2010 - Human-Animal Medicine

Human-Animal
Medicine
Clinical Approaches to Zoonoses, Toxicants,
and Other Shared Health Risks
Peter M. Rabinowitz, MD, MPH
Associate Professor of Medicine
Director of Clinical Services
Yale Occupational and Environmental Medicine Program
Yale University School of Medicine
New Haven, Connecticut
Lisa A. Conti, DVM, MPH, DACVPM, CEHP

Director
Division of Environmental Health
Florida Department of Health
Tallahassee, Florida
with more than 400 illustrations

3251 Riverport Lane
Maryland Heights, Missouri 63043
HUMAN-ANIMAL MEDICINE: CLINICAL APPROACHES TO ZOONOSES, ISBN 978-1-4160-6837-2

TOXICANTS, AND OTHER SHARED HEALTH RISKS
Copyright © 2010 by Saunders, an imprint of Elsevier Inc.
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Knowledge and best practice in this field are constantly changing. As new research and experience broaden
our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate.
Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the
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and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on
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The Publisher
Library of Congress Cataloging-in-Publication Data

Rabinowitz, Peter MacGarr.
Human-animal medicine: clinical approaches to zoonoses, toxicants, and other shared health risks /
Peter M. Rabinowitz, Lisa A. Conti.
p. ; cm.
Includes bibliographical references.
ISBN 978-1-4160-6837-2 (hardcover : alk. paper)
1. Zoonoses. 2. Environmental health. I. Conti, Lisa A. II. Title.
[DNLM: 1. Communicable Diseases–epidemiology. 2. Bonding, Human-Pet. 3. Communicable Diseases–
veterinary. 4. Environmental Monitoring–methods. 5. Sentinel Surveillance–veterinary. 6. Zoonoses–
epidemiology. WC 100 R116h 2010]
RA639.R33 2010
614.5′6–dc22
2009040249
Cover image (woman with cat) © Inti St. Clair/Corbis.

Internal images © Graham Bell/Corbis; Shutterstock; and AFI/Getty Images.
Vice President and Publisher: Linda Duncan

Senior Acquisitions Editor: Anthony Winkel
Developmental Editor: Maureen Slaten
Publishing Services Manager: Patricia Tannian
Project Manager: Carrie Stetz
Designer: Jessica Williams
Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1
This book is dedicated to Ronald M. Davis, MD (1956-2008), immediate past
president of the American Medical Association and Director of the Center for
Health Promotion and Disease Prevention at the Henry Ford Health System
in Detroit. Dr. Davis was a One Health champion, a public health advocate,
and an inspiration to all his friends and colleagues. His work established a
standard of excellence and collaboration for generations to come.
Contributors
Matthew S. Alkaitis Russell W. Currier, DVM, MPH, DACVPM

Dartmouth College Executive Vice President
Hanover, New Hampshire American College of Veterinary Preventive
Zoonoses: Orf Medicine
Des Moines, Iowa
Lorraine C. Backer, PhD, MPH Zoonoses: Scabies
Team Leader
National Center for Environmental Health Tracy DuVernoy, DVM
Centers for Disease Control and Prevention Veterinary Medicine Officer, Food and Drug Administration
Atlanta, Georgia Center for Food Safety and Applied Nutrition
Toxic Exposures: Harmful Algae Blooms College Park, Maryland
Zoonoses: Rift Valley Fever
Carina Blackmore, MS VetMed, PhD, DACVPM
State Public Health Veterinarian Lora E. Fleming, MD, PhD
State Environmental Epidemiologist Professor
Chief, Bureau of Environmental Public Health Medicine Departments of Epidemiology & Public Health and Marine
Division of Environmental Health Biology & Fisheries
Florida Department of Health Miller School of Medicine and Rosenstiel School of Marine
Tallahassee, Florida and Atmospheric Sciences
Zoonoses: Influenza, West Nile Virus and Other Arbovirus Infections Miami, Florida
Toxic Exposures: Harmful Algae Blooms
Roger I. Ceilley, MD
Dermatology and Syphology Elena Hollender, MD
The University of Iowa Director of Clinical Services
Iowa City, Iowa A.G. Holley State Tuberculosis Hospital
Zoonoses: Scabies Lantana, Florida;
Voluntary Assistant Professor of Medicine
Lisa A. Conti, DVM, MPH, DACVPM, CEHP Division of Pulmonary and Critical Care Medicine
Director Miller School of Medicine
Division of Environmental Health University of Miami
Florida Department of Health Miami, Florida;
Tallahassee, Florida Courtesy Assistant Professor of Medicine
Legal and Ethical Issues in Human-Animal Medicine Southeastern National Tuberculosis Center at the University
Establishing a New Approach to Clinical Health History of Florida
Sentinel Disease Signs and Symptoms Department of Medicine
The Built Environment and Indoor Air Quality School of Medicine
Toxic Exposures: Healthy Homes, Carbon Monoxide, Lead, Gainesville, Florida;
Pesticides, Envenomations Courtesy Assistant Professor
Zoonoses: Overview, Anthrax, Bartonella Infections, Department of Epidemiology and Biostatistics
Brucellosis, Campylobacteriosis, Chlamydophila Psittaci College of Public Health and Health Professions
and Related Infections, Cryptosporidiosis, Dermatophytosis, University of Florida
Dipylidiasis, Echinococcosis, Ehrlichioses and Anaplasmosis, Gainesville, Florida
Escherichia Coli Infection, Giardiasis, Hantavirus Infections, Zoonoses: Tuberculosis and Other Mycobacterial
Hookworm Infection, Leishmaniasis, Leptospirosis, Infections
Lyme Disease, Methicillin-Resistant Staphylococcus
Aureus Infection, Orf, Plague, Q fever, Rabies, Rocky Rebecca A. Johnson, PhD, RN, FAAN
Mountain Spotted Fever and Other Rickettsial Infections, Millsap Professor of Gerontological Nursing
Salmonellosis, Toxocara Infestation, Toxoplasmosis, Director, Research Center for Human-Animal
Transmissible Spongiform Encephalopathies, Tularemia Interaction
Infectious Disease Scenarios College of Veterinary Medicine
Foodborne Illness University of Missouri
Occupational Health of Animal Workers Columbia, Missouri
Public Health and Human-Animal Medicine Psychosocial and Therapeutic Aspects of Human-Animal
Shared Strategies to Maximize Human and Animal Health Interaction
vi
Contributors vii
Laura H. Kahn, MD, MPH, MPP, FACP Establishing a New Approach to Clinical Health History
Research Staff Sentinel Disease Signs and Symptoms
Program on Science and Global Security The Built Environment and Indoor Air Quality
Woodrow Wilson School of Public and International Affairs Allergic Conditions
Princeton University Toxic Exposures: Healthy Homes, Carbon Monoxide, Lead,
Princeton, New Jersey Pesticides, Envenomations
The Convergence of Human and Animal Medicine Zoonoses: Overview, Anthrax, Bartonella Infections,
Brucellosis, Campylobacteriosis, Chlamydophila
Bruce Kaplan, DVM, Daves (Hon) Psittaci and Related Infections, Cryptosporidiosis,
Sarasota, Florida Dermatophytosis, Dipylidiasis, Echinococcosis, Ehrlichioses
The Convergence of Human and Animal Medicine and Anaplasmosis, Escherichia Coli Infection, Giardiasis,
Hantavirus Infections, Hookworm Infection, Influenza,
Hugh M. Mainzer, MS DVM, DACVPM Leishmaniasis, Leptospirosis, Lyme Disease, Methicillin-
Captain, U.S. Public Health Service Resistant Staphylococcus Aureus Infection, Orf, Plague,
Chief Veterinary Officer, U.S. Public Health Service Q fever, Rabies, Rocky Mountain Spotted Fever and Other
Division of Emergency and Environmental Health Services Rickettsial Infections, Salmonellosis, Toxocara Infestation,
Centers for Disease Control and Prevention Toxoplasmosis, Transmissible Spongiform Encephalopathies,
Atlanta, Georgia Tuberculosis and Other Mycobacterial Infections,
Public Health and Human-Animal Medicine Tularemia
Infectious Disease Scenarios
Clifford S. Mitchell, MS, MD, MPH Foodborne Illness
Director, Environmental Health Coordination & Preventive Occupational Health of Animal Workers
Medicine Residency Programs Public Health and Human-Animal Medicine
Maryland Department of Health and Mental Hygiene Shared Strategies to Maximize Human and Animal Health
Baltimore, Maryland
The Built Environment and Indoor Air Quality Carol Norris Reinero, DVM, PhD, DACVIM
Allergic Conditions Assistant Professor, Small Animal Internal Medicine
Department of Veterinary Medicine and Surgery
Ben Hur P. Mobo, Jr., MD College of Veterinary Medicine
Assistant Professor of Medicine University of Missouri
WHVAMC Columbia, Missouri
West Haven, Connecticut The Built Environment and Indoor Air Quality
Occupational Health of Animal Workers Allergic Conditions
Thomas P. Monath, MD Judy Sparer, CIH, MSCE

Partner Industrial Hygienist
Kleiner Perkins Caufield & Byers Yale Occupational and Environmental Medicine Program
Pandemic & Biodefense Fund Yale University School of Medicine
Harvard, Massachusetts New Haven, Connecticut
The Convergence of Human and Animal Medicine The Built Environment and Indoor Air Quality
Lynda U. Odofin, DVM, MSPH Oyebode A. Taiwo, MD, MPH

Yale School of Public Health Assistant Professor of Medicine
Yale University Director, Occupational and Environmental Medicine
New Haven, Connecticut Fellowship Training
Zoonoses: Lymphocytic Choriomeningitis Yale Occupational and Environmental Medicine Program
Natasha Rabinowitz New Haven, Connecticut
Mount Holyoke College Occupational Health of Animal Workers
South Hadley, Massachusetts
Zoonoses: Orf Julia Zaias, DVM, PhD
Research Assistant Professor, Comparative Pathology
Peter M. Rabinowitz, MD, MPH Department of Pathology
Associate Professor of Medicine Miller School of Medicine
Director of Clinical Services University of Miami
Yale Occupational and Environmental Medicine Miami, Florida
Yale University School of Medicine Toxic Exposures: Harmful Algae Blooms
New Haven, Connecticut
Legal and Ethical Issues in Human-Animal Medicine
Reviewers
Alina Alonso, MD Emily Beeler, DVM

Medical Director Los Angeles County Department of Public Health
Palm Beach County Health Department Veterinary Public Health and Rabies Control Program
West Palm Beach, Florida Downey, California;
College of Veterinary Medicine
Larry Anderson, DVM, MD Western University of Health Sciences
Family Practitioner Pomona, California
Family Care Center
Wellington, Kansas Jeff B. Bender, DVM, MS, DACVPM
Veterinary Public Health
Fred Angulo, PhD, DVM Center for Animal Health and Food Safety
Acting Associate Director for Science, NCEH/ATSDR College of Veterinary Medicine
Centers for Disease Control and Prevention University of Minnesota
Atlanta, Georgia St. Paul, Minnesota
Philip W. Askenase, MD Tegan K. Boehmer, PhD, MPH

Section of Allergy and Clinical Immunology LCDR U.S. Public Health Service
Department of Medicine Epidemiologist
Yale University School of Medicine Air Pollution and Respiratory Health Branch
New Haven, Connecticut National Center for Environmental Health
Centers for Disease Control and Prevention
Paul Auerbach, MD Atlanta, Georgia
Professor of Surgery—Emergency Medicine
Stanford University School of Medicine Jonathan Borak, MD, DABT, FACP, FACOEM
Stanford, California Clinical Professor of Epidemiology & Public Health
Clinical Professor of Medicine
Connie C. Austin, DVM, MPH, PhD Yale University School of Medicine
State Public Health Veterinarian New Haven, Connecticut
Division of Infectious Disease
Illinois Department of Public Health Edward B. Breitschwerdt, DVM
Springfield, Illinois Professor of Medicine and Infectious Diseases
Nili Avni-Magen, DVM North Carolina State University
Head Veterinarian Raleigh, North Carolina
Tisch Family Zoological Gardens
Jerusalem, Israel Anne Brewer, MD
Associate Director
Sarah L. Babcock, DVM, JD Family Medicine Residency Program
Animal & Veterinary Legal Services The Stamford Hospital
Harrison Township, Michigan Stamford, Connecticut
Michele Barry, MD, FACP Victoria E. Bridges, DVM, MS

Senior Associate Dean of Global Health Veterinary Epidemiologist
Health Consultant Overseas Program, Ford U.S. Department of Agriculture
Foundation; Fort Collins, Colorado
Director of Global Health Programs in Medicine
Director, Yale/Stanford Johnson & Johnson Global Health Sondra Brown, DVM, MS
Scholars Program, Stanford University Site Northwood Animal Hospital and
Professor, Department of Medicine The Animal Hospital & Pet Resort at Southwood
Stanford University School of Medicine Tallahassee, Florida
Stanford, California
viii
Reviewers ix
Stanley D. Bruntz, DVM, MPH Paul Ettestad, DVM, MS

MAHRS Coordinator State Public Health Veterinarian
National Surveillance Unit Epidemiology and Response Division
Centers for Epidemiology and Animal Health New Mexico Department of Health
U.S. Department of Agriculture, Animal and Plant Health Santa Fe, New Mexico
Inspection Service Veterinary Service
Fort Collins, Colorado Durland Fish, PhD
Professor of Epidemiology and Public Health
Arlene Buchholz, DVM, MPH, DACVPM
Professor of Forestry and Environmental Studies
Veterinary Medical Officer
School of Public Health;
Hawaii State Department of Health
Director
Honolulu, Hawaii
Yale Institute for Biospheric Studies Center for
Danielle Buttke, DVM, PhD Candidate EcoEpidemiology
The Baker Institute for Animal Health Yale University
College of Veterinary Medicine New Haven, Connecticut
Cornell University
Ithaca, New York Renée Funk, DVM, MPH & TM, DACVPM
Bryan Cherry, VMD, PhD LCDR, United States Public Health Service
State Public Health Veterinarian Emergency Preparedness and Response Office NIOSH
New York State Department of Health Centers for Disease Control and Prevention
Albany, New York Atlanta, Georgia
James E. Childs, ScD
Senior Research Scientist/Scholar Paul Garbe, DVM, MPH
Department of Epidemiology and Public Health Chief, Air Pollution and Respiratory Health Branch
Yale University School of Medicine Division of Environmental Hazards and Health Effects
New Haven, Connecticut National Center for Environmental Health
Kerry L. Clark, MPH, PhD Atlanta, Georgia
Associate Professor and MPH Program Director
Epidemiology & Environmental Health
Department of Public Health Gary Ginsberg, PhD
Brooks College of Health Division of Environmental and Occupational Health
University of North Florida Connecticut Department of Public Health
Jacksonville, Florida Hartford, Connecticut
Mark R. Cullen, MD
Chief, Division of General Internal Medicine Carol Glaser, DVM, MPVM, MD
Stanford University School of Medicine Viral and Rickettsial Disease Laboratory
Stanford, California California Department of Health Services
Richmond, California
Radford Davis, DVM, MPH, DACVPM
Associate Professor of Public Health
Larry Glickman, VMD, DrPH
Department of Veterinary Microbiology and Preventive
Professor of Epidemiology
Medicine
Department of Emergency Medicine
University of North Carolina;
Iowa State University
Senior Epidemiologist
Ames, Iowa
OneEpi Consulting
F. Joshua Dein, VMD, MS Pittsboro, North Carolina
Veterinary Medical Officer
USGS National Wildlife Health Center Jerome Goddard, PhD
Madison, Wisconsin State Medical Entomologist
Mississippi State Department of Health
Millicent Eidson, MA, DVM, DACVPM (Epidemiology)
Jackson, Mississippi
State Public Health Veterinarian and Director, Zoonoses
Program
New York State Department of Health; Robert P. Gordon, DVM
Associate Professor Owner and Director
Department of Epidemiology and Biostatistics Oakland Animal Hospital
School of Public Health Oakland, New Jersey
State University of New York
Albany, New York
x Reviewers
Zimra J. Gordon, DVM, MPH Anne E. Justice-Allen, DVM

Private Practice Wildlife Health Specialist
Stamford, Connecticut Arizona Game and Fish Department
Phoenix, Arizona
Marilyn Goss Haskell, DVM, MPH
NCDHHS Public Health Veterinarian Bruce Kaplan, DVM, DAVES (Hon)
Epidemiology, CD Medical Unit Sarasota, Florida
Raleigh, North Carolina
Jeffrey D. Kravetz, MD
Ellis C. Greiner, PhD Veterans Affairs Healthcare System
Professor, Parasitology West Haven, Connecticut;
Department of Infectious Diseases and Pathology Yale University School of Medicine
College of Veterinary Medicine New Haven, Connecticut
University of Florida
Gainesville, Florida Charlotte A. Lacroix, DVM, JD
Owner and CEO
Sharon Gwaltney-Brant, DVM, PhD, DABVT, DABT Veterinary Business Advisors, Inc.
Vice President & Medical Director Whitehouse Station, New Jersey
ASPCA Animal Poison Control Center
Urbana, Illinois Mira J. Leslie, DVM, MPH
Public Health Veterinarian
Steven A. Hale, MD Ministry of Agriculture and Lands
Senior Physician Abbotsford, British Columbia
Orange County Health Department Canada
Orlando, Florida
Joann M. Lindenmayer, DVM, MPH
Michael L. Haney, PhD, NCC, LMHC Associate Professor of Public Health
Division Director for Prevention and Intervention Department of Environmental
Children’s Medical Services and Population Health
Florida Department of Health Cummings School of Veterinary Medicine
Tallahassee, Florida Tufts University
North Grafton, Massachusetts
Frederick G. Hayden, MD, FACP
Professor of Medicine, Infectious Disease and International Jean Malecki, MD, MPH, FACPM
Health Director
University of Virginia School of Medicine Palm Beach County Health Department
Charlottesville, Virginia West Palm Beach, Florida
Robert Hood, PhD, CIP Leonard C. Marcus, VMD, MD

Ethics and Human Research Protections Program Assistant Travelers’ Health and Immunization Services
Director Newton, Massachusetts
Office of Public Health Research
Florida Department of Health Rosanna Marsella, DVM, DACVD
Tallahassee, Florida Professor
Department of Small Animal Clinical Sciences
Martin E. Hugh-Jones, Vet MB, MA, MPH, PhD College of Veterinary Medicine
Coordinator of the World Health Organization Working University of Florida
Group on Anthrax Research and Control Gainesville, Florida
Geneva, Switzerland;
Professor Emeritus Catherine McManus, VMD, MPH, DACVPM
Department of Environmental Sciences Veterinary Epidemiologist
School of the Coast and Environment Division of Environmental Epidemiology
Louisiana State University Virginia Department of Health
Baton Rouge, Louisiana Richmond, Virginia
Suzanne R. Jenkins, VMD, MPH, ACVPM CDR David McMillan, MD, MPH, ACOEM
State Public Health Veterinarian (Retired) Head, Navy Occupational Medicine Programs and Policy
Virginia Department of Health Navy Surgeon General’s Office
Richmond, Virginia Washington, DC
Reviewers xi
Jennifer McQuiston, DVM, MS, DACVPM Mark A. Pokras, DVM

Epidemiology Team Lead, Rickettsial Zoonoses Branch Associate Professor
National Center for Zoonotic, Vector-Borne, and Enteric Department of Environmental and Population Health
Diseases Wildlife Medicine
Centers for Disease Control and Prevention Wildlife Clinic & Center for Conservation Medicine
Atlanta, Georgia Cummings School of Veterinary Medicine
Tufts University
Laura Mulford, RN, MPH North Grafton, Massachusetts
Nursing Consultant
Office of Public Health Nursing Burt Pritchett, DVM, MS
Florida Department of Health Division of Animal Feeds
Tallahasee, Florida Center for Veterinary Medicine
Food and Drug Administration
Elizabeth Mumford, DVM, MS Rockville, Maryland
Scientist
Global Influenza Programme Carrie A. Redlich, MD, MPH
World Health Organization Professor of Medicine
Geneva, Switzerland Yale Occupational and Environmental Medicine Program
and Section of Pulmonary & Critical Care Medicine
Julia M. Murphy, DVM, MS, DACVPM Yale University School of Medicine
State Public Health Veterinarian New Haven, Connecticut
Virginia Department of Health
Richmond, Virginia
Ralph C. Richardson, DVM, DACVIM (Oncology, Internal
Paul Nicoletti, DVM, MS Medicine)
Emeritus Professorship Dean
College of Veterinary Medicine College of Veterinary Medicine
University of Florida Kansas State University
Gainesville, Florida Manhattan, Kansas
Richard A. “Ran” Nisbett, PhD, MSPH Charles E. Rupprecht, VMD, MS, PhD
Global Health Practices Track Chief, Rabies Program
Department of Global Health Centers for Disease Control and Prevention
College of Public Health Atlanta, Georgia
University of South Florida
Tampa, Florida Emi Kate Saito, VMD, MSPH, DACVPM
Veterinary Epidemiologist
Kenneth E. Nusbaum, DVM, PhD National Surveillance Unit
Professor USDA/APHIS/VS Centers for Epidemiology and Animal
Department of Pathobiology Health
College of Veterinary Medicine Fort Collins, Colorado
Auburn University
Auburn, Alabama Peter Schantz, VMD, PhD
Senior Service Fellow
W. John Pape, BSc Division of Parasitic Diseases
Epidemiologist Centers for Disease Control and Prevention
Colorado Department of Public Health and Environment Atlanta, Georgia
Denver, Colorado
Matthew L. Scotch, PhD, MPH
Daniel Parker, MSP Associate Research Scientist
Sustainability Director Center for Medical Informatics
Division of Environmental Public Health Yale University School of Medicine
Florida Department of Health New Haven, Connecticut
Tallahassee, Florida
Kanta Sircar, PhD
Gary J. Patronek, VMD, PhD
Epidemiologist
Vice President for Animal Welfare and New Program
Los Angeles County Department of Public Health
Development
Los Angeles, California
Animal Rescue League of Boston
Boston, Massachusetts
xii Reviewers
Kathleen A. Smith, DVM, MPH †

Jeff W. Tyler, DVM, MPVM, PhD, DACVIM
State Public Health Veterinarian Professor
Ohio Department of Health Director of Strategic Program Initiatives
Reynoldsburg, Ohio Director of Clinical Research
Department of Veterinary Medicine and Surgery
Andre N. Sofair, MD, MPH College of Veterinary Medicine
Associate Professor of Medicine, Epidemiology, and Public University of Missouri
Health Columbia, Missouri
New Haven, Connecticut Mark Jerome Walters, DVM
Associate Professor
Daniel L. Sudakin, MD, MPH, FACMT, FACOEM Department of Journalism & Media Studies
Associate Professor University of South Florida
Department of Environmental and Molecular St. Petersburg, Florida
Toxicology
College of Veterinary Medicine Kalman L. Watsky, MD
Oregon State University Clinical Professor of Dermatology
Corvallis, Oregon Yale University School of Medicine;
Section Chief of Dermatology
Hospital of Saint Raphael
David E. Swayne, DVM, PhD, DACPV
Laboratory Director New Haven, Connecticut
Southeast Poultry Research Laboratory
J. Scott Weese, DVM, DVSc, DACVIM
USDA/Agricultural Research Service
Department of Pathobiology
Athens, Georgia
Ontario Veterinary College
University of Guelph
Wendy T. Thanassi, MA, MD Guelph, Ontario
Chief, Occupational Health Services Canada
Palo Alto VA Health Care System;
Clinical Assistant Professor of Surgery (Emergency Sara C. Wilson, RN/CNS, MSN, APHN-BC
Medicine) Registered Nursing Consultant
Stanford Hospitals and Clinics and Lucile Packard Office of Public Health Nursing
Children’s Hospital Tallahassee, Florida
Stanford University School of Medicine
Stanford, California James C. Wright, DVM, PhD, DACVPM
Associate Professor
Greg Troll, MD Veterinary Public Health
Associate Dean Department of Pathobiology
Faculty & Curriculum Development College of Veterinary Medicine
Touro University College of Osteopathic Medicine Auburn University
Sebastopol, California Auburn, Alabama
†
Deceased.
Preface
We believe that human and animal health clinicians have an

Introduction and How to Use This Book important role to play in identifying specific factors affecting
the health of their patients. Public health professionals can
This book is designed to help clinicians and public health look at factors affecting both animals and human beings in
professionals manage a wide range of clinical problems at their communities and take steps to ameliorate conditions.
the intersection of human and animal health. It presents a Informed communities can work on a policy and practical
“One Health” approach to such problems, in recognition that level to implement a variety of solutions.
the health of human beings, animals, and their environments In the future, we envision the need for an expanded cadre
is interrelated. of veterinarian “specialists” in human-animal medicine con-
cepts who can function as part of integrated clinical care and
prevention teams for human health. We also see the possibil-
Background and Conceptual Approach ity for human health clinicians who receive special veterinary
medical training to better deliver services such as occupa-
The relevance of nonhuman animals to human health takes tional health care to persons with animal contact and evalu-
at least three basic forms. First, a number of health risks ation of environmental hazards affecting both human beings
are related to animal contact, including zoonotic infectious and other animals. The escalating role of veterinarians in
diseases transmitted from animals to human beings; ani- public health over the last several years is just the first step
mal allergens that cause allergic disease in human beings; in a necessary and ongoing process that is detailed in several
and animal bites, stings, and other direct trauma. Second, sections of this book.
important psychosocial effects of the human-animal bond We hope this book can provide additional impetus to this
may have physical benefits as well. Third, animals may serve evolution.
as “sentinels” for toxic or infectious health hazards in the
environment that are also a risk for human beings.
Despite the fact that the majority of American households
include at least one animal, communication between the vet- Who Will Benefit From This Book
erinarian caring for the family pets and the human health
care providers treating the human household members is • For human health clinicians, including primary care pro-
currently limited. Similarly, there may be limited contact viders, home health care providers, and specialists in
between public health professionals and their animal health infectious disease, allergy, dermatology, and psychiatry,
counterparts. The growing recognition of the links among this book provides a core body of knowledge regarding
human health, animal health, and the environment requires the role of animals in human infectious and allergic dis-
new tools for cooperation and communication between ease, the psychosocial aspects of human-animal contact,
professionals working in these sectors. Such intersectoral and the potential for animals to serve as sentinels for toxic
cooperation demands further development of a common and other environmental health risks to human beings.
body of knowledge (what we call human-animal medicine) Armed with such knowledge, human health clinicians can
and a common scientific and clinical vocabulary for under- more effectively screen for human-animal health prob-
standing diseases affecting both human beings and animals lems and make appropriate referrals to both veterinarians
that often are related to environmental factors. This book and public health departments.
is an attempt to outline this body of knowledge and sug- • For physicians and other clinicians providing occupational
gests practical steps for implementing the concept of “One health services to persons with animal contact, includ-
Health” in the daily practice of human and animal medicine ing farmers, veterinarians, zookeepers, pet store employ-
and public health. ees, and laboratory animal workers, this book details the
Emerging infectious diseases such as SARS, West Nile Virus special risks of injury, allergy, infection, and psychoso-
infection, and avian/swine influenza have focused attention cial stress that these workers may experience. It provides
on infectious diseases that cross between animals and human guidelines for designing and implementing appropriate
beings; we believe that many of these diseases are manifes- preventive services for these occupational risk groups.
tations of important environmental changes related to land • For veterinarians in community-based practice, this book
use, climate change, intensification of food production, and outlines the human health implications of zoonotic dis-
other factors. Therefore preventing such diseases must involve eases, animal allergy, and human-animal interaction.
creating and maintaining healthy environments. Other envi- It provides guidelines for communication with clients
ronmental health risks that may be shared by human beings and human health care providers about reducing animal-
and animals include toxicants, allergens, and psychosocial related disease risk, and how to recognize when animals
issues. Working to improve such environments is a complex may be serving as potential sentinels of environmental
process that involves both professionals and communities. health risks. It also details some of the legal and ethical
xiii
xiv Preface
ramifications of veterinarians playing a greater role in Chapter 12 outlines the occupational hazards facing workers
human health care. who handle animals on a regular basis and provides guide-
• For public health professionals in environmental health, lines for preventive health care services for such individuals.
the book explains how specific hazards in the home and Chapter 13 discusses the special role that public health agen-
environment can affect the health of human beings and cies play in the prevention and management of disease risk
animals in the community, and how animals can serve as facing human and animal populations. Chapter 14 concludes
sentinels for human health risks, and vice versa. the book with practical suggestions for integrated primary,
• For public health officials engaged in disease surveillance, secondary, and tertiary disease prevention activities among
the book provides examples of how outbreaks in ani- the human health, animal health, and public health sectors as
mal populations can provide information about human well as templates for communication between professionals
disease risk and how to investigate the human health working in these sectors.
implications of such outbreaks, in cooperation with We have endeavored to make this book as evidence based
agricultural and other animal health agencies. as possible by referencing, when available, original studies in
the biomedical literature in support of specific recommen-
dations. At the same time, we acknowledge that for many
Organization human-animal health issues there are important gaps in
knowledge, and much of the available evidence is anecdotal
To address these needs, this book attempts to outline clini- in nature. A notable exception is the recommendations of
cally important areas where human and animal health are the U.S. Public Health Service in “Guidelines for Preventing
linked and some key similarities and differences in the ways Opportunistic Infections Among HIV-Infected Persons” (see
that human and animal health is affected by environmen- Chapter 10).1 It is our hope that such evidence-based rec-
tal factors. For each area, we have enumerated specific roles ommendations can serve as a model for future guidelines on
for human health, veterinary health, and public health pro- other human-animal medicine issues.
fessionals in the detection, management, and prevention of
disease.
Chapter 1 outlines the factors driving the convergence Distinctive Features
of human, animal, and environmental health as well as the
“One Health” concept that has been proposed to encourage For each clinical problem covered, the book presents:
greater cross-specialty interaction on vital issues of emerg-
ing diseases and environmental change. Chapter 2 provides • Comparative charts of the presentation and treatment of
some cautionary guidance regarding potential legal and ethi- the disease in human beings and nonhuman animals.
cal pitfalls that must be faced and avoided during this process • Specific steps for human health, animal health, and pub-
of increasing intersectoral collaboration. Chapter 3 provides lic health professionals to take to prevent and manage the
a guide to the history that both human and animal health particular condition.
clinicians can incorporate into their daily care of patients • The role of environmental factors in the causation of the
to identify important human-animal health links. Chapter clinical problem.
4 provides charts of important sentinel signs in human Other features include:
beings and animals that could indicate human-animal health
risks. Chapter 5 outlines the different facets of the psycho- • Treatment of emerging disease issues, including emerg-
social bonds between human beings and animals and how ing zoonoses, harmful algae blooms, and animal-related
human-animal interaction can be a therapeutic tool as well pesticides.
as an important factor to consider in a wide range of clinical • Legal and ethical aspects of greater interaction between
situations. Chapter 6 highlights the need to consider health human and animal health professionals.
effects from indoor and other built environments. Chapter • Sample protocols for professional communication between
7 deals with allergens related to human-animal contact and veterinarians, human health clinicians, and public health
clinical manifestations of allergic disease in human beings professionals.
and animals. Chapter 8 provides an overview of important
clinical syndromes in human beings and animals related to
acute and chronic exposure to toxic hazards in the environ- Reference
ment, the ability of animals to serve as sentinels for human
environmental health hazards from toxicants, and preven- 1. Mofenson LM, Brady MT, Danner SP et al: Guidelines for the preven-
tion and treatment of opportunistic infections among HIV-exposed and
tive steps for toxicant avoidance. Chapter 9 reviews selected HIV-infected children: recommendations from the CDC, the National
zoonotic diseases of importance, and Chapter 10 presents Institutes of Health, the HIV Medicine Association of the Infectious
particular infectious disease risk scenarios, including travel Diseases Society of America, the Pediatric Infectious Diseases Society,
and immunocompromised individuals. Chapter 11 provides and the American Academy of Pediatrics, MMWR Recomm Rep 58
(RR-11):1-66, 2009.
an overview of common issues regarding foodborne illness.
Acknowledgments
Because this is a book about partnerships, it could not have those who generously helped provide coverage during Peter’s
been created without the help of many individuals and sabbatical included Patrick O’Connor, Mark Cullen, Carrie
organizations to whom we would like to express our deep Redlich, Oyebode Taiwo, Mark Russi, Martin Slade, Sharon
appreciation. Kirsche, Deron Galusha, Lynda Odofin, Frank Nusdeu, and
The concept for the book grew out of discussions over Judy Sparer.
a number of years with some wonderfully original think- Any acknowledgments are inadequate to the large team of
ers, including Zimra Gordon, Joshua Dein, Thomas Chase, coauthors and chapter reviewers whose names appear else-
Augustus Ben David II, Jakob Zinsstag, Juan Lubroth, where in the book. A special thanks is due to the members of
Elizabeth Mumford, Alonzo Aguirre, Peter Daszak, William the National Association of Public Health Veterinarians who
Karesh, Lonnie King, Don Levy, Mark Pokras, Stephan consistently responded to requests for assistance in review-
Delaroque, Katinka deBalough, Michael Perdue, and Craig ing chapters. These individuals took time away from other
Stephens. duties to provide text and unsparing but always constructive
Bruce Kaplan drew on his many professional contacts critiques for the section drafts. We are incredibly fortunate to
to introduce the authors to each other and to encourage have been able to tap some of their vast funds of knowledge.
the development of the book throughout its many stages. Responsibility for any errors in the final version rests, how-
His partners in the One Health initiative, Laura Kahn and ever, with us, not them.
Thomas Monath, have tirelessly worked to explore many of Although it may be a cliché to mention long-suffering
the themes that appear in the book. family members, there are no words to describe the sup-
Katherine Quesenberry helped introduce the idea of the port, understanding, and insight provided by Peter’s wife
book to Elsevier, where editor Anthony Winkel took it under Nelly, who lived and breathed every step of the book’s cre-
his wing. Catherine Bowers helped with organization of ation; children Aaron and Natasha, who waited patiently for
early drafts. Maureen Slaten, our developmental editor, used the end of writing sessions; stepsons Sasha and Eliosha, who
unimaginable patience and perseverance to help us mold the provided long-distance encouragement; and parents Alan
many different sections into a consistent format and a rec- and Andrea, who always had useful advice. Lisa’s husband
ognizable whole, aided by Brandi Graham, Brian Dennison, Tommy offered empathy, strength, and encouragement dur-
and many others. Publisher Penny Rudolph assumed respon- ing the process; son Dane allowed his mom nights and week-
sibility for the project in its later stages and helped finalize ends to attend to the project; and Aunt Mary brightened any
the many remaining decisions. day with her sanguine disposition.
The work on the book drew us away from other profes- We hope that this book does justice to the efforts and
sional responsibilities, and we are indebted to the supportive inspiration provided by these wonderful friends, family, and
colleagues who helped make this possible. At Yale, some of colleagues.
xv
Foreword: Clinical Perspective
Ronald Davis, MD, MPH, and Roger Mahr, DVM
Serving as presidents of our respective national associations, nineteenth century, and Assistant Surgeon General James Steele
the American Medical Association (AMA) and the American and Dr. Calvin Schwabe in the twentieth century, have signifi-
Veterinary Medical Association (AVMA), and representing cantly influenced the development of comparative medicine
our professions around the world, was, for us, the honor of and biomedical research and advanced the prevention and
a lifetime. control of zoonotic diseases internationally.
As each of us prepared to assume our presidencies, we As we face the challenges of the twenty-first century, it is
focused on our respective Association missions and contem- imperative that One Health become a central focus within each
plated the following question: What are the values and respon- health science profession. While the AVMA and AMA will con-
sibilities of our professions to global society? tinue to be key advocates for this effort, the success of the One
We believe that animal and human health are at a cross- Health Initiative will depend on the collaboration of various
roads. The convergence of animal, human, and environmen- health science professional associations, academic institutions,
tal health dictates that the “One Health” concept be embraced governmental agencies, nongovernmental organizations, and
and that the health science professions assume major leader- industries.
ship roles to translate that concept from a vision to reality. It is most fitting and timely that Human-Animal Medicine:
It was on that basis of value to global society, and that Clinical Approaches to Zoonoses, Toxicants, and Other Shared
sense of responsibility to the future, that we articulated our Health Risks be written collaboratively by a physician, Dr. Peter
collective vision for a One Health Initiative. We have traveled Rabinowitz, and a veterinarian, Dr. Lisa Conti. This book
the world, meeting and talking with veterinarians, physicians, promises to be a valuable contribution to the One Health
public health professionals, academicians, students, govern- Initiative and will serve to demonstrate the significant benefit
ment officials, legislators, and other stakeholders about the of interdisciplinary collaboration. In addition, it will further
interrelationships among health science professions. underscore the importance of coordination, communication,
Through our respective leadership roles, we were able to and cooperation among multiple disciplines, professions, and
achieve a collaborative relationship between the AVMA and organizations.
AMA. In April 2007, the AVMA Executive Board took offi- This clinical guide is well designed and written for human
cial action to establish the AVMA One Health Initiative Task health, animal health, public health, environmental health,
Force. The charge to the Task Force was to study the feasi- and wildlife professionals. Through our individual careers as
bility of a One Health Initiative that would facilitate collab- a clinical veterinary practitioner and a public health and pre-
oration and cooperation among health science professions, ventive medicine physician, we appreciate the value this book
academic institutions, governmental agencies, and industries will offer to students, practitioners, educators, researchers,
and that would help with the assessment, treatment, and and other professional disciplines. It can also be used as a
prevention of cross-species disease transmission and mutu- resource to help the general public develop an awareness and
ally prevalent, but nontransmitted, human and animal dis- understanding of One Health.
eases and medical conditions. In June 2007, the AMA House It is our fervent hope that professionals engaged in the
of Delegates approved a resolution calling for the AMA to health sciences will work to bring our disciplines into closer
support the One Health Initiative and to engage in a dialogue harmony, which will surely demonstrate that an integrated
with the AVMA to discuss means of enhancing collaboration One Health enterprise is stronger and more valuable than
between the two professions in medical education, clinical care, the sum of its parts. Drs. Rabinowitz and Conti have pro-
public health, and biomedical research. vided evidence of that synergy through their collaboration
We were privileged to serve as liaisons to the One Health in the publication of this extraordinary book.
Initiative Task Force and are proud of the dedicated efforts of
its visionary members. We are enthusiastic about the poten- †
Ronald Davis, MD, MPH
tial impact of this initiative throughout the world. One Health Past President
has been defined as the collaborative efforts of multiple dis-
American Medical Association
ciplines—working locally, nationally, and globally—to attain
optimal health for people, animals, and our environment.
Certainly the One Health concept is not new. The pioneering Roger Mahr, DVM
efforts of many health science professionals in the past, including Past President
Sir William Osler, Rudolph Virchow, and Louis Pasteur in the American Veterinary Medical Association
Deceased.
†
xvi
Foreword: Public Health
Perspective
James H. Steele, DVM, MPH, and Lonnie King, DVM, MS, MPA
While the foundation for the One Health concept as a tools and insights into the convergence of human, animal, and
convergence of human and animal health has been well environmental health and have reinforced a growing scientific
articulated by key champions in the past, we are now foundation that further undergirds the principles of One Health.
entering a new era of awareness among public health The scope, scale, and global implications of emerging infec-
professionals, clinicians, and the public about the inextri- tious diseases and other contemporary public health chal-
cable links of human, animal, and environmental health. lenges demand that scientists, researchers, health care
This era is making the One Health concept more expansive, workers, and practitioners move beyond the confines of
accepted, global, and evidence based rather than charac- their own disciplines and explore new models of team sci-
terized by single events. Understanding the One Health ence as well as establish new working relationships among
paradigm and our ability to effectively work at the human- human, animal, and environmental professionals, especially
animal interface is now a new dictum for health profes- between veterinary practitioners and physicians. Thus a
sionals. The publication of this book is further evidence of One Health construct is now essential for us to target earlier
this transformation. interventions and new p revention strategies.
In the nineteenth century, Louis Pasteur confirmed that There is every indication that the driving forces that
disease transmitted by microbes could affect both human have dramatically resulted in a new and profound era
beings and animals. This laid the groundwork for cross-dis- of emerging infections will continue to grow even more
ciplinary cooperation in public health research and prac- complex, challenging, and important to our work and lives.
tice, with veterinarians and physicians working side by side. Thus this book is especially timely and relevant. We now live
It was a veterinary student named Daniel Salmon who iso- in a world where we must prepare for an H5N1 pandemic,
lated the enteric organism that now carries his name—Sal- appreciate our rapidly growing and expanding global food
monella. One of the first activities of the Veterinary Public system, understand the importance of emerging zoonoses,
Health program at the then Centers for Disease Control grow increasingly concerned about antimicrobial resis-
(CDC, now Centers for Disease Control and Prevention) tance, and acknowledge new threats from the expansion of
was to investigate the possibility that Salmonella was an vector-borne, foodborne, and water-borne diseases both
important human pathogen. At that time, poultry and meat domestically and globally.
producers argued that Salmonella did not cause infection This book is especially beneficial to raise the awareness
in human beings. CDC investigators, however, were able to and appreciation of private practitioners, both veterinary
confirm that the bacteria were indeed an important cause of and human, to envision themselves and their clinical work
human enteric disease. Today, we have more sophisticated as key to putting One Health into practice. At the same time,
diagnostic tools and growing technological capacities that the book is enormously helpful in building momentum
enable us to gain more insights into the complex dynamics toward a more universal acceptance of One Health and
and full dimensions of human-animal health links. Over a encourages us to work across disciplines, professions, and
decade ago, the CDC introduced a new DNA fingerprint- organizations. Just as important, the book is instructive to
ing diagnostic system termed PulseNet. Working with state help us shift from the concept of One Health to actually
public health laboratories, PulseNet has enabled us to bet- implement daily actions and strategies that bring the nexus
ter diagnose multistate foodborne outbreaks and better of human, animal, and environmental health into better
understand the ecology and epidemiology of these out- focus to ensure positive and real health impact.
breaks. Salmonella in peanut butter, peppers, and pot pies Furthermore, this book serves as a wonderful contribu-
and Escherichia coli in spinach are just a few examples of tion for educating public and animal health professionals
discovering new vehicles for foodborne pathogens and help- and practitioners about working together at the human-ani-
ing reveal the importance of understanding how microbes mal interface. Yet much more needs to be done to ensure that
are transmitted and maintained in the environment and our researchers, diagnosticians, laboratory scientists, and
readily move across species lines. The use of microarrays practitioners take a more holistic view of health and realize
and new molecular diagnostics has also helped us elucidate the many overlaps between human and animal medicine and
the science of infectious disease ecology. We now appreciate health. We appreciate that the authors have demonstrated
that bats may harbor Ebola, Hendra, Nipah, and Marburg the benefits of working together and have encouraged us to
viruses and that H5N1 avian influenza is found in mul- be part of a larger community with mutual respect and new
tiple wild bird and domestic poultry species and popula- tools and thinking that will continue to improve human, ani-
tions worldwide. Technological advances have given us new mal, and environmental health. We are grateful for both the
xvii
xviii Foreword: Public Health Perspective
intellectual and practical contributions of this book and will

use the examples and ideas contained in it to better prepare
us to address the threats and challenges of the future. Lastly,
this book will also be enormously helpful to stimulate us to
continue our pioneering efforts and leadership in public and
animal health to create a more integrated worldview of One
Health.
James H. Steele, DVM, MPH

Chief Veterinary Officer
Assistant Surgeon General
U.S. Public Health Service
Lonnie King, DVM, MS, MPA

Director of National Center for Zoonotic, Vector-Borne
and Enteric Diseases
Atlanta, Georgia
The Convergence of
Human and Animal 1
Medicine
Laura H. Kahn, Bruce Kaplan, and Thomas P. Monath
How human and animal health Food Animals

converge
On a global scale, the growing human population has
led to a rapid and unprecedented increase in the num-
The relationship between human and animal health is becom-
bers and density of animals raised for food production in
ing increasingly complex and includes biological, chemical,
many parts of the world and the United States (see Chapter
physical, and social factors (Figure 1-1). Both endemic and
11). The rearing, transportation, marketing, and process-
newly emerging infectious diseases have grabbed headlines
ing of these animals have significant implications for the
and heightened awareness of the role of wild and domes-
occupational health of the human beings working with
tic animal populations in transmitting diseases to human
the animals (Figure 1-3); wildlife that may have contact
beings. Although the importance of zoonotic disease is not
with such animals; as well as the air, soil, and water qual-
new—approximately 60% of all infectious pathogens of
ity of agricultural areas (see Chapter 12). The widespread
human beings are zoonotic in origin—an even higher per-
outbreaks of avian influenza among domestic poultry and
centage of newly emerging diseases over the past 2 decades
the threat of the emergence of new strains with pandemic
are zoonoses, many originating from wildlife (Figure 1-2).1
potential are a reminder of these connections. In addi-
All but one of the bioterrorism agents considered to have the
tion, the increasing reliance on bush meat consumption
highest potential for use as a weapon of biological warfare
in many developing countries affects wildlife populations
are zoonotic pathogens.
and species diversity and exposes human beings to zoonotic
disease threats.3
Pets and Wildlife
More than half of households in the United States own
a dog, cat, or both. In addition, millions of exotic wild The importance of environmental
animals, birds, and reptiles are kept in U.S. households as health to human beings and other
pets, and the worldwide trade in such animals is accelerat- animals
ing (see Chapter 10).2 Therefore the average patient visiting
his or her health care provider is likely to share his or her Zoonotic disease represents just one of the ways that the
living space with a pet, and the health of the pet (which health of companion animals, livestock, and wildlife is inex-
may have originated in a wildlife population across the tricably linked with human health. The global environment
globe) may hold clues to health or disease issues that the is rapidly changing, and animals and human beings are
patient is experiencing. Furthermore, as suburban develop- exposed to shared environmental health risks. Environmental
ments encroach on wildlife habitat (see Chapter 6), con- disasters such as Hurricane Katrina wreak havoc on both
tact with domestic animals, wildlife, and insect vectors may human and animal populations. Many zoonotic diseases
be frequent, allowing pathogens to pass in both directions are emerging as a result of environmental factors, including
and bringing human beings into the mix. At the same time, climate change, deforestation, alterations of wildlife habi-
veterinarians in small animal practice have understood tat, and other land use change4; human population growth;
for years that pets contribute to improved human mental movement of human beings and animals across borders;
health and well-being and that the benefits of compan- and increased production of food animals. The built envi-
ion animals usually far exceed the risks of zoonotic dis- ronment may contribute to a sedentary lifestyle and mani-
ease. A growing body of research now supports the concept fest as an obesity epidemic in both human beings5 and their
of this “human-animal bond phenomenon”; avenues for pets (Figure 1-4). Animals and human beings often share
physician-veterinarian cooperation to maximize these exposure risks from noninfectious disease threats, such as
benefits are detailed in Chapter 5. air and water quality problems, pesticides, lead, and carbon
1
2 Human-Animal Medicine
Environmental health (biologic,

chemical, physical, and social factors)
“Shared risk” and

sentinel health events
Human health Animal health
Figure 1-3 n Removing the breast and leg meat from a bird without
using gloves. (Courtesy Melissa Anderson. From Auerbach PS: Wilderness
medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.)
Figure 1-1 n Relationships among environmental, human, and animal

health.
EXAMPLES OF ROUTES BY WHICH ZOONOSES ARE ACQUIRED
Direct Contact with Contact Fecal–oral Bites and Via Eating Ingestion Respiratory
contact animal with urine route scratches ectoparasites under- of milk route
products carrying cooked
pathogens meat, fish
Dermatophytes Anthrax Leptospirosis Salmonellosis Rabies Ticks: Rocky Trichinellosis Mycobacterium Histoplasmosis
Mountain bovis
Tularemia Toxoplasmosis
spotted fever,
Streptococcus
tularemia, Taenia solium
zooepidemicus
Lyme disease,
babesiosis
Fleas: Plague
Figure 1-2 n Examples of routes by which zoonoses are acquired by human beings. (From Cohen J, Powderly
WG: Infectious diseases, ed 2, London, 2003, Mosby Elsevier.)
onoxide. Just as canaries once warned coal miners of the

m a diagnosed disease that provides information about an
presence of deadly gases and dead songbirds sent a mes- environmental risk to animals living nearby. Chapter 4 in
sage to human beings about the risks of pesticides in Rachel this book, as well as the disease-specific chapters, provide
Carson’s Silent Spring, a disease occurrence in an animal can many examples of sentinel events and how clinicians and
be a “sentinel event” warning human beings of an environ- public health professionals can detect them and act on such
mental threat.6 Alternatively, at times a human being has information to p
revent further cases.
Chapter 1 n The Convergence of Human and Animal Medicine 3
in important ways. Table 1-1 outlines some of the key points

differentiating the groups.
Despite many curricular similarities between human
medical and veterinary medical schools, veterinarians
receive more training in zoonotic diseases, whereas medical
students learn virtually nothing about animal health issues.
Both groups receive only limited training in public health
theory and practice.
After completing their training, physicians in practice
rarely make home or worksite visits to directly see the
environments where their patients live and work, whereas
large animal veterinarians frequently visit farms. Public
health professionals may be more likely to visit locations
where environmental health threats have been identified.
The rate at which veterinarians perform necropsies on
animals that have died may be higher than the rate at which
Figure 1-4 n Obese Savannah monitor (Varanus exanthematicus). physicians perform autopsies. As a result of these training
(Courtesy S.J. Hernandez Divers. From Mader DR: Reptile medicine and sur- and practice differences, the approaches to detecting and
gery, ed 2, St Louis, 2005, Saunders Elsevier.) preventing problems related to interactions among human
beings, animals, and the environment may differ greatly
Similarities and differences among among these groups.
the training and practice of human
health, animal health, and public Role of Veterinarians in Human Health
health professionals
Many physicians may not be aware of the routine contri-
The training and practice patterns of human health care pro- butions made by practicing veterinarians to human health.
viders, veterinarians, and public health professionals differ Veterinarians regularly educate pet owners and farmers
Table 1-1 n Training and Practice Statistics: Veterinary Medicine, Human Medicine, and Public Health
Veterinary Medicine Human Health
Category (DVM/VMD)7 (MD, DO)7 Public Health (MPH, DrPH)
Minimum years of 4 4 2-4
professional school Approximately 2 years basic Approximately 2 years basic Studies include epidemiology,
sciences + 2 years clinical studies sciences + 2 years clinical studies biostatistics, and public health
Curricula comparable to medical Curricula comparable to administration
schools veterinary medical schools
Amount of training in Moderate Minimal Varies
zoonotic diseases
Amount of training in animal High8 None Varies (e.g., there are combined
health issues DVM/MPH programs)
Curriculum hours in public Minimal Minimal High
health
Number of practitioners in the Approximately 69,170 (active)8* 633,000 †
United States
Specialties 70% of private practice Primary care professions Includes environmental health,
veterinarians focus on small Specialists occupational health, maternal
animal medicine/surgery and child health, infectious
(dogs, cats, etc.) diseases, biostatistics
Board certifications in various
specialties
Practice organization Prevailing model solo or Increasing role of health Public health agency
small group practices with some maintenance organizations
evolving large group practices
House calls/site visits Large animal DVMs/VMDs visit MDs rarely make house calls Some public health
farms; rare for small animal Home health care nurses professionals perform site
practitioners (via mobile provide many services in visits
veterinary clinics) homes
Licensing agency in states Departments of consumer affairs, professional regulation, or departments of public health (usually the
same department in state)
*As of October 31, 2007.

†Data not available.
about the risks of acquiring zoonotic diseases. They reduce health issues. They often interact with their federal colleagues
transmission risks to human beings by vaccinating large at the CDC and other professionals in state and federal
numbers of pets and livestock against zoonotic diseases. departments of agriculture on issues related to food safety,
Many are involved in caring for wildlife and exotic animals. importation of animal diseases, bioterrorism preparedness,
The expanding role of veterinarians at the U.S. Centers for pandemic preparedness, environmental health, and many
Disease Control and Prevention (CDC, http://www.cdc.gov) areas of shared concern (see Chapter 13).
reflects a growing trend to create joint teams of veterinarians
and human health professionals to deal with human-animal Other Professionals Critically Involved With
health issues. The team approach has proved synergistic; more Human-Animal Medicine Issues
rapid and precise evaluations enhance more efficacious con-
trol. At the time of this writing, approximately 90 veterinarians In addition to physicians, veterinarians, and public health
work at the CDC.9 The CDC’s National Center for Zoonotic, professionals, many other professionals play key roles in
Vector-Borne, and Enteric Diseases (NCZVED) provides lead- human and animal health and should be considered in any
ership, expertise, and service in laboratory and epidemiological discussion of how these fields converge. A significant percent-
science, bioterrorism preparedness, applied research, disease age of health care services in the United States is provided by
surveillance, and outbreak response for infectious diseases. Its advanced practice registered nurses (APRNs) or physician
ecological framework includes human beings, animals, and assistants (PAs), and hospital-based and home health nurses
plants interacting in the complex, changing natural environ- perform frequent health assessments and contribute to the
ment. Until September 1, 2009, NCZVED was directed and development of care plans. On the veterinary side, veterinary
administered by a veterinarian with previous experience as technicians and other veterinary staff provide many animal
administrator of the U.S. Department of Agriculture’s (USDA) health care services, as do wildlife rehabilitators. Public
Animal and Plant Health Inspection Service (APHIS). health efforts to manage zoonotic disease risk and other
From 1953 through 2008, more than 228 veterinarians environmental health issues require the expertise of vector
have completed the Epidemic Intelligence Service (EIS) ecologists, wildlife biologists, disease ecologists, environ-
training at the CDC (Figure 1-5). The EIS represents the mental health professionals, industrial hygienists, toxicolo-
U.S’s critical unit for investigating the causes of major epi- gists, anthropologists, farmers, and agricultural extension
demics. Over the past 50 years, EIS officers have played cru- officers, among others. Although human health and animal
cial roles in combating the root causes of epidemics of major health clinicians may detect sentinel cases of disease related
consequence. The EIS has served as a model for similar ser- to environmental factors, the actual intervention to improve
vices in about 25 other countries worldwide. such environments requires a team approach of diverse pro-
The Special Pathogens Unit at the CDC concerns itself fessionals, as is described in other sections of this book.
with the investigation of the highly pathogenic, zoonotic viral
hemorrhagic fevers, such as Ebola virus, Marburg hemor-
rhagic fever, and Lassa fever. The unit is currently directed by Efforts to bridge the gaps between
a veterinarian and includes a number of physicians who col- human and animal health
laborate on laboratory and field research aimed at elucidating
the reservoirs of infection in nature, transmission of viruses Communication Between Human and Animal
to human beings, the control of outbreaks, and ground- Health Care Providers
breaking research on diagnostic methods and vaccines.
Outside the CDC, state public health veterinarians (http:// The convergence of these health issues involving human
www.nasphv.org) are involved in a wide range of public beings and other animals would seem to demand ongoing
Figure 1-5 n A CDC investigator examines a calf as part of an outbreak investigation. (Courtesy Centers for
Disease Control and Prevention, Atlanta, Ga.)
Chapter 1 n The Convergence of Human and Animal Medicine 5
and substantive interactions between human health care as conservation medicine,13 Ecohealth,14 and “One World,
providers and veterinarians, as well as a shared body of One Health.”15 The common theme of these diverse efforts
knowledge regarding health links between human beings is that the health of human beings, wildlife, domestic ani-
and animals. Yet professional interaction of this type is often mals, and the environment is vitally interconnected and
limited. Research indicates that many physicians and other future efforts to improve global health must take these
health care providers may be uncomfortable discussing ani- interrelationships into account.
mal health issues with their patients.10 Veterinary medi- Recently the American Medical Association (AMA)
cal health care providers may be cautious about discussing and American Veterinary Medical Association (AVMA)
human health issues with their clients, in some circumstances began collaborative efforts on a One Health Initiative (also
because of caution to not overstep professional boundaries referred to as One Medicine, One Medicine-One Health, and
and possibly because of concerns about malpractice liability One World One Medicine One Health). The One Health
or privacy issues (see Chapter 2). Both human health and Initiative promotes the model of physicians, veterinarians,
veterinary clinicians may be unfamiliar with public health and allied medical and environmental scientists in clini-
and environmental health concepts and their relevance to cal, public health, and biomedical research settings working
their practices. more closely together than in the past to better understand,
Some of the key differences among the professions, as well manage, and prevent health risks involving animals, human
as the One Health Initiative aimed at overcoming professional beings, and their environments (Figure 1-6).11,16
barriers to communication and collaboration, are described A joint One Health Task Force created by the AMA and
below. AVMA was formed to study ways to facilitate collabora-
tion and cooperation among human health and animal
health professions, educational institutions, and agencies
Collaborations Between Animal and Human to improve assessment, treatment, and prevention of cross-
Health Care Providers species disease transmission and mutually prevalent nonin-
Historical precedents do exist for productive collabora- fectious human and animal diseases and medical conditions.
tion between animal and human health care providers. The recommendations of the One Health Task Force were
The nineteenth-century physician pathologist Dr. Rudolf published in 2008 (available online at http://www.avma.
Virchow (who coined the term zoonosis) emphasized the org/onehealth).17 Key recommendations of the task force
need for medical scientists to learn from comparative medi- included a call for a national research agenda for One Health
cine approaches to research. Sir William Osler (called the and outreach efforts to involve medical, veterinary medical,
“Father of Modern Medicine”), a physician who studied with and public health students and their respective organizations
Virchow, helped establish the first departments of veteri- in One Health concepts.
nary pathology in North America in the late nineteenth cen- Similarly, a consultation document, “Contributing to
tury. Drs. Theobald Smith, a physician, and F. L. Kilborne, a One World, One Health: Strategic Framework for Reducing
veterinarian, discovered that Babesia bigemina, the cause of Risks of Infectious Diseases at the Animal-Human-
cattle fever, was transmitted by ticks. Their work set the stage Ecosystems Interface,” was produced by the Food and
for Walter Reed’s discovery of yellow fever transmission via Agriculture Organizations of the United Nations (FAO),
mosquitoes.11 More recently, Rolf Zinkernagel, a physician, World Organization for Animal Health (OIE), World
and Peter C. Doherty, a veterinarian, shared the 1996 Nobel Health Organization (WHO), United Nations System Influ
Prize for their discoveries of how the body’s immune system enza Coordination, United Nations Children’s Emergency
distinguishes normal cells from virus-infected cells. Funds (UNICEF), and the World Bank (see http://www.
o i e . i n t / d ow n l d / AV I A N % 2 0 I N F LU E N ZA / OWO H /
OWOH_14Oct08.pdf).
One Health Initiative The six specific objectives suggested for prioritization by
national authorities are as follows:
In the 1960s, veterinarian Dr. Calvin W. Schwabe, a para-
sitologist and veterinary epidemiologist, coined the term 1. Develop international, regional, and national capacity in
One Medicine in his textbook, Veterinary Medicine and surveillance, making use of international standards, tools,
Human Health.12 Schwabe proposed a collaborative effort and monitoring processes
between veterinary and human health professionals to 2. Ensure adequate international, regional, and national
combat zoonotic diseases. In recent years, a number of capacity in public and animal health—including com-
organizations and collaborations have sought to build on munication strategies—to prevent, detect, and respond to
and further expand this model, producing concepts such disease outbreaks
Figure 1-6 n The One Health Initiative logo. (From B. Kaplan, http://www.onehealthinitiative.com.)
3. Ensure functioning national emergency response capacity book provides numerous practical suggestions for helping
as well as a global rapid response support capacity such professionals retool and implement One Health con-
4. Promote interagency and cross-sectoral collaboration and cepts into their daily practice routines, which could enhance
partnership the preventive and therapeutic care they provide and lead to
5. Control highly pathogenic avian influenza and other further convergence between the disciplines.
existing and potentially re-emerging infectious diseases
6. Conduct strategic research
References
Research approaches linking human and animal health in
a One Health model hold great promise. Improved vaccine 1. Woolhouse ME, Gowtage-Sequeria S. Host range and emerging and
development and delivery for animal diseases such as brucel- reemerging pathogens. Emerg Infect Dis. 2005;11(12):1842–1847.
2. Chomel BB, Belotto A, Meslin FX. Wildlife, exotic pets, and emerging
losis and avian influenza may reduce human risk from these zoonoses. Emerg Infect Dis. 2007;13(1):6–11.
diseases. Conversely, the conservation of great apes in Africa, 3. Wolfe ND, Daszak P, Kilpatrick AM, et al. Bushmeat hunting, defor-
currently affected by outbreaks of Ebola virus, could ben- estation, and prediction of zoonoses emergence. Emerg Infect Dis.
efit if a human vaccine were developed. Similarly, pharma- 2005;11(12):1822–1827.
ceutical developments and sustainable environmental health 4. Patz JA, Daszak P, Tabor GM, et al. Unhealthy landscapes: policy
recommendations on land use change and infectious disease emergence.
practices often have benefits across species. Environ Health Perspect. 2004;112(10):1092–1098.
The Human Genome Project has resulted in the avail- 5. Wakefield J. Fighting obesity through the built environment. Environ
ability of sequencing the genomes of multiple animal species Health Perspect. 2004;112(11):A616–A618.
and an understanding of epigenetics. These molecular tools 6. Carson R. Silent spring. Boston: Houghton Mifflin; 1962.
7. Bureau of Labor Statistics, U.S. Department of Labor. Occupational out-
are helping define the similarities and differences between look handbook, 2008-09 edition. http://www.bl.gov/oco/ocos076.htm.
species with regard to host-environment interactions as well Accessed August 26, 2008.
as drug pharmacodynamics and pharmacokinetics. 8. National Research Council, Committee on the National Needs for
Disease surveillance represents another area of improved Research in Veterinary Science. Critical needs for research in veterinary
collaboration between human and animal health. Improved science. Washington, DC: National Academies Press; 2005.
9. King LJ. Personal communication. 2008.
early warning systems for disease risk that use both human 10. Grant S, Olsen LW. Preventing zoonotic diseases in immunocompromised
and animal data could help highlight environmental factors persons: the role of physicians and veterinarians. EID. 1999;5(1):159–163.
driving disease outbreaks in wildlife, domestic animals, and 11. Kahn LH, Kaplan B, Steele JH. Confronting zoonoses through closer
human beings, leading to better disease prevention. collaboration between medicine and veterinary medicine (as “one med-
icine”). Veterinaria Italiana. 2007;43(1):5–19.
A better understanding of disease ecology and the impact 12. Schwabe CW. Veterinary medicine and human health, ed. 3. Baltimore:
of environmental change on disease risk for both animals Williams & Wilkins; 1984.
and human beings is essential to the One Health approach. 13. Aguirre AA, Ostfeld RS, Tabor GM, et al. Conservation medicine: ecologi-
As clinicians become increasingly aware that the diseases cal health in practice. New York: Oxford University Press; 2002.
observed in their human and animal patients are related to 14. Wilcox B, Kueffer C. Transdisciplinarity in EcoHealth: status and future
prospects. EcoHealth. 2008;5(1):1–3.
shared environmental health risks, this can create synergy in 15. Wildlife Conservation Society. The Manhattan principles on “One World-
collaboration with environmental health and disease ecology One Health.” http://www.oneworldonehealth.org/index.html. Accessed
experts to reduce such risks. August 11, 2008.
In the midst of such developments, human and animal 16. Kahn LH, Kaplan B, Monath TP, et al. Teaching “one medicine, one
health.” Am J Med. 2008;121(3):169–170.
health professionals working on the front lines of clinical 17. King LJ, Anderson LR, Blackmore CG, et al. Executive summary of
and public health practice will play an important role in the the AVMA one health initiative task force report. J Am Vet Med Assoc.
recognition and management of a wide range of health issues 2008;233(2):259–261.
involving overlaps between human and animal health. This
Legal and Ethical Issues
in Human-Animal 2
Medicine
Peter M. Rabinowitz and Lisa A. Conti
The concept of increasing communication and collaboration • Do not treat animals or give veterinary medical advice
among public health, human health, and animal health pro- because these activities fall outside the scope of prac-
fessionals in a One Health model has numerous advantages. tice for human medical licensure.
Important legal and ethical issues apply to such professional • Provide medical services that promote public health,
interactions. Clinicians and public health professionals need such as preventive care for zoonotic disease.
to be aware that such issues can be complex and are continu-
ing to evolve. This chapter outlines some of these issues.
Veterinary Clinicians
Health care providers should query local authorities such
as health department attorneys, risk managers, and their • Comply with the state’s scope of veterinary practice.
professional associations about state and local regulations. • Counsel clients about zoonotic disease risks and how to
Although some international disease reporting requirements reduce such risks. Document in the veterinary medical
apply to animal and human health in the United States, pro- record all public health advice given to clients.
fessionals in other countries also will need to be informed • Provide clients with written information on zoonotic
about country and region-specific regulations. and other animal-related disease risks (such as the
CDC Pets-Scription), including advice about seeking
Key Points for Clinicians and Public Health medical care if clinical signs develop.
Professionals • Provide competent preventive care for zoonotic dis-
ease prevention.
• If clients decline preventive, diagnostic, or treatment ser-
Public Health Professionals vices for their animals for zoonotic disease, request that
they sign a waiver documenting refusal of these services.
• Educate human health and veterinary clinicians about • Avoid giving human medical advice but offer to assist
requirements for reporting certain diseases to public in communication with physicians or other human
health authorities. health care providers regarding zoonotic or other ani-
• Facilitate communication between animal and mal-related health risks.
human health professionals while protecting patient • Request permission of client before discussing the cli-
confidentiality. ent’s animals with human health care providers.
• Respect the confidentiality of client medical informa-
Human Health Clinicians tion and do not include protected health information
(PHI) about clients and their families in a veterinary
• Report notifiable diseases to public health authorities. medical record.
• Become knowledgeable about zoonotic and other • Report suspected animal abuse to appropriate authorities.
animal-related disease risks. Competently assess such • Provide veterinary medical services that promote pub-
risks during the care of patients. lic health, such as strategic deworming and vaccina-
• Provide written information on zoonotic and other tion against zoonotic diseases.
animal-related disease risks (such as the CDC’s Pets-
Scription: http://www.cdc.gov/healthypets/health_
prof.htm#petscription) to patients with animal Legal considerations
contact. Information if include advice about seeking
medical care if symptoms develop. The convergence of animal health and human health
• Respect patient confidentiality when communicating described in Chapter 1 raises a number of potentially
with veterinary professionals and abide by applicable important legal issues of which human health and veterinary
laws and professional guidelines. providers should be aware.
7
Scope of Practice
BOX 2-1 DEFINITION OF THE “PRACTICE OF
In some instances, physicians have been asked to treat ani- VETERINARY MEDICINE” FROM THE AVMA
mals belonging to their patients. Likewise, veterinarians have MODEL
been asked to treat people or provide medical advice and/
or medications that could be used for human beings as well
as other animals, especially when dealing with zoonotic dis-
eases. Both human and veterinary health professionals need
to be aware of the concept of professional scope of practice
and the need not to overstep professional bounds in such
situations.
Physicians and other human health care providers, includ-
ing nurse practitioners and physician assistants, are licensed
to evaluate and treat diseases in human beings. Individuals
without such licenses who provide medical treatment (such
as administration of prescription medication or performing
a surgical procedure such as suturing a wound) are “practic-
ing medicine without a license,” which is a violation of state
professional licensing (and possibly criminal) statutes. The
justification for licensing professionals is in part to ensure
they are appropriately qualified and can provide necessary
care. The exact scope of practice of physicians and other
medical professionals is determined by medical examining
boards of individual states and therefore can vary among
states. For example, licensed psychologists have the authority
to prescribe medications in some states but not in many oth-
ers.1 Obviously, the scope of practice for medical care provid- From American Veterinary Medical Association: Model Veterinary Practice Act, http://
ers does not include providing veterinary care for animals. www.avma.org/issues/policy/mvpa.asp.
Similarly, veterinarians are licensed to evaluate and treat

animals other than human beings. Veterinary practice acts
in different states define the practice of veterinary medicine BOX 2-2 VETERINARIAN’S OATH
and the scope of practice for veterinary professionals in that
state, including veterinarians and associated providers such
as veterinary technicians. Someone who diagnoses and treats
an animal (other than one he or she owns) without such
licensing is at risk of being charged with “practicing veteri-
nary medicine without a license.” The American Veterinary
Medical Association (AVMA) publishes a Model Veterinary
Practice Act (MVPA) that has been used by some states in
drafting scope of practice legislation.2 Veterinary providers
should be aware of their state’s current definition of veteri-
nary medicine and scope of veterinary practice. The defini- From http://www.avma.org/careforanimals/animatedjourneys/aboutvets/aboutvets.asp.
tion of veterinary practice in the MVPA is shown in Box 2-1.
of a veterinarian to perform such activities could potentially
Veterinary Practice Act lead to legal liability (see below). Veterinarians consequently
must carefully consider ways to fulfill their public health
As shown in Box 2-1, the “rendering of advice or recommen- obligations while not exceeding their professional scope of
dation” about animal diseases is part of the practice of vet- practice.3
erinary medicine, and this should be kept in mind by human
health care providers who are discussing animal health issues
with their patients. The MVPA does not include any provi-
Malpractice Liability
sions for veterinarians offering medical advice to their clients Both physicians and veterinarians are liable for malprac-
regarding human diseases. However, in addition, the oath of tice (damages awarded for professional negligence). Many
practice that veterinarians take when entering the profes- human health and veterinary providers carry malpractice
sion (Box 2-2) includes a commitment to “the promotion insurance, but such insurance covers only activities within
of public health, and the advancement of medical knowl- the scope of practice for that professional.
edge.” Therefore counseling clients about reducing zoonotic There is a growing realization of particular risks to both
disease risk, providing preventive care to reduce such risk, human and veterinary medical providers related to zoonotic
and notifying public health departments in a timely manner diseases in terms of malpractice liability related to human-
about human health risks would appear to be an intrinsic animal medicine issues, although legal precedent in this area
part of good preventive veterinary care. Failure on the part remains sparse. There is potential malpractice liability for
Chapter 2 n Legal and Ethical Issues in Human-Animal Medicine 9
physicians and other human health care providers who fail to Management techniques to avoid these malpractice liabil-
correctly diagnose an animal-related disease such as a zoono- ities include the following:
sis in their patients because they failed to take an adequate his-
1. Educating clients about the risks of zoonotic disease
tory of animal exposures or otherwise consider the diagnosis.
and methods to reduce such risks, and documenting
For example, a physician who fails to obtain a history of bird
such education. To supplement such teaching, hand-
contact in the household and consequently fails to correctly
outs about zoonotic disease risks can be given to clients
diagnose a disease such as psittacosis in a person who shares
by veterinarians to educate them. An example of such
the household with the bird could be at risk of being sued for
a handout is the “Pet-Scription” and “Pet-Scription for
negligence (see Chapter 9). Management of this liability can
Reptile Owners” available from the CDC Healthy Pets
include training for physicians and other medical providers
Healthy People website. Discussions about zoonotic
in the recognition of zoonotic disease risk and other animal-
disease risk should be documented in the veterinary
related risks.
medical record.
Veterinarians are in a knowledgeable position to warn cli-
2. Asking clients who decline preventive treatment (such
ents about the risks of zoonoses and control the risk to human
as routine deworming) for their animals to sign a waiver
beings by competently managing disease in the animal popu-
documenting the refusal of such treatment. Examples
lation. Consequently, there appear to be a number of areas of
of such legal consent forms are available, but veterinari-
potential malpractice liability for veterinarians related to neg-
ans should seek advice from a local attorney about such
ligence in the management of zoonotic disease.
documentation because local statutes may vary.3
The first area of potential negligence is the failure to cor-
3. Increasing direct professional communication between
rectly diagnose a zoonotic disease in an animal. For example,
human health care providers and veterinarians. Direct
if a veterinarian fails to detect dermatophytosis in a cat used
physician-veterinarian contact offers several advan-
for animal therapy (see Chapter 5) and an immunocompro-
tages, including ensuring that diagnostic and thera-
mised person who is in contact with the cat becomes infected
peutic information is accurately conveyed, learning of
with Microsporum as a result (see Chapter 9), the veterinarian
other animal-human interaction health concerns, and
could be blamed for failing to diagnose the zoonotic risk. In
increasing dual awareness on the part of both types of
the past, it may have been more difficult to definitively link
practitioners about the health issues related to animal-
an animal infection to a subsequent infection in a human,
human contacts. Many sections of this book contain
but the use of molecular techniques to characterize particu-
specific suggestions for the content of direct commu-
lar strains of an organism crossing from animals to human
nication between human and animal professionals.
beings now allows such causative linkages to be made. Such
Such communications, however, need to consider con-
evidence could surface in a medicolegal setting.3
cerns about patient confidentiality (see below).
Another area of malpractice liability for veterinarians
related to zoonotic disease is the failure to recommend
preventive measures for common zoonotic diseases. This Workers’ Compensation Liability
situation could occur if a veterinarian failed to isolate an
unvaccinated stray cat with bite wounds with the subsequent Employers of animal workers, including owners of vet-
need for rabies postexposure prophylaxis among human erinary practices, zoos, and animal care facilities, are lia-
contacts if the cat develops rabies (see Chapter 9). In such a ble for work-related diseases in employees as a result of
case, the veterinarian could be held liable for not taking steps human-animal contact. Examples of potentially compens-
to control the zoonotic risk. Another example would be if a able diseases in animal workers include skin rashes, asthma
veterinarian diagnosed leptospirosis in a dog, failed to ade- or other allergy, animal bites, and zoonotic infections as
quately warn the owner regarding the zoonotic risk of dis- well as diseases resulting from exposure to anesthetic gases,
ease, and leptospirosis that could be traced back to the strain cleaning agents, and workplace noise. Incidents of work-
that infected the dog later develops in the owner. related injury and illness are compensable under state
In the case of exotic and wildlife pets that could harbor workers’ compensation statutes, with the employee being
unusual zoonotic diseases (such as monkeypox) or pose enven- potentially eligible for reimbursement of medical expenses,
omation risks (such as venomous reptiles), a veterinarian could lost work time, and other awards related to the illness or
be held liable for not warning clients about the dangers of keep- injury. Veterinarians and other employers of animal work-
ing such animals. Even in the case of rare and unusual zoonoses ers can manage liability for work-related illness and injury
and other disease risks related to exotic pets with which a vet- by taking steps to reduce risks in the workplace through
erinarian may be less familiar, it could be argued that the engineering and work practice controls for biological,
veterinarian should have referred the owner to a specialist for chemical, physical, and psychosocial hazards and by ensur-
diagnosis or treatment of a species or condition that was not ing the provision of adequate occupational health services
within the practitioner’s expertise (see Chapter 10). 3 for such workers (see Chapter 12).
An additional potential area of veterinarian malpractice
liability involves a failure to advise a client to seek care from Other Liability
a physician for diagnosis and treatment of a zoonotic disease.
This could occur if a client reports certain symptoms such as Veterinarians may be liable for physical injury to a human
fever or diarrhea to a veterinarian after an exposure to a sick (such as a dog bite) if it could be shown that the veterinarian
animal and the veterinarian fails to counsel that person to failed to properly counsel owners about ways to reduce the
seek medical care. risk of such injury and failed to intervene appropriately in
the care of a potentially dangerous animal. Again, educating Notification and Reporting
owners about warning signs of behavioral problems in dogs
and other animals and steps to take to reduce risks of aggres- Both human health care and veterinary providers are required
sive animals, and documentation of such education, is one by state and federal regulations to report certain diseases and
way to manage liability. conditions to the appropriate health agencies, although the
lists of reportable human and animal diseases have areas of
overlap and some differences (see Chapter 13 for a listing of
Confidentiality and the Health Insurance nationally notifiable human and animal diseases). Whereas
Portability and Accountability Act human health providers must report notifiable diseases to
public health authorities, veterinarians may need to report
The Health Insurance Portability and Accountability Act animal and other diseases to agriculture departments, public
(HIPAA, known as the Privacy Rule) has tightened the rules health departments, or both (see Chapter 13).
regarding the release and sharing of personal health informa- In addition to reportable diseases, other medical condi-
tion (PHI) by medical providers treating patients. This rule tions require notification by health professionals. Human
also applies to health plans and health care clearinghouses.4 health care providers are required to report cases of sus-
PHI refers to health information that can be linked to an pected child abuse. Similarly, in some states veterinarians are
identifiable individual and that relates to the following: required to report suspected animal abuse (see Chapter 5).8
1. Past, present, or future physical or mental health or If human health care providers, veterinary providers,
condition of the individual or their employees incur an occupational injury or ill-
2. Provision of health care to the individual ness, including animal bites and zoonotic or allergic dis-
3. Payment for the provision of health care to the individual ease among workers in an animal hospital or other animal
care facility, such incidents need to be recorded on the
“Covered entities” under HIPAA include persons, busi- Occupational Safety and Health Administration (OSHA)
nesses, or agencies that furnish, bill, or receive payment for reporting log of work-related injuries and illnesses for
health care in the normal course of business.5 The Privacy that facility (see Chapter 12). Instructions regarding
Rule does not directly address confidentiality in veterinary OSHA reporting can be found at http://www.osha.gov/
practices. Provisions of the Privacy Rule allow PHI to be doc/outreachtraining/htmlfiles/cfr1904.html.
released to public health authorities for the purpose of sur-
veillance and disease control. However, public health author-
ities must take steps to preserve the confidentiality of such
information.6
Ethical issues
Veterinarians also have laws that govern the confiden-
tiality of veterinarian-client interactions.7 In some states, Professionalism
veterinarians are forbidden to release details regarding
One set of ethical issues concerns professionalism and expec-
the treatment of an animal without the written permis-
tations of practitioners. For example, patients have an expec-
sion of the animal’s owner. Although exceptions allow
tation that health care providers are honest and truthful, are
for communications between veterinarians or between
knowledgeable and current in their field, and act in the best
veterinarians and human health professionals or animal
interests of their patients. The idea that professionals act in
control officers, in general veterinarians should obtain
the best interests of their patients is both a legal and ethi-
the permission of their clients before releasing informa-
cal obligation known as a fiduciary duty. This duty refers to
tion about an animal’s diagnosis and treatment.7 HIPAA
the relationship of trust or confidence between professionals
legislation does not specifically mention veterinarians,
and their patients or clients. Professionals are expected to be
but some communications of health information between
loyal, not put personal interests above those of the patient or
veterinarians and human health care providers could
client, and not profit from the relationship unless the patient
involve HIPAA-defined PHI (see Chapter 3). For exam-
or client consents. An implication of this last point is the
ple, if a client mentions to the veterinarian that he or she
expectation that professionals minimize and disclose con-
has a medical condition that could predispose others to
flicts of interests.
zoonotic infection (see Chapter 10), such information
could be considered PHI.
Guidelines for practice in this environment for veterinar- Ethical Principles in Human Health
ians include the following:
Another set of issues concerns ethical principles regard-
• Excluding identifiable health information about clients ing the conduct of human medical and veterinary practice.
or other persons in the household that could be consid- These can be characterized in ethical codes, in general prin-
ered PHI from the veterinary record (see Chapter 3) ciples, or by reference to cases (cases of good behavior and
• Refusing to provide medical advice to human beings cases of nonoptimal behavior). Because a profession may
(see also the scope of practice discussion above) have more than one code of ethics (for example, there are a
• Offering assistance to speak with the person’s physi- number of codes in medicine, some tailored to the particular
cian, with the person’s permission practice specialty), one broad approach to ethics is to iden-
• Educating the physician or other human health care tify and analyze practice using general ethical principles. In
provider on questions he or she may have regarding medicine there is widespread agreement on three principles:
pets, zoonoses, and pet care respect for persons (autonomy), beneficence, and justice.9
Chapter 2 n Legal and Ethical Issues in Human-Animal Medicine 11
Respect for persons means that health care professionals rec- be to use the least-intrusive methods out of concern to mini-
ognize the ability of patients to make their own choices and mize suffering and to exercise respect for animals.
exercise personal autonomy. Even when patients are not able Applying the principle of justice with regard to animal
to exercise autonomy (for example, in cognitively impaired welfare ethics presents several challenges. The idea that all
populations), clinicians have an obligation to involve patients people deserve equal moral consideration (which may result
as much as their abilities permit and to pay particular atten- in different treatment to serve the people’s different needs)
tion to dissent. Beneficence means that the benefits of medi- is generally accepted. However, there is no general consensus
cal treatments should outweigh the harms. Justice means that that animals deserve equal consideration, either with peo-
patients are treated fairly and receive equal moral consider- ple or with respect to other kinds of animals. For example,
ation, and that nonmedical criteria such as financial ability in many states, agricultural animals are exempt from ani-
to pay for care do not influence treatment decisions by the mal cruelty laws. At the same time, agricultural animals may
clinician. In addition, there is a recognition that additional be viewed by some to have greater moral importance than
principles may apply to certain areas, such as public health. In indigenous predatory animals such as wolves. One way of
public health an additional principle is the idea of proportion- thinking about the idea of justice in veterinary medicine is
alism, which means that public health officials should use the that interventions should minimize unfair treatment of both
least-intrusive means to achieve a public health goal. Another people and animals. For example, as a matter of justice it may
principle important in public health is the idea of transpar- be the right thing for a government to compensate those who
ency and public disclosure about public health interventions. own animals if there is a need to cull such animals for public
health purposes, such as in an outbreak of avian influenza.
Overarching ethical principles for public health and
Ethical Principles in Animal Health
clinical considerations include eliminating environmental
General ethical principles also can be applied to the care of pollution and addressing habitat restoration. Focusing on
animals.10 The concept of respect for animals involves con- environmental health is beneficial for human and other ani-
sideration of their general welfare. The principles of animal mal populations.
welfare have been summarized as “five freedoms,” which
were developed as goals for farm animal husbandry but are References
applicable to the care of other animals.11 These freedoms are
listed in Box 2-3. 1. American Psychology Association. Louisiana becomes second state to
The ethical concept of beneficence may be applied to the enact prescription privileges law for psychologists. http://www.apa.org/
releases/louisianarx. Accessed September 23, 2008.
treatment of animals and human beings. As with medical 2. American Veterinary Medical Association. Model veterinary practice act.
treatment of human beings, veterinary treatments for indi- http://www.avma.org/issues/policy/mvpa.asp. Accessed September 23,
vidual animals should be grounded in the idea that bene- 2008.
fits should outweigh harms. However, in addition to treating 3. Babcock S, Marsh AE, Lin J, et al. Legal implications of zoonoses for
particular animals, veterinarians also may be called on to clinical veterinarians. J Am Vet Med Assoc. 2008;233(10):1556–1562.
4. US Department of Health and Human Services. Health information
address the welfare of populations of animals as part of pub- privacy. http://www.hhs.gov/ocr/hipaa/. Accessed September 23, 2008.
lic health. Control of zoonotic diseases may require inter- 5. US Department of Health and Human Services. Covered entity charts.
ventions to separate infected populations from uninfected http://www.cms.hhs.gov/HIPAAGenInfo/Downloads/CoveredEntity
populations and may require various control measures of charts.pdf. Accessed September 23, 2008.
6. Centers for Disease Control and Prevention. HIPAA privacy rule and
infected populations. When dealing with populations of ani- public health. Guidance from CDC and the U.S. Department of Health
mals, the principle of proportionality is important to animal and Human Services. MMWR Morb Mortal Wkly Rep. 2003;52(suppl
ethics, just as it is relevant to public health ethics focusing on 1–17):19–20.
the health of people. For example, if intrusive control mea- 7. Babcock SL, Pfieffer C. Laws and regulations concerning the confi-
sures, such as culling, are necessary, the requirement would dentiality of veterinarian-client communication. J Am Vet Med Assoc.
2006;229(3):365–369.
8. Babcock SL, Neihsl A. Requirements for mandatory reporting of animal
cruelty. J Am Vet Med Assoc. 2006;228(5):685–689.
9. American Medical Association. Principles of medical ethics. http://www.
ama-assn.org/ama/pub/category/2512.html. Accessed June 19, 2008.
BOX 2-3 THE “FIVE FREEDOMS” OF ANIMAL WELFARE
10. American Veterinary Medical Association. Principles of veterinary medi-
cal ethics of the AVMA. http://www.avma.org/issues/policy/ethics.asp.
Accessed June 19, 2008.
11. Webster AJ. Farm animal welfare: the five freedoms and the free market.
Vet J. 2001;161(3):229–237.
From Webster AJ: Farm animal welfare: the five freedoms and the free market, Vet J.
161(3):229-37, 2001.
Establishing a New
Approach to Clinical 3
Health History
Despite the growing sophistication of medical technologies 1. To identify possible zoonotic disease risks, thereby
for imaging and chemical diagnosis of disease states in both facilitating the diagnosis and prevention of disease
human and veterinary patients, the clinical history remains a transmission from animals to the patient.
critical part of medical decision making in human and ani- 2. To determine whether animals nearby could be a
mal health care. In an era when human health care provid- source of allergen exposure (see Chapter 7).
ers and veterinarians rarely visit the homes, neighborhoods, 3. To understand the patient’s psychosocial issues, including
and workplaces of their clients, the process of history tak- the emotional bond between a patient and one or more
ing remains the principal method of gathering information companion animals, the effect of animal care and feeding
about environmental factors that could be relevant to the on daily routines, and the warning signs of neglect or abuse
health status of the patient. of an animal. Animals may be more significant in a patient’s
Despite a growing realization of connections between life than other social support networks that are routinely
the health of human beings and other animals living in asked about in the social history (see Chapter 5).
close proximity, the idea of a human health care provider 4. Asking about the health of animals living nearby could
including in the evaluation of a patient any directed ques- provide information about toxic and infectious expo-
tions about the contact with companion and other animals sures in the environment as well as whether animal
may seem foreign to many clinicians. Animal exposures are medications are stored in the house and could pose a
often overlooked during medical evaluations. A study of pri- risk to human beings.
mary care physicians found that the majority of the time they
In addition, asking about animal contacts may increase
failed to take a history of animal exposures when evaluating
the rapport between clinician and patient, allow a better
patients with presumed infectious gastroenteritis and diar-
understanding of family relationships and health beliefs, and
rhea.1 Possible exposures to pet shops, exotic and domestic
provide additional information about the patient’s daily rou-
pets, farm animals/environments, and zoos and other wild-
tine and environment.
life centers, although apparently clinically relevant, were rou-
tinely omitted in the medical history. As a result, the study
authors concluded that a significant number of zoonotic dis- Animal Contact History as Part of the Acute
ease events are missed. As explained in Chapter 2, potential Care Visit
exists for both missed diagnoses2 and medicolegal liability in
During an acute care visit, time available for history taking
overlooking the importance of animal exposures when taking
can be limited and priority must be given to the most impor-
a medical history. For the veterinary clinician as well, there
tant medical information gathering. At the same time, failure
is some potential legal liability for overlooking a zoonotic or
to gather important information about animal contacts, espe-
other human-animal–related health risk.
cially if no baseline data exist in the chart, can increase the risk
This chapter outlines essential elements of human-animal
of missing important clues to the correct diagnosis and treat-
health concerns that should be (1) included in the clinical
ment of the acute condition. Therefore it may be appropriate
history taken by human health care providers and (2) asked
to ask several brief screening questions about animal contacts
of animal owners by veterinary health professionals.
as part of the history of a patient with an acute illness.
Some patients may be surprised by their health care pro-
vider asking questions about family pets or other animals. The
Animal health information in
health care provider can begin these questions with an explan-
the human medical history
atory statement, such as:
Human health care providers should routinely ask questions These days, we are discovering that several diseases may
about animal contacts as part of the medical history for four pass between people and pets or other animals. I’m going
major reasons: to ask you some routine questions about pets in the house
12
Chapter 3 n Establishing a New Approach to Clinical Health History 13
Table 3-1 n Screening and Follow-Up Questions Home Health Assessment of Companion Animals
and Human Health
for the Acute Care Visit
Screening and Follow-Up Questions About Animal Contacts
A home visit, such as during the delivery of visiting nurse
or other home health care services, provides an important
If the following screening Ask these follow-up opportunity to identify health risks and other issues relat-
questions are answered “yes,” questions: ing to pets in the house. As before, these include zoonotic,
allergic, psychosocial, and toxic risks. Figure 3-2 provides a
1. Do you have pets or other If yes, go to #2. form for home health care workers to complete as part of a
contact with animals? home health risk assessment. A key aspect of such an assess-
2. Are the pets or other animals Please describe specific signs ment is whether there is a “mismatch” between the patient
showing signs of illness? and any diagnoses and and animals in the house in terms of an animal that poses a
current treatment.
direct health risk to the patient or indicates that the patient
3. Do you think that your illness What exactly is your is becoming unable to care for and handle.
is related to your pet or other concern?
animals?
4. Do your animals need Do you know which
vaccinations or deworming to vaccinations are not up Human-animal contact information in
be up to date? to date? the veterinary history
5. Has your veterinarian Name and telephone
mentioned any human health number of veterinarian, For veterinary health care providers, the important
care concerns? exact concern mentioned, categories of human-animal contact information that
and recommended course should be included in the veterinary history are similar to
of action.
those for human health providers. If a known zoonotic dis-
ease is diagnosed in an animal with close human contact, the
veterinarian should inform the client of common human
and any other animal contacts that you may have, and symptoms of the disease and direct the animal owner to his
whether your pets have had any health problems. This or her physician if such symptoms have been noted in the
information can help me know whether there could be human beings sharing the animal’s environment or if any
any connection between the health of animals that you persons in the home are at increased risk for the disease.
live with and your health concerns. The veterinarian can stress preventive steps to reduce expo-
Table 3-1 lists screening and follow-up questions for the sure risks. Similarly, if the animal’s disease is likely from an
acute care visit. The general screening questions can be mod- environmental exposure, the veterinarian can recommend
ified for the particular situation, and examples of modified that persons in the household be screened and/or help elim-
screening questions appear throughout this book (see, for inate the household exposure. For the well-being of the pet
example, Chapter 10). If the response to any of the screening or other animal, it is also important for the veterinarian
questions is “yes,” additional follow-up questions are indi- to know information about human-animal bonding and
cated. Specific follow-up questions are mentioned in other potential for abuse and neglect.
sections of this book.
Baseline Human Health History for Veterinarians
Baseline Information for the Medical Chart Just as with the primary care medical visit and the animal
An important setting for incorporating animal health infor- health history, having baseline information in the veteri-
mation into the human health medical record is baseline nary medical chart regarding medical issues in persons liv-
medical information gathered for the patient’s inpatient or ing in proximity of a particular animal can be useful. Certain
outpatient chart. Because time is often limited for health care individuals, including infants, young children, and persons
professionals to take an extensive inventory of animal con- with impaired immune function, can be at increased risk of
tacts, one way to gather such information may be through a zoonotic diseases. Conversely, human beings with commu-
self-administered checklist completed by the patient (Figure 3-1). nicable diseases can pose a risk to nearby animals. Allergy in
This can be completed while other baseline medical infor- a human household member may be related to the presence
mation is being gathered and incorporated later into an elec- of an animal in the house. Smokers in the house may put
tronic or paper medical record. the animals at risk of health complications. Numerous other
In addition to asking about pets, the primary care assess- examples can be found throughout this book. However, any
ment of zoonotic and other animal contact disease risks discussion of which aspects of human health history can be
should include asking about wildlife and farm animal con- obtained by veterinarians and recorded in a veterinary medi-
tacts for both human beings and pets living with them. This cal record leads rapidly to a consideration of patient medical
type of questioning has particular importance if a person’s record privacy rules and regulations, in particular the Health
home is situated near wildlife habitat, on or near a farm, and/ Insurance Portability and Accountability Act (HIPAA) (see
or when pets living in the house are allowed to roam free Chapter 2). To date, the extent to which HIPAA applies to
outdoors where they might come in contact with wildlife or the veterinary health care setting is unclear because it was
livestock. written to focus on health care settings such as hospitals and
outpatient medical offices where patients are often covered
Baseline Animal Health History Checklist (to be completed by the patient)
Date: Name and telephone number of veterinarian:
Animal contacts:
Please list all the different pets that live in your home and indicate whether they have had any health problems.
In the past year,
has the pet been Currently taking
Type of pet (cat, Roams free treated for any medication? If
Approximate
dog, bird, rabbit, outside? infections or had so, please list
age (years)
reptile, etc.) (yes/no) any other health (prescription and
problems? If so, nonprescription).
please list.
1.
2.
3.
4.
5.
6.
Does your work involve contact with animals? Y N
If yes, please describe.
Do you frequently visit any of the following and have direct contact with animals (check all that apply)?
Farms where animals are kept Y N
Pet stores Y N
Petting zoos Y N
Animal markets Y N
Residential contact with wildlife:
Dwelling (check one): House Apartment Other
Size of property: acres
Property is: Urban Suburban Rural
Please note which of the following are within 100 yards of your house:
Lawn Woods Pond or other wetlands
Is property fenced? Y N
Have you noticed ticks around your yard? Y N
Do you have a bird feeder? Y N If yes, how far from your home?
Have you noticed mice or rats near your home? Y N
Figure 3-1 n Self-administered checklist for a patient’s animal contact history.

Please state which wildlife species can be found either on your property or in a half-mile vicinity:
Deer Coyotes Foxes Canada geese
Other (please specify):
Farm animals:
On property or immediate vicinity, please state whether the following exist, and how many:
Chickens Ducks Other poultry Horses Goats Sheep Domestic rabbits Pigs
Number:
Hunting and other wild game exposures:
Please check which of the following apply.
I or another household member regularly hunt for:
Deer Waterfowl Other gamebirds Rabbits Feral hogs
Such hunting involves:
Skinning carcasses without gloves or other protection Eating wild meat
Figure 3-1 n Cont’d
by health insurance. In such settings, HIPAA sets clear guide- to record the names and contact information of health care
lines for the protection of personal health information (PHI) providers, such as pediatrician, family physician, physician
that includes identifiable information about the health of assistant, nurse practitioner, obstetric health provider, and
individuals. Detailed information can be found at http:// so on. This information can be recorded in the chart in an
www.hhs.gov/ocr/hipaa/. For example, even if no names are anonymous manner as shown in Figure 3-3.
recorded in a written record at a veterinary office, noting that
a 29-year-old woman in the house has diabetes constitutes Health Assessment During the Sick Animal Visit
PHI because the person is potentially identifiable by address,
age, and gender. In general, therefore, it is best that the veteri- As with human health care, the acute care animal visit takes
narian not record confidential human medical information place in a time-limited environment, and any attempt to
in a veterinary medical record. gather information about the health of human beings in the
Figure 3-3 is an example of a human health questionnaire household must be streamlined. This can be accomplished
that can be completed by a client without revealing confi- by using screening questions listed in Table 3-2.
dential medical information about individuals. This base- More detailed screening and follow-up questions can
line information is potentially useful if the client agrees to be found in the sections of the book relating to particular
complete the form. For a single household, it may be useful conditions.
Animal Health Risk Assessment Form
1. Inventory of animals in the home:
# Cats # Dogs # Birds
Other pets (please specify):
Animals share living space with persons in house
Pets allowed to roam outside
2. Zoonotic risks: Is there evidence of a high-risk animal or high-risk situation for zoonotic disease transmission (such as
poor hygiene around puppies or kittens)? Check all that apply:
Exposure to animal feces
Pets share dishes with persons
High-risk animal (reptile, puppy or kitten, duckling, sick animal)
3. Allergic issues: Are there animals that could be causing allergy?
Visible accumulation of pet hair, dander, or feathers
4. Psychosocial: Significant bonding between patient and animals, or evidence of abuse or neglect?
Patient appears attached to particular animal (please specify):
Evidence of neglected or abused animals
5. Toxic issues: Are there veterinary medications unsecured that could be confused with human medications, or other
toxic exposures?
List veterinary medications in the home
6. Other mismatch between animal(s) and patient:
Patient increasingly unable to care for pets
Type of pet inappropriate for patient (example: dog too active or large, animal in need of great deal of care)
Figure 3-2 n Animal health risk assessment form for home health nurses and other home health care providers.
Human-Animal Disease Risk Survey
The following questions will help indicate whether people in your household are at increased risk of animal-related
disease. Please answer the following questions. All information will be kept confidential.
Type of pet or other animal:
Name of family health care provider and contact information:
Number of persons in the household:
Dwelling: House Apartment Other
In the household are there:
Any children under 5 years of age? Y N
Any people with immune problems or chronic health problems? Y N
Any woman who may be or is planning to become pregnant? Y N
Any smokers? Y N
Any person(s) with allergies to animals? Y N
If yes, list animals known to be source of allergy for person:
Would you like more information about pet-related health issues? Y N
If yes, please specify:
Figure 3-3 n Human health risk survey completed by animal owner to include in the veterinary chart.
Table 3-2 n Human Health Risk Screening References

Questions for the Sick Animal Visit 1. Warwick C. Gastrointestinal disorders: are health care professionals
missing zoonotic causes? J R Soc Health. 2004;124:137–142.
Screening and Follow-Up Questions About Health 2. Mohapatra PR, Janmeja AK, Kaur R. The answer you get depends on the
Problems in Pet Owners and Other Household Members question you ask. Am J Med. 2006;119(3):e19.
If the following screening Ask these follow-up

questions are answered“yes,” questions:
1. Are any persons in the If yes, go to #2.

household sick?
2. Has this animal had contact Please describe specific
with household members or types of contact, including
other people? frequency.
3. Do you have any concerns What exactly is your
about human health problems concern?
related to your animal’s illness?
4. Has your health care provider Name and telephone
mentioned any concerns number of health care
regarding the animals in the provider, exact concern
household? mentioned.
Sentinel Disease Signs
and Symptoms
4
Key Points for Clinicians and Public Health Signs of illness in animals that may be
Professionals relevant to human health
As mentioned in Chapter 3, in providing their medical his-

Public Health Professionals tories, human patients may spontaneously mention par-
ticular health problems that have developed in their pets
• Investigate human cases of zoonotic disease when ani- or other animals, perhaps thinking their own condition
mal zoonoses are reported. may be associated in some way with an ill animal. They
• Consider potential for biological or chemical threat. may also provide information about the health of their
animals in response to the directed questions listed in
Chapter 3. Although a human health care provider should
Human Health Clinicians not attempt to offer advice about veterinary treatment (see
Chapter 2), there are fundamental steps that he or she can
• Consider information about clinical disease in ani- take that may enhance the opportunities for early detec-
mals as potentially relevant to human disease (do not tion and prevention of human disease. In the case of the
diagnose disease in animals or discuss specific animal release of biological or chemical agents, either intentional
treatments). or accidental, it is possible that sudden animal mortality
• Report diseases of public health significance to local or or morbidity clusters could be an early warning sentinel
state public health authorities.* event that would need to be recognized and acted on as
• Consider contacting a veterinarian to coordinate dis soon as possible to reduce human health risks (see Chapter
ease control efforts. 13). The following section provides an overview of com-
mon clinical signs in animals, potential etiological agents,
clinical and public health implications, and the next steps
Veterinary Clinicians that human and animal health care providers should take
if they learn of such conditions.
• Pursue etiologic diagnosis of disease in animals for
appropriate treatment and determination of public
health risk.
• Provide pet owners information concerning public Types of Animal Diseases That May Be Important
health aspects of zoonoses and document this infor- to Human Health Care Providers
mation in the medical record (do not diagnose dis- In general, the human health consequences of a particu-
eases in human beings or discuss specific human lar animal illness fall into two main categories (Figure 4-1).
treatments). The first category is direct infection risk. The clinical sign is
• Report diseases of public health significance to local or related to an infectious agent that could pass from the ani-
state public health authorities. mal to the person, with the animal serving as a source for the
zoonotic infection risk. An example may be the direct infec-
tion of a person tending a calf with cryptosporidial diarrhea
after fecal material splashes directly into the person’s mouth.
The second is as an environmental sentinel event. The clinical
*Each state has a listing of reportable conditions. Contact your state epidemi- signs of the animal disease provide an indication of an envi-
ologist for more information; http://www.cste.org/dnn/StateEpidemiologists/ ronmental hazard, either infectious or toxic, to which human
tabid/80/Default.aspx. beings may also be exposed. For example, identification of
18
Chapter 4 n Sentinel Disease Signs and Symptoms 19
Examine person for

sign of infection, review
hygiene practices,
notify health department
Zoonosis risk (who will determine the
Clinical sign in animal; need for further investigation)
refer animal for
veterinary care if Human health risk
not already done Sentinel event for Check person for
environmental corollary disease, discuss
health risk environmental interventions,
(including notify health department
psychosocial) (who will determine the
need for further investigation)
Figure 4-1 n Relationship between clinical signs in animals and human health risks.
Rocky Mountain spotted fever in dogs has led to the discov- on reported signs, but reports of certain symptom complexes
ery and treatment of disease in a human patient.1 Similarly, a in human beings should trigger steps, such as advising the
dog that becomes ill after ingesting toxic berries on an orna- client to contact a human health care provider for follow-
mental plant signals a potential danger for children who up, as well as possibly affect the type of animal health care
could inadvertently ingest the berries. Elevated blood lead required.
levels in pets are an indicator of lead exposure risk in chil-
dren living nearby.
Types of Human Disease Symptoms That May Be
Important to Veterinarians
Specific Signs in Animals and Appropriate
Follow-up Steps for Human Health Professionals Table 4-2 includes human diseases for which a veterinarian
may take appropriate action. The relevance to animal health
Table 4-1 includes selected animal disease conditions for professionals of a particular disease or symptom in human
which a heightened index of suspicion for human disease risk beings can be classified into several categories:
is warranted, potential etiological agents and public health
implications, and next steps for the human health care pro- • Zoonotic disease acquired from an animal. This may neces-
vider in protecting public health. A diagnosis in the animal sitate referral of a person to a health care provider, eval-
should be pursued and human case findings similarly inves- uation of suspect animal(s), and a review of hygienic
tigated while considering a common source of exposure. and biosafety practices and other preventive measures.
Immunocompromised persons (e.g., from chemother-
apy, chronic debilitation) are at increased risk of severe
Human disease symptoms that may be complications from a zoonotic disease, and there is conse-
relevant for animal health quently a need for increased vigilance to prevent zoonotic
transmission from a pet-related infection such as diag-
Just as animals can serve as sentinels of human health risk, nosing and treating any animal infections and reviewing
it is conceivable that disease symptoms in the owner of an infection hygienic practices.
animal being treated or in human beings in the community • Reverse zoonoses (disease passing from the human to the ani-
could have important ramifications for veterinarians and mal). This could require screening the animal for infection
animal health. It is possible that clients will spontaneously as well as ensuring that the human being receives appro-
volunteer information about a medical condition they or priate treatment and review of infection control practices
household members are experiencing, and they may provide and prevention measures.
information in response to the directed questions listed in • Potential environmental sentinel event. Signaling a risk of
Chapter 3. Veterinarians should not provide medical advice biological, chemical, or physical hazards in the environment
or otherwise attempt to diagnose disease in a person based to which animals or other people may also be exposed and
Table 4-1 n Clinical Signs in Animals That Patients May Report and Possible Human Health Care
Provider Responses
Possible Causes (Differential
Diagnosis) With Human Health Appropriate Actions for Human
Sign in Animal Animal Species Implications Health Care Providers*
Diarrhea Dogs, cats, livestock Bacterial: Campylobacter,

Escherichia coli, Salmonella, Counsel about hygiene with excretions,
Yersinia avoid close contact; hand hygiene;
consider common food source (see
Parasitic: Ancylostoma, Chapter 11)
Cryptosporidium, Giardia
Toxic: Pesticides, human Ensure children are not at risk for ingesting
medications toxins
Vomiting Dogs, cats Lead poisoning, ingestion of Check lead level and report to public
toxic substances such as human health department if elevated; provide
medications or poisonous plants guidance for identification and removal of
substances that can put children at risk
Upper respiratory signs Cats Chlamydophila felis, SARS
(coughing, nasal or sinus (Coronavirus), Francisella Counsel about hygiene with secretions,
congestion, sneezing) tularensis, Yersinia pestis avoid close contact; hand hygiene; ask
Ferrets, chickens/ducks Influenza about respiratory symptoms in human
beings; consider increased zoonotic
Birds Chlamydophila potential in immunocompromised persons
Dogs Bordetella
Labored breathing, wheezing Cats, dogs, horses, Environmental sentinel (not well Ask about respiratory problems in human
cattle documented): environmental beings sharing living space; eliminate
allergens, irritants possible irritants from the household or
barn; eliminate indoor tobacco smoke
Nonhealing wounds Dogs, cats Methicillin-resistant Staphylococcus Zoonotic and reverse zoonotic risks; hand
aureus, mycobacteriosis hygiene; disinfection of or exposure
reduction to contaminated environment
Hemorrhage Dogs, cats Toxin: coumarin derivatives, Ensure children are not at risk of ingesting
arsenic, lead, zinc rodent poison or heavy metals
Infection: Leptospira Consider zoonotic risks
Trauma Consider risk of violence
Neuropathology (ataxia, Cats, raccoons, skunks, Rabies
somnolence) bats, foxes, coyotes,
dogs, bobcats
Cattle BSE
Evaluate possible human exposures;
Horses Equine encephalitis
contact public health officials
Dogs, cats, birds Carbon monoxide, lead
Dogs, cats, cattle, Cyanobacteria (in stagnant fresh
horses, sheep, pigs, water)
rabbits, geese
Skin rashes, crusting Dogs, cats, rodent Dermatophytes (Figure 4-2), Ask about lesions in human contacts, contact
pets, hedgehogs, Leishmania, allergies veterinarian for coordinated household
horses treatment; counsel about handwashing
and other methods of transmission risk
Sudden death Pet birds Teflon fumes
Wild birds West Nile virus Eliminate exposure, immediately assess risk
to human beings; ask about breathing
Cattle, sheep, goats Bacillus anthracis problems in human beings; contact
Horses Venezuelan equine encephalitis public health officials
virus
Neoplasia (weight loss, Dogs Indoor air carcinogens (sinonasal Consider obtaining an environmental
weakness, fatigue) cancer), asbestos (mesothelioma), assessment, screening for disease in
pesticides (lymphomas) human beings
Fetal losses Cattle, goats, sheep, Brucella, Coxiella Assess associated disease symptoms in
dogs human beings
Signs of trauma, neglect, or Dogs, cats, other Domestic violence, family Screen for domestic violence or other
abnormal behavior animals dysfunction, neglect psychosocial problems
*These actions should also include recommending that patients consult their veterinarians.
BSE, Bovine spongiform encephalopathy; SARS, severe acute respiratory syndrome.
Table 4-2 n Human Disease Signs and Symptoms and Appropriate Actions for Veterinarians
Human Symptom or Sign Reported by Client Possible Causes (Differential Steps for Veterinary Professionals to
or Other Human Beings in Household Diagnosis) Consider*
Diarrhea Bacterial: Salmonella, Campylobacter, Request examination and treatment

Yersinia, Giardia of animals with clinical signs; review
biosafety practices (hand hygiene);
consider food safety issues
Vomiting Staphylococcal food poisoning Inquire about any shared food, vomiting
in animals
Upper respiratory symptoms (nasal Influenza If in risk area for zoonotic influenza, ensure
congestion, sore throat) human being is receiving care, look for
evidence of infection in animals; may be
a reverse zoonosis for pet ferrets
Hypersensitivity reaction: air quality, Ask about indoor air quality and other
brevitoxins, animal allergy, pneumonitis environmental conditions; consider
consulting health department; evaluate
signs in animals; consider allergy to
pet and methods to reduce allergens;
eliminate tobacco smoke
Acute lower respiratory tract symptoms Chlamydophila, Francisella, Yersinia pestis, Review zoonotic disease risks
(cough, shortness of breath, fever) Hantavirus
Chronic lower respiratory tract Mycobacterium tuberculosis Ensure person is receiving follow-up and is
symptoms (chronic cough, weight loss) aware of reverse zoonosis risk
Nonhealing wound Methicillin-resistant Staphylococcus aureus Consider culture of companion animals
Mycobacteriosis if this is a recurring issue in the person
and other household members have had
cultures
Consider a common source of exposure for
companion animal
Hematochezia, hemoptysis Poisoning with coumarin derivatives Consider whether companion animals
could have ingested poison as well
Skin rash Rocky Mountain spotted fever Ectoparasite and endoparasite control and
Excoriations (maculopapular [Figure 4-4]), Borrelia prevention; counsel about zoonotic risks;
Serpiginous rash, especially on feet burgdorferi (ECM rash [Figure 4-5]), examine animal; consider presumptive
Papules dermatophytes treatment
Eschar Ectoparasites (scabies, other mites)
Cutaneous larva migrans
Flea (Figure 4-6), ant/mosquito bites
Anthrax (Figure 4-7)
Trauma (broken bones, bruises, bruises Accidents, domestic violence Look for signs of physical or behavioral
in unusual places or not consistent Psychosocial dysfunction in household trauma in pet or signs of neglect; referral
with history of trauma) for social services
Behavior problems in children or adults
Pregnancy Agents that could complicate pregnancy Review hygiene/biosafety practices,
(Toxoplasma, Salmonella, Coxiella, particularly of food preparation and
Listeria) avoidance of handling animal waste, and
appropriate pet selection
Weight loss, weakness, fatigue Cancer, HIV, other immunosuppression Review hygiene/biosafety; ensure pets are
adequately treated for infection
Arthritis Borrelia burgdorferi Tick control for pets, environment around
house
*In all cases, recommend that the client consult a human health care provider.
HIV, Human immunodeficiency virus; ECM, erythema chronicum migrans.
Figure 4-2 n A guinea pig with a crusted area on the dorsal pinna consistent with dermatophytosis. A Trichophyton organism was cultured from the site. (From Mitchell M,
Tully TN Jr: Manual of exotic pet practice, St Louis, 2008, Saunders Elsevier.)
Diagnose and treat animal,

review biosafety practices
(hand hygiene, etc.)
Zoonosis
Human being with Examine animal for
disease symptoms;
Reverse zoonosis Animal health sign of infection, review
refer to health care infection control
provider if not
already done
Sentinel event for
environmental Check animal for
health risk corollary disease, discuss
(including environmental interventions,
psychosocial) notify the health department
or proper authority
Figure 4-3 n Human disease symptoms, according to animal health ramifications.
Figure 4-4 n Child’s right hand and wrist displaying the characteristic
spotted rash of Rocky Mountain spotted fever. (From Centers for Disease Figure 4-5 n Lyme disease rash. (From Cohen J, Powderly WG: Infectious
Control and Prevention Public Health Image Library, Atlanta, Ga.) diseases, ed 2, Philadelphia, 2003, Mosby.)
Figure 4-7 n Cutaneous anthrax on an employee of a goat-hair processing

mill spinning department. (From Centers for Disease Control and Prevention
Public Health Image Library Atlanta, Ga.)
Figure 4-6 n Flea bites in human. (From Habif TP: Clinical dermatol-
ogy: a color guide to diagnosis and therapy, ed 4, St Louis, 2003, Mosby.)
at risk. This should initiate a search for the environmental Reference

hazard, examination of the animal(s) to see whether corol-
1. Paddock CD, Brenner O, Vaid C, et al. Short report: concurrent Rocky
lary disease is present, notification of the health department Mountain spotted fever in a dog and its owner. Am J Trop Med Hyg.
and/or state veterinarian’s office, if indicated, and con- 2002;66(2):197–199.
sideration of ways to reduce the environmental risk. This
category includes allergic disease, neglect, and domestic vio-
lence. These possibilities are summarized in Figure 4-3.
Psychosocial and
Therapeutic Aspects 5
of Human-Animal
Interaction
Rebecca A. Johnson
People derive physiological and psychological benefits from

interactions with animals. Animals can play a therapeu-
tic and health-promoting role in a wide variety of human • Encourage routine animal wellness examinations and
health conditions and in settings ranging from the com- zoonotic disease screening for animals used in thera-
munity to primary, inpatient, and long-term health care. peutic settings.
Human and veterinary health care providers need to be • Become familiar with the American Veterinary Medical
aware of the potential health benefits of human-animal Association (AVMA) Guidelines for Animal-Assisted
interaction (HAI) and the important role that the human- Activity, Animal-Assisted Therapy and Resident Animal
animal bond may play in the health status of patients. This Programs.1
chapter outlines some of the therapeutic uses of animals • Provide training to veterinary staff in the provision of
and other psychosocial issues related to the human-animal pet loss support services.
bond (Figure 5-1). • Report animal abuse to appropriate authorities and
consider signs of abuse in pets as a possible warning of
Key Points for Clinicians and Public Health domestic violence risk to human beings in the house-
Professionals hold (see also Chapter 2).
• Keep current on zoonoses prevention, such as for
• Educate human health and veterinary clinicians about methicillin-resistant Staphylococcus aureus (MRSA)
ways to maximize public health benefits of HAI. (e.g., http://www.avma. org/reference/backgrounders/
• Support policies that encourage appropriate infec- mrsa_bgnd.pdf).
tion control and other safeguards for animal assisted-
therapy and other forms of HAI.
• Support developed environment enhancements that Human-animal interaction:
encourage physical activity for people and compan- Animal-assisted activity, animal-assisted
ion animals (e.g., parks, sidewalks, landscaping, traffic therapy, and service dogs defined
calming).
Human-animal interaction (HAI) is the term used to encom-
Human Health Clinicians pass the human-animal bonds developing from pet owner-
ship, uses of animals for recreation (such as horseback riding),
• Be aware of indications and precautions for the animal husbandry, and therapeutic settings. Perhaps the first
therapeutic use of animal-assisted activity (AAA), therapeutic use of animals was Florence Nightingale’s intro-
animal-assisted therapy (AAT), and pet ownership for duction of birds as distractions for hospital patients in the
patients. mid-1800s. The practice of facilitating HAI for therapeutic
• Coordinate AAA, AAT, and pet ownership referrals purposes has expanded in recent years, in advance of consis-
with social workers, physical or occupational thera- tent research-based evidence supporting the health benefits
pists, and veterinarians. of HAI. Today, HAI is used in countless clinical settings and
• Ensure that animals used in therapy have been is generally believed to improve patient outcomes.
screened by veterinarians and are used by certified Animal-assisted activity (AAA) refers to relatively brief visits
AAT professionals. (usually lasting up to 1 hour) occurring in a variety of settings in
• Consider human-animal bond issues when dealing which people talk to, pet, groom, offer treats to, and/or play with
with acute illness or disaster response involving sepa- companion animals with the animal’s human handler present.
ration of patients from pets. Animal-assisted therapy (AAT) refers to structured encoun-
• Consider the psychological impact of the death or loss ters in which the animal with its handler becomes part of a
of a pet on the owner and family. treatment plan for a particular patient. In this instance, the
24
Chapter 5 n Psychosocial and Therapeutic Aspects of Human-Animal Interaction 25
BOX 5-1 USES OF AAA, AAT, AND SERVICE DOGS
Current Uses of AAA

Social interaction
• Instructional purposes in school classrooms
• Social purposes in nursing homes, retirement facilities,
hospitals, prisons
• Instructional purposes with social and service organizations
Companionship purposes with shut-ins
Current Uses of AAT
Rehabilitation
• Cerebrovascular accident or traumatic brain injury
• Behavioral and other psychotherapy contexts, including
depression
• Child abuse
• Autism spectrum disorder
Figure 5-1 n A child interacting with her dog. (From Centers for Disease Current Uses of Service Dogs
Control and Prevention: Healthy pets, healthy people: infants and young chil-
dren. http://www.cdc.gov/healthypets/child.htm.) Leading a person who has a visual impairment around obstacles
to destinations (e.g., seating, across street, to/through door, to/into
elevator)
patient may walk with, reach out to, groom, or engage in vari- Sound discrimination to alert a person with a hearing impair-
ous games with the animal, with all such activities designed ment to the presence of specific sounds, such as the following:
to address particular functional deficits in the person. These • Smoke/fire/clock alarms
activities may be included as goals in the patient’s plan of • Telephone
care. Thus the animal becomes an instrument through which • Baby crying
a patient’s progress may be measured (e.g., a patient goal may • Sirens
be to daily increase the number of strokes brushing the dog • Another person
using an impaired hand or arm). The most common situa- • Timers buzzing
tions in which AAT is used are in cerebrovascular accident or • Knocks at door
• Unusual sounds (things that go bump in the night, mice in
traumatic brain injury rehabilitation or in various behavioral
the cabinet, etc.)
and other psychotherapy contexts, such as with depressed
General Assistance, Including
• Mobility (helping person balance for transfer/ambulation,
pulling wheelchair, helping person rise from sitting or fallen
position)
• Retrieval (getting items that are dropped or otherwise out
of reach, carrying items by mouth)
• Miscellaneous (e.g., open/close doors and drawers, help
person undress/dress, carry items in backpack, act as
physical buffer to jostling by others, put clothes in washer/
remove from dryer, bark to alert for help)
Sense and alert owners to oncoming seizures. It is currently
unknown why or how some dogs are able to do this, but a number of
dogs have demonstrated the ability to warn their owners of oncoming
seizures, enabling the owners to position themselves safely.
From the Delta Society, Bellevue, Wa.
adults, children who have been abused, or those with autism

spectrum disorder.
As Box 5-1 demonstrates, service dogs (Figure 5-2) are
currently used in long-term patient-animal relationships
for a variety of health care settings, both in institutional and
home-based care.
Health benefits of human-animal

interaction
Figure 5-2 n Service dog with a visually impaired person. (From

Research into the health benefits of HAI began in the late
Centers for Disease Control and Prevention Public Health Image Library, 1970s with a study of nursing staff perceptions of psychoso-
Atlanta, Ga.) cial benefits of older adults interacting with a cat mascot in
long-term care.2 Subsequently, despite a growing number and

Table 5-1 n Research Evidence Showing
wide range of studies that have been conducted with varying
populations, there remain methodological issues associated Physiological Benefits of HAI
with small samples, nonexperimental designs, nonrandom- Pet Ownership
ized treatment groups, and the influence of confounding Benefit Population (O), AAA, or AAT
variables.3
One problem commonly seen in literature discussing Decreased cortisol Adults with own O
benefits of HAI is the assumption that similar health effects levels or unfamiliar pet
are found in pet ownership (or with service animals) and Decreased blood Adults O, AAA
more casual pet interaction contexts, such as AAA or AAT. pressure and heart
It is important to identify the distinction and to clarify these rate/cardiovascular
reactivity
terms because pet/service animal ownership implies a longer,
more committed relationship than what can be relatively Increased Adults O, AAA
brief encounters in other pet interactions. In many cultures, parasympathetic
nervous system
companion animals are viewed as family members, occu- activity
pying homes, sleeping on human beings’ beds, and sharing
Increased Adults with own O, AAA
food and recreational activities—they are treated almost as phenylethylamine, or unfamiliar
children.4,5 The distinction is made between this long-term prolactin, oxytocin, pet
relationship and more casual encounters in which people serotonin
interact with companion animals in public or in therapeu- Decreased pain, Adults AAA
tic contexts, such as schools, clinics, or a range of health care analgesia use, anxiety,
facilities (AAA and AAT). and epinephrine levels
Several physiological benefits of HAI have been found Decreased cholesterol Adults O
in AAA, AAT, and pet ownership contexts (Table 5-1). and triglyceride levels
The strong bond that human beings can develop with ani- Better 1-year survival Adults O
mals may stem from an innate human affinity with nature, after myocardial
including animals (termed biophilia, the love of living infarction
things6), predicated on the dependence of human beings on Buffered blood pressure Adults O
animals for food throughout history.7 This natural tendency response to stress in
may help to provide an understanding of some of the effects hypertensive patients
of HAI. treated with lisinopril
Fewer patient-initiated Elderly O
physician visits
AAA and AAT: Psychological and Psychosocial
Improved self-perceived Elderly O
Effects health
Clinical evidence indicates that even in therapeutic settings, Increased physical Adults and O, AAA
in relatively short encounters with varying degrees of fre- activity levels and elderly
quency, an intense attachment can rapidly develop between weight loss with dog
walking
people and pets. In a laboratory setting serum cortisol levels
were found to decrease when people interacted quietly with Increased longevity Elderly O
a dog.9 During this interaction, additional beneficial changes Increased food intake Elderly AAA
in neurohormones were found (phenylethylamine, prolac- (with aquarium
tin, oxytocin, dopamine, and endorphin levels increased sig- watching)
nificantly), as was a significant decrease in blood pressure. A Decreased muscle Children with AAA, AAT
parallel result was found in the dogs during the interaction, spasticity cerebral palsy
suggesting that they also benefited. Similarly, investigators
found significantly smaller increases in blood pressure and
heart rate when a dog was present during challenging math- In clinical settings, hospitalized patients reported less pain
ematical tasks than when either a friend or an investigator and used fewer analgesics during and after an animal visit,13
was present.10 and patients with heart failure had decreased anxiety and epi-
In a therapeutic horsemanship context, a relaxation nephrine levels during and after an animal visit.14 For older
response was observed in children with spastic cerebral adults with dementia in long-term care settings, watching fish
palsy who experienced 8 minutes of riding. Electromyogram swim in an aquarium at mealtimes was associated with lon-
readings showed improved symmetry in muscle activity ger periods sitting to eat and greater nutritional intake (Figure
both during and for some time after the riding episodes.11 5-3).15 Newly admitted nursing home residents exposed to
Improved walking and muscle coordination also has been a series of dog visits were found to have lower cortisol levels
found in disabled children after therapeutic horseback rid- than those who had human visitors.16
ing.12 Generally, children have been an understudied pop- Among community-dwelling older adults, walking with
ulation in the HAI literature. Preliminary findings seem a “loaner” dog was associated with significantly greater
promising but additional data are needed to clarify the most parasympathetic nervous system activity (high-frequency
beneficial contexts for AAT and AAT in children. heart rate variability) than walking without a dog.17 When
Table 5-2 n Psychosocial Benefits of HAI
Pet Ownership
Benefit Population (O), AAA, or AAT
Decreased Elderly, patients O, AAA, AAT

depression with AIDS
Decreased anxiety Adults and patients O, AAA, AAT
with psychiatric
disorders
Decreased loneliness Adults, elderly O
Improved morale Elderly O
Fun, relaxation Elderly O
Unconditional love Elderly, cancer O
and support patients
Pets perceived as Adults O
Figure 5-3 n Watching fish swim in an aquarium has a relaxing effect family members
on human beings. (From Mitchell M, Tully TN Jr: Manual of exotic pet prac- Improved “prosocial” Elderly AAA, AAT
tice, St Louis, 2008, Saunders Elsevier. Photo courtesy Trevor Zachariah.) behaviors in nursing
home
participants interacted quietly with the dog while it visited Increased social Adults O, AAA, AAT
them in their own home, this activity increased by 1.87 times interaction (pets
as catalysts)
over their levels while at home without the dog. In overweight
residents of public housing, an adherence rate of 72% and Increased interaction Adults AAA
between staff and
average weight loss of 14 pounds in a “loaner” dog-walk- nursing home
ing program was demonstrated because the participants residents
believed that “the dogs need us to walk them.” Participants
Facilitators of Children O
in a community shelter dog-walking program were moti- attachment
vated to increase their exercise outside the walking program.
Investigators found a significant increase in exercise and phys- AIDS, Acquired immunodeficiency syndrome.
ical activity stage of change (participants went from vigorous
exercise less than three times per week or moderate exercise
less than five times per week to 30 minutes a day of moderate Among children with autism spectrum disorder, investi-
exercise five or more days per week for 1 to 5 months).18 gators found that children were more attentive to and likely
A variety of psychosocial benefits have been reported by to respond appropriately in therapy sessions involving a live
investigators studying outcomes of AAA and AAT (Table dog than with either a stuffed toy dog or a ball.29 Given the dif-
5-2).19 These benefits include increased social contact, ficulty of children with autism attending to faces, one fruitful
reduced loneliness and depression in hospitalized patients area of inquiry in this topic might be to investigate the extent
and homeless persons,20,21 and decreased anxiety in psy- to which an animal face is more likely than a human face to
chiatric patients.22 The most commonly studied context is receive the children’s attention.
long-term care. For example, one study found nursing home Generally, clinical evidence supports that people receiving
residents’ prosocial behavior (e.g., smiles, looks, leaning in, AAA or AAT benefit from the following:
and touching) toward the animal and toward others ben-
• Distraction from their own circumstances by interact-
efited from the presence of a visitor dog or a resident dog.23
ing with the pet
Nursing home staff interacted more and in more positive
• Feelings of being accepted by the animal
ways with each other and with residents when a dog was
• Feeling happy, less lonely, and more included
present. However, another study found that nursing home
• Having something pleasant to look forward to in antici-
residents enjoyed a visit from a “happy” human visitor as
pating subsequent visits by the animal and its handler
much as one from a dog and its handler.24 Similarly, in a
small study, investigators found that human visits were as Pet owners experiencing AAA commonly engage in remi-
favorable as dog/handler visits on nursing home residents’ niscence about a previous pet or in comparison with a current
daily hassles, daily uplifts, mood, and social support.25 pet. Stimulation of this activity may be beneficial in itself and
Patients with cancer showed no significant differences in could benefit from scientific scrutiny.
mood and social support when they received a series of dog/
handler visits, human visits, or participated in quiet read- Pet Ownership: Physiological and Psychosocial
ing.26 Interaction with animals in AAA has been associated Effects
with prosocial behaviors and decreased agitation among
older adults with dementia.27,28 Clinical evidence has shown It may seem commonsense that the mutual attachment
that they are more likely to verbalize (even appropriately) in between a pet and its human family would be stronger and
response to visiting with an animal. thus more powerful in promoting beneficial outcomes
than in short-term interactions common in AAA and Older pet owners have been found to function better in
AAT. Research has shown significant benefits in several activities of daily living than nonowners when studied over a
parameters indicative of health. Early research findings 1-year period46 and to have fewer patient-initiated physician
showed lowering of blood pressure and a relaxation appointments than non–pet owners, irrespective of the num-
response when people interacted with pets.30-32 For ber and type of stressful life events they experienced during
example, physiological arousal decreased in response to the study period.47
the presence of one’s dog even while the human being Pet attachment was related to decreased depression (par-
was engaged in a stressful situation such as completing ticularly in older adult pet owners,48 people with acquired
a difficult mathematical task.33 Beneficial responses in immunodeficiency syndrome [AIDS]49) and in another study
neurohormonal changes were similar in direction (and to improved morale. When people have a positive affect and
even stronger) when people interacted with their own morale, they are more likely to engage with others socially, to
dogs.9 Other investigators found pet ownership associ- participate in recreational activities, and to avoid sedentary,
ated with lower triglyceride and cholesterol levels, par- isolated situations.50 This mind-body connection has been
ticularly among women.34 The 1-year survival rate was well established in research and can be a factor in maintain-
positively associated with dog ownership among patients ing older adults’ health and thus preventing or minimizing
discharged from a coronary care unit irrespective of age, disability.
severity of illness, or comorbid conditions.35 Data on 4435 Pets have been extensively written about as sources of
adults showed that the relative risk of death from heart unconditional love and support51 and facilitators of attach-
attack was 40% higher for those who had never owned a ment in children52 and were viewed as fun, dependent, and
cat.36 The findings may have significant implications for relaxing.53 Other authors reported on the multiple health
health care expenditures. Older adult pet owners were benefits of pet ownership, many of which involved less-
found to have fewer patient-initiated physician visits and ened anxiety, depression, and social isolation and increased
better health. Pet owners were healthier and made fewer physical activity.54 Dogs were found to be catalysts for social
physician visits, accounting for an estimated savings of interactions (Figure 5-4).55 People walking their dogs in a
$988 million in health care expenditures in Australia over park had significantly more chance conversations with other
a 1-year period.37 The finding was similar in an analy- park users than when they walked the same route alone.56
sis of German data, in which people who continuously A person’s perceived likeability by others was increased by
owned pets were found to be the healthiest and to have the presence of a dog.57 These findings were extended more
15% fewer physician visits.38 The investigators controlled recently when investigators in Australia identified that pet
for previous health and a wide range of other potentially owners scored higher than non–pet owners on social cap-
confounding variables to address directional causality or ital (defined as social engagement, social reciprocity or
the criticism of HAI research that healthier people are doing favors for each other, trusting others, a sense of com-
more likely to acquire pets. munity, and civic engagement). The findings are relevant
Older adult pet owners walked longer and had lower for health care professionals advising clients about how
triglyceride and cholesterol levels than non–pet owners.39 to become more physically and socially active because pet
Commitment to dogs involves exercising them and thus owners indicated that they had met and had varying lev-
may lead to healthier physical activity patterns. Dog walk- els of interaction with other pet owners, but also that they
ing may be one factor motivating increased physical activity.
In Australia, dog owners walked 18 minutes per week more
than non–dog owners and were more likely to meet physi-
cal activity recommendations of 150 min/wk.40 A study in
the United Kingdom found that dog owners accumulated
significantly more exercise than either cat owners or adults
without pets.41 Findings from the National Household
Travel Survey in the United States revealed that nearly half
of adults who walked dogs in 2001 accumulated at least 30
minutes of walking in bouts of at least 10 minutes daily.42 An
intervention trial in the United States found that obese pet
owners increased their moderate physical activity over that
of non–pet owners and that the majority of this increase
resulted from dog-related activities. The study concluded
that companion dogs can serve as social support for weight
loss and 1-year weight maintenance.43 These patterns may
differ across ethnic groups, which is a topic that has received
little study. For example, although Latino elders expressed
a very strong bond with their pet dogs, they did not nec-
essarily exercise with them.44 The implications for main-
taining function among older adults who exercise with pets Figure 5-4 n A puppy party can combine an open house with an enter-
taining and informative session about puppy socialization, play, and training.
are being tested.45 Dog walking may have a role in prevent- The trainer demonstrates the power of positive reinforcement at a puppy party
ing disability and functionally limiting effects of chronic at the Doncaster Animal Clinic. (From Landsberg GM: Handbook of behavior
illnesses. problems of the dog and cat, ed 2, Oxford, 2008, Saunders Elsevier.)
Chapter 5 Psychosocial and Therapeutic Aspects of Human-Animal Interaction
n 29
had met others because of their dogs. Pet owners were 57% AAA or AAT to identify the proper mechanism for this in
more likely to engage in volunteer work, school-related their own institution. If no existing AAA or AAT program
activities, or sports and recreational clubs and activities operates in the facility, referral can result in an affiliation of
than were non–pet owners. Pet ownership was significantly the facility with the nearest animal visitation group. There
and positively related to reciprocity (giving and receiv- are many such groups throughout North America. If health
ing favors from others). Pet owners attributed feeling safe care professionals in the facility are interested in starting
in their homes and when out walking their dogs. Further, an AAA/AAT program by affiliating with an animal visita-
sense of community was significantly higher in pet owners, tion group, the resources identified in this chapter provide
who reported it less difficult than non–pet owners to gen- a starting point for developing policies and procedures to
erally get to know others.58 Similar findings held in disabled guide such a program.
persons accompanied by a service dog; the dog was found As a discipline, the field of social work has a grow-
to facilitate social interaction.59-61 ing affiliation with AAA/AAT groups and facilitating the
human-animal bond and education of veterinary medical
students about the bond through their practice in teaching
Facilitating Human-Animal Interaction hospitals of veterinary medicine. For example, the Denver
University Graduate School of Social Work offers an ani-
Referral for AAA or AAT mal-assisted intervention certification program preparing
social workers to use animals in their practice. The pro-
Applying the extant research and clinical evidence on ben- gram is sought by students seeking a master’s degree in
eficial effects of HAI, it is possible to make some guarded social work and by those seeking a post-master’s certifica-
recommendations for facilitating AAA and AAT with par- tion or doctorate.
ticular patient populations and situations (Table 5-3).
Patients may benefit from AAA if they are experiencing
anxiety-inducing disease states or treatment protocols, Medical Recommendations for Pet Ownership
such as patients with cancer undergoing chemotherapy or All human health histories should include questions about
radiation treatments. In this population, AAA may pro- patients’ pets given the beneficial findings about pet own-
vide support and distraction.41 In populations needing ership and health as well as the possible health risks (see
companionship, AAA or pet ownership may be benefi- Chapter 3). Care must be taken when health care profes-
cial to increase social interaction and decrease loneliness, sionals recommend pet ownership to patients. In particu-
anxiety, and depression.26 In obese patients, AAA or pet lar, it is important to ascertain to what extent the patient
ownership can provide motivation for increasing physi- is physically and cognitively able or has sufficient sup-
cal activity.18,59 port systems (e.g., home helpers or family) to enable the
However, AAA or AAT may not be appropriate for various proper care of the animal. When a patient’s disability is sig-
patient populations, or special precautions may need to be nificant and support is minimal, a dog, cat, or bird may
taken. In particular, if a patient is significantly immunocom- not be an appropriate recommendation; a self-cleaning
promised, introduction of animals may not be appropriate aquarium may be a better option. Similarly, the costs of
or special precautions may be needed. providing proper veterinary care, feeding, grooming, and
The most common way to make a referral for AAA or AAT training must be considered. To date, little financial assis-
is through a social worker or department of social work. In tance is available for low-income pet owners to offset the
some inpatient facilities, the department of physical or occu- costs of keeping pets. Clinical evidence of pet owners with-
pational therapy may be the correct conduit through which holding food themselves to provide care for their pet has
to prescribe AAA or AAT. It is incumbent on health care pro- been reported. Finally, during impending hurricanes, some
fessionals who are in a position to recommend or prescribe pet owners have elected to stay in harm’s way rather than
leave their pets when no pet-friendly shelter options were
available.
Physical and cognitive disability must be considered
Table 5-3 n Guidelines for Recommending AAA, in recommending pet ownership. When patients are
AAT, or Pet Ownership immunocompromised, certain pets—such as reptiles—
are off-limits due to the risk of Salmonella infection (see
Clinical Indication AAA, AAT, or Pet Ownership (O)*
Chapters 9 and 10). However, when precautions are taken,
Anxiety-inducing disease AAA and/or O (cat, bird, dog, such as keeping cats indoors, good handwashing after
states or treatment or self-contained aquarium if handling pets, wearing gloves when cleaning cat litter
protocols for distraction dementia is present) boxes, and regular screening of the cat or dog for patho-
Settings or populations AAA and/or O (cat, bird, or dog) gens by a licensed veterinarian, risk of infection may be
needing social interaction minimized.62
(animals to facilitate) When a patient needs increased physical activity, exercising
Situations where AAA and/or O (cat, bird, or dog) a dog may be recommended with or without recommending
companionship is needed pet ownership. If pet ownership is desirable, breed recom-
Obesity/sedentary lifestyle AAA and/or O (dog) mendations must be made carefully. It may seem intuitive
to recommend a breed requiring considerable exercise or of
*If patient is physically able to care for a pet. great athleticism. However, matching the breed characteristics
with the expectations of the prospective owner may be a e xposure to a variety of breeds and possibly can learn what
more effective approach than trying to make the animal fit breed might be preferred. Second, the person can begin a reg-
the maximum therapeutic level of physical activity desired. imen of increased physical activity gradually without putting
Most reputable animal shelters have surveys that attempt to an animal’s health at risk if he or she does not follow through
identify an owner-breed match (http://www.hsus.org/pets/ with the prescribed exercise regimen.
pet_adoption_information/choosing_the_right_dog.html). Clearly a team approach is needed involving physicians,
Given that the most common reasons for pet relinquishment nurses, physical therapists, social workers, and veterinar-
to animal shelters are behavior problems that often have not ians (Table 5-4) to help assess the factors that may impede
been approached with proper owner training, ensuring that or facilitate pet ownership. This approach to recommending
prospective owners are aware of likely breed-specific behav- pet ownership will have greater likelihood of success for both
ior is a must. When the health care professional is unsure of the patient and the pet.
the patient’s motivation to increase physical activity, it may
be beneficial to recommend that the person volunteer to
walk dogs at a local animal shelter as an intermediate step Credentialing for AAA and AAT Programs
to owning a dog that needs regular exercise. This may serve In both AAA and AAT, the animal and handler are trained
two important purposes. First, the person can have regular to engage in the activities. The handler commonly joins an
Table 5-4 n Types of Behavioral Services Offered by the Veterinary Practice
Approach Considerations
Preselection consultation Consult with prospective pet owners to help them select an appropriate pet for their
circumstances. Advise the owner about the health, behavior, and nutritional requirements of
their new pet so that the home and family can be prepared in advance.
Preventive counseling Counsel owners to raise their pet to minimize behavioral problems. Use handouts, pamphlets,
books, and videos. Take full advantage of puppy and kitten vaccination visits to educate the
family.
Puppy parties/training Encourage owners to participate in puppy programs to enhance early socialization and provide
training advice. If you have the space and expertise, consider offering classes in the clinic.
Behavior management Recommend and supply appropriate training devices (leashes, halters, chew toys, motion-activated
products alarms, etc.) to prevent or correct undesirable behaviors. If you do not recommend the right
products, the owners may make improper decisions.
Surgery Neutering can prevent estrous cycles in females and in males may reduce behavior problems
associated with the effects of androgens, such as sexual attraction to females, roaming, marking,
masturbation, mounting, and some forms of aggression.
Basic behavior counseling As puppies and kittens mature, undesirable behaviors may develop. Intervene early and dedicate
sufficient time to counseling for each specific behavior problem. If managed unsuccessfully,
consider an anesthesiologist referral before the behavior becomes even more ingrained and the
family becomes more frustrated.
Behavioral screening Diseases of any organ or body system can cause or contribute to changes in behavior. Therefore
screening for behavior problems and any behavioral changes is an important component of each
health care visit and can aid in the early identification and diagnosis of medical conditions.
Medical history and Practice good-quality medicine and complete medical assessment on all patients routinely. Perform
diagnostics a medical workup on every patient that requires a behavioral assessment. Run appropriate
diagnostics to rule out all possible medical problems for the presenting behavioral signs.
Behavioral history and Once medical problems for behavioral signs have been ruled out (or resolved), the behavioral
diagnostics diagnosis requires some knowledge and expertise in history-taking and familiarity with the
differential diagnoses for the presenting signs. A videotape, interactive discussion with the owner,
observation of the pet and owner, and a written history might all be used.
Advanced behavioral Make sure you feel competent in performing behavior counseling for advanced problems, such as
consultations aggression or phobic behaviors. If in doubt, contact a behavior referral center for advice or refer
the case. Inappropriate counseling benefits neither the patient nor the veterinary practice.
Pharmacological Drug therapy (as well as alternative therapies such as nutritional management and supplements)
management can be an important component or even a necessity for the successful resolution of many
behavior problems. This might be the case if there are medical conditions causing or
contributing to the signs (e.g., pain management, interstitial cystitis, seizure focus). Psychotropic
drugs may be a useful therapeutic option or an integral part of the treatment program for some
problems.
From Landsberg GM: Handbook of behavior problems of the dog and cat, ed 2, 2004, Oxford, Saunders.
established animal visitation group that has affiliations with

health care facilities and may provide some assistance with BOX 5-2 COMPONENTS OF A HEALTH CLEARANCE
EXAMINATION FOR SERVICE ANIMALS
liability insurance. Most importantly, the visitation groups
have health screening, certification, and AAA/AAT imple-
mentation guidance and standards. Persons who want to
become registered as a pet-visitor team typically ensure
that their animals are in good health (based on recent
examination by a licensed veterinarian, including screen-
ing for internal and external parasites and administration
of needed vaccinations; see below). The animal and handler
must complete obedience training (in the case of dogs), and
the dog must pass the American Kennel Club’s Canine Good
Citizen test. This test is offered by certified testers through-
out the United States and identifies the dog’s basic level of
obedience mastery. Next, the pair must complete a training
and testing protocol to ensure readiness to make visits in
health care facilities. A commonly used training and regis-
tration protocol in the United States is the Delta Society’s
Pet Partners Program (http://www.deltasociety.org/) in
which the handler and dog must complete course materi-
als and training exercises and the dog must undergo a tem-
perament and behavior examination. The purpose of this
examination is to identify the dog’s suitability to behave
reliably and under control of the handler, accept awkward
handling, loud noises, and rapidly changing situations. Cats
are similarly tested. Upon completion of the Pet Partners
Program, in accordance with the rules of their animal visi-
tation group, the handler and dog or cat may begin making
visits in facilities either already affiliated with or making a
new affiliation with the animal visitation group. Many ani-
mal visitation groups in the United States follow the stan-
Adapted from AAA/AAT guidelines; http://www.avma.org/issues/policy/animal_assisted_
dards manual (based on compilation of existing research activity.asp.
evidence and consensus of health care professionals) cre-
ated by the Delta Society. The book Standards of Practice for
Animal-Assisted Activities and Therapy63 provides a guide for
animal visitation groups and health care facilities in devel- and Pasteurella.66 It is important that animals used for AAA
oping policies and procedures for AAA and AAT. The stan- or AAT receive an appropriate veterinary health assessment
dards include topics such as animal grooming standards, (Box 5-2). This assessment also should include a behavioral
areas within facilities appropriate for accessibility to AAA evaluation to ensure that the animal is suitable for working
and AAT teams, selection of the most (and least) applicable with a variety of human encounter situations (Figure 5-5).
patient situations, successful implementation of visits, and An interdisciplinary working group of health care profes-
lines of accountability. sionals (in veterinary medicine, AAA/AAT, infection con-
No national service animal certification currently exists, trol, and public health) developed standards for AAA and
although several groups can assist with specific instruction AAT in health care facilities.62 The AAA/AAT standards rec-
and training. The Americans with Disabilities Act requires ommend exclusion of reptiles, amphibians, nonhuman pri-
businesses to permit people to be accompanied by their ser- mates, recently domesticated species, and other animals that
vice animals “regardless of whether [their animals] have been cannot be litter trained (Table 5-5). The standards also rec-
licensed or certified by a state or local government.”64 ommend exclusion of animals receiving a raw meat diet (due
to the risk of shedding E. coli and other pathogens), those
coming directly from animal shelters, dogs and cats younger
than 1 year, or animals not in a permanent home for at least
Minimizing Infectious Disease and Other Risks 6 months. Detailed recommendations are made about hand-
in AAA and AAT washing and other components of the AAA and AAT patient-
The use of animals for therapy of persons with underlying animal encounters. Adherence to such standards helps to
medical problems involves a certain risk of zoonotic disease ensure that AAA or AAT do not occur thoughtlessly or with-
transmission. There is also a risk of animals becoming infected out significant commitment and contribution on the part of
from human beings. For example, a human epidemic strain animal handlers and animal visitation groups. This helps to
of Clostridium difficile, an emerging pathogen in health care reassure those working in health care facilities regarding the
settings, has been found in a visitation dog.65 Other patho- likely safety of patients receiving AAA or AAT and maximizes
gens reported in visitation dogs include antibiotic-resistant the probability that patients will receive the benefits of this
Escherichia coli, Salmonella, Giardia, Toxocara, Ancylostoma, human–companion animal interaction.
Initial observations:
Animal friendly? Y N
Animal appears responsive? Y N
Any sign of aggression or fear when approached? Y N
Overactive or highstrung? Y N
Behavioral examination: Any adverse reactions with the following:
Door slamming? Y N
Pulling of hair or ears or tail? Y N
Being petted aggressively? Y N
Being hugged? Y N
When someone approaches animal’s owner? Y N
Figure 5-5 n Example of behavioral evaluation for therapy dog.
Table 5-5 n Exclusion Criteria for AAA and AAT

animals
Criterion Exclusion
Species Reptiles, amphibians, nonhuman primates;

recently domesticated species; other
animals that cannot be litter trained
Age Dogs and cats younger than 1 year
Origin Directly from animal shelters
Permanent home for less than 6 months
Health issues Being fed a raw-meat diet
Immunocompromised
Lack of complete vaccinations certified by
a licensed veterinarian
Affiliation Not affiliated with a visitation group
Not registered by an AAA or AAT training
program
Behavior Any aggressive incident in a health care Figure 5-6 n A paretic patient acclimated to a wheelchair or cart.
facility The cart can be used as a therapy tool in the absence of aquatic ther-
apy or as an ambulation aid at home if improvement is not expected.
(From Fossum TW: Small animal surgery, ed 3, St Louis, 2007, Mosby
Elsevier.)
Health Effects of loss of or separation
from a pet
As with human health care, improvements in veteri- Human health care providers need to understand the
nary care have increased the longevity of companion magnitude of the loss of a pet on psychosocial and phys-
animals (Figure 5-6). Nevertheless, both human health iological functioning.
care professionals and veterinary professionals may Despite the rapidly growing popularity of pet owner-
need to assist patients in ultimately dealing with pet ship, many health care providers may not recognize that
loss. Pet owners who have lost a beloved pet often indi- pet loss can be as traumatic as or even more traumatic
cate that they feel ashamed to mention their feelings of than losing a human family member. One study showed
loss because they fear they will be treated insensitively. that nearly 30% of owners recently bereaved of a pet
e xperienced severe grief. The most apparent risk factors 87% of the women, the animal was identified as very close
for grief were level of attachment, euthanasia, societal atti- to them.68 Animal abuse also presents serious problems for
tudes toward pet death, and professional support from the children who witness this violent and manipulative behav-
veterinary team.67 In addition to grief, patients may feel ior in adult role models and may learn to imitate what they
guilt at not providing better care or making the determi- see. Experts in the field of animal and domestic violence
nation to euthanize the pet, denial that the pet is actually and abuse agree that children exposed to domestic violence
gone, and anger. These emotions may lead to sleep distur- are more likely to be cruel to animals and that battered
bances, depression, or anxiety. women and children may be more likely to stay in abusive
During acute illness episodes requiring hospitalization, homes to protect their pets, thereby exposing themselves to
patients may experience significant psychosocial stress further abuse.69
related to separation from the pet. Sources of stress may Health care professionals who encounter such abuse
include concerns over the pet’s welfare and loss of com- have significant responsibilities. Human health care pro-
panionship. This is one justification for inquiring about pet fessionals are mandated to report child and elder abuse
ownership in the evaluation of a hospitalized patient (see to law enforcement agencies. Veterinarians have an ethical
Chapter 3). responsibility to report suspected child and elder abuse
During natural disasters such as hurricanes and earth- but may not be mandatory reporters. More than 42 states
quakes, separation from pets and other animals can be asso- have delineated various forms of animal abuse as felo-
ciated with similar stress reactions (see Chapter 13). nies.70 However, animal cruelty laws are inconsistent across
Sensitivity of human health and veterinary care providers states, and such crimes are commonly prosecuted only in
during the process of pet euthanasia or other events leading extreme cases. Some states have mandated that veterinar-
to the death of a pet is crucial. If the euthanasia occurs in ians report animal abuse (termed nonaccidental injury)
the veterinary clinic, the owner may want to bring the ani- to authorities designated in their respective statutes. The
mal’s favorite bedding, toy, or treat to provide comfort dur- rules vary considerably so it is incumbent on veterinary
ing the process. It is important that the owner not feel rushed health care professionals to know the expectations in their
and that the veterinary staff are kind and respectful of the particular state. The issues associated with veterinarians
pet and the owner’s need to be present if that is his or her reporting animal abuse are similar to those encountered
preference. as child protection laws were being created. The role of the
Encouraging owners to express their feelings of loss and veterinarian in diagnosing the abuse is undisputed, but the
reassuring them that it is normal to feel such loss will help process of diagnosis is not so clear-cut. The Tufts Animal
them to progress through the grief process. Listening while Care and Condition Scales help to provide consistent,
they reminisce about their pet and acknowledging the pet’s objective criteria for the diagnosis.71 However, veterinar-
importance to them may be of further help. The veterinarians may not feel sufficiently trained to identify, intervene,
ian may be the only health care professional with whom and report such cases. A recent study indicated that vet-
the owner talks about this loss. This conversation may erinarians in Australia believed that they should intervene
stimulate memories and discussion of previous losses of in animal and child abuse cases but felt ill-equipped to
both pet and human family members. A follow-up phone do so.72 Along with diagnosis, the issues for veterinarians
call to the owner a few days to a week later is important to reporting animal abuse parallel those encountered when
express care and concern and to rule out signs of extreme health care providers in human medicine report child,
grief (owner unable to leave home, eat, dress, or do usual domestic partner, or elder abuse. Specifically, the issues
daily activities; extreme crying; statements about life being reflect concern about making a valid diagnosis, confiden-
not worth living or about thoughts of suicide). If the tiality with clients, liability of reporting suspected cases,
owner identifies suicidal intentions, asking the name of the the ethical duty to report, involvement of the veterinar-
owner’s physician, and contacting the physician to share ian in the investigative and court process after reporting
this information or calling 911 may save the owner’s life. occurs, and the practical implications of all of these issues
If nonsuicidal extreme grief is identified, the veterinarian on the veterinary practice and business.73 However, the
may encourage the owner to contact his or her physician AMVA’s position is that veterinarians have the responsi-
for an appointment and may call a second time a few days bility to report cases of animal abuse or neglect.73
later to check on the owner. The Humane Society of the United States developed
the “First Strike” campaign in 1997 to increase aware-
ness about animal abuse and neglect and the connection
between this type of abuse and domestic violence. A variety
Pets as indicators of human behavior of materials are available on their Web site to help health
and domestic violence care professionals who need information about this con-
nection, how to report such violence, and what steps can
There is little doubt that violence toward animals and other be taken in communities to prevent it. The following URL
forms of domestic violence occur in tandem. In a recent may be of assistance: http://www.hsus.org/hsus_field/
study, investigators found that 54% of women participants first_strike_the_connection_between_a nimal_cruelty_
who were staying in domestic violence shelters reported and_human_violence/. Box 5-3 lists warning signs asso-
pet abuse in their households. The animal abuse included ciated with possible abuse and domestic violence related
injury, torture, permanent loss of function, or death. In to animals.
cortisol in response to the work, yet behavioral assessments

BOX 5-3 POSSIBLE WARNING SIGNS OF ANIMAL ABUSE revealed that the dogs commonly abstained from food and
AND DOMESTIC VIOLENCE slept for an additional 2 to 3 hours after a day of visiting
patients with cancer.26 Yet clinical reports indicate that
• Unexplained death of an animal
dogs sometimes have aversive responses to dying patients.
• Unusual fractures
• Unexplained weight loss
The extent to which an animal may seek out or avoid par-
• Anxiety symptoms ticular patients has not been studied, nor has the mecha-
• Incontinence in an animal that was formerly housebroken nism through which this selection/aversion process occurs.
• Animal hoarding (accumulating large numbers of cats or other Areas in need of investigation in the case of service dogs
domestic animals) relate to their responses to their work and measures taken
to minimize work-related stresses. For example, in service
dogs working with children with autism, lack of rest and
recreation, aggressive behavior toward the dog, and lack of
Research needs predictability of daily routines have been identified as fac-
tors contributing to the dog’s behavior, welfare, and perfor-
Although the body of evidence continues to grow, clearly mance, as well as parental satisfaction with the dog.74 These
more research about the health benefits of HAI is needed areas have not been addressed in the AAA/AAT context and
with robust designs and larger samples. But many areas would enhance our understanding of the AAA/AAT experi-
about which we know relatively little—from either a clinical ence for the dog.
or empirical evidence point of view—need to be investigated. The field of HAI continues to grow rapidly in a clini-
For example, research is needed to investigate the extent to cal sense (more programs for AAA and AAT emerge almost
which one species may be more effective than another in par- daily), but the research evidence base is growing slowly.
ticular clinical settings for AAA and AAT. Interaction with a Many aspects of the complex interactions between human
dog or cat is significantly different than what can be accom- beings and animals are still unknown (a 1987 National
plished with a bird or fish in an aquarium. However, benefi- Institutes of Health expert panel called for animal-related
cial outcomes have been shown with all of these species. It is variables in every major health study in the United States).
unclear to what extent individual preference may play a role The research is growing such that it is possible to begin to
in the efficacy of AAA and AAT. If we believe in the placebo guide practice relying on this evidence. The ultimate goal of
effect in setting the stage for any intervention to be effec- evidence-based study—clinical observations and practical
tive (as any nurse can attest to the importance of introduc- application—is to optimize health through human animal
ing a “take as needed” analgesic as “a very powerful drug that interactions.
I think will help you,” in predicting the efficacy of the drug),
then individual preferences may be important in clinical pre-
scriptions of AAA and AAT. References
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1997;5(3):267–280.
The Built Environment
and Indoor Air Quality 6
Clifford S. Mitchell, Carol Norris Reinero,
Peter M. Rabinowitz, Lisa A. Conti, and Judy Sparer
Our health is inextricably linked to both the natural and built • Encourage physical activity, including activities with
environments. The built environment is defined as manmade healthy companion animals.
surroundings ranging from individual buildings to develop • Be alert to sentinel cases of disease in human beings
ments and communities. The challenge is to design new, or related to the built environment or indoor air quality.
retrofit existing, built environments to be sustainable and • Report possible cases of environmentally induced or
health promoting. Indoor air quality refers to gases and par exacerbated disease to the health department.
ticulates or physical components of interior air that relate to • If treating patients with diseases possibly related to
building occupants’ health and comfort. This chapter identi the built environment or indoor air quality, inquire
fies certain links between clinical diseases in human beings whether animals are also experiencing problems. This
and other animals relating to built environments and indoor could help identify causative links.
air quality. Disease development in an animal or human being • Consider building or retrofitting health care facilities
may be a sentinel sign of an environmental health hazard. to become certified.2
Key Points for Clinicians and Public Health Veterinary Clinicians

Professionals
• Advocate for (re)development in the community that
promotes healthy living, such as walking/biking and
addition/maintenance of green spaces and parks.
Public Health Professionals
• Encourage physical activity with healthy companion
• Monitor the health of the community and determine animals.
health associations with the built environment, includ • Be alert to sentinel cases of disease in animals related to
ing neighborhood and street planning and design of the built environment and indoor air quality problems.
buildings. • Report possible cases of environmentally induced or
• Work with urban planners, transportation engineers, exacerbated disease to the health department.
environmental health specialists, and disease ecologists to • If treating patients with problems possibly related to
implement improvements in neighborhoods and com the built environment or buildings, inquire whether
munity design.1 Resources are available at http://www. human beings in area are also experiencing problems.
cdc.gov/healthyplaces, http://www.usgbc.org, http:// This could help identify causative links.
www.smartgrowth.org, and http://www.epa.gov/dced.
• Provide technical advice to homeowners, contractors,
and clinicians about ways to improve indoor air qual Built environments and active living
ity in homes and worksites.
• Provide information on energy conservation and sus On a large scale, habitat destruction affects species diversity;
tainability such as Leadership for Energy and Environ this results in loss of access to traditional medicines and novel
mental Design (LEED)-certified2 status and LEED for pharmaceuticals as well as infectious disease emergence and
Neighborhood Development (LEED-ND; see http:// spread.3-5 Recent years have seen increasing realization that the
www.usgbc.org/DisplayPage.aspx?CMSPageID=148). design of neighborhoods and community environments has
a profound impact on human health.6 Moreover, issues such
as traffic safety and injury risk, communities that sprawl (i.e.,
Human Health Clinicians
single-use development with design around the automobile),
• Advocate for (re)development in the community that obesity,7 and lack of exercise opportunities leading to inactiv
promotes healthy living, such as walking/biking and ity have all been cited as important public health threats. These
addition/maintenance of green spaces and parks. threats can eventually manifest as clinical problems, including
37
Figure 6-2 n The deer mouse, Peromyscus maniculatus, is a hantavirus

carrier that becomes a threat when it enters human habitation in rural and
suburban areas. (From Centers for Disease Control and Prevention Public
Health Image Library, Atlanta, Ga. Photo courtesy James Gathany.)
Figure 6-1 n Tree-lined, designated pedestrian paths increase the likeli

hood of walking. (From Centers for Disease Control and Prevention: Healthy and that should make clinicians consider this possibility.
community design. http://www.cdc.gov/healthyplaces/docs/Healthy%20 Similar clinical conditions can arise in both human beings
Community%20Design.pdf.)
and companion animals.
The impact of the built environment on health is complex.
diabetes, asthma, hypertension, and stress-related illness.8,9 Nevertheless, identifying individuals with medical problems
Societal reductions of physical activity contributing to these apparently related to the built environment can contribute to
poor health outcomes have been linked with designing our raising awareness in the community about specific environ
communities around motorized transportation and failing to mental health issues.
design communities to promote neighborhood interaction.
Active living is defined as participating in at least 30 minutes of
physical activity on most days.10 Research indicates that envi Building healthy communities
ronmental factors, including accessibility (e.g., safe pedestrian
and bike paths, parks, stores, churches, schools, libraries, and Public health and health care involvement in community
so on within safe walking distance), opportunities (e.g., side design is critical to addressing and improving population
walks, a walkable neighborhood environment), and aesthetic health. Activity-promoting environments are those with
attributes (e.g., tree-lined pedestrian paths, free of litter, with pedestrian-centric design and aesthetic appeal, and are joined
enjoyable scenery; Figure 6-1) all have a significant effect on with historic core public health issues such as water, soil, and
the likelihood of engaging in physical activity,11–13 “aging in air quality concerns.19 Urban designers and planners, with
place,”*,14 and community resiliency.15 their roots in public health protection, can be advocates in
Less well considered is that companion animals and wild concert with public health professionals and clinicians to alter
life are also affected by changes in the built environment zoning codes to encourage working, shopping, and attend
and, in turn, may contribute to human health issues. Human ing school within neighborhoods and to provide green space
health care providers may not be aware that pet obesity is with its attendant violence prevention and mental health
an increasing problem, presumably due to factors similar to improvements.20 Veterinarians, wildlife biologists, and other
those driving the rise in obesity prevalence in human beings, animal health professionals can play key roles in this effort by
including lack of exercise related in part to neighborhood working with planners, land use experts, and developers to
design and their owners’ sedentary habits. The interactions help design and build environments that encourage healthy
between built environments with nearby wildlife areas can pet ownership, including adequate sidewalks and paths for
affect the risk of zoonotic disease transmission among wild pet walking (Figure 6-3), parks that encourage pet sanitation,
life, domestic animal, and human populations (Figure 6-2). and approaches to limit forest fragmentation and problems
such as peridomestic rodent infestation and disease vector
abundance. Specific guidelines for reducing rodent infesta
Clinical conditions in human beings tion and tick control are found in Chapter 9.
and other animals related to built
environments
Indoor environments
Table 6-1 lists conditions in human beings and other animals
that could be related to problems with built environments Americans spend the majority of each day indoors21 both at
home and at work, and the indoor environment is becoming
*Older adults continuing to live independently rather than moving to an recognized as an important factor in respiratory, allergic, and
institutional care setting. other health issues.22,23 Many companion animals are kept
Chapter 6 n The Built Environment and Indoor Air Quality 39
Table 6-1 n Health Hazards and Clinical Conditions Related to the Built Environment
Health Hazard Associated With Sentinel Health Event in Human or

Built Environment Companion Animal Mitigation
Lack of safe pedestrian areas Pedestrian, bicyclist, or animal injured by Provide safe walking paths for people and pets
motorist (Figure 6-3); (re)design communities for
pedestrians rather than automobiles, mixed-
Lack of exercise areas and Obesity and chronic disease16,17 use and higher-density zoning and design
opportunities (for sprawl); protection and creation of green
Lack of green space or other aesthetic Reduction in physical activity11,18 spaces
attributes
Suburban encroachment on wildlife Tick-borne disease (such as Lyme disease or Management of open space and wildlife habitat
habitat Rocky Mountain spotted fever) near housing, integrated pest management
techniques
Rodent infestation in and around Rodent-associated illness (such as
buildings hantavirus)
Inadequate policies on pet sanitation Hookworm disease, toxoplasmosis Policies addressing pets in public areas (e.g.,
in playgrounds and public areas picking up after pets to keep areas free of feces)
Table 6-2 n Common Contaminants in Indoor Air
Class of Hazard Hazard Sources
Volatile organic Plywoods, particle board; new vinyl

compounds flooring, rubber-backed nylon
(formaldehyde carpeting; adhesives, paints, resins,
and others) solvents; printed materials, printer
and photocopier emissions; cleaning
chemicals, personal products,
fragrances, pesticides, cooking fumes
Dust Dirt, house dust, construction, paper
dust, paint dust (lead)
Fibers Insulation (asbestos, fiberglass)
Bioaerosols Bacteria, fungi/molds, dust mites,
viruses, pollen, human skin particles,
animal and insect dander and excreta
Entrapped outdoor Vehicle exhaust (including carbon
sources monoxide, ozone, and particulate
matter), industrial exhaust
Physical factors Temperature, humidity, noise, lighting
Other chemicals Cooking odors, combustion products,
radon, pesticides, cleaning agents,
environmental tobacco smoke,
building materials
Adapted from Hodgson M, Addorisio MR. Exposures in indoor environments. In:

Rosenstock L, Cullen MR, Redlich C, et al, eds: Textbook of clinical occupational and
Figure 6-3 n Dog-walking provides exercise and stress reduction for environmental medicine, ed 2, Philadelphia, 2004, Saunders.
both people and their pets.
chemicals are described in Chapter 8. In most living areas,
indoors because of lifestyle (apartment living), to avoid injury the total loading of chemicals is not high compared with an
(from automobiles or other animals), or to minimize contact industrial environment, but low levels of chemicals with
with zoonotic disease threats from wildlife and arthropod out good ventilation have an effect on health. In addition, as
vectors (as recommended in some sections of this book). As a described in Chapter 7, animals and people are exposed to
result of these changes in the Western lifestyle, human beings each other’s allergens. Animal dander has been linked to an
and other animals share indoor environments to a signifi increasing prevalence of asthma and other allergic conditions
cant extent and are exposed to many similar indoor air health in human beings in developed countries.24 In a similar man
hazards. These hazards include chemicals from cleaning, ren ner, human dander has been associated with feline asthma25
ovation, pesticides, personal care products, and even cook and canine eosinophilic bronchopneumopathy.26
ing; allergens; and infectious pathogens (Table 6-2). Specific As Table 6-2 shows, indoor air environments can con
infectious diseases are discussed in Chapter 9, and the shared tain complex mixes of contaminants, often caused by inad
exposures of animals and human beings to specific toxic equate ventilation. Persistent water intrusion from leaks
or condensate can lead to mold growth (Color Plate 6-1).

Sources of potential contaminants include renovation and BOX 6-1 DIAGNOSTIC CHECKLIST FOR ASSESSING
POTENTIAL human ILLNESS ASSOCIATED
remodeling materials, cleaning compounds, pesticides, paint,
WITH INDOOR AIR QUALITY
carpet or flooring, improperly stored volatile material, glue,
copy machines, printers, and perfumes. Any water leaks are
• When did the [symptom or complaint] begin?
also of concern because molds can find hospitable growth • Does the [symptom or complaint] exist all the time, or does it
conditions in damp carpet, ceiling tile, or even wallboard. The come and go? That is, is it associated with times of day, days of
resulting exposures can produce certain nonspecific clinical the week, or seasons of the year?
syndromes. • If so, are you usually in a particular place at those times?
• Does the problem abate or cease, either immediately or gradually,
when you leave that location? Does it recur when you return?
Clinical Conditions in Human Beings and Other • What is your work? Have you recently changed employers or
Animals Related to Indoor Air Quality assignments, or has your employer recently changed location?
Not surprisingly, human beings and other animals exposed • If not, has the place where you work been redecorated or
refurnished, or have you recently started working with new
to indoor air contaminants can develop a number of health
or different materials or equipment? (These may include
conditions (Figure 6-4). In human beings, the nonspecific pesticides, cleaning products, craft supplies, and so on.)
cluster of symptoms known as “sick building syndrome” or • What is the smoking policy at your workplace? Are you exposed
nonspecific building-related illness (NSBRI) can include to environmental tobacco smoke at work, school, home, or
itching, watery eyes, nasal congestion, headaches, fatigue, other places?
and pruritus.27 The causes of NSBRI appear to be multifac • Describe your work area.
torial, including low-level exposure to airborne irritants and • Have you recently changed your place of residence?
temperature and humidity fluctuations. Symptoms often • If not, have you made any recent changes in, or additions to,
improve with increased fresh air ventilation. A key factor in your home?
improving conditions is the opinion of the health care pro • Have you or anyone else in your family recently started a new
hobby or other activity?
fessional about the relationship between reported illness
• Have you recently acquired a new pet?
and the indoor air environment. Box 6-1 provides suggested • Does anyone else [or any pets] in your home have a similar
intake questions to assist with this determination. problem? How about anyone with whom you work? (An
Less is known about diseases in other animals related to affirmative reply may suggest either a common source or a
indoor air environments, but it appears that some conditions communicable condition.)
experienced by human beings may have corollaries in pets
From Environmental Protection Agency: Indoor air pollution: an introduction for health
(Table 6-3). Importantly, pets tend to spend a greater portion professionals. http://www.epa.gov/iaq/pubs/hpguide.html.
of each day inside the home compared with human beings
and consequently experience greater exposure to many
indoor air contaminants. Therefore signs of ill health in
animals may be an indication of a health risk to the human
beings, and vice versa, making diagnosis in one species
relevant to the health of the other.
Building-related illness associated with indoor air quality
tends to improve when human beings and animals are away
from the building and recur after returning to the building.
CC CC Evaluation and Improvement of Indoor

Air Quality
GC The health of occupants in indoor environments—whether
human or other animal—depends on the same factors: the
creation of an environment that is well ventilated and rela
tively free of agents that are harmful to the biological organ
GC
ism. The goal is not to create a sterile environment but one
that promotes comfort and health. The U.S. Green Building
Council has established the LEED rating system, a set of stan
Figure 6-4 n Primary bronchus epithelium (×2000). This scanning dards based primarily on energy conservation and sustain
electron micrograph illustrates the surface of a primary bronchus; the film able construction, although it offers some encouragement to
of surface mucus has been removed. The ciliated epithelial cells (CC) have improve air quality. New or renovated buildings may apply
numerous surface cilia, each several microns long, that move in a coordi
nated fashion to sweep mucus up the bronchus. Scattered goblet cells (GC) for LEED certification that its standards have been met.38
are recognizable by their bulbous surface outline, lack of cilia, and the pres
ence of small surface projections associated with mucus secretion. The frag
ile cilia are particularly vulnerable to damage and destruction by inhaled Evaluating Indoor Air Problems
toxic chemicals (cigarette smoke, car exhaust fumes) and by bacterial and
viral infections. (From Young B, Lowe JS, Stevens A, et al: Wheater’s func-
Indoor air quality evaluations, which can be performed by an
tional histology: a text and colour atlas, ed 5, Edinburgh, 2006, Churchill industrial hygienist, usually focus on two aspects of a building.
Livingstone Elsevier.) The first is the identification and evaluation of potential
Chapter 6 n The Built Environment and Indoor Air Quality 41
Table 6-3 n Conditions in Human Beings and Other Animals Related to Indoor Air Quality Problems
Indoor Air Quality Problem Sentinel Event in Human Beings Sentinel Event in Other Animals
Allergens (see Chapter 7), including Asthma, rhinitis, atopic dermatitis Allergic skin disease,28 feline asthma (possible),
those to chemicals in personal canine eosinophilic bronchopneumopathy, equine
and pet care products hypersensitivity pneumonitis due to mold, dermatitis
Environmental tobacco smoke, Bronchitis, rhinitis, pharyngitis, Nasal neoplasia29 and possible chronic bronchitis30 in
a major source of indoor air asthma, lung cancer, conjunctival dogs; oral squamous cell carcinoma31 and malignant
contamination irritation, headache lymphoma in cats32; pneumotoxicity in birds33; possible
chronic respiratory conditions in captive reptiles34
Radon Lung cancer Lung cancer in rats35
Inadequate ventilation, VOCs, “Sick building syndrome” Calves grouped indoors are at increased risk for exposure
temperature and humidity (nonspecific building-related to ammonia fumes and subsequent Pasteurella multocida
fluctuation illness) colonization of the lungs36; increased mastitis rates in
cattle37
sources of contaminants in the air (see Table 6-2). The other humidity (above 60%) encourages the growth of mold. Levels
important aspect affecting indoor air quality is the ventila of airborne mold are sometimes measured but levels are not
tion system. To achieve good air quality, the system must be yet sufficiently understood to predict illness. Mold is always
able to supply sufficient fresh air to all occupied spaces and present in both indoor and outdoor air and varies tremen
remove the contaminants. An evaluation includes determi dously from season to season and place to place. A history of
nation of how much fresh air is being provided, the quality water damage is generally more helpful in identifying a mold
of that fresh air, and how well the distribution system func problem than measuring mold levels. Therefore mold mea
tions. The air system must be balanced, delivering enough surements are not recommended. Any porous materials that
air to each room, and must ensure mixing of new and old have become damp with water for any reason should be dried
air within each space for proper cleaning and temperature immediately. If they have been wet for a prolonged period,
equilibrium. they should be removed and replaced because effective mold
Sometimes measurements of carbon dioxide, total air removal from porous materials is extremely difficult.
borne hydrocarbons, or airborne molds are taken to help The American Society of Heating, Ventilating,
determine ventilation effectiveness. The carbon dioxide Refrigerating and Air Conditioning Engineers (ASHRAE)
measurement is used as a marker. If the air circulation is recommends that a minimum of 20 cubic feet per minute
poor and the fresh air insufficient, carbon dioxide, derived (cfm) of fresh outdoor air per occupant be provided in busi
primarily from occupants’ breathing, builds up (carbon ness offices and 15 cfm per occupant in reception areas. Any
dioxide is not a good marker of air quality if there are few additional sources of air contaminants increase the demand
people or animals present and breathing in the space). for fresh air. There is no specific recommendation for phy
Carbon dioxide serves as an easily measured marker for sicians’ or veterinarians’ offices, but hospitals and nursing
poor ventilation, which is often associated with com homes are recommended to provide 25 cfm per occupant
plaints of fatigue, dry or irritated eyes, scratchy throat, or for patients’ rooms, 15 cfm for medical procedure rooms,
headache. (Although the Occupational Safety and Health 30 cfm for operating rooms, and 15 cfm for recovery rooms,
Administration [OSHA] standard for carbon dioxide intensive care units, and autopsy rooms. Many homes, espe
is 5000 parts per million [ppm], when indoor levels rise cially older ones and stand-alone homes, do not have a regu
above 700 to 800 ppm, building occupants report discom lar source of fresh air but depend on leakage, open windows,
fort. For reference, carbon dioxide levels outdoors are usu or the opening and closing of doors to provide adequate
ally between 250 and 450 ppm, depending on traffic or ventilation.
other sources of combustion.) In many situations the principles of good practice listed
Particulates (airborne dust particles) are a common prob in Box 6-2 can prevent the indoor environment from causing
lem in indoor air environments. If the ductwork or unit ven health problems for human beings and companion animals.
tilators have become dirty, the filters overloaded or breached, Clinicians may often feel ill-equipped to make recom
or some part of the structure (sometimes the insulation of mendations or initiate interventions to improve indoor air
the ductwork) has deteriorated, the ventilation system itself quality. The environmental health division of the local health
can become a source of contamination. It is not unusual for department may be able to offer technical advice to home
construction dust to enter the ventilation system. Systems owners, contractors, and clinicians about improving indoor
designed with an open return plenum are especially suscep air quality. The Environmental Protection Agency (EPA) also
tible. Poorly maintained fuel-burning heating systems can be has useful educational materials on its Web site (http://www.
a source of carbon monoxide. Systems should have annual epa.gov/iaq/pubs). Human health clinicians and veterinar
maintenance. ians may be able to collaborate to work toward improve
Excessive dryness (relative humidity below 30%) adds to ment of a particular building where both human beings and
winter discomfort from respiratory complaints. Excessive animals are affected.
12. Gauvin L, Riva M, Barnett T, et al. Association between neigh

BOX 6-2 INTERVENTIONS TO IMPROVE INDOOR AIR borhood active living potential and walking. Am J Epidemiol.
ENVIRONMENTS 2008;167(8):944–953.
13. Wells NM, Ashdown P, Davies EHS, et al. Environment, design, and
obesity. Environ Behav. 2007;39(1):6–33.
Reduce or Eliminate Sources of Indoor Air Pollution 14. Michael YL, Green MK, Farquhar SA. Neighborhood design and active
• Perform regular maintenance on home heating systems to aging. Health Place. 2006;12(4):734–740.
reduce potential carbon monoxide exposure. 15. Campanella TJ. Planning for postdisaster resiliency. Ann Am Acad Pol
• Minimize the use of products that become airborne, such as Soc Sci. 2006;604(1):192–207.
cleaning chemicals with VOCs, personal products and per 16. McCann BA, Ewing R. Measuring the health effects of sprawl: a national
fumes, air fresheners, and pesticides. Renovation and deco analysis of physical activity, obesity and chronic disease. Smart Growth
America Surface Transportation Project; 1993. http://www.smart
rating materials may also “off-gas” VOCs for some time.
growthamerica.org/report/HealthSprawl8.03.pdf.
• Prohibit smoking in buildings and away from entrances and 17. German AJ. The growing problem of obesity in dogs and cats. J Nutr.
air intakes. 2006;136(suppl 7):1940S–1946S.
• Keep the home as free as dust and allergens as possible by: 18. Farley TA. Prescription for a healthy nation: a new approach to living our
 Frequent cleaning lives by fixing our everyday world. Boston: Beacon Press; 2005.
 Putting walk-off mats by entrances, wiping pets’ feet 19. Prevention Institute. The built environment and health: 11 profiles
when returning from walks of neighborhood transformation. http://www.preventioninstitute.org/
 Using vacuums with HEPA filters rather than regular builtenv.html.
vacuum cleaners or brooms 20. Jackson RJ, Kochtitzky C. Creating a healthy environment: the impact
of the built environment on public health. Washington DC: Sprawl
 Using microfiber dust cloths rather than traditional
Watch. http://www.cdc.gov/healthyplaces/articles/Creating%20A%20
dusters Healthy%20Environment.pdf.
 Furnishing with items that are easily cleaned and do not 21. Leech JA, Nelson WC, Burnett RT, et al. It’s about time: a comparison
become reservoirs for dust and allergens of Canadian and American time-activity patterns. J Expo Anal Environ
• Develop an integrated pest management program to Epidemiol. 2002;12(6):427–432.
effectively control pests while minimizing the use of toxic 22. Wu F, Jacobs D, Mitchell C. Improving indoor environmental quality
pesticides. for public health: impediments and policy recommendations. Environ
• Prevent mold by promptly fixing water leaks and dry Health Perspect. 2007;115(6):953–957.
ing spills. Any absorbent material that has been damp for 23. National Institute for Occupational Health and Safety. Indoor environ-
mental quality. http://www.cdc.gov/niosh/topics/indoorenv.
longer than 48 hours can become an indoor source of mold.
24. Liccardi G, Cazzola M, D’Amato M, et al. Pets and cockroaches: two
• Test and mitigate for radon. increasing causes of respiratory allergy in indoor environments.
Ensure Proper Ventilation Characteristics of airways sensitization and prevention strategies. Respir
Med. 2000;94(11):1109–1118.
• Good ventilation is essential to removing contaminant-
25. Corcoran BM, Foster DJ, Fuentes VL. Feline asthma syndrome: a retro
laden air and bringing in fresh outdoor air. spective study of the clinical presentation in 29 cats. J Small Anim Pract.
1995;36(11):481–488.
VOC, Volatile organic compound; HEPA, high-efficiency particulate air.
26. Clercx C, Peeters D, German AJ, et al. An immunologic investiga
tion of canine eosinophilic bronchopneumopathy. J Vet Intern Med.
References 2002;16(3):229–237.
27. Burge PS. Sick building syndrome. Occup Environ Med. 2004;61(2):185–190.
1. Jacobs DE, Kelly T, Sobolewski J. Linking public health, housing, 28. August JR. Consultation in feline internal medicine. 5th ed. St. Louis:
and indoor environmental policy: successes and challenges at local Saunders; 2006.
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2007;115(6):976–982. dures and emergency treatment. 8th ed. St Louis: Saunders; 2006.
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org/DisplayPage.aspx?CMSPageID=1765. ed. St Louis: Saunders; 2006.
3. Cassis G. Biodiversity loss: a human health issue. MJA. 1998;169:568–569. 31. Bertone ER, Snyder LA, Moore AS. Environmental and lifestyle risk fac
4. Grifo F, Rosenthal J, eds. Biodiversity and human health. Washington tors for oral squamous cell carcinoma in domestic cats. J Vet Intern Med.
DC: Island Press; 1997. 2003;17:557–562.
5. Swaddle J, Calos S. Increased avian diversity is associated with lower 32. Bertone ER, Snyder LA, Moore AS. Environmental tobacco smoke
incidence of human West Nile infection: observation of the dilution and risk of malignant lymphoma in pet cats. Am J Epidemiol.
effect. PLoS ONE. 2008;3(6):e2488. 2002;156:268–273.
6. Jackson RJ. The impact of the built environment on health: an emerging 33. Plumlee K. Clinical veterinary toxicology. St Louis: Mosby; 2004.
field. Am J Public Health. 2003;93(9):1382–1384. 34. Mader DR. Reptile medicine and surgery. 2nd ed. St Louis: Saunders;
7. Frances L, Gordenard B, Jalaludin B. Impact of urban sprawl on over 2006.
weight, obesity, and physical activity in Sydney, Australia. J Urb Health. 35. Collier CG, Strong JC, Humphreys JA, et al. Carcinogenicity of radon/
2008;186(1):19–30. radon decay product inhalation in rats—effect of dose, dose rate and
8. Rutt C, Dannenberg AL, Kochtitzky C. Using policy and built environ unattached fraction. Int J Radiat Biol. 2005;81(9):631–647.
ment interventions to improve public health. J Public Health Manag 36. Divers TJ, Peek SF. Rebhun’s diseases of dairy cattle. 2nd ed. St Louis:
Pract. 2008;14(3):221–223. Saunders; 2008.
9. University of Colorado Denver. Children, youth, and environments center 37. Radostits OM, Gay CC, Hinchcliff KW, eds. Veterinary medicine: a text-
for research and design. http://www.cudenver.edu/Academics/Colleges/ book of the diseases of cattle, horses, sheep, pigs and goats. 10th ed. Oxford:
ArchitecturePlanning/discover/centers/CYE/Pages/index.aspx. Saunders Elsevier Ltd.; 2007.
10. Active Living by Design. http://www.activelivingbydesign.org. 38. US Green Building Council. LEED. http://www.usgbc.org/DisplayPage.
11. Sallis J, Cervera R, Archer W, et al. An ecological approach to creating aspx?CategoryID=19.
active living communities. Ann Rev Pub Health. 2006;27:297–332.
Allergic Conditions
7
Carol Norris Reinero, Clifford S. Mitchell, and Peter M. Rabinowitz
Although concern is ongoing about the risks of zoonotic dis- health of the animals. Animals may also manifest clini-
ease transmission from animal exposure, allergic diseases cal reactions to environmental allergens.
caused by animal allergens may be a greater public health
and clinical problem because of the prevalence of disease
and potential for mortality. Diagnosing and managing ani-
mal allergy can be challenging in part because many people • Communication with human health clinicians can
are reluctant to give up their pets. help explore alternatives to removing a pet from the
Pets and other animals can develop allergic conditions household of an allergic person.
that may be triggered by the allergens that cause problems • Allergic conditions in an animal may suggest an
in people. In addition, because of the similarity of animal indoor air contaminant with human health relevance.
and human disease, animals serve as research models for Veterinarians treating an animal with an allergic con-
human beings. Therefore increased communication among dition can inquire about human beings with problems
public health, human health, and veterinary clinicians may related to allergies or airborne contaminant exposures
lead to improved management and prevention of allergic and whether causative agents have been identified.
conditions. Contact with the treating health care provider may
help coordinate household allergen management.
Key Points for Clinicians and Public Health
Professionals
Animal allergy in human beings
Public Health Professionals Human beings can become sensitized to a wide range of
animal allergens (Table 7-1). As much as 10% of the general
• Educate the public that exposure to allergens can be population and 50% of persons with atopy (allergic predis-
a significant contributor to rates of asthma and other position) may be sensitized to dogs and cats. Other animals
allergic conditions in the community.1 causing significant allergy in human beings include rodents,
• Support surveillance and analysis of asthma data (for horses, insects, and birds.5
case definition, see http://www.cste.org/ps/1998/1998- Much symptomatic animal allergy is associated with pet
eh-cd-01.htm). ownership, but allergy can also be a significant occupational
problem for individuals working with animals, including
Human Health Clinicians laboratory animal workers3 and veterinarians (see Chapter 12).
Occupational allergens include rodent urine, cat dander, and
• Allergen exposure reduction is a part of a comprehen- horse dander. Because animal allergens may persist in the
sive management program for asthma and allergies. environment long after elimination of a pet and can be car-
Pets may be an important source of allergens, but elim- ried distances in dust, cat and dog allergens may be present
ination of the pet may not be the only therapeutic option in homes where no pets are present and in schools.
and should be considered in light of a comprehensive
treatment and prevention approach. Clinicians may wish
Allergy to Cats and Dogs
to discuss options with the family veterinarian. (Note:
Cat allergens can persist in the environment years after A common misconception is that human beings are aller-
the elimination of the pet.) Other animals such as rats gic to cat and dog hair and that short-haired breeds of cats
and mice also can contribute to indoor air allergen load. and dogs are less allergenic than long-haired breeds. In fact,
• When evaluating a patient with allergic symptoms, human allergy to cat and dogs is related to specific protein
inquire also about contacts with animals and the allergens, such as Fel d 1 and Can f 1, respectively, rather than
43
Table 7-1 n Sources of Animal Allergens

Clinical conditions related to animal
allergy
Associated with Human Allergy
Animal Species Source of Allergen Rhinitis and Upper Airway Symptoms

Rats and mice Urine, hair, saliva Rhinitis and upper airway symptoms are among the most
common complaints in outpatient medical practice. The
Guinea pigs Urine, dander, saliva, hair
prevalence in the general population is as high as 20%, but
Rabbits Urine, saliva, hair in patients with asthma the prevalence is generally much
Cats Dander, saliva higher. Symptoms include sneezing, nasal passage obstruc-
Dogs Dander tion, lacrimation, and itching of the nasopharynx. The diag-
nosis is generally made by history and physical examination.
Birds Feathers, serum
One of the most important distinctions to make in chronic
Horses Serum, dander rhinitis and sinusitis is whether it is allergic or nonaller-
Cattle Hair, dander gic. Nonallergic rhinitis and rhinosinusitis can occur in the
Reptiles Scales3
context of exposure to airborne irritants in the environment.
Especially if these irritant exposures continue, this condition
Nonhuman primates Hair is less amenable to treatment with pharmacotherapy.
Cockroaches Feces, saliva, debris from dead Diagnostic testing for rhinitis and other allergic condi-
animals4 tions related to indoor air exposure can include skin prick
Mites Feces or blood testing for IgE antibodies to specific antigens.
Skin prick testing involves noting the immediate wheal-
and-flare reaction to antigens introduced under the skin.
hair per se. For this reason, despite advertising claims to the Blood testing using radioallergosorbent testing (RAST)
contrary, there are currently no “nonallergenic” breeds of cats can screen for a wide number of IgE antibodies to specific
and dogs. However, some species appear to provoke allergies antigens. Both skin testing and RAST testing are associ-
in certain individuals and efforts are under way to develop ated with false-positive and false-negative results, and this
breeds with lower allergenic potential. Cats produce a num- possibility must be considered in reviewing the results of
ber of proteins that can act as human allergens. The one con- such testing.
sidered the most important, Fel d 1, is produced by sebaceous Management of upper airway disorders is generally a
and salivary glands, basal squamous epithelial skin cells, and combination of exposure reduction and pharmacotherapy.
anal glands of cats.6 It can be carried on particles less than 5 Exposure reduction typically involves multiple measures,
microns in diameter that can remain airborne for long peri- such as eliminating irritating chemicals, cleaning more fre-
ods of time.7 A naturally selected line of cats with deficient quently and/or adopting changes in cleaning techniques, and
Fel d 1 is being developed.2 Dog breed, gender, and seborrhea (if relevant) removing or isolating pets from the bedroom
appear to influence the levels of Can f 1 allergen detected on and removing fabrics that retain dander and allergens. These
fur.8 Cat and dog allergens may persist for extended periods measures have been effective in reducing allergen exposure
in a house even after a pet has left, and both Fel d 1 and Can and improving symptoms in the aggregate but not neces-
f 1 have been detected in homes without pets.9 sarily in the individual patient. Pharmacotherapy includes
nasal steroid sprays and antihistamines to control allergic
Risk Factors for Pet Allergy symptoms.
Despite the prevalence of pet allergy, it is not clear whether

having a pet in the house increases the overall risk of allergy.
Asthma
Host factors play an important role, especially the presence of Human asthma is characterized by bronchoconstriction and
atopy, defined as “the genetic propensity to develop immuno- inflammation with airway secretions, leading to obstruction
globulin E [IgE] antibodies in response to exposure to aller- of the airways. Clinically, the hallmark symptoms of asthma
gen.”10 Studies have shown that children born into families are wheeze, cough, and dyspnea. The pathogenesis of asthma
that already own dogs (where there is no history of atopy) involves reversible airway obstruction, and treatment with
have a lower risk of allergic disease by 2 years of age compared both short- and long-acting medications can reverse or pre-
with families that did not have a dog.11 The genetic basis of vent the symptoms. A variety of allergens can lead to sensitiza-
allergic predisposition is a subject of active scientific investi- tion and new onset of asthma, or exacerbation of underlying
gation. The timing of allergen exposure also appears to play a asthma in previously sensitized individuals, including ani-
role. Although it has been reported that early exposure to cats mal-related allergens such as dander, cockroach excreta, and
can increase the risk of early sensitization and development dust mites. The role of domestic animals in asthma causa-
of an immune response to cat allergens, other studies have tion and prevention is complex. Some studies show that pos-
shown a protective effect for pet ownership early in life, and session of pet dogs and cats may be associated with a lower
still others have demonstrated inconsistent results regard incidence of early childhood asthma, whereas other studies
ing the development of early clinical allergic disease (particu- suggest that pet possession may lead to an increased risk of
larly asthma).12,13 Farm exposure in early life is also associated asthma. These differences may be due in part to the nature
with an allergy-protective effect in human beings.14 of the population in question. The effect seems to vary with
Chapter 7 n Allergic Conditions 45
the age of the children, whether they are in environments from other birds, especially psittacine birds such as parakeets
with high or low prevalence of pet ownership, and whether and parrots (“bird fancier’s lung”).
there is a family history of allergic disorders.15 At this time, HP can have both an acute and insidious onset pattern.
therefore, it is not possible to offer general recommendations Acute symptoms may follow an exposure to antigen, such
regarding ownership of pets for young families if there is no as cleaning an animal’s cage, and can include cough, short-
current asthma or atopy in the family. ness of breath, and fever. Many cases are misdiagnosed and
In evaluating a patient with suspected asthma, it is impor- treated as pneumonia because chest radiographs may show
tant to confirm that reversible airway disease is present. If a fleeting infiltrates (Figure 7-1).17 HP also can be mistaken
patient has spirometry showing obstruction, reversibility can for other forms of interstitial lung disease. Some exposed
be demonstrated by improvement in spirometry flow rates patients may not notice acute effects but instead have grad-
after bronchodilator administration. If spirometry is nor- ual onset of shortness of breath and progressive fatigue. If
mal at baseline, a methacholine challenge test can document exposure continues, the pulmonary inflammation may lead
abnormal bronchial reactivity. to irreversible fibrosis and restrictive lung disease and even
As with rhinitis, allergic asthma must be distinguished respiratory failure.
from nonallergic asthma. Nonallergic asthma may be due HP can be difficult to recognize and diagnose. The diagno-
to exposure to chemical irritants. Diagnostic testing often sis of HP relies partly on a history of exposure to an antigen.
involves skin prick or RAST testing. A variety of agents are Pulmonary function testing classically shows a restrictive pat-
available for asthma treatment, including inhaled cortico tern, although obstruction also can be seen, particularly with
steroids, bronchodilators, leukotriene inhibitors, and mast avian exposures. Like other interstitial disease, the diffusion
cell stabilizers. capacity of carbon monoxide is reduced. Serum precipitins
may be positive but have low sensitivity and depend on the
laboratory and preparation of standards.18 Bronchoalveolar
Anaphylaxis
lavage (BAL) shows a predominance of lymphocytes (30%
Anaphylaxis is an acute, severe, IgE-mediated reaction to to 90%) and macrophages. Computed tomographic scans
environmental allergens that can occur in sensitized indi- may show a characteristic alveolitis pattern. Referral and co-
viduals. The clinical presentation of anaphylaxis can involve management with a specialist in occupational pulmonary
swelling of the lips and throat with progressive airway edema diseases are recommended.
leading to obstruction and respiratory collapse and death if The treatment of HP requires removal from exposure.
not treated. Patients may be reluctant to give up their animals or oth-
Anaphylaxis can occur as a result of exposure to insect erwise take steps to reduce exposure and need to be coun-
stings (see Chapter 8) but can also occur with exposure seled that they risk potentially fatal lung disease. Unlike
to other animal allergens. Anaphylactic reactions can also some allergic conditions mentioned in this chapter, elimina-
occur when the immediate precipitating factor is unknown. tion of the exposure is generally required for patients with
The diagnosis is typically made by clinical history; labora- HP because of the risk of irreversible complications. Other
tory testing is of limited value. Although tryptase or hista- adjuncts to treatment include oral steroids, although there is
mine levels may be elevated acutely after an anaphylactic no supporting evidence that this affects the natural history
episode, they usually return to normal by the time of a of the disease.
clinical evaluation. The presence of elevated serum IgE
to a specific antigen can be of benefit in a patient with a
history of anaphylactic episodes, but it is of limited value
in predicting whether an asymptomatic patient is at risk of
future anaphylaxis because many people with elevated IgE
levels do not have anaphylactic symptoms. Although the
negative predictive value of IgE is relatively high, occasion-
ally people with normal IgE levels can have anaphylactic
reactions to an antigen.16 The treatment of anaphylactic
episodes may include epinephrine, antihistamines, and
steroids.
Hypersensitivity Pneumonitis
Hypersensitivity pneumonitis (HP), also known as extrinsic
allergic alveolitis, is an inflammatory reaction of the lower
airways to a variety of environmental allergens. Also encoun-
tered in the occupational setting, HP can be caused by expo-
sure to thermophilic bacteria in moldy hay (“farmer’s lung”),
mushrooms (“mushroom worker’s lung”), and a large num-
ber of other animal and plant allergens, including wood dust.
It can also be caused by certain chemicals such as isocyanates. Figure 7-1 n Chest radiograph of acute hypersensitivity pneumonitis.
Animal allergens that have been implicated in HP include (From Adkinson NF Jr: Middleton’s allergy: principles and practice, ed 6,
pigeon antigens (pigeon breeder’s lung) and feather dander St. Louis, 2003, Mosby.)
An accurate history can reveal important details about

the circumstances of exposure (see Chapter 3). The timing of
symptom onset with the acquisition of a pet or contact with
the pet or specific areas where the pet spends the most time
can be helpful in making the association. It is also impor-
tant to ask about occupation and possible association with
occupational exposures. It is important to have a history of
possible comorbid conditions and to establish which medi-
cations are already in use or have been tried. A family history
and history of tobacco use are also essential.
It is important to inquire about any previous symptoms
of anaphylactic reactions to animal contact or other allergens
in taking the history of allergy.
Diagnostic testing for animal allergy can involve skin
prick testing, RAST for animal-specific IgE, and/or a serum
IgG panel for suspected HP. Chest radiographs often are use-
ful for HP. Pulmonary function tests are helpful to establish
baseline function and to distinguish obstructive disease from
restrictive or mixed patterns but are not generally helpful in
distinguishing allergic from other disorders.
If airway involvement is suspected (bronchial asthma),
an adjunct to the patient history can be a peak flow diary,
Figure 7-2 n Hand eczema. (From Habif TP: Clinical dermatology: a
in which the patient records peak flow rates several times a
color guide to diagnosis and therapy, ed 4, St Louis, 2004, Mosby.) day for 2 weeks to help determine whether decreases in peak
flows are related to times of animal exposure.20
Trials of avoidance for animal allergy can be both diag-
Eczema/Dermatitis nostic and therapeutic. In the home setting, they involve
either removing the animal from the house for a period to
Eczema, also known as atopic dermatitis, is a skin disorder see whether symptoms improve or having the person spend
(Figure 7-2) characterized by pruritus and scratching that time in another house or other environment free from the
often affects flexor surfaces and usually appears before the presumptive allergen. Removal of the animal for a few days
age of 5 years. Because it is associated with an atopic pre- or weeks may not be sufficient because 20 weeks or longer
disposition, in many children with eczema allergic rhinitis, may be required for levels of animal antigen to fall to back-
asthma, or both eventually develop. The condition often per- ground levels, and allergens may be highly transportable.21
sists into adulthood. The diagnosis is usually made by history
and physical examination. As with other allergic disorders, it
has been suggested that early exposure (indicated by owner- Management options for allergy
ship of a furry pet) may have a protective effect against the to animals
development of eczema, but this result is inconsistent and
could have other explanations such as avoidance behavior.19 Once it is clear that an individual has allergies and is sensi-
Management of eczema includes topical steroids and tized to a pet in the house, there are three basic management
newer nonsteroidal antiinflammatory agents. Treatment may options: (1) removal of the animal or person, (2) reduction
be required for secondary effects such as infection. Known of the allergen load without removal of the animal or per-
triggers can be avoided but this is often not effective, and son, and (3) desensitization therapy. Robust evaluation of
there are few data on either allergen reduction or removal of the differential effectiveness of these measures is lacking.22
pets in eczema.
Other dermatitis conditions related to animal allergy
Removal of the Animal or Person
include acute development of hives and itching following
allergen exposure; such skin reactions may be accompanied The National Asthma Education and Prevention Program
by anaphylaxis (see below). Expert Panel Report 3 recommends animal removal as the
treatment of choice for those with known animal dander sensi-
Diagnosing Allergy to Animals tization. If removal is not acceptable to the patient, then expo-
sure should be minimized by keeping the pet out of the patient’s
When faced with a patient who may have an animal allergy, room, keeping the bedroom door closed, removing upholstered
clinicians should take a detailed history of exposures and furniture and carpeting, or keeping the pet from those items.23 It
symptoms, perform diagnostic testing for response to anti- is important to stress that this should be done as part of a com-
gens, and consider a trial of exposure reduction. It is simple prehensive program of exposure reduction and effective medi-
to assume that a person with allergic symptoms who shares cal management. Removal of the pet will reduce but may not
a house with an animal must be having allergic reactions to eliminate an individual’s total allergen exposure. This is espe-
that animal, but this is not always the case. Another allergen cially important in cases of anaphylaxis, as well as HP and severe
exposure could be the causative agent instead. asthma, for which the outcomes can be irreversible or fatal.24
Allergen Reduction
Selected allergic conditions in animals
The role of allergen load reduction in asthmatic patients with
known sensitization to animal dander is well established. A number of conditions in companion animals may be
Studies of allergen reduction have generally demonstrated related in part to allergens and could be corollaries of allergic
that multifaceted strategies are required to achieve significant conditions in human beings (Table 7-2). With more owners
reductions in allergen load. These strategies include thorough seeking veterinary medical care for their pets, the recogni-
cleaning with high-efficiency particulate (HEPA) vacuum tion of these diseases is increasing.
cleaners (to avoid resuspending particulates), removing car-
peting and upholstered furniture from the bedroom, washing Feline Asthma
and covering bedding with impermeable covers, using HEPA
air filtration, and keeping the pet out of the bedroom.25 In As in human beings, feline asthma is associated with eosino-
one study, routinely washing cats resulted in only a short- philic airway inflammation, reversible airway obstruction,
lived (24-hour) reduction in Fel d 1 and was therefore not airway hyperreactivity, and airway remodeling. Aeroallergens
considered efficacious.26 Although individually it is difficult are believed to drive the Th2 immune response leading to
to document how much each of these strategies adds to the clinical signs of cough, wheeze, and episodic respiratory
total, the reductions in allergen loads are significant. distress. Cats have tested positive to a variety of allergens
(including weeds, trees, grasses, fungi, and house dust mites)
using IgE serology and intradermal skin testing (Figure
Desensitization
7-3).29-31 Cats may also develop clinical signs after exposure
Allergen desensitization therapy has been used extensively to nonallergen irritants such as cigarette or fireplace smoke,
to treat patients with more severe allergic conditions such as various sprays (e.g., hairspray, deodorant, flea spray, deodor-
insect venom allergy. A recent innovation in immunother- izer), and dust from cat litter. Some cats have responded well
apy is the use of sublingual administration in addition to the to allergen avoidance.32,33
more traditional injections. Much of the data on the effective- The diagnosis of feline asthma is usually made clinically.
ness of immunotherapy concerns allergens that pose signifi- Thoracic radiographs may show signs of a bronchial or bron-
cant risks to patients or cannot be easily avoided, such as dust chointerstitial pattern with evidence of lung lobe collapse (due
mite, pollens, or bee stings. Some data show the effectiveness to mucus plugging of the major bronchus) or hyperinfla-
of immunotherapy for animal allergens, but this is not seen as tion (due to air trapping secondary to bronchoconstriction).
a first-line therapy.27 One question that remains unanswered However, thoracic radiographs may also be unremark-
is how long immunotherapy must be maintained.28 able despite pronounced airway inflammation. Eosinophilic
Table 7-2 n Common Allergic Diseases in Companion Animals
Potential
Species Disease Clinical Manifestations Diagnosis Treatment Causative Factors
Cats Asthma Cough, wheeze, Thoracic radiographs, Bronchodilators, Aeroallergens

respiratory distress airway cytology, ancillary steroids (presumptive)
diagnostics
Dogs Canine Cough, respiratory Thoracic radiographs, Steroids (with or without Aeroallergens (?)
eosinophilic distress, nasal discharge airway cytology, exclusion antibiotics as indicated)
broncho of known causes of
pneumopathy eosinophilic airway
(eosinophilic inflammation
bronchitis/
pneumonia)
Cats, Atopic Pruritus, redness, scaling, Intradermal skin Steroids, allergen Molds; tree,
dogs dermatitis hyperpigmentation, testing (see Figure 7-3), avoidance, allergen- weed, and
hair loss RAST test specific immunotherapy, grass pollens;
essential fatty animal and
acids, cyclosporine, human dander;
antihistamines fabrics (wool)
Horses Recurrent airway Coughing, airway History, physical Environmental Molds, stable
obstruction obstruction, exercise examination, airway modification, dusts
(heaves) intolerance cytology bronchodilators, steroids
Cattle Hypersensitivity Weight loss, coughing, Tracheal wash, positive Corticosteroids for acutely Dusts from
pneumonitis granulomatous serology to Micropolyspora affected or severely moldy hay
inflammation, alveolitis, faeni suggestive, lung recurrent cases, change (thermophilic
interstitial fibrosis biopsy in management (e.g., actinomycetes
turning cattle outside) spores)
Atopic Dermatitis
Dogs and cats commonly develop allergic skin disease associated
with elevated IgE to a variety of indoor and outdoor environmen-
tal allergens. Along with elevations in allergen-specific IgE, other
contributing factors thought to contribute to atopic dermatitis
include increased susceptibility to bacterial and yeast infections
(Figure 7-4), abnormal epidermal barrier function, T helper 2
cell polarity, and/or defective T-cell regulatory function.
The diagnosis of atopic dermatitis involves performing
a careful clinical history and physical examination (Figure
7-5). It is necessary to exclude other disorders causing similar
clinical signs, including ectoparasites, flea allergic dermatitis,
adverse food reactions, and dermatophytosis. Intradermal
skin testing and serum allergen-specific IgE testing are
important aids to identifying specific allergens in making a
diagnosis of atopic dermatitis in dogs and cats.
Figure 7-3 n Allergy skin testing in a cat. The positive reactions are well- In dogs and cats, treatment for atopic dermatitis includes
demarcated erythematous wheals, which have the appearance of bee stings. avoidance of identified allergens when possible, topical ther-
(From Medleau L, Hnilica KA: Small animal dermatology: a color atlas and apy (such as hypoallergenic and colloidal oatmeal–containing
therapeutic guide, ed 2, St Louis, 2006, Saunders Elsevier.) shampoos) to remove allergens from the skin and prevent
dry skin, antiinflammatory drugs (steroids, fatty acids,
cyclosporine), and allergen-specific immunotherapy.
a irway inflammation can be seen on lavage cytology. A positive
response to a treatment trial of oral or inhaled glucocorticoids
and bronchodilators is also helpful in the diagnosis of feline
asthma. Unlike in human asthma, pulmonary function testing
is not routinely performed in pet cats.
Canine Eosinophilic Bronchopneumopathy

Dogs are not known to develop asthma, although they do
develop a syndrome more analogous to eosinophilic bron-
chitis in human beings that is characterized by eosinophilic
airway inflammation without spontaneous airway obstruc-
tion or consistent hyperreactivity.34 In contrast to what is
seen in human beings, simultaneous bronchial and pul-
monary parenchymal infiltration by eosinophils is usually Figure 7-4 n Generalized alopecia in a dog secondary to atopy. (From
present in dogs. Eosinophils and CD4+ T lymphocytes in Medleau L, Hnilica KA: Small animal dermatology: a color atlas and therapeutic
bronchoalveolar lavage fluid support an allergic cause for guide, ed 2, St Louis, 2006, Saunders Elsevier.)
this disorder. Intradermal skin testing in dogs with eosino-
philic bronchopnemopathy has shown positive reactions
against mites, human dander, and mixed feathers.35
Radiographic and bronchoalveolar lavage results support
diagnosis. Thoracic radiographs show infiltrates centered
around the airways and/or in the interstitium or alveolar
spaces with bronchiectasis in many chronic cases. Lavage
cytology demonstrates an increased eosinophil count. Other
causes of airway eosinophilia (e.g., parasites) should be ruled
out by blood or fecal testing or with a course of an appropri-
ate antihelminthic.
Glucocorticoids are the mainstay of therapy of canine
bronchopneumopathy. During clinical presentation, second-
ary infection may exacerbate disease, and a course of antibi-
otics based on culture results should be considered. Because
it is suspected that aeroallergens may be responsible for
eosinophilic bronchopnemopathy, hyposensitization/desen- Figure 7-5 n Feline atopy. Alopecia and early eosinophilic plaques on the
sitization therapy based on intradermal skin testing results abdomen of an allergic cat. (From Medleau L, Hnilica KA: Small animal derma-
can be tried.34 tology: a color atlas and therapeutic guide, ed 2, St Louis, 2006, Saunders Elsevier.)
Heaves in Horses at age 5 years in an inner-city cohort. J Allergy Clin Immunol.

2008;121(4):1047–1052.
Heaves (also called recurrent airway obstruction and formerly 13. Brussee JE, Smit HA, van Strien RT, et al. Allergen exposure in infancy
called equine chronic obstructive pulmonary disease) appears and the development of sensitization, wheeze, and asthma at 4 years.
J Allergy Clin Immunol. 2005;115(5):946–952.
to be a form of chronic allergic asthma or severe asthma 14. Vogel K, Blümer N, Korthals M, et al. Animal shed Bacillus licheniformis
that develops as a hypersensitivity reaction to mold and sta- spores possess allergy-protective as well as inflammatory properties.
ble dusts. Unlike the case in cats and many human beings J Allergy Clin Immunol. 2008;122(2):307–312.
in which eosinophils are the predominant inflammatory 15. Chan-Yeung M, Becker A. Primary prevention of childhood
asthma and allergic disorders. Curr Opin Allergy Clin Immunol.
cell, the neutrophil is the main cell type in equine heaves and 2006;6(3):146–151.
eosinophils are rare. 16. Simons FE, Frew AJ, Ansotegui IJ, et al. Risk assessment in anaphylaxis:
current and future approaches. J Allergy Clin Immunol. 2007;120
(suppl 1):S2–24.
Bovine Hypersensitivity Pneumonitis 17. Rosenstock L, Cullen MR, Redlich C, et al., eds. Textbook of clinical occu-
pational and environmental medicine. 2nd ed. Philadelphia: Saunders;
Cattle can develop a respiratory condition that is similar to 2002.
HP in human beings as a result of exposure to moldy hay. 18. Fenoglio CM, Reboux G, Sudre B, et al. Diagnostic value of serum
The presentation may be acute or chronic and includes precipitins to mould antigens in active hypersensitivity pneumonitis.
cough, fever, and respiratory distress. The chronic form can Eur Respir J. 2007;29(4):706–712.
19. Langan SM, Flohr C, Williams HC. The role of furry pets in eczema:
involve anorexia and weight loss. Interstitial fibrosis of the a systematic review. Arch Dermatol. 2007;143(12):1570–1577.
lung may be found on necropsy. Treatment with steroids may 20. Plaschke P, Janson C, Balder B, et al. Adult asthmatics sensitized to cats
lead to clinical improvement, but affected cattle can improve and dogs: symptoms, severity, and bronchial hyperresponsiveness in
markedly when turned out to pasture in the spring.36 patients with furred animals at home and patients without these ani-
mals. Allergy. 1999;54(8):843–850.
21. American Academy of Allergy, Asthma, and Immunology (ACAAI).
Resources Advice from your allergist…pet allergy. http://www.acaai.org/public/
advice/pets.htm. Accessed August 20, 2008.
• National Institutes of Health, National Heart, Lung, and 22. Morris A. ABC of allergology: aero-allergen avoidance measures—
Blood Institute: Guidelines for the diagnosis and manage- effective or futile? Curr Allergy Clin Immunol. 2008;21(2):101–102.
23. National Heart, Lung, and Blood Institute; National Asthma Education
ment of asthma (http://www.ncbi.nlm.nih.gov/bookshelf/ and Prevention Program. Expert panel report 3: guidelines for the diag-
picrender.fcgi?book=asthma&blobtype=pdf) nosis and management of asthma. http://www.nhlbi.nih.gov/guidelines/
• Centers for Disease Control and Prevention: Asthma asthma/asthgdln.pdf. Accessed July 26, 2008.
(http://www.cdc.gov/asthma) 24. Shirai T, Matsui T, Suzuki K, et al. Effect of pet removal on pet allergic
asthma. Chest. 2005;127(5):1565–1571.
25. Eggleston PA. Improving indoor environments: reducing allergen expo-
References sures. J Allergy Clin Immunol. 2005;116(1):122–126.
26. Nageotte C, Park M, Havstad S, et al. Duration of airborne Fel d 1
1. Institute of Medicine. Clearing the air: asthma and indoor air exposures. reduction after cat washing. J Allergy Clin Immunol. 2006;118(2):
Washington DC: National Academy Press. http://www.nap.edu/catalog. 521–522.
php?record_id=9610. 27. Alvarez-Cuesta E, Berges-Gimeno P, González-Mancebo E, et al.
2. Ferguson BJ. Environmental controls of allergies. Otolaryngol Clin North Sublingual immunotherapy with a standardized cat dander extract:
Am. 2008;41(2):411–417, viii–ix. evaluation of efficacy in a double blind placebo controlled study.
3. San Miguel-Moncín MM, Pineda F, Río C, et al. Exotic pets are new Allergy. 2007;62(7):810–817.
allergenic sources: allergy to iguana. J Invest Allerg Clin Immunol. 28. Cox L, Cohn JR. Duration of allergen immunotherapy in respira-
2006;16(3):212–213. tory allergy: when is enough, enough? Ann Allergy Asthma Immunol.
4. Adkinson Jr NF. Middleton’s allergy: principles and practice. 6th ed. 2007;98(5):416–426.
St Louis: Mosby; 2003. 29. Halliwell RE. Efficacy of hyposensitization in feline allergic diseases
5. Elliott L, Heederik D, Marshall S, et al. Progression of self-reported based upon results of in vitro testing for allergen-specific immunoglob-
symptoms in laboratory animal allergy. J Allergy Clin Immunol. 2005; ulin E. J Am Anim Hosp Assoc. 1997;33(3):282–288.
116(1):127–132. 30. Moriello KA, Stepien RL, Henik RA, et al. Pilot study: prevalence of pos-
6. Liccardi G, Cazzola M, D’Amato M, et al. Pets and cockroaches: two itive aeroallergen reactions in 10 cats with small-airway disease without
increasing causes of respiratory allergy in indoor environments. concurrent skin disease. Vet Derm. 2007;18(2):94–100.
Characteristics of airways sensitization and prevention strategies. Respir 31. Norris Reinero CR, Decile KC, Berghaus RD, et al. An experimental
Med. 2000;94(11):1109–1118. model of allergic asthma in cats sensitized to house dust mite or bermuda
7. Bateman BJ, Dean TP. The Cheshire cat’s grin—is cat allergy here to grass allergen. Int Arch Allergy Immunol. 2004;135(2):117–131.
stay? Clin Exp Allergy. 1999;29(6):725–728. 32. Prost C. Treatment of feline asthma with allergen avoidance and specific
8. Ramadour M, Guetat M, Guetat J, et al. Dog factor differences in Can f immunotherapy: experience with 20 cats. Revue Française d’Allergologie
1 allergen production. Allergy. 2005;60(8):1060–1064. et d’Immunologie Clinique. 2008;48(5):409–413.
9. Arbes Jr SJ, Cohn RD, Yin M, et al. Dog allergen (Can f 1) and cat aller- 33. Corcoran BM, Foster DJ, Fuentes VL. Feline asthma syndrome: a retro-
gen (Fel d 1) in US homes: results from the National Survey of Lead and spective study of the clinical presentation in 29 cats. J Small Anim Pract.
Allergens in Housing. J Allergy Clin Immunol. 2004;114(1):111–117. 1995;36(11):481–488.
10. Arshad SH, Tariq SM, Matthews S, et al. Sensitization to common aller- 34. Clercx C, Peeters D. Canine eosinophilic bronchopneumopathy. Vet
gens and its association with allergic disorders at age 4 years: a whole Clin North Am Small Anim Pract. 2007;37(5):917–935.
population birth cohort study. Pediatrics. 2001;108(2):E33. 35. Clercx C, Peeters D, German AJ. An immunologic investigation
11. Pohlabeln H, Jacobs S, Bohmann J. Exposure to pets and the risk of of canine eosinophilic bronchopneumopathy. J Vet Intern Med.
allergic symptoms during the first 2 years of life. J Invest Allerg Clin 2002;16(3):229–237.
Immunol. 2007;17(5):302–308. 36. Kahn CM, Line S. The Merck veterinary manual. 9th ed. Whitehouse
12. Perzanowski MS, Chew GL, Divjan A, et al. Cat ownership is a risk Station, NJ: Merck; 2005.
factor for the development of anti-cat IgE but not current wheeze
Toxic Exposures
8
sections provide specific information on toxicity caused by
Healthy Homes carbon monoxide, lead, animal-related pesticides, envenoma-
tions, and harmful algae blooms (HABs).
The concept of a “healthy home” as promoted by the U.S.
Department of Housing and Urban Development (HUD)
Professionals
and other federal agencies involves not only aspects of the
built environment (see Chapter 6), but also creating homes
that are safe in terms of toxic hazards such as carbon mon-
oxide and pesticides.1 This concept is one in which human
health care providers, public health professionals, and vet- • Educate the public on principles for a safer, healthier
erinarians can actively collaborate because it seems clear that home:
what is good for the human beings in the household in terms Eliminate tobacco smoking from the home.
of toxic hazard reduction is also good for animals living in Use safer substances for general cleaning (e.g., vin-
the household. egar, lemon juice).
In the early part of the twentieth century, miners in the Store medications out of reach of children and pets.
United States and Great Britain brought caged canaries into Eliminate toxic substances from the home or store
mines to provide an early warning of the presence of deadly them out of reach of children and animals.
gases such as carbon monoxide and methane. Studies had Use nontoxic plants in and around the home.
shown that the canaries were more sensitive than other spe- Use integrated pest management (IPM) techniques
cies to the effects of these gases,2 and a canary becoming ill for rodent, weed, and insect control to reduce de-
and falling from its perch was sufficiently recognizable to pendence on toxic substances. (See, for example,
warn the miners of the hazard. In the same way, animals liv- http://www.epa.gov/pesticides/factsheets/ipm.
ing in or near a household can serve as “sentinels” for human htm.) IPM is a commonsense and environmentally
health hazards related to toxic exposures in the home and sensitive approach to pest management that uses
other environments. Much of what is known about the toxic current, comprehensive information on the life cy-
properties of environmental chemicals is based on studies cles of pests and their interaction with the environ-
of laboratory animals such as rats and mice. However, pets, ment.
other domestic animals, and wildlife can provide both clini-
cally important information to human health as well as use-
ful “animal models” of cancer and other environmentally
induced disease.3 • Consider toxic exposures in the differential diagnosis
At times it is the human being who first presents to medi- of both acute and chronic medical problems.
cal care with a toxic syndrome that is relevant to animals in • If unusual health events are occurring in pets and/or
the household. Greater access to medical care and diagnos- other animals, consider whether this could be a sentinel
tic services may result in diagnosis in the human case before event warning of human health risk from an environ-
related animal cases. mental toxic hazard.
This chapter outlines acute poisoning and chronic toxic • An acute poisoning episode in a pet could be a warning
exposure situations for human beings and other animals and of inappropriate access to hazardous substances and
indicates certain scenarios in which a toxicant-related dis- the need for steps to prevent exposures to children.
ease event in one species could be an indicator of risk for • Counsel smokers on the importance of smoking cessa-
other species. This section provides an overview of acute tion to benefit their own health and the health of oth-
and chronic toxic exposures in different species. Subsequent ers in the household (including pets).
50
Chapter 8 n Toxic Exposures 51
• Be aware of cultural and ritualistic use of toxic sub- Judiciously Prescribe Medications
stances such as mercury, which may endanger household
members and companion animals (see http://www.epa. Human and veterinary clinicians should weigh the relative
gov/superfund/community/pdfs/merc_rep05.pdf). value of prescribing medications by considering such issues
• Judiciously prescribe medications and counsel patients as antibiotic resistance, drug interactions, entrance of phar-
to keep medications and other toxic hazards stored out maceuticals into community drinking water, and assurance
of the reach of children and companion animals. that drugs are taken only by the individuals for whom they
are prescribed. Patient/owner education should be care-
fully reviewed such that judiciously prescribed medications
should never be administered to other people, household
• Consider toxic exposures in the differential diagnosis pets, or other animals. In addition, over-the-counter medi-
of both acute and chronic animal illness. cations should be administered only to a companion animal
• If toxic exposures are identified in animal patients, based on the veterinarian’s treatment plan for that animal.
consider whether human beings could also be at risk
and contact public health authorities. Substitution: “Green” Chemistry
• An acute poisoning episode in a pet could be a warning
of inappropriate access to hazardous substances and One way to reduce the risk of acute and chronic poisoning
the need for steps to prevent exposures to children. is to consider less-toxic substitutes for many household uses.
• If owners report toxic exposures diagnosed in human In general, keeping the residence uncluttered, food sources
beings in the household, consider whether animals are appropriately stored, and surfaces clean and dry will elimi-
also at risk. nate much of the need for more-toxic substances. In addi-
• Judiciously prescribe medications and counsel owners tion, “green” or “sustainable” chemistry encourages the
to keep medications stored out of the reach of children design and use of products that ultimately eliminate the need
and companion animals. for hazardous substances.
• Counsel owners not to use any medications in their The public should use caution with herbal remedies in the
animals unless prescribed by a veterinarian. belief that these substances as substitutes for conventional
• Counsel owners about the least-toxic chemicals for pharmacology. Adverse events may occur and antidotes may
pest control and the use of IPM techniques. not be available.
Primary prevention of toxic exposure Animals as sentinels for human toxic

exposure risk
Human health and veterinary health clinicians can recom-
mend a number of preventive steps to their patients and Six years before the detection of Minamata disease, an out-
clients, respectively, to reduce the risk of toxic exposures to break of severe methyl mercury poisoning among families
human beings and other animals. living near Minamata Harbor in Japan, strange clinical signs
were seen in local cats that ate diets high in fish from the
Pet Proofing and Child Proofing bay. This “dancing cat disease” included twitching, spasms,
Pets and children share the potential for accidentally ingest- abnormal movements, and convulsions. Only later was the
ing toxic substances left around a house or yard. Keep toxic association made between the neurological signs in the cats
substances such as cleaning solutions, flea and tick prepara- and the devastating signs of mercury poisoning in children
tions, other pesticides, and all medications out of reach of and adults (who also ate mercury-contaminated fish from
pets and children. Encourage smoking cessation to protect the bay) that included mental retardation, seizures, and other
the health of the smoker and human beings and animals neurological damage.4
exposed to secondhand smoke (Figure 8-1). The inappropriate use of melamine as a filler substance in
pet foods has been blamed for thousands of animal deaths
from renal failure.5 Unfortunately, this scandal did not pro-
tect against the subsequent unscrupulous use of the “protein
booster” in powdered baby formula in China, which led to
illness and death in human infants the following year.6
A National Academy of Sciences panel has concluded
that domestic animals and wildlife could serve as useful sen-
tinels of human environmental health hazards because they
may develop recognizable signs or biomarkers of toxicity in a
timely way to provide a warning to human beings and to assist
in human risk assessment.7 Animals may function as sentinels
when there are differences between animals and human beings
regarding exposure, susceptibility, or latency to a particular
hazard. At times, an unusual cluster of disease in an animal
Figure 8-1 n Eliminate tobacco smoke in the house. (From Centers for population may suffice to draw attention to a particular haz-
Disease Control and Prevention Public Health Image Library, Atlanta, Ga.) ard. For example, when horses (and dogs) in Times Beach,
Missouri, began to die after their stable area was sprayed with
oil to control dust, it was discovered that the oil was contami-
nated with dioxin.8 The Times Beach incident was the largest
community-wide exposure to dioxin in the United States.
Routes of Exposure
Perhaps the most likely opportunity for animals to serve as
sentinels of household toxic exposures is by their greater
exposure risk. Dogs are well known for their propensity to
ingest a wide variety of substances, including lead-containing
dusts and household cleaning agents, and therefore may be
the first in a household to manifest signs. Household pets also
spend more time in the home environment and thus could
have a higher exposure risk to a number of substances present
in the home. For example, cats and dogs may have increased Figure 8-2 n Canaries are popular caged birds that are revered for their
exposure to dust compared with human beings because they beauty and singing qualities. (From Tully TN Jr: Birds. In Mitchell MA,
Tully TN Jr (eds): Manual of exotic pet practice, St Louis, 2008, Saunders
live close to the floor level and often lick their fur during Elsevier.)
grooming (especially cats). Dust in a household may contain
accumulations of chemicals, including flame retardants, lead,
mercury, phthalates, and perfluorochemicals (used in non- anatomical differences that allow different degrees of contact
stick cookware) and can lead to significant toxic exposures in between carcinogenic air pollutants such as polyaromatic
human beings and other animals in the house. A recent study hydrocarbons (PAHs) and the lining of their nasal passages
of levels of chemicals in the blood and urine of dogs and cats compared with short-nosed dogs.12 An increased risk of
found levels of flame retardants in cats more than 20 times the bladder cancer has been reported in obese female dogs; the
average level in human populations, levels of mercury more reasons for this are not clear.12
than five times as high, and levels of perfluorochemicals in An example of interspecies differences in susceptibility to
dogs more than double that found in the general human pop- toxic exposures can be seen in the list of human foods that
ulation.9 These finding indicate that pets may have increased are toxic to some companion animals (Table 8-1) and com-
exposure to many toxicants found in household dust and mon human medications that may be highly toxic to pets at
fumes compared with human beings and therefore may be at relatively low doses.
risk of showing signs sooner or with greater severity.
Outdoors, dogs and cats may dig in the soil around a house Latency
or in adjacent neighborhoods, exposing themselves to lead, pes-
ticides, arsenic, and other toxic chemicals that could be in soil. Another way in which animals may be a sentinel for human
Some authorities have expressed concern that pets could then illness is if they develop signs in a shorter period of time
track such contaminated soil into a house on their paws and (latency). This may be more important for chronic rather
fur, potentially increasing the exposure risk for children and than acute toxic exposures. Most companion animals have
other inhabitants.10 Wildlife and livestock often live continu- a shorter average lifespan than human beings. Therefore
ously in outdoor environments near human beings and may be chronic disease effects from environmental exposures tend
exposed to toxicants in water, air, soil, and food sources, includ- to have a shorter latency. An example is the finding of meso-
ing vegetation, at much higher levels than human beings. thelioma in dogs whose owners had occupational or hobby
exposure to asbestos (which resulted in secondary exposure
of the household dog and other human beings in the house-
Metabolic Fate/Susceptibility hold) (Color Plate 8-1). The average age of the dogs at time
Physiological differences in metabolism in some animals of diagnosis was 8 years (48 “dog years”), whereas mesothe-
may make them more sensitive than human beings to cer- lioma in human asbestos exposure has a usual latency (time
tain toxicants. Canaries were found to be more sensitive than since asbestos exposure) in excess of 20 years.14
human beings to the toxic effects of carbon monoxide and
methane gas in coal mines, allowing them to provide early
warning to miners if they began to act sick (Figure 8-2). Dogs Acute toxic exposures
lack the metabolizing enzyme rhodanese and therefore may
have effects of cyanide poisoning at lower doses than human Accidental poisoning is a major cause of acute injury and
beings. Birds appear to be more sensitive than human beings death in the United States. The national network of poi-
to inhalation of fumes from burning polytetrafluoroethylene son control centers in the United States provides emergency
(PTFE; Teflon [DuPont, Wilmington, Del.]).11 advice to individuals and health care professionals about
Susceptibility to acute and chronic exposure to toxicants human poisonings (800–222–1222).15
may vary within species according to breed, sex, age, neuter- Each year more than 2 million cases of acute toxic expo-
ing status, or other differences. For example, the risk of nasal sures are reported to regional poison control centers, and
cancer in dogs (which has been linked to indoor air pollu- many others are treated in emergency departments with-
tion; see below) may be higher in long-nosed dogs because of out formal reporting.16 The majority of human poisonings
Table 8-1 n Partial List of Foods Toxic to Table 8-2 n Top 25 Substances Involved in Human
Companion Animals Exposures Reported to American Association of
Poison Control Centers, 2006
Food Toxic Effect in Toxic Effect in
(Ingredient) Dogs Cats Substance No. %*
Alcoholic beverages Ataxia, respiratory Ataxia, Analgesics 284,906 11.9

(ethanol) depression, cardiac respiratory
abnormalities, depression, Cosmetics/personal care 214,780 8.9
death (acute cardiac products
toxicity with 5-8 abnormalities, Cleaning substances 214,091 8.9
mL/kg; oral LD50 death (acute (household)
5500 mg/kg in toxicity with
dogs) 5-8 mL/kg) Sedative/hypnotics/ 141,150 5.9
antipsychotics
Avocado (persin) Vomiting, diarrhea None known
Foreign bodies/toys/ 120,752 5.0
Chocolate Vomiting, diarrhea, Vomiting, miscellaneous
(theobromine) tremors, seizures, diarrhea,
death (250-500 tremors, Cold and cough 114,559 4.8
mg/kg LD50 in seizures, death preparations
dogs) (200 mg/kg
Topical preparations 108,308 4.5
LD50 in cats)
Pesticides 96,811 4.0
Coffee (all forms) Vomiting, diarrhea, Vomiting,
(caffeine) tremors, seizures, diarrhea, Antidepressants 95,327 4.0
death (LD50 tremors,
140-150 mg/kg in seizures, death Bites and envenomations 82,133 3.4
dogs) (LD50 100-150 Cardiovascular drugs 80,426 3.3
mg/kg in cats)
Alcohols 76,531 3.2
Fatty foods Steatorrhea, Steatorrhea,
diarrhea, obesity, diarrhea, Antihistamines 75,070 3.1
pancreatitis obesity Food products/food 66,115 2.8
Macadamia nuts Vomiting, None known poisoning
depression, ataxia Antimicrobials 66,017 2.7
(2.2 g/kg)13
Plants 64,236 2.7
Moldy foods Muscle tremors, Muscle tremors,
(tremorgenic seizures seizures Vitamins 63,331 2.6
mycotoxins) Hormones and hormone 51,875 2.2
Onions, onion Hemolysis (11 g raw Hemolysis (28 g antagonists
powder, garlic, onions/kg) raw onion/kg) Gastrointestinal 50,914 2.1
leeks, chives preparations
(propyl disulfide)13
Hydrocarbons 49,526 2.1
Raisins and grapes Acute renal failure None known
(no apparent dose Chemicals 47,557 2.0
response)
Stimulants and street 46,239 1.9
Yeast dough Abdominal Abdominal drugs
(ethanol) distention, ethanol distention,
Anticonvulsants 40,476 1.7
toxicosis ethanol
toxicosis Fumes/gases/vapors 39,586 1.6
LD50, Median lethal dose.

Arts/crafts/office supplies 37,990 1.0
*Percentages are based on the total number of human exposures (2,403,539) rather
than the total number of substances.
involve young children, and the most common source of From Bronstein AC, Spyker DA, Cantilena LR Jr et al: 2006 annual report of the
poisoning is from prescription medications. However, other American Association of Poison Control Centers’ National Poison Data System (NPDS),
common exposures include cleaning substances and pes- Clin Toxicol (Phil) 45(8):815-917, 2007.
ticides. Table 8-2 shows the substances most commonly
involved in human exposures reported to poison control
centers. tices and a network of animal poison control centers in the
Animals also experience acute poisoning episodes. In United States and other countries. The American Society
fact, a significant number of calls to human poison con- for the Prevention of Cruelty to Animals (ASPCA) main-
trol centers involve nonhuman animals. As Table 8-3 shows, tains the national Animal Poison Control Center, a 24-hour
reported poisoning in dogs is much more frequent than in resource for practitioners managing acute toxic exposures in
cats, and poisonings in other species, including livestock and animals.17 An online information system has been developed
wildlife, are much less likely to be reported.11 In addition to in Switzerland for the management of poisoning in large and
animal reports to human poison control centers, acute poi- small animals (http://www.clinitox.ch).18 France also has a
soning episodes in animals are reported to veterinary prac- national service (http://www.vet-lyon.fr).19
Clinical management of acute toxic exposures involves

Table 8-3 n Nonhuman Exposures by Animal
identification of the exposure, reduction of the exposure,
Type Reported to American Association of administration of specific antidotes if available, and sup-
Poison Control Centers portive care. In-depth discussion of treatment protocols for
the complete range of specific chemical exposures is beyond
Animal No. %
the scope of this book, but a number of common toxic
Dog 114,599 89.3 exposures found in homes are covered, in addition to those
in the sections on carbon monoxide, lead poisoning, pesti-
Cat 12,002 9.4
cides, e nvenomations, and HABs.
Bird 482 0.4
Rodent/lagomorph 417 0.3
Horse 264 0.2
Common Medications and Their Toxicity
in Human Beings and Animals
Sheep/goat 105 0.1
Cow 41 0
Acetaminophen
Aquatic 40 0
Acetaminophen, a principal component of a large number
Other 403 0.3
of analgesic medications, is an excellent example of differ-
Total 128,353 100 ential interspecies susceptibility to toxic exposures. The
drug is metabolized in the liver by uridine diphosphate
From Bronstein AC, Spyker DA, Cantilena LR Jr et al: 2006 annual report of the
American Association of Poison Control Centers’ National Poison Data System (NPDS), (UDP)–glucuronyl transferase 1,6 to glucuronide and
Clin Toxicol (Phil) 45(8):815-917, 2007. excreted via the kidneys. Another detoxification pathway
is sulfation. Acetaminophen can also be oxidized through
the cytochrome P450 (CP450) system to N-acetyl-p-
Table 8-4 shows the distribution of substances account- benzoquinone imine, which is toxic to the liver. Cats have
ing for toxic exposures in animals reported to poison control only one tenth of the glucuronyl transferase activity com-
centers and veterinary practices in 2006. Chocolate inges- pared with dogs and are therefore highly susceptible to
tion, rodenticide exposure (also a hazard to children in a acetaminophen toxicity. The clinical signs of toxicity dif-
house), and medications (especially analgesics) account for fer somewhat among human beings and dogs and cats;
the majority of animal poisoning reports. Animals can be in human beings, the principal complication of over-
exposed to pharmaceuticals from ingesting human medica- dose is liver toxicity, whereas in cats methemoglobinemia
tions that are left unsecured within a household and from predominates. Both hepatocellular injury and methemo-
inappropriate administration of human or veterinary med- globinemia develop in dogs.11
ications by human beings. Inappropriate ingestion also Treatment of acetaminophen poisoning is similar in
accounts for much of exposure to rodenticides, pesticides human beings and other animals and involves decontami-
(including slug bait), poisonous plants, and cleaning prod- nation with stomach evacuation and administration of acti-
ucts.20,21 An acute toxic poisoning in an animal can therefore vated charcoal to bind unabsorbed medication, as well as the
be a warning sign of inappropriate access to hazardous prod- use of the antidote: N-acetylcysteine, which prevents oxida-
ucts. This situation should alert human health and animal tive damage to the liver.
health care providers to take steps to avoid further pet or
children’s exposures. Aspirin
Aspirin (acetylsalicylic acid) is another common analgesic
present in both over-the-counter and prescription analge-
Table 8-4 n Exposures of Animals to Various sics. As with acetaminophen, cats are more susceptible than
Toxic Agents Reported by Veterinary Clinics dogs or human beings, and fairly low doses can be fatal. The
and Poison Control Centers major complication of aspirin toxicity is gastrointestinal
(GI) irritation and bleeding, but at higher doses it can cause
Agent Relative Frequency (%) metabolic acidosis and central nervous system (CNS) tox-
icity. Treatment involves gastric evacuation if a recent large
Chocolate 26 ingestion is suspected, followed by activated charcoal, fluids,
Rodenticides 26 and alkalinization of urine.
Pharmaceuticals 22
Pesticides 13 Nonsteroidal Antiinflammatory Drugs
Plants 5 Nonsteroidal antiinflammatory drugs (NSAIDs), such as ibu-
Miscellaneous 3 profen and naproxen, can cause GI irritation and bleeding in
human beings, dogs, and cats. Dogs can be highly susceptible
Glycols 1
to the toxic effects of NSAIDs (Figure 8-3).11 Table 8-5 lists
Adapted from Gwaltney-Brandt SM: Epidemiology of animal poisonings. In Gupta RC the toxic effects in human beings and companion animals of
(ed): Veterinary toxicology: basic and clinical principles, New York, 2007, Academic Press. several common analgesics.
cats. The most common source is antifreeze, which is approx-

imately 95% EG. Its sweet taste is attractive, and EG can be
found stored in many households. Exposure is usually by
ingestion, although cutaneous exposure has been reported
to cause toxicity in cats.22
Acute EG ingestion causes a toxicosis with CNS depres-
sion and gastric irritation. EG is metabolized in the liver by
enzymes such as alcohol dehydrogenase to metabolites includ-
ing glycoaldehyde and glyoxylate that can lead to further tox-
icity, including an anion gap metabolic acidosis, renal failure,
and deposition of oxalic acid crystals in the kidney and other
tissues.23 Fomepizole (4-methylpyrazole) is an alcohol dehy-
drogenase inhibitor that is indicated for suspected or con-
firmed cases of EG (or methanol) toxicity in human beings.24
It is also used in dogs. In cats, fomepizole is ineffective at the
canine dosage and ethanol is used. Once renal failure devel-
ops in dogs and cats, the prognosis is poor. In contrast, the use
of dialysis in human beings is one reason why renal insuffi-
ciency in EG poisoning has a relatively good prognosis.
Cleaning Products (Bleach, Ammonia, Others)

Figure 8-3 n Gastric ulcer resulting from NSAID use in a dog. (From Cleaning products such as hypochlorite bleach and ammo-
Peterson ME, Talcott PA: Small animal toxicology, ed 2, St Louis, 2006, Saunders nia are toxic to animals and human beings through inges-
Elsevier. Courtesy Dr. M. Kern.) tion, inhalation of fumes, or skin contact. Ingestion by pets
can occur through drinking from toilet bowls or other li-
Other Household/Environmental Sources of quids treated with cleaners and can lead to GI distress, includ-
Acute Toxic Exposures ing vomiting and irritation. Respiratory exposure can result
in irritation and difficulty breathing and the development or
worsening of asthma symptoms. Dermal exposure leads to an
Ethylene Glycol
irritative dermatitis. Treatment involves removal from expo-
Ethylene glycol (EG) toxicosis is relatively common in both sure, substitution with less-irritating chemical cleaning agents,
human beings and domestic animals, especially dogs and and symptomatic treatment of airway, skin, or GI irritation.
Table 8-5 n Common Medications and Their Toxic Effects in Human Beings and Pets
Medication Toxic Effect in Human Beings Toxic Effect in Dogs Toxic Effect in Cats Treatment
Acetaminophen Liver failure at high Toxic dose 100 mg/kg22 Toxicity reported with Decontamination
doses (acute intake of Hepatocellular injury, doses of 10 mg/kg, most (emetics, gastric
>150 mg/kg in methemoglobinemia, poisonings due to doses lavage, activated
children) anorexia, abdominal >50 mg/kg charcoal)
pain, brown blood Methemoglobinemia at Antidote:
60 mg/kg (brown blood, N-acetylcysteine
mucous membranes)
Depression, weakness,
hyperventilation, death,
hepatic injury can also
occur
Aspirin Potentially acute toxic Gastric ulcers with doses Doses between 100 and Gastric evacuation for
dose 150 mg/kg/day13 of 75-105 mg/kg/day11 110 mg/kg/day fatal11 large recent ingestion,
Anion gap Depression, gastric activated charcoal,
Metabolic acidosis, ulceration, liver necrosis, fluids, alkalinize urine
respiratory alkalosis, fever, seizures, coma,
GI bleeding death
NSAIDs GI irritation, bleeding, renal Dogs extremely susceptible GI irritation Gastric evacuation for
toxicity to ibuprofen, naproxen large recent ingestion,
toxicosis; toxicity with activated charcoal,
ibuprofen >5 mg/kg/day11 fluids, H2 blockers,
Vomiting, diarrhea, nausea, sucralfate
abdominal pain, ulcers,
anemia (see Figure 8-3)
H2, Histamine; NSAIDs, nonsteroidal antiinflammtory drugs.

Metaldehyde Table 8-6 n Top 25 Poisonous Plant Exposures

Metaldehyde is a bait used to kill slugs, snails, and other gar- Reported to American Association of Poison
den pests. Baits in pellet form resemble dog food and are Control Centers, 2006
flavored with sweeteners such as molasses to attract snails.
Botanical (Common) Name No.
This can lead to poisoning in dogs, cats, birds, and other
wildlife. Human poisoning can also occur, especially in chil- Spathiphyllum spp. (peace lily) 2133
dren who accidentally ingest pellets, but such incidents are
Euphorbia pulcherrima (poinsettia) 1615
less common in human beings than in other animals. Human
poisonings are usually not serious. Metaldehyde is a neuro- Ilex spp. (holly) 1572
toxin and exposure results in vomiting, tachycardia, tremors, Philodendron spp. (philodendron) 1514
seizures, and death.11 Susceptibility varies slightly by species. Phytolacca americana (American pokeweed) 1358
Treatment involves removal of the agent from the GI tract, use
of activated charcoal, and control of medical complications, Toxicodendron radicans (poison ivy) 1194
including seizures and acidosis. Schlumbergera bridgesii (Christmas cactus) 705
Ilex opaca (American holly) 608
Poisonous Plants Crassula argentea (jade plant) 604
A wide variety of plants used as houseplants or in home land- Plants—cardiac glycosides 583
scaping are toxic to human beings and other animals if they Malus spp. (crabapple) 582
are ingested. Exposures to leaves, stems, and berries of poi- Taraxacum officinale (dandelion) 581
sonous plants are a significant cause of poisoning in animals
Pepper mace 566
and can also pose a risk to children. Each year more than
100,000 calls to poison control centers involve plant expo- Epipremnum aureum (silver vine, money plant) 566
sures.25 Table 8-6 shows the most common types of plant Plants—cyanogenic glycosides 555
exposures involved in human poison center calls. Plants—pokeweed 543
Most poisonous plant exposures to human beings are non–
life-threatening because the quantities ingested by children are Mold 538
usually small. Certain plants, however, have high levels of toxins. Caladium spp. (elephant ear) 533
An example is poisonous oleander (Nerium oleander) (Color Nandina domestica 530
Plate 8-2). The leaves of the oleander plant contain cardiac gly-
Narcissus pseudonarcissus (wild daffodil) 474
coside chemicals resembling digoxin. The toxicity of oleander
in human beings and other animals resembles digoxin toxicity, Spinacia oleracea (spinach) 467
with GI distress, nausea, and tachycardia and other arrhythmias. Cactus (unknown type or name) 460
Treatment is with the digoxin-specific Fab antibody fragment.25 Rosa spp. (rose) 450
Ingestion of mushrooms and toadstools is another seri-
Quercus spp. (oak) 447
ous cause of plant poisonings in human beings and animals.
The majority of human fatalities and serious dog poisonings Hedera helix (common ivy) 446
as a result of mushroom poisoning involve mushrooms of
From Bronstein AC, Spyker DA, Cantilena LR Jr et al: 2006 annual report of the
the genus Amanita that contain Amanita toxin (Figure 8-4). American Association of Poison Control Centers’ National Poison Data System
Ingestion by human beings or animals leads to hepatocellular (NPDS), Clin Toxicol (Phil) 45(8):815-917, 2007.
injury and liver and kidney failure. Puppies and children may
be at increased risk. Treatment is supportive and involves gas-
tric decontamination and activated charcoal for recent inges-
tion followed by management of medical complications.
Rodenticides
Rodenticides, used to control rats and mice around dwell-
ings, represent another example of a potent toxic hazard to
which animals are more often exposed than human beings.
Rodenticides are often placed near places where rodent
infestation exists but where pets and wildlife may also have
access. The toxic elements in rodenticides are anticoagulants,
including warfarin and related compounds, that kill rodents
by causing internal bleeding. The symptoms of rodenticide
ingestion are bleeding complications, including hematomas
(Color Plate 8-3), GI bleeding, hematuria, anemia, and pro-
longation of the international normalized ratio. Treatment
consists of administration of vitamin K to reverse the warfa- Figure 8-4 n Amanita rubescens. (From Auerbach PS: Wilderness medi-
rin effect on the coagulation pathway. cine, ed 5, Philadelphia, 2007, Mosby Elsevier.)
cough have been reported. Treatment for inhalation of PTFE

fumes is supportive.
Table 8-7 summarizes the comparative presentation and
treatment of common toxic exposures in human beings and
other animals. Consultation with a poison control center is
recommended for serious acute poisoning exposures.
Identification of Exposure
Identification of the toxic exposure can involve checking
product labels and searching online or through the dis-
tributing company for a copy of the material safety data
sheet (MSDS) regarding the suspected chemical expo-
sure (see the Resources section for Web site resources for
MSDSs and other toxic hazards). During the medical eval-
uation of the exposure, specialized toxicologic testing may
be indicated. Table 8-8 summarizes analytical toxicologic
testing in animals. Similar testing can be performed in
human beings.
In addition to eliminating the offending exposure and
treating the patient, human health and veterinary clinicians
can contact the environmental health officer in the local
health department to report suspected environmental haz-
ards to human beings or other animals.
A veterinarian who sees a pet animal with a toxic exposure
that could also endanger the owner and family should con-
sider directly contacting the human health care provider for
the family to communicate this concern. Similarly, human
health clinicians who identify environmental health hazards
in the setting of pet ownership should counsel patients to
contact their veterinarian or should contact the veterinar-
ian directly.
Figure 8-5 n Hindlimb ataxia with decreased conscious proprioception

in a cat 5 days after ingestion of bromethalin (found in rodenticides) (dose
0.45 mg/kg). (From Dorman DC: Emerging neurotoxicities. In August JR Chronic toxic exposures and health
(ed): Consultations in feline internal medicine, vol 2, Philadelphia, 1994, WB effects
Saunders.)
Toxic exposures at levels below those associated with acute
poisoning can produce long-term toxic effects in both human
beings and other animals. Studies have linked certain low-
A newer rodenticide agent, bromethalin, is a neurotoxic dose household toxic exposures to chronic health effects in
agent that uncouples oxidative phosphorylation in the mito- animals, suggesting that animals in a household could serve as
chondria of the CNS. Animals poisoned with bromethalin sentinels for human beings exposed to the same substances.
develop cerebral edema and neurological signs including
ataxia and paralysis (Figure 8-5). Human cases are rare to
date, but a fatality has been reported.26 It is anticipated that Cancer
treatment in human beings will be modeled after treatment
in animals, including GI decontamination and treatment of A number of studies have found associations between expo-
cerebral edema.26 sure to chemical and physical hazards and cancer in animals,
especially in dogs. Table 8-9 lists some of these reported
associations. Many of these associations are based on limited
PTFE Fumes case-control studies or descriptive case reports and remain
inconclusive. One obstacle to connecting animal cancers to
Nonstick cooking pans containing PTFE (Teflon) release environmental exposures is the existence of fewer tumor
fumes (perfluorooctanoic acid [PFOA]) when overheated. registries for domestic animals compared with human
These fumes are highly toxic to caged birds, and there are beings. Another is the lack of detailed data on environmen-
numerous reports of pulmonary hemorrhage and death. tal exposures; often data are not obtained for animals diag-
A syndrome known as polymer fume fever can develop in nosed with cancer. Much remains unknown regarding the
human beings exposed to fumes of burning PTFE and Teflon- linkages between animal risk and human risk of carcino-
containing sprays.27,28 Flulike symptoms of fever, chills, and genesis, including reasons why the most common types and
Table 8-7 n Comparative Presentation and Treatment of Common Toxic Exposures in Human Beings
and Other Animals
Toxic Exposure Human Beings Dogs Cats Birds29 Treatment*
Ethylene glycol Intoxication/ (LD 4.4 cc/kg) (LD 1.4 cc/kg) (poultry LD 7-8 Fluids, supportive
(antifreeze) CNS depression, 30 min-12 hr after 30 min-12 hr after cc/kg)23 care
metabolic acidosis, ingestion: polyuria, ingestion: CNS CNS depression, In human beings
oxalate crystals in polydipsia, CNS depression, ataxia, ataxia and dogs,
urine, respiratory/ depression, ataxia, vomiting, polyuria, fomepizole to
cardiac difficulty, vomiting, oxalate oxalate crystals in inhibit ADH
renal failure, crystals in urine urine In cats, ethanol to
cerebral edema 36-72 hr after 12–24 hr after inhibit ADH
ingestion: oliguria, injection: oliguria, Dialysis effective for
lethargy, coma lethargy, coma, renal insufficiency
swollen/ painful in human beings
kidneys23
Household cleaners Inhalation: respiratory Ingestion: vomiting, Pulmonary irritation, Respiratory irritation, Removal from
Chlorine bleach, irritation (fumes): hypersalivation, retching, coughing death23 exposure,
ammonia, others coughing, gagging, depression Concentrated substitution of less
sneezing, asthma Inhalation: coughing, ammonia: seizures irritating cleaning
Ingestion: GI distress, gagging, sneezing and death within agents, supportive
vomiting 5 minutes13 care of irritation
Dermal: skin irritation
Slug bait Toxic level not Immediate to 3 hr after ingestion: LD50 500 mg/kg Remove from GI
(metaldehyde) known; most Convulsions, tremors, hyperthermia, (chickens) tract, activated
ingestions not hyperpnea, vomiting, cyanosis, depression, charcoal; control
serious ataxia, seizures, death seizures, spasms;
Salivation, nausea, LD50 (ingestion) 100 mg/kg in dogs, treat acidosis
vomiting, 207 mg/kg cats11
abdominal pain,
tachycardia can
occur
Plants Many plants with Many plants toxic to animals, including lilies, azaleas,
low toxicity rhododendron
Oleander (cardiac Dizziness, nausea, Vomiting, diarrhea, cardiac toxicity (tachycardia, heart block) GI decontamination,
glycosides) cardiac arrhythmias activated charcoal
Cardiac monitoring,
digoxin-specific
Fab fragment
Mushrooms, Amanita: Liver, kidney toxicity: vomiting, pain, jaundice GI decontamination,
toadstools (Amanita activated charcoal
toxin; see Figure
8-4)
Rodenticides
Warfarin and related Bleeding Anemia, spontaneous bleeding, hematomas, GI decontamination,
compounds melena (see Color Plate 8-3) charcoal, vitamin K
Bromethalin Altered mental Hindlimb ataxia (see Figure 8-5), tremors, GI decontamination,
status, seizures26 hyperthermia, seizures, coma treatment of
cerebral edema
Teflon fumes (PFOA) Polymer fume fever None known Respiratory distress, Remove from
(flulike symptoms) death30 exposure,
supportive care
ADH, Antidiuretic hormone; CNS, central nervous system; GI, gastrointestinal; LD, lethal dose; LD50, median lethal dose.
*Poison center consultation recommended.
sites of cancer may vary among species and differing biology Breast cancer in female dogs spreads to bone, just as it does
of particular cancers across species.12 Therefore linking the in women. The most frequent tumor in dogs, osteosarcoma,
occurrence of animal cancers to either environmental expo- is an important tumor that affects young people. Such obser-
sures or human risks remains extremely difficult. vations have led to the development of the field of “compar-
Nevertheless, considering the relationships between ative oncology.” A growing amount of research is studying
human and companion animal cancers may be of both clin- similarities and differences between tumors of human beings
ical and scientific value. Dogs and human beings are the and domestic animals, and new cancer registries for pet can-
only animals that naturally develop lethal prostate cancers. cers are being established to better understand links between
Table 8-8 n Samples That May Be Needed for Analytical Toxicology Testing*
Sample Amount Condition Examples of Toxicoses
Antemortem
Whole blood 1-3 mL EDTA or heparin anticoagulant Lead, arsenic, mercury, selenium,
pesticides, anticoagulants
Urine 10-50 mL Plastic screw-capped vial Drugs, some metals, paraquat, alkaloids
Serum 5 mL Remove from clot; element tubes Trace metals (no rubber contact
if testing for zinc), some drugs,
ethylene glycol, electrolytes,
botulinum, iohexol
Cerebrospinal fluid 1 mL Clot tube Sodium
GI contents 100 g Obtain representative sample Pesticides; plant-, metal-, and feed-
related poisons
Body fluids 10-20 mL Clot tubes Anticoagulants
Hair 1-5 g Rarely useful Call laboratory; chronic selenosis
Postmortem
Urine, serum, body fluids 1-50 mL Same preparation and tests as for Drugs, arsenic
antemortem samples; get serum from
heart clot
Liver 100 g Plastic (foil for organics) Pesticides, metals, botulinum
Kidney 100 g Plastic (foil for organics) Metals, compound 1080 (sodium
monofluoroacetate), calcium,
ethylene, glycol, cholecalciferol
Brain 50% Cut sagittally; put half in plastic for Organochlorines, sodium, bromethalin
analysis (fix other half for pathologic
examination)
Fat 100 g Foil in plastic Organochlorines
Lung 100 g Plastic Paraquat
Pancreas 100 g Plastic Metals (zinc)
GI contents 100 g Obtain representative sample Pesticides/baits; plant- metal-, or feed-
related toxicants
Bone 100 g One long bone Fluoride
Miscellaneous Injection sites, spleen Some drugs (barbiturates in spleen)
Environmental
Baits/sources 200 mL or g Clean glass jar (liquid); plastic vial (write Unidentified chemicals, organics
chemical name if available)
Feed 1 kg Plastic, box; must be representative Mycotoxins, feed additives, plants,
pesticides
Plants Entire plant Fresh or pressed, send all parts Identification, chemical assay
Water 1L Clean mason jar; foil under lid for Metals, nitrates, pesticides, algae, salt,
organics, plastic jar for metals organics
EDTA, Ethylenediamine tetraacetic acid.

*Submit samples frozen except for blood or if very dry. Amounts given are optimum amounts; smaller samples may be accommodated (call laboratory about testing for smaller
samples). Appropriate tissue samples should be fixed in formalin for histological analysis as well. Do not submit material in syringes.
Modified from Galey FD: Effective use of an analytical laboratory for toxicology problems. In Kirk RW, Bonagura JD, editors: Current veterinary therapy, small animal practice,
vol XI, Philadelphia, 1992, WB Saunders. In Peterson ME, Talcott PA: Small animal toxicology, ed 2, St Louis, 2006, Saunders Elsevier.
environments and cancers.37 Some studies have attempted determine whether a suspected environmental cause of a
to assess human environmental cancer risk by monitor- pet cancer exists. If there appears to be grounds for con-
ing biomarkers such as lymphocyte micronucleus testing in cern, the physician or veterinarian can contact the envi-
dogs living near Environmental Protection Agency (EPA) ronmental health department of the local or state health
Superfund sites to determine the extent of exposure to mix- department or one of the regional clinics in the Association
tures of chemicals that could be carcinogenic.38 of Occupational and Environmental Medicine Clinics
When patients report a history of cancer in a pet, human (AOEC) to assess any possible human risk related to the
health clinicians may wish to contact the veterinarian to exposures.
Table 8-9 n Reported Associations Between

Cancer in Animals and Environmental Exposures
Associated
Type of Environmental
Species Neoplasia Exposure Comments
Cats Oral Environmental Tonsillar

squamous tobacco form is more
cell smoke31 common in
carcinoma urban cats
than rural cats Figure 8-6 n Fluorosis in cheek teeth of a cow. The enamel is chalky and
weak and the teeth are usually rapidly worn down. (From McGavin MD,
Dogs Bladder Pesticides Higher risk in Zachary JF: Pathologic basis of veterinary disease, ed 4, St Louis, 2007, Mosby
cancer obese female Elsevier. Courtesy Dr. L. Krook, College of Veterinary Medicine, Cornell
dogs32 University.)
Nasal Indoor coal Evidence
carcinoma or kerosene stronger for
heaters33 long-nosed Table 8-10 n Noncancer Outcomes in Animals and
breeds Implicated Chronic Environmental Exposures
Lymphoma Lawn pesticide Concern
application,34 that such Species Type of Disease Exposure Implicated
electromagnetic exposures
fields35 cause cancer Cat Hyperthyroidism Flame-retardant
in human (PBDE) from carpet
beings and furniture43
Dogs Testicular Vietnam service Exposed to Mercury poisoning Fish consumption
(military) cancer variety of Dog Lung disease Ambient air
chemicals, pollutants42
infections, and
medications Cattle, horses, Fluorosis of bones Exposure to fluoride
during military deer and teeth in pastures
service36 contaminated from
nearby factories
Horses, dogs Sudden death Exposure to dioxin
Noncancer Outcomes from contaminated
oil used to spray
Just as with cancer, a number of other diseases in animals roads, stables8
have been attributed to chronic exposures to toxicants, and Cattle Cadmium-induced Cadmium in feed and
there is evidence that animals can serve as sentinels for renal disease pastures irrigated
human beings. Recently an association has been reported with sewage sludge
between hyperthyroidism in cats and high levels of the flame
retardant polybrominated diphenyl ether (PBDE) related to
house dust and diet exposures.39 This association is an exam-
ple of the current scientific controversy regarding the poten- Web Resources
tial of chemicals in the environment to cause alterations in
endocrine function (“endocrine disruption”) in animals and • National Healthy Homes Training Center and Network
possibly human beings. http://www.healthyhomestraining.org/
As previously described, cats were sentinels of methyl • Environmental Protection Agency
mercury poisoning in Minamata, Japan, and the deaths of Using Toxics and Pesticides Safely: http://www.epa.gov/
dogs and horses provided warning of a human health risk epahome/home.htm#safe
from dioxin in oil sprayed for dust control in Times Beach, • TOXNET Toxicology Data Network
Missouri. Other examples of animals providing sentinel infor- http://toxnet.nlm.nih.gov/
mation about chronic toxic exposures in homes and outdoor • Agency for Toxic Substances Disease Registry (ATSDR)
environments include horses and deer that develop fluorosis Toxicological Profiles
of their bones and teeth while grazing near areas of fluoride- http://www.atsdr.cdc.gov/toxpro2.html
contaminated soil in the vicinity of aluminum smelters and • The Canary Database (animals as sentinels of human
other industrial sources (Figure 8-6).40 In a similar fashion, environmental health hazards)
livestock can develop signs of cadmium toxicity when graz- http://canarydatabase.org
ing on cadmium-contaminated soils.41 Dogs have been used • Tox Town (consumer resource for information regarding
to monitor the effects of air pollution on lungs and cardiac environmental health concerns and toxic chemicals)
function.42 Table 8-10 lists some of these reported associa- http://toxtown.nlm.nih.gov/index.php
tions between environmental toxic exposures and noncancer • Material Safety Data Sheets
outcomes in animals that have potential sentinel value for Available through University of Vermont SIRI MSDS
human health. database: http://siri.org/msds/
References 22. Kahn CM, Line S. ed. The Merck veterinary manual. 9th ed. Whitehouse
Station, NJ: Merck; 2005.
1. U.S. Department of Housing and Urban Development. Healthy Homes 23. Ford MD, Delaney KA, Ling L, et al. Clinical toxicology. Philadelphia:
Initiative. http://www.hud.gov/offices/lead/hhi/index.cfm. Accessed April 5, Saunders; 2001.
2009. 24. Holstege CP, Dobmeier SG, Bechtel LK. Critical care toxicology. Emerg
2. Burrell G, Seibert F. Experiments with small animals and carbon mon- Med Clin North Am. 2008;26(3):715–739, viii–ix.
oxide. J Ind Eng Chem. 1914;6(3):241–244. 25. Froberg B, Ibrahim D, Furbee RB. Plant poisoning. Emerg Med Clin
3. Bukowski JA, Wartenberg D. An alternative approach for investigating North Am. 2007;25(2):375–433.
the carcinogenicity of indoor air pollution: pets as sentinels of environ- 26. Pasquale-Styles MA, Sochaski MA, Dorman DC, et al. Fatal bromethalin
mental cancer risk. Environ Health Perspect. 1997;105(12):1312–1319. poisoning. J Forensic Sci. 2006;51(5):1154–1157.
4. Eto K, Yasutake A, Nakano A, et al. Reappraisal of the historic 1959 27. Patel MM, Miller MA, Chomchai S. Polymer fume fever after use of a
cat experiment in Minamata by the Chisso Factory. Tohoku J Exp Med. household product. Am J Emerg Med. 2006;24(7):880–881.
2001;194(4):197–203. 28. Son M, Maruyama E, Shindo Y, et al. Case of polymer fume fever with
5. Thompson ME, Lewin-Smith MR, Kalasinsky VF, et al. Characterization interstitial pneumonia caused by inhalation of polytetrafluoroethylene
of melamine-containing and calcium oxalate crystals in three (Teflon) [in Japanese]. Chudoku Kenkyu. 2006;19(3):279–282.
dogs with suspected pet food-induced nephrotoxicosis. Vet Pathol. 29. Animal Forum. Animal poison control center offers pet poison safety tips
2008;45(3):417–426. for bird owners. http://www.animalforum.com/birdpoison.htm. Accessed
6. Lattupalli R, Yee J, Kolluru A. Nephrotoxicity of mala fide melamine: April 5 2009.
modern era milk scandal. Scientific World Journal. 2008;8:949–950. 30. Stoltz JH, Galey F, Johnson B. Sudden death in ten psittacine birds
7. National Research Council. Animals as sentinels of environmental health associated with the operation of a self-cleaning oven. Vet Hum Toxicol.
hazards. Washington DC: National Academies Press; 1991. 1992;34(5):420–421.
8. EPA Superfund Record of Decision. Shenandoah Stables. http://www. 31. Snyder LA, Bertone ER, Jakowski RM, et al. P53 expression and envi-
epa.gov/superfund/sites/rods/fulltext/r0790042.pdf. Accessed October ronmental tobacco smoke exposure in feline oral squamous cell carci-
28, 2008. noma. Vet Pathol. 2004;41(3):209–214.
9. Environmental Working Group. Polluted pets: high levels of toxic indus- 32. Glickman LT, Raghavan M, Knapp DW, et al. Herbicide exposure and
trial chemicals contaminate cats and dogs. http://www.ewg.org/book/ the risk of transitional cell carcinoma of the urinary bladder in Scottish
export/html/26238. Terriers. J Am Vet Med Assoc. 2004;224(8):1290–1297.
10. Ginsberg G, Toal B. What’s toxic, what’s not. New York: Berkeley Books; 2006. 33. Bukowski JA, Wartenberg D, Goldschmidt M. Environmental causes for
11. Gupta RC. Veterinary toxicology: basic and clinical principles. New York: sinonasal cancers in pet dogs, and their usefulness as sentinels of indoor
Academic Press; 2007. cancer risk. J Toxicol Environ Health A. 1998;54(7):579–591.
12. Kelsey JL, Moore AS, Glickman LT. Epidemiologic studies of risk factors 34. Hayes HM, Tarone RE, Cantor KP, et al. Case control study of canine
for cancer in pet dogs. Epidemiol Rev. 1998;20(2):204–217. malignant lymphoma: positive association with dog owner’s use of
13. Peterson ME, Talcott PA. Small animal toxicology. 2nd ed. St Louis: 2,4-dichlorophenoxyacetic acid herbicides. J Natl Cancer Inst. 1991;83(17):
Saunders Elsevier; 2006. 1226–1231.
14. Glickman LT, Domanski LM, MacGuire TG, et al. Mesothelioma 35. Reif JS, Lower KS, Ogilvie GK. Residential exposure to magnetic fields
in pet dogs with exposure of their owners to asbestos. Environ Res. and risk of canine lymphoma. Am J Epidemiol. 1995;141(4):352–359.
1983;32(2):305–313. 36. Hayes HM, Tyrone RE, Casey HW. Excess of seminoma observed
15. American Association of Poison Control Centers. Poison Centers Can in Vietnam service U.S. military working dogs. J Natl Cancer Inst.
Help. http://www.aapcc.org/dnn/Home/tabid/36/Default.aspx. Accessed 1990;82(12):1042–1046.
April 5, 2009. 37. Waters DJ, Wildasin K. Cancer clues from pet dogs. Sci Am. 2006;295(6):
16. Bronstein AC, Spyker DA, Cantilena Jr LR, et al. 2006 Annual report of 94–101.
the American Association of Poison Control Centers’ National Poison 38. Backer LC, Grindem CB, Corbett WT, et al. Pet dogs as sentinels for envi-
Data System (NPDS). Clin Toxicol (Phila). 2007;45(8):815–917. ronmental contamination. Sci Total Environ. 2001;274(1–3):161–169.
17. Khan SA, Schell MM, Trammel HL, et al. Ethylene glycol exposures 39. Dye JA, Venier M, Zhu L, et al. Elevated PBDE levels in pet cats: senti-
managed by the ASPCA National Animal Poison Control Center from nels for humans? Environ Sci Technol. 2007;41(18):6350–6356.
July 1995 to December 1997. Vet Hum Toxicol. 1999;41(6):403–406. 40. Vikoren T, Stuve G. Fluoride exposure in cervids inhabiting areas
18. Kupper J, Hellwig B, Demuth D, et al. Computer-based information adjacent to aluminum smelters in Norway. II. Fluorosis. J Wildl Dis.
system (clinitox) for the management of poisoning in small animals [in 1996;32(2):181–189.
German]. Schweiz Archiv Tierheilkd. 2004;146(3):127–134. 41. Kessels BG, Wensing T, Wentink GH, et al. Clinical, chemical, and
19. Burgat V, Keck G, Guerre P, et al. Glyphosate toxicosis in domestic animals: hematological parameters in cattle kept in a cadmium-contaminated
a survey from the data of the Centre National d’Informations Toxico area. Bull Environ Contam Toxicol. 1990;44(2):339–344.
logiques Veterinaires (CNITV). Vet Hum Toxicol. 1998;40(6):363–367. 42. Calderon-Garciduenas L, Mora-Tiscareno A, Fordham LA, et al. Canines
20. Cope RB, White KS, More E, et al. Exposure-to-treatment interval and as sentinel species for assessing chronic exposures to air pollutants: part
clinical severity in canine poisoning: a retrospective analysis at a Portland 1. Respiratory pathology. Toxicol Sci. 2001;61(2):342–355.
veterinary emergency center. J Vet Pharmacol Ther. 2006;29(3):233–236. 43. American Chemical Society. Cat disease linked to flame retardants in
21. Hornfeldt CS, Murphy MJ. American Association of Poison Control furniture and to pet food. ScienceDaily. http://www.sciencedaily.com/
Centers report on poisonings of animals, 1993–1994. J Am Vet Med releases/2007/08/070815122354.htm. Accessed February 3, 2009.
Assoc. 1998;212(3):358–361.
Carbon Monoxide
Peter M. Rabinowitz and Lisa A. Conti deaths each year are attributed to non–fire-related acciden-
tal CO poisoning.2 Because the gas has no warning odor or
(ICD-10 T58.0 Toxic Effect of Carbon Monoxide)
color and the symptoms are often subtle and nonspecific,
Carbon monoxide (CO) is the most common cause of the true incidence of CO poisoning in human beings may
poisoning-related death.1 Each year in the United States, be much higher. In fact, CO has been termed the “unnoticed
several thousand individuals die or are hospitalized with CO poison of the twenty-first century.”3 CO is an example of a
poisoning related to smoke inhalation, and more than 400 toxicant for which companion animals could provide early
warning of human exposure risk. However, it is likely that Human Health Clinicians
just as in human beings, the diagnosis is often overlooked.
The classic animal sentinel for CO poisoning is the canary. • Provide the national or state poison control number to
Canaries were brought into mines in the United States patients.
and Great Britain in the first half of the twentieth century • In taking a history of a patient with suspected CO poi-
to provide early warning to miners of CO and other toxic soning, ask about abnormal signs in household pets.
gases. Canaries were chosen after experiments on this spe- • Have a high index of suspicion in the autumn when home
cies, as well as guinea pigs, rabbits, chickens, dogs, mice, and heating units are turned on, after storms when generators
pigeons, revealed that either canaries or mice were most suit- are used, or when gasoline-powered appliances are used.
able, with canaries more sensitive than mice to the effects of • Encourage CO testing of pets as well as human beings.
CO.4 Canaries developed recognizable signs of toxicosis suf-
ficiently early to allow the miners to take preventive steps Veterinary Clinicians
to avoid further exposure. In the home setting as well, dogs
and cats may sometimes serve as sentinels. Human cases of • In taking a history about an animal with suspected CO
CO poisoning have been detected because the family dog poisoning, ask about any similar symptoms (see Table
and family members were displaying signs of intoxication.5 8-11) in people living in the household.
Additionally, the 2007 ASPCA Cat of the Year award was • Consider the diagnosis in unexplained sudden deaths
given to a 2-year-old domestic short-hair cat that scratched of pets, and alert human beings living nearby as well as
at her sleeping owner’s face to arouse her and save her from health professionals responsible for their care.
death from CO intoxication.6 • Have a high index of suspicion for the diagnosis of CO
intoxication in pets after storms, at the beginning of
heating season, and for pets living in an economically
depressed area.
Professionals
• Encourage testing of human beings and animals when
intoxication is suspected.
• Provide the national or state poison control number to
clients.
• Educate the public on preventive measures (Box 8-1).
• Maintain heightened alertness at the onset of the win- Agent
ter heating season as well as after natural disasters and
emergencies such as power outages, hurricanes, and CO is an odorless, colorless, nonirritating gas that is produced
earthquakes. by the incomplete combustion of fuels. Common sources
• Consider CO exposure in unexplained deaths of ani- include malfunctioning and improperly vented heating
mals or human beings. furnaces, automobile exhaust, and propane-powered equip-
• Monitor poison control data. ment such as forklifts, generators, space heaters, and floor pol-
• Consider adding CO intoxication as a reportable con- ishers (Figure 8-7).8 CO is also a component of air pollution,
dition if it is not already. leading to population-wide low-level exposures. CO is slightly
lighter than air, so it tends to rise through a building.
Box 8-1 YOU CAN PREVENT CARBON MONOXIDE Routes of exposure and metabolic fate
EXPOSURE
The primary route of CO exposure is inhalation. Levels of
• Do have your heating system, water heater, and any other CO in ambient air are usually less than 10 ppm but may be
gas, oil, or coal-burning appliances serviced by a qualified higher in urban areas. The Occupational Safety and Health
technician every year. Administration (OSHA)-permissible exposure level for CO
• Do install a battery-operated CO detector in your home and exposures in the workplace is 50 ppm. After a gas stove is
check or replace the battery when you change the time on used for cooking, nearby air levels may exceed 100 ppm.1 CO
your clocks each spring and fall. (Some states have passed laws inhaled into the lungs binds tightly to hemoglobin in red
requiring their installation.7) If the detector sounds, leave your blood cells (RBCs) to form carboxyhemoglobin (COHb).
home immediately and call 911.
This process displaces oxygen from the hemoglobin-binding
• Do seek prompt medical attention if you suspect CO poisoning
and are feeling dizzy, lightheaded, or nauseated.
sites because it binds to hemoglobin more than 200 times
• Don’t use a generator, charcoal grill, camp stove, or other more avidly than oxygen.3 This reduces the oxygen-carrying
gasoline- or charcoal-burning device inside your home, capacity of the bloodstream, causing tissue hypoxia, partic-
basement, or garage or near a window. ularly of the heart and brain. COHb is bright red in color,
• Don’t run a car or truck inside a garage attached to your house, which is why tissues of a CO-poisoned individual may be
even if you leave the door open. “cherry red.” The half-life of COHb in the human blood-
• Don’t burn anything in a stove or fireplace that is not vented. stream is approximately 4 to 5 hours when the person is
• Don’t heat your house with a gas oven. breathing room air. However, if 100% oxygen is administered,
Modified from Centers for Disease Control and Prevention: Carbon monoxide poison- the half-life has been reported to shorten to 47 to 80 minutes9
ing: prevention guidelines. http://www.cdc.gov/co/guidelines.htm. and is even shorter in a hyperbaric oxygen environment.
O2 saturation of available Hb (% max)

with COHb
normal
0 50 100 pO2
A
% of CO in inhaled air
0.01 0.03 0.1 0.3

% Hb as COHb
0 50 100
Headache
(mild)
Headache
(severe)
Nausea and vomiting
Weakness
Figure 8-7 n CDC flyer on the proper use of generators and pressure Syncope
washers. (From Centers for Disease Control and Prevention, Atlanta, Ga.
Tachycardia
Coma
Convulsions
The level of COHb in the blood helps determine the Cardiovascular
degree of toxicity. Smokers may have chronically elevated collapse
levels around 7% to 12%. Normal levels in nonsmokers are Death
generally less than 2%.10 B
Figure 8-8 n Effects of carboxyhemoglobin (COHb) on oxygen dissocia-
Groups at risk tion from hemoglobin (A), and the symptoms associated with carbon mon-
oxide (CO) poisoning (B). The affinity of CO for hemoglobin (Hb) is 220
times higher than for oxygen, thereby decreasing the oxygen-carrying capac-
Individuals at high risk of CO poisoning include workers who ity of blood. In addition, COHb shifts the oxyhemoglobin–oxygen saturation
use propane- or gasoline-powered equipment and individuals curve to the left, making oxygen release during hypoxia more difficult. This
who improperly use propane- or gasoline-fired generators, space is illustrated in the upper panel, which is normalized to 100% maximum. If
heaters, or other heating devices, including wood- and coal- the data were expressed as absolute oxygen content, the values in the pres-
ence of COHb would be decreased compared with normal. (From Page CP,
burning stoves. Use of such equipment may increase in areas that Hoffman B, Curtis M et al: Integrated pharmacology, ed 3, Edinburgh, 2006,
have experienced natural disasters. Individuals with increased Mosby Elsevier.)
susceptibility include elderly people, individuals with cardiovas-
cular disease, infants, and pregnant women (risk to the fetus). exposure. Low-level chronic exposure, as from a slowly leak-
Pets such as dogs may be at increased exposure risk rela- ing furnace, can cause headaches, fatigue, malaise, dizziness,
tive to human beings because of their faster breathing rate chest pain, and abdominal pain. These nonspecific symp-
and smaller volume of distribution. Birds have increased toms can easily be attributed to other causes, and the diag-
susceptibility relative to human beings because of their effi- nosis may therefore be overlooked. Elevations in the COHb
cient gas exchange and higher mass-specific ventilation of level to between 5% and 20% may be associated with subtle
tissues.11 Pregnant animals and pets with underlying cardiac changes such as headache and behavioral changes. Chronic
disease are at increased risk. exposures are believed to predispose human beings to the
development of cardiovascular disease and memory loss.
Acute, high-level exposure with COHb levels greater than
Toxicity in human beings 20% produces symptoms as described above, as well as ataxia,
confusion, slurred speech, disturbances of visual or audi-
CO can produce both acute and chronic effects (Figures 8-8 tory function and, with increasing intoxication, eventual
and 8-9).3 Because of their high metabolic activity and oxygen loss of consciousness. If exposure continues, death can result
demand, the brain and heart are the organs most affected by from respiratory arrest (Color Plate 8-4). The skin color of
Toxicity in animals
Dogs appear to be more resistant to COHb than human

beings.13 Acute signs include lethargy, incoordination,
cherry-red mucous membranes, dyspnea, coma, and death.
Tachycardia has been reported in dogs at levels of 15%
COHb.14 Chronic exposure in dogs and cats can manifest as
decreased exercise tolerance and gait problems.
Birds exhibit drowsiness, difficulty breathing, weakness,
ataxia, and seizures.11 Chickens may become exposed in
enclosed facilities and during transport in trucks. This can
result in high mortality rates, with bright pink coloration
of the viscera at necropsy.15 Spontaneous abortion has been
noted in sows that have experienced CO intoxication.12 Table
8-11 shows key aspects of CO toxicity in human beings and
other animals.
Diagnosis
The cornerstone of diagnosis is the history of exposure and a

COHb level. The COHb level should be measured as soon as
Figure 8-9 n Magnetic resonance imaging of the brain shows areas of the diagnosis is suspected because the half-life is 4 to 5 hours.
infarction after carbon monoxide poisoning. This T2-weighted image shows A history of similar illness resembling CO intoxication in
abnormally high signal intensity in the basal ganglia, right frontal lobe, and both animals and people is supportive of the diagnosis.
cerebral cortex. (From Yanoff M, Duker J: Ophthalmology, ed 2, St Louis, Measurement of air levels of CO in the area where the
2004, Mosby.)
exposure occurred should also be done as soon as possible.
Many fire departments or public health departments are able
CO-poisoned individuals usually is normal. The pulse oxim- to obtain such measurements. Although CO standards have
etry reading can be falsely elevated because conventional oxi- yet to be set for indoor air, the U.S. National Ambient Air
meters cannot distinguish between oxyhemoglobin and COHb. Quality Standards are 9 ppm for 8 hours and 35 ppm for 1
There may be electrocardiographic abnormalities includ- hour for outdoor air.18
ing arrhythmias and ischemia. Magnetic resonance imaging
(MRI) of the brain may show white matter high-signal inten-
sities resulting from impaired diffusion.3 Low-attenuation Management of CO poisoning
lesions in the globus pallidum have been reported.
Individuals who have recovered from acute episodes of
intoxication may have long-term sequelae including chronic Treatment in Human Beings
encephalopathy, parkinsonism, memory loss, and other signs The principal approach to management of acute CO poison-
of dementia. ing is to remove the patient from exposure, ensure adequate
Table 8-11 n Comparative Toxicity of Carbon Monoxide in Human Beings and Other Animals
Species Risk Factors Toxic Level Clinical Manifestations Diagnostic Findings
Human Inadequate ventilation COHb >10% Lethargy, cherry-red Elevated COHb level,
beings when operating propane mucous membranes, pulse O2 usually normal,
or gasoline appliances; headaches, visual, auditory abnormal MRI, abnormal
pregnancy disturbances, confusion, ECG
ataxia, somnolence
Dogs, cats16 Impaired cardiac or >15% COHb Acute: lethargy, incoordination, Elevated creatine kinase,
pulmonary function cherry-red mucous whole blood COHb,
membranes, dyspnea, coma blood pH lowered due
death to metabolic acidosis,
Chronic: exercise intolerance, ECG consistent with
gait abnormalities anoxia
Birds Varying sensitivity in 20% COHb associated with Drowsiness, respiratory Bright pink viscera on
different species, canaries motor impairment11 difficulty, lethargy, seizures, necropsy
very sensitive17 sudden death
Pigs Unknown Spontaneous abortion
CO EXPOSURE
Oxygen 100% by Prevent further

non-rebreather exposure and
SYMPTOMATIC?
mask YES NO protect
cohabitants
Poisoning unlikely Obtain COHb

Syncope,
unless many Not level Elevated seizure,
hours elapsed Elevated coma?
NO YES
HBO
COHb > 15% or fetal distress

Continue face
Pregnancy test if
mask oxygen
NEGATIVE female POSITIVE
for 2-4 hours
COHb < 15%
Still symptomatic Prolonged O2

(headache, confusion, therapy
ataxia)?
NO YES
Discharge with
HBO
precautions for
exposure site and
cohabitants
Figure 8-10 n Suggested algorithm for the management of carbon monoxide poisoning. (From Ford MD,
Delaney KA, Ling L et al: Clinical toxicology, Philadelphia, 2001, Saunders.) HBO, Hyperbaric oxygen.
oxygenation, and eliminate COHb from the body (Figure promotes recovery. Treatment should also include elimination
8-10). All patients should receive 100% oxygen. Patients with of exposure. Response to therapy should be evident within
significant symptoms (such as loss of consciousness with or 4 hours of treatment. Physical activity should be limited for
without neurological deficits) levels of COHb greater than 2 weeks after exposure. After acute treatment, rehabilitation
25% and all pregnant patients are candidates for hyperbaric may be required for chronic neurological effects, which may
oxygen therapy, but hyperbaric oxygen therapy should be become evident days to up to 6 weeks after exposure.
considered on a case-by case-basis in all patients in consulta-
tion with a bariatric medicine specialist.
Electrolytes should be monitored for the presence of lac- Web resources
tic acidosis as a result of tissue hypoxia. Cardiac function
should be monitored continuously during treatment. After • CDC: Carbon Monoxide Poisoning
the acute treatment, follow-up care should assess the impact http://www.cdc.gov/co/basics.htm
on neuropsychiatric functioning. Follow-up MRI imaging • EPA: An Introduction to Indoor Air Quality: Carbon
of the brain and formal neuropsychiatric testing may be Monoxide (CO)
indicated. http://www.epa.gov/iaq/co.html
• Consumer Product Safety Commission: Carbon
Monoxide Detectors Can Save Lives
Treatment in animals http://www.cpsc.gov/cpscpub/pubs/5010.html
• U.S. Fire Administration (USFA): Exposing an Invisible
Treatment of CO poisoning in animals also depends on the Killer: The Dangers of Carbon Monoxide
COHb level and primarily involves restoration of oxygen to http://www.usfa.dhs.gov/citizens/all_citizens/co/fswy17.
heart and brain tissue. Hyperbaric oxygen, when available, shtm
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occupational and environmental medicine. 2nd ed. Edinburgh:
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2. Centers for Disease Control and Prevention (CDC). Carbon monoxide- York: Academic Press; 2007.
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States Bureau of Mines; 1914. 14. Farber JP, Schwartz PJ, Vanoli E, et al. Carbon monoxide and lethal
5. The Boston Channel. Dog helps alert family to carbon monoxide arrhythmias. Res Rep Health Eff Inst. 1990;(36):1–17, discussion
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by ASPCA after rescuing their masters. http://www.msnbc.msn.com/ Station, NJ: Merck; 2005.
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8. Washington State Department of Labor and Industries. Carbon monoxide. model for studies of respiratory toxicosis and for monitoring air quality.
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Saunders; 2001.
Lead
Peter M. Rabinowitz and Lisa A. Conti Human Health Clinicians

(ICD-10 T56.0 Toxicity Due to Lead) • Report cases to the health department.
• Gather medical history information about possible
lead exposure risks, including older homes, dishes or
Other Names in Human Beings: Plumbism, Lead Colic glassware containing lead, and lead in toys or hobbies.
• Have a high index of suspicion in high-risk areas and
with groups and individuals with occupational and
Other Names in Animals: Lead Poisoning environmental risk (painters, battery workers, old
homes with peeling paint, etc.) and recent immigrants
Lead is a common exposure in the environment. As a heavy from countries with environmental exposure risk.
metal, it has the ability to accumulate over time in bones and • When evaluating a suspected human case, inquire
soft tissues, leading to a chronic body burden and a wide whether any animals are exposed and showing signs of
range of clinical effects in human beings and other animals. illness.
It is an example of toxicant for which there are numerous • Encourage testing of pets as well as human beings.
documented episodes of animals serving as sentinels provid-
ing warning of human exposure risk. Veterinary Health Clinicians
• Gather history information about lead exposure risks
in indoor and outdoor environments.
• Have a high index of suspicion in pets that are younger
Professionals
than 1 year, live in an economically depressed area, or
are in an old house or building that is being renovated.
• When treating an animal with lead poisoning, encour-
age the client to contact a health care provider to get
• Ensure remediation for contaminated buildings and children (and possibly adults) in the household tested.
other sites in the health district. • Contact the local health department to inform them of
• Perform follow-up investigations of cases identified in cases of lead poisoning diagnosed in animals.
human beings and animals.
• Educate human health clinicians and veterinarians
about the need to communicate about cases. Agent
• Provide lead alerts for toys, candies, candles, and other
product recalls. Lead is a toxic metal that is widely distributed in the environ-
• Educate human health clinicians and veterinarians ment. It the most common cause of heavy metal toxicity in
about risks in the home or environment; see http:// human beings.1 It is most commonly found in the inorganic
www.cdc.gov/nceh/lead/. form (Pb) but also can exist as an organic compound, such as
the tetraethyl lead in leaded gasoline (phased out of use in the lead is absorbed from the GI tract by adults (absorption
United States beginning in 1976 but still in use in many other in children may be as high as 50%1) and is absorbed even
countries). The most significant source of environmental expo- faster in the presence of nutritional deficiencies. The second
sure for children in the United States is lead-based paint. It is most important exposure pathway is inhalation of dust and
estimated that more than 27 million housing units built before vapors containing lead. Up to 100% of inhaled lead is taken
1950 still contain such paint.2 Other sources in the environ- up by the body. Dermal exposure plays a much smaller role,
ment include batteries; lead solder in plumbing joints; lubricat- and inorganic lead is absorbed less through the skin than
ing compounds; putty; tar paper; contaminated soil from paint, organic lead. Once lead enters the bloodstream, it binds to
paint residues, or dusts, linoleum, solder, mining tailings, and red blood cells. The half-life in the blood is approximately
industrial facility waste; and lead objects such as fishing sinkers. 30 to 60 days.1 The body distributes lead among the blood,
In households, plates, glassware, cans, and cooking vessels con- soft tissues (such as kidney and liver), and bone. Lead can
taining lead may contaminate food, water, and other beverages. pass the blood-brain barrier and affect the CNS. Once lead
Some folk remedies and herbal medicines may contain signifi- is taken up by bone, it remains as part of the bony matrix
cant amounts of lead. Other household risks include drapery for many years. In growing bones, “lead lines” can be seen
weights, stained glass, and the home use of lead for hobbies and at the ends of long bones (Figure 8-12). Lead is eliminated
home repair. Lead is a very stable compound and persists in the from the body in the urine, but this is a slow process and,
environment for a long time. It also tends to accumulate in the if exposure is ongoing, urinary excretion cannot keep pace
body of human beings or other animals, with a long half-life for with accumulation of the lead body burden.
elimination. As a result, even small exposures over a prolonged
period can lead to significant body burdens.
Routes of exposure and metabolic fate
The primary route of lead exposure in most cases is inges-

tion (Figure 8-11). Approximately 10% to 15% of ingested
Figure 8-11 n Abdominal radiograph shows lead in the intestines. (From

Ford MD, Delaney KA, Ling L et al: Clinical toxicology, Philadelphia, 2001, Figure 8-12 n Lead lines in the distal radius. (From Ford MD, Delaney
Saunders.) KA, Ling L et al: Clinical toxicology, Philadelphia, 2001, Saunders.)
Groups at risk Centers for Disease Control and Prevention (CDC) to repre-
sent overexposure, evidence suggests that the target level in
Among the general population, children have the highest children should be lowered further.10,11 Even at higher lead
risk of lead exposure and toxic effects of lead. It is estimated levels requiring chelation therapy (see below), many chil-
that more than 300,000 U.S. children have blood lead lev- dren may have minor or only vague symptoms, reinforcing
els in excess of 10 mcg/dL.3 Children living in houses with the importance of a high index of clinical suspicion. Rarely,
old peeling paint or dust or soil that contains lead are at children will present with extremely high lead levels and
risk because of their tendency to play on floors and on the symptoms of severe toxicity, including mental confusion,
ground and to ingest dirt and dust (especially if they have weakness, abdominal pain, and vomiting and seizures.
pica) through such activities. In addition, children are more In adults, subclinical neurological toxicity can manifest as
susceptible than adults to the neurotoxic effects of lead depression, problems with memory and learning, headaches,
exposure. fatigue, and abdominal discomfort. Peripheral nervous sys-
Among adults, certain occupations and hobbies place tem effects include a motor neuropathy with weakness of the
individuals at increased risk. Occupational hazards include wrist and ankle extensor muscles. Encephalopathy and sei-
sanding old paint from houses and other structures (Color zures can occur with severe cases of lead poisoning (blood lev-
Plates 8-5 and 8-6), making or recycling batteries, welding, els generally in excess of 70 mcg/dL). A frequent toxic effect of
or using solders that contain lead. Such workers can bring lead is anemia, produced through a number of effects on the
home lead dust on their clothes or shoes, posing a risk for hematological system including impairment of hemoglobin
other family members and family pets. Hunters who eat game synthesis and a destabilization of RBC membranes, thus lead-
with lead shot are also at risk.4 Anyone using lead for hobbies ing to hemolysis. The toxic effect of lead on the bone marrow
including stained glass or the home melting of lead to make can result in coarse basophilic stippling of RBCs seen on the
such items as fishing gear, hunting gear, or dive weights may peripheral blood smear (Color Plate 8-7).
be at risk. The kidney is another target of lead toxicity. In children,
Similarly, pets such as dogs may be at increased risk acute lead poisoning can lead to the development of Fanconi
because of their tendency to also ingest dust and dirt around syndrome. In adults, chronic lead exposure can increase the
a house or yard. Dogs living in industrial areas have been risk of hyperuricemic gout, chronic lead nephropathy, renal
found to have higher lead levels than those in rural areas.5 failure, and hypertension.
Licking of contaminated fur, such as cats cleaning them- Lead can cause a number of GI effects, including nausea,
selves, may be one source of ingestion of lead in dust and vomiting, constipation, and abdominal pain or “lead colic”
dirt. Lead intoxication in caged birds is well recognized.6 Pet as a result of the effects of lead on bowel smooth muscle.
birds may ingest paint, lead in stained glass windows, and At high exposure levels, lead may deposit along the gums
lead curtain weights. Pocket pets such as gerbils that gnaw producing a “lead line.” Other reported manifestations of
on articles may also become lead poisoned.6 Poultry living in toxicity include infertility caused by the effects on sperm
areas of contaminated soil or old coops with lead paint can counts and the risk of spontaneous abortion, hearing loss,
also become fatally intoxicated.6 and thyroid dysfunction.
There are a number of case reports of pets serving as early- In children, lead toxicity may affect school performance
warning sentinels of lead exposure risks to human beings liv- and behavior. Acute significant toxicity can present with
ing nearby. In one case, a dog developed persistent vomiting abdominal pain, irritability, and muscle cramps. Pregnant
and weight loss 1 month after renovation of the home. After the women can pass lead to their developing fetus, increasing the
dog was diagnosed with lead poisoning, the two young children risks for premature birth, low birth weight, and neurological
living in the home were tested and found to have lead toxicity as damage. After birth, lead can be passed from the mother to
well.7 In another case, a pregnant woman was becoming over her newborn in breast milk.
exposed to lead by removing paint from interior walls but real-
ized this danger to herself and her fetus only after her two cats
were hospitalized with lead poisoning.8 Reported cattle deaths Toxicity in animals
from lead poisoning related to contamination from mining
have provided warning of the risk to children in the area.9 As in human beings, lead exposure can produce both acute
and chronic signs, some of which may be nonspecific and
easily missed by veterinarians. Companion animals such as
Toxicity in human beings cats and dogs can exhibit anorexia, abdominal discomfort,
nausea and vomiting, seizures, and blindness. Cats can also
Lead exposure produces toxic effects in a range of organs and manifest vestibular signs.
a different spectrum of clinical effects in children and adults. Large animals can develop lead poisoning; horses may
Although acute toxicity can occur, chronic effects are more be more sensitive than cattle. These animals can develop
common. Importantly, many patients with lead poisoning may laryngeal paralysis, colic, abnormal bellowing, and seizures
have nonspecific symptoms, and medical care providers can (Figure 8-13).12
miss the condition if a careful exposure history is not taken. In birds, signs can include emaciation, anorexia, tremors
In children, subclinical effects of lead neurotoxicity may and leg weakness, loss of vision, wing drooping, reproductive
occur at blood lead levels of 10 mcg/dL or lower. These effects failure, and death. Anemia and renal dysfunction may occur.
include impaired school performance, attention problems, Such signs can be seen in caged birds and wild and domes-
and aggressive behavior.2 Therefore, although blood lev- tic waterfowl that ingest lead in fishing sinkers and lead shot
els in excess of 10 mcg/dL in children are considered by the from hunting.
Figure 8-13 n Lead poisoning causing recumbency, blindness, and bel-

lowing. This 16-month-old heifer also showed uncontrolled, jerky move-
ments. (From Divers TJ, Peek SF: Rebhun’s diseases of dairy cattle, ed 2, St.
Louis, 2008, Saunders Elsevier.)
Reported cases of lead poisoning in reptiles are rare, but

captive iguanas have been found to have toxic levels of lead
(Figure 8-14). Wild snapping turtles that ingested lead sink-
ers have been observed to have weakness, difficulty walking,
and CNS dysfunction.13 Table 8-12 shows the comparative
clinical presentations of lead toxicity in human beings and
other animals. Figure 8-14 n Radiograph shows metallic densities in a green iguana
(Iguana iguana) with lead poisoning. Blood lead levels were measured at 600
mcg/dL The source of lead was never determined. (From Mader DR: Reptile
medicine and surgery, ed 2, St Louis, 2006, Saunders Elsevier.)
Table 8-12 n Comparative Toxicity of Lead in Human Beings and Other Animals
Species Risk Factors Toxic Level Clinical Manifestations Laboratory Findings
Human Children: lead paint (in U.S. 25-40 mcg/dL (adults) Children: learning problems, Elevated blood lead level,
beings houses built before 1950), 10 mcg/dL or below confusion, seizures, renal ZPP, anemia, basophilic
soil, lead objects, water (children) dysfunction stippling of RBCs,
Adults: lead paint, water, Adults: lethargy, depression, abnormal liver and renal
occupational or hobby abdominal pain, anorexia, function tests, “lead
exposure, folk medicines CNS effects, weakness, lines” in radiographs of
renal toxicity long bones, elevated
bone lead by x-ray
fluorescence
Dogs, cats Exposure to old paint in >40 mcg/dL Anorexia, colic, emesis, Basophilic stippling of
buildings or soil diarrhea, constipation, RBCs, nucleated RBCs,
CNS depression or hepatocyte intranuclear
excitation, ataxia, inclusion bodies, abnormal
nystagmus, convulsions14,15 liver function tests
(elevated AST and ALT),
elevated blood lead levels
Birds Caged: lead around Varies with species: 20-40 Regurgitation, depression, Hemoglobinuria, anemia,
windows, curtains, pet toys mcg/dL weakness, excitability, elevated liver and kidney
Wild: ingestion of lead sinkers, seizures, wasting, death function tests
lead shot by waterfowl
Cattle, Forage contaminated with 35 ppm Anorexia, colic, constipation, Anemia, basophilic
horses lead from agriculture, ataxia, muscle tremors, stippling of RBCs
calves at increased risk, convulsions
ingestion of lead from
batteries or shot in soil
Reptiles Lead fishing sinkers, other Insufficient evidence Abnormal behavior, Elevated blood lead level
lead ingestion weakness, gait difficulties
ALT, Alanine aminotransferase; AST, aspartate aminotransferase; CNS, central nervous system; PPM, parts per million; RBCs, red blood cells; ZPP, zinc protoporphyrin.
Diagnosis
Box 8-2 QUESTIONS FOR THE MEDICAL HISTORY
REGARDING LEAD EXPOSURE RISKS
The cornerstone of diagnosis of lead poisoning in human
beings and other animals is obtaining an accurate expo-
The following are some issues a physician might discuss with the
sure history and documenting elevated blood lead levels. patient and/or family:
The two principal tests are the venous lead level and the zinc • Condition of household pets
protoporphyrin (ZPP) level. The ZPP level is a measure of • Drinking water source and type of pipes
the impact of lead on RBC synthesis and reflects exposures • Family history, including possibility of maternal/family exposure
over a period of several months. Therefore the finding of an and potential use of unusual medicines or home remedies
elevated level of venous lead but a normal ZPP test result • Hobbies of all family members
suggests acute rather than chronic exposure. Normal values • Home-remodeling activities
of ZPP are usually below 35 mcg/dL. Other conditions that • Location, age, physical condition of current residence, school,
elevate ZPP levels are iron deficiency anemia and hereditary and day-care center, and so on (to identify potential for lead
paint, as well as proximity to industrial facilities, hazardous
porphyria. Urine lead is sometimes measured but is consid-
waste sites, and other potential lead sources)
ered to be variable and does not accurately reflect the body • Nutritional status
lead burden. Similarly, analysis of lead in hair and nails is • Occupational history of all home occupants
considered unreliable. • Past living conditions (international background is important)
For individuals with long-term exposure, it is sometimes • Siblings or playmates in whom a diagnosis of lead poisoning
useful to assess the body lead burden. Chelation challenge has been made
with ethylenediamine tetraacetic acid (EDTA) is the most • Use of imported or glazed ceramics
common method. This test measures the urinary excretion From Agency for Toxic Substances and Disease Registry: Lead toxicity: how should
of lead after administration of the chelating agent EDTA. patients exposed to lead be evaluated? http://www.atsdr.cdc.gov/csem/lead/pbpatient_
EDTA challenge appears especially useful for assessing the evaluation2.html. Accessed February 15, 2008.
burden of lead in soft tissues.
Another method to assess body lead burden is K-shell
x-ray fluorescence (XRF) measurement of lead in bone. This Table 8-13 n Guidance for Treatment Actions
test is not widely available. In birds and other animals that According to Blood Lead Level
have ingested lead objects, radiographs may reveal accumu-
lation of lead in the digestive system. However, many birds Blood Lead Level
and wild animals have lead toxicosis without radiographi- (BLL) (mcg/dL) Treatment Actions
cally visible metallic objects.
10-19 Provide lead education and referrals
Provide diagnostic testing within 3 months and
follow-up testing within 2 to 3 months
Management of lead toxicity Proceed according to guidelines in 20-44
mcg/dL range if BLLs persist in 15-19 mcg/
dL range
Treatment in Human Beings (The presence of a large proportion of children
in the 10-14 mcg/dL range should trigger
The fundamentals of management of lead poisoning in human community-wide lead poisoning prevention)
beings are elimination of further exposure, removal of any metal- 20-44 Provide lead education and referrals
lic lead from the GI tract, and chelation therapy, which is gener- Provide coordination of care (case management)
ally reserved for children and acute severe toxicity in adults. Perform clinical evaluation and management
Provide diagnostic testing (from within
Removing an individual from exposure allows the body to 1 month to within 1 week) and follow-up
slowly eliminate the body’s accumulation of lead through the testing (every 1 to 2 months)
urine over time. It is therefore imperative to identify and elim- Perform aggressive environmental intervention
inate exposure sources by removal of the individual from the 45-69 Provide lead education and referrals
environment and/or environmental decontamination. Even if Provide coordination of care (case
the source of exposure is clear, a complete history should be management) within 48 hr
obtained to rule out other concurrent exposures (Box 8-2). Perform clinical evaluation and management
within 48 hr
The health department should be contacted for assistance Provide diagnostic testing within 24-48 hr
in identifying and eliminating the exposure. Table 8-13 pro- and follow-up testing (in accordance with
vides guidelines for ongoing management of lead poisoning chelation therapy, at least once a month)
in human beings based on the venous lead level and the clini- Perform aggressive environmental intervention
cal status of the patient. Provide appropriate chelation therapy
Chelation is never a substitute for aggressive environmental ≥70 (or in case This is a medical emergency
intervention to eliminate all further exposure. Chelation should of enceph Perform diagnostic testing immediately as
alopathy) an emergency lab test
not be given if there is persistent lead exposure or residual lead Hospitalize and begin immediate chelation
in the GI tract. In addition, periodic monitoring is necessary therapy
to ensure that blood lead levels are declining. Table 8-14 lists Begin other activities as above
guidelines for chelation therapy in human beings and animals.
For high-level exposure and/or significant symptoms, BLL, Blood lead level.
From Agency for Toxic Substances and Disease Registry: Lead toxicity: how should
treatment with a chelating agent may be indicated. Possible patients exposed to lead be treated and managed? http://www.atsdr.cdc.gov/csem/lead/
indications for chelation in adults include blood lead level pbmanage_therapy2.html. Accessed March 2, 2008.
greater than 70 mcg/dL, ongoing hemolysis, and encephal- http://www.epa.gov/opptintr/lead/index.html

opathy. In children, oral chelation with dimercaptosuccinic • HUD: Office of Healthy Homes and Lead Hazard Control
acid (DMSA) is indicated for blood levels in excess of 45 http://www.hud.gov/offices/lead/
mcg/dL. For extremely high lead levels, intravenous chela-
tion with CaNa2EDTA is recommended.2 Na2EDTA (diso-
dium ethylenediamine tetraacetic acid or edetate disodium) References
should not be used for chelation in children because it can
1. Ford MD, Delaney KA, Ling L, et al. Clinical toxicology. Philadelphia:
cause fatal hypocalcemia.17 Other risks of chelation include Saunders; 2001.
worsening of lead toxicity and hepatic effects of DMSA. 2. Moline JM, Landrigan PJ. Lead. In: Rosenstock L, Cullen MR, Brodkin
Before initiating chelation therapy, consultation with a CA, et al., eds. Textbook of clinical and occupational environmental medi-
regional poison center or pediatric or adult toxicology unit cine. 2nd ed. Edinburgh: Saunders; 2005.
should be obtained. 3. Centers for Disease Control and Prevention. Lead: topic home. http://
www.cdc.gov/lead/. Accessed December 12, 2008.
4. Guitart R, Serratosa J, Thomas VG. Lead-poisoned wildfowl in Spain:
Treatment in Animals a significant threat for human consumers. Int J Environ Health Res.
2002;12(4):301–309.
Treatment in animals depends on the blood lead level. 5. Ghisleni G, Spagnolo V, Roccabianca P, et al. Blood lead levels, clinico-
Treatment must involve elimination of exposure. Lead objects pathological findings and erythrocyte metabolism in dogs from differ-
in the GI tract should be removed and, in a haired animal ent habitats. Vet Hum Toxicol. 2004;46(2):57–61.
6. Kahn CM, Line S. The Merck veterinary manual. 9th ed. Whitehouse
such as a dog or cat, it is necessary to remove possible lead Station, NJ: Merck; 2005.
contamination from the coat. Cathartics such as magnesium 7. Dowsett R, Shannon M. Childhood plumbism identified after lead poi-
sulfate (400 mg/kg orally) can remove lead from the GI tract soning in household pets. N Engl J Med. 1994;331(24):1661–1662.
if acute ingestion is suspected in cattle.6 Balanced electrolyte 8. Doumouchtsis SK, Martin NS, Robins JB. Veterinary diagnosis of lead
poisoning in pregnancy. BMJ. 2006;333(7582):1302–1303.
solutions to replace hydration deficit, gastric lavage, and sei- 9. Feely E, Garavan C, Kelleher K. Dead cattle, lead and child health. Ir
zure control may be necessary. Chelation therapy should be Med J. 2003;96(8):232–234.
considered for severe animal toxicity cases. 10. Agency for Toxic Substances and Disease Registry. Lead toxicity: what
are the physiological effects of lead exposure? http://www.atsdr.cdc.
gov/csem/lead/pbphysiologic_effects2.html. Accessed February 15,
Web resources 2008.
11. Centers for Disease Control and Prevention. Preventing lead poison-
ing in young children. http://www.cdc.gov/nceh/lead/publications/
• CDC: Lead Poisoning Prevention Program PrevLeadPoisoning.pdf. Accessed December 12, 2008.
http://www.cdc.gov/nceh/lead/ 12. Gupta RC, ed. Veterinary toxicology: basic and clinical principles. New
• EPA: Lead Awareness Program York: Academic Press; 2007.
Table 8-14 n Chelation Guidelines for Lead Toxicity in Human Beings and Other Animals
Species Blood Level or Signs Primary Alternative
Adult human Consider chelation for markedly Succimer (DMSA) 10 to 30 mg/kg/day Ca-EDTA chelation
beings elevated blood lead level (>80 for 5 days
mcg/dL)1, ongoing hemolysis,
encephalopathy
Children >45 mcg/dL (see Table 8-12) Succimer (DMSA) safety and
effectiveness in pediatric patients
younger than 12 months have not
been established
Dose: 10 mg/kg or 350 mg/m2 q8h
for 5 days, then 10 mg/kg or 350
mg/m2 q12h for 14 days
Dogs >40 mcg/dL or Ca-EDTA 25 mg/kg d-Penicillamine 10-15 mg/kg PO
>20 mcg/dL with evidence of clinical diluted in D5W q6h for 5 days q12h × 2 weeks (do not give if
signs and exposure Or succimer 10 mg/kg PO tid × there is lead in the GI tract)
10 days16
Cats Ca-EDTA 25 mg/kg diluted in D5W
SC, IM, IV q6h for 5 days
Cattle Ca-EDTA 110 mg/kg/day IV/SC
divided and diluted in D5W bid × 3
days, repeat after 2 days,6 thiamine
2-4 mg/kg/day SC
Birds Ca-EDTA 30-50 mg/kg diluted in D5W d-Penicillamine 30-50 mg/kg bid
IM or SQ, bid, or tid 5-7 days
After a 5- to 7-day rest, repeat
treatment may be warranted6
D5W, 5% dextrose in water.

13. Wellehan JFX, Gunkel CI. Emergent diseases in reptiles. Seminars in 16. Ramsey DT, Casteel SW, Faggella AM, et al. Use of orally administered
Avian and Exotic Pet Medicine. 2004;13(3):160–174. succimer (meso-2,3-dimercaptosuccinic acid) for treatment of lead poi-
14. De Francisco N, Ruiz Troya JD, Agüera EI. Lead and lead toxicity in soning in dogs. J Am Vet Med Assoc. 1996;208(3):371–375.
domestic and free living birds. Avian Pathol. 2003;32(1):3–13. 17. Brown MJ, Willis T, Omalu B, et al. Deaths resulting from hypocalce-
15. Knight TE, Kumar MS. Lead toxicosis in cats—a review. J Feline Med mia after administration of edetate disodium: 2003–2005. Pediatrics.
Surg. 2003;5(5):249–255. 2006;118(2):e534–e536.
Pesticides
Lisa A. Conti and Peter M. Rabinowitz

Pesticides (ICD-10: T60.0 Toxic Effect of
Organophosphate and Carbamate Insecticides;
T60.2 Toxic Effect of Other Insecticides; T60.8 Toxic
Effect of Other Pesticides; T60.9 Toxic Effect of
Pesticide, Unspecified)
Pesticides are chemicals, biologicals, antimicrobials, or disin-

fectants used to control insects, weeds, mollusks, mammals,
fish, birds, nematodes, plant pathogens, and microbes.
Historically, pesticides have been a common cause of poison-
ing in human beings and other animals. In recent years the
number of serious poisonings reported to U.S. poison con-
trol centers appears to be declining,1 related in part to phasing
out of several toxic organophosphate insecticides (including Figure 8-15 n An ideal flea and tick control is one that is specific to
target the organism and safe for nontarget species such as human beings
chlorpyrifos) for residential use and an increased interest in and companion animals. (From Centers for Disease Control and Prevention
using “green” products. Yet pesticide poisoning remains an Public Health Image Library, Atlanta, Ga.)
important clinical problem in the United States and world-
wide. Although pesticides are usually developed and mar- spectra of toxic effects, many commercial formulations con-
keted for specific purposes, their toxic effects may cross many tain mixtures of different compounds, resulting in complex
species. In addition, trace amounts may find their way into clinical syndromes. In addition, symptoms of pesticide tox-
drinking water with as yet unknown effects from chronic icity are often nonspecific, and it is likely that many cases of
exposure. Differences in toxicokinetics (and toxicodynamics) mild toxicity are never reported.
between human beings and other animals can result in dif-
ferential susceptibility (a pesticide may be more or less toxic,
depending on the species that has been exposed).
Professionals
This section focuses on toxic hazards associated with
animal-related pesticides. Some of the zoonotic diseases
discussed in this book are controlled through the use of Public Health Professionals
pesticides applied directly to animals or their bedding or
by the use of insect repellents applied to human skin or • Ensure that local animal care facilities and extermi-
clothing. Such uses can involve a risk of toxicity to both nators are using only approved pesticides for flea and
human beings and animals. In recent years the U.S. EPA tick control and are storing and using them with strict
has taken steps to phase out of commercial use a number adherence to the product labeling instructions.
of pet-related pesticides, especially organophosphate com- • Educate human health clinicians to communicate about
pounds such as chlorpyrifos, because of concerns about cases and veterinarians to contact public health if there
the short- and long-term health effects in human beings is a possibility of human exposure from these products.
and other animals (Figure 8-15). Other groups, such as the • Educate the public about the judicious use of prod-
Humane Society of the United States, have recommended ucts. See “Using Pesticides Safely” (http://www.epa.
that newer, apparently less-toxic pesticides be used for ani- gov/opp00001/health/safely.htm), which includes
mal care.2 Perhaps in part as a result of such actions, in links to documents on protecting pets, children, and so
2006 fewer than 200 human exposures to veterinary insect forth with an emphasis on the importance of compli-
repellents were reported to U.S. poison control centers.3 In ance with labeling instructions for pesticide products
addition, animals may become sickened through inappro- in human beings and other animals.
priate use of a human insect repellent on a pet, although  Always store pesticides and other household chemi-
this appears to be a rare occurrence. cals away from children and animals.
Although there are several major classes of pesticides (and  Read the label.
some of the newer pesticides are in entirely new chemical  Before applying pesticides or other household chemi-
classes) with markedly different chemical composition and cals remove children, pets, and toys from the area.
 Never transfer pesticides to another container. of the U.S. population uses some quantity of DEET.5 In 2006,
• Report incidents to the EPA via the National Pesticide more than 8000 exposures to DEET were reported to U.S.
Information Center; see http://oregonstate.edu/npmmp/ poison control centers.3 Although residues of DEET have
contact.php (general information: http://npic.orst.edu/). been identified in environmental water samples, the impact
on the ecosystem is considered to be minimal.8 The EPA rec-
Human Health Clinicians ommendations for safe use of DEET products are listed in
Box 8-3.
• Encourage the use of cleanliness and sanitation around
the home in lieu of the use of pesticides. Integrated
pest management emphasizes using a combination Picaridin
of approaches toward taking care of pest problems Picaridin (2-(2-hydroxyethyl)-1-piperidinecarboxylic acid
(not just using pesticides). See http://www.epa.gov/ 1-methylpropyl ester) was registered as an insect repel-
opp00001/factsheets/ipm.htm. lent with the EPA in 2001 and is thus a much newer agent
• For patients who own pets or farm animals, inquire than DEET. It is believed to have comparable efficacy, have
about pesticide use practices and storage and counsel very low toxicity, and be safe for human use as directed.9
about symptoms of toxicity. Advantages over DEET include the fact that it is odorless,
• Have a high index of suspicion in persons occupation- less greasy, and does not damage clothing.
ally exposed or otherwise exposed to pet pesticides.
• Counsel pet owners not to use N,N-diethyl-meta-
toluamide (DEET)-containing products on pets. Pyrethroids/Permethrin
• Report incidents to state or local public health officials Permethrin is a synthetic chemical compound, along with
and the EPA via the National Pesticide Information other pyrethroids, similar to that produced by pyrethrum
Center; see http://oregonstate.edu/npmmp/contact. flowers (Chrysanthemum cinerariifolium and C. coccineum).
php (for general information, see http://npic.orst.edu/). These chemicals are poorly absorbed by the skin but can
The EPA’s Recognition and Management of Pesticide cause hypersensitivity reactions. These chemicals are neuro-
Poisonings is a good resource for information about the toxic to insects by maintaining patency in sodium channels
clinical toxicology of pesticides and is available online in neuronal membranes.
at http://npic.orst.edu/rmpp.htm.
Oil of Lemon Eucalyptus
Oil of lemon eucalyptus is a plant-based repellent that the
• Encourage pet owners to use appropriate alternatives CDC considers to be an alternative to DEET as an insect repel-
to pesticides or lower toxicity pesticides to control fleas lent. The active ingredient is p-methane 3,8-diol (PMD). The
and ticks and to keep cats indoors. mechanism of action is unclear, and aside from eye irritation
• Discourage the use of organophosphate or carbamate no significant toxicity has been reported.7 However, accord-
pesticides for animals. ing to the product labeling, products containing oil of lemon
• Ensure that veterinary workers applying flea or mite dips eucalyptus should not be used on children younger than 3
and other treatments are adequately protected and trained years.10
in the proper handling and storage of these products. Other products are being developed with regard to safety
Consider use of less-toxic compounds for such purposes. and efficacy.11,12
• Report incidents to the EPA via the National Pesticide
Information Center; see http://oregonstate.edu/npmmp/
contact.php (general information: http://npic.orst.edu/).
Pesticides used on animals
In addition to being nuisances, fleas, ticks, and mosquitoes are

Insect repellents used on human beings carriers of disease agents such as plague (fleas), Rocky Mountain
spotted fever (ticks; Figure 8-20), and arboviral disease (mos-
Table 8-15 lists agents for prevention of insect bites for quitoes). Table 8-16 provides information about the pesticides
human beings (Figures 8-16 and 8-17). The EPA reviews the used on companion animals to control these arthropods.
use of particular compounds as insect repellents.4 Most of
these repellents do not work on lice or fleas (Figure 8-18).
Pesticides With Low Relative Mammalian
Toxicity
DEET
Fipronil is an N-phenylpyrazole compound that was intro-
DEET was developed for use by the U.S. Army in 1946 and duced in 1996. When applied to a dog or cat, it spreads
approved for use by the general public in 1957. It is one of over the skin and accumulates in sweat glands, where it is
the insect repellents judged by the EPA to provide longer- slowly released over time. Skin absorption is thought to
lasting protection than some others. It is considered safe for be minimal. It acts by blocking gamma-aminobutyric acid
use by both adults and children 2 years and older when used (GABA) receptors in insects, disrupting nervous system
as directed (Figure 8-19). Each year, approximately one third function. It appears to have less affinity for mammalian
Table 8-15 n Agents for Prevention of Insect Bites for Human Beings
Compound Use Insects Comment
DEET (e.g., Off, Cutter, Repel, Apply to clothing or exposed skin Flies, mosquitoes, ticks Combined sunscreen/DEET
many other products, some Note: DEET (along with the other products not recommended6,7
combined with sunscreen)5 repellents) should not be applied DEET products should not be
under clothing (on unexposed used on animals
areas); applying underneath Not to be used on children
clothing can increase the extent <2 years
of absorption and is more likely
to result in irritant reactions
Picaridin (e.g., Cutter Apply to clothing and skin Biting flies, mosquitoes, chiggers,
Advanced) ticks, fleas
Pyrethroids/permethrin Apply to clothing and gear but Mosquitoes, ticks, other
not skin arthropods
Oil of lemon eucalyptus (e.g., Apply to skin and clothing Mosquitoes, ticks (not yet Not to be used in children
Repel Lemon Eucalyptus studied in malaria mosquitoes) younger than 3 years old
Insect Repellent)
DEET, N,N-diethyl-m-toluamide.
Figure 8-16 n Mosquito about to take a blood meal. (From Centers for Figure 8-18 n Flea. Thin wingless insects with very hard bodies and
Disease Control and Prevention Public Health Image Library, Atlanta, Ga. large hind legs adapted for jumping. (From Habif TP: Clinical dermatology:
Courtesy James D. Gathany.) a color guide to diagnosis and therapy, ed 4, St Louis, 2004, Mosby. Courtesy
Ken Gray, Oregon State University Extension Services.)
Figure 8-17 n A mother applying mosquito repellent to her child’s skin to

prevent mosquitoes from biting, thereby, preventing many arboviral infections Figure 8-19 n Applying DEET repellent to clothing. (From Centers for
such as West Nile virus. (From Centers for Disease Control and Prevention Disease Control and Prevention Public Health Image Library, Atlanta, Ga.
Public Health Image Library, Atlanta, Ga. Courtesy James D. Gathany.) Courtesy James D. Gathany.)
Box 8-3 EPA GUIDELINES FOR SAFE USE OF DEET-

CONTAINING PRODUCTS
Consumers can reduce their own risks when using DEET by

reading and following product labels. All DEET product labels
include the following directions:
• Read and follow all directions and precautions on the product
label.
• Do not apply over cuts, wounds, or irritated skin.
• Do not apply to hands or near eyes and mouth of young children.
• Do not allow young children to apply this product.
• Use just enough repellent to cover exposed skin and/or clothing.
• Do not use under clothing.
• Avoid overapplication of this product.
• After returning indoors, wash treated skin with soap and water.
• Wash treated clothing before wearing it again.
• Use of this product may cause skin reactions in rare cases.
The following additional statements appear on the labels of all
aerosol and pump spray formulation labels:
• Do not spray in enclosed areas.
• To apply to face, spray on hands first and then rub on face. Do Figure 8-20 n This illustration depicts a dorsal view of a female “hard”
not spray directly onto face. or Ixodidae, “American dog tick” (wood tick), Dermacentor variabilis. (From
Centers for Disease Control and Prevention Public Health Image Library,
From Environmental Protection Agency: The insect repellent DEET. http://www.epa. Atlanta, Ga.)
gov/pesticides/factsheets/chemicals/deet.htm. Accessed April 14, 2008.
Table 8-16 n Pesticides Used on Animals
Compound Uses Dogs Cats Other LD50
Fipronil (e.g., Frontline, Top Flea and tick control X X Dermal dose: >5000 mg/kg in rats
Spot) Orally: 750 mg/kg in rats
Imidacloprid (e.g., Advantage, Flea control X X Dermal dose: >5000 mg/kg in rats
Advantix [which also includes Orally: 450 mg/kg in rats
permethrin])
Spinosad (e.g., Comfortis) Flea control X Orally: >3000 mg/kg in rats;
>2000 mg/kg in rabbits
(translates to over 30 times
recommended oral dose)
Metaflumizone (with Amitraz) Flea control X X Metaflumizone: >5000 mg/kg
(e.g., ProMeris) Tick control X dermally in rats
Amitraz: 515-938 mg/kg orally in
rats; 100 mg/kg orally for dogs
Selamectin (e.g., Revolution) Endoparasites and ectoparasites X X Dermal dose: >1600 mg/kg in rats
(heartworm, roundworm,
hookworm, mites)
Nitenpyram (e.g., Capstar) Fleas X X Orally: 1575 mg/kg in rats
Lufenuron (e.g., Program, Fleas (sterilization) X X Orally: >2000 mg/kg in rats
Sentinel [and milbemycin for
additional parasites])
Pyrethrins/pyrethroids (e.g., Tick and flea control, mite and X X Orally: 430-4000 mg/kg in rats
permethrin, phenothrin, lice (birds)
cyphenothrin)
Organophosphates (e.g., low Tick and flea control X X Orally: 22 to >1000 mg/kg in rats
toxicity: tetrachlorvinphos;
moderately toxic: diazinon,
chlorpyrifos; extremely toxic:
coumaphos)
Carbamates (e.g., low toxicity: Tick and flea control X X Orally: 4-850 mg/kg in rats
propoxur, carbaryl; extreme
toxicity: carbofuran)
LD50, Median lethal dose.
GABA receptors and is considered to have low acute tox- Pesticides With High Relative Mammalian
icity. The major acute sign appears to be skin and eye Toxicity
irritation. In young rabbits, however, there have been
anecdotal reports of anorexia, lethargy, seizures, and Organophosphate compounds phosphorylate and inac-
death. Fipronil is classified as a possible human carcino- tivate acetylcholinesterase and pseudocholinesterase
gen based on studies in rats showing an increase in thy- enzymes that are responsible for breaking down acetyl-
roid tumors.13 choline (ACh) in nerve endings, RBCs, and muscle. As a
Imidacloprid is a chloronicotinyl nitroguanidine com- result, ACh accumulates, resulting in disruption of nor-
pound. It acts by blocking nicotinic acetylcholine receptors mal nerve stimulus control and excess stimulation of
in the insect nervous system and, like fipronil, appears to both central and peripheral nerve junctions, including
have less affinity for mammalian receptors. It is capable of muscarinic and nicotinic receptors. (Note: Cats have
being absorbed through the skin but appears to have low most of their cholinesterases in their plasma rather
acute toxicity. Animals fed significant amounts of imida- than RBCs like most other species. Measuring RBCs for
cloprid over time have developed thyroid disturbances. It cholinesterase activity in cats detects only the pseudocho-
is classified as having evidence of noncarcinogenicity in linesterase activity, which can drop to zero by exposure
human beings.13 to subtoxic doses of ACh inhibitors. Plasma ACh activ-
Spinosad is a macrolide insecticide derived from a ity, not RBC ACh, should therefore be measured in cats
naturally occurring actinomycete bacterium that acti- to reduce false-positive findings due to the inhibition of
vates nicotinic acetylcholine receptors by a novel mecha- RBC pseudocholinesterases.)
nism. It also has effects on GABA receptor function that N-methyl carbamates cause reversible carbamylation of
may contribute further to its insecticidal activity. It has a acetylcholinesterase (AChE) and therefore cause clinical
low mammalian toxicity. It requires topical application syndromes similar to organophosphates, with muscarinic,
and spreads in the skin oils (requiring a day or two for nicotinic, and CNS effects. However, inhibition of AChE is
distribution). more reversible than organophosphate poisoning, resulting
Metaflumizone is a semicarbazone insecticide derived in shorter duration of signs and somewhat easier treatment.
from the pyrazolone sodium channel blocker insecticides
discovered in the early 1970s. Metaflumizone has greatly
improved mammalian safety over its ancestors. Groups at risk
Nitenpyram is a neonicotinoid chemical, interfering with
nerve transmission in the flea but not the pet. Children, the elderly, and pregnant women may be at par-
Luferuron is an insect growth regulator through chitin inhi- ticularly high risk for toxicity from pesticides and insect
bition. Therefore lufenuron does not kill adult fleas. repellents. Individuals at increased risk of exposure to pet
Selamectin is a semisynthetic avermectin developed for pesticides include pet groomers and handlers, pet parlors,
use in dogs and cats. It treats a wide range of ectoparasites pet store employees, veterinary workers, agricultural work-
and endoparasites. It affects chloride channels in the nervous ers, and children who pet animals that have been topically
system of insects, producing paralysis, and has less effect treated with pesticide.
on mammalian nerves. It is applied topically and absorbed Pet groomers and veterinary workers have become poi-
systemically, where it acts in both the intestine and the skin soned after skin contact with flea dips containing phosmet
glands to eliminate parasites. It is considered to have low tox- (organophosphate). In one case the dog being bathed shook
icity in human beings, cats, and dogs. The major side effect his coat and showered the worker with fluid from the dip.16
is skin irritation. Symptoms included skin irritation, shortness of breath,
abdominal cramping, and nausea. In another case, a pet store
employee sprayed her face with a solution containing pyre-
Pesticides With Moderate Relative Mammalian thrins while spraying a flea-infested house. She developed
Toxicity eye irritation and wheezing.
Beginning in 2000, the EPA acted to phase out the use of Certain animals have increased susceptibility to partic-
organophosphate insecticides in residential environments. ular pesticides. For example, cats are particularly sensitive
As a result, the number of pyrethrin- and pyrethroid- to carbamates and permethrins. The pyrethroids are also
related exposures reported to poison control centers has very toxic to aquatic species, which is important to mention
increased in recent years.14 Pyrethrins are derived from the to people who have aquariums or fish ponds at home. In
chrysanthemum plant. They have a quick onset of para- addition, animals may be susceptible to toxicity from insect
lytic action on insects and are often used in household repellents used on human beings. Therefore such com-
settings. However, they break down quickly in sunlight. pounds should never be used on animals unless specifically
Synthetic pyrethrins (pyrethroids) are more stable and labeled for such use.
have wider use in agricultural applications and mosquito
control. Pyrethrins are poorly absorbed across the skin and
are rapidly broken down in the mammalian digestive sys- Toxicity in human beings
tem.15 Pyrethrins are often used with potentiating agents
such as piperonyl butoxide, which inhibit breakdown of the Table 8-17 compares clinical manifestations of acute pesti-
compound by inhibiting mixed function oxidase action in cide poisoning in human beings and other animals. Acute
insects. organophosphate poisoning in human beings manifests as
Table 8-17 n Clinical Manifestations of Acute Pesticide Poisoning in Human Beings and Other Animals
Type of Pesticide Human Beings Dogs Cats Birds
Organophosphates Hypersalivation, Hypersalivation, miosis, diarrhea, vomiting, colic, Diarrhea, ataxia,

lacrimation, urination, bradycardia, dyspnea, ataxia, hyperthermia, tremors, seizures,
miosis, bradycardia, excessive bronchial secretions (thick, ropy mucus dyspnea, respiratory
blurred vision, mental blocking the respiratory tract is one of the more failure, increased
status changes, depressed common causes of death in dogs and cats), secretions, paralysis
cholinesterase levels CNS stimulation progressing to seizures followed
by onset of weakness and paralysis, respiratory
depression, depressed cholinesterase levels22
Carbamate Resembles organophosphate poisoning but shorter lived; seizures; bradycardia less
frequent
Pyrethrin/pyrethroids Allergic symptoms (crude Mild: hypersalivation, fasciculation Depression, weakness;
pyrethrum), respiratory Moderate: vomiting, diarrhea, depression, ataxia, tremors possible tremors,
irritation, paresthesias, Severe: seizures or death (cats are more sensitive than seizures23
seizures (rare) dogs)
signs of cholinergic overstimulation, including salivation, parasympathetic stimulation. Toxicity occurs with inappro-
sweating, lacrimation, urination, diarrhea, bradycardia, mus- priate application: overuse or use of yard products as topical
cle twitching, and nausea. CNS effects include headache and insecticides or dog products used on cats, and with acciden-
agitation. In severe cases, there can be respiratory depres- tal ingestion of lawn products (typically out of containers by
sion, seizures, and loss of consciousness. Miosis may occur. dogs) or cats walking through wet, recently treated areas and
Cholinesterase levels are depressed. grooming the product off their coats.
Carbamate toxicity resembles organophosphate poison- Cats are quite sensitive to the effects of concentrated
ing but tends to be shorter lived. Bradycardia and seizures pyrethroids such as permethrin (e.g., >10% permethrin;
are less frequent. Cholinesterase levels may be “falsely nor- dog products are 20% to 85% permethrin). Despite label
mal” in the setting of carbamate toxicity because of the warnings, cats are poisoned by permethrin spot-on treat-
presence of a carbamylated enzyme that can be reactivated ments for ticks and fleas that were intended for use on dogs.
in vitro. Young, old, or debilitated animals are also more likely to suf-
Crude pyrethrum and, to a lesser extent, purified pyre- fer ill effects. Signs result from idiosyncratic and neurotoxic
thrin preparations and pyrethroids may cause allergic reac- reactions and include twitching, muscle spasms and fascicu-
tions including skin and eye irritation and asthma.17 The lations, and seizures.19 Hypothermic patients are more likely
chief effect of pyrethroids appears to be on the nervous to show signs.
system. In mild cases, nausea and paresthesia can occur (at DEET at very high oral doses (400 mg/kg/day) has been
the site of contact, which generally resolve within 24 hours reported to cause vomiting, ataxia, tremors, and convulsions
after exposure). Seizures have been reported in more severe in dogs,20 and a DEET/fenvalerate topical product for dogs
exposures. has resulted in seizures. However, the ASPCA Animal Poison
There are case reports of DEET toxicity in human beings, Control Center has issued a press release that recommends
including CNS effects such as slurred speech and seizures; not using DEET on companion animals because of the risk
these have generally been the result of ingestion of large of neurologic effects in dogs and cats.21
doses,18 and the anecdotal nature of these reports requires
caution in interpretation. Dermal application has been
reported to rarely cause rashes, itching, and mucosal irrita-
tion; eye and skin irritation are considered the major pos- Diagnosis
sible side effects of conventional DEET use.7
No major toxic effects of picaridin or lemon eucalyptus Diagnosis of pesticide poisoning is often a clinical diagnosis
oil have been reported to date. Both are believed to cause less made when typical symptoms or signs develop after exposure.
skin and eye irritation than DEET. However, long-term tox- Organophosphate pesticides depress serum and RBC cholin-
icity studies are lacking. esterase levels (<25%). Any patient with organophosphate
toxicosis should have blood levels determined immediately
because the administration of pralidoxime hydrochloride
Toxicity in animals can normalize test results. As stated previously, cholinesterase
levels may be spuriously normal in carbamate intoxication.
Organophosphates and carbamates have higher toxicity in Cholinesterase levels are also useful in the diagnosis of animal
animals with lower cholinesterase activity. Cats are more intoxication. (Care must be used when interpreting cholin-
sensitive to these products than dogs. Young and leaner ani- esterase activity results between species. Use toxicologist and
mals are more susceptible. Signs include predominantly laboratory normal values for comparison.)
Table 8-18 n Treatment of Acute Pesticide Poisoning in Human Beings and Other Animals
Type of Pesticide Human Beings Dogs Birds
Organophosphate Moderately severe Atropine sulfate 0.2 mg/kg (¼ given Atropine sulfate 0.01-0.02 mg/kg
Adult: Atropine sulfate 2-4 mg IV IV and the remainder SC) q3-6h SC, IM (most species, ranges up
q15min until decreased secretions, should be given only to relieve to 0.5 mg/kg) or pralidoxime
pulse 140. excessive bronchial secretions or severe 10-100 mg/kg IM q24-48h or
Children <12 years: 0.05-0.1 mg/ bradycardia. (Over-atropinization is repeat once in 6 hr (use lower
kg body weight, minimum dose a common cause of serious illness dose in combination with
0.1 mg and death in dogs and cats when atropine)24
Severe poisoning: atropine is given without regard
Adults: Pralidoxime 1-2 mg IV slowly for the condition of the animal.
Children <12 years: 20-50 mg/kg body Unfortunately, over-atropinzied
weight (depending on severity of animals may display CNS signs that
poisoning) IV, in 100 mL of normal resemble some of the CNS effects
saline infused over 30 min15
of the OP/carbamate, which may
result in yet more atropine being
administered.)
Pralidoxime chloride 10-15 mg/kg IM
or slow IV (over 5-10 min) q8-12h
until recovery
If seizures, diazepam (0.05-1 mg/kg IV) or
phenobarbital (3-30 mg/kg IV) to effect
Carbamates Atropine, anticonvulsants, as with organophosphates
Pyrethrin/pyrethroids Antihistamines for allergic Bathe with a mild detergent Bathe with mild detergent,
reactions If tremors or seizures, methocarbamol diazepam 0.5-1.0 mg/kg IM,
55-220 mg/kg IV not to exceed 330 IV q8-12h as anticonvulsant24
mg/kg/day, diazepam to control
seizures
OP, Organophosphate; IV, intravenous; SC, subcutaneous; IM, intramuscular.
2. Humane Society of the US. What you should know about flea and tick
Management of animal-related pesticide products. http://www.hsus.org/pets/pet_care/what_you_should_know_
poisoning about_flea_and_tick_products/. Accessed February 20.
3. Bronstein AC, Spyker DA, Cantilena Jr LR, et al. 2006 Annual Report of
Management of acute pesticide exposures involves assessment the American Association of Poison Control Centers’ National Poison
of exposure amount and route, decontamination (removal Data System (NPDS). Clin Toxicol (Phila). 2007;45(8):815–917.
4. Environmental Protection Agency. How to use insect repellent safely.
of clothing, washing, etc.), supportive measures, and consid- http://www.epa.gov/pesticides/health/mosquitoes/insectrp.htm.
eration of specific antidotes. Contact the poison control cen- Accessed April 14, 2008.
ter at 800-222-1222 or the Animal Poison Control Center at 5. Environmental Protection Agency. The insect repellent DEET. http://www.
888-426-4435 (a fee may apply to the latter call). Table 8-18 epa.gov/pesticides/factsheets/chemicals/deet.htm. Accessed April 14, 2008.
6. Centers for Disease Control and Prevention. Insect repellent use and safety:
presents treatment options of acute pesticide poisoning in using repellents properly. http://www.cdc.gov/ncidod/dvbid/westnile/qa/
human beings and other animals. insect_repellent.htm#proper. Accessed April 14, 2008.
7. Kendrick DB. Mosquito repellents and superwarfarin roden-
ticides—are they really toxic in children? Curr Opin Pediatr.
Web resources 2006;18(2):180–183.
8. Costanzo SD, Watkinson AJ, Murby EJ, et al. Is there a risk associated with
the insect repellent DEET (N,N-diethyl-m-toluamide) commonly found
• National Pesticide Information Center in aquatic environments? Sci Total Environ. 2007;384(1-3):214–220.
http://npic.orst.edu 9. Environmental Protection Agency. New pesticide fact sheet: Picadirin.
• CDC: Insect Repellent Use and Safety (including dura- http://www.epa.gov/opprd001/factsheets/picaridin.pdf. Accessed April
14, 2008.
tion of effectiveness) 10. Centers for Disease Control and Prevention. Insect repellent use and
http://www.cdc.gov/ncidod/dvbid/westnile/qa/insect_ safety. http://www.cdc.gov/ncidod/dvbid/westnile/qa/insect_repellent.
repellent.htm htm. Accessed September 15, 2008.
• EPA: Ten Tips to Protect Children from Pesticide and 11. Schwantes U, Dautel H, Jung G. Prevention of infectious tick-borne
Lead Poisonings diseases in humans: comparative studies of the repellency of different
dodecanoic acid-formulations against Ixodes ricinus ticks (Acari:
http://www.epa.gov/pesticides/factsheets/child-ten-tips. Ixodidae). Parasit Vectors. 2008;1(1):8.
htm 12. Thorsell W, Mikiver A, Tunón H. Repelling properties of some plant mate-
rials on the tick Ixodes ricinus L. Phytomedicine. 2006;13(1–2):132–134.
13. Hovda LR, Hooser SB. Toxicology of newer pesticides for use in dogs
References and cats. Vet Clin North Am Small Anim Pract. 2002;32(2):455–467.
14. Power LE, Sudakin DL. Pyrethrin and pyrethroid exposures in the
1. Blondell JM. Decline in pesticide poisonings in the United States from United States: a longitudinal analysis of incidents reported to poison
1995 to 2004. Clin Toxicol (Phila). 2007;45(5):589–592. centers. J Med Toxicol. 2007;3(3):94–99.
15. Reigart JR, Roberts JR. Recognition and management of pesticide poisoning. 20. Schoenig GP, Osimitz TG, Gabriel KL, et al. Evaluation of the chronic
5th ed. Washington DC: U.S. Environmental Protection Agency; 1999. toxicity and oncogenicity of N,N-diethyl-m-toluamide (DEET). Toxicol
16. Centers for Disease Control and Prevention. Illnesses associated with Sci. 1999;47(1):99–109.
occupational use of flea-control products—California, Texas, and 21. The American Society for the Prevention of Cruelty to Animals
Washington, 1989–1997. MMWR. 1999;48(21):443–447. (ASPCA). Press release: the ASPCA Animal Poison Control Center Alerts
17. Franzosa JA, Osimitz TG, Maibach HI. Cutaneous contact urticaria to Dog Owners to Important Information Regarding West Nile Virus. http://
pyrethrum—real? common? or not documented? An evidence-based www2.aspca.org/site/News2?page=NewsArticle&id=10900&news_iv_
approach. Cutan Ocul Toxicol. 2007;26(1):57–72. ctrl=1101. Accessed April 14, 2008.
18. Koren G, Matsui D, Bailey B. DEET-based insect repellents: safety 22. Kahn CM, Line S. eds. The Merck veterinary manual. 9th ed. Whitehouse
implications for children and pregnant and lactating women. CMAJ. Station, NJ: Merck; 2005.
2003;169(3):209–212. 23. Willis GA. Hamilton & District Budgerigar Society, Inc: Avian poisoning.
19. Sutton NM, Bates N, Campbell A. Clinical effects and outcome of feline per- http://www3.sympatico.ca/davehansen/avpoison.html. Accessed April 14,
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Envenomations

(ICD-10 T63.0 Toxic Effect of Contact With Venomous • When appropriate, help coordinate with regional poison
Animals) control centers and emergency medical providers to ensure
A wide variety of animals are equipped with venom of access to antivenin and other information necessary to treat
different types for protective and sometimes feeding pur- possible envenomations that may occur locally.7
poses. Human beings and other animals may be exposed • Increase the public’s awareness of the risks of venom-
to such venoms through bites, stings, and ingestion.1 ous animals kept as pets and in the wild.
Envenomation may be a complication to consider in eval-
uating a patient who seeks emergency care after an animal
bite (see Chapter 10). Human Health Clinicians
Envenomation scenarios often illustrate the overlap • When taking a history of animal exposures (see
between human and veterinary medicine. For a number Chapter 3), ask about any venomous pets. If patients
of hazards, such as snakebite, poisoning episodes are much report such a history, ensure they are aware of emer-
more common in dogs than in human beings because of gency procedures if envenomation should occur. If
greater exposure to snakes in the wild. For example, several patients have questions about a particular animal, con-
thousand human beings are bitten by poisonous snakes each sult the patient’s veterinarian.
year in the United States, but the number of dogs and cats • In evaluating a patient with an animal bite, determine
that sustain snakebites annually may be as high as 150,000.2 the species responsible and the possibility for enveno-
Pets can therefore serve as sentinels about the environ- mation. Consult a regional poison control center.
mental risk of venomous animals. For marine envenoma- • Counsel travelers about the risk of animal envenom-
tions, documented cases in companion animals or wildlife ation (including in exotic foods) and necessary steps
are uncommon. When cases of poisoning do occur in ani- to take in case of envenomation in countries that the
mals, they often closely resemble the clinical picture in patient plans to visit.
human beings. In terms of treatment, moreover, veterinar-
ians must sometimes rely on the use of antivenin developed
for human beings when treating poisoned animals. A sig- Veterinary Clinicians
nificant issue for both human health and veterinary clini-
• Recognize the envenomation potential of particu-
cians is the risk of poisoning from exotic pets (see Chapter
lar species kept as pets. Discuss with clients the risk
10), such as reptiles,3 amphibians, and invertebrates such as
to companion animals in the house, and counsel cli-
scorpions.4 Many owners are unaware that these pets pose
ents to discuss human health risks with their medical
an envenomation risk to human beings and other animals
provider.
living in the house.5 Another issue is the potential for animal
• Only highly trained individuals should handle venom-
envenomation during foreign travel from bites, stings, and
ous animals.
even exotic foods such as toad soup.6
• Counsel pet owners with venomous animals on enveno-
mation risks and methods to reduce them (bite preven-
Key Points for Clinicians and Public Health tion; see Chapter 10 on animal bites), as well as the need
Professionals to seek immediate medical care if envenomation occurs.
• Ensure that the local emergency departments and
regional poison control centers are aware of certain
venomous animals being housed in the community, as
• Describe the public health risk in the community from well as venomous wildlife species, and that steps are
venomous animals, both wild and captive, including being taken to prepare for an envenomation incident
pet swap meets and private collectors. (such as availability of appropriate antivenin).
• When treating a dog or other animal for envenoma- a large ant colony. Treatment is supportive with cool com-
tion from a snake or other venomous animal, consider presses, antihistamines, and topical steroids if necessary.
the risk to human beings as well and counsel owners Individuals with Hymenoptera allergy should carry epi-
on risk reduction. nephrine in an injectable form (Epi-Pen, DEY L.P., Napa,
• If a pet is traveling to another country or region, coun- Calif.) (Figure 8-22) whenever there is potential for stings
sel the owner about local envenomation risks and steps to occur.
to take in an emergency. In animals, anaphylactic reactions to hymenopteran
stings have been reported in dogs but not in livestock.10 Local
reactions (pain and swelling) from stings in dogs, cats, and
other mammals resemble those in human beings (Figure
Hymenopteran envenomation 8-23), and systemic reactions can occur with multiple stings.
Treatment is similar to that in human beings and involves
Stings from insects of the order Hymenoptera (bees, yellow antihistamines, corticosteroids, and fluids (see Table 8-20).
jackets, wasps, and ants) can cause reactions ranging from Epinephrine is used for suspected anaphylactic reactions.
mild local discomfort to life-threatening systemic reactions
in human beings and other animals. They are the most fre-
quent arthropod-associated envenomation seen in U.S. poi- Lepidopterism
son control centers, with more than 4000 reported cases in
2005.8 Honeybees have a barbed stinger that is left in the Certain species of caterpillars are capable of producing
skin, eviscerating the insect. Honeybees are attracted to car- minor envenomations (lepidopterism) on direct skin contact.
bon dioxide, bright colors, and sweet odors but are usually Symptoms include local redness and irritative dermatitis
docile unless provoked.9 Africanized bees, in contrast, may (Color Plate 8-9). Other caterpillars can inflict painful stings
be aggressive and cause mass envenomations. Yellow jackets (Color Plate 8-10).
and hornets may be more aggressive than honeybees and
have nonbarbed stingers that can sting repeatedly and deliver
more venom than a bee sting (Figure 8-21). Hymenoptera
stings usually result in local redness, pain, and swelling.
A small number of persons have Hymenoptera allergy and
are at risk of severe allergic reactions that can include ana-
phylaxis (see Chapter 7 on allergic conditions). Even without
allergy, systemic reactions can occur including nausea, dizzi-
ness, and vomiting, especially after m
ultiple stings.
Treatment involves local measures, including ice and topi-
cal steroids or oral antihistamines. Anaphylaxis needs to be
treated promptly with epinephrine and steroids. Honeybee
stingers should be removed using a credit card or fine
tweezers to remove the apparatus without expressing addi-
tional venom into the wound.9 Figure 8-22 n EpiPen preloaded delivery system for injection of aque-
ous epinephrine.
Other hymenopterans capable of significant envenom-
ations include fire ants, which can give painful stings pro-
ducing a ring of small pustules (Color Plate 8-8). Mass
envenomation can occur when a child or animal disturbs
Figure 8-23 n Angioedema. Severe swelling of the face and periocular

tissue developed after a venomous insect sting. (From Medleau L, Hnilica
Figure 8-21 n Yellow jacket, Vespula maculiforma. (From Auerbach PS: KA: Small animal dermatology: a color atlas and therapeutic guide, ed 2, St.
Wilderness medicine, ed 5, Philadelphia, 2007, Mosby.) Louis, 2006, Saunders Elsevier.)
painless but later cause local tissue necrosis. Systemic reac-

Spider bites tions (loxoscelism) can include fever, jaundice, vomiting,
convulsions, rash, and intravascular hemolysis.11 The bite
More than 34,000 species of spiders exist worldwide, but only typically first appears as an erythematous bull’s-eye lesion
a small percentage can penetrate the skin of a large mammal that then progresses over days and weeks to a necrotic ulcer.11
and cause envenomation.11 Antivenin has been developed for The wound margin and necrosis may take weeks to fully
three of the most dangerous spiders: the brown recluse, the develop, and follow-up with a plastic surgeon is advisable for
black widow, and the funnel-web spider. However, such anti- wound care.9
venin may not be widely available. Brown recluse bites to companion animals produce simi-
Tarantulas are found in parts of the United States and are lar pathology and are treated in a similar manner with local
frequently sold as pets. Tarantula bites usually do not cause wound care and pain control.10
significant envenomations but may cause local tissue swell- Bites of the female black widow spider and related widow
ing. Another hazard of tarantulas is that contact with the spiders (Latrodectus spp.; Figure 8-25) result in a neurotoxic
hairs of the back, which are released when the tarantula is envenomation caused by α-latrotoxin. α-Latrotoxin is a
distressed, can cause local skin reactions as well as a granu- polypeptide that binds to nerve receptors at the neuromuscular
lomatous reaction of the cornea and conjunctiva of the eye junction and in the autonomic nervous system, producing
(ophthalmia nodosa) that requires urgent ophthalmologic excess acetylcholine at the synapse. Clinical manifestations
attention.9 Dogs or cats that attempt to eat tarantulas may include abdominal pain and rigidity, headache, hyperten-
gag or vomit.10 sion, and nausea, vomiting, and diaphoresis that can be mis-
Bites of the brown recluse spider (Loxosceles reclusa, also taken for appendicitis or other acute medical problems.9
known as the fiddleback spider because of the violin-shaped Most widow spider envenomations are not life threaten-
dark band on its cephalothorax; Figure 8-24) are initially ing. Supportive measures can include pain control and mus-
cle relaxants (benzodiazepines). However, for serious cases,
the Food and Drug Administration (FDA) has approved an
equine-derived antivenin for black widow spider enveno-
mation. Indications for the use of the antivenin include
predisposing conditions (cardiovascular disease, pregnancy,
chronic obstructive pulmonary disease, elderly or very young
patients) as well as failure of supportive treatment.11 In
Figure 8-24 n The brown recluse spider is 10 to 15 mm long, light to

dark brown, and has a species-specific dorsal, dark, violin-shaped band.
(From Dillaha CJ, Jansen GT, Honeycutt WM et al: North American loxos- Figure 8-25 n Black widow spider. (From Ford MD, Delaney KA, Ling L
celism. Necrotic bite of the brown recluse spider, JAMA 188:33–36, 1964.) et al: Clinical toxicology, Philadelphia, 2001, Saunders.)
patients with known horse allergy, the risks of allergic reac-

tion versus the benefits of the antivenin must be weighed,9 Reptile evenomations
and resuscitation equipment and medications should be
available to handle a severe allergic reaction.1 It has been estimated that worldwide each year more than
Cats are very sensitive to black widow envenomation and 5 million individuals are bitten by snakes, resulting in
have a high fatality rate. There are case reports of cats being more than 2.5 million cases of envenomation and as many
successfully treated with antivenin.10 as 125,000 deaths.12 A large number of snakes worldwide
Funnel-web spiders are found in Australia and produce possess significant venom and their bites can lead to seri-
a neurotoxic venom. Symptoms of a funnel-web spider bite ous complications and mortality. As stated previously, many
include painful lymphadenopathy, headache, nausea, sweat- more dogs and cats than human beings are bitten by venom-
ing, and muscle spasms of the legs and abdomen. Renal fail- ous snakes each year in the United States. In many parts of
ure, hypertension, and cardiovascular collapse can occur. the world, venomous snake bites are an occupational hazard.
The bite can be fatal within 2 hours, and elderly and very Examples of groups at risk include rice farmers and plan-
young victims are at increased risk. An antivenin has been tation workers in Asia, farmers in West Africa, herdspeople,
developed but is not commercially available in the United persons catching snakes in China for human consumption,
States.11 Susceptibility to funnel-web spider bites appears fishermen in Asia encountering sea snakes, wildlife biolo-
to vary among species, with human beings very sensitive, gists, forestry workers, zoo workers, and pet store workers.
whereas dogs and cats experience only mild and transient Snakebites can occur during recreational activities, includ-
effects. In animals, the bite of the male spider appears to be ing wilderness travel to many regions (see Chapter 10 on
more potent than that of the female.10 travel and animal contact). The increasing number of rep-
tile enthusiasts who keep venomous snakes as exotic pets in
their homes has created new risk groups in the United States
Scorpion stings (see Chapter 10).11 Table 8-19 shows the number of indig-
enous and exotic snake envenomations reported to the Toxic
Most scorpion stings cause only local pain and swelling Exposure Surveillance System (TESS), a database of poison
and respond to local measures such as cold compresses and center calls.
wound care. A number of species, however, possess potent Venomous snakes are members of four families:
venom and can cause significant envenomations. These spe- Viperidae, Elapidae, Colubridae, and Atractaspididae.7 In
cies include the bark scorpion (Centruroides spp.) found in North America, indigenous venomous snakes include pit
the Southwestern United States (Figure 8-26 and Color Plate vipers of the family Viperidae (subfamily Crotalinae) and
8-11), scorpions of the genus Tityus in the Caribbean, and coral snakes (of the family Elapidae, which also includes
members of the genera Androctonus, Buthus, and Parabuthus cobras, sea snakes, and others). The clinical manifestations
in Africa. Such scorpion stings can result in excess cholin- and treatment of their bites vary by species. Antivenin is a
ergic activity with symptoms of delirium, nausea, bradycar- key part of treatment of snakebite, but in the United States
dia, salivation, and sweating. With some species, adrenergic only antivenin for Crotaline and coral snake envenomations
toxicity and tissue necrosis can also occur. Treatment is sup- are approved by the FDA for commercial use. However, the
portive. An antivenin has been developed for Centruroides FDA allows zoos to keep stocks of antivenin for exotic species
stings but is not often used because of the frequency of aller- in case of occupational exposure. The Association of Zoos
gic hypersensitivity reactions.7
There is a lack of evidence that scorpion envenomation in
dogs and cats is a significant concern.10
Table 8-19 n Snakebites Reported to Toxic
Exposure System in United States (2003–2005)
Snake 2003 2004 2005
Copperhead 997 1098 1051

Coral 97 99 58
Cottonmouth 175 192 194
Crotaline: unknown 397 431 413
Rattlesnake 1245 1178 1255
Venomous exotic snake 126 131 98
Nonvenomous exotic snake 138 131 42
Unknown exotic 9 2 6
Nonvenomous snake 1818 1803 1552
Unknown snake 1887 2147 1972
Figure 8-26 n Centruroides exilicauda (C. sculpturatus), the bark scor-
pion of Arizona. (From Auerbach PS: Wilderness medicine, ed 5, Philadelphia, From McNally J, Boesen K, Boyer L: Toxicologic information resources for reptile
2007, Mosby Elsevier.) envenomations, Vet Clin North Am Exot Anim Pract 11(2):389–401, viii, 2008.
and Aquariums (AZA) maintains an electronic database of

these stockpiles known as the Antivenom Index that is avail-
able to regional poison control centers.7
Pit Vipers
The Crotalinae subfamily of pit vipers includes venomous snakes
such as copperheads, water moccasins, and rattlesnakes. The
name pit vipers comes from heat-sensing glands (pits) located
on either side of the triangle-shaped head (Figure 8-27).
The fangs of pit vipers are hollow and can deliver a dose
of venom deep into tissues. Pit viper venom is a highly com-
plex mix of toxins, including metalloproteinases that cause
local tissue destruction and thrombin-like proteins that
cause a coagulopathy. Some species have venom with signifi-
cant amounts of neurotoxins such as a phospholipase A2 that
blocks nerve transmission. The Mojave rattlesnake, Crotalus A
scutulatus, produces a potent neurotoxin that is a compound
of phospholipase A2 and an acidic subunit (Mojave toxin). As
a result, victims of pit viper bites can have complicated clin-
ical syndromes involving local pain, tissue swelling, edema,
and necrosis (Figures 8-28, 8-29, and Color Plate 8-12) as well
as hemorrhage, shock, and signs of neurotoxicity, including
paresthesias and respiratory failure. Renal failure as a result of
rhabdomyolysis can occur. Other complications can include
allergy to components of the toxin and bacterial wound infec-
tion. Laboratory findings include leukocytosis and elevated
creatine phosphokinase.
Although controlled studies are few, it is not clear whether
first-aid measures for snake bites are beneficial. Such mea-
sures include incising and suctioning of the wound or the
B
Pit Vipers
Figure 8-28 n Crotalid envenomation. A, Photograph taken 60 minutes
after bite. Marked swelling and ecchymosis are apparent. Fang marks are
barely visible. B, In the same patient, the back of the hand shows extensive
swelling. (From Wolf MD: Envenomation. In Halbrook PR, editor: Textbook
of pediatric critical care, Philadelphia, 1993, WB Saunders.)
Triangular head
Keeled scales
Elliptical pupil
Nostril
Pit
Figure 8-27 n Pit viper’s head. Note the elliptical pupil and the heat-
sensing pit for which these reptiles are named. Viewed from above, the head
has a distinctly triangular shape. Many nonvenomous snakes also possess
triangular heads; therefore this is not a reliable means of differentiation. Figure 8-29 n Local tissue necrosis from a copperhead (Agkistrodon con-
(From Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007, Mosby tortrix) envenomation. (From Ford MD, Delaney KA, Ling L et al: Clinical
Elsevier. Courtesy Marlin Sawyer.) toxicology, Philadelphia, 2001, Saunders.)
use of a tourniquet. In fact, such measures could worsen less sensitive than other species to Crotaline venom but are
outcomes.11 Most bites are to extremities, and the extremity more likely to be bitten on the abdomen, with severe conse-
should be immobilized in the field and the victim taken to a quences. Cats also tend to run and hide after a bite, delaying
hospital. Hospital care includes wound treatment, support- veterinary treatment. The local and systemic effects of pit
ive care to prevent shock, and management of swelling and viper bites in animals resemble those in people (Table 8-20
other medical complications. Specific treatment involves the and Figure 8-32). Treatment of Crotaline bites in animals is
administration of Crotaline antivenin. The FDA-approved similar to that in human beings (see Table 8-20). A rattle-
antivenin is an ovine-derived Fab immunoglobulin fragment snake vaccine has recently been developed for dogs (Crotalus
(CroFab; Protherics US Inc., Brentwood, Tenn.).1 Indications atrox toxoid; Hygeia Biological Laboratories, Woodland,
for antivenin use include significant progression of swelling, Calif.), and twice-yearly vaccination is recommended for
coagulopathy, neuromuscular paralysis, and cardiovascular dogs that have potential for rattlesnake exposure.10
collapse.1
Among domestic animals, dogs are most frequently bit-
ten by pit vipers. Dogs are commonly bitten on the front legs Elapids
and head (Figure 8-30 and Color Plate 8-13), horses are bit-
The family Elapidae includes cobras, mambas, and sea
ten most often on the muzzle (Figure 8-31), and cattle tend
snakes (see Marine Envenomations). In North America,
to be bitten on the tongue or muzzle. Cats are believed to be
the family is represented by the coral snake Micrurus spp.
(Color Plate 8-14). The venom of many members of the
elapid family is predominantly neurotoxic. The bite of an
elapid such as a coral snake can produce local pain (but
usually not swelling), headache, nausea, paresthesias,
cranial nerve involvement, altered mental status, and respi-
ratory failure. As with pit viper bites, medical care should
be sought immediately. Treatment involves administration
of a Micrurus-specific antivenin as soon as possible. Some
evidence suggests that pressure and immobilization of the
wound area until antivenin can be administered is benefi-
cial for the outcome of elapid bites. This treatment method
is shown in Figure 8-33.
Coral snake bites also cause significant morbidity and
mortality in cats and dogs. As with human beings, neuro-
toxic effects predominate and treatment is based on the use
of antivenin.10
Figure 8-30 n Swelling on the muzzle resembling angioedema caused

by a snakebite. (From Medleau L, Hnilica KA: Small animal dermatology: a Poisonous Lizards
color atlas and therapeutic guide, ed 2, St Louis, 2006, Saunders Elsevier.)
North America is home to the only poisonous lizards: the
Gila monster (Heloderma suspectum) and the Mexican
beaded lizard (Heloderma horridum). Their bite is often
complicated by local tissue trauma owing to the chewing
action of their powerful jaws. The venom is similar to pit
viper venom in causing local tissue destruction and swelling.
Treatment is supportive; no specific antivenin is available.
Human fatalities have not occurred in the past 50 years.
Among domestic animals, dogs are the most likely to be
bitten by poisonous lizards, but in general envenomation of
pets by Heloderma spp. is rare (Figure 8-34).10
Amphibian intoxications
Toads (genus Bufo) produce a potent toxin (bufotoxin)

in their parotid gland that is similar to cardiac glycosides
such as digoxin. Human cases of intoxication are rare, but
in Asia ingestion of toad egg soup has led to significant
toxicity. Treatment involves gastric decontamination and
Figure 8-31 n Face of a horse after being bitten by an Eastern diamond- management of arrhythmias. In serious human poison-
back rattlesnake. (From Reed S, Bayly WM, Sellon DC: Equine internal med- ings a digoxin antidote (digoxin-specific Fab fragment) has
icine, ed 2, St Louis, 2004, Saunders.) been used.
Table 8-20 n Terrestrial Envenomations in Human Beings and Companion Animals
Particular Species and

Venomous Animal Geographic Location Symptoms and Treatment in Human Beings Clinical Signs and Treatment in Other Animals
Arthropods
Hymenopterans Worldwide Local pain, redness, swelling, anaphylaxis in allergic Urticaria, peripheral edema, anaphylaxis in sensitized animals
(wasps, bees, ants) individuals Treatment: Antihistamines, steroids
Treatment: Antihistamines, steroids Anaphylactic shock: epinephrine (1-5 mL of 1:10,000 SC)
For treatment of severe allergy: 0.1% adrenaline
(0.5-1.0 mL for adults, 0.01 mL/kg for children)13
Spiders Brown recluse spiders, widow Local tissue necrosis, anaphylaxis, systemic conditions, Tissue necrosis
spiders, funnel-web spiders, including muscle spasms and abdominal pain, Systemic signs may develop after 3-4 days
wandering spiders (South hypertension, cardiovascular collapse Treatment: Early application of cold packs, steroids to prevent
America) Treatment: Supportive treatment, tetanus prophylaxis, necrosis; consider dapsone (4,4′-diaminodiphenylsulfone),
antivenin (widow spider) a leukocyte inhibitor, 1 mg/kg q8h for 10 days (dogs),14
antibiotics to animals not treated with dapsone
Restlessness, muscle rigidity, severe cramping
Treatment: Black widow antivenin given slowly IV diluted in
crystalloid solution. Monitor the inner pinna for evidence
of hyperemia as an indicator for allergic response to
antivenin (envenomation in cats is usually fatal without
antivenin), treat intractable hypertension with sodium
nitroprusside, methocarbamol for spasms, analgesia,
diazepam, tetanus prophylaxis14
Scorpions North and South America, Local: pain, swelling, redness Pain, swelling
Africa, Middle East, South Asia Systemic: cholinergic phase (vomiting, sweating, salivation, Treatment: Antihistamine
bradycardia, hypotension) followed by adrenergic phase
(hypertension, tachycardia, cardiac failure)
Treatment: Pain control, tetanus prophylaxis, control blood
pressure; in United States, consider antivenin13
Chapter 8
Reptiles
Crotalids (pit vipers) In United States: rattlesnakes, Local pain, swelling, tissue destruction, some neurotoxicity Dogs and cats: Pain, weakness, dizziness, nausea, severe
Responsible for most water moccasin, and with certain species hypotension, thrombocytopenia; clinical signs can last
human snakebites copperhead Treatment: Immobilization in field, followed by antivenin up to 1½ weeks; may be fatal
n
in United States; (consult with poison control on urgent basis for specific Treatment: Crystalloid fluids IV, 1 vial of antivenin2
Toxic Exposures
approx. 6000 cases antivenin by species) mixed with 200 mL crystalloid fluids and given slowly
annually,1 and IV, monitoring the patient for hypersensitivity to the
150,000 dog or cat antivenin; vaccine available for dogs
cases annually in Horses: Pain, swelling, systemic signs, rarely fatal unless bite
United States to head/neck
Treatment: Supportive measures, antivenin if available15
Continued
85
86
Human-Animal Medicine
Table 8-20 n Terrestrial Envenomations in Human Beings and Companion Animals—cont'd
Particular Species and
Venomous Animal Geographical Location Symptoms and Treatment in Human Beings Clinical Signs and Treatment in Other Animals
Reptiles—cont'd
Elapidae Coral snakes (United States), Neurotoxicity Neurotoxicity, bites often occur on the lip, clinical signs can last
cobras (Asia) Treatment: Antivenin (check with poison control for specific for up to 1½ weeks, bulbar paralysis with respiratory collapse
species), supportive care as primary cause of fatality
Treatment: Administer 1-2 vials of antivenin. If no antivenin
available, provide ventilator support for several days in a
critical care facility, broad-spectrum antibiotics for 7-10
days
Lizards (Heloderma) The only two poisonous lizards Venom effect similar to many rattlesnakes: local pain, swelling, Bleeding from the site of the bite, ptyalism, hypotension
in the world are in southwest tissue destruction; bite can be tenacious with chewing Treatment: Flush bite site with lidocaine and probe for tooth
United States and Mexico: Gila and tissue destruction; dislodge lizard with hot water or fragments, soak bitten area with Burrow’s solution; pain
monster and Mexican beaded instrument; wound cleansing and irrigation important; no control, broad-spectrum antibiotics
lizard commercially available antivenin, no human fatalities in past
50 years11
Amphibians
Toads (especially U.S. marine toad and Colorado Toxic ingestion of toad eggs reported, may resemble digitoxin Profuse hypersalivation after an exposure, brick-red buccal
Bufo marinus and River toad produce defensive overdose: nausea, tachycardia, arrhythmias, hyperkalemia membranes
Bufo alvarius) toxin from the parotid glands: Treatment: Emesis/gastric decontamination, cardiac Marine toad contact is a medical emergency with a high
indole alkyl amines (similar to monitoring, electrolyte monitoring and correction; consider fatality rate, whereas Colorado River toad fatalities are
LSD), cardiac glycosides, and digoxin-specific Fab fragment antidote if syndrome of uncommon after decontamination
noncardiac sterols digoxin toxicity6 Treatment: Flush mouth with copious amounts of water for
10 min, monitor temperature (cool bath for hyperthermic
animal >105 °F), atropine (0.04 mg/kg IM, SC), cardiac
monitoring
LSD, Lysergic acid diethylamide; IV, intravenous; SC, subcutaneous; IM, intramuscular.
Figure 8-32 n Photomicrograph of canine renal tissue after exposure Figure 8-34 n Training technicians to handle reptiles and provide for
to snake venom. Three glomeruli have varying degrees of hemorrhage and their daily needs is critical to successful treatment. This experienced techni-
necrosis (mesangiolysis) (×10). (From Plumlee K: Clinical veterinary toxi- cian is handling a venomous Gila monster (Heloderma suspectum) for treat-
cology, St. Louis, 2004, Mosby.) ment. (From Mader DR: Reptile medicine and surgery, ed 2, St Louis, 2006,
Saunders Elsevier.)
Fang marks
4
1
3
Figure 8-33 n The Australian pressure-immobilization technique. This technique has proved effective in the
management of elapid and sea snake envenomations. Its efficacy in Viperid bites has yet to be fully evaluated clini-
cally. (From Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.)
to two main groupings: Scyphozoa (true jellyfish) and

Hydrozoa. Scyphozoa found in U.S. waters include sting-
ing nettles, the chirodropid box jellyfish (Chironex spp.;
Figure 8-36), and the purple jellyfish (Pelagia noctiluca).
The class Hydrozoa includes both the Portuguese man-o-
war (Physalia physalis) and fire coral. The types of jellyfish
associated with fatal envenomations in the United States are
the box jellyfish and Portuguese man-o-war. In Australia,
jellyfish of the Carybdeid family cause a systemic syndrome
called Irukandji syndrome, with catecholamine release lead-
ing to tachycardia, muscle cramps, hypertension, and cere-
bral edema.1
The venom of jellyfish is released by nematocysts—
stinging organelles found in cells on the tentacles that
are capable of stinging even when a tentacle has become
detached (Figure 8-37). The venom is a complex mixture
of proteins and polypeptide compounds that have antigenic
and toxic effects. One of the toxic effects is disturbance
of the sodium-potassium pump of cell membranes.1 The
effects of jellyfish stings range from local pain and rash to
tissue necrosis (Color Plate 8-16), cardiac effects, fatal ana-
phylaxis, and other systemic reactions.
Treatment of jellyfish envenomation involves rinsing
the skin with sea water to remove any nematocysts. If a box
jellyfish sting is suspected, the skin can be decontaminated
Figure 8-35 n Bufo marinus (cane or marine toad). (From Peterson ME, first with 5% acetic acid (vinegar) for 5 to 10 minutes to
Talcott PA: Small animal toxicology, ed 2, St Louis, 2006, Saunders Elsevier.) inactivate any undischarged nematocysts before attempting
to remove tentacles (Figure 8-38).
For stings from other jellyfish, the skin can be decon-
taminated by flooding the skin with vinegar, baking soda, or
¼-strength ammonia. After decontamination, any remaining
Poisoning by toads is a significant problem in dogs that tentacles should be removed by scraping and the area should
try to ingest them. Large toads such as the marine toad (Bufo be treated again with the decontamination solution. Pain can
marinus; also known as cane toads or giant neotropical toads) be treated with topical lidocaine and allergic reactions con-
carry a higher load of venom (Figure 8-35). trolled with antihistamines. For persistent pain, a hot shower
Mouthing of the toad by the dog releases toxin into the may inactivate heat-labile venom.1
dog’s mouth and contact with mucous membranes, leading
to systemic absorption. Poisoned dogs develop excess saliva-
Anthozoa (Sea Anemones)
tion, anxiety, and vomiting almost immediately, and death
can occur within 15 minutes after exposure. Treatment Sea anemones live in tidal pools and have tentacles that con-
involves decontamination of the oral cavity through irriga- tain nematocysts. An anemone sting presents as an erythema-
tion with water and forced emesis if a toad has been swal- tous ring around a pale center. Such lesions usually resolve
lowed. Endoscopic or surgical removal of the toad may be within 48 hours, although vesicles can form and ulceration
necessary. If cardiac complications develop in a dog, the use can occur.
of digoxin-specific Fab fragment should be weighed against
its high cost.10 Bradycardia can be treated with atropine
Larvae (Sea Bather’s Eruption)
(0.04 mg/kg IM, SC).
Larvae of certain jellyfish such as thimble jellyfish, as well as
sea anemones, can get under a swimmer’s bathing suit or a
Marine envenomations diver’s wet suit. Trapped by the clothing, the nematocysts of
the larvae release venom, create stinging and a rash known as
Marine envenomations are more of a threat to human health sea bather’s eruption that spares uncovered areas (Color Plate
than animal health (Table 8-21), although a case of a horse 8-17). Treatment is similar to that for jellyfish stings.
envenomation by a stingray has been reported.16 A number
of invertebrate and vertebrate organisms are capable of sig-
Echinodermata (Sea Urchins)
nificant envenomations (Color Plate 8-15).
Sea urchin spines can inject venom if a person inadvertently
Coelenterates makes contact with them. The spines can break off in the skin.
Sea urchin venom contains heat-labile proteins that can have
Jellyfish can cause significant envenomations when encoun- neurotoxic activity. Clinical manifestations include immedi-
tered in the water or washed up on a beach. Jellyfish belong ate pain at the site, followed in some cases by systemic effects
Table 8-21 n Marine Envenomations in Human Beings
Organism Geographic Distribution Clinical Manifestations Treatment
Scyphozoa (true U.S.: stinging nettles, box jellyfish (Chironex spp.) Local tissue effects: stinging, redness, swelling, Rinse area with sea water
jellyfish) purple jellyfish (Pelagia noctiluca) sometimes with necrosis Chironex suspected: flood with vinegar
Systemic envenomation with potentially fatal effects Others: use vinegar, baking soda, or dilute
(box jellyfish) ammonia,1 then remove tentacles, immerse
limb in hot water (45° C) to inactivate toxin;
antivenin available for Chironex poisoning13
Carybdeid species: Australia Irukandji syndrome (catecholamine release— First-aid as above, supportive care
tachycardia, muscle cramps)
Hydrozoa (Portuguese Atlantic, Indopacific ocean Local tissue effects, stinging, redness, swelling, Decontaminate skin (vinegar, baking soda, dilute
man-o-war) sometimes with necrosis ammonia), remove tentacles,1 immerse in hot
Systemic envenomation with potentially fatal water, pain control, other supportive measures
effects: GI distress, altered mental status, including steroids for skin irritation13
respiratory arrest
Anthozoa (sea Worldwide Local pain, redness, swelling Often no treatment required; topical steroids,
anemones) Larval forms (under bathing suits): sea bather’s pain control, remove clothing, shower, skin
eruption: tingling, burning, pain, itching, redness decontamination with vinegar, topical steroids
(spares exposed areas) if necessary for itching
Echinodermata (sea Worldwide Sea urchins associated with spine puncture Hot shower, remove spines, antiinflammatory if
urchins) wounds: pain, swelling at site of puncture necessary1
Systemic envenomation can occur with multiple
wounds
Fish Stingrays: worldwide in oceans, some freshwater Stingray most common source of fish Immerse stung limb in hot water (45° C) for
Chapter 8
species envenomation in U.S.1 30 min
South America: Weever fish Pain, tissue damage, systemic effects Antivenin for stone fish sting, tetanus
Mediterranean and eastern Atlantic: lionfish Wound infection can occur prophylaxis, surgery if necessary for retained
(aquariums, introduced into the Atlantic), fragments of spines, supportive care for
toadfish, scorpion fish (non-U.S.), stone fish systemic envenomation13
n
(non-U.S.), catfish
Toxic Exposures
Sea snakes (Elapidae) Subtropical and tropical waters of Indian Ocean Originally painless, then pain, paralysis, respiratory Pressure immobilization, antivenin, supportive
and Pacific Ocean difficulty, myoglobinuria with rhabdomyolysis, measures (dialysis if necessary)
and renal failure13
89
Figure 8-36 n Box jellyfish (Chironex fleckeri), swimming just beneath

the surface of the water. (From Auerbach PS: Wilderness medicine, ed 5,
Philadelphia, 2007, Mosby Elsevier. Courtesy John Williamson, MD.)
Tube
Operculum Onidocil
(lid) (trigger hair) } Spines Figure 8-38 n Surf lifesavers pour vinegar on the leg of a simulated
box jellyfish envenomation. Note how they restrain the victim’s arms to
Capsule prevent him from handling the harmful tentacles. (From Auerbach PS:
Spines Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier. Courtesy John
Capsule Williamson, MD.)
Tube
most marine fish envenomations occur in waters outside
Nucleus the United States, some of these poisonous fish, including
Nucleus
A B lion fish (Color Plates 8-18 and 8-19) and catfish, are popu-
lar aquarium fish, and envenomations have occurred during
Figure 8-37 n Structure of a typical nematocyst from a cnidarian
shown before (A) and after (B) discharge. (From Ford MD, Delaney KA,
handling of captive fish.
Ling L et al: Clinical toxicology, Philadelphia, 2001, Saunders.) Clinical manifestations of fish envenomation can include
severe local pain, nausea, vomiting and, in severe cases, car-
diac arrhythmias. Allergic reactions can occur. Treatment of
of the envenomation including weakness, muscle spasms, fish envenomations involves removal of the barb or spine
and difficulty breathing. Immersion in hot water may inacti- and supportive care. Hot water may inactivate the toxin.
vate the venom. Spines should be removed with care because An antivenin is available for stone fish envenomations, which
they can break easily. Surgical removal may be necessary if tend to produce the most severe reactions.
joints or nerves are involved. Tetanus prophylaxis should be
given if indicated. Sea Snakes
Poisonous Fish Sea snakes are members of the Elapid family that are found
in the Indian and Pacific oceans. They are perhaps the most
Fish with significant venom include stingrays, lion fish, scor- abundant reptiles on earth, and all 52 species are venomous,
pion fish, stone fish, weever fish, and catfish. All of these fish with several species capable of severe envenomation. Their
species possess heat-labile toxins. The stingray has a barbed venom is highly toxic but the actual bite may be painless.
tail that can puncture skin and inject venom, while the other Fishermen may be bitten when encountering sea snakes in
fish deliver venom injections through their spines. Although nets. Signs and symptoms develop in minutes to hours and
include dizziness, nausea, weakness, difficulty speaking or 7. McNally J, Boesen K, Boyer L. Toxicologic information resources
swallowing, pain, altered mental status, coma, and respira- for reptile envenomations. Vet Clin North Am Exot Anim Pract.
2008;11(2):389–401.
tory collapse. Rhabdomyolysis can occur with myoglobinuria 8. Lai MW, Klein-Schwartz W, Rodgers GC, et al. 2005 Annual report of
and renal failure. Treatment involves pressure administration the American Association of Poison Control Centers’ national poi-
as for other Elapid bites (see Figure 8-33), supportive mea- soning and exposure database. Clin Toxicol (Phila). 2006;44(6–7):
sures, administration of sea snake antivenin if available, and 803–932.
9. Rangan C. Emergency department evaluation and treatment for chil-
dialysis if necessary.11 dren with arthropod envenomations: immunologic and toxicologic
considerations. Clin Ped Emerg Med. 2007;8(2):104–110.
References 10. Gupta RC. Veterinary toxicology: basic and clinical principles. New York:
Academic Press; 2007.
1. Singletary EM, Rochman AS, Bodmer JC, et al. Envenomations. Med 11. Auerbach PS. Wilderness medicine. 5th ed. Philadelphia: Mosby Elsevier;
Clin North Am. 2005;89(6):1195–1224. 2007.
2. Peterson ME. Snake bite: pit vipers. Clin Tech Small Anim Pract. 12. Chippaux J-P. Snake-bites: appraisal of the global situation. Bull WHO.
2006;21(4):174–182. 1998;76(5):515–524.
3. Warrell DA. Treatment of bites by adders and exotic venomous snakes. 13. Junghanss T, Bodio M. Medically important venomous animals: biol-
BMJ. 2005;331(7527):1244–1247. ogy, prevention, first aid, and clinical management. Clin Infect Dis.
4. Rein JO. Exotic invertebrates—a health problem? [in Norwegian]. 2006;43(10):1309–1317.
Tidsskr Nor Laegeforen. 2002;122(30):2896–2901. 14. Kahn CM, Line S. The Merck veterinary manual. 9th ed. Whitehouse
5. Fitzgerald KT, Newquist KL. Poisonings in reptiles. Vet Clin North Am Station, NJ: Merck; 2005.
Exot Anim Pract. 2008;11(2):327–357. 15. Landolt GA. Management of equine poisoning and envenomation. Vet
6. Kuo HY, Hsu CW, Chen JH, et al. Life-threatening episode after inges- Clin North Am Equine Pract. 2007;23(1):31–47.
tion of toad eggs: a case report with literature review. Emerg Med J. 16. Riggs CM, Carrick JB, O’Hagan BJ, et al. Stingray injury to a horse in
2007;24(3):215–216. coastal waters off eastern Australia. Vet Rec. 2003;152(5):144–145.
Harmful Algal Blooms*
Julia Zaias, Lorraine C. Backer, and Lora E. Fleming E860-E869 Accidental Poisoning by Other Solid and
(ICD-10: Note: There is no specific ICD-10 code for Liquid Substances, Gases, and Vapors
many of the harmful algae blooms (HAB) illnesses;
therefore the following injury codes should be
considered as possible HAB illnesses) E865 Accidental Poisoning from Poisonous
Foodstuffs and Poisonous Plants
E928 Other and Unspecified Environmental and

Accidental Causes
E865.1 Shellfish
E928.6 Environmental Exposure to Harmful Algae

and Toxins; Algae Bloom NOS E865.2 Other Fish
• Blue-green algae bloom
• Brown tide
• Cyanobacteria bloom 988 Toxic Effect of Noxious Substances Eaten
• Florida red tide as Food
• Harmful algae bloom
• Pfiesteria piscicida
• Red tide 988.0 Fish and Shellfish
*This work was funded in part by the following sources: the National
Center for Environmental Health (NCEH); CDC; Florida Department
of Health (FL DOH); Florida Department of Environmental Protection E865 Accidental Poisoning from Poisonous
(FL DEP); Florida Red Tide Control and Mitigation; the National
Science Foundation (NSF) and the National Institute of Environmental
Foodstuffs and Poisonous Plants
Health Sciences (NIEHS); Oceans and Human Health Center at the
University of Miami Rosenstiel School (NSF 0CE0432368, NIEHS 1 P50
ES12736); and the NIEHS Aerosolized Florida Red Tide PO1 (P01 ES
10594). E865.2 Other Fish
example, one of the most common first indicators of a toxin-

V70-V82 Persons Without Reported Diagnosis
producing bloom in freshwater lakes and ponds is a report of
Encountered During Examination and Investigation
a dog dying shortly after swimming.7
of Individuals and Populations
Better communication between veterinarians and local
public health officials could mean that not only are people
protected from toxic blooms subsequent to observing animal
V82.5 Chemical Poisoning and Other Contamination,
morbidity or mortality, but also that local HAB data from
Poisoning from Contaminated Water Supply
monitoring and bloom detection activities can be shared
with the veterinary, public health, and human health com-
Algal blooms are exuberant growths of microalgae such munities to protect animals and human beings in the com-
as dinoflagellates, diatoms, and cyanobacteria (blue-green munity. This would allow veterinarians and physicians to
algae; Color Plate 8-20). Harmful algal blooms (HABs) have a high index of suspicion that HAB-related toxins may
are intense blooms that cause harm to people, animals, or be the cause of illness in patients with symptoms related to
the local ecology, for example, by producing toxins or by an environmental exposure, such as swimming.1 For exam-
inducing hypoxia. HABs occur in all aquatic environments, ple, in August 1984 in Montana, people who had been swim-
including freshwater, estuaries, and the oceans. In marine ming in a lake contacted the local health department to report
environments, they are also generally called red tides, dead cattle in and near the lake and to ask about their own
although the causative organism, the color of the water, the risks of becoming ill.8 Investigation of the incident found
particular threats, and subsequent effects of the HABs vary that wind had concentrated a toxin-producing bloom of sev-
greatly.1-4 eral cyanobacteria, Anabena flos-aquae, Microcystis aerugi-
The primary effects of HABs on human beings and nosa, and Aphanizomenon flos-aquae, against the shore of the
other animals occur through exposure to the toxins pro- lake where the cattle had been drinking. Because people had
duced by the HAB-forming organisms. These toxins are been swimming in another part of the lake, their exposure
some of the most potent natural substances known, cre- was limited and no bloom-associated human illnesses were
ating untoward effects in nanogram to picogram doses. reported.
These toxins can target multiple organ systems, including Although we are only beginning to understand the
the nervous system, the liver, the skin, and the respira- dynamics of bloom formation and senescence, we know
tory tract. The HAB toxins are most infamous for their enough to make some recommendations. For example,
acute health effects that range from severe gastroenteri- lakes and ponds with a low rate of flushing are likely to
tis to respiratory illness, and even death from respiratory experience dense blooms during the summer when tem-
paralysis. However, these toxins can also induce chronic peratures increase, particularly right after rains when
illnesses, including long-term neurologic disease and excess nutrients can enter the water. Thus the medical and
genotoxic damage. Some of the toxins can act as tumor veterinary communities can remind patients and owners
promoters, thus increasing cancer risks.1-5 to limit exposure to water bodies with dense blooms dur-
Although it has been known for decades, if not centuries, ing the summer.7
that exposure to certain HAB toxins causes adverse health
effects, studies designed to more fully characterize these
acute and chronic effects have only recently begun. Until
Professionals
recently, it has been difficult to measure these potent tox-
ins because even picogram doses can cause adverse health
effects. Furthermore, the symptoms of the illnesses associ-
ated with exposure to HABs and their toxins are common
symptoms associated with other acute diseases, including • Educate human health and veterinary clinicians about
upper respiratory tract infections, food poisoning, and per- the need to communicate about suspect cases.
haps even chronic diseases, including chronic fatigue syn- • If animal cases of disease related to HABs are reported
drome. Thus unless a physician or veterinarian considers in the community, consider whether such cases could
HAB-related poisonings as part of a patient’s differential be sentinels for human risk.
diagnosis, it is likely that the event will be misdiagnosed and • Coordinate with agricultural agencies monitoring for
thus not identified as HAB related. For example, ciguatera paralytic shellfish poisoning (PSP), neurotoxic shell-
fish poisoning is often diagnosed only as “food poisoning.” fish poisoning (NSP), amnesic shellfish poisoning
Despite the difficulties in collecting accurate informa- (ASP), diarrheic shellfish poisoning (DSP), ciguatera
tion about HAB disease occurrence and diagnoses, recent fish poisoning, and other HABs associated with con-
research suggests that there are measurable and increasing taminated seafood to educate the public about marine
societal impacts from HABs manifested as adverse human areas to avoid.
and animal health events as well as adverse impacts on eco- • Collect implicated seafood and human/animal sam-
nomic and social resources.1-4,6 ples for testing at FDA laboratories.
From the point of view of the health care provider, the • Support policies that discourage the application of
diagnosis, treatment, and reporting of HAB-related illnesses potential nutrients, such as fertilizers, in areas where
can be improved in a number of ways. One of the most runoff can affect the nearby aquatic environment.
important is increased communication across the human, • Educate the public about avoiding swimming in ponds
public health, and animal medical care communities. For or lakes with visible “pond scum.”
• Monitor the National Oceanographic and Atmospheric

Administration (NOAA) HAB Bulletin; see http://tide- Box 8-4 FLORIDA RED TIDE AND MARINE MAMMALS
AS SENTINEL SPECIES
sandcurrents.noaa.gov/hab/bulletins.html.
Shellfish can bioaccumulate brevetoxins during Florida red tides. By
Human Health Clinicians contrast, until recently it was assumed that exposure to brevetoxins
from Florida red tide instantly killed all fish by paralyzing their gills.
• Have a high index of suspicion in persons who con- Thus it was also assumed that exposure to brevetoxins would not
sume seafood or who are exposed to water bodies. occur through the fin-fish food web, and public health advisories did
• Report suspected cases to state or local public health not recommend against eating fresh fish caught during established
officials. Florida red tides. However, between 2002 and 2004 in two separate
• Be aware of cases in the community of adverse effects but large mortality events, 34 Florida manatees (Trichechus manatus
of HABs in human beings and animals. latirostris) and 107 bottlenose dolphins (Tursiops truncatus) died
in waters off the Florida coast. In both of these unusual mortality
events, extensive water surveys revealed only low concentrations of
Veterinary Clinicians Karenia brevis and brevetoxins. However, analysis of the stomach
contents of the dead animals detected high concentrations of
• Discourage pet owners from allowing their animals to brevetoxins in the fish and seagrasses eaten by the dolphins and
swim or drink water containing any pond scum. manatees, respectively. This bioaccumulation was verified in
• Report suspected cases to state or local public health laboratory experiments. Although most of the brevetoxins were
officials. found in the fish organs and not in the muscle (the part of the fish
usually eaten by people), these findings suggest the need to revise the
public health recommendations for eating fresh fish caught in waters
Primary prevention affected by established Florida red tides. 10,11
Primary prevention of HAB-related illness in human beings

and other animals consists of preventing exposure to the may adversely affect the health of marine mammals. Because
HAB organisms and their toxins. In some cases, this is rela- people are exposed to a similar array of environmental con-
tively easy if it is known that HAB organisms and their toxins taminants, these marine mammals may serve as sentinels for
are in the environment. For example, given the ubiquity of potential human combination exposures and subsequent
the cyanobacteria in all aquatic environments, it is reasonable disease.4,5
to warn people that they, their pets, and other animals may be Another component of primary prevention is identification
at risk of exposure to cyanobacteria and their toxins if they and prevention of the actual causes of the blooms and of toxin
swim or drink from areas with obvious pond scums (even production. There is no single reason why HAB organisms
though not all pond scums are necessarily toxic). As another bloom and produce these potent natural toxins. Some organ-
example, in areas with frequent HABs, such as coastal New isms, such as the cyanobacteria, seem to bloom when high nutri-
England and the Pacific Northwest (from the dinoflagellate ent concentrations (such as nitrates or phosphates) exist in the
Alexandrium spp.) and the Gulf of Mexico (from the dino- aquatic environment; thus there is growing interest in prevent-
flagellate Karenia brevis), local governments have instituted ing the dispersion of nutrients into waterways. Unfortunately,
shellfish monitoring programs. If the organisms or toxins are the environmental factors associated with blooming and
detected in the shellfish beds at concentrations above specific toxin production for most HAB organisms are still unknown.
limits, the beds are closed to commercial harvest. These clo- However, even when solid evidence linking HAB formation
sures are the primary prevention of cases of PSP and NSP, with high nutrient concentrations is lacking, repeatedly affected
respectively. However, even when shellfish beds are closed communities may institute regulations (e.g., Ordinance 2007–
to commercial harvesting, tourists or isolated ethnic groups 062 Sarasota County, FL, Fertilizer and Landscape Management
may be unaware of these closures and unknowingly harvest Code) and outreach programs to discourage the application of
toxic seafood.1-4,9 In addition, HAB organisms can occur in potential nutrients, such as fertilizers, in areas where runoff can
previously unaffected geographic regions; even in areas where affect the nearby aquatic environment.12-14
blooms are anticipated, local resources for expensive envi-
ronmental monitoring may be limited or intermittent. Thus
monitoring alone cannot protect public health. Early detection, surveillance, and
Primary prevention is possible for companion animals, education
but it is particularly difficult for wild animals, even highly
protected ones such as marine mammals. Millions of fish In addition to ongoing and periodic environmental HAB
die every year in all aquatic environments from exposure to monitoring programs (Figure 8-39), the oceanographic and
a range of HAB organisms and their toxins. Even more dis- public health communities continue to develop partner-
tressing are the acute and chronic illnesses and deaths of ships directed at the early detection and forecasting of HABs.
aquatic birds and marine mammals through the inadvertent These efforts were originally aimed at predicting local effects
or unavoidable consumption of HAB toxin–contaminated of Florida red tides, HABs that seem to be annual events
food and/or exposure to contaminated aerosols and water (Box 8-5). These efforts have been extended to the early detec-
(Box 8-4). Some evidence also indicates that the combination and forecasting of Florida red tides (K. brevis) in the Gulf
tion of exposures to the HAB toxins, microbes (including of Mexico, red tides (Alexandrium and Pseudo-Nitzschia) in
antibiotic-resistant pathogens), and anthropogenic chemicals the Pacific Northwest, and now cyanobacteria in Florida; they
Box 8-5 FLORIDA RED TIDE: HAB DETECTION,

SURVEILLANCE, OUTREACH, AND EDUCATION
Florida red tides are annual blooms of the marine dinoflagellate

Karenia brevis in the Gulf of Mexico. The organism produces a
group of highly potent natural neurotoxins called brevetoxins.
Brevetoxins cause massive fish kills, neurotoxic shellfish
poisoning, and respiratory distress, particularly in people
with asthma. The public health challenge is to provide timely
preventive information for Florida’s dynamic resident and
tourist populations about the exposures and health effects
of Florida red tide.15 In a unique collaboration, the Florida
Department of Health (FDOH), CDC, NOAA, and public
and private partners have established a linked network of
public health information resources and exposure and disease
surveillance on Florida red tide.
NOAA (coastwatch.noaa.gov/hab/bulletins_ns.htm) and
Florida Fish and Wildlife Research Institute (FWRI) (tele-
Figure 8-39 n Lifeguard during Florida red tide bloom. (Courtesy phone 866-300-9399) produce weekly reports of red tide loca-
Florida Red Tide Research Group.)
tions based on remote sensing, oceanographic conditions, and
extensive water monitoring for K. brevis available by phone and
are published as the NOAA HAB Bulletin (see link above). Internet.16,17 Dead fish reports can be given and received via
Florida FWRI Marine Fish Kill Hotline (telephone 800-636-
The NOAA HAB Bulletin uses environmental monitoring 0511). The South Florida Poison Information Center Aquatic
and oceanographic data to attempt to predict the location Toxins Hotline (telephone 888-232-8635) provides 24-hour/day
and future direction of HABs. The predictions based on these toll-free health information on exposure and health effects in
models are available to beach and resource managers and the human beings and other animals of Florida red tide and other
public health community. In the future, these bulletins could HABs in multiple languages; the Hotline also reports cases to the
be used to provide early warnings that threatening local HABs FDOH and to the ongoing CDC Harmful Algal Bloom Incidence
are likely to develop as well as track their progress. Surveillance System (HABISS). In addition, daily reports of
In general, health care providers are not legally required to respiratory irritation, dead fish, and other beach conditions from
report HAB-related illnesses to local or state health agencies or to Gulf Coast beaches can be obtained from the Beach Conditions
the CDC. However, marine toxin seafood diseases are reportable Reporting of the Mote Marine Laboratory (www.coolgate.mote.
org/beachconditions).
to state health agencies and the CDC as foodborne outbreaks if Currently researchers are working to incorporate the respi-
more than one person becomes ill. In addition, individual cases ratory irritation reports from the Aquatic Toxins Hotline and
of ciguatera are reportable in Florida and Hawaii, cases of NSP from the Beach Conditions Report into the NOAA HAB Bulletin
are reportable in Florida, and cases of PSP are reportable in for use in modeling and to provide an early warning system.
Washington, Oregon, California, Maine, and Massachusetts. The early-warning time frame is important because people in
coastal areas may experience the respiratory irritation even
before K. brevis is measured in the water or dead fish are found
Actions to prevent eutrophication on the beaches.18 In addition, the CDC, FDOH, Mote Marine
Laboratory, FWRI, the University of Miami, and other col-
It appears that worldwide, HABs are occurring more fre- laborators have ongoing research studies into the causes of the
quently, lasting longer, and occurring over larger geographic Florida red tide and its potential human health effects (www.
areas. This may be a response to the overall increase in nutri- isurus.mote.org/niehsredtidestudy/). Finally, the FDOH (http://
ents and other anthropogenic inputs into all aquatic envi- www.doh.state.fl.us/environment/community/aquatic/index.
html), the grassroots organization, START (http://www.start1.
ronments worldwide, global warming, growth of coastal com), and their partners have developed beach signage, museum
populations, seafood harvesting, and international com- displays, information cards, and a traveling exhibit to advertise
merce. Part of this apparent increase could be ascribed to this up-to-date information to Florida’s tourists and residents.
increased detection efforts. However, evidence suggests that There is even education targeted specifically for health care pro-
these blooms are occurring in areas where they were previ- viders on HAB exposure and health effects available through the
ously undocumented; again, human beings may have inad- Florida Poison Information Center (http://www.med.miami.
vertently introduced these HAB organisms into new areas edu/poisoncontrol/x57.xml).
through mechanisms such as ship ballast water or the trans-
port of living marine organisms.4,5,13,14
The medical, veterinary, and public health communities
could address eutrophication (the increase in nutrients in CAUSATIVE Agents
water) by reminding patients about good environmental stew-
ardship. For example, the health threats represented by certain The main effect of HABs on human beings and other ani-
local HABs may be mitigated if community members carefully mals seen by the medical community is through exposure to
consider their own behavior, including minimizing the use of their natural toxins (Tables 8-22, 8-23, and 8-24). These tox-
lawn and garden fertilizers and taking care not to contaminate ins are some of the most potent natural substances known
local streams and rivers with HAB-inducing nutrients. and can affect human beings and other animals in nanogram
Table 8-22 n HAB Toxin and Disease Information (Not Including Cyanobacteria)
Saxitoxin Brevetoxin Okadaic Acid Domoic Acid Ciguatoxin
Associated PSP NSP DSP ASP Ciguatera fish poisoning

diseases in Certain puffer fish poisonings Aerosolized respiratory irritation Cancer (?)
human beings Brevetoxin fish poisoning (?)
Skin irritation (?)
Associated Fish deaths Fish deaths Fish deaths Death and severe Fish behavior changes (?)
diseases in Marine bird deaths Cancer (?) encephalopathy in sea lions Illness and death in domestic
other animals Brevetoxicosis and deaths Death in pelicans animals
in marine mammals
(dolphins, manatees)
Dog morbidity and mortality (?)
Main area with Temperate areas worldwide Gulf of Mexico, southeast U.S. Europe, Japan East and west coasts of North Tropical coral reefs (although
endemic coast, New Zealand America, South America, transported through trade
disease Northern Europe and tourism throughout the
world)
Associated Bivalve shellfish Bivalve shellfish Bivalve shellfish Bivalve shellfish Large reef fish (e.g.,
transvectors Specific herbivorous fish and Marine aerosols Some fish species barracuda, grouper, red
crabs Fish species (?) snapper, and amberjack)
Seaweed (?)
Acute signs or Gastrointestinal: diarrhea, Gastrointestinal: diarrhea, Gastrointestinal: nausea, Gastrointestinal: diarrhea, 1-6 hr postexposure:
symptoms/ nausea, vomiting nausea, vomiting vomiting, diarrhea, vomiting, abdominal pain Gastrointestinal: diarrhea,
conditions Respiratory: shortness of breath, Cardiovascular: arrhythmias, abdominal pain Respiratory: shortness of breath, nausea, vomiting
progressing to paralysis hypertension, or hypotension Other: chills, headache progressing to paralysis Respiratory: shortness of
Cardiovascular: arrhythmias, Neurological: paresthesias of Cardiovascular: arrhythmias, breath, progressing to
hypertension or hypotension mouth, lips, tongue, and hypertension or hypotension paralysis
Neurologic: paresthesias of throat; dizziness; reversal Neurological: paresthesias 3 hr postexposure:
mouth and lips, weakness, of hot and cold sensations (especially reversal of hot Neurological: paresthesias,
Chapter 8
dysphasia, dysphonia Other: muscular aches, skin and cold sensation), burning reversal of hot/cold, pain,
rashes in teeth or extremities, weakness, coma
With aerosol exposure, confusion, memory loss, 1-5 days postexposure:
respiratory: shortness disorientation, seizure, and Cardiovascular: bradycardia,
of breath particularly in coma hypotension, increase in
asthmatics T-wave abnormalities
n
(Note: Pacific ciguatera
Toxic Exposures
may present with only
neurological symptoms)
Chronic signs Unknown Pneumonia, bronchitis (?) Unknown Amnesia (?) Paresthesias, extreme fatigue
or symptoms/ Possible carcinogen
conditions
Continued
95
Table 8-22 n HAB Toxin and Disease Information (Not Including Cyanobacteria)—cont'd
Saxitoxin Brevetoxin Okadaic Acid Domoic Acid Ciguatoxin
Treatment Supportive care Supportive care Supportive care Supportive care, IV mannitol
Possibly respiratory support Possibly respiratory support Possibly respiratory support Supportive care
Possibly antihistamines, especially for elderly and Tricyclic antidepressants for
bronchodilators for people with underlying chronic symptoms (?)
respiratory symptoms after chronic diseases such as renal Food avoidance (alcohol,
aerosol exposure disease caffeine, nuts, chocolate) (?)
Possibly brevenal, particularly Possibly brevenal (?)
for brevetoxicosis in marine
mammals
Possibly IV mannitol for NSP
Incubation time 5-30 min 30 min-24 hr <24 hr <24 hours <24 hr
Duration Days Days Days Weeks to years (?) Weeks to months to years (?)
Death rate 1%-14% 0% 0% 3% 0.1%- 12%
Toxin-producing Dinoflagellates: Dinoflagellate: Dinoflagellates: Diatoms: Epibenthic dinoflagellates:
organism Gymnodinium catenatum, Karenia brevis (formerly Dinophysis spp., Prorocentrum Pseudo-Nitzschia spp. Gambierdiscus toxicus, possibly
Pyrodinium bahamense var. Gymnodinium breve) lima Ostreopsis spp, Coolia spp,
compressum, Alexandrium spp. or Prorocentrum spp
Molecular Na+ channel blocker Na+ channel activator Phosphorylase phosphatase Glutamate receptor agonist Na+, Ca++ channel activators
mechanism(s) inhibitor
Data from Backer LC, Schurz-Rogers H, Fleming LE et al: Marine phycotoxins in seafood. In Dabrowski W, Sikorski ZE, editors: Toxins in food, Boca Raton, FL, 2005, CRC Press.
Table 8-23 n Cyanobacteria Responsible for Toxic Freshwater HABs Associated With Human Illness3,19,23
Signs and Symptoms of
Toxin Toxicologic End Points* Organisms Acute Effect Mechanism of Action Intoxication Therapy
Anatoxin-a 1. 250 μg/kg Anabaena flos-aquae Neurotoxicity Blocks postsynaptic Progression of muscle No known therapy
2. 2.5 mg/kg/day (mouse, short-term Anabaena spiroides depolarization fasciculations, decreased Respiratory support
studies) Anabaena circinalis Mimics acetylcholine movement, abdominal may allow time for
3. 0.5 mg/kg/day (rat, subchronic Oscillatoria breathing, cyanosis, detoxification and
studies) Aphanizomenon convulsions, death (animals); respiratory recovery
4. 3 × 10–3 mg/kg/day Cylindrospermopsis also opisthotonos (S-shaped
neck) (birds)
Anatoxin-a 40 μg/kg Anabaena flos-aquae Neurotoxicity2 Anticholinesterase Hypersalivation, mucoid Has not been
nasal discharge, tremors, thoroughly
fasciculations, ataxia, investigated
diarrhea, recumbency
(pigs); also regurgitation,
paresis, opisthotonos, clonic
seizures (ducks); lacrimation,
hypersalivation, urination,
defecation, death from
respiratory arrest (mice); also
red-pigmented tears (rats)
Cylindrospermopsin 1. 2100 μg/kg1 24 hr LD50 200 μg/kg2 Cylindrospermopsis Hepatotoxicity Inhibition of protein, Huddling, anorexia, slight Has not been
5-6 d LDμ racborskii Chromosome phosphatases diarrhea, gasping, respiration investigated
2. 0.15 μg/kg/day (mouse) breakage, Cumulative toxicity (mice)
3. 0.05 mg/kg/day (short-term studies, aneuploidy Enlarged liver, malaise, anorexia,
mouse liver); 0.3 mg/kg/day (short- vomiting, headache (human
term studies, mouse spleen) beings)
4. 3 × 10–5 mg/kg/day
Chapter 8
Microcystins 1. 45-1000 μg/kg Microcystis Hepatotoxicity Alterations of actin Weakness, reluctance to move, Powdered charcoal,
2. 3 μg/kg (nasal lesions, mouse) aeruginosa microfilaments, anorexia, pallor of extremities cholestyramine,
3. 200-500 μg/kg (short-term studies, Microcystis viridis destruction of and mucous membranes therapeutic support
mouse) Microcystis parenchymal cells, (animals) mental derangement
4. 6 × 10–6 mg/kg/day wesenbergii lethal hemorrhage or (animals)
n
Anabaena hepatic insufficiency Survivors (animals) may
Inhibition of protein experience photosensitization
Toxic Exposures
phosphatases, Elevated alanine amino-transferase
tumor-promoter (mice, human beings)
activity Elevated gamma-glutamyl
transpeptidase (human beings)
Embryo lethality, teratogenicity
(rats)
Continued
97
Table 8-23 n Cyanobacteria Responsible for Toxic Freshwater HABs Associated With Human Illness—cont'd
Signs and Symptoms of
Toxin Toxicologic End Points* Organisms Acute Effect Mechanism of Action Intoxication Therapy
Nodularin 1. 30-50 μg/kg Nodularia Hepatotoxicity Inhibition of protein Skin and eye irritation (dermal Therapeutic support
spumigena phosphatases, contact, human beings)
tumor-promoter
activity
Saxitoxin, 1. 10-30 μg/kg Aphanizomenon Neurotoxicity Sodium channel Incoordination, recumbency, Activated charcoal,
neosaxitoxin flos-aquae (New blocker respiratory failure (animals), artificial respiration
Hampshire, U.S.) death; paresthesia and
Anabaena circinalis numbness of lips, mouth
(Australia) within 30 min to 3 hr,
extending to face, neck,
extremities, motor weakness,
incoordination, respiratory and
muscular paralysis (human
beings)
*1. LD50 (i.p. mouse) of pure toxin; 2. NOAEL; 3. LOAEL; 4. Estimated short-term RfD.
Table 8-24 Comparative Effects of Selected Harmful Algal Bloom Toxins in Humans and Other Animals
Species Route of Exposure Clinical Manifestations Laboratory Findings
Brevetoxins
Human beings Ingestion NSP With NSP, may have brevetoxin
metabolites in urine by ELISA
Inhalation Shortness of breath Decreased FEV1
Skin Rash, hives
Dolphins, manatees Inhalation, ingestion Neurological signs including muscle Congestion, edema, and catarrhal
fasciculations, incoordination, and inflammation of nasopharyngeal,
inability to maintain righting reflex tracheal, and bronchial mucosa;
(e.g., listing in water) pulmonary congestion; nonsuppurative
leptomeningitis
May have brevetoxin metabolites in urine
by ELISA
Seabirds Weakness, reluctance to fly, slumping Pulmonary hemorrhage and congestion,
of head, broad-based stance, clear hepatic and splenic hemosiderosis,
nasal discharge, excessive lacrimation, cholangitis, nephritis
diarrhea, dyspnea, tachypnea,
tachycardia, decreased blood pressure,
hypothermia, dehydration, diminished
reflexes, seizures, death
Cyanobacterial Toxins
Human beings Ingestion Acute hepatitis, kidney failure, death Increased liver function tests
Inhalation Respiratory irritation
Skin Rash, hives, blistering
Cattle Ingestion Microcystin and nodularins: diarrhea, Toxins in tissues
vomiting, piloerection, weakness, Microcystin and nodularins: hepatic
pallor, death congestion, hepatitis, and hemorrhage;
Anatoxin, saxitoxin: muscle weakness, hemorrhagic shock; hypoglycemia,
paralysis, dyspnea, hypersalivation, death hyperkalemia, bilirubinemia
Lyngbyatoxin, aphysiatoxin: skin, eye, and Anatoxin, saxitoxin: few if any
respiratory irritation Lyngbyatoxin, aphysiatoxin: dermatitis
Clindrospermopsin: acute death
Ducks, eagles Ingestion b-methylamino-l-alanine (BMAA) (?): Avian Vacuolar myelinopathy (?)
vacuolar myelinopathy BMAA in tissues (?)
Domoic Acid
Human beings Ingestion Acute: vomiting, diarrhea, seizures, Neuronal necrosis
lethargy, death
Chronic: memory loss (?)
Sea lions Ingestion Acute: seizures, lethargy, inappetence, Neuronal necrosis, astrocytosis; abnormal
vomiting, muscle twitching, blindness, EEG, MRI
blepharospasm, abnormal behaviors, Toxin found in placenta and fetus
abortion, stillbirths, premature births,
death
Chronic: seizures/epilepsy (1 yr later)
Pelicans Ingestion Disorientation, ataxia, agitation, Neuronal necrosis, astrocytosis
difficulty swimming, inability to right
themselves, death
EEG, Electroencephalogram; ELISA, enzyme-linked immunosorbent assay; FEV 1, forced expiratory volume in the first second; BMAA, b-methylamino-l-alanine; MRI, magnetic
resonance imaging.
to picogram doses (Color Plate 8-21 and Figure 8-40). In gen- Routes of exposure and metabolic fate
eral, these are tasteless, odorless, and very stable toxins that
are highly resistant to heat, acid, and freezing. Thus they can- Exposure to HABs can occur through a variety of routes, includ-
not be eliminated from foods with normal preparation and ing skin contact, eating contaminated food, drinking contami-
storage methods, and the toxin-contaminated food appears nated water, and inhaling aerosolized HAB toxins. Some HAB
to be normal, reportedly smelling and tasting delicious when toxins can bioconcentrate in the aquatic food web, exposing
consumed. top predators to particularly high doses. For example, the
Neurotoxic shellfish poisoning

Paralytic shellfish poisoning
Amnesic shellfish poisoning
Ciguatera fish poisoning
Pfiesteria complex
Brown tide
Macroalgae proliferation
Fish, bird, mammal and
submerged aquatic
vegetation kills
P.R.
Figure 8-40 n Sites and types of harmful algal blooms along U.S. coast. (Note: This figure is a summary of
verified HABs in marine waters and does not capture HABs verified in the Great Lakes or in inland waters; see
Color Plate 8-20). (From Mandell GL, Bennett JE, Dolin R: Principles and practice of infectious diseases, ed 6, New
York, 2005, Churchill Livingstone.)
ciguatoxins associated with ciguatera fish poisoning biocon- nated sources. People who live in coastal areas with aerosolized
centrate in the food web, making barracuda and other top-reef HABs (such as K. brevis and its brevetoxins), particularly those
predators some of the most highly toxic fish.19 Another exam- with underlying respiratory diseases, are also at risk. Many
ple of a HAB toxin that is bioconcentrated is β-methylamino- of the known HAB toxins are neurotoxins; therefore persons
l-alanine (BMAA), a nonprotein amino acid elaborated by with underlying neurologic disease and infants and young
many cyanobacterial species. BMAA is also found in the cycad children may be at greater risk from these toxins. Consumers
plant, which is consumed by fruit bats in Guam. Both cycads of seafood derived from all aquatic environments are at risk
and fruit bats are eaten by the Chamorro people of Guam, for exposure to HAB toxins. In particular, tourists traveling to
among whom a high number have exhibited degenerative areas where HABs are endemic and isolated racial and ethnic
neurologic symptoms. Subsequent studies of these individuals groups who are unaware of local HAB-related risks may be
and others support the hypothesis that BMAA may be associ- particularly at risk for exposure and illness.1,4
ated with amyotrophic lateral sclerosis–parkinsonism demen- Domestic animals and pets are at particular risk from
tia complex (ALS/PDC). In South Carolina, BMAA elaborated exposure to cyanobacterial toxins by dermal contact and
by cyanobacteria is believed to be transferred through water by drinking contaminated water from streams, ponds, and
plants eaten by ducks and subsequently to eagles that ate lakes.7 As previously discussed, through consumption of
the ducks. Both bird species have developed avian vacuolar contaminated seagrasses, seafood, and possibly through
myelinopathy (AVM)20–22 (R. Bidigare, University of Hawaii, respiratory contact, marine mammals, marine birds, and fish
personal communication, 2008). are particularly vulnerable to coastal HABs that may last for
Several HAB toxins are lipophilic and thus pass easily months in large geographic areas (see Box 8-4). Domestic
through the blood-brain barrier (including ciguatoxin, bre- animals are also at risk from marine HABs. For example, dog
vetoxin, and domoic acid). They are stored in fatty tissues morbidity and possibly mortality associated with Florida
and, during pregnancy, may be mobilized to pass directly red tide have been reported (J. Landsberg, Florida Fish and
into the fetus through the placental barrier. Newborns may Wildlife Commission, personal communication, 2008).
be exposed through breast milk.1,3,19,23
Toxicity in human beings

Groups at risk
Skin toxicity, ranging from mild irritation to hives to blistering,
Human beings are exposed to HABs and their toxins through has been reported with direct contact with almost all the HAB
recreational activities (swimming and boating) and occupa- toxins in contaminated water (Color Plate 8-22). However, this
tions (such as lifeguards or fishermen) and through drinking phenomenon has not been well studied and might actually
water and possibly irrigation water derived from contami- be due to the lipopolysaccharides of some HAB organisms.1,4
Many HAB-related illnesses, such as ciguatera fish poison-

ing and the shellfish-associated diseases (such as PSP, NSP,
ASP, and DSP; see Tables 8-22, 8-23, and 8-24), are diagnosed
simply as “food poisoning” because victims present with sig-
nificant GI symptoms within minutes to hours of consum-
ing implicated seafood and usually have no fever. However,
because these illnesses have a neurologic component, they
may be distinguished from microbial food poisoning or sea-
food allergy by the concomitant or subsequent onset of neu-
rologic symptoms such as paresthesias and confusion. Other
presenting signs and symptoms (also neurologic in origin)
can be cardiovascular (including labile hypotension and
arrhythmias) and respiratory (including respiratory depres-
sion), and may require intensive care unit and respiratory
support for several days.1,4,9,19
Most HAB toxin–related illnesses present as acute, self-
limiting cases of disease. However, there is evidence that
ciguatera fish poisoning and possibly ASP produce lingering Figure 8-41 n Fish kill during Florida red tide bloom. (Courtesy Florida
neurologic symptoms in human beings (i.e., paresthesias and Red Tide Research Group.)
possibly short-term memory loss) that may last from weeks
to months and even years.1,19,24 Although controversial, it is
possible that exposure through contaminated food to BMAA Toxicity in animals
may lead to an increased risk for ALS, Parkinson’s disease,
and even Alzheimer’s dementia. However, although the genes
Wildlife
needed to produce BMAA have been found in every species of
cyanobacteria tested so far, it is not clear that all cyanobacte- Reports of livestock and wild animals poisoned by toxic
ria produce the toxin. Thus it is not known whether the gen- cyanobacteria after drinking from small ponds have been in
eral population could be exposed via the food web, whether the veterinary literature for years. Affected animals showed
this exposure is limited to specific groups, or whether health neurological signs or died from acute effects.30 Animals
effects occur only in sensitive subpopulations.20,21 appear to be more frequently and more seriously poisoned
A number of illness outbreaks associated with exposure to by freshwater HABs than are human beings. This may be
cyanobacterial toxins in drinking water have been reported because thirsty animals are more likely to drink water that
in wild animals, domestic animals, and people. Severe GI ill- people would not use because of foul taste, smell, or pres-
ness associated with acute and chronic liver disease and subse- ence of surface scum.31,32 In addition, grooming and licking
quent kidney disease has been reported in people exposed to of their coats also contributes to the toxin load ingested by
cyanobacterial toxins in drinking water. In more than one epi- dogs and other animals.
sode in Brazil, dialysis patients received microcystin-contam- The most dramatic toxicity in animals from the HAB tox-
inated dialysis water. The affected patients experienced severe ins is the acute death of millions of fish exposed to marine
acute hepatitis and most died. It is important to remember HABs producing saxitoxin or brevetoxins. The first sign of a
that these dialysis patients received an intraperitoneal dose that red tide event along the Florida Gulf coast can be dead fish
was equivalent to the mouse oral median lethal dose (LD50).25 washing ashore (Figure 8-41). Exposure to these neurotoxins
More recently, upper and lower respiratory tract symptoms results in loss of equilibrium, erratic swimming behaviors,
(such as cough, shortness of breath, or chest tightness) have and rapid respiratory paralysis.10,33
been associated with exposure to aerosolized Florida red tide Marine seabird deaths (including species such as pelicans,
brevetoxins, particularly among those with underlying respi- cormorants, mergansers, and scaup) have been reported
ratory disease such as asthma. Some evidence indicates that during HAB events from seabirds inhaling toxic aerosols or
prolonged exposure to these aerosolized toxins, particularly eating contaminated fish.34,35 Typical clinical signs included
among coastal residents, is associated with increased emer- weakness, reluctance to fly, clear nasal discharge, excessive
gency department admissions for respiratory illness (includ- lacrimation, dyspnea, diminished reflexes, ataxia, seizures,
ing pneumonia, bronchitis, and asthma).26-28 There have also and death. The majority of bird deaths in these events were
been anecdotal reports of respiratory illness in persons exposed ascribed to toxicity from the consumption of contaminated
to aerosols from irrigation systems using pond water with active fish; many of the affected cormorants were juveniles; as
algae blooms (John Burns, personal communication, 2005). inexperienced foragers, they may have eaten dead or dying
Several HAB toxins are at least in vitro carcinogens: oka- fish. This event suggests trophic biotoxin transfer of HAB
daic acid and microcystin. There is some research to suggest toxins.34
that chronic exposure to microcystin in contaminated drinking The deaths of numerous marine mammals (e.g., bottlenose
water may be associated with an increased risk for hepatocel- dolphins, manatees, sea lions, whales) have been ascribed, at
lular carcinoma, whereas okadaic acid may be associated with least in part, to intoxication with HAB toxins after both acute
increased prevalence of tumors in shellfish, which one author and chronic exposure over many years. More recently, with
speculated might be relevant to an increased risk of tumors in improved toxicologic and necropsy testing, individual and
human beings who consume toxin-contaminated seafoods.1,4,29 group deaths of many marine mammals have been linked to
HAB toxins, particularly those that accumulate through the of these illnesses are misdiagnosed or completely unidentified
food web.10,11,36,37 It is now clear that toxins such as domoic because of the relatively common presenting signs and symp-
acid and brevetoxins can enter and be transmitted through toms and the specialized toxicologic testing required to make
the food web (including via seagrasses and fish), be biocon- a definitive diagnosis. In addition, the exposure history is cru-
centrated within the marine mammals over time, and induce cial, particularly exposure to possibly contaminated aquatic
subsequent neurological illness and death even when there is environments and seafood. Reporting suspected HAB-related
not an active bloom (see Box 8-4).10 illnesses to local health authorities may prevent additional
Particularly dramatic episodes of severe neurological ill- cases in other people or animals by alerting local officials to
ness and death have been reported in California sea lions after destroy the c ontaminated seafood or test local water bodies.1,4
they ate fish contaminated with domoic acid. In addition to It is important in all cases of a suspected HAB-related ill-
acute effects of intoxication (e.g., ataxia, seizures, abortion, ness to obtain a sample of the contaminated food or water for
stillbirths, premature births, death), chronic effects (e.g., sei- testing. For example, in the case of suspected HAB food poi-
zures that continued to occur more than 1 year after expo- soning, a representative from the state or local health agency
sure) have been documented in sea lions exposed to domoic should obtain a sample of the suspected seafood. The sam-
acid at relatively low levels over a long period.38 In addition, ple should be handled and shipped appropriately for analysis
both brevetoxins and domoic acid have been shown to cross by specialized laboratories such as the FDA. Establishing the
the placenta in rats and have been recovered from sea lion link between illness and a contaminated source of exposure
fetuses and placental tissues.23,36 is critical not only in terms of the appropriate diagnosis of
Data from marine mammal strandings during HAB events the etiology in the particular patient, but also in potentially
have also indicated that intoxication may be either a function preventing additional cases of illness.4,19
of current immune status of the animal (i.e., that the animal In the case of affected animals, stomach contents and tis-
was immunosuppressed or ill when exposed) or may in fact sue samples should also be collected for testing for the HAB
cause immune suppression. Experimental intratracheal expo- toxins. Testing can be done through one of the specialized
sure of sheep with purified brevetoxin PbTx-3 demonstrated laboratories at the NOAA or the FDA.19
decreased phagocytic activity by alveolar macrophages in
vitro.39 These findings, in combination with the documenta-
tion of lymphoid depletion and uptake of brevetoxin in lym- Management of HAB toxicity
phoid cells from exposed dolphins and manatees in the wild,
are suggestive of immune system dysfunction associated with No specific antidotes for HAB-related toxins are currently
brevetoxin poisoning in marine mammals.39 available for general use. In addition, few specific treatments
Finally, as noted, it is now believed that consumption of have been identified for HAB-related illnesses. Thus, in gen-
BMAA-contaminated water plants may be the cause of the eral, the treatment of HAB-related illnesses is supportive in
AVM noted in water fowl and eagles that feed on these water- both human beings and other animals. Obviously, preventing
fowl. However, research on the exposures and acute and any additional exposure to the toxins for the patient and for
chronic health effects of BMAA in human beings and other other human beings and animals through the original trans-
animals is in its infancy (R. Bidigare, University of Hawaii, vector or environmental pathway is part of the management
personal communication, 2008).20–22 of and public health response to HAB-related illnesses.1
Companion Animals Treatment in Human Beings

There have been some reports of dogs becoming gravely ill In the case of the acute neurological diseases such as PSP,
after consuming dead fish they found on a marine beach. In ASP, NSP, and ciguatera fish poisoning, it is important to be
one case, brevetoxins were detected in the dog’s urine using aware of the possible need for intensive care and respiratory
ELISA (J. Landsberg, Florida Fish and Wildlife Commission, support, particularly in the first few days of illness.1,8,19
personal communication, 2008). However, another pos- Almost no formal research has been conducted regarding
sible explanation of the dogs’ responses is secondary bacte- the treatment of HAB diseases. Intravenous mannitol (1 g/kg)
rial growth and subsequent bacterial toxin production in the has been evaluated in two small randomized trials and sev-
dead fish. Despite the lack of documentation of health effects eral case series of ciguatera fish poisoning. This treatment
on pet birds and other animals in areas known for repeated was efficacious in decreasing or even eliminating the symp-
aerosol exposure to toxins (e.g., gulf coast of Florida), pets toms and in preventing the chronic neurological symptoms
may be repeatedly exposed to low levels of aerosolized toxin. when used within a few days of exposure. Of note, because
Clinical veterinarians should be aware of HAB events in their brevetoxins and ciguatoxin are structurally very similar,
area as this can be a differential diagnosis or compounding it is possible that intravenous administration of manni-
factor in pet illnesses. tol may also be efficacious for the treatment of acute NSP.
Many other medications for ciguatera poisoning have been
tried but without appropriate randomized evaluation, such
Diagnosis as tricyclic antidepressants and selective serotonin reuptake
inhibitors. Anecdotally, avoidance of certain foods (i.e., alco-
The most important aspect of diagnosing HAB-related illness hol, caffeine, nuts, chocolate, and fish) and maintenance of
in human beings and other animals is to consider the possibil- hydration seems to speed recovery from the chronic neuro-
ity of HAB toxin exposure and illness in the first place. Many logical symptoms.19
Based on a sheep model of human asthma, albuterol, 11. Naar JP, Flewelling LJ, Lenzi A, et al. Brevetoxins, like ciguatoxins,
diphenhydramine, and corticosteroids have been dem- are potent ichthyotoxic neurotoxins that accumulate in fish. Toxicon.
onstrated to prevent and mitigate the onset of the bron- 2007;50:707–723.
choconstriction associated with exposure to aerosolized 12. Viviani R. Eutrophication, marine biotoxins, human health. Sci Total
Environ. 1992;S1:631.
brevetoxins.40,41 Recently a natural antagonist to brevetoxin, 13. Brand LE, Compton A. Long-term increase in Karenia brevis abundance
brevenal, has been demonstrated to prevent the onset of along the southwest Florida coast. Harmful Algae. 2006;7:232–252.
bronchoconstriction caused by inhalation of aerosolized bre- 14. Vargo GA, Heil CA, Fanninge KA, et al. Nutrient availability in support
vetoxins in asthmatic sheep. It is also possible that brevenal of Karenia brevis on the central west Florida shelf: what keeps Karenia
blooming? Cont Shelf Res. in press.
may be efficacious in the treatment of ciguatera fish poison- 15. Reich A, Backer LC, Kirkpatrick B, et al. Public health and Florida red
ing given the structural similarity between the brevetox- tide: from remote sensing to poison information (published abstract).
ins and ciguatoxin (D. Baden, UNC–Wilmington, personal In: Am Public Health Association Annual Meeting. Boston, MA, 2006.
communication, 2008).40 16. Stumpf RP, Culver ME, Tester PA, et al. Monitoring Karenia brevis
blooms in the Gulf of Mexico using satellite ocean color imagery and
other data. Harmful Algae. 2003;2:147–160.
Treatment in Animals 17. Fisher KM, Allen AL, Keller HM, et al. Annual report of the Gulf of
Mexico Harmful Algal Bloom Operational Forecast System (GOM HAB-
As for human beings, treatment of affected animals involves OFS). NOAA Technical Report NOS CO-OPS 047. Silver Spring, MD:
treating signs and removing the source of exposure. Data NOAA.
18. Kirkpatrick B, Currier R, Nierenberg K, et al. Florida red tide and
from marine mammal deaths during HAB events and from human health: a pilot beach conditions reporting system to minimize
laboratory animal studies indicate that at least brevetoxico- human exposure. Sci Total Environ. 2008;402(1):1–8.
sis may be responsible for some immunosuppression39,42; 19. Friedman MA, Fleming LE, Fernandez M, et al. Ciguatera fish poison-
thus animals under treatment should be given prophylac- ing: treatment, prevention and management. Marine Drugs (special
tic antibiotics for secondary bacterial infections. Restoration issue on marine toxins), in press.
20. Cox PA, Banack SA, Murch SJ. Biomagnification and Chamorro neuro-
of appropriate hydration, fluid support to flush toxins, degenerative disease. PNAS. 2003;100:13380–13383.
and medications to treat neurological signs are the most 21. Cox PA, Banack SA, Murch SJ, et al. Diverse taxa of cyanobacteria pro-
important treatment modalities. duce Beta-N-methylamino-L-alanine, a neurotoxic amino acid. PNAS.
Recently brevenal has been approved as a specific anti- 2005;102(14):5074–5078.
22. Rao SD, Banack SA, Cox PA, et al. BMAA selectively injures
dote by the FDA for use on a compassionate basis in marine motor neurons via AMPA/kainate receptor activation. Exp Neurol.
mammals diagnosed with brevetoxicosis. Based on the bio- 2006;201(1):244–252.
logic activity of brevetoxins and brevenal, the drug is likely 23. Benson JM, Gomez AP, Statom GL, et al. Placental transport of breve-
to be most effective at the very early stages of intoxication toxin-3 in CD1 mice. Toxicon. 2006;48:1018–1026.
(D. Baden, UNC–Wilmington, personal communication, 24. Friedman M, Levin BE. Neurobehavioral effects of harmful algal
bloom (HAB) toxins: a critical review. J Int Neuropsychol Soc.
2008).40 However, until there is a source of sufficient quanti- 2005;11:331–338.
ties of brevenal, its use will be limited. 25. Azevedo SMFO, Carmichael WW, Jochimsen EM, et al. Human intoxi-
cation by microcystins during renal dialysis treatment in Caruaru—
Brazil. Toxicology. 2002;181–182:441–446.
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red tide toxins: exposures and effects. Environ Health Perspect.
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eds. Neurotoxicology handbook. vol. 1. Towata, NJ: Humana Press; to Florida red tides: effects on emergency room respiratory diagnoses
2002. admissions. Harmful Algae. 2006;5:526–533.
2. Backer LC, Fleming LE, Rowan AD, et al. Epidemiology and public 28. Fleming LE, Kirkpatrick B, Backer LC, et al. aerosolized red tide toxins
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Hallegraeff GM, Anderson DM, Cembella AD, eds. IOC manual on 29. Landsberg J. Neoplasms and biotoxins in bivalves: is there a connection?
harmful marine microalgae. Geneva: UNSECO; 2003. J Shellfish Res. 1996;15(2):203.
3. Backer LC, Schurz-Rogers H, Fleming LE, et al. Marine phycotoxins in 30. Briand JF, Jacquet S, Bernard C, et al. Health hazards for terrestrial ver-
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FL: CRC Press; 2005. 2003;361–377.
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Zoonoses
Peter M. Rabinowitz and Lisa A. Conti 9
Overview INFECTIOUS DISEASES IN HUMANS
AND OTHER ANIMALS: FROM “US VERSUS
Key Points for Clinicians and Public Health THEM” TO “SHARED RISK”
Professionals
The history of contact between animals and humans has
always involved infectious diseases, and today more than
Public Health Professionals half of the infectious diseases of humans are zoonotic in ori-
• Establish or refresh lines of communication among gin. In fact, the majority of “emerging” infectious diseases in
the human health and veterinary clinicians within the past three decades are zoonotic. Therefore the control
the community (e.g., provide continuing education, and prevention of these diseases can be accomplished only
update distribution list information). through improving approaches to reducing disease transmis-
• Routinely disseminate information about reportable sion among humans and other animals.
diseases to the human health and veterinary community. Despite the great deal of attention that has been focused
• Consider providing emerging disease exercises that on emerging infectious zoonotic diseases, including severe
involve the human health and veterinary community. acute respiratory syndrome (SARS), West Nile virus, mon-
keypox, and avian influenza, there has been less discus-
sion and effort targeted at the environmental “drivers” of
Human Health Clinicians such diseases. One possible reason is that the traditional
• Consider zoonotic diseases in the differential diagno- approach of the human health community to zoonotic dis-
sis of a wide range of medical complaints, and counsel ease has been an “us versus them” approach. The problem
clients about risk. is viewed as an infectious animal reservoir that then poses
• Reassure owners about non-zoonoses in terms of an infectious risk to humans—either through direct con-
human risk. tact with infected animals and their excretions, meat, milk,
• Consider inviting veterinary clinicians and veterinary or other tissues, or via a vector transmission bringing the
professionals in the community to a joint continuing pathogen from the animal population into human hosts.
education meeting regarding zoonoses. The control of such “us versus them” diseases has tradition-
ally involved measures such as control of the animal reser-
Veterinary Clinicians voir (through culling, quarantine, or vaccination) or vector
control (through pesticides and personal protection). For
• Consider the zoonotic potential of animal infectious many zoonotic diseases, however, such approaches are lim-
diseases and whether an infection in an animal indicates ited because the ultimate causes of infection in the ani-
environmental risk shared by humans as well. mals may not be addressed sufficiently. For example, Nipah
• Consider inviting human health clinicians and veteri- virus emerged as a deadly pathogen in Malaysia when pig
nary professionals in the community to a joint continu- farms were built close to forest areas frequented by fruit bats
ing education meeting regarding zoonoses. (Figure 9-1 and Color Plate 9-1). These fruit bats, natural
105
Therefore, for many infectious diseases that cross between

animals and humans, it is advisable for human health profes-
sionals to move beyond an “us versus them” view of animals
and infections and to instead join veterinarians and public
health professionals to examine the environmental forces
driving disease emergence that constitute a “shared risk” of
infection for both humans and animals.2 Figure 9-2 outlines
these relationships.
This chapter presents this shared risk approach for a num-
ber of zoonotic diseases. For each disease, environmental risk
factors (drivers) of infectious risk are discussed, as well as
practical steps that public health, human health, and animal
health professionals can take to prevent, control, diagnose,
and treat such infections. A key step with each disease is pro-
viding accurate information about risk to clients and other
members of the health professions.
NON-ZOONOSES (FOR NOW)
Infection in animals can be a warning signal of infectious dis-

Figure 9-1 n Collection of oral swab from anesthetized spectacled fly- ease risk to humans, and sometimes the converse is true. At the
ing fox (Pteropus conspicillatus) for Hendra virus antigen detection. (From same time, many animal diseases currently are not believed to
Fowler ME, Miller RE: Zoo and wild animal medicine: current therapy, ed 6, pose a threat to humans, and many human infectious diseases
St Louis, 2008, Saunders Elsevier. Courtesy Jack Shield.) do not appear to infect pets and other animals.
Experience has shown that this situation may change as
organisms continue to adapt to new environments and acquire
hosts for Nipah and other henipaviruses, had sufficient mutations that allow them to cross species barriers. Nonetheless,
contact with the pig farms to allow the virus pathogen to human health clinicians should (1) be aware of animal dis-
“spill over” from the wildlife reservoir into the domestic pig eases that, based on current knowledge, do not appear to
population, causing mortality for pigs and humans (and cause disease in humans and (2) be able to reassure patients
cats) in contact with them.1 who express such concerns. Similarly, clinicians can correct
Figure 9-2 n Relation between environmental drivers of infectious disease and health outcomes in humans
and animals. (From Rabinowitz PM, Odofin L, Dein FJ: From “us vs. them” to “shared risk”: can animals help link
environmental factors to human health? Ecohealth 5(2):224, 2008.)
Chapter 9 n Zoonoses 107
Table 9-1 n Common Infectious Diseases of Companion Animals Not Currently Believed to Be Zoonotic
Disease Agent Species Affected Signs/Comment
Feline Feline immunodeficiency virus: Cats Infected cats are at risk of opportunistic infections.
immunodeficiency retrovirus in the same genus FIV is used as a research model for HIV.
virus infection as HIV, the causative agent of
(feline AIDS) AIDS in humans3
Canine parvovirus Canine parvovirus 2 (CPV-2), Dogs (especially Cause of acute debilitating diarrhea and death in
infection DNA virus puppies) untreated young dogs.
Related to feline panleukopenia virus causing “feline
distemper.”
In humans, a different strain of parvovirus (parvovirus
B19) causes fever and rash (fifth disease) in children
and serious infection in pregnancy.
Canine distemper Canine distemper virus (CDV): Dogs and other Febrile disease, often fatal neurological involvement;
Morbillivirus (Paramyxovirus carnivores, including respiratory signs can occur.
family), related to measles ferrets, raccoons, Humans may become subclinically infected.3
virus skunks, foxes, large “Feline distemper” of domestic cats is a panleukopenia
felines, seals virus, similar to canine parvovirus.
Feline leukemia virus Feline leukemia virus (FeLV) Cats Used as natural model for human cancer; zoonotic
infection potential is controversial.
isinformation regarding species-specific human diseases that

m maintain an awareness of possibly increasing zoonotic dis-
patients may believe come from animal contact. For example, ease risk. Table 9-3 lists a number of currently recognized
human pinworm infection is not a zoonotic disease. Table 9-1 zoonotic pathogens and some of the species for which the
lists some of these non-zoonoses. As this list shows, many of pathogen has been reported.
these agents, while currently not considered zoonotic to any
significant degree, bear some relation to human pathogens. References
1. Daszak P, Cunningham AA, Hyatt AD. Anthropogenic environmental
change and the emergence of infectious diseases in wildlife. Acta Trop.
DISEASES TO WATCH 2001;78(2):103.
2. Rabinowitz PM, Odofin L, Dein FJ. From “us vs. them” to “shared
risk”: can animals help link environmental factors to human health?
The sections in this chapter present individual descriptions EcoHealth. 2008;5(2):224.
of zoonotic diseases that human health and veterinary clini- 3. Barr SC, Bowman DD. 5-minute veterinary consult clinical companion
cians and public health professionals in the United States may canine and feline infectious disease and parasitology. Ames, IA: Wiley-
encounter in their clinical work. It has been estimated, however, Blackwell; 2006.
4. Theis JH. Public health aspects of dirofilariasis in the United States. Vet
that there are more than 1600 known zoonotic pathogens, some Parasitol. 2005;133(2–3):157.
of which are considered to be “emerging” in terms of expand- 5. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
ing their geographical range or pathogenicity to other species. Station, NJ: Merck; 2005.
Our knowledge of the zoonotic potential of many infectious 6. Liu W, Chemaly RF, Tuohy MJ, et al. Pasteurella multocida urinary tract
pathogens is continually changing as new evidence, some based infection with molecular evidence of zoonotic transmission. Clin Infect
Dis. 2003;36(4):E58.
on improved techniques of molecular diagnosis, appears. 7. Dvorak GA, Rovid-Spickler A, Roth JA, eds. Handbook for zoonotic dis-
Table 9-2 presents a number of pathogens and diseases eases of companion animals. Ames, IA: The Center for Food Security &
for which clinicians and public health professionals should Public Health; Iowa State University; 2006:234.
108
Table 9-2 n Diseases and Agents “to Watch” in Terms of Zoonotic Potential
Disease Agent Animal Hosts Zoonotic Transmission Route Clinical Manifestations Comments
Bordetella Bordetella Dogs, rabbits, guinea Respiratory Cough, fever; disease A cause of “kennel cough” in
bronchiseptica pigs seen mostly in immune- dogs
bacteria compromised humans
Chagas disease Trypanosoma cruzi Rodents rabbits, Organism in feces of Triatoma Fever, myocarditis, Dogs exhibit clinical signs similar
protozoa opossums, dogs, cats, bug (“kissing” bug or “assassin” hepatosplenomegaly to those in humans
armadillos bug) can enter wound; blood Other animals are carriers; dogs
transfusion infected in southern United
States; dogs may be extending
the range of this disease
Chikungunya Chikungunya virus Humans, rodents, birds, Aedes mosquito vector (present in Fever, rash, arthralgia Seen in returning travelers, new
primates United States) cases in Europe
Dirofilariasis Dirofilaria immitis Dogs, cats, ferrets, Mosquito vector Fever, cough, “coin lesion” Parasite not known to complete
(“heartworm” in dogs) roundworm raccoons, bears in lung due to vasculitis, its life cycle in humans
reported involvement of
extrapulmonary sites (CNS,
liver)4
Erysipeloid (human Erysipelothrix Pigs, sheep, turkeys, Direct contact Cellulitis Occupational disease of farmers,
disease) rhusiopathiae pigeons, marine butchers, cooks
bacteria mammals, fish
Feline cowpox Feline cowpox virus Cats are principal host; Direct contact Skin ulcer resembling anthrax Distribution is Eurasia
rodents, cows, and
humans are accidental
hosts
Pseudomembranous Clostridium difficile Cattle Ubiquitous organism; may preset Diarrhea, abdominal pain Emerging community-acquired
colitis bacteria with overuse of antibiotics infection
Strains in humans recently found
to match those in cattle
Glanders Burkholderia mallei Horses, mules, donkeys Direct contact Four forms of disease: Category B bioterrorism agent
bacteria septicemia, pulmonary
infection, local infection,
chronic infection
Helicobacter infection Helicobacter: gram- Dogs, cats, birds Ingestion Peptic ulcer disease, gastritis,
negative bacteria: gastric neoplasia in humans
H. pylori (humans),
H. felis (cats), H. canis
(dogs)3
Monkeypox Monkeypox virus African rodents (able Bites, aerosols, direct contact Flulike symptoms, rash Caused outbreak in humans
to infect prairie dogs, and pet prairie dogs related
rats, mice, squirrels), to importation of Gambian
primates, rabbits rats and other African rodents
intended as exotic pets
Melioidosis Pseudomonas Rodents, goats, sheep, Acquired from the environment Infection of skin, lung, hepatitis Category B bioterrorism agent,
(pseudoglanders) pseudomallei bacteria horses, swine, occurs in zoo animals5
primates, dogs, birds,
dolphins, tropical fish
Pasteurellosis Pasteurella multocida Dogs, cats, other Scratch, bite, but also secretions Wound infection, but UTI
bacteria animals recently reported6
Rat-bite fever (Haverhill Streptobacillus Rodents, including Bites and scratches, ingestion Uncommon; risk to laboratory
fever) moniliformis bacteria laboratory and wild animal workers
animals
Streptococcosis Streptococcus suis Pigs Direct contact, aerosols, fomites Fever, endocarditis 35 serotypes; type 2 is most
(and other species) frequently isolated from pigs
bacteria with clinical signs and from
humans7; occupational disease
of pig handlers
Yersiniosis Yersinia enterocolitica Pigs Ingestion, especially of Diarrhea, abdominal pain
bacteria undercooked pork
CNS, Central nervous system; UTI, urinary tract infection.
Chapter 9
n
Zoonoses
109
110
Table 9-3 n Chart of Species and Associated Pathogens
Domestic
Dogs
Cats
Ferret
amphibians
Reptiles and
Caged birds
Rabbits
(rodents)
Pocket pets
Fish
Horses
Cattle
Goats
Sheep
Swine
Poultry
Mink
primates
Nonhuman
alpacas
Camels, llamas,
Raccoons
Squirrels
Other wild rodents
Wild birds
Marine mammals
Wild cats
wild canids
Foxes, coyotes,
Bats
Skunks
Opossums
Elephants
Beavers
Deer
herbivores
Other wild
Disease
Arthropods
Scabies X X X X X X X X X
Other acariasis X X X X X X X X X X X X X X
Bacterial
Anthrax X X X X X X X X X X X
Bartonellosis X X
Bordetella bronchiseptica X X X
Botulism X X X X X X X X
Brucellosis X X X X X X X X X X X X X
Campylobacteriosis X X X X X X X X X X X X X X
Chlamydophila infection X X X X X X X X X X X X
Ehrlichiosis and X X X X X X X X X X X X X
anaplasmosis
Escherichia coli O157 X X X X X X
infection
Erysipeloid X X
Leptospirosis X X X X X X X X X X X X X X X
Lyme disease X X X X X X X X X X
Melioidosis X X X X X X
MRSA X X X X X X X X
Mycobacteriosis other X X X X X X
than TB
TB X X X X X X X
Pasteurellosis X X
Plague X X X X X X
Q Fever X X X X X X X X X X X X X X X X
Rat-bite fever X X X X X X X X
Rocky Mountain spotted X X X X X
fever
Salmonellosis X X X X X X X X X X X X X X X X X X X X X X X
Tularemia X X X X X X X X X X X X X
Yersiniosis X X X X X X
Fungal
Cryptococcosis X
Dermatophytosis X X X X X X X X X X X X X X X X X X
Sporotrichosis X X X X X X X X X X
Histoplasmosis X X
Parasitic
Baylisascariasis X X X X X
Chagas’ disease X X X X X X X X X
(trypanosomiasis)
Cysticercosis (Taenia X X X X X X
infection)
Cryptosporidiosis X X X X X X X X X X X X X X X X X X X X X X X X X
Dipylidiasis X X X
Dirofilariasis X X X X X
Echinococcosis X X X X X X X X X X X X X X
Giardiasis X X X X X X X X
Hookworm infestation X X X X X X
Chapter 9
Leishmaniasis X X X X X X X
Toxocariasis X X X X X X X X X X X
Toxoplasmosis X X X X X X X X X X X X X
Trichinellosis X X X X X X
n
Zoonoses
Prion
Transmissible spongiform X X X X X X
encephalopathy
Viral
Hantavirus infection X X
Herpes B
111
Continued
112
Table 9-3 n Chart of Species and Associated Pathogens—cont’d
Domestic
Dogs
Cats
Ferret
amphibians
Reptiles and
Caged birds
Rabbits
(rodents)
Pocket pets
Fish
Horses
Cattle
Goats
Sheep
Swine
Poultry
Mink
primates
Nonhuman
alpacas
Camels, llamas,
Raccoons
Squirrels
rodents
Other wild
Wild birds
Marine mammals
Wild cats
wild canids
Foxes, coyotes,
Bats
Skunks
Opossums
Elephants
Beavers
Deer
herbivores
Other wild
Disease
Influenza (human) X X
Influenza (avian) X X X X X X X X X X X X
Lymphocytic X X X X X
choriomeningitis
Monkeypox X X X X
Orf X X X
Rabies X X X X X X X X X X X X X X X X X X
Rift Valley fever X X X X X X X X X X
West Nile virus infection X X X X X X X X X X X X
Adapted from Kahn CM, Line S (eds): The Merck veterinary manual, ed 9, Whitehouse Station, NJ, 2005, Merck; Dvorak GA, Rovid-Spickler A, Roth JA (eds): Handbook for zoonotic diseases of companion animals, The Center for Food Security
& Public Health, Ames, IA, 2006, Iowa State University; Forrester DJ: Parasites and diseases of wild mammals in Florida, Gainesville, FL, 1992, University Press of Florida.
MRSA, Methicillin-resistant Staphylococcus aureus; TB, tuberculosis.
ANTHRAX
Peter M. Rabinowitz and Lisa A. Conti • Counsel travelers to endemic areas about risk reduc-
tion and monitoring for symptoms.
Cutaneous anthrax (ICD-10 A22.0), Pulmonary anthrax • If providing occupational health services to workers
(A22.1), Gastrointestinal anthrax (A22.2) at risk, ensure that they are educated about symptoms
of the disease, use adequate protective equipment, and
Other names in humans: wool sorter’s disease, charbon, that efforts are taken to reduce potential of infection
malignant carbuncle, Siberian ulcer (such as disinfection of animal hides with formalin).
• Consider vaccine for high-risk groups,5 including lab-
Other names in animals: splenic fever, Milzbrand oratory workers and persons who handle potentially
infected animals and animal products in high-incidence
Anthrax is a fatal disease of herbivores. Most human cases areas where safety standards are insufficient to prevent
result from direct contact with sick or dead animals or con- exposure to anthrax spores.6 Military personnel7
taminated animal products. The causative agent, Bacillus deployed to areas with high risk for biological warfare
anthracis, is a Centers for Disease Control and Prevention may require vaccination.
(CDC) Category A bioterrorism agent, and the anthrax-
tainted letters mailed in the United States in 2001 were a
reminder of its potential for deliberate release. In the United
States, anthrax outbreaks in wildlife and livestock occur annu- • Do not perform a necropsy on suspected animal cases.
ally but human cases are rare.1 Veterinary and human health • Annually vaccinate cattle, sheep, horses, goats, and
care professionals need to recognize the clinical signs of dis- swine in endemic areas using the Sterne strain vaccine.8
ease and report suspected cases to public health authorities. Treat infected and potentially infected animals. During
quarantine these animals should not be used as food.
• Report suspected cases to agricultural health authori-
Key Points for Clinicians and Public Health ties who can quarantine premises to prevent spread of
Professionals disease.
• Veterinarians who work with potentially infected animals
Public Health Professionals in high-incidence areas should consider vaccination.
• Avoid contact with blood and bloody discharges. Keep
• Characterize the risk in the community, including whether flies and scavengers from carcasses. Infected carcasses
cases have been reported in livestock or wildlife and whether should be burned (preferred) to destroy spores or bur-
there is a possibility of environmental contamination. ied in quick lime. To kill spores use 2% glutaraldehyde
• Work with veterinary authorities to control disease in or 5% formalin for several hours. Heat sterilization at
animals. 121° C for 30 minutes can also be used.
• Conduct immediate investigation of human cases to • Notify health department immediately if cases are
determine whether they are related to zoonotic trans- diagnosed in animals. Such cases could both pose a
mission or deliberate toxin release. risk to humans and be a sentinel warning of deliberate
• Ensure that potentially exposed individuals receive release of toxin.
postexposure prophylaxis (PEP).
• Counsel people who contact spores to wash hands with
soap and water, followed by an organic iodine solution Agent
immersion. Clothing should be washed and boiled. The bacterium B. anthracis is a spore-forming, nonmotile,
• Recommend that imported animal hides be disinfected gram-positive bacillus 3 to 5 microns long. When the vegetative
before use. The U.S. Department of Agriculture (USDA) form is exposed to air, it sporulates to form infectious spores.
Animal and Plant Health Inspection Service (APHIS) The spores may survive for decades in soil (Figure 9-3).
regulates importation of all animal hides but does not
mandate screening of imported hides for B. anthracis.
In addition, some hides may be imported illegally.2 Geographical Occurrence
• Reduce environmental exposure risk through disinfec- National disease control programs have reduced the global inci-
tion where possible. dence of anthrax. It remains common in some Mediterranean
• Provide guidance for environmental sampling and countries, localized areas of Canada and the United States,
environmental cleanup.3,4 parts of Central and South America, central Asia, parts of sub-
Saharan Africa, and western China.9 An epizootic among cattle
Human Health Clinicians in South Dakota in 2000 resulted in 157 cattle deaths and one
human case of cutaneous anthrax.10 Human anthrax resulting
• Consider the diagnosis in all patients with livestock from exposure to infected livestock remains rare in the United
contact or travel to endemic countries. States but occurs more commonly in less-developed countries.
• Report suspicion of disease immediately to public In many regions, the true incidence is not known because many
health authorities. cases in animals and humans probably go unreported.
In the 2001 intentional use of anthrax in mail, postal

workers were an occupational risk group. No animals were
affected in these attacks.
Hosts, Reservoir Species, Vectors

The reservoir for anthrax is the environment, where the
spores can survive for years in alkaline calcium-rich soil.
Anthrax is principally a disease of livestock, including
cattle, sheep, goats, and camels. Wild ruminants such as
antelope and bison can also be infected and pose a risk to
livestock.11 However, all mammals are susceptible,12 and
horses, pigs, dogs, cats, and humans can be incidentally
infected. Because of their higher body temperatures birds
are normally resistant, but ostriches are susceptible. In
some settings, biting flies may serve as vectors for anthrax
Figure 9-3 n Photomicrograph depicting a number of gram-positive, transmission.9
endospore-forming Bacillus anthracis bacteria.
In the 1979 accidental release of aerosolized anthrax in
Sverdslovsk, Russia, cattle and sheep died as far as 50 km
downwind from the release site, while human cases of
inhalation anthrax occurred only up to 4 km downwind
from the release.13 The fact that animals became sickened
Groups at Risk over a wider geographical area than did humans may
Anthrax can be an occupational disease of workers who pro- reflect their increased susceptibility and increased expo-
cess carcasses and hides of infected animals, including farm- sure risk, making animal cases sentinels for human risk.
ers, abattoir workers, butchers, and workers in factories that
process hides. Veterinarians who handle sick animals are also
Mode of Transmission and Life Cycle
at risk, as are laboratory workers who routinely work with
B. anthracis. Cases of both inhalation and cutaneous anthrax Infected animals release vegetative bacteria into the environ-
have developed in travelers and drum makers who have ment. As the bacteria are exposed to air, they sporulate and
bought drums or hides originating from infected animals. the spores can survive for years. Ruminant animals grazing
In 2007, two cases of cutaneous anthrax in Connecticut were on areas contaminated by spores can ingest the spores and
tied to importation of infected goat hides for drum-making become infected. This can lead to further contamination of the
(Figure 9-4).2 environment and additional animal cases (Figure 9-5). Biting
flies appear to play a role in large outbreaks by facilitating ani-
mal-animal transmission, sometimes over significant distances
(5 to 15 km). Direct animal-animal transmission among her-
bivores is considered insignificant,9 but if carnivores eat the
flesh of infected animals, they can become infected.
Transmission from animal to human usually involves
direct contact with spores because the vegetative form of the
microbe is not as infectious. Spores may be present on an
infected animal’s hide, in meat that has been in contact with
air and has developed spores, or as an aerosol from infected
animal hide or tissues or from the environment.
Most human infection occurs through direct contact with
animals or animal products. Such transmission is more likely
when there are breaks in the skin and leads to the cutaneous
form of the disease (Figure 9-6).
Airborne transmission from animals to humans can occur
when spores are aerosolized during the processing or han-
dling of contaminated animal hair, wool, hides, and bones.
Improvements in working conditions have reduced this risk.
Airborne transmission can also occur during the deliberate
release of the agent.
Humans can also become infected through ingestion
Figure 9-4 n Bacillus anthracis–contaminated drum head made from of tissue from an infected animal, leading to development
goat hide from Guinea; Connecticut, 2007. (From Centers for Disease
Control and Prevention: Cutaneous anthrax associated with drum mak- of gastrointestinal or oropharyngeal anthrax. Human-to-
ing using goat hides from West Africa—Connecticut, 2007, MMWR Morbid human transmission is considered rare and has been reported
Mortal Weekly Rep 57(23):628, 2008.) only with cutaneous anthrax.
From terminally infected animal,

or carcass after death
Cutaneous Biting fly
Germination and multiplication

in lymphatics and spleen.
Vegetative forms released
Pulmonary in massive numbers into
(spore-laden dust) blood in final hours of life
Gastrointestinal Spores
(infected meat, Ingested
contaminated water?) (grazing, browsing,
drinking). Inhaled
sometimes?
Cutaneous Sporulate on (spore-laden dust)
(via lesion) exposure to O2
Vegetative forms
(shed at death in
Haemorrhagic exudate
from nose, mouth or anus
or in spilt blood)
Enviromental drivers:
Soil types Rainfall patterns Season
Figure 9-5 n Cycle of anthrax infection. (Modified from Guidelines for the surveillance and control of anthrax in humans and animals, ed 4, Geneva, 2008,
World Health Organization. Available at http://www.who.int/csr/resources/publications/anthrax/whoemczdi986text.pdf.)
life species have been linked to climate factors such as hot,

dry weather following spring flooding.11 Heavy rainfall may
increase the population of biting flies that can amplify animal
outbreaks and may lead to spores being brought to the soil
surface.9,12
Anthrax spores can contaminate indoor environments.
One of the recent cases in Connecticut tied to imported drum
hides was the child of the drum maker, who became infected
through contamination of the household environment.2
Disease in Humans
There are three main forms of the disease: cutaneous,
inhalational, and gastrointestinal. In naturally occurring
human disease, more than 95% of cases are the cutaneous
Figure 9-6 n Cutaneous anthrax in a child. (From Roche KJ, Chang
form. Inhalational anthrax is the next most common form.
MW, Lazarus H: Images in clinical medicine: cutaneous anthrax infection, Gastrointestinal anthrax has never been reported in the
N Engl J Med 345:1611, 2001.) United States. Table 9-4 shows the comparative clinical pre-
sentations of anthrax in humans and animals.
Environmental Risk Factors
Cutaneous Anthrax
The persistence of spores in the environment depends on a
number of factors, including temperature, humidity, soil pH, Cutaneous anthrax begins 1 to 7 days after inoculation with
calcium and other cations in soil, and the abundance of soil a small, painless, pruritic papule that is often asymptomatic
bacteria that could break down spores.14 Outbreaks in wild- and does not lead to an infected individual seeking medical
Table 9-4 n Anthrax: Clinical Presentations in Humans and Other Animals
Incubation
Species Risk Factors Period Signs and Symptoms Diagnostic Findings
Humans: cutaneous Contact with infected 2-6 days Painless, pruritic papule followed Organisms seen on methylene
(95% of naturally animal or animal by vesicles, edema, ulcer, and blue stain, culture, or by PCR
occurring human products eschar; bacteremia or ELISA
cases)
Inhalational Aerosol from processing 4-6 days Malaise, fever, cough, followed Chest radiograph may show
hides, wool, deliberate by acute onset of respiratory widened mediastinum,
release distress pleural effusion
Gastrointestinal Ingestion of infected 3-7 days9 Fever, abdominal pain, nausea, Identification of bacteria in
meat vomiting, bloody diarrhea, blood or other fluid samples
oropharyngeal swelling
Cattle, sheep goats, Grazing on areas 1-20 days Fever, depression, staggering, Demonstration of bacteria by
other herbivores contaminated by collapse, edema, abortion, culture, PCR, fluorescent
spores, biting flies sudden death antibody of blood or tissue
Pigs Contact with 7-14 days Often a milder form of disease Demonstration of bacteria by
contaminated soil with systemic symptoms and culture, PCR, fluorescent
cervical lymphadenopathy antibody of lymphoid or
other tissue
Acute septicemia with
oropharyngeal swelling and
death may occur
Dogs, cats, wild Ingestion of tissue from 1-14 days Resembles disease in pigs
carnivores infected animal
Horses Grazing on 1-20 days Fever, colic, diarrhea, swelling of
contaminated pasture neck, belly, genitalia
ELISA, Enzyme-linked immunosorbent assay; PCR, polymerase chain reaction.
care. Over a period of days, vesicles develop with surround-

ing edema, which then rupture to form an ulcer covered by a
black eschar. A significant degree of edema develops around
the eschar and can be severe. Most cutaneous lesions are
on the hands and arms. If the head and neck are involved,
breathing may be compromised by the swelling. Bacteremia
can develop, leading to systemic complications. Without
antibiotic treatment the mortality rate is approximately
20%.15 Figure 9-6 shows cutaneous anthrax in a child.
Inhalational Anthrax
Inhalational anthrax often begins with nonspecific malaise,
mild fever, and nonproductive cough 1 to 6 days after expo-
sure. After several days, a second phase of the disease begins
abruptly with high fever, dyspnea, cyanosis, and stridor. A
hemorrhagic lymphadenitis can develop with mediastinal
widening (Figure 9-7). Without treatment, respiratory dec-
ompensation soon occurs. In up to half of cases, anthrax
meningitis may also be present, with meningeal signs and Figure 9-7 n Chest radiograph of a patient with inhalational anthrax in
2001. The arrows emphasize the widened mediastinum caused by the char-
altered consciousness.15 Mortality rate is high even with anti- acteristic mediastinal adenopathy. (From Borio L, Frank D, Mani V et al:
biotic treatment. Death due to bioterrorism-related inhalational anthrax: report of 2 patients,
JAMA 286:2554, 2001.)
Gastrointestinal Anthrax
Gastrointestinal anthrax is characterized by fever, abdominal Disease in Animals
pain, and bloody diarrhea that develop 2 to 5 days after inges-
tion of contaminated meat (to date, it has not been reported Cattle and sheep develop an acute form of anthrax that is usu-
in the United States). Oropharyngeal involvement can pro- ally rapidly fatal. Clinical signs include fever, depression, stag-
duce swelling with respiratory compromise. The mortality gering, difficulty breathing, and collapse. Subcutaneous edema
rate can be 25% to 75%.16 may be present. Pregnant animals may abort before dying.
Infected horses can also develop acute disease with fever,

colic, diarrhea, weakness, and swelling of the neck, sternum,
belly, and genitalia. The disease is also rapidly fatal.
Pigs are considered to be more resistant to the disease
compared with ruminants. Although pigs may develop an
acute septicemia with sudden death and/or oropharyngitis
with throat swelling and suffocation, a chronic form of dis-
ease is more common, with mild systemic signs and cervical
lymphadenopathy.
Dogs, cats, nonhuman primates, and wild carnivores can
develop disease resembling that in pigs (Figure 9-8).15
Diagnosis
Diagnosis in Humans
The differential diagnosis of cutaneous anthrax in humans
includes boils, cellulitis, spider bite, rickettsial disease, Figure 9-8 n Gross pathologic posterior oblique view of inhalation
anthrax in a chimpanzee’s lungs. (From Centers for Disease Control and
ulceroglandular tularemia, rat-bite fever, leishmaniasis, and Prevention Public Health Image Library, Atlanta, Ga. Courtesy U.S. Army,
human orf. A history of exposure to livestock or livestock Arthur E. Kay.)
products, the presence of extensive edema, and the lack of
pus and pain can provide clues to the diagnosis.
Inhalational anthrax can present with nonspecific symp- inhalation anthrax has been proposed by a consensus report
toms and may be confused with other causes of pneu- (Figure 9-9). This protocol is based on history of exposure
monitis, including community-acquired pneumonia and and the presence of clinical signs.
influenza. In the second, severe stage of illness, possible con- Gastrointestinal anthrax, though rare, typically presents
siderations include aortic dissection, pneumonic plague, and as a cluster of cases of acute abdominal pain and diarrhea
hantavirus pulmonary syndrome. A screening protocol for following ingestion of food from a common source. It can
Epidemiologic factors or Clinical factors
• History of exposure Symptoms

• Occupational or • Fever
environmental risk • Sweats (often drenching)
• Fatigue
• Cough
• Chest discomfort, pleuritic pain
• Nausea/vomiting
• Headache
• Dyspnea
• Myalgias
• Abdominal pain
• Confusion
Signs
• Fever (low grade, mean
temperature 38º C)
• Tachycardia (mean heart
rate 121 beats/min)
Clinical presentation consistent

with inhalation anthrax
• 5 symptoms (see above)
• Fever
• Tachycardia
NO YES
• Observe closely with

definite follow-up
• Provide antimicrobial Diagnostic testing Public health
prophylaxis if exposure • Laboratory studies • Inform appropriate
is confirmed • Radiologic imaging public health agency
Figure 9-9 n Revisions to the Centers for Disease Control and Prevention (CDC) interim inhalation anthrax
screening guidelines. (From Stern EJ, Uhde KB, Shadomy SV et al: Conference report on public health and clinical
guidelines for anthrax, Emerg Infect Dis 14(4):pii: 07-0969, 2008.)
therefore be confused with other causes of food-borne Table 9-5 shows the recommended initial treatment regi-
illness. mens. Although quinolones or doxycycline are first-line
The differential diagnosis of oropharyngeal anthrax agents, if the infecting strain is found to be susceptible to
includes streptococcal pharyngitis and Ludwig’s angina.9 penicillin, penicillin can be substituted.
The laboratory diagnosis of anthrax involves identifica-
tion of the capsulated organism in blood or tissues using Treatment in Animals
methylene blue (M’Fadyean)-stained smears or through bac-
terial culture of blood or other specimens.16 Rapid tests that Control of anthrax in animals may involve a combination of
are increasingly available include polymerase chain reaction vaccination, quarantine, PEP of subclinically exposed ani-
(PCR), enzyme-linked immunosorbent assay (ELISA), and mals, antibiotic treatment, or euthanization of sick animals
immunohistochemical staining. Diagnostic testing for sus- and disposal of carcasses by burning. Cattle at risk should
pected inhalation anthrax in humans should include chest receive a full course of antibiotics, followed by vaccination 7 to
radiography and/or chest computed tomographic (CT) 10 days later. Vaccination and antibiotics should not be given
scanning to look for mediastinal widening.1 concurrently. Animals under treatment should be moved to a
new pasture that is free from possible contamination.
Carcasses of animals that have died of anthrax should not
Diagnosis in Animals
be necropsied or otherwise opened to prevent sporulation of
In cattle, anthrax can be confused with other causes of sudden the bacteria and further cycles of infection.
death, including lightning strikes, poisonings, leptospirosis,
anaplasmosis, and clostridial infections. In pigs, other diag-
noses to consider include classical or African swine fever and Additional Resources
pharyngeal malignant edema. In dogs, other systemic infec-
tions or causes of pharyngeal edema should be considered. CDC Advisory Committee on Immunization
Diagnostic testing can be performed on a swab of blood Practices Recommendations for Use of Anthrax
that is allowed to air-dry, resulting in sporulation of the bac- Vaccine
teria and death of other bacteria and contaminants. In pigs,
lymph tissue should be sent for studies. Bacterial culture, • Use of Anthrax Vaccine in Response to Terrorism
PCR, and fluorescent antibody stains can demonstrate the (2002)
organism in blood and tissues.17 http://www.cdc.gov/mmwr/preview/mmwrhtml/
mm5145a4.htm
• Use of Anthrax Vaccine in the United States (2000)
Treatment
http://www.cdc.gov/mmwr/preview/mmwrhtml/
rr4915a1.htm
• MMWR Notice to Readers: Occupational Health
Treatment in Humans
Guidelines for Remediation Workers at Bacillus anthracis–
Treatment of anthrax in humans involves treatment with contaminated Sites—United States, 2001-2002 (MMWR
antibiotics as soon as the disease is suspected or as PEP. 6;51(35), 786-789, 2002)
Table 9-5 n Initial Treatment of Anthrax in Human Beings and Animals
Species Primary Treatment Alternative Treatment
Humans:
Cutaneous Ciprofloxacin 500 mg PO bid or levofloxacin Doxycycline 100 mg PO bid × 60 days
500 mg IV/PO bid × 60 days Children >8 yr and >45 kg: doxycycline 100 mg PO bid × 60 days
Children <50 kg: ciprofloxacin 20-30 mg/kg/ <8 yr: doxycycline 2.2 mg/kg PO bid × 60 days18
day divided q12h PO (maximum 1 gm/day)
× 60 days or levofloxacin 8 mg/kg PO q12h ×
60 days
Inhalational and Adult: Ciprofloxacin 400 mg IV q12h or levofloxacin Children: ciprofloxacin 10 mg/kg IV q12h or 15 mg/kg PO q12h
gastrointestinal 500 mg IV q24h PLUS clindamycin 900 mg IV or doxycycline (>8 yr and >45 kg) 100 mg IV q12h, PLUS
q8h and/or rifampin 300 mg IV q12h; treatment clindamycin 7.5 mg/kg IV q6h and/or rifampin 20 mg/kg
duration 60 days; switch to PO when able (maximum 600 mg) IV q24h; treatment duration 60 days19
Postexposure Ciprofloxacin 500 mg PO bid or levofloxacin Doxycycline 100 mg PO bid × 60 days
prophylaxis 500 mg PO q24h × 60 days Children >8 yr and >45 kg: doxycycline 100 mg PO bid
Children: ciprofloxacin 20-30 mg/kg/day divided <8 yr: doxycycline 2.2 mg/kg PO bid × 60 days
q12h × 60 days
Cow, sheep, goat, Penicillin Oxytetracycline
horse
Dog19 Oxytetracycline 5 mg/kg IV q24h Enrofloxacin 5 mg/kg q24h
Potassium penicillin G at 20,000 U/kg IV q8h
http://www.cdc.gov/mmwr/preview/mmwrhtml/ 4. National Institute for Occupational Safety and Health. NIOSH respi-
mm5135a3.htm ratory diseases research program: evidence package for the National
Academies’ Review 2006–2007: 6.2 Anthrax. http://www.cdc.gov/niosh/
• Bacterial Agents: Anthrax. In Biosafety in microbiology nas/RDRP/ch6.2.htm; Accessed August 11, 2008.
and biomedical laboratories, ed 5, pp. 122-124, 2007) 5. Use of anthrax vaccine in the United States: recommendations of the
http://www.cdc.gov/OD/OHS/biosft y/bmbl5/ Advisory Committee on Immunization Practices. MMWR Recomm Rep.
BMBL_5th_Edition.pdf 2000;49(RR15):1.
6. Notice to readers. Use of anthrax vaccine in response to terror-
ism: supplemental recommendations of the Advisory Committee on
Antimicrobial Prophylaxis Immunization Practices. MMWR. 2002;51:1024. Available at http://
www.cdc.gov/mmwr/preview/mmwrhtml/mm5145a4.htm.
• Antimicrobial Prophylaxis to Prevent Anthrax Among 7. Military Vaccine Agency. Anthrax vaccine immunization program. http://
Decontamination/Cleanup Workers Responding to an www.anthrax.osd.mil; Accessed August 11, 2008.
Intentional Distribution of Bacillus anthracis (2002): 8. United States Department of Agriculture. Animal and Plant Health
Inspection Service: APHIS factsheet: anthrax—general information and
http://emergency.cdc.gov/agent/anthrax/exposure/ vaccination. http://www.aphis.usda.gov/publications/animal_health/
cleanupprophylaxis.asp content/printable_version/fs_ahanthravac.pdf. Accessed August 11,
• Responding to Detection of Aerosolized Bacillus anthra- 2008.
cis by Autonomous Detection Systems in the Workplace 9. World Health Organization. Anthrax in humans and animals. http://
www.who.int/csr/resources/publications/anthrax/whoemczdi986text.
(MMWR 2004/53(early release);1-11, April 30, 2004) pdf.
http://www.cdc.gov/mmwr/preview/mmwrhtml/ 10. Centers for Disease Control and Prevention. Human anthrax associated
rr53e430-2a1.htm with an epizootic among livestock—North Dakota, 2000. MMWR Morb
Mortal Wkly Rep. 2001;50(32):677.
11. Nishi JS, Dragon DC, Elkin BT, et al. Emergency response planning for
Personal Protective Equipment anthrax outbreaks in bison herds of northern Canada. Ann N Y Acad Sci.
2002;969:245.
• Protecting Investigators Performing Environmental 12. Hugh-Jones ME, de Vos V. Anthrax in wildlife. Rev Sci Tech Off Int Epiz.
Sampling for Bacillus anthracis: Personal Protective 2002;21:359.
Equipment (Nov. 6, 2001): http://emergency.cdc.gov/ 13. Meselson M, Guillemin J, Hugh-Jones M, et al. The Sverdlovsk anthrax
agent/anthrax/environment/investigatorppe.asp outbreak of 1979. Science. 1994;266(5188):1202.
14. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
• Interim Recommendations for the Selection and Use of and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington, DC:
Protective Clothing and Respirators Against Biological Pan American Health Organization; 2001.
Agents (Oct. 25, 2001): http://www.bt.cdc.gov/docu- 15. Swartz MN. Recognition and management of anthrax—an update. N
mentsapp/Anthrax/Protective/10242001Protect.asp Engl J Med. 2001;345(22):1621.
16. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
References 17. US Food and Drug Administration, Center for Biologics Evaluation
and Research. Anthrax. http://www.fda.gov/cber/vaccine/anthrax.htm
1. Shadomy, TLSmith SV. Zoonosis update: Anthrax. J Am Vet Med Assoc. Accessed August 11, 2008.
2008;233(1):63. 18. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti-
2. Centers for Disease Control and Prevention (CDC). Cutaneous anthrax microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
associated with drum making using goat hides from west Africa— 2009.
Connecticut, 2007. MMWR Morb Mortal Wkly Rep. 2008;57(23):628. 19. Langston C. Postexposure management and treatment of anthrax
3. Meehan PJ, Rosenstein NE, Gillen M, et al. Responding to detection in dogs—executive councils of the American Academy of Veterinary
of aerosolized Bacillus anthracis by autonomous detection systems in Pharmacology and Therapeutics and the American College of Veterinary
the workplace. http://www.cdc.gov/mmwr/preview/mmwrhtml/rr53e4 Clinical Pharmacology. http://www.aapsj.org/view.asp?art=aapsj070227.
30-2a1.htm; Accessed August 11, 2008. Accessed August 11, 2008.
BARTONELLA INFECTIONS
Peter M. Rabinowitz and Lisa A. Conti Bartonella infection is an occupational risk for veterinary
workers (including one reported case of Bartonella clarridge-
Bartonella infection (ICD-10 A28.1) iae) and one of the more common infections associated with
cat ownership.
Other names in humans: cat-scratch fever, cat-scratch dis-
ease, benign lymphoreticulosis, Parinaud’s oculoglandular
syndrome, bacillary angiomatosis, bacillary parenchymatous
peliosis (peliosis hepatis), recurrent rickettsemia
Professionals
Other names in animals: bartonellosis
Bartonella henselae, the causative agent for cat-scratch disease
(CSD), is usually associated with self-limited infection in • Educate community about avoiding cat scratches and
humans and subclinical disease in cats, but it is capable of seri- bites (particularly kittens), thorough cleaning of wounds
ous systemic infection in humans. Other Bartonella species to reduce infection, discouraging cats from licking a per-
may be emerging pathogens for humans and other animals. son’s skin or opens wounds, and flea and tick control.1
identified. B. henselae, B. vinsonii, and B. elizabethae are

known to infect both human and animal hosts.3
• Be alert to diagnosis in persons with unexplained
lymphadenopathy or fever of unknown origin.
• Counsel immunocompromised patients to avoid cat Geographical Occurrence
scratches, thoroughly clean wounds after a scratch or B. henselae is found worldwide.
bite, and to not allow cats to lick a person’s skin or
open wounds.
• Consider risk of infection in any patient bitten or Groups at Risk
scratched by a cat or with flea or tick bites. CSD can be an occupational disease of veterinarians and others
• Counsel occupationally exposed workers (e.g., zoo- providing care to cats. Studies of zookeepers have revealed sero-
keepers) and persons owning cats to avoid and seek prevalence rates for past Bartonella infection as high as 65%,4
care for bites and scratches and to be alert to signs and while a convenience survey of veterinarians and veterinary
symptoms of infection. workers found Bartonella species seroprevalence of only 7%.
• Report cases to health department if required in state.
• No human vaccine is currently available.
Veterinary Clinicians Bartonella species have been found in a wide range of sub-
clinically infected mammals, including rodents, rabbits, deer,
• Ensure flea control for cats.
elk, bighorn sheep, cattle, foxes, dogs, and coyotes.5 Domestic
• Counsel cat owners, especially immunocompromised
cats are considered the principal reservoir for B. henselae.6
patients, about avoiding cat scratches and bites, thor-
Seroprevalence studies have shown rates of antibody positiv-
ough cleaning of cat infected wounds, and not allowing
ity in cats in the range of 40%.7 However, infection in cats is
cats to lick a person’s skin or open wound. Although
considered either subclinical or subtle, even in the setting of
declawing has not been associated with preventing
chronic bacteremia. B. henselae has also been isolated from
infection, some recommend trimming cats’ nails rou-
cat fleas, dog fleas, and a number of other vectors.8 Dogs may
tinely. Some suggest keeping cats indoors.
also be infected with B. henselae. Recent data show that ticks
• A vaccine has been developed (though not currently
may play a role in transmission to humans.9
marketed).
B. quintana at present is known to have only a human
reservoir and is spread by the human body louse. B. vinsonii
Agent and B. elizabethae have been found in asymptomatic rodent
reservoirs, including rural mice (B. vinsonii)10 and urban rats
B. henselae is a gram-negative bacillus in the fam-
(B. elizabethae).11 Infection to humans may occur through
ily Bartonellaceae. This family shares some features with
vectors or direct contact.
rickettsial organisms but has been removed from the order
Rickettsiales. The genus Bartonella includes at least 20 spe-
cies, five of which (B. henselae, B. quintana, B. bacilliformis,
B. vinsonii subspecies arupensis, and B. elizabethae) are
recognized human pathogens (Table 9-6).2 At present, no Despite the fact that B. henselae can occur in vectors,
animal reservoirs of B. quintana or B. bacilliformis have been transmission to humans is thought to be mainly mechanical
Table 9-6 n Pathogenic Bartonella Species
Bartonella Species Disease(s) Reservoir(s) Arthropod Vector(s)
B. bacilliformis Oroya fever and verruga peruana Humans Sandflies

B. clarridgeiae Cat-scratch disease; canine valvular Domestic cats ?
endocarditis
B. elizabethae Human endocarditis Norway rat ?
B. grahamii Human neuroretinitis Rodents Fleas
B. henselae Human, canine cat-scratch fever, Domestic cats; dogs (?) Cat flea
endocarditis, peliosis hepatitis
B. quintana Human trench fever Humans Body lice
B. vinsonii subsp. arupensis Human endocarditis Mice, voles ?
B. vinsonii subsp. berkhoffii Human, canine endocarditis; canine Rodents, dogs Ticks
granulomatis lymphadenitis, rhinitis,
peliosis hepatitis
B. washoensis Human myocarditis Ground squirrels ?
From Songer JG, Post KW: Veterinary microbiology: bacterial and fungal agents of animal disease, St Louis, 2005, Saunders Elsevier.
through a scratch or bite or licking of an open wound or and hepatic abscesses. In many but not all cases, CSD pre-
rubbing the eyes with contaminated hands (Figure 9-10). cedes the development of more serious complications. In the
The role of fleas in transmission is not well understood. elderly, B. henselae endocarditis may be found more frequently
(a common cause of culture-negative endocarditis), whereas
CSD is less frequent than in younger individuals.12
Environmental Risk Factors In immunocompromised individuals, complications of
infection can include bacillary angiomatosis (Color Plate 9-3).
Flea infestation is a definite risk factor for both feline and Peliosis hepatis, a condition characterized by fever, chills,
zoonotic infection because cats infested with fleas have hepatosplenomegaly, and gastrointestinal symptoms, can
higher seroprevalence of Bartonella infection. develop in immunocompromised patients. Like B. henselae,
B. quintana causes a number of conditions, including trench
fever, endocarditis, bacillary angiomatosis, and peliosis
Disease in Humans hepatitis.11
Cat scratch infection produces an inoculation at the point At present. case reports of bacteremia and endocarditis
of injury, with inflammation of nearby lymph nodes several in humans resulting from infection with B. vinsonii10 and
weeks later (Color Plate 9-2). The lymph swelling often is self- B. elizabethae are limited.13 Antibodies to B. elizabethae have
limited over a period of months in immunocompetent hosts been found in urban homeless and drug users,14 but the clin-
(Figure 9-11). In up to one sixth of cases the lymph nodes sup- ical significance remains poorly understood.
purate. Other symptoms can include malaise, fatigue, fever,
and rash.3 Disease in Animals
Atypical presentations of B. henselae infection include
Parinaud’s oculoglandular syndrome (granulomatous con- B. henselae causes subclinical infection in cats, including
junctivitis accompanied by pretragal lymphadenopathy).3 chronic bacteremia. Between 5% and 60% of cats may be
Even in immunocompetent patients, serious complications of seropositive depending on the geographical area. There is
B. henselae infection can occur, such as central nervous system a case report of B. henselae infection in a Golden Retriever
(CNS) involvement (including encephalopathy and myelitis)12 causing pelosis hepatitis (Figure 9-12 and Color Plate 9-4).15
Table 9-7 provides comparative clinical manifestations in
humans and other animals.
Mechanical injury
Infected cat (scratch, bite), Human being
licking of wound Diagnosis
? Diagnosis in humans is based on the clinical picture of local
lymphadenopathy, especially in the setting of a history of
Nonimmune cat Infected fleas cat contact. Bartonella species are difficult to grow in cul-
ture; therefore other diagnostic techniques such as PCR
Figure 9-10 n Life cycle of Bartonella henselae infection. and serology are often required (e.g., immunofluorescent
antibody [IFA] titer ≥1:64 to B. henselae).19 Cross-reactions
can occur among Bartonella species and Chlamydia and
Figure 9-12 n Ultrasonographic appearance of the liver of a dog with

Figure 9-11 n Papular lesion and enlarged lymph nodes in a person peliosis hepatis associated with B. henselae infection showing hypoechoic
with cat scratch disease. (From Long SS, Pickering LK, Prober CG (eds): areas (arrows) representing vascular peliosis. (From Greene CE: Infectious
Principles and practice of pediatric infectious diseases, ed 3, Philadelphia, diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier. Courtesy
2008, Saunders Elsevier.) Barbara Kitchell, University of Illinois, Urbana, Ill.)
Table 9-7 n Bartonella Infections: Comparative Clinical Presentations in Humans

and Other Animals16
Incubation
Species Risk Factors Period Clinical Manifestations Laboratory Findings
B. Henselae
Humans Cat scratch or bite, 3-10 days Lymphadenopathy, fever, culture- Leukocytosis, elevated
immunocompromised negative endocarditis; rare sedimentation rate,
individuals at complications including bacillary serology (IFA or ELISA),
increased risk angiomatosis, neurological PCR
involvement, endocarditis, Parinaud’s
oculoglandular syndrome
Cats 2-16 days Subclinical or mild symptoms, Blood culture, serology
(experimental uveitis (?) (IFA)
infection)
B. Vinsonii Subsp. Berkhoffii
Humans Bacteremia and endocarditis reported17
Isolated in healthy animals
Dogs and coyotes Canine granulomatous rhinitis (?), liver

disease, endocarditis, fever, death
B. Vinsonii Subsp. Arupensis
Humans Rodent exposure (?) Bacteremia, endocarditis reported18
Rodents Subclinical
B. Elizabethae
Humans Rodent exposure14 Endocarditis reported13
Rodents Subclinical
ELISA, Enzyme-linked immunosorbent assay; IFA, immunofluorescent antibody; PCR, polymerase chain reaction.
Coxiella. PCR of tissue and fluid obtained from lymph antibiotics.20 Table 9-8 outlines treatment guidelines for
node biopsy can often identify the organism. Disease in symptomatic disease in humans. There are no treatment
animals can be diagnosed by blood culture or serology (IFA protocols for animals.
or ELISA) and PCR.
Treatment References
In humans, some cases of CSD in an immunocompetent 1. Carr RM, Mohrman L, Arelli V, et al. Update on cause and management
of catscratch disease. Infect Med. 2008;25:242.
host may not require antibiotic treatment.12 However, 2. Koehler JE, Duncan LM. Case records of the Massachusetts General
any immunocompromised patient, as well as any patient Hospital. Case 30-2005. A 56-year-old man with fever and axillary
with extralymphatic involvement, should be treated with lymphadenopathy. N Engl J Med. 2005;353(13):1387.
Table 9-8 n B. Henselae Treatment in Humans and Other Animals21
Species Primary Treatment Alternative

Humans
Cat-scratch disease (immunocompetent) Adults: azithromycin 500 mg × 1, then Consider no treatment since often
250 qd × 4 days self-limited
Children (≤45.5 kg): liquid azithromycin
10 mg/kg ×1, then 5 mg/kg/day × 4
days12
Bacillary angiomatosis, peliosis hepatitis, Clarithromycin 500 mg bid or Erythromycin 500 mg PO qid or doxycycline
immunocompromised patients clarithromycin ER 1 gm PO q24h 100 mg PO bid × 8 weeks, or if severe,
or azithromycin 250 mg q24h or combination of doxycycline 100 mg PO/IV
ciprofloxacin 500-750 mg PO bid × 8 wk12 bid and rifampin 300 mg PO bid
Cats, Dogs (With Clinical Signs) Azithromycin 5-10 mg/kg once a day × 7
days and every other day × additional 5
weeks22
3. Mandell GE, Bennett JE, Dolin R. Principles and practice of infectious dis- 12. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to antimicro-
eases. 6th ed. Philadelphia: Churchill Livingstone Elsevier; 2000. bial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy; 2009.
4. Juncker-Voss M, Prosl H, Lussy H, et al. Screening for antibodies against 13. Daly JS, Worthington MG, Brenner DJ, et al. Rochalimaea elizabethae sp. nov.
zoonotic agents among employees of the Zoological Garden of Vienna, isolated from a patient with endocarditis. J Clin Microbiol. 1993;31:872.
Schönbrunn. Austriac. 2004;117(9–10):404. 14. Comer JA, Diaz T, Vlahov D, et al. Evidence of rodent-associated Bartonella
5. Breitschwerdt EB, Kordick DL. Bartonella infection in animals: carri- and Rickettsia infections among intravenous drug users from Central and
ership, reservoir potential, pathogenicity, and zoonotic potential for East Harlem, New York. Am J Trop Med Hyg. 2001;65(6):855.
human infection. Clin Microbiol Rev. 2000;13(3):428. 15. Kitchell BE, Fan TM, Kordick D, et al. Peliosis hepatis in a dog infected
6. Acha PN, Szyfres B. Zoonoses and communicable diseases common to with Bartonella henselae. J Am Vet Med Assoc. 2000;216(4):519–523 517.
man and animals: vol. 2: chlamydioses, rickettsioses, and viroses. 3rd ed. 16. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic dis-
Washington DC: Pan American Health Organization; 2003. eases of companion animals. Ames, IA: The Center for Food Security and
7. Fabbi M, Vicari N, Tranquillo M, et al. Prevalence of Bartonella hense- Public Health, Iowa State University; 2008.
lae in stray and domestic cats in different Italian areas: evaluation of 17. Roux V, Eykyn SJ, Wyllie S, et al. Bartonella vinsonii subsp. berkhoffii
the potential risk of transmission of Bartonella to human beings. as an agent of afebrile blood culture-negative endocarditis in a human.
Parassitologia. 2004;46(1–2):127. J Clin Microbiol. 2000;38(4):1698.
8. Maurin M, Birtles R, Raoult D. Current knowledge of Bartonella species. 18. Fenollar F, Sire S, Raoult D. Bartonella vinsonii subsp. arupensis as
Eur J Clin Microbiol Infect Dis. 1997;16(7):487. an agent of blood culture-negative endocarditis in a human. J Clin
9. Breitschwerdt EB, Maggi RG, Duncan AW, et al. Bartonella species in Microbiol. 2005;43(2):945.
blood of immunocompetent persons with animal and arthropod con- 19. Heymann DL. Control of communicable diseases manual. 19th ed.
tact. Emerg Infect Dis. 2007;13(6):938. Washington DC: American Public Health Association; 2008.
10. Welch DF, Carroll KC, Hofmeister EK, et al. Isolation of a new subspecies, 20. Boulouis HJ, Chao-chin C, Henn JB, et al. Factors associated with
Bartonella vinsonii subsp. arupensis, from a cattle rancher: identity with the rapid emergence of zoonotic Bartonella infections. Vet Res.
isolates found in conjunction with Borrelia burgdorferi and Babesia microti 2005;36:383.
among naturally infected mice. J Clin Microbiol. 1999;37(8):2598. 21. Rolain JM, Brouqui P, Koehler JE, et al. Recommendations for treatment of
11. Comer JA, Paddock CD, Childs JE. Urban zoonoses caused by Bartonella, human infections caused by Bartonella species. http://www.pubmedcentral.
Coxiella, Ehrlichia, and Rickettsia species. Vector Borne Zoonotic Dis. nih.gov/articlerender.fcgi?artid=415619 Accessed September 11, 2008.
2001;1(2):91. 22. Breitchwerdt E. Personal communication. August 21, 2008.
BRUCELLOSIS
Peter M. Rabinowitz and Lisa A. Conti • Educate the public (especially travelers to endemic
countries) on risk of infection from unpasteurized
Brucellosis due to Brucella melitensis (ICD-10 A23), Brucellosis dairy products.
due to Brucella abortus (A23.1), Brucellosis due to Brucella • Encourage public health measures to avoid consump-
suis (A23.2), Brucellosis due to Brucella canis (A23.3) tion of unpasteurized dairy products.
• Educate hunters of feral swine and other potentially
Other names in humans: undulant fever, Mediterranean infected wildlife (e.g., elk, bison) about infection
fever, Malta fever control precautions, including gloves and protective
clothing while preparing carcasses and burying of all
Other names in animals: Bang’s disease (cattle), epizootic remains to avoid scavenging.
abortion, contagious abortion • If disease is present in livestock population, educate farm-
ers and livestock workers regarding personal protection
Brucellosis is an important bacterial disease of ruminants when handling strain 19 vaccine, potentially infected tis-
worldwide and an occupational disease for humans working sue, and adequate ventilation in abattoir environments.
closely with infected animals. Many human cases are related • Sentinel human cases may indicate problems with food
to foodborne exposures to unpasteurized dairy products. safety, infection in local livestock, or inadequate safety
Brucellosis prevention demands a “One Health” approach controls for workers and require public health follow-up.
between animal and human health disciplines because • Educate local veterinary and human health clinicians
the human health risk can be reduced only by controlling about groups at risk, signs of disease, and to consider
the disease in animals.1 Brucellosis can be passed between the possibility of intentional exposure activity.
domestic cattle and wildlife such as bison, where it can be
difficult to control.
Key Points for Clinicians and Public Health • Screen for exposure risk factors: ingestion of unpas-
Professionals teurized dairy products, contact with potentially
infected animals, recent travel to endemic areas, and
Public Health Professionals animal contact during travel.
• Human cases should immediately be reported to local
• Describe the local incidence and prevalence in health officials.
human, domestic animal, and wildlife populations • When treating human cases, while rarely transmitted
using cooperative veterinary/human disease surveil- person to person, counsel about safe sex precautions
lance systems.2 to prevent secondary transmission.
• In endemic areas, coordinate with local agricultural • Ensure that workers in high-risk occupations (includ-
and wildlife agencies regarding vaccination, testing, ing veterinarians and laboratory workers) are using
and control in domestic livestock and wildlife. appropriate biosafety procedures.
• Consider brucellosis in workup of fever of unknown Between 1986 and 2007, fewer than 150 human cases were
origin. reported annually in the United States.8,9 As a result, many
• Offer PEP and management to exposed laboratory human health clinicians in the United States have never seen
workers and veterinary workers with vaccine exposure. a case. In the United States, the highest incidence rates are
• Counsel patients to avoid consuming unpasteurized in states bordering Mexico, including California and Texas.
dairy products and to use protective clothing (rubber The most common Brucella species for human infections
boots, gloves, goggles) if they must come in contact in the United States are B. abortus and B. melitensis.10 The
with infected livestock, wild ruminants, or wild dogs. occurrence of human brucellosis is higher in other countries
• Consider a 3- to 6-week prophylactic antibiotic course where livestock infection is not as well controlled, including
for a needlestick injury with a veterinary vaccine, labo- Mexico, other Latin American countries, the Mediterranean
ratory, or bioterrorism exposure.3 basin, Eastern Europe, Asia, Africa, and the Middle East. The
• No human vaccine is available. United Nations’ Food and Agriculture Organization has set a
goal for worldwide eradication of brucellosis.
Groups at Risk
• Isolate and screen herd replacements.
• Quarantine infected herds, test and slaughter to eradi- Worldwide, brucellosis is considered largely an occupational
cate infection, and disinfect facility where infected ani- disease of workers exposed to cattle and other large animals
mals have been housed. through animal husbandry, dairy, and slaughter operations.
• Report animals with positive screenings to agriculture Such workers include herdsmen, slaughterhouse work-
officials. ers, and veterinarians. Handling of infected aborted fetuses
• Vaccinate cattle, sheep, and goats against Brucella.* and newborn animals is considered a particularly high-risk
• Ensure proper biosafety procedures are followed in activity. Another risk is sharing living spaces with potentially
veterinary facility and that staff are aware of symptoms infected animals; high rates of brucellosis infection have
of infection. been reported among goat-herding families that bring goats
• If diagnosing animal case, discuss zoonotic risk with into family bedrooms during the winter.11
owner; offer direct communication with human health A rare occurrence among veterinarians is the self-inocula-
clinician caring for family. tion (needlestick, splash or spray to mucous membranes, or
• Disinfect with 1% sodium hypochlorite, 70% ethanol, broken skin) of vaccine strains of Brucella (RB51 or B. abor-
or iodine solutions. Brucella can also be inactivated by tus strain 19, or B. melitensis Rev-1) during animal vaccina-
several hours of direct sunlight.3 Replacement swine tion; this represents one of the rare reported occupational
herds can be placed on ground that has been free of risks of animal vaccination.12 Outbreaks have occurred in
pigs for a minimum of 30 days. laboratory workers who handled Brucella cultures outside
biological safety cabinets,9 and dog handlers are considered
to be at risk from B. canis. However, analysis of recent cases
Agent in the United States indicates that brucellosis is increasingly
Brucellosis is caused by Brucella species, which are gram- a foodborne disease associated with ingestion of unpasteur-
negative coccobacilli. A number of species in the genus have ized dairy products from infected animals.10
affinities for particular animal hosts. These species have been
further subdivided into biologically distinct strains (bio- Hosts, Reservoir Species, Vectors
vars).6 At least four species of Brucella are found in animals
and man; these include Brucella abortus (cattle), B. melitensis The species and biovars of Brucella are adapted to particular
(goats), B. suis (swine),* and B. canis (dogs). There have been animals that serve as definitive hosts. However, as shown in
several reported isolations of bacteria from marine mammals, Tables 9-9 and 9-10, cross-species infections can occur, with
including seals, whales, and dolphins that are currently clas- humans and dogs particularly susceptible to infection by a
sified in the genus Brucella. However, the human zoonotic number of different Brucella species.
potential of these new agents remains to be established.7
Geographical Occurrence Table 9-9 n Hosts for Brucella Species

Brucellosis is found worldwide, but its prevalence depends
Species Animal Hosts
largely on the state of control in domestic animals. In the
United States, bovine brucellosis control programs have Brucella abortus Cattle, elk,13 bison, water buffalo,14
reduced the frequency of infection in both cattle and humans. goats,4 horses,15 dogs,4 coyotes16
Brucella melitensis Goats, sheep, cows, dogs4
*A number of vaccines are available for different animal species. In cattle, Brucella suis Pigs, feral swine and wild boar,
vaccination with B. abortus strain 19 or RB51 increases resistance to infec- horses, cattle,4 dogs4
tion.4 The same vaccines have been used to attempt to control outbreaks in Brucella ovis Sheep
wildlife species, including coyotes, elk, and bison.5 Goats can be vaccinated
with the Revl strain of B. melitensis. There is no vaccine for Brucellosis in Brucella canis Dogs
swine. In dogs, brucellosis vaccine has not been found to be effective.4
Table 9-10 n Brucellosis: Comparative Clinical Presentations in Humans and Other Animals
Species Risk Factors Incubation Period Clinical Manifestations Laboratory Findings
Humans (B. abortus, Ingestion of Variable, usually 5-60 Fever, joint pain, Elevated IgG; other
B. melitensis, B. suis, unpasteurized dairy days20 abdominal pain, laboratory values
B. canis) products, occupational weight loss, fatigue, may be normal
exposure to animal arthritis, endocarditis, or leukopenia,
tissue, fluids, aerosol epididymitis/orchitis thrombocytopenia,
abnormal liver
function may occur;
positive blood culture
Dogs (B. canis, B. abortus, Ingestion of infected tissue Variable, related to stage Usually asymptomatic CBC usually normal,
B. melitensis, B. suis) of gestation, often or vague signs, positive serology,
Sexual contact months but lethargy, positive blood or tissue
Transplacental lymphadenopathy, culture
back pain, weakness,
glomerulonephritis,
discospondylitis may
occur21
Females: abortion,
infertility
Males: Epididymitis,
testicular atrophy
Sheep, goats Direct contact, sexual Variable, related to stage Abortion Positive serology
(B. melitensis, B. abortus) transmission of gestation, often
months
Sheep (B. ovis) Epididymitis
Cattle (B. abortus) Ingestion of Variable, related to stage Abortion, epididymitis, Positive serology,
contaminated tissue, of gestation, often arthritis Brucella ring test
feed, water months
Swine (B. suis) Ingestion of infected Variable, related to stage Abortion, orchitis, Brucellosis card test
tissue, sexual contact of gestation, often spondylitis, sterility4
months
CBC, Complete blood cell count.
with mucous membranes (Figure 9-13). It can also be acquired

by ingestion of contaminated foods. Aerosol transmission
Brucellosis is transmitted by direct contact with infected tissues can easily occur. It is thought that a small number of inhaled
or secretions and enters the body by breaks in the skin or contact organisms can lead to human infection, as seen in outbreaks
Transplacental, sexual contact,

ingestion of contaminated tissue
Infected host animal Nonimmune

(definitive host) host animal
Products of
conception, feces Ingestion
Contaminated environment
(pastures, water, soil)
Direct contact with tissue, secretions,

ingestion of milk or other dairy
products, infected meat or other
tissue, inhalation of aerosol
Human being or other

nonimmune accidental host
Environmental factors: Contamination of water, pastures, climate

Figure 9-13 n Transmission and life cycle of Brucellosis.
of infection among laboratory workers. Brucella consequently

requires biosafety level 3 containment in laboratories.
Transmission in cattle occurs through ingestion of con-
taminated pasture forage or water, as well as through lick-
ing and other direct contact of infected calves, fetuses, and
afterbirths. Transmission in dogs is due to ingestion of or
other contact with contaminated tissue, including sexual
contact. The risk of transmission of brucellosis from dogs to
humans is considered low and related to frequent close con-
tact with blood, birth tissues, or other infected secretions.17
In humans, person-to-person infection has been reported
through breastfeeding, childbirth, bone marrow transplants,
sexual contact, and transfusions, but these modes of trans-
mission are considered exceptional.6

Brucella may survive for months in the environment in water
and other media that are not exposed to direct sunlight or
heat. Pastures can become contaminated by feces, products of
conception, and vaginal discharges of infected animals, lead-
ing to spread of infection in herds of grazing animals. Brucella
organisms have been recovered from cow manure that has
remained in a cool environment for longer than 2 months.4
Disease in Humans
Five to 60 days after infection, Brucella can cause a febrile
illness that may be abrupt or gradual. Symptoms are often
nonspecific and include fever, headache, night sweats, fatigue,
arthralgia, myalgia, joint pain, anorexia, abdominal pain, diar- Figure 9-14 n Radiograph of lumbar spine showing discitis and spon-
dylitis due to brucellosis. Note reduced disk space and the destruction of
rhea, vomiting, and weight loss. Depression may be a prom- articular margins at L3-L4 (arrows). (From Cohen J, Powderly WG: Infectious
inent feature. The fever may be “undulant” in patients who diseases, ed 2, St Louis, 2004, Mosby Elsevier.)
remain untreated. Clinical findings may be unremarkable, but
in 20% to 30% of patients hepatosplenomegaly and/or lymph-
adenopathy may develop. Osteoarticular involvement of the
spine and large weightbearing joints (Figure 9-14) is com-
mon.18 Rarely, more severe infection can lead to epididymi-
tis, orchitis, uveitis, endocarditis, and meningitis. A review of
human cases found B. melitensis was more likely than B. abor-
tus to cause abdominal pain and tenderness, hepatomegaly,
splenomegaly, thrombocytopenia, pancytopenia, and hepatic
dysfunction.10 Laboratory findings are usually mild or absent
but may include elevation of liver function test results, throm-
bocytopenia, and other hematologic abnormalities.
Disease in Animals
In most animals, spontaneous abortion is the most common
manifestation of Brucella infection. Infection may be chronic Figure 9-15 n Fistulous withers in a horse. (From Auer JA: Equine
and poorly responsive to treatment. surgery, ed 3, Philadelphia, 2006, Saunders Elsevier.)
In pregnant cows, B. abortus causes placental infection
leading to abortion in the second half of gestation. It also
causes reduced milk yield, testicular abscesses and epididy Horses develop a rare bursitis condition known as poll evil
mitis in bulls, and (rarely) joint involvement with long- or fistulous withers that may be caused by B. abortus or occa-
standing infection.4 Infection in goats, sheep, and pigs is sim- sionally B. suis (Figure 9-15).4
ilar to that in cattle. In dogs, the most common recognized sign and symptom
In sheep, B. ovis causes epididymitis in rams but abor- are abortion and infertility. Females may have a prolonged
tions and stillbirths in ewes (Color Plate 9-5).4 vaginal discharge following abortion. Lymphadenitis may
be seen. In males, orchitis, epididymitis, and prostatitis may

Table 9-11 n Brucellosis Treatment in Humans
occur. Spondylitis resulting in back pain and weakness, and
uveitis are reported complications (Color Plate 9-6).4 and Other Animals
Cats are apparently resistant to Brucella infection.19 Species Primary Treatment Alternative
Diagnosis Humans (adult or Doxycycline 100 mg Doxycycline 100 mg

child >8 yr23) bid × 6 wk PLUS PO bid PLUS
The differential diagnosis of brucellosis in humans is exten- gentamicin × 7 rifampin 600-
sive and includes other causes of fever, including influenza, days or doxycycline 900 mg PO
100 mg PO bid q24h × 6 wk or
mononucleosis, human immunodeficiency virus (HIV), × 6 wk PLUS trimethoprim-
and malaria. A history of contact with animals, laboratory streptomycin 1 gm sulfamethoxazole
exposure, or consumption of unpasteurized dairy prod- IM q24h × 2-3 wk 1 DS tab (160 mg
ucts should make clinicians suspect brucellosis. Diagnosis TMP) PO qid
× 6 wk PLUS
in humans is based on culturing the organism from blood, gentamicin × 2 wk
bone marrow, or other tissue, and/or serology. Cultures may
be slow to grow and require caution in handling. Elevated Humans Trimethoprim-sulfamethoxazole 5 mg/kg
(child <8 yr) PO q12h × 6 wk PLUS gentamicin 2 mg/kg
immunoglobulin G (IgG) antibodies titers by ELISA or other IV/IM q8h × 2 wk23
tests including serum agglutination (SAT) are often key to
Postexposure Doxycycline 100 mg Trimethoprim-
the diagnosis, as active infection titers often exceed 1:160. prophylaxis PO bid PLUS sulfamethoxazole
Infection with B. canis may produce antibodies that do not rifampin 600 mg (160 mg/800 mg)
react with standard Brucella test antigens; therefore specific PO qd × 3 wk × 3 wk
B. canis serology must be requested if this infection is sus- (doxycycline alone
pected. PCR techniques have shown promising results but if exposed to strain
are still in development.21 B. abortus RB51)9
In dogs, cultures of blood and tissue are also used. Dogs Doxycycline 12-15 mg/kg PO q12h × 4 wk
There are several serological tests. The RSAT test has a PLUS gentamicin 5 mg/kg SC q24h at 0
and 1 wk21
high sensitivity but low specificity. The mercaptoethanol
test also has low specificity; positive results must be con-
firmed by other tests such as the agar-gel immunodiffu-
sion (AGID) test.4 In animals, treatment can be unsuccessful even after
Possible herd infection in cattle is diagnosed using the rolonged administration of antibiotics. Therefore euthanasia
p
Brucella milk ring test, which is sensitive but not specific (Color and culling are often used as a means of brucellosis control.
Plate 9-7).4 Blood samples are collected from slaughtered ani- Animals may still be infectious to other animals (and humans)
mals. Further tests are used to confirm positive results. despite treatment, and this should be considered before
attempting treatment of a pet dog. Neutering of infected dogs
Postexposure Prophylaxis is sometimes performed to achieve infection control.
In cattle, antibiotic treatment is considered practical.4
Following laboratory or vaccine exposure to Brucella spe-
cies, 100 mg of doxycycline twice daily and rifampin 600 mg/
day should be taken for 21 days. Trimethoprin sulfamethox- References
azole is an alternative for those with a contraindication to 1. Zinsstag J, Schelling E, Roth F, et al. Human benefits of animal interven-
doxycycline. Doxycycline alone should be given if the expo- tions for zoonosis control. Emerg Infect Dis. 2007;13(4):527.
sure was to Brucella abortus strain RB51, which is resistant 2. Food and Agriculture Organization (FAO). Guidelines for coordi-
to rifampin.9 Baseline serum drawn for Brucella serology nated human and animal brucellosis surveillance. http://www.fao.org/
docrep/006/y4723e/y4723e00.htm; Accessed September 4, 2008.
with repeat serology at 2, 4, 6, and 24 weeks can be used to 3. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases
monitor for evidence of infection. Such monitoring is not of companion animals. Ames, IA: The Center for food security and public
recommended for exposures to vaccine RB51, which does health, Iowa State University College of Veterinary Medicine; 2008.
not elicit an antibody response on available assays. Exposed 4. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse
pregnant women should consult their obstetric care provider Station, NJ: Merck; 2005.
5. Kreeger TJ, DeLiberto TJ, Olsen SC, et al. Safety of Brucella abortus
regarding PEP. Exposed persons should be monitored on a strain RB51 vaccine in non-target ungulates and coyotes. J Wildl Dis.
regular basis for the development of fever and other clinical 2002;38(3):552.
signs of infection.9 6. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington, DC:
Pan American Health Organization; 2001.
Treatment 7. Godfroid J, Cloeckaert A, Liautard JP, et al. From the discovery of the
Malta fever’s agent to the discovery of a marine mammal reservoir,
Antibiotic therapy for brucellosis infection in humans and brucellosis has continuously been a re-emerging zoonosis. Vet Res.
other animals is outlined in Table 9-11 below. In humans, 2005;36(3):313.
relapse and prolonged convalescence may occur after antibi- 8. Chang MH, Glynn MK, Groseclose SL. Endemic, notifiable bioterrorism-
related diseases, United States, 1992–1999. Emerg Infect Dis. 2003;9:556.
otic treatment. Patients with focal complications including 9. Centers for Disease Control and Prevention. Laboratory-acquired bru-
spinal or neurological involvement may require a more pro- cellosis—Indiana and Minnesota, 2006. MMWR Morb Mortal Wkly Rep.
longed course of treatment. 2008;57(2):39.
10. Stephanie B, Troy SB, Rickman LS, et al. Brucellosis in San Diego epide- 17. Centers for Disease Control and Prevention. Brucellosis. http://www.
miology and species-related differences in acute clinical presentations. cdc.gov/ncidod/dbmd/diseaseinfo/Brucellosis_g.htm#mydog. Accessed
Medicine. 2005;84:174. July 27, 2008.
11. Acha PN, Szyfres B. Zoonoses and communicable diseases common to 18. Mandell GE, Bennett JE, Dolin R. Principles and practice of infectious dis-
man and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington eases. 6th ed. Philadelphia: Churchill Livingstone; 2000.
DC: Pan American Health Organization; 2001. 19. Colville J, Berryhill D. Handbook of zoonoses: identification and preven-
12. Berkelman RL. Human illness associated with use of veterinary vaccines. tion. St Louis: Mosby Elsevier; 2007.
Clin Infect Dis. 2003;37(3):407. 20. Heymann DL. Control of communicable diseases manual. 19th ed.
13. Rhyan JC, Aune K, Ewalt DR, et al. Survey of free-ranging elk from Washington DC: American Public Health Association; 2008.
Wyoming and Montana for selected pathogens. J Wildl Dis. 1997;33:290. 21. Barr SC, Bowman DD. 5-Minute veterinary consult clinical companion
14. Nishi JS, Stephen C, Elkin BT. Implications of agricultural and wildlife canine and feline infectious disease and parasitology. Baltimore: Wiley-
policy on management and eradication of bovine tuberculosis and bru- Blackwell; 2006.
cellosis in free-ranging wood bison of northern Canada. Ann N Y Acad 22.Vrioni G, Pappas G, Priavali E, et al. An eternal microbe: Brucella
Sci. 2002;969:236. DNA load persists for years after clinical cure. Clin Inf Dis. 2008;
15. Acosta-Gonzalez RI, Gonzalez-Reyes I, Flores-Gutierrez GH. Prevalence 46(12):e131.
of Brucella abortus antibodies in equines of a tropical region of Mexico. 23. Gilbert DN, Moellering RC Jr, Eliopoulos GM, et al. The Sanford guide
Can J Vet Res. 2006;70:302. to antimicrobial therapy, 2009. 39th ed. Sperryville, VA: Antimicrobial
16. Davis DS, Boeer WJ, Mims JP, et al. Brucella abortus in coyotes. I. Therapy; 2009.
A serologic and bacteriologic survey in eastern Texas. J Wildl Dis.
1979;15(3):367.
CAMPYLOBACTERIOSIS
Peter M. Rabinowitz and Lisa A. Conti • Educate food handlers to avoid cross-contamination
of foods—use separate cutting boards.
Campylobacter enteritis (ICD-10 A 04.5) • Pursue public health measures to control local con-
sumption of unpasteurized dairy products.
Other names in humans: Campylobacter enteritis, vibriosis • Prevent infected health care workers from providing
direct patient care.
Other names in animals: bovine genital campylobacteriosis, • Educate local human health and veterinary clinicians
vibriosis, epizootic infertility, epizootic ovine abortion and public about risk of infection in puppies and
kittens. Stress the need for handwashing and other
Campylobacter species (C. jejuni and C. coli) are now con- hygiene after contact with pets and poultry. Prevent
sidered the leading cause of bacterial enteritis in humans children from handling sick animals.
(Campylobacter enteritis).1 They are also found in a large • Work with agricultural agencies and local farms to
number of animal species. Collaborative research between reduce incidence of Campylobacter in poultry at all
human health and veterinary researchers led to the rela- phases of rearing and production.
tively recent discovery of Campylobacter species as significant • Educate local veterinary and human health clinicians
human pathogens. Improving diagnostic methods continue about groups at risk and symptoms of disease and
to shed light on the prevalence and clinical importance of importance of handwashing for people with diarrhea.
Campylobacter species, including the high zoonotic potential • Coordinate with agriculture officials and veterinarians to
of these agents. receive information about outbreaks of C. fetus in local
Campylobacter fetus is associated with less common, but livestock herds so that agricultural workers can be edu-
severe, infections in immunocompromised persons. Cattle, cated about disease and need for biosafety on farms.
sheep, and goats are generally infected by contact with repro-
ductive discharges and feces. C. fetus also is a sexually trans-
mitted disease among cattle. Traditional culture methods Human Health Clinicians
for other Campylobacter may not detect C. fetus; therefore
its true clinical importance remains poorly understood and • Report cases to health department if required in state.
probably underestimated. • Interview infected individuals about exposure risk
factors, such as recent travel to developing country;
ingestion of unpasteurized dairy products or under-
cooked meat; and contact with poultry or poultry
Key Points for Clinicians and Public Health products, dogs and cats (especially kittens and pup-
Professionals pies), or other potentially infected animals. Notify
public health authorities of ongoing risk to other
Public Health Professionals humans.
• Counsel immunocompromised patients to avoid con-
• Educate public (especially travelers to endemic coun- tact with puppies, kittens, dogs, and cats with diarrhea;
tries) on the risk of infection from untreated drinking poultry; unpasteurized dairy products; or undercooked
water, unpasteurized dairy products, and uncooked meat.
poultry, including handwashing and food preparation • When treating an infected human, ensure enteric
precautions. infection control precautions are used. Exclude the
symptomatic individual from food handling or care of placentas and fetuses), and that staff are aware of
sick individuals or contact with immunocompromised symptoms of infection.
individuals. Stress proper hand hygiene. • Quarantine infected animals. Ensure proper treatment
• Ensure that workers in high-risk occupations (includ- of bulls if indicated.
ing poultry workers and veterinarians) use appropriate • No animal vaccine is currently available for enteritis,
biosafety procedures, including handwashing. but C. fetus bacterin can prevent abortions in sheep
• A candidate vaccine has been developed by the Navy and genital campylobacteriosis in cattle.4
Medical Research Institute.2
Agent
Veterinary Clinicians Campylobacter species are spiral, S-shaped, or curved, gram-
negative rods (Figures 9-16, 9-17, and 9-18). More than 20
• If treating an infected animal, counsel owner regarding strains have been described, including C. jejuni, C. coli,
zoonotic risk and need for adequate handwashing and C. upsaliensis, C. larii, C. fetus, and C. helveticus.5 Most cases
disposal of feces. Offer direct communication with of Campylobacter enteritis in humans are believed to be due
human health clinician caring for family. to C. jejuni or C. coli. However, when more sensitive isola-
• Discourage feeding raw diets to pets or allowing pets to tion techniques are used, some cases have been found to be
hunt.
• Exclude wild birds and rodents and control insects
from poultry facilities.
• Ensure disinfection of kennel or other facility where
infected animals have been housed. Disinfectants
include 1% sodium hypochlorite, 70% ethanol, 2%
glutaraldehyde, and iodine-based solutions.3
• Ensure proper biosafety procedures are followed in
veterinary facility or farm (e.g., sterilization of instru-
ments used on possibly infected animals, proper dis-
posal of potentially infected tissue such as aborted
Box 9-1 Case Study: Campylobacter jejuni
Campylobacter jejuni was diagnosed in a child by her physician.

The child was exposed to a puppy that was mildly ill a few weeks
previously and recovered fine. No specific diagnostic tests were
performed on the puppy; it was treated symptomatically and
recovered. The physician is concerned about the possibility of the
puppy being the source of the Campylobacter. The puppy has had
all routine dewormers and vaccinations and is in good health now.
Question/concern: The puppy is part of a much larger group
of dogs and puppies (~100) that are currently being rehabilitated
in foster homes. All were mixed together when they were removed
Figure 9-16 n Campylobacter species viewed by dark-field microscopy.
from a common source environment several months ago. There
Note the chaining of individual organisms, which are often mistaken for spi-
have been no reports of diarrhea in other puppies or human rochetes. (From Songer JG, Post KW: Veterinary microbiology: bacterial and
household members among children or parents caring for the pup- fungal agents of animal disease, St Louis, 2005, Saunders Elsevier. Courtesy
pies over the past several months. Would a fecal culture now reveal J. Glenn Songer.)
Campylobacter? Would there be any value in screening other pup-
pies, or should we just have Campylobacter on the differential and
perform appropriate diagnostics should any other puppies become
ill in the future?
Response: There have been several studies demonstrating the
link of Campylobacter and illness in children. The population
attributable risk is in the range of 5% to 7%. Campylobacter shed-
ding is more frequent in kittens and puppies versus adult animals.
At least in kittens, an average carriage of about 4 to 6 weeks was
observed (unknown in dogs). Treatment for animals with diarrhea
is appropriate because it likely decreases the days of shedding and
the number of organisms shed. Appropriate hand hygiene is criti-
cal in households with foster puppies. Treatment for asymptom-
atic dogs would probably not be appropriate (because of antibiotic
resistance issues) even though a fair number of puppies and kittens
shed Campylobacter when they are asymptomatic. Likely the quan-
tity of organisms is less, and studies seem to support contact with
dogs with diarrhea as a source.23 Figure 9-17 n Electron micrograph of Campylobacter. (From Centers
for Disease Control and Prevention, Atlanta, Ga.)
identified have been drinking unpasteurized milk, con-

tact with farm animals, and eating poultry in restaurants.11
Campylobacter is an important cause of travelers’ diarrhea in
travelers to countries with poor sanitation (Color Plate 9-8).
Ownership of cats and dogs (especially puppies and kittens)
is considered a risk factor for infection, although the extent
of pet-to-human transmission remains unknown.12
Most human cases of C. fetus to date have occurred in
immunocompromised persons, although cases in healthy
individuals have been recorded.13 Risk factors include
hepatic cirrhosis, HIV infection, diabetes, and systemic lupus
erythematosus.

C. jejuni and C. coli occur across a range of species and par-
ticular strains appear able to cross species barriers. Surveys
Figure 9-18 n Campylobacter species: canine fecal smear (Wright’s of poultry, such as chickens and turkeys, have found coloni-
stain, ×100). Fecal smear shows numerous Campylobacter species organisms
(lighter-staining smaller bacteria), a mixed population of bacterial rods, and
zation rates up to 100%, and contaminated chicken meat is
two degenerating neutrophils. The characteristic “gull wing” formations (visi- considered a major source of infection for humans.
ble on the surface of the neutrophil) are chains of three to five of these slender, A survey of dogs and cats in Switzerland found coloniza-
gram-negative, comma-shaped, or curved motile rods. The organisms have tion rates of 41% in dogs and 42% in cats.14 A Taiwan survey
the same morphologic characteristics in all species of animals. Campylobacter reported higher rates in stray dogs versus nonstrays.15
are often overlooked because of their small size. Animals can be carriers, in
which case usually only very low numbers are seen. These organisms can C. fetus is widespread in cattle and sheep. It also occurs in
be either the primary cause of diarrhea or act as secondary pathogens in reptiles. Unlike C. jejuni, it is not commonly recognized in
conjunction with other enteric bacteria. Campylobacter species are difficult to poultry, and therefore poultry may not be a major source of
culture. Neutrophils are not seen in normal stool and indicate an active infec- human infection.16
tion. (From Quesenberry K, Carpenter JW: Ferrets, rabbits and rodents: clinical
medicine and surgery, ed 2, St Louis, 2004, Saunders Elsevier.)
caused by C. larii and C. fetus. Fluoroquinolone-resistant C. jejuni and C. coli are transmitted by consumption of con-
Campylobacter infections are more likely to be severe with taminated food, such as undercooked poultry or unpasteurized
bloody diarrhea. dairy products. It can also be transmitted by fecal-oral contact
C. fetus is a gram-negative, motile bacteria. Based on cur- (Figure 9-19). Waterborne transmission is also possible.
rent knowledge, it has distinctive epidemiological and clini- The source of many human C. fetus infections is unknown,
cal features. C. fetus has a tendency to invade the vascular and the mechanism of transmission from animals to humans
endothelium6 in humans and is an opportunistic pathogen remains unclear.8 In cattle, C. fetus venerealis is a sexually trans-
causing mainly systemic infection. In animals, Campylobacter mitted disease. However, cows and ewes may be chronically
fetus subspecies fetus (intestinalis) is thought to be primar- infected and may have colonization of the gallbladder, leading
ily an intestinal pathogen (although it has been associated to fecal elimination. In sheep transmission is fecal-oral, with
with infertility4), whereas C. fetus venerealis infects the geni- sexual transmission apparently not playing a role.8
tal tract. Selective media used to culture other Campylobacter
species use antibiotics that may inhibit C. fetus.7 C. fetus also Environmental Risk Factors
grows at a lower incubation temperature (25° C vs. 42° C)
than other Campylobacter species.8 Normal isolation tech- Environments contaminated by poultry manure, such as
niques may not detect C. fetus, and as diagnostic methods occurs in backyard poultry rearing, could propagate C. jejuni
improve, our understanding of Campylobacter infections and C. coli infection. Because Campylobacter organisms can
will continue to evolve. survive in water, the bacteria circulate in wild bird popula-
tions such as waterfowl and shorebirds.17 Surface water can
become contaminated with infected feces of wild and domes-
Geographical Occurrence
tic birds; therefore pollution of water bodies is a potential
C. jejuni, C. coli, and C. fetus are found worldwide. In the source of infection.
developing world, C. jejuni and C. coli infections are consid- Transmission of C. fetus in sheep and cows is thought to
ered to be mostly diseases of young people. The incidence of involve environmental contamination of grazing areas by
C. fetus in humans is uncommon but believed to be much infected tissues and feces.8
higher than recorded.8
Disease in Humans
Groups at Risk
Campylobacter enteritis in humans is an acute but usu-
Because poultry flocks have high rates of colonization with ally self-limited diarrheal illness characterized by abdomi-
Campylobacter, persons engaged in poultry raising and pro- nal cramping, diarrhea, and fever. The incidence is higher
cessing are at increased risk of infection.10 Other risk factors among infants and young adults ages 15 to 44 years.
Due to Campylobacter jejuni or Campylobacter coli
Infected feces; ingestion

Infected host animal Host animal
of contaminated tissue,
(definitive host) (including human being)
milk, or water supplies
Due to Campylobacter fetus
Environmental contamination
by placental tissue, feces from Ingestion Sheep, cattle, goats
poultry or other infected animal
Infected host animal

Sexual transmission (cattle) Cattle
(cattle, sheep, goats)
Human being
Ingestion of
contaminated tissue (?)
Environmental factors: Contamination of water supplies

Figure 9-19 n Life cycle, campylobacteriosis.
In many cases, blood or mucus is noted in the feces, indica

Disease in Animals
ting colorectal inflammation.18 The abdominal pain may
mimic appendicitis. Usually the diarrhea resolves after sev- Campylobacter may be present in animals without signs or
eral days without specific treatment, but other symptoms it may cause diarrhea. Adult animals and poultry older than
may persist longer. 1 week are usually subclinical carriers.3,18,19 The diarrhea is
Bacteremia and other extraintestinal manifestations are usually most severe in young animals (e.g., in puppies and kit-
rare, but complications of infection may include erythema tens from birth to 6 months) or in debilitated animals.4,20 The
nodosum, uveitis, meningitis, and reactive arthritis. Guillain- diarrhea can range from watery to mucus with blood or bile
Barré syndrome occurs in approximately 1 of 1000 cases of streaking. Affected animals may have reduced appetite and,
C. jejuni infection.19 rarely, vomiting. Tenesmus is common. Diarrhea also occurs
C. fetus is an opportunistic pathogen in humans typically after infection in cattle (especially calves), primates, ferrets, and
presenting as an acute or chronic bacteremia or thrombophle- mink.4 In sheep, C. jejuni infection is associated with abortion
bitis. Complications include myocarditis, endocarditis, men- (Color Plate 9-9).21
ingitis, and abortion (Figure 9-20). C. fetus is an important cause of infertility and abor-
tions in cattle and sheep. In cattle, bovine genital campy-
lobacteriosis presents with early fetal death, infertility, and
abortion.4
Table 9-12 shows comparative clinical presentations of
campylobacteriosis in humans and other animals.
Diagnosis
Diagnosis in humans is based on culturing the organism
from feces, blood, bone marrow, or other tissue using correct
media and incubation procedures. It should be recognized
that the selective media may inhibit the growth of certain
Campylobacter species such as C. fetus, leading to false-negative
results. Identification of organisms in feces using phase-contrast
or dark-field microscopy can be used to make a presumptive
diagnosis.5 PCR techniques have recently been developed and
may play a greater role in diagnosis in the future.
In animals, cultures and microscopic examination of feces
Figure 9-20 n Human cardiac abscess from C. fetus bacteremia. AB,
Abcess; RA, right atrium; RV, right ventricle; TV, tricuspid valve. (From
or reproductive discharges are also used. Agglutination and
Peetermans WE, De Man F, Moerman P et al: Fatal prosthetic valve endo- ELISA tests are used on vaginal mucus of cows suspected to
carditis due to Campylobacter fetus, J Infect Dis 41(2):180, 2000.) be infected.
Table 9-12 n Campylobacteriosis: Comparative Clinical Presentations in Humans and Other Animals
Humans (Campylobacter Infants and young adults; 2-5 days18 Diarrhea, often with mucus Fecal leukocytes, organisms
jejuni, C. coli) travelers to developing or blood, abdominal seen on Gram stain, dark-
countries; ingestion of cramping, fever field or phase-contrast
contaminated meat, microscopy of feces, fecal
unpasteurized dairy culture
products; occupational
exposure to animal
feces, exposure to sick
or colonized pet
C. fetus Immunocompromised, 3-5 days Gastrointestinal symptoms, Blood culture
diabetes, cirrhosis bacteremia, endocarditis
infection, SLE, cancer
Dogs, cats, cattle, Ingestion of contaminated 3 days4 Diarrhea, usually mild, may CBC may show
sheep, chickens, food or water have mucus or blood; loss leukocytosis
turkeys, mink, ferrets, Young animals, stressed of appetite, occasional Fecal leukocytes,
pigs, nonhuman or debilitated animals at vomiting, and fever8 organisms seen on Gram
primates, others increased risk In sheep, abortion near end stain or phase-contrast
(C. jejuni, C. coli) of pregnancy, stillbirth16 microscopy of stool, fecal
Mastitis in cattle culture
Sheep (C. fetus) Ingestion of infected 7-25 days Abortion near end of Dark-field and phase-
material pregnancy, stillbirth8 contrast microscopy
of placenta, fetal
abomasums, and uterine
discharge3
Cattle (C. fetus) Ingestion of infected Subclinical carriage Vaginal mucus
material, sexual Endometritis, embryonic agglutination test, ELISA
transmission death, prolonged estrous test of vaginal mucus
cycles, abortions
CBC, Complete blood cell count; SLE, systemic lupus erythematosus.
Treatment
Table 9-13 n Campylobacteriosis Treatment in
Treatment in Humans Humans and Other Animals
Most human enteritis cases are self-limited and resolve Primary

with only supportive therapy such as replacement of fluid Species Treatment Alternative
and electrolytes, lactose-free diet, and avoidance of caffeine.
Humans (adults) Azithromycin mg Erythromycin stearate
Antibiotic treatment is reserved for more severe cases, (Campylobacter PO q24h x 3 500 mg PO qid x
including six or more unformed stools per day, and/or tem- jejuni) days 5 days
perature of 101.5° F or more, and significant persistent tenes-
(C. fetus) Gentamicin Ampicillin,
mus, stool blood, and leukocytes. Immunocompromised chloramphenicol,
patients (e.g., individuals who are HIV positive) should be erythromycin9
treated with antibiotics to prevent systemic complications18 Dog and cat Erythromycin Tylosin 11 mg/
Treatment in humans is outlined in Table 9-13. Although in (C. jejuni, C. coli) 10-20 mg/kg PO kg PO q8h × 7
the past ciprofloxacin has been used as a primary therapeutic q8h × 5 days days or neomycin
agent, high rates of resistance to fluoroquinolones have been 10-20 mg/kg PO
observed in certain settings.22 q8h × 5 days13
Bull (C. fetus) Streptomycin Tylosin 11 mg/
20 mg/kg SC, kg PO q8h × 7
1-2 treatments, days or neomycin
Treatment in Animals streptomycin 10-20 mg/kg PO
As in humans, many enteritis cases in dogs and cats are self- in oil-based q8h × 5 days
suspension
limited. When signs are severe (e.g., high fever or dehydration), applied to the
persist beyond 5 days, or are present in immunocompro- penis × 3 days
mised patients, treatment with antibiotics is recommended.
Erythromycin is the drug of choice.20 Antibiotics may pre- 11. Friedman CR, Hoekstra RM, Samuel M, et al. Emerging Infections
vent abortions in sheep or prevent the spread of genital Program FoodNet Working Group. Risk factors for sporadic
Campylobacter infection in the United States: a case-control study in
campylobacteriosis by treating infected bulls.3 Good hygiene FoodNet sites. Clin Infect Dis. 2004;38(suppl 3):S285.
is critical for prevention. In cattle herds, antibiotic treatment 12. Damborg P, Olsen KE, Moller Nielsen E, et al. Occurrence of
is not considered practical.4 Campylobacter jejuni in pets living with human patients infected with
C. jejuni. J Clin Microbiol. 2004;42(3):1363.
13. Zonios DI, Panayiotakopoulos GD, Kabletsas EO, et al. Campylobacter
References fetus bacteraemia in a healthy individual: clinical and therapeutical
implications. J Infect. 2005;51(4):329.
1. Altekruse SF, Stern NJ, Fields PI, et al. Campylobacter jejuni—an emerging 14. Wieland B, Regula G, Danuser J, et al. Campylobacter spp. in dogs and
foodborne pathogen. Emerg Infect Dis. 1999;5(1):28. cats in Switzerland: risk factor analysis and molecular characterization
2. World Health Organization. http://www.who.int/vaccine_research/ with AFLP. J Vet Med. Series B 2005;52(4):183.
diseases/diarrhoeal/en/index2.html. Accessed May 12, 2009. 15. Tsai HJ, Huang HC, Lin CM, et al. Salmonellae and campylobacters
3. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic in household and stray dogs in northern Taiwan. Vet Res Comm.
diseases of companion animals. Ames, Iowa: The Center for Food 2007;31(8):931.
Security and Public Health, Iowa State University College of Veterinary 16. Kempf I, Dufour-Gesbert F, Hellard G, et al. Broilers do not play a dom-
Medicine; 2008. inant role in the Campylobacter fetus contamination of humans. J Med
4. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse Microbiol. 2006;55(Pt 9):1277.
Station, NJ: Merck; 2005. 17. Waldenstrom J, On SL, Ottvall R, et al. Species diversity of campy-
5. Heymann DL. Control of communicable diseases manual. 19th ed. lobacteria in a wild bird community in Sweden. J App Microbiol.
Washington DC: American Public Health Association; 2008. 2007;102(2):424.
6. Peetermans WE, De Man F, Moerman P, van de Werf F. Fatal prosthetic 18. Butzler JP. Campylobacter, from obscurity to celebrity. Clin Microbiol
valve endocarditis due to Campylobacter fetus. J Infect. 2000;41(2):180. Infect. 2004;10(10):868.
7. Kalka-Moll WM, Van Bergen MA, Plum G, et al. The need to differenti- 19. Allos BM. Association between Campylobacter infection and Guillain-
ate Campylobacter fetus subspecies isolated from humans. Clin Microbiol Barré syndrome. J Infect Dis. 1997;176(suppl 2):S125.
Infect. 2005;11(4):341. 20. Barr SC, Bowman DD. 5-Minute veterinary consult clinical companion
8. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man canine and feline infectious disease and parasitology. Baltimore, MD:
and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington DC: Pan Wiley-Blackwell; 2006.
American Health Organization; 2001. 21. Colville J, Berryhill D. Handbook of zoonoses: identification and preven-
9. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti- tion. St Louis: Mosby Elsevier; 2007.
microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy; 22. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti-
2009. microbial therapy 2007. 37th ed. Sperryville, VA: Antimicrobial Therapy;
10. Potter RC, Kaneene JB, Hall WN. Risk factors for sporadic Campylobacter 2007.
jejuni infections in rural Michigan: a prospective case-control study. Am 23. NASPHV listserv. Personal communication, August 2008.
J Public Health. 2003;93(12):2118.
CHLAMYDOPHILA PSITTACI AND RELATED INFECTIONS
Peter M. Rabinowitz and Lisa A. Conti New molecular evidence is broadening our understanding
of the host range and clinical spectrum of Chlamydophila
Chlamydophila psittaci and related infections (ICD-10 infections.2 Therefore clinicians should maintain a high
A70 Psittacosis; ICD-10 A74 Other diseases caused by index of suspicion in the appropriate settings where
chlamydiae) infection can occur.
Other names in humans: psittacosis, ornithosis, chlamydio- Key Points for Clinicians and Public Health
sis, parrot fever Professionals
Other names in animals: avian chlamydiosis; mammalian
chlamydiosis, chlamydial conjunctivitis, feline chlamydial Public Health Professionals
pneumonitis, septic abortion of sheep and goats
• Characterize the risk in the community related to
Chlamydophila (formerly Chlamydia) psittaci infection pet shops, aviaries, bird ownership, and poultry
from exposure to birds causes disease in humans rang- production.
ing from mild flulike signs to severe pneumonia and sep- • Become familiar with the National Association of State
sis. Although fewer than 50 human cases of psittacosis are Public Health Veterinarians Compendium of Measures to
reported yearly in the United States,1 it is likely that many Control Chlamydophila psittaci Infection Among Human
cases go undetected. C. psittaci commonly infects psitta- Beings (Psittacosis) and Pet Birds (Avian Chlamydiosis).3
cine (parrot family) birds that are used as pets, but domes- These measures are summarized in Box 9-2.
tic poultry flocks, especially turkeys and ducks, can develop • Conduct an investigation of human cases, includ-
widespread infection with significant flock mortality and ing surveillance of pet shops and poultry farms, to
occupational risk to poultry workers. Human disease detect sources of infection and other human cases. If
with mammalian chlamydiae (i.e., C. abortus, C. felis, and infected birds are found, ensure that they are treated
C. pneumoniae) is rarely reported. The diagnosis of chla- or destroyed and the area is decontaminated with a
mydiosis can be challenging in humans and other animals. disinfectant.4
Box 9-2 Measures for Psittacosis Prevention
Adapted from Compendium of measures to control Chlamydophila psittaci infection among human beings (psittacosis) and pet birds (avian chlamydiosis), 2008, National Association
of State Public Health Veterinarians.
• Coordinate with agriculture officials to control the Veterinary Clinicians

disease in bird populations.
• Ensure that poultry workers with occupational risk for • Counsel bird owners on the signs of psittacosis, how to
C. psittaci infection are informed about the disease and protect their birds from exposure, and how to reduce
its prevention through exposure controls and protec- risks to humans, especially if owners are immuno
tive equipment. compromised.
• Consider the diagnosis of chlamydiosis in any sick
bird with lethargy and nonspecific signs, especially if
recently purchased or stressed (e.g., transported).
• Consider the diagnosis in all patients with bird contact • Follow local and state reporting regulations; con-
(avian chlamydiosis) who present with respiratory tact local health department or Department of
symptoms or fever, as well as patients with keratocon- Agriculture.
junctivitis (or rarely endocarditis and glomerulone- • Train veterinary personnel in biosafety measures,
phritis) and cat contact (mammalian chlamydiosis). such as wearing masks and gloves when working with
• Report suspected cases to public health authorities. See potentially infected birds, and use of strict personal
CDC case definition: http://www.cdc.gov/ncphi/disss/ hygiene (e.g., handwashing and cleaning/disinfecting
nndss/casedef/psittacosiscurrent.htm. footwear) to prevent spreading the organism to other
• Counsel patients with psittacine birds to take steps to animals.
protect their birds from exposure to C. psittaci and to • If a case is diagnosed in a cat, immunize cats in the
seek veterinary care for ill birds, especially if owners are household or cattery using C. psittaci vaccine. A live C.
immunocompromized. Other risk reduction measures abortus vaccine may reduce shedding in sheep.
include avoiding mouth-to-beak contact and appropri-
ate personal protective equipment (PPE) when cleaning Agent
cages or handling dead birds (see Box 9-2).
• If caring for workers with occupational exposure C. psittaci is an intracellular bacterium closely related to
to birds (e.g., pet shop workers, poultry workers), the human pathogen Chlamydia trachomatis (causes vene-
ensure that they immediately report symptoms of real infection in humans) and other zoonotic Chlamydiae
fever, myalgias, and cough, and that the workplace is (Table 9-14). A number of different strains (serovars) of C.
adopting preventive practices (see Box 9-2), including psittaci have been described; the majority are avian patho-
respiratory protection for workers who are working gens. The strains vary in virulence and zoonotic poten-
with ill or potentially exposed birds. tial; for example, the turkey strain may be more virulent
• Counsel pregnant patients to avoid contact with preg- than serovars that affect pigeons and ducks.5 Mammalian
nant or aborting sheep and goats. strains of zoonotic Chlamydiaceae are Chlamydophila felis
Table 9-14 n Comparison of Classification of Chlamydophila and Chlamydia
Hosts Preferential Tissues Before 1999 After 1999
Chlamydophila
Birds Genital, lung, internal organs Chlamydia psittaci psittaci
Cattle, sheep Brain, eye, joints Chlamydia pecorum pecorum
Humans, koalas, horses Lung, joints, endothelial Chlamydia pneumoniae pneumoniae
Sheep, mammals Intestines, placenta Chlamydia psittaci abortus
Guinea pigs Bladder, eye, spleen Chlamydia psittaci caviae
Cats Eye, genital, joints, lungs Chlamydia psittaci felis
Chlamydia
Humans Ocular and urogenital, neonatal lung Chlamydia trachomatis trachomatis
Rodents Many internal organs Chlamydia trachomatis muridarum
Swine Eye, intestines, lung Novel species suis
Adapted from Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier.
(formerly Chlamydia psittaci, feline strain, causes conjuncti- rate of fulminant diseases in birds. Wildlife may serve as a
vitis in cats), C. abortus (formerly Chlamydia psittaci, mam- reservoir and pose an infectious threat to domestic poultry.5
malian abortion strain or serotype 1, causes abortion in
ruminants, especially sheep and goats), and C. pneumoniae Mode of Transmission and Life Cycle
(formerly Chlamydia pneumoniae, previously considered a
human pathogen, but has been isolated from horses, reptiles, Chlamydiae exists in two forms, an infectious but metaboli-
and amphibians).6 cally inactive elementary body that is relatively stable in the
The CDC considers C. psittaci a category B biological war- environment, and the metabolically active but noninfectious
fare agent because of its ability to be produced and dissemi- reticulate body (Figure 9-21).5 Infection is initiated by the
nated in quantities sufficient to affect large populations.7 elementary body attaching to susceptible cell membranes,
primarily in the respiratory and later gastrointestinal tracts.13
Transformation of the elementary body to the reticulate body
Geographical Occurrence occurs within several hours, after which the reticulate body
Worldwide. creates progeny that differentiate into elementary bodies and
are released from infected cells. The bacteria can be shed in
the feces, leading to fecal-oral transmission5; in addition,
Groups at Risk nasal, ocular, and uterine discharges can lead to direct inocu-
Groups at increased risk for C. psittaci infection include lation into mucous membranes or aerosol transmission.
owners of birds, pet store workers, veterinarians, zookeepers, Bird species implicated in zoonotic aerosol transmission
live poultry and poultry processing workers, and diagnostic include psittacine birds, poultry, shorebirds, and raptors.3
laboratorians. Recent studies have found seroprevalence rates Direct handling of an infected bird or cat followed by self-
as high as 15% in workers at pet bird breeding facilities.8 inoculation of conjunctiva or other mucous membranes is
Seroprevalence rates of 15% have been reported in live- another potential route of animal-human transmission, as
stock farmers.9 Pregnant women have developed severe infec- is beak-to-mouth contact (kissing a pet bird). Person-to-
tion with C. abortus, including sepsis, stillbirth, and abortion person transmission has been reported in close contacts of
after contact with birth products of sheep and goats, but infected persons.14
such cases are considered rare.10
Hosts, Reservoir Species, Vectors Under certain conditions, the bacterial elementary body can
C. psittaci occurs in most birds. One serovar is found in a persist for prolonged periods in the environment. This can
wide range of psittacine birds, including parrots, parakeets, lead to reinfection of poultry flocks or pet birds through
and cockatiels (Color Plate 9-10). Another infects turkeys both oral and respiratory routes.
and ducks and, rarely, chickens. Certain Chlamydiae infect
mammals, and a high rate of subclinical carriage has been Disease in Humans
reported in rodents.11 Prevalence rates of 5% to 10% in cats
have been reported, and exposure to infected cats has been C. psittaci can cause an acute febrile syndrome with head-
linked to human infection.12 ache, myalgias, cough, and photophobia. Respiratory
Many animals shed the organisms in the absence of clini- symptoms may be mild in relation to the chest x-ray find-
cal signs. Crowding and other stressors appear to increase the ings, which may appear worse than the patient’s condi-
Susceptible
Infected bird
Direct contact with secretions, human being
beak-mouth contact
Feces, nasal or Inhalation of

ocular secretions aerosolized bacteria
Contaminated
environment
Ingestion, inhalation
Susceptible bird
Environmental Stress, crowding Poor sanitation, ventilation

factors:
Figure 9-21 n Life cycle, Chlamydophila psittaci infection.
tion appears (Figure 9-22). Sputum production is often Many aspects of the disease remain incompletely under-
scant. Hepatomegaly and pharyngeal erythema often stood, including an association with ocular adnexal
occur. The pulse may be paradoxically slow in relation to lymphoma, and indolent lymphoma from chronic avian
the degree of fever. Skin signs include Horder’s spots, a chlamydiosis.10,16,17 These associations, if true, may lead to
pink, blanching maculopapular rash.15 Keratoconjunctivitis preventive therapies for these lymphomas.
has been reported in cases of contact with infected cats.15 Severe complications including sepsis, stillbirth, and mis-
Complications of infection include hepatitis, splenomegaly, carriage can develop in pregnant women infected with
hemolytic anemia, disseminated intravascular coagulation C. abortus from contact with pregnant sheep and goats.18
(DIC), endocarditis, myocarditis, pericarditis, and glomer- The role of other Chlamydiae and Chlamydia-like organisms
ulonephritis. Neurological complications including hearing in obstetrical pathology is emerging.19
loss, cranial nerve palsy, cerebellar symptoms, and confu-
sion can also occur. Disease in Animals
In more severe cases, progressive pneumonia and acute
respiratory distress syndrome (ARDS) develop with multio- Many birds and mammals shed Chlamydiae without any
rgan failure. Infection in pregnancy can cause severe com- signs. However, C. psittaci can cause morbidity and mortal-
plications including DIC and fetal death. Past infection does ity in psittacine birds, with malaise, weight loss, diarrhea,
not appear to confer subsequent immunity.15 and conjunctivitis. Stress and crowding appear to increase
the prevalence of clinical disease.5 As in humans, previously
infected animals may become reinfected.
Cats typically develop conjunctivitis and mild upper
respiratory disease. Conjunctivitis may also be seen in other
species (Figures 9-23 and 9-24). Kittens 2 to 6 months old
are more likely to be infected. C. abortus is a major cause
of reproductive failure and abortion in sheep and goats.
Chlamydial infection has been associated with horses with
recurrent airway obstruction.20 Table 9-15 provides clini-
cal presentations of chlamydiae infections in humans and
other animals.
Diagnosis
The differential diagnosis in humans includes other causes
of atypical pneumonia, including Legionella, Mycoplasma,
C. pneumoniae, Coxiella, and influenza. The clinical presen-
tation of an atypical pneumonia in the setting of a history
Figure 9-22 n Chest radiograph of a 9-year-old girl with a 2-week of exposure to birds should lead clinicians to strongly con-
history of fever, headache, and hacking cough. She was the caretaker of the sider the diagnosis of psittacosis.
family’s cockatoo. Serum complement fixation antibody titer for C. psittaci
was 1:256. (From Long SS, Pickering LK, Prober CG (eds): Principles and Confirmation of the diagnosis is usually by serology, using
practice of pediatric infectious diseases, ed 3, Philadelphia, 2008, Saunders either complement fixation or microimmunofluorescence
Elsevier. Courtesy of S.S. Long.) (MIF). Serology specimens should be obtained acutely and
Figure 9-24 n Severe conjunctivitis and periocular edema in a Morelet’s

crocodile (Crocodylus moreletii). (From Bewig M: Manual of exotic pet prac-
Figure 9-23 n Acute Chlamydia species conjunctivitis in a heifer. (From
tice, St Louis, 2009, Saunders Elsevier.)
Fubini S: Farm animal surgery, Philadelphia, 2004, Saunders Elsevier.)
2 to 3 weeks later. Because antibiotics may blunt the antibody • Presence of immunoglobulin M antibody against
response, a third set of serologic tests may be obtained 4 to C. psittaci by MIF to a reciprocal titer of ≥16.21
6 weeks after the acute sample if the results of the second set
Culture of the organism is difficult and poses a risk to
are equivocal.
laboratory personnel and therefore should be performed
CDC surveillance criteria for a confirmed case of psitta-
only in qualified laboratories. A PCR test is available
cosis are as follows:
through the CDC.
• Isolation of C. psittaci from respiratory secretions, or In birds, the diagnosis can be challenging, especially in
• Fourfold or greater increase in antibody against asymptomatic cases. A combination of culture, antibody
C. psittaci by complement fixation or MIF to a recipro- testing, and antigen detection is recommended.
cal titer of ≥32 between paired acute- and convalescent- For necropsy diagnosis, tissue specimens from the liver
phase serum specimens, or and spleen are preferred. In live birds, conjunctival, choanal,
Table 9-15 n Chlamydiae Infections: Comparative Clinical Presentations in Humans

and Other Animals
Humans Contact with sick birds and 5-15 days15 Headache, fever, myalgias, Pulmonary infiltrates on x-ray,
their environment cough, photophobia, scant elevated WBC, erythrocyte
sputum, shortness of breath; sedimentation rate, serology
rarely endocarditis, hepatitis, (CF, IFA), PCR, culture
neurological complications
Contact with cats Conjunctivitis (exposure to C. felis) PCR (may not distinguish
experiencing species), culture
keratoconjunctivitis
Pregnant women working Miscarriage (exposure to C. abortus)
with sheep and goats
Birds Crowding, other stressors 3 days to weeks Often subclinical Culture and serology (IFA,
Latent infections Lethargy, diarrhea, malaise, ELISA)
possible conjunctivitis, ruffled feathers, Antigen, PCR
ocular or nasal discharge
Cats Crowding 3-10 days12 Often subclinical Culture, serology, IFA
Chronic conjunctivitis,
photophobia, pneumonitis,
sneezing
Sheep, goats Parturition Months May be subclinical Culture, serology
Spontaneous abortion
CF, Complement fixation; WBC, white blood cell count.

and cloacal swab specimens or liver biopsy specimens can

Treatment
be used. Fecal specimens can be collected over several days
and pooled for increased sensitivity. As with diagnosis of Treatment in humans depends on whether the diagnosis is
human disease, the culture of C. psittaci requires specialized suspected or confirmed. If the diagnosis is not certain, the
laboratory facilities to minimize risk to laboratory person- patient should receive antibiotics to cover the spectrum of
nel. Conjunctival scrapings of various animals may reveal ele- organisms causing community-acquired pneumonia, with
mentary bodies in epithelial cells (Figure 9-25). the regimen adjusted to the severity of disease and exist-
Serological tests available include elementary body ing comorbid conditions such as alcoholism or chronic
agglutination (EBA) for detection of IgM antibodies, obstructive lung disease. Once the diagnosis is confirmed,
and indirect fluorescent antibody test (IFA) to detect IgG more specific therapy can be given as outlined in Table 9-16.
antibodies. Doxycyline and tetracycline are the mainstay of treatment
Complement fixation (CF) is more sensitive than agglu- in humans but are contraindicated in children younger than
tination methods. Antigen tests include ELISA tests that 8 years and pregnant women, for whom a macrolide anti-
were originally developed for identification of Chlamydia biotic such as erythromycin may be considered. However,
trachomatis in humans and IFAs to detect antigen. PCR is erythromycin may be less efficacious in severe cases and it
available in a number of diagnostic laboratories to detect C. may not protect the fetus of a pregnant patient.15
psittaci DNA in samples. Care is necessary in the prepara- Treatment in animals also relies on antibiotics of the
tion of samples for PCR testing to prevent environmental tetracycline class. Euthanasia may be considered as a control
contamination.3 measure during outbreaks. In cats, a vaccine is available that
does not prevent disease but may reduce the severity and
duration of illness.12
References
1. Centers for Disease Control and Prevention. Disease listing, psittacosis,
technical information: CDC bacterial, mycotic diseases. http://www.cdc.
gov/ncidod/dbmd/diseaseinfo/psittacosis_t.htm. Accessed May 30, 2008.
2. Bodetti TJ, Jacobson E, Wan C, et al. Molecular evidence to support
the expansion of the hostrange of Chlamydophila pneumoniae to include
reptiles as well as humans, horses, koalas and amphibians. Syst Appl
Microbiol. 2002;25(1):146.
3. National Association of State Public Health Veterinarians. Compendium
of measures to control Chlamydophila psittaci infection among humans
(psittacosis) and pet birds (avian chlamydiosis). http://www.nasphv.
org/Documents/Psittacosis.pdf. Accessed May 30, 2008.
4. Heymann DL. Control of communicable diseases manual. 19th ed.
Washington DC: American Public Health Association; 2008.
5. Acha PN, Szyfres B. Zoonoses and communicable diseases common to
man and animals: vol. 2: chlamydioses, rickettsioses, and viroses. 3rd ed.
Washington DC: Pan American Health Organization; 2003.
6. Sykes JE. Feline chlamydiosis. Clin Tech Small Anim Pract. 2005;20:129.
7. Biological and chemical terrorism: strategic plan for preparedness and
Figure 9-25 n Conjunctival scraping from a cat with chlamydial con- response. Recommendations of the CDC Strategic Planning Workgroup.
junctivitis. Elementary bodies of Chlamydophila felis are found in an epi- Morb Mortal Wkly Rep. 2000;49:1.
thelial cell (arrows). (Wright’s stain, original magnification ×1000.) (From 8. Vanrompay D, Harkinezhad T, van de Walle M, et al. Chlamydophila
Young KM, Taylor J: Laboratory medicine: yesterday, today, tomorrow: eye psittaci transmission from pet birds to humans. Emerg Infect Dis.
on the cytoplasm, Vet Clin Pathol 35:141, 2006.) 2007;13:1108.
Table 9-16 n Treatment of Chlamydophila Psittaci Infection in Humans and Other Animals
Humans: adult Doxycycline 100 mg PO or IV q12h × 10-21 days22 Tetracycline 500 mg PO q6h × 10-21 days22
<8 yr, pregnancy Doxycycline, tetracycline contraindicated; consider
macrolide (erythromycin), specialist consultation
Birds Doxycycline 25-50 mg/kg q24h PO for 30-45 days (dose 1% Chlortetracycline in medicated feed; some
and time are species dependent) injectable doxycyclines (consult with avian
veterinarian)
Cats Doxycycline 5 mg/kg PO q12h × 3-4 wk Tetracycline 22 mg/kg PO q8h × 3-4 wk22 (may
Ophthalmic ointments containing tetracycline q8h affect growing teeth of young kittens)
Sheep, goats Long-acting oxytetracycline 20 mg/kg, with a second Tetracycline21
injection 3 weeks later
9. Fenga C, Cacciola A, Di Nola C, et al. Serologic investigation of the prev- 16. Ferreri AJM, Dolcetti R, Magnino S, et al. A woman and her canary: a
alence of Chlamydophila psittaci in occupationally-exposed subjects in story of chlamydiae and lymphomas. http://jnci.oxfordjournals.org/cgi/
eastern Sicily. Ann Agric Environ Med. 2007;14:93. content/extract/99/18/1418. Accessed August 11, 2008.
10. Walder G, Hotzel H, Brezinka C, et al. An unusual cause of sepsis during 17. Husain A, Roberts D, Pro B, et al. Meta-analyses of the associa-
pregnancy: recognizing infection with chlamydophila abortus. Obstet tion between Chlamydia psittaci and ocular adnexal lymphoma and
Gynecol. 2005;106:1215. the response of ocular adnexal lymphoma to antibiotics. Cancer.
11. Cisláková L, Stanko M, Fricová J, et al. Small mammals (Insectivora, 2007;110(4):809.
Rodentia) as a potential source of chlamydial infection in East Slovakia. 18. Portlock CS, Hamlin P, Noy A, et al. Infectious disease associations in
Ann Agric Environ Med. 2004;11:139. advanced stage, indolent lymphoma (follicular and nonfollicular):
12. Barr SC, Bowman DD. 5-Minute veterinary consult clinical companion developing a lymphoma prevention strategy. Ann Oncol. 2008;19:254.
canine and feline infectious disease and parasitology. Ames, IA: Wiley- 19. Theegarten D, Sachse K, Mentrup B, et al. Chlamydophila spp. infec-
Blackwell; 2006. tion in horses with recurrent airway obstruction: similarities to human
13. Vanrompay D, Mast J, Ducatelle R, et al. Chlamydia psittaci in turkeys: chronic obstructive disease. Respir Res. 2008;9:14.
pathogenesis of infections in avian serovars A, B and D. Vet Microbiol. 20. Centers for Disease Control and Prevention. Case definitions for infectious
1995;47:245. conditions under public health surveillance. http://www.cdc.gov/ncphi/
14. Hughes C, Maharg P, Rosario P, et al. Possible nosocomial transmission disss/nndss/casedef/psittacosiscurrent.htm. Accessed June 19, 2008.
of psittacosis. Infect Cont Hosp Epidemiol. 1997;18:165. 21. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse
15. Baud D, Regan L, Greub G. Emerging role of Chlamydia and Chlamydia- Station, NJ: Merck; 2005.
like organisms in adverse pregnancy outcomes. Curr Opin Infect Dis. 22. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
2008;21:70. diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005.
CRYPTOSPORIDIOSIS
Peter M. Rabinowitz and Lisa A. Conti Public Health Veterinarians Compendium of Measures
to Prevent Disease Associated with Animals in Public
Cryptosporidiosis (ICD-10 A07.2) Settings, 2009; http://www.nasphv.org/Documents/
AnimalsInPublicSettings.pdf).
Like Giardia, Cryptosporidium species are a common para- • Disinfect the environment of oocysts using 5% ammo-
sitic cause of infectious diarrhea in humans and are found nia solution.2 Recognize the limited efficacy of disin-
in many vertebrate species. Many episodes of infection are fection procedures and place emphasis on thorough
mild enough that they do not come to medical attention. Yet cleaning.
because of its capability to cause massive human outbreaks • Provide preventive guidance for day care facilities, rec-
through waterborne exposure, it is considered a category reational water facilities, and boil water notification.
B bioterrorism agent. In immunocompromised patients, Remove reservoirs (recently infected people) from
cryptosporidiosis can cause serious and even fatal disease. contact with susceptible populations. Exclude children
A growing body of knowledge supports the importance with diarrhea from school or child care centers, water
of cross-species transmission between animals, especially parks, swimming pools, and so on.
calves, and humans. • Support policies to keep public areas free of animal
feces.
• Consider efficacy of local water treatment procedures
Key Points for Clinicians and Public Health with regard to removal of oocysts (i.e., chlorination
Professionals lacks efficacy; therefore alternative disinfection proce-
dures such as filtration or ozonation may be required).
• Be familiar with CDC guidelines: “Cryptosporidiosis
Outbreak and Response Evaluation.”1 • Report cases to public health authorities: http://www.
• Analyze and report trends from compulsory reports of cdc.gov/mmwr/preview/mmwrhtml/00047449.htm.
human disease. • Include questions about animal contact for every
• In the event of a case report, determine risk factors for patient presenting with diarrhea.
infection and conduct additional case finding. • Consider occupational exposure of cattle workers and
• Public health laboratories should determine the geno- animal shelter workers.
type to assist with source tracking. • Person-to-person transmission is possible; counsel
• Consider zoonotic sources of infection (farm animals/ infected persons about hand hygiene and avoiding
petting zoos, water supplies with animal contact) in fecal exposure during sexual activity.
addition to human-to-human spread (especially in
day care settings). Veterinary Clinicians
• Educate the public, veterinarians, and human
health clinicians about risk factors for transmis- • Counsel owners and any others in contact with infected
sion. Highlight the need for strict hygiene measures animals about the zoonotic risk, need for hand hygiene
for, or restrictions on, petting zoos and other ani- after handling pet, feces, pet toys, and other objects
mal settings (see the National Association of State that are potentially infected with cysts.
• Decontaminate infected animal’s coat with shampoo

Table 9-17 n Cryptosporidium Species Infecting
and kennels or other environments with an 18-hour
exposure to 5% ammonia, 10% formol saline, or 3% Humans and Other Animals
hydrogen peroxide.2 Host Major Species Minor Species
• Counsel persons who work with young ruminants or
animal shelters of the increased potential for exposure Humans C. hominis, C. parvum C. meleagridis,
and provide a clean birthing environment. Neonates C. felis, C. canis,
should receive colostrum, segregate calves from other C. suis, C. baileyi,
calves for the first 2 weeks of life, and maintain hygienic cervine genotype
husbandry practices including fly and rodent control. Cats C. felis
• Counsel immunosuppressed persons regarding the Cattle C. parvum, C. bovis, C. suis
risks of animal exposures. C. andersoni deer-like
genotype
Agent Chickens C. baileyi C. meleagridis, C.

galli
Cryptosporidia are protozoan parasites of the coccidia group Deer C. parvum, deer genotype
in the phylum Apicomplexa (Figure 9-26). At least 30 species
Dogs C. canis
of Cryptosporidium and multiple genotype variations have
been described in a wide number of animal species (Table Horses Horse genotype
9-17). The two species believed to cause most cases of human Lizards C. serpentis, C. varanii Lizard genotype
infections are C. hominis (formerly known as C. parvum Mice C. muris, mouse genotype
anthroponotic genotype or genotype 1) and C. parvum.
Sheep Cervine genotypes 1-3,
C. hominis is a human pathogen, although infection has bovine genotype
Snakes C. serpentis C. varanii, snake
genotype
Squirrel C. muris, squirrel
genotype
Swine C. suis Pig genotype II
Turkey C. meleagridis, C. baileyi
Adapted from Fayer R, Xiao L: Cryptosporidium and cryptosporidiosis, Boca Raton,

FL, 2007, CRC Press, p 11.
A
been found in lambs, cattle, and other mammals. C. parvum
infects humans, cattle, and other ruminants. Other species
reported in humans include C. canis (dogs), C. felis (cats),
and C. meleagridis (birds).
Cryptosporidia colonize the intestinal and biliary tracts
but can also be found in the lungs. The organism reproduces
in the intestinal tract to produce oocysts. Oocysts are imme-
diately infectious as shed in feces. The oocysts measure 2.5
to 5 microns in diameter and can survive in moist environ-
ments, including water supplies, for several months. They are
resistant to chlorination but are inactivated by boiling water
or ozonation.
C. parvum occurs worldwide in animals and humans. Human
B prevalence is greater in developing countries with poor sani-
tation practices. Reported rates of infection in human popu-
Figure 9-26 n Cryptosporidiosis, small intestine. A, Cow. Cryptosporidia
(arrow) are attached to the microvillus border of the enterocyte mem-
lations range from 20% in developing countries to 1% to 4%
brane. Plastic-embedded, toluidine blue–stained section. B, Rabbit. The in developed countries.3
Cryptosporidia form a trilaminated enveloping membrane upon fusion
with the enterocyte membrane. Their location is thus intracellular, but
extracytoplasmic. Microvilli are effaced. Transmission electron micrograph,
Groups at Risk
uranyl acetate and lead citrate stain. (From McGavin MD: Pathologic basis of Children younger than 2 years, their caregivers, and immu-
veterinary disease, ed 4, St Louis, 2006, Mosby Elsevier. A, Courtesy Dr. A.R.
Doster, University of Nebraska; and Noah’s Arkive, College of Veterinary nocompromised persons have an increased risk of infection.
Medicine, The University of Georgia. B, Courtesy Dr. H. Gelberg, College of Other risk groups include animal handlers, travelers, con-
Veterinary Medicine, Oregon State University.) tacts of infected persons, and men who have sex with men.
the sporozoites are released and invade the mucosa of the

intestinal tract. Sporozoites mature into trophozoites that
Humans are the reservoir for C. hominis, whereas humans, multiply asexually first. Then these trophozoites undergo
cattle, and other ruminants (e.g., goats, sheep, deer, elk) sexual reproduction (meronts) to produce sporozoites, most
appear to be major reservoirs for C. parvum.4 C. muris of which acquire a protective cover to form an oocyst. These
infects mice and cattle gastric glands, and chickens are the oocysts are passed in the feces, where they are immediately
reservoir for C. baileyi. In many individuals and species, infective. Sporozoites that remain in the intestine without
asymptomatic carriage may occur with the ability to trans- developing a cyst wall are able to reinfect the host, perpetuat-
mit the infection to others and the environment. The ing infection.5 The infectious dose is about 130 organisms to
zoonotic potential of avian Cryptosporidia has not been initiate a C. parvum infection in 50% of healthy volunteers.6
fully elucidated. Cattle can shed up to 1 million organisms per gram of feces.
Most transmission appears to occur through ingestion
of oocysts. Vehicles of transmission include drinking water,
direct fecal-oral contamination, foodborne exposure, or con-
Each oocyst contains four sporozoites that are the infective tact with contaminated objects leading to ingestion (Figure
phase of the parasite (Figure 9-27). When shed in feces, the 9-28). Infected drinking water and freshwater bathing areas
oocysts are immediately infective. Upon ingestion by a host, have been the sources of large human outbreaks, such as the
i
3 Thick-walled oocyst
injested by host
Recreational water Drinking water

2 Contamination of water
and food with oocysts
i  Infective stage
1 Thick-walled oocyst d i
d  Diagnostic stage (sporulated) exits host
j Thick-walled a Oocyst b
Sporozoite c Trophozoite d
Type I Meront
oocyst (sporulated) e
exits host
Asexual Cycle
k
Thin-walled
oocyst Merozoite
(sporulated)
Microgament
Microgametes
f
g Undifferentiated
Gamont
Type II Meront
Merozoites
Microgamont Sexual Cycle
Zygote h
i
Enviromental factors: Water sanitation, manure-spreading practices

Figure 9-27 n Cryptosporidiosis transmission/life cycle. (Modified from Centers for Disease Control and
Prevention Public Health Image Library, Atlanta, Ga.)
A B
Figure 9-28 n A, Photomicrograph of Cryptosporidium parvum oocysts in stool smear, acid fast stain. B, Water
fountain with sign that water is unsafe. (From Centers for Disease Control and Prevention Public Health Image
Library, Atlanta, Ga.)
sickening of more than 400,000 people in Milwaukee, Wis.,

Disease in Humans
due to improperly treated municipal water supply in 1993.7
A secondary means of transmission is by inhalation of aero- The majority of the North American population has
solized oocysts. been exposed to the infection at some time. Cryptospori
Calves are accepted as a source for human infection. dium infection in immunocompetent humans can be
A study in Wisconsin using PCR analysis of human isolates asymptomatic.
concluded that most sporadic cases of cryptosporidiosis in The major symptom is diarrhea—often explosive, pro-
that state were zoonotic in origin, with cattle and other rumi- fuse, and watery with mucus—accompanied by abdominal
nants the main source.8 The types of zoonotic transmission pain and cramping, vomiting, and weight loss.3 Low-grade
that occur appear to differ by geographical area, with less fever may occur. The diarrhea is self-limiting in healthy
zoonotic transmission occurring in urban areas. The risk of people, lasting 8 to 20 days. In patients infected with HIV
human infection by dogs and cats is believed to be small in and in other immunodeficient patients, symptoms can be
industrialized countries. C. canis, C. felis, and C. meleagridis more severe and chronic and include massive diarrhea and
are responsible for as much as 20% of human infection in involvement of the respiratory and biliary tracts.5
some developing countries, but some evidence indicates that
although diseases originates in animals, these strains are being
transmitted person to person.4 Data from the Milwaukee out- Disease in Animals
break and others suggest two thirds of water-source human
outbreaks are not of animal origin. Transmission in animals, In dogs and cats, the disease is often subclinical. Puppies and
as in humans, occurs through ingestion and possibly inhala- kittens are more likely than adults to show intestinal signs
tion of oocysts. of infection. In cats and dogs, most clinical cases are associ-
ated with immunosuppression, such as with feline leukemia
virus, canine distemper virus, canine parvovirus, and intesti-
nal lymphosarcoma, and can manifest as intestinal, hepatic,
pancreatic, or respiratory disease.10 Calves may exhibit diar-
Cryptosporidium cysts, like Giardia, can contaminate rhea, anorexia, and weight loss. Adults are often asymptom-
water supplies and other moist environments for months. atic. Cryptosporidiosis commonly causes vomiting in snakes
Environments where manure is spread have been associated (Color Plate 9-11). Table 9-18 provides a comparison of clin-
with increased risk of human infection.9 ical manifestations in humans and other animals.
Table 9-18 n Cryptosporidiosis: Comparative Clinical Presentations in Humans and Other Animals
Species Risk Factors Incubation Period Clinical Manifestations
Humans Children and their caretakers 1-12 days3 Asymptomatic or acute watery
Farm animal contact diarrhea, coughing and low-grade
fever
Dogs, cats, ruminants, mice, Neonates, immunocompromised 5-10 days Often asymptomatic in older and
horses (Cryptosporidium. spp. at increased risk of symptomatic immunocompetent animals
can infect reptiles and birds) disease Small-bowel diarrhea, diarrhea,
tenesmus, dehydration, weight loss
Table 9-19 n Antibiotic Treatment of Cryptosporidiosis in Humans and Other Animals
Humans: Supportive care

immunocompetent Nitazoxanide 500 mg PO bid × 3 days11
Adult with HIV infection Effective antiretroviral therapy best treatment
Dogs, cats Supportive care
Paromomycin 125-165 mg/kg PO bid × 5 days (may cause Tylosin 11 mg/kg q12h × 28 days
nephropathy in young animals)
Cattle Supportive care, hyperimmune bovine colostrum
antibiotics are registered for treatment of Cryptosporidium

Diagnosis
in animals. Monitor fecal oocyst shedding 14 days after
In human beings, cases are diagnosed by IFA visualization of treatment.
oocysts in feces. An ELISA test is also available. Many labora-
tories do not routinely test for Cryptosporidium, so a special
request may be necessary. References
Animal diagnosis involves testing for oocysts in feces 1. Centers for Disease Control and Prevention. Cryptosporidiosis outbreak
with sucrose or zinc sulfate solution with visualization after response & evaluation. http://www.cdc.gov/crypto/pdfs/core_guidelines.
modified acid-fast staining, a procedure typically performed pdf.2.
2. Dvorak GA, Rovid-Spickler A, Roth JA, eds. Handbook for zoonotic dis-
by a veterinary laboratory rather than by the private practi eases of companion animals. Ames, IA: The Center for Food Security &
tioner (Color Plate 9-12). Routine in-house flotation tests Public Health, Iowa State University; 2006.
often fail because cysts are small (4 to 5 microns in diame- 3. Heymann DL. Control of communicable diseases manual. 19th ed.
ter). To inactivate potential cysts and submit fecal samples to Washington DC: American Public Health Association; 2008.
an appropriate laboratory, mix one part 100% formalin with 4. Xiao L, Feng Y. Zoonotic cryptosporidiosis. FEMS Immunol Med
Microbiol. 2008;52(3):309.
nine parts feces. Oocysts are not shed continuously; there- 5. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
fore repeat samples may be necessary. and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington DC: Pan
American Health Organization; 2001.
6. Dupont HL, Chappell CL, Sterling CR, et al. The infectivity of Cryptosporidium
parvum in healthy volunteers. N Engl J Med. 1995;332:855.
7. MacKenzie WR, Hoxie NJ, Proctor ME, et al. A massive outbreak in
Treatment Milwaukee of Cryptosporidium infection transmitted through the public
water supply. N Engl J Med. 1994;331(3):161.
Acute cryptosporidiosis is treated with supportive care 8. Feltus DC, Giddings CW, Schneck BL, et al. Evidence supporting
including rehydration. Antibiotics are indicated for symp- zoonotic transmission of Cryptosporidium spp. in Wisconsin. J Clin
Microbiol. 2006;44(12):4303.
tomatic patients. In patients with HIV infection, adequate 9. Lake IR, Harrison FC, Chalmers RM, et al. Case-control study of
antiretroviral therapy is essential to reducing the morbidity environmental and social factors influencing cryptosporidiosis. Eur J
of cryptosporidiosis infection (Table 9-19). Epidemiol. 2007;22(11):805.
In immunocompetent animals the disease is usually 10. Barr SC, Bowman DD. 5-minute veterinary consult clinical companion
canine and feline infectious disease and parasitology. Ames, IA: Wiley-
self-limiting and may include oral glucose-electrolyte solu- Blackwell; 2006.
tion. Severe diarrhea warrants parenteral fluids. If there are 11. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to antimicro-
zoonotic concerns, a trial of antibiotics may be warranted. No bial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy; 2009.
DERMATOPHYTOSIS
Peter M. Rabinowitz and Lisa A. Conti • Counsel pet owners and clinic employees to disinfect
contaminated equipment, bedding, and the environ-
Dermatophytosis (ICD-10 B35) ment with dilute bleach solution (1:10).
• Consider the possibility of rodents spreading the
Other names in humans: ringworm infection, tinea infection, disease to pets and other animals.
dermatomycosis, trichophytosis, microphytosis • If dermatophytosis is diagnosed in a pet, treat the animal
and advise the owner and family members of the zoonotic
Other names in animals: ringworm, keratinophilic mycosis risk and to seek medical care if symptoms are noticed.
• Isolation may be advisable for an animal that is under
Dermatophytosis is a skin infection caused by members treatment due to the zoonotic nature of the disease.
of three genera of fungi: Epidermophyton, Microsporum, • An attenuated vaccine for cattle is available in Europe,
and Trichophyton. Because all domestic animals are sus- where it has been reported to reduce the incidence of
ceptible to dermatophytosis and many dermatophytes can zoonotic disease in animal care workers3; it is not cur-
pass between species, dermatophytosis is probably one rently available in the United States.
of the most common pet-associated and occupational • Therapy cats should be tested biannually.4
zoonoses. It has been estimated that approximately 2 mil-
lion people in the United States are infected each year as
Agent
a result of contact with animals.1 The true prevalence is
probably greater than recognized; the signs of disease may Fungi that cause dermatophytosis are spore-producing patho-
be mild, so infected individuals may not seek medical care gens that may be classified according to mode of transmission
and the condition is often not reported to local health as anthropophilic (preferring humans), zoophilic (preferring
authorities. animals), or geophilic (preferring soil environments). Although
zoophilic species often can pass from animals to humans, they tend
Key Points for Clinicians and Public Health to not be readily transmissible from human to human. Table
Professionals 9-20 lists the main species and their type.5
Public Health Professionals Geographical Occurrence

• Provide descriptive epidemiology about the disease. These pathogenic fungi are found worldwide and the inci-
• Educate the public on modes of transmission and risk dence is generally higher in hot and humid climates.
factors for infection. Trichophyton tonsurans is commonly found in urban areas
• Raise awareness of the disease among high-risk groups in the eastern United States, Puerto Rico, Mexico, the United
such as animal workers and in school settings. Kingdom, and Australia. T. verrucosum and T. mentagro-
• Make recommendations for environmental cleanup of phytes are common in rural areas2 as is Microsporum canis.
contaminated surfaces and fomites with dilute bleach M. audonii is more common in West Africa.
solution (1:10).
Groups at Risk
Human Health Clinicians Dermatophytoses from animals are an occupational risk for
• When taking a history on a patient with a rash for veterinary health care workers and other animal workers. Pet
which dermatophytosis is suspected, inquire about pet owners, children, and immunocompromised individuals are
and other animal exposures. at increased risk of infection,2 as are humans living in close
• Teach patients to always wash their hands after contact quarters (such as military personnel, athletes, school chil-
with pets and other animals.2 dren, and inner-city residents) who are at risk for human-to-
• Encourage infected patients with dogs and cats to seek human transmission.
veterinary evaluation of their pets.
• No human vaccine is available. Hosts, Reservoir Species, Vectors
Table 9-20 lists the principal animal reservoir species for
the T. mentagrophytes zoophilic dermatophytoses. The
• Ensure that owners bring affected animals for prompt different species of fungi tend to vary in their host specific-
treatment; be aware that there are inapparent carriers ity. M. nanum, an infection of pigs, tends not to infect other
and that use of corticosteroids may prolong species,4 whereas T. mentagrophytes has a much wider host
infection. range, infecting rodents, dogs, cats, rabbits, horses, humans,
• Counsel clients and veterinary care staff about hand- hedgehogs,6 and other animals. Mechanical vectors include
washing and other measures to avoid zoonotic furniture, animal bedding, hair care articles (scissors, combs,
transmission. and brushes), clothing, and hats.
Table 9-20 n Classification of the Major Dermatophytes
Zoophilic
Anthropophilic Geophilic Organism Sources
Trichophyton concentricum Trichophyton ajelloi Trichophyton erinacei * Hedgehogs

T. gourvilii T. terrestre T. equinum Horses
T. mentagrophytes interdigitale* Microsporum fulvum T. mentagrophytes* Rodents
T. megnini M. gypseum T. quinckeanum* Mice
T. rubrum T. simii Monkeys
T. schoenleinii T. verrucosum Cattle
T. soudanense Microsporum canis Cats, dogs
T. tonsurans M. gallinae Chickens
T. violaceum M. nanum Pigs
T. yaoundei M. persicolor Bank voles
Microsporum audouinii
M. ferrugineum
Epidermophyton floccosum
*These organisms are part of the “mentagrophytes” complex and may be classified as a single species.
From Mandell GE, Bennett JE, Dolin R (eds): Principles and practice of infectious diseases, ed 6, Philadelphia, 2000, Churchill Livingstone Elsevier.
Mode of Transmission and Life Cycle Table 9-21 n Clinical Features of Dermatophytes
Transmission occurs through direct skin-to-skin and skin- Based on Mode of Transmission
to-hair contact with infected animals or humans and indirect Mode of Transmission Clinical Features
contact with the infectious arthrospores in the environment
or on fomites (Figure 9-29). An infected human or animal Human-to-human Mild to noninflammatory, chronic
can generate an aerosol of infectious arthrospores.2 The
Animal-to-human Intense inflammation (pustules
infectious spores germinate in the keratinized layers of skin, and vesicles possible), acute
hair, and nails.7
Soil-to-human or animal Moderate inflammation
The mode of transmission also helps determine the
severity of clinical disease. In general, animal-to-human From Bolognia JL, Jorizzo JL, Rapini RP (eds): Dermatology, ed 2, London, 2003,
transmission produces some of the most severe clinical syn- Mosby Elsevier.)
dromes, as shown in Table 9-21.
growth of fungi and persistence of spores on surfaces and
Environmental Risk Factors articles. Environmental samples such as soil and clothing
associated with human and other animal cases have spore
The fungi and infectious spores can survive on surfaces and positivity rates as high as 100%.8 Contamination with multi-
in desquamated skin for months.2 Therefore environmental ple dermatophyte species has been found on veterinary clinic
contamination can play an important role in transmission. floors, producing an environmental risk of infection for both
In general, moist, warm environmental conditions favor the animals, clients, and the veterinary staff.2
Infected animal
or human being
Direct contact with Susceptible human
Fungal reproduction, skin or hair, aerosol being or animal
production of arthrospores
Contact with skin
Soil, articles, surfaces

contaminated with fungi or spores
Environmental factors: Climate, temperature, humidity, crowding

Figure 9-29 n Transmission of dermatophytosis in animals and humans.
In immunocompromised individuals, T. mentagrophytes

Disease in Humans
and M. canis can cause disseminated skin infection.
The incubation period in humans is 10 to 14 days. Infection
in humans usually begins with a small area of erythema that Disease in Animals
develops into a patch of annular scaling skin with a raised bor-
der that then slowly spreads peripherally. Infections are usually The incubation period in animals is generally 1 to 2 weeks.
accompanied by pruritus, which can lead to excoriation and The infection in dogs may begin as alopecia (Figure 9-31).
secondary bacterial infections. As shown in Table 9-21, zoo- Erythema, scaling, and pruritus may develop around the
philic fungi are more likely than anthropophilic or geophilic lesions. In some dogs clinical signs do not develop yet the
fungi to produce severe inflammatory changes in humans, dogs are capable of shedding spores into the environment.
often with pustular lesions (kerion).9 The location of the infec- In immunocompromised animals, these infections can be
tion determines the name of the dermatophytosis. severe (Color Plate 9-14).
Tinea capitis is an infection of the scalp that occurs most Up to 90% of infected cats show no clinical signs of
commonly in children. It is caused by only two genera: disease. Clinical infections are more common in kittens
Trichophyton and Microsporum. In the United States, T. ton- and long-haired breeds of cats. Clinical signs include a poor
surans is the most common cause and M. canis is the second hair coat or circular skin lesions, usually on the face or paws
most common.9 Tinea capitis can produce localized hair loss, (Color Plate 9-15).
pustules, and scarring (Figure 9-30). Infections are more common when cattle are stabled
Tinea corporis is an infection of the trunk and extremities indoors. Lesions often begin as gray-white areas that thicken,
that does not involve the hair, palms, soles, or groin. Worldwide, scab, and slough, leaving an area of alopecia. Infection is
it is most commonly caused by T. rubrum followed by T. men- often self-limited over several months (Color Plate 9-16).3
tagrophytes.9 It can present in a variety of ways dependent in Horses tend to become infected at areas of contact with a
part on the mode of transmission, but classically causes a cir- harness. The disease manifests as areas of localized alopecia
cular annular lesion with scaling (Color Plate 9-13). with skin thickening (Figure 9-32 and Color Plate 9-17).3
Tinea pedis is an infection of the toes and feet caused
T. rubrum, T mentagrophytes, Epidermophyton floccosum,
and T. tonsurans.9
Other dermatophyte infections include tinea barbae, an
infection of the beard area; tinea cruris, an infection of the groin
and perianal area; and tinea manum, an infection of the hand.
Figure 9-31 n Dermatophytosis. Focal alopecia on the muzzle of a

Dachshund. This is a typical location for dogs that frequently dig in soil.
(From Medleau L, Hnilica KA: Small animal dermatology: a color atlas and
therapeutic guide, ed 2, St Louis, 2006, Saunders Elsevier.)
Figure 9-30 n Tinea capitis due to M. canis infection. (From Mandell Figure 9-32 n Classic signs of dermatophytosis (ringworm) in a horse.
GE, Bennett JE, Dolin R: Principles and practice of infectious diseases, ed 6, (From Reed SM, Warwick MB, Sellon DC: Equine internal medicine, ed 2, St
Philadelphia, 2000, Churchill Livingstone Elsevier.) Louis, 2004, Saunders Elsevier.)
Table 9-22 n Dermatophytosis: Comparative Clinical Presentations in Humans and Other Animals
Humans Children, crowding, 10 days to 2 wk Erythema, itching, scaling KOH preparation may show
contact with animals, lesion of skin hyphae; Wood’s lamp may
immunocompromised fluoresce; fungal culture
Dogs or cats Crowding, young animals, 1-4 wk Alopecia or poor hair
immunodeficiency coat, scales, erythema,
asymptomatic
Cattle Stabling indoors, calves Gray-white areas that scab M. canis may fluoresce under
and fall off, leaving alopecia Wood’s lamp, microscopic
examination10
Horses Friction from harnesses Dry, scaling, thickened areas Fungal culture
Rodents Often no clinical signs, white
scabby lesions of head and
trunk
KOH, Potassium hydroxide.
Rodents such as mice may show no evidence of disease Scrapings or clippings can be placed in 10% to 20% potas-
or may have white scabbing lesions on the head and trunk sium hydroxide solution and examined microscopically.
(Color Plate 9-18). Hyphae can appear as chains (Figure 9-33). Conidae (spores)
Table 9-22 shows the comparative clinical presentations can also be recognized by microscopy (Figures 9-34 and 9-35).
in humans and animals. In addition to microscopy, fungal culture is often worth-
while to confirm the diagnosis and the fungal species
(Color Plate 9-19). Similar diagnostic tests are used in other
Diagnosis
animals.
In humans the diagnosis can be made clinically based on the
typical appearance of lesions and a history of contact with Treatment
an infected person or animal. The differential diagnosis may
include eczema, impetigo, and conditions causing localized Table 9-23 outlines treatment guidelines in humans and
alopecia, such as cutaneous lupus. The sensitivity and speci- other animals. Many human cases of dermatophytosis are self-
ficity of the Wood’s lamp test is limited because only some limited and do not require treatment. However, treatment
dermatophytes will fluoresce; therefore this test should be
used only as part of a screening process. Wood’s lamp–pos-
itive areas can be used to guide scrapings for microscopic
examination and/or culture. Samples of skin and hair should
be taken from the periphery of lesions where infection is
active.
Figure 9-33 n Photomicrograph of the fungus Trichophyton menta-

grophytes. This dermatophyte is a zoophilic species that commonly inhab- Figure 9-34 n Trichophyton mentagrophytes in culture. Spherical micro-
its mice, guinea pigs, kangaroos, cats, horses, sheep, and rabbits. Members conidia and one thin-walled, multicellular, cigar-shaped macroconidium
of the genus Trichophyton are common causes of hair, skin, and nail infec- (lactophenol analine blue, ×2000). (From Greene CE: Infectious diseases of
tions in humans. (From Centers for Disease Control and Prevention Public the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier. Courtesy Spencer
Health Image Library, Atlanta, Ga. Courtesy Dr. Leonor Haley.) Jang, University of California, Davis.)
may shorten the duration of infection and reduce the pos-

sibility of further transmission.
Companion animals with positive culture findings should
be treated because of the zoonotic disease risk.11 However,
eradicating the disease may be a challenge if multiple animals
are housed together. Response to therapy is monitored by
dermatophyte culture as many animals will remain culture
positive while improving clinically.
For mild skin infections, topical medication may be
sufficient. More extensive infections may require systemic
treatments. In food-producing animals, treatment options
may be limited because of food safety concerns.
References
1. Stehr-Green JK, Schantz PM. The impact of zoonotic diseases transmit-
ted by pets on human health and the economy. Vet Clin N Am Small
Anim Pract. 1987;17:1.
and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington DC: Pan
American Health Organization; 2001.
4. Greene CE. Infectious diseases of the dog and cat. 3rd ed. St Louis:
Figure 9-35 n M. canis in culture. Rough and thick-walled multicellu- Saunders Elsevier; 2006.
lar spindle-shaped macroconidia. Note curved, pointed ends (lactophenol 5. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infec-
analine blue, ×2000). (From Greene CE: Infectious diseases of the dog and cat, tious diseases. 6th ed. Philadelphia: Churchill Livingstone Elsevier;
ed 3, St Louis, 2006, Saunders Elsevier. Courtesy Richard Walker, University 2005.
of California, Davis.) 6. Rosen T. Hazardous hedgehogs. South Med J. 2000;93(9):936–938.
Table 9-23 n Dermatophytosis Treatment in Humans and Other Animals
Humans: tinea corporis, tinea Topical antifungal, drying powder Terbinafine 250 mg PO × 4 wk or ketoconazole
cruris, tinea pedis 200 mg PO q24h × 4 wk or fluconazole
150 mg PO 1×/wk for 2-4 wk or griseofulvin:
Adults: 500 mg PO q24h × 4-6 wk
Children: 10-20 mg/kg/day 2-4 wk for T. corporis,
4-8 wk for T. pedis
Humans: tinea capitis Adults: Terbinafine 250 mg PO × 4 wk Itraconazole 3-5 mg/kg PO qd × 30 day or
(T. tonsurans) or 4-8 wk (M. canis) fluconazole 8 mg/kg (max 150 mg) PO qwk ×
8-12 wk griseofulvin: Adults: 500 mg PO q24h
Children: 125 mg or 6-12 mg/kg PO qd12 × 4-6 wk
Children: 10-20 mg/kg/day until hair regrows12
Dogs and cats Topical miconazole or clotrimazole10 Ketoconazole (not labeled for use in dogs and
Griseofulvin microsized formulation 25-60 mg/kg cats in the United States) 10 mg/kg PO q24h
(Note: Spontaneous remission PO q12h × 4-6 wk (fed with a fatty meal helps or divided twice per day for 3-4 wk; acid meal
may occur in short-haired cats increase absorption) (add tomato juice) will enhance absorption
in a single-cat environment Ultramicrosized formulation 2.5-5.0 mg/kg PO Itraconazole 10 mg/kg PO q24h or 5 mg/kg
and in dogs; environmental q12-24h q12h
treatment is important; use Pediatric suspension 10-5 mg/kg PO q12h Spot treatment not recommended11
dilute bleach [1:10]; multi- Lufenuron (Program) 100 mg/kg for 2 doses at
cat environments can be 2-week intervals, then treat monthly
complicated.) Clipping and topical therapy: lime sulfur (1:16)
or miconazole shampoo
Cattle Washes or sprays of 4% lime sulfur, 0.5% sodium Treat individual lesions with miconazole or
hypochlorite bleach, 0.5% chlorhexidine, 1% clotrimazole lotions
povidone-iodine, natamycin, and enilconazole
(not available in the United States)
Horses Topical clotrimazole or miconazole
Lambs Sodium hypochlorite washes or enilconazole
rinses11
7. Van Rooij P, Detandt M, Nolard N. Trichophyton mentagrophytes of 10. Barr SC, Bowman DD. 5-minute veterinary consult clinical companion
rabbit origin causing family incidence of kerion: an environmental study. canine and feline infectious disease and parasitology. Ames, IA: Wiley-
Mycoses. 2006;49(5):426–430. (Erratum in Mycoses 2007;50(2):160.) Blackwell; 2006.
8. Cafarchia C, Romito D, Capelli G, et al. Isolation of Microsporum canis 11. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse
from the hair coat of pet dogs and cats belonging to owners diagnosed Station, NJ: Merck; 2005.
with M. canis tinea corporis. Vet Derm. 2006;17(5):327–331. 12. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti-
9. Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. London: microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
Mosby Elsevier; 2008. 2009.
DIPYLIDIASIS
Peter M. Rabinowitz and Lisa A. Conti Veterinary Clinicians

Dipylidiasis (ICD-10 B71.1) • Counsel pet owners to practice flea control.
• Deworm all dogs and cats in the household when
Other names in humans: dog tapeworm infection is identified in one animal (typically because
of passage of tapeworm segments in stool).
Other names in animals: dog tapeworm, dog cestodiasis • Counsel owners of pets that have been diagnosed with
tapeworms or fleas to watch for signs of infection in
The dog tapeworm (Dipylidium caninum) is a common par- children in the household.
asite of dogs and cats. The cat flea (Ctenocephalides felis)
and dog flea (Ctenocephalides canis, relatively rare in North Agent
America)1 are important intermediate hosts in the life cycle.
Human infection is apparently a rare event that occurs when The double-pored dog tapeworm (D. caninum) is a Cestode
children ingest fleas containing tapeworm eggs.2 Although that is the most common tapeworm of dogs and cats.3 The adult
infection in both humans and other animals is usually worms may be as long as 70 cm and can live in the small intestine
asymptomatic, the white, seedlike, motile proglottids are for up to 3 months. The adult worms consist of a head (scolex),
passed in the stool, causing concern. neck, and chain of segments known as proglottids (Figure 9-36).
New segments form at the neck and older segments are pushed
back.4 Each proglottid contains both male and female elements
Key Points for Clinicians and Public Health and can become full of eggs (gravid) and break off from the rest
Professionals of the worm, to be shed in the feces. Fleas play an important role
in the life cycle of the worm as intermediate hosts.
Public Health Professionals Geographical Occurrence

• Educate the public about the need for routine flea Worldwide.
control.
• Ensure policies are in place for proper disposal of
animal feces. Groups at Risk
Young children appear to represent most human cases
because of their close contact with pets and greater likelihood
• The veterinarian caring for the family pets should be
contacted to ensure that pets receive treatment.
• The appearance of proglottids in the stool of a child
may be a sentinel event indicating probable flea infes-
tation in the house as well as infection of a house-
hold pet. Human health clinicians should counsel
adult patients or parents of pediatric patients to seek
veterinary advice and preventive services to ensure
that the house and pets of a patient are treated for
fleas.
• Children should wash their hands after playing
with pets. Children with pica behavior require care-
Figure 9-36 n Adult Dipylidium caninum with detaching proglottids.
ful supervision when playing in environments with (From Centers for Disease Control and Prevention Public Health Image
pets. Library, Atlanta, Ga.)
of ingesting fleas directly or in food. A case in a 5-week-old

infant has been reported.5

Dogs and cats are the principal reservoirs, although wild
carnivores have also been found to be infected. Humans are
accidental hosts.

The adult worms live in the intestine of the reservoir host (Figure
9-37). Gravid proglottids are released in the feces (Figure 9-38).
In the environment the proglottids break down, releasing the
eggs. If the eggs are ingested by a larval cat or dog flea, the eggs
hatch and turn into cysticercoids as the flea develops. Dogs and
cats may ingest a flea as a defensive behavior. Children may Figure 9-38 n Micrograph depicting a proglottid (i.e., a tapeworm seg-
ingest a flea accidentally when playing with or handling a dog ment) from the Cestode Dipylidium caninum. Such proglottids, which when
mature average 12 mm × 3 mm, are passed with feces and often resem-
or cat or by ingesting food containing a flea (Figure 9-39). Once ble rice grains when dried. Each proglottid contains egg packets that are
the flea is ingested, cysticercoids are released into the small intes- held together by an outer embryonic membrane. (From Centers for Disease
tine, where they develop into adult worms within 20 days.6 Control and Prevention Public Health Image Library, Atlanta, Ga.)
Figure 9-37 n Life cycle, dipylidiasis. (From Centers for Disease Control and Prevention Public Health Image
Figure 9-39 n A 20-month-old girl was seen in consultation because of “moving rice” in
the stool on the diaper. A, A grain of rice from the hospital cafeteria is seen on the left, and
the patient’s “rice” on the right. B, A drop of iodine shows the typical carbohydrate blackening
of rice on the left. Note the 7-cm vase shape of patient’s “rice” on the right. C, Histologic sec-
tion of “rice” shows typical structure of Dipylidium caninum. D, Typical egg packet of D. cani-
num is seen from patient’s stool specimen. E, The family dog. (From Long SS, Pickering LK,
Prober CG (eds): Principles and practice of pediatric infectious diseases, ed 3, Philadelphia, 2008,
Churchill Livingstone Elsevier. Courtesy Joel E. Mortensen and Sarah S. Long, St. Christopher’s
Hospital for Children, Philadelphia, PA.)
Table 9-24 n Dipylidiasis in Humans and Animals
Species Risk Factors Incubation Period Clinical Signs Diagnostic Findings
Humans Fleas in house, children Adult worms develop in Usually asymptomatic, Proglottids in stool
at increased risk of 20 days may have abdominal
ingesting fleas pain
Dogs, cats Flea contact, ingestion No symptoms or perianal
pruritus
Environmental Risk Factors Table 9-25 n Treatment of Dog and Cat

Tapeworm Infection in Humans
The key environmental risk is flea infestation of a house or
other living environment. and Other Animals
Primary Alternative
Species Treatment Treatment
Disease in Humans
Based on existing case reports, human infection with dipy- Humans Praziquantel 5-10 mg/
kg PO × 1 dose
lidiasis is usually asymptomatic. The proglottids appear in
the stool as white, rice-like motile objects and may be shed Dogs* Praziquantel 5 mg/kg Praziquantel*/
PO, SC once pyrantel/febantel
over a number of months. In one report, dipylidiasis was PO once
misdiagnosed as recurrent pinworm (Enterobius vermicu-
laris) infection and therefore incorrectly treated.7 Abdominal Flea control Epsiprantel 5.5 mg/
kg PO once
discomfort may occur, as well as abdominal distension, appe-
tite disturbances, and insomnia.6 Accompanying neurologi- Fenbendazole
50 mg/kg PO q24h
cal symptoms including vertigo and light-headedness have × 5 days
been described.8
Cats* Praziquantel 5 mg/kg Praziquantel/pyrantel
PO, SC once PO once
Flea control Epsiprantel 2.8 mg/
Disease in Animals kg PO once10
The infection in dogs and cats is considered to cause few
*Not for puppies or kittens younger than 3 weeks or weighing less than 2 lb.
clinical signs. Perianal pruritus may be present. Infected
dogs may therefore “scoot,” dragging their anus along the
ground to relieve the itching. The most significant finding is
the sight of proglottids in the feces, emerging from the anus
or stuck to perianal hairs. These appear as white, crawling References
rice-like segments on the fur or in feces or on the perianal
area. 1. Goddard J. Physician’s guide to arthropods of medical importance. 5th ed.
Boca Raton, FL: CRC Press; 2007.
2. Figueroa HM, Augilar FJ. The first case of dipylidium caninum found
and identified in a human being in Guatemala. Am J Trop Med Hyg.
Diagnosis 1956;5:269-71
3. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse
The diagnosis is usually made clinically by identifying the Station, NJ: Merck; 2005.
motile proglottids and obtaining a history of contact with 4. Colville J, Berryhill D. Handbook of zoonoses: identification and preven-
fleas or a dog or cat. In animals, visualizing the proglottids of tion. St Louis: Mosby Elsevier; 2007.
D. caninum is diagnostic. Table 9-24 shows the manifestation 5. Minnaganti VR. Dipylidiasis. http://www.emedicine.com/med/
of disease in humans and other animals. TOPIC573.htm. Accessed August 13, 2008.
and animals: vol 3: chlamydioses, parasitoses. 3rd ed. Washington DC:
Pan American Health Organization; 2003.
Treatment 7. Samkari A, Kiska DL, Riddell SW, et al. Dipylidium caninum mimick-
ing recurrent Enterobius vermicularis (pinworm) infection. Clin Pediatr
The goal of treatment in humans and other animals is the (Phila). 2008;47:397-9.
elimination of the cestodes. Table 9-25 summarizes rec- 8. Cirioni O, Giacometti A, Burzacchini F, et al. Unusual neurological pre-
ommended treatment regimens for dipylidiasis in different sentation of dipylidiasis in a child. Eur J Ped. 1996;155(1):67.
species. 9. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to antimicro-
bial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy; 2009.
Flea control is also important for dogs and cats. This can 10. Barr SC, Bowman DD. 5-minute veterinary consult clinical companion
be accomplished with monthly treatments of selamectin, canine and feline infectious disease and parasitology. Ames, IA: Wiley-
lufenuron, imadacloprid, fipronil,10 or spinosad. Blackwell; 2006.
ECHINOCOCCOSIS
Peter M. Rabinowitz and Lisa A. Conti • Regularly examine and treat high-risk dogs and cats
(e.g., sheep dogs).
Echinococcosis (ICD10B-67) • An experimental recombinant vaccine is available for
sheep in high-risk areas.
Echinococcosis due to Echinococcus granulosus (ICD-10
B67-67.4), echinococcosis due to Echinococcus multilocularis
(ICD-10 B67.9) Agent
Other names in humans: hydatid disease, cystic hydatid The causative agent of echinococcosis in humans is the lar-
disease, alveolar hydatid disease, echinococciasis val (hydatid) phase of Cestodes (tapeworms) in the genus
Echinococcus, including E. granulosus, E. multilocularis, E. oli-
Other names in animals: hydatid disease, hydatid cyst, uni- garthrus, and E. vogelii (Figures 9-40 and 9-41).1 Cystic echi-
locular hydatid disease, cystic echinococcosis, hydatidosis nococcosis is causes by E. granulosus, whereas E. multilocularis
causes alveolar echinococcosis.
Echinococcosis is a potentially fatal zoonotic tapeworm
infection. Dogs and other canids are the definitive host of
Echinococcus granulosus; therefore cases in humans are typ- Geographical Occurrence
ically related to contact with domestic dogs. The types of E. granulosus is found on every continent except Antarctica.
human-dog contact and the way that dogs are raised and fed In the United States, human cases are more likely to be found
determine the degree of human risk. in areas where there is contact between dogs and sheep,
such as in the western states. In Alaska, a sylvatic strain of E.
granulosus is found in caribou and moose; dogs that eat the
Key Points for Clinicians and Public Health viscera of these infected animals can then infect humans.2,3
Professionals E. oligarthus and E. vogelii are found only in Central and
South America. Alveolar echinococcosis caused by E. mul-
Public Health Professionals tilocularis is restricted to the northern hemisphere.
• Provide descriptive epidemiology regarding the risk in
the community. Groups at Risk
• Prevent dogs, cats, and foxes from contaminating play-
grounds and other public areas with feces. Echinococcosis tends to occur in well-defined groups who have
• Educate the public to thoroughly wash all fruits and contact with dogs that ingest the raw viscera of infected ani-
vegetables before consuming them. mals. These include sheepherders who use dogs and persons in
• Educate pet owners to not allow dogs and cats to roam Alaska who allow dogs to feed on entrails of wild caribou and
outside or feed on raw carcasses. moose. Many of the cases diagnosed in the United States are in
• Ensure that workers with occupational risk for immigrants from countries where contacts between dogs and
Echinococcus infection (e.g., sheep ranchers, wild- sheep and cattle are common.4 Children may be at greater risk
life rehabilitators) receive adequate surveillance and of infection because of close contact with dogs.
reduction of exposure risk through exposure controls
and protective equipment.

• Disease is reportable in some states.
• Counsel dog owners to wash hands after handling pet
and to avoid contact with animal feces.
• Counsel all patients to thoroughly wash vegetables and
fruits before consumption.
• Ensure that high-risk groups (e.g., veterinarians, labo-
ratory workers, and wildlife rehabilitators) frequently
exposed to foxes and wild animals use protective mea-
sures (gloves and handwashing).
• Counsel clients to avoid feeding raw meat to dogs and
cats and to not allow pets to hunt.
• Train veterinary personnel in biosafety measures to Figure 9-40 n Scolex from hydatid cyst. (From Centers for Disease
reduce risk from infected dogs and wild animals. Control and Prevention Public Health Image Library, Atlanta, Ga.)
intestinal wall, they lodge in the liver, lung, or other tissues.

There they form cysts containing protoscolices. E. granulosus
tends to form large, slowly growing unilocular cysts with a
well-defined limiting membrane. By contrast, E. multilocu-
laris form multilocular cysts, also known as “alveolar” cysts,
without a limiting membrane and grow more aggressively.4
This results in the potential for E. multilocularis to cause
more serious complications. When dogs feed on the carcass
of an intermediate host containing cysts, the protoscolices
develop into adult worms in the dog intestine (Color Plate
9-20).

Contamination of the environment by egg-containing feces
of infected canids is an important factor in transmission of
Echinococcus. Feces containing eggs can contaminate grazing
areas of sheep and other ruminants, leading to infection of
these animals.8 Echinococcus eggs can survive in the environ-
ment for weeks to months under optimal conditions.9
Dogs that defecate near vegetable gardens or otherwise
contaminate sources of food and water can be a source of
infection for humans. Factors that increase the abundance
of foxes and rodents (potentially infected with E. multilocu-
laris) around dwellings can increase the risk of infection to
Figure 9-41 n Echinococcus granulosus (Taeniidae), entire worm (×44).
(From Bowman DD: Georgis’ parasitology for veterinarians, ed 8, St Louis,
humans and domestic animals; these can include the pres-
2003, Saunders Elsevier.) ence of food sources including pet food and bird seed from
bird feeders.
Reported risk factors for E. multilocularis infection Disease in Humans

include owning dogs that kill game or roam outdoors, living
in a farmhouse or near a field, growing vegetables, owning Table 9-26 shows the clinical features of Echinococcus infec-
outdoor cats, or eating unwashed fruit.5 tion in humans and other animals.
Hosts, Reservoir Species, Vectors Echinococcosis Caused by E. granulosus (Cystic or

Unilocular Hydatid Disease)
Dogs and wild canids are the definitive hosts for E. granulo-
sus. The adult tapeworms reproduce in the dog intestine and The cysts tend to be slow growing, unilocular, and often
shed gravid proglottids or eggs in the feces. These eggs can asymptomatic for many years. The size may reach 15 cm
remain viable in moist conditions with moderate tempera- or larger. Many cysts are discovered only during imaging
tures for months. Intermediate hosts include a wide variety performed for other reasons (Figure 9-43). The severity of
of herbivores as well as mongooses, non-human primates, disease depends largely on the organ involved and cyst size
and humans. and number. Most hydatid cysts are found in the liver (50%
The growing urban populations of red and arctic foxes, to 70%) and lungs (20% to 30%) but more rarely can involve
the primary definitive host for E. multilocularis, increase spleen, muscles, heart, kidney, and even the brain. Symptoms
concern for human risk of infection.6 The intermediate develop if a cyst becomes large enough to affect organ func-
hosts for E. multilocularis are usually rodents, including tion or cause pain or if cysts rupture or become superin-
mice, shrews, lemmings, and voles.7 In addition to foxes, fected. Liver cysts can cause abdominal pain, whereas lung
dogs and cats that hunt such animals can subsequently cysts can cause chest pain, cough, hemoptysis, and embo-
infect humans.8 lism.7 Cyst rupture or leak suddenly, producing anaphylactic
reactions, release of protoscolices, eosinophilia, and second-
Mode of Transmission and Life Cycle ary infectious complications.8
The adult tapeworms living in the intestine of a dog or Echinococcosis Caused by E. multilocularis
other carnivore release eggs that are shed in the feces (Figure
9-42). Human infection occurs by ingesting these eggs, either Cysts tend to grow more aggressively than those of E. granu-
through contamination of food or by direct contact with dogs losus, almost always involving the liver, but capable of form-
or other definitive hosts. Children are often infected because ing metastases in other organs (Figure 9-44). Symptoms can
of more intimate contact with dogs and frequent hand-to- include pain, jaundice, weight loss, and hepatic obstruction,
mouth contact. Once ingested, the eggs hatch into larvae with sometimes fatal complications. The clinical picture
(oncospheres) in the small intestine. Migrating through the can thus resemble hepatic carcinoma. The World Health
Figure 9-42 n Life cycle/transmission, Echinococcus granulosus infection. 1, Adult worms in bowels of definitive host.
2, Eggs passed in feces, ingested by humans or intermediate host. 3, Onchosphere penetrates intestinal wall, carried via
blood vessels to lodge in organs. 4, Hyatid cysts develop in liver, lungs, brain, and heart. 5, Protoscolices (hydatid sand)
ingested by definitive host. 6, Attached to small intestine and growth to adult worm. (Modified from Centers for Disease
Control and Prevention Public Health Image Library, Atlanta, Ga.)
Table 9-26 n Clinical Presentation of Echinococcosis in Humans and Other Animals
Species Risk Factors Incubation Period Clinical Manifestations Diagnostic Findings
Humans: hydatid cyst Children in rural areas, 12 months to years Often asymptomatic, Cyst seen on imaging,
disease sheep herders with abdominal pain serology
contact with dogs that
feed on carcasses
Echinococcus Proximity to fox populations, Pain, jaundice, weight Elevated bilirubin levels
multilocularis ownership of dogs or cats loss, hepatic Irregular cysts on
that roam outside and obstruction imaging, may have
feed on rodents calcifications
Dogs Feeding on infected Adult worms produce Usually asymptomatic, Fecal examination for
carcasses or rodents eggs 27-61 days after enteritis with high eggs, adult worms, or
infection1 parasite load proglottids
Sheep, goats, pigs, Pastures contaminated Months to years Usually asymptomatic, Cysts on necropsy
horses with dog feces bloating may occur
Wild caribou, Grazing areas contaminated
moose by wolf, dog feces
Rodents Areas contaminated by Months Symptomatic, fatal cysts
feces of definitive host may occur
Figure 9-43 n CT image of large hydatid cyst in liver caused by Echinococcus

granulosus. The membranes of multiple internal daughter cysts are visible
within the primary cyst structure. (From Kliegman RM, Behrman RE, Jenson
HB et al: Nelson textbook of pediatrics, ed 18, Philadelphia, 2007, Saunders
Elsevier. Courtesy John R. Haaga, University Hospitals, Cleveland, Ohio.)
Figure 9-45 n A hydatid cyst (Echinococcus granulosus) in the liver

of a horse (about natural size). This horse displayed no clinical signs of
hepatic involvement despite the presence of 20 to 30 cysts like the one illus-
trated. (From Bowman DD: Georgis’ parasitology for veterinarians, ed 8,
St Louis, 2003, Saunders Elsevier.)
Intermediate hosts for E. granulosus, including sheep,

goats, and horses, develop cystic disease that is generally
subclinical, although jaundice, ascites, bronchopneumonia,
decreased growth, and lameness have been reported (Figure
9-45 and Color Plate 9-21).12 Rodents may develop clinical
cystic disease from E. multilocularis.1 Nonhuman primate
deaths have been reported from zoologic institutions.
Figure 9-44 n CT image of alveolar cyst due Echinococcus multilocu-
laris in right lobe of liver. Note irregular densities and areas of calcification. Diagnosis
(From Long SS, Pickering LK, Prober CG: Principles and practice of pediatric
infectious disease, ed 3, Edinburgh, 2008, Churchill Livingstone Elsevier.) The initial diagnosis is often made using ultrasound, com-
puted tomography (CT), or magnetic resonance imaging
(MRI). The differential diagnosis in human beings includes
Organization (WHO) has devised a clinical staging system
tumors, abscesses, and tuberculosis. When echinococcosis is
for alveolar echinococcosis based on parasitic mass, nodes,
suspected, serologic testing is performed using immunoblot
and metastases (PNM) similar to cancer tumor staging.10
or ELISA but is not 100% sensitive. Fine-needle aspiration of
cyst contents can help make the diagnosis in equivocal cases
by demonstrating protoscolices in the cyst fluid but carries a
Polycystic Hydatid Disease Cause by E. vogelii and risk of cyst rupture and leakage.
E. oligarthus In definitive host animals, arecoline purgatives can result
These are comparatively rare infections that usually involve in finding adult parasites or proglottids. In an experienced
the liver or lungs and are characterized by the development laboratory, fecal examination can reveal tapeworm eggs.
of multiple microcysts. A stool-based PCR test (copro-PCR) is also available.13 In inter-
mediate hosts, diagnosis can be made on histologic samples.
Disease in Animals Treatment

Adult Cestode worms in the intestine of dogs, cats, and other Treatment of hydatid cyst disease in humans depends on
definitive hosts rarely cause serious disease,11 although large the location of the cyst. While treatment is often surgical,
parasite burdens can result in signs of enteritis. the technique of puncture-aspiration-injection-reaspiration
Table 9-27 n Echinococcus Infection: Treatment in Humans and Other Animals
Disease Agent Species Primary Alternative
E. granulosus Humans Puncture-aspiration-injection-reaspiration with albendazole Surgical drainage

before and after drainage (>60 kg; 400 mg PO bid;
<60 kg; 15 mg/kg/day divided bid and for 28 days after15)
E. multilocularis Wide surgical excision, albendazole as for hydatid disease
can be tried but efficacy unclear15
Dogs* Praziquantel 5 mg/kg PO, SC once Epsiprantel 5.5 mg/kg PO once
Cats* Praziquantel 5 mg/kg PO, SC once Epsiprantel 2.8 mg/kg PO once16
*Not in animals younger than 4 weeks.
(PAIR) with the adjunctive use of an antihelminthic appears 5. Kern P, Ammon A, Kron M, et al. Risk factors for alveolar echinococ-
promising as an alternative for the treatment of uncompli- cosis in humans. Emerg Infect Dis. 2004;10(12):2088.
6. Deplazes P, Hegglin D, Gloor S, et al. Wilderness in the city: the urbaniza-
cated cysts.14 Albendazole is given before the procedure; then tion of Echinococcus multilocularis. Trends in Parasitol. 2004;20(2):77.
the cyst is aspirated and injected with hypertonic saline solu- 7. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
tion or alcohol and is then reaspirated with final irrigation. handbook for primary care. St Louis: Mosby Elsevier; 2006.
Albendazole treatment is then continued for 28 days. Such 8. Heymann DL. Control of communicable diseases manual. 19th ed.
treatment produces cure in more than 90% of cases.15 The 9. Veit P, Bilger B, Schad V, et al. Influence of environmental factors
treatment for alveolar echinococcosis is wide surgical exci- on the infectivity of Echinococcus multilocularis eggs. Parasitology.
sion, although albendazole can be tried in similar doses to 1995;110(Pt 1):79.
that used in E. granulosus infection. 10. Kern P, Wen H, Sato N, et al. WHO classification of alveolar echinococ-
In the definitive animal host, tapeworms are treated with cosis: principles and application. Parasitol Int. 2006;55(suppl):S283.
11. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse
antihelminthics. Table 9-27 provides treatment information Station, NJ: Merck; 2005.
for humans and other animals. 12. Dvorak GA, Rovid-Spickler A, Roth JA, eds. Handbook for zoonotic
diseases of companion animals. The Center for Food Security & Public
Health. Ames, IA: Iowa State University; 2006.
References 13. Craig PS, McManus DP, Lightowlers MW, et al. Prevention and control
of cystic echinococcosis. Lancet Infect Dis. 2007;7(6):385.
1. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man 14. Nasseri Moghaddam S, Abrishami A, Malekzadeh R. Percutaneous
and animals: vol 3: chlamydioses, parasitoses. 3rd ed. Washington DC: needle aspiration, injection, and reaspiration with or without benz-
Pan American Health Organization; 2003. imidazole coverage for uncomplicated hepatic hydatid cysts. Cochrane
2. Moro P, Schantz PM. Cystic echinococcosis in the Americas. Parasitol Database Syst Rev. 2006;(2):CD003623.
Int. 2006;55(suppl):S181. 15. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti-
3. Schantz PM. Echinococcosis. In: Steele JH, ed. CRC handbook series microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
in zoonoses, Section C: Parasitic zoonoses. Vol. 1. Boca Raton, FL: CRC 2009.
Press; 1982:231–277. 16. Barr SC, Bowman DD. 5-minute veterinary consult clinical companion
4. Chrieki M. Echinococcosis—an emerging parasite in the immigrant canine and feline infectious disease and parasitology. Ames, IA: Wiley-
population. Am Fam Physician. 2002;66(5):817. Blackwell; 2006.
EHRLICHIOSES AND ANAPLASMOSIS
Peter M. Rabinowitz and Lisa A. Conti Ehrlichiosis and anaplasmosis refer to several potentially
serious tickborne diseases caused by related members of
Erlichioses and anaplasmosis (ICD-10 A79.8) the family Anaplasmataceae. These diseases are transmit-
ted to people and domestic animals by specific ticks that
Other names in humans: human monocytic ehrlichiosis become infected by feeding on wildlife reservoirs. Recent
(HME), human granulocytic anaplasmosis (HGA), ehrlichi- taxonomic changes have reclassified some of these agents
osis ewingii formally broadly called Ehrlichia into two genera; Ehrlichia
and Anaplasma. New accepted terminology to describe these
Other names in animals: canine monocytic ehrlichiosis, diseases in humans includes ehrlichiosis to refer to diseases
canine hemorrhagic fever, tropical canine pancytopenia, caused by infection with Ehrlichia chaffeensis and Ehrlichia
canine rickettsiosis, tracker dog disease, canine typhus, tick- ewingii, and anaplasmosis to describe disease caused by
borne fever, pasture fever, equine anaplasmosis, Potomac horse Anaplasma phagocytophilum. There are a number of simi-
fever, equine monocytic ehrlichiosis, infectious canine cyclic lar diseases in dogs and other animals. Anaplasmataceae
thrombocytopenia provide an excellent example of the need for animal and
human health professionals to work together since they

were recognized as animal pathogens several decades before Box 9-3 Integrated Pest Management to Reduce
Tick Populations Around Dwellings
being described in human infection.1 As with several other
zoonotic diseases, recent advances in molecular diagnostics
Some actions to consider in an integrated pest management
are shedding new light on the true prevalence of infection
approach include:
and the degree of overlap between human and animal ehrli- • Keep grass mowed.
chioses. Discoveries using animal models of infection with • Remove leaf litter, brush, and weeds at the edge of the lawn.
these agents also may further our understanding of diagnos- • Restrict the use of groundcover, such as pachysandra, in areas
tic and treatment options in humans. frequented by family and pets.
• Remove brush and leaves around stone walls and wood piles.
• Discourage rodent activity. Clean up and seal stone walls and
small openings around the home.
Key Points for Clinicians and Public Health • Move firewood piles and bird feeders away from the house.
Professionals • Use veterinary-approved tick prevention products on pets;
perform daily tick checks on pets and safely remove and
dispose of ticks.
Public Health Professionals • Use plantings that do not attract deer, or exclude deer through
various types of fencing.
• Provide epidemiologic analysis of these reportable • Move children’s swing sets and sand boxes away from the
diseases and assessment of local ehrlichiosis and ana- woodland edge and place them on a wood chip or mulch-type
plasmosis disease risk for the health district. foundation.
• Educate the public to: • Trim tree branches and shrubs around the lawn edge to let in
 Avoid tick-infested areas, but if this is not possible, more sunlight.
wear appropriate clothing (long sleeves, long pants, • Adopt hardscape and xeriscape (dryer or less water-
tuck pants legs into socks, and wear light-colored demanding) landscaping techniques with gravel pathways and
mulches. Create a 3-foot or wider wood chip, mulch, or gravel
clothing to visualize ticks). Wash clothes with hot
border between lawn and woods or stone walls.
water.2 • Consider areas with decking, tile, gravel, and border or
 Use CDC-recommended tick repellents such as container plantings in areas by the house or frequently traveled.
DEET or permethrin (apply to clothes, not skin) • Widen woodland trails.
where ticks are abundant. Be sure to follow label • Consider a least-toxic pesticide application to tick-infested
instructions before using any repellent. areas of high human exposure.
 Do frequent tick checks to remove even tiny imma-
Adapted from Stafford KC: Tick management handbook: an integrated guide for home
ture-stage ticks. owners, pest control operators, and public health officials for the prevention of tick-associated
 Encourage adults to inspect children at least once disease, revised edition, 2007, The Connecticut Agricultural Experiment Station, The
Connecticut General Assembly, Bulletin No. 1010.
daily for ticks. When in heavily infested areas,
inspect children every 3 to 4 hours.
 Use appropriate technique to remove ticks. Wear
gloves or grasp tick with tweezers as close to the
skin as possible and pull gently, or use a tick-remov- tickborne disease prevention measures and are taking
al spoon. Follow-up by cleaning the area, applying precautions.
antibiotic topical on tick bite site, and washing • Ask patients about occurrence of tickborne disease in
hands.3 their pets.
 Discourage the use of matches, petroleum products, • No ehrlichial vaccine is currently commercially avail-
or nail polish as tick removal methods.3 able for humans.
 Implement integrated pest management tech-
niques including landscape management (Box Veterinary Clinicians
9-3). Counsel pet owners to discuss tickborne dis-
ease prevention strategies with their veterinarian. • Counsel clients to use protection (e.g., gloves, tick
• Work with local planning agencies on smart growth to removal devices) when removing ticks from pets.
avoid fractionating forested areas (see Chapter 6, Built • Counsel owners about the potential for human infec-
Environment). tion related to shared environmental exposures, espe-
cially upon identification of seropositive pets.
• Treat pets preventively against ectoparasites.
• An equine vaccine against Neorickettsia risticii (formerly
• Report cases of disease to public health authorities Ehrlichia risticii) is commercially available in the
using the appropriate case definition: http://www. United States.
cdc.gov/ncphi/disss/nndss/casedef/ehrlichiosis_2008.
htm. Agent
• Counsel patients to avoid tick exposure or advise about
use of appropriate tick repellents. A number of related agents cause ehrlichioses and anaplas-
• Inquire about occupational risk factors for infection mosis in humans and other animals. These agents are gram-
and ensure that workers at risk are educated about negative, obligate intracellular coccobacilli bacteria that
now includes the agent formerly called E. equi) also infects

neutrophils. The disease in humans was formerly termed
human granulocytic ehrlichiosis (HGE); it is now referred to
as human granulocytic anaplasmosis (HGA) or, most com-
monly, simply anaplasmosis. Strains of A. phagocytophilum
also cause disease in dogs, horses, ruminants and, rarely,
cats.5 A. platys is a canine pathogen that infects platelets and
causes a disease known as infectious canine cyclic thrombocy-
topenia; it is not thought to be a significant human patho-
gen. Another canine pathogen, E. canis, causes ehrlichiosis
in dogs; although it is not considered a highly likely zoonotic
agent, at least one case of human infection with E. canis has
been reported.6 Neorickettsia sennetsu causes a febrile syn-
drome (sennetsu fever) that is rare outside Asia.7
Figure 9-46 n A canine neutrophil containing an Ehrlichia ewingii

morula. (Wright’s stain, original magnification ×250.) (From Cowell RL, Geographical Occurrence
Tyler RD, Meinkoth JH et al (eds): Diagnostic cytology and hematology of the
dog and cat, ed 3, St Louis, 2008, Mosby Elsevier.) The distribution of both human and domestic animal cases
of the various ehrlichioses and anaplasmosis varies largely
depending on the distribution of tick vector and reservoir
species (Color Plate 9-22). For instance, although human
cases of E. chaffeensis have been reported in almost every
state in the United States, cases are most frequently reported
from the southeastern and Midwestern states where white-
tailed deer (Odocoileus virginianus) and Lone Star ticks
(Amblyomma americanum) coexist. E. chaffeensis is restricted
to the United States. A. phagocytophilum is found interna-
tionally in association with the distribution of Ixodes ticks. In
the United States, human cases of A. phagocytophilum occur
particularly in the upper Midwest, Northeast, and West
Coast, where the primary vectors Ixodes scapularis and Ixodes
pacificus exist; the distribution of infection is similar to that
of Lyme disease. Although dogs seropositive for E. canis have
been found throughout most of the United States, most
canine cases occur in areas with an increased concentration
of the brown dog tick (Rhipicephalus sanguineus) such as the
southeastern states and the Southwest. In the United States,
E. canis is mainly found in the Gulf Coast states and Eastern
Seaboard, Midwest, and California.8
Figure 9-47 n Ehrlichia inclusion in the mononuclear cell of a cat. (From
Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders
Elsevier. Courtesy Mike Lappin, Colorado State University, Fort Collins,
Colo.) Groups at Risk
As in other tickborne diseases, the risk of ehrlichioses and
anaplasmosis varies between and within regions and is gen-
parasitize leukocytes, erythrocytes, endothelial cells, or plate- erally related to the abundance of host ticks that can carry
lets (Figures 9-46 and 9-47). The bacteria within the family the disease. Individuals living in areas of high tick abundance
Anaplasmataceae that have been documented to cause dis- are at increased risk. Immunocompromised individuals are
ease in humans are Ehrlichia chaffeensis, Anaplasma phagocy- at risk of infection with severe disease.
tophilum, Ehrlichia ewingii, Ehrlichia canis, and Neorickettsia
sennetsu. Hosts, Reservoir Species, Vectors
E. chaffeensis affects monocytic phagocytes, and the dis-
ease it causes in humans was formerly termed human mono- Infected animals are not believed to pose a substantial direct
cytic ehrlichiosis (HME) but is now most commonly referred zoonotic risk to humans. In general, animal infections serve
to as ehrlichiosis. E. chaffeensis is mainly a human pathogen as a means of sustaining infections in tick vectors, and
but also causes diseases in dogs. E. ewingii is found in neu- humans and other animals acquire infection from tick bites.
trophils, especially in immunocompromised patients.4 It was White-tailed deer (O. virginianus) are considered a likely
formerly in the disease category “human ehrlichiosis, unspec- major reservoir for E. chaffeensis and E. ewingii,4 and dogs
ified” and now is described as E. ewingii ehrlichiosis when it may also play a role. The primary reservoir for A. phagocy-
causes disease in humans; it has also been found to cause tophilum consists of small mammals, including deer mice
canine infections. The organism A. phagocytophilum (which (Peromyscus) and wood rats (Neotoma), although deer may
also play a role.9 Vectors of A. phagocytophilum are ticks of infection for E. chaffeensis. Most infections in the United
the genus Ixodes, including I. scapularis, I. ricinus, I. pacifi- States occur between May and August, coincident with peri-
cus, I. triangulaceps, I. spinipalpis, and I. persulcatus (Color ods of peak tick feeding activity.9 Direct transmission between
Plate 9-23).4 These hard ticks are also the vector for Borrelia humans and other mammals has not been reported.
burgdorferi, Babesia microti, and tickborne encephalitis;
therefore coinfection is common. The vector for E. chaffeen-
sis and E. ewingii is the Lone Star tick (A. americanum). In Environmental Risk Factors
dogs, the brown dog tick (R. sanguineus) is the principal vec-
tor for A. platys and E. canis.10 Dermacentor variabilis, the The relation of environmental factors to the risk of anaplas-
American dog tick, can also be a vector of E. canis infection.11 mosis and ehrlichiosis may resemble that for Lyme disease,
Accidental hosts for these agents include humans, dogs, cats, with landscape modification in the United States related to
and ruminant animals. suburbanization of the human population playing a signifi-
cant role. These suburban developments encroach into land
that was previously forest habitat and result in “fragmenta-
tion” of forests (see Chapter 6). This provides habitat for deer
Most ehrlichioses are tickborne infections. The larval, and small mammals that can serve as reservoirs for certain
nymphal, and adult forms of the tick vectors are capable of Ehrlichia and Anaplasma and also increases tick abundance
transmitting infections. Figure 9-48 shows the life cycle of and infection rates.
Figure 9-48 n Life cycle/transmission, E. chaffeensis. Noninfected larvae obtaining blood from a bacter-
emic vertebrate reservoir host (e.g., white-tailed deer [shaded]), become infected, and maintain Ehrlichieae to
the nymphal stage. Infected nymphs may transmit E. chaffeensis to susceptible reservoir hosts (unshaded) or to
humans during acquisition of blood. Infected adult ticks, having acquired Ehrlichieae either by transtadial trans-
mission from infected nymphal stage or during blood meal acquisition as noninfected nymphs on infected deer,
may also pass E. chaffeensis to humans or other susceptible reservoirs. Transovarial transmission has not been
demonstrated, and eggs and unfed larvae are presumably not infected. (From Paddock CD, Childs JE: Ehrlichia
chaffeensis: a prototypical emerging pathogen, Clin Microbiol Rev 16(1):37, 2003.)
Climate change with warmer winters may also be leading including fever, anorexia, pale mucous membranes, and
to increased tick abundance during the following spring and weight loss has been described. 16 A few cases of feline
summer.12 Wild birds may play a role in dispersing the Ixodes A. phagocytophilum infections, also known as feline granulo-
tick vectors that can transmit A. phagocytophilum.13 cytotropic anaplasmosis, have been described in cats. Clinical
signs associated with these infections include fever, anorexia,
and lethargy.
Disease in Humans A. phagocytophilum causes tickborne fever (also known as
pasture fever) in cattle, sheep, and other ruminants, predomi-
Human ehrlichioses caused by E. chaffeensis, E. ewingii, or
nantly in Europe (Figure 9-49). The clinical signs are listed in
E. canis and anaplasmosis (HGA) caused by A. phagocytophi-
Table 9-28. Equine anaplasmosis (formerly equine ehrlichio-
lum can present as clinical syndromes that share a number of
sis) is also caused by A. phagocytophilum (formerly E. equi)
common features, including fever, headache, and myalgias,
and consists of a febrile disease resembling human anaplas-
with laboratory findings of thrombocytopenia, leukopenia,
mosis. Table 9-28 shows the comparative clinical presenta-
and elevated liver function test results.
tions in humans and other animals.
Rash is not a common feature of all ehrlichioses and ana-
plasmosis, although it may occur in up to 30% of children with
E. chaffeensis infections. When present, it is maculopapular, Diagnosis
not petechial.14 E. chaffeensis may cause more severe disease
than the other pathogens, and CNS involvement may occur
in up to 20% of cases, including meningitis and meningoen- Diagnosis in Humans
cephalitis. Septic shock and respiratory distress syndrome can
also develop in patients with E. chaffeensis. Severe complica- Ehrlichial infections in humans can resemble other tickborne
tions and even death are more common among immunocom- febrile syndromes. A history of a tick bite and thrombocy-
promised patients. The overall mortality rate of E. chaffeensis topenia, leukopenia, and elevated liver function test results
disease is approximately 3%.9 Coinfections with other agents favor the diagnosis. Unlike Rocky Mountain spotted fever
sharing the same tick vector are not uncommon; therefore (RMSF), vasculitis is not present in ehrlichial infections.14
Lyme disease, babesiosis, or tickborne encephalitis may be In HME, rapid laboratory diagnosis is possible when cellular
seen in up to 10% of E. chaffeensis cases.9 stippling of intracytoplasmic inclusions (morulae) in mono-
Peripheral neuropathy may develop in patients with cytes are seen, although this is uncommon (see Figure 9-49),
A. phagocytophilum, but severe complications and fatalities while in HGA, morulae in neutrophils and bands can be seen
are less common (case fatality rate approximately 0.7%) than more commonly (in up to 20% to 80% of cases14; Color Plate
with E. chaffeensis. 9-28 and Figure 9-50). A PCR test using ethylenediamine
tetraacetic acid (EDTA) or citrate-anticoagulated blood is
becoming the standard method of diagnostic confirmation
Disease in Animals for both conditions.14 The organisms can also be grown in
cell cultures but this may take several weeks. Serologic tests
Canine ehrlichiosis is a multisystemic disorder that can cause
using a fluorescent antibody reaction can be used to compare
a variety of clinical signs, including fever, anorexia, CNS signs,
acute and convalescent titers, and demonstration of a four-
hemorrhagic conjunctivitis, vasculitis, splenomegaly, and
fold change in titers is considered the most sensitive method
lymphadenopathy (Color Plates 9-24 to 9-27). The course of
of detecting infection, although the test may cross-react with
the infection may be subclinical, acute, or chronic.15 Although
cases of canine ehrlichiosis confirmed via cytology or serol-
ogy have been attributed to E. canis, it is now thought that
some cases may have been related to infections with E. chaf-
feensis, E. ewingii, or A. phagocytophilum.16 Doberman pin-
schers and German shepherd dogs are considered by some
to be more likely than other breeds to have severe chronic
E. canis infection.15 E. ewingii causes polyarthritis with fever
and hepatosplenomegaly in dogs.15 Concurrent infection
with other Ehrlichia, Anaplasma, Babesia, Haemobartonella,
or Hepatozoon organisms can worsen the clinical course of
ehrlichiosis in dogs.
Canine anaplasmosis caused by A. phagocytophilum is
thought to produce a milder clinical syndrome with fever,
lethargy, and thrombocytopenia. A. platys causes a moderate
to severe cyclic thrombocytopenia in dogs; however, bleeding
complications are rare.15
Clinical ehrlichiosis has also been described in cats.
Although the species of Ehrlichia that naturally infects cats Figure 9-49 n Chronic weight loss in a goat as a sequela to anaplasmosis.
(From Pugh DG: Sheep & goat medicine, St Louis, 2002, Saunders. Courtesy
has not been fully determined, clinical illness with signs Tom Powe and D.G. Pugh, Auburn University, Auburn, Ala.)
Table 9-28 n Ehrlichioses and Anaplasmosis: Comparative Clinical Presentations in Humans and
Other Animals
Incubation Clinical
Species Agent Risk Factors Period Manifestations Lab Findings
Humans
Human ehrlichiosis Ehrlichia chaffeensis, Tick exposures 7-10 days Fever, myalgias, rash, Thrombocytopenia,
(HME) E. ewingii respiratory distress, leukopenia, elevated liver
CNS and hepatic function tests, morulae
E. canis17 involvement in monocytes (rare)
Human anaplasmosis Anaplasma 7-14 days4 Fever, myalgias, Thrombocytopenia,
(HGA) phagocytophilum peripheral leukopenia, morulae
neuropathies seen in neutrophils,
bands (20%-80% of
cases)14; elevated liver
function tests4
Dogs
Canine ehrlichiosis E. canis, E. chaffeensis, Tick exposures, 1-3 weeks15 May be subclinical, acute, Leukopenia, anemia
E. ewingii animals allowed or chronic; vasculitis,
to roam outdoors ataxia, hemorrhagic
conjunctivitis,
hepatosplenomegaly,
lymphadenopathy,
polyarthritis
Canine anaplasmosis
A. phagocytophilum Mild illness: fever, Thrombocytopenia15
lethargy
Infectious cyclic canine A. platys Moderate to severe Thrombocytopenia

thrombocytopenia thrombocytopenia,
bleeding rare
Cats A. phagocytophilum, Tick exposures, Rare; fever, anorexia, Thrombocytopenia,
E. canis animals allowed lethargy leukopenia, anemia
to roam outdoors
Cattle, Sheep,
Goats, Deer
Tickborne fever A. phagocytophilum Tick exposures in 2-6 days Fever, lethargy, weight Neutropenia,
(Pasture fever) endemic areas loss, decreased lymphocytopenia,
lactation, abortion, thrombocytopenia10
lymphadenopathy
Horses
Equine anaplasmosis A. phagocytophilum 10-45 days Fever, ataxia, Morulae seen in
depression neutrophils
other diseases, including Lyme disease and RMSF.9 PCR test- and organism cultivation may be useful in confirming the
ing may help resolve problems of cross-reactivity between diagnosis.
species that can occur with serology testing.
Treatment
Diagnosis in Animals
Antibiotic treatment of ehrlichial infection in humans and
In dogs, serology using IFA is commonly used with titers is other animals is shown in Table 9-29.
more reliable 3 weeks after infection. Although IFA is sensi-
tive, the test may not be very specific because of cross-reac- Treatment in Humans
tivity between E. ewingii and E. canis, as well as E. canis and
A. phagocytophilum. Standardized serologic tests for feline Because of the serious nature of Ehrlichia and Anaplasma
patients are needed. Depending on the ehrlichial species, infections, early initiation of antibiotic treatment is rec-
cytology may be a useful tool for detecting the presence of ommended when the diagnosis is suspected. Doxycycline
morulae in blood or tissue smears. Depending on the type is considered the first line of treatment (see Table 9-29).
of animal and ehrlichial species, any one or a combination In pregnancy, rifampin has been recommended by some
of other testing such as PCR, serology, immunoblotting, authorities.
acute disease and prompt treatment. Prognosis is poor for

dogs with E. canis infection that progresses to hypoplas-
tic marrow; anabolic steroids may be needed to stimulate
bone marrow production. In ruminants, administration
of oxytetracycline early in the course of the disease may
be beneficial. Tick and infection control strategies are con-
sidered effective herd health strategies to prevent clinical
cases.18 Previous infection can produce immunity in horses
for several years.10
References
1. Maeda K, Markowitz N, Hawley RC, et al. Human infection
with Ehrlichia canis, a leukocytic rickettsia. N Engl J Med. 1987;
316(14):853.
2. Centers for Disease Control and Prevention. Division of Vector Borne
Figure 9-50 n Peripheral blood smear showing intracellular inclusion Infectious Diseases; Lyme disease. http://www.cdc.gov/ncidod/dvbid/
within a neutrophil of a patient with human granulocytic anaplasmosis lyme/Prevention/ld_Prevention_Avoid.htm. Accessed September 28,
(arrows). (Wright stain, ×1000.) (From Mandell GL, Bennett JE, Dolin R 2008.
(eds): Principles and practice of infectious diseases, ed 6, Philadelphia, 2005, 3. Placerville Veterinary Clinic. Tick removal tools: what should I use
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5. Magnarelli LA, Bushmich SL, Ijdo JW, et al. Seroprevalence of antibod-
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Infection in Humans and Other Am J Vet Res. 2005;66(11):1895.
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Animals parison of Ehrlichia canis isolates from dogs, ticks, and a human in
Venezuela. J Clin Microbiol. 2001;39(8):2788.
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Species Treatment Treatment eases, Ehrlichiosis. http://www.cdc.gov/ticks/diseases/ehrlichiosis.
Accessed December 15, 2008.
Humans: Doxycycline 100 mg Tetracycline 500 mg 8. Bockino L, Krimer PM, Latimer KS, et al. An overview of canine ehrli-
ehrlichiosis PO/IV bid × 7-14 PO qid × 7-14 chiosis, veterinary clinical pathology clerkship program. http://www.vet.
and days (not during days (not for uga.edu/vpp/clerk/Bockino. Accessed October 4, 2008.
anaplasmosis pregnancy) children or during 9. Dumler JS, Madigan JE, Pusterla N, et al. Ehrlichioses in humans: epide-
Children should receive pregnancy)19 miology, clinical presentation, diagnosis, and treatment. Clin Infect Dis.
doxycycline per 2007;45(suppl 1):S45.
standard guidelines 10. Kahn CM, Line S, eds. 9th ed.The Merck veterinary manual. Whitehouse
During pregnancy, Station, NJ: Merck; 2005.
consider treatment 11. Waner T. Hematopathological changes in dogs infected with Ehrlichia
with rifampin19 canis. Israel J Vet Med. 2008;63(1). http://www.isrvma.org/arti-
cle/63_1_3.htm. Accessed December 15, 2008.
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PO q12h or 10 mg/ dipropionate 5 mg/ sis in southern Sweden following mild winters and during warm, humid
kg PO q24h × 28 kg IM for 2 doses summers. Eur J Clin Microbiol Infect Dis. 2006;25(7):426.
days (give IV for 5 14 days apart15,20 13. Ogden NH, Lindsay LR, Hanincová K, et al. Role of migratory birds
days if the dog is or oxytetracycline in introduction and range expansion of Ixodes scapularis ticks and of
vomiting) and tetracycline Borrelia burgdorferi and Anaplasma phagocytophilum in Canada. Appl
22 mg/kg PO q8h Environ Microbiol. 2008;74(6):1780.
× 28 days 14. Mandell GL, Bennett JE, Dolin R, et al. Principles and practice of infec-
Horses Oxytetracycline 7 mg/ tious diseases. 6th ed. Philadelphia: Churchill Livingstone Elsevier;
kg IV SID × 8 days 2005.
15. Barr SC, Bowman DD. 5-minute veterinary consult clinical companion
canine and feline infectious disease and parasitology. Ames, IA: Wiley-
Blackwell; 2006.
16. Greene CE. Infectious diseases of the dog and cat. 3rd ed. St Louis:
Saunders Elsevier; 2006.
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Treatment in Animals accompanied by clinical signs in Venezuela (Abstract). Ann N Y Acad
Sci. 2006;1078:110.
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2009.
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ESCHERICHIA COLI INFECTION
Peter M. Rabinowitz and Lisa A. Conti for months in feces and soil. Disinfection agents
include 1% sodium hypochlorite, 70% ethanol, and
Escherichia coli infection (ICD-10 A04.0-A04.4) iodine-based solutions.7
• Ensure that local petting zoos and other areas where
Other names in humans: E. coli O157:H7, hemorrhagic the public has contact with animals have policies and
colitis procedures in place to reduce the risk of infection. This
includes providing access to handwashing stations,
Other names in animals: colibacillosis proper manure disposal, and separation of animals
from food areas.
The gram-negative bacterium Escherichia coli has hundreds • Provide descriptive epidemiology of disease in local
of different strains. These strains can be separated into three human and animal populations.
categories: (1) nonpathogenic, existing as commensal organ- • Coordinate with agriculture officials to ensure that
isms in the normal gut flora; (2) intestinal pathogenic, caus- food safety and farm safety measures are in place.
ing diarrhea in humans, including enterohemorrhagic E.
coli (EHEC); enterotoxigenic E. coli (ETEC); enteroinvasive Human Health Clinicians
E. coli (EIEC), enteropathogenic, enteroaggregative, and dif-
fuse-adherent1; and (3) capable of causing extraintestinal • Ensure adequate hydration and consider hospitalization
pathologenic E. coli (ExPEC). Case reports have linked entero- to reduce the risk of hemolytic uremic syndrome.1
pathogenic E. coli causing canine enteritis in a dog to colo- • Report cases immediately to local health authorities.
nization in a child,2 an outbreak of necrotizing pneumonia • Institute enteric precautions for patients.
in cats to a strain of ExPEC with molecular features resem- • Educate patients about personal hygiene and proper
bling human strains,3 and cases of edema in pigs tied to toxin- handwashing techniques.
producing strains resembling those occurring in humans.4 • Avoid the use of antibiotics in patients with Shiga
Urinary tract infections in humans have been linked with toxin–producing E. coli infections.
E. coli from food sources.5 It is likely that additional patterns
of interspecies transmission of E. coli infection will be recog- Veterinary Clinicians
nized in the future6; however, this chapter emphasizes cur-
rent knowledge regarding enterohemorrhagic strains, such as • Counsel animal handlers about hygiene, handwashing,
O157:H7. Pathogenic E. coli strains, particularly those that are and avoiding direct contact with feces.
antibiotic resistant, from the food supply are a public health • Prevent infection in puppies and kittens by cleaning
and economic concern. and disinfecting the parturition environment (1:32
dilution of bleach), ensuring adequate colostrum
intake, ensuing that the bitch/queen is in good health,
and washing hands/changing clothes and shoes before
Key Points for Clinicians and Public Health handling neonates.
Professionals • Counsel pet owners to avoid feeding raw or under-
cooked meat to dogs and cats.
Agent
• Ensure that health professionals know how to report
cases to the local health authorities. E. coli is a gram-negative bacillus that is a lactose fermenter
• Exclude infectious patients from child care or patient and a normal inhabitant of the intestinal tract of most mam-
care facilities and food production facilities. mals (Figure 9-51). The classification into different sero-
• Educate the public on modes of transmission and the groups is based on the O polysaccharide antigen. Further
preventive measures that they can use, including the differentiation into serotypes is based on the H (flagellar)
following: antigen.8 The most common serotype of EHEC in human
 Discourage consumption of undercooked ground infections is O157:H7. This serotype does not ferment
meat and unpasteurized dairy products or juices. sorbitol, so this aids in the identification of the organism.
 Encourage washing raw fruits and vegetables before EHEC organisms are capable of producing potent cytotox-
consumption. ins known as Shiga toxins 1 and 2 (also known as verocyto-
• Monitor the chlorination of public water supplies and toxins). Shiga toxin 1 is also produced by Shigella dysenteriae
pools. (see Chapter 11).
• Identify the source of an outbreak and institute control
measures to prevent transmission, including transmis- Geographical Occurrence
sion by contaminated food, direct animal contact, or
person-person transmission. EHEC strains have been identified in North America and South
• Institute environmental cleanup of contaminated areas. America, Europe, Japan, and southern Africa. The distribution
The organism can be maintained in the environment of these strains in other parts of the world is unknown.1

Transmission occurs through direct contact with feces or
through the ingestion of meat, dairy products, produce, or
water that is contaminated with feces (Figure 9-52). The
infective dose is estimated to be fewer than 10 organisms.12
Subclinically infected animals may shed organisms in their
feces for prolonged periods.
Significant outbreaks have been linked to contami-
nated beef, vegetables and fruit, and unpasteurized juice
and dairy products. Contaminated dust settling into drinks
has been suspected in outbreaks associated with fairs and
petting zoos. Contaminated swimming pools and drink-
ing water supplies have been associated with waterborne
transmission of the bacterium.13 After the organisms have
Figure 9-51 n At an extremely high magnification (×44,818), this scan- been ingested, they reproduce in the intestinal tract. The
ning electron micrograph revealed some of the morphologic details dis- incubation period to clinical illness is between 2 to 10 days.1
played by a single gram-negative Escherichia coli bacterium. This bacterium Infected humans may then shed organisms in their feces for
was a member of the strain O:169 H41 ETEC (enterotoxigenic E. coli). (From several weeks.
Atlanta, Ga. Courtesy J.H. Carr.)
Shiga toxin–producing E. coli result in cytotoxic effects on
intestinal epithelia that cause characteristic bloody diarrhea.
Shiga toxins systemically cause renal endothelial damage and
possible HUS.
Groups at Risk
Although E. coli infections can occur in persons of all ages,
children younger than 5 years are at increased risk of develop- E. coli has been shown to persist in contaminated environ-
ing serious complications from EHEC infections, including ments for prolonged periods.14 The organism may persist for
hemolytic uremic syndrome (HUS). In the elderly, thrombo- longer periods in the soil in cold climates.
cytopenic purpura may develop. Forty-two weeks after an outbreak of human illness at a
fair in Ohio, E. coli O157:H7 was able to be recovered from
the sawdust in the implicated barn.15 Campers have become
Hosts, Reservoir Species, Vectors infected by camping and contacting mud and soil in pastures
Cattle are the principal reservoir for EHEC. Other ruminants where livestock such as sheep have grazed in the past.12
may also be reservoirs. EHEC strains have been identified in
sheep, goats, turkeys, chickens, cats, deer, swine, horses, and
Disease in Humans
dogs.9,10 Contaminated meat and other food are major vehi-
cles for human infection. Human-to-human transmission E. coli O157:H7 and other EHEC strains of E. coli cause vary-
is common. When a subclinically infected cat was found to ing infections that can range from asymptomatic to fatal.
have the same strain of O145:H-EHEC as a child with bloody Common symptoms include watery diarrhea, often (in more
diarrhea, it was not possible to determine the direction of than half of cases16) followed by large amounts of blood,
the transmission, so human-to-animal transmission may be abdominal cramping, and colitis (Color Plate 9-29). Fever is
possible as well.11 either low grade or absent.
Infected cattle or other Direct contact with feces

Infected human being
asymptomatic animal
Direct contact with feces

Ingestion
Fecal-oral, person to person
Fecal contamination
Contaminated meat, dairy

Uninfected animal Infected human being
products, produce, dust, soil
Environmental factors: Soil, water contamination

Figure 9-52 n Life cycle of E. coli O157:H7 infection.
In most cases, the disease can resolve in 5 to 10 days with- adult dogs and cats. Table 9-30 compares clinical presenta-
out antibiotics.17 Severe complications are more common in tions of E. coli infection (enterohemorrhagic) in humans and
children and the elderly and include HUS in approximately other animals.
10% of cases, acute renal failure, coagulopathies, and ane-
mia.18 E. coli O157:H7 is the major cause of HUS in the
United States and the most common cause of acute renal Diagnosis
failure in children. Fecal samples should be cultured on sorbitol/MacConkey’s
media. All EHEC strains should be sent to a public health
Disease in Animals laboratory for serotyping to characterize the strain and detect
possible outbreaks. There are also commercial assays for
Cattle are typically subclinical carriers for E. coli O157:H7 Shiga toxins and DNA probe for specific genes.1 Subtyping
(Figure 9-53). Herd prevalence rates in excess of 40% have been of E. coli O157:H7 can be done using pulsed gel electropho-
reported. Studies of calves have shown EHEC prevalence rates resis to further detect outbreaks.
of almost 70%.19 Sheep (rates in excess of 30%), dogs, deer,
swine, and other animals may also subclinically carry EHEC.
ETC, EPEC, uropathogenic E. coli, and cytotoxic necrotiz- Treatment
ing factor E. coli have been recovered from dogs, while EPEC,
VTEC, and uropathogenic E. coli organisms have been recov- Many human cases of EHEC infection are self-limiting and
ered from cats. Many of the E. coli strains that have been do not require medical intervention. Even in more serious
recovered from dogs and cats are hemolytic. cases, it is believed that antibiotic treatment and antimotility
Neonates that have not had adequate amounts of colos- agents may increase the release of toxins and increase the risk
trum are more susceptible to enteritis or septicemia caused of HUS.16 Supportive measures include fluid and electrolyte
by β-hemolytic E. coli. Sporadic cases of E. coli enteritis, replacement and monitoring of hematologic and renal func-
cystitis, endometritis, pyelonephritis, prostatitis, or masti- tion for the development of HUS. HUS often requires trans-
tis have also been reported in puppies and kittens, as well as fusion, dialysis, and intensive care.20
In adult animals the disease may be self-limiting; however,
animals with clinical signs may need intensive supportive
care. Antibiotic therapy protocols should be based on cul-
ture results and sensitivity testing. Trimethoprim-sulfa can
be used at 30 mg/kg orally every 12 to 24 hours or amoxicil-
lin can be used at 10 to 20 mg/kg orally every 8 to 12 hours.
The prognosis for neonates with clinical signs is often poor.
Web Resources
• Diagnosis and Management of Foodborne Illnesses: http://

Figure 9-53 n Cattle are typically subclinical carriers of E. coli. (From
www.cdc.gov/mmwr/preview/mmwrhtml/rr5304a1.htm
Divers TJ, Peek SF (eds): Rebhun’s diseases of dairy cattle, ed 2, St Louis, 2008, • E. coli Resources for Clinicians: http://www.cdc.gov/ecoli/
Saunders Elsevier. Courtesy Robert O. Gilbert.) clinicians.htm
Table 9-30 n E. coli (Enterohemorrhagic): Comparative Clinical Presentations in Humans and
Other Animals
Humans Children; crowding; contact 2-10 days Watery diarrhea, bloody Positive fecal culture
with feces; consumption diarrhea, abdominal
of undercooked meat or cramping
unpasteurized milk, cider,
HUS, renal failure Leukocytosis, anemia,
or juice; ingestion of water
thrombocytopenia, abnormal
from lakes and pools while
renal function tests
swimming
Cattle, poultry, Neonates with inadequate Subclinical carriage; Positive fecal culture
deer, swine colostrum/immune system neonates with diarrhea,
dehydration, and
depression; hypovolemic
shock
Dogs, cats Neonates, inadequate Subclinical carrier, diarrhea Positive fecal culture, cytotoxin
colostrum intake assays
References 11. Busch U, Hormansdorfer S, Schranner S, et al. Enterohemorrhagic

Escherichia coli excretion by child and her cat. Emerg Infect Dis.
1. Heymann DL. Control of communicable diseases manual. 19th ed. 2007;13(2):348.
Washington DC: American Public Health Association; 2008. 12. Strachan NJ, Fenlon DR, Ogden ID. Modelling the vector pathway and
2. Rodrigues J, Thomazini CM, Lopes CA, et al. Concurrent infection infection of humans in an environmental outbreak of Escherichia coli
in a dog and colonization in a child with a human enteropathogenic O157. FEMS Microbiol Lett. 2001;203(1):69.
Escherichia coli clone. J Clin Microbiol. 2004;42(3):1388. 13. Rangel JM, Sparling PH, Crowe C, et al. Epidemiology of Escherichia
3. Sura R, Van Kruiningen HJ, DebRoy C, et al. Extraintestinal pathogenic coli O157:H7 outbreaks, United States, 1982–2002. Emerg Infect Dis.
Escherichia coli-induced acute necrotizing pneumonia in cats. Zoonoses 2005;11:603.
Pub Health. 2007;54(8):307. 14. National Association of State Public Health Veterinarians et al. Com
4. Barth S, Tscholshiew A, Menge C, et al. Virulence and fitness gene pat- pendium of measures to prevent disease associated with animals in public
terns of Shiga toxin-encoding Escherichia coli isolated from pigs with settings, 2007: National Association of State Public Health Veterinarians,
edema disease or diarrhea in Germany. Berl Munch Tierarztl Wochenschr. Inc. Morb Mortal Wkly Rep Recomm Rep. 2007;56(RR-5):1.
2007;120(7–8):307. 15. Varma JK, Greene KD, Reller ME, et al. An outbreak of Escherichia coli
5. Warren RE, Ensor VM. Imported chicken meat as a potential source O157 infection following exposure to a contaminated building. JAMA.
of quinolone-resistant Escherichia coli producing extended-spectrum 2003;290(20):2709.
β-lactamases in the UK. J Antimicrob Chemo. 2008;61(3):504. http://jac. 16. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti-
oxfordjournals.org/cgi/content/abstract/61/3/504. Accessed October microbial therapy, 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
2008. 2009.
6. Smith JL, Fratamico PM, Gunther NW. Extraintestinal pathogenic 17. Centers for Disease Control and Prevention. Disease listing: Escherichia
Escherichia coli. Foodborne Pathog Dis. 2007;4(2):134. coli general information: CDC DFBMD. http://www.cdc.gov/ncidod/
7. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases dbmd/diseaseinfo/escherichiacoli_g.htm. Accessed February 12, 2008.
of companion animals. Ames, IA: The Center for Food Security and Public 18. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
Health, Iowa State University College of Veterinary Medicine; 2008. handbook for primary care. Philadelphia: Mosby Elsevier; 2005.
8. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man 19. Wieler LH, Sobjinski G, Schlapp T, et al. Longitudinal prevalence study
and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington DC: Pan of diarrheagenic Escherichia coli in dairy calves. Berl Munch Tierarztl
American Health Organization; 2001. Wochenschr. 2007;120(7–8):296.
9. Colville J, Berryhill D. Handbook of zoonoses: identification and preven- 20. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
tion. St Louis: Mosby Elsevier; 2007. diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005.
10. Doane CA, Pangloli P, Richards HA, et al. Occurrence of Escherichia coli
O157:H7 in diverse farm environments. J Food Prot. 2007;70(1):6.
GIARDIASIS
Peter M. Rabinowitz and Lisa A. Conti • Ensure public water supplies are not contaminated
with human or other animal waste and that water
Giardiasis (ICD-10 A07.1) treatment includes filtration.
• In the event of a case report, determine risk factors for
Other names in humans: lambliasis, backpacker’s disease, infection and whether others are at risk.
beaver fever, traveler’s diarrhea • Consider zoonotic sources of infection (e.g., pets,
farm animals/petting zoos, water supplies with animal
Other names in animals: giardosis, lambliasis, lambliosis contact).
• Educate the public, veterinarians, and human health
Giardia intestinalis (also known as Giardia lamblia, Lamblia clinicians about risk factors for transmission, includ-
intestinalis, Giardia duodenalis)1 is a common parasitic cause ing not drinking untreated surface water.
of infectious diarrhea in humans. Human cases are thought to • Support policies to clean up dog feces and other ani-
be a result of person-to-person transmission, either directly or mal waste in public areas.
through contaminated water supplies. The importance of ani- • Ensure that day care center staff have proper training
mals, including dogs and cats, as disease reservoirs and sources to avoid outbreaks.
of zoonotic transmission of the disease remains incompletely
understood and potentially overlooked by human health clini- Human Health Clinicians
cians and public health authorities. Recent advances in molec-
ular genotyping hold promise for clarifying the risk of Giardia • Check with your state health office to determine
infection related to human-animal contact. whether the disease is reportable to public health
authorities using the case definition; see http://www.
cdc.gov/mmwr/preview/mmwrhtml/ss5607a2.htm.
• Include questions about animal contact in every
patient presenting with diarrhea. If pets are in the
Professionals
house, suggest a consultation with the family veteri-
narian. Human Giardia may be able to infect pets.
• Person-to-person transmission is possible. Counsel
infected persons about handwashing, avoiding swim-
• Disease is reportable to public health authorities in ming for 2 weeks after symptoms end, and avoiding
some states. fecal exposure during sexual activity.
• Counsel owners and any others in contact with infected
animals about the zoonotic risk, need for handwashing
after handling pet, feces, pet toys, and other objects that
are potentially infected or contaminated with cysts.
• Decontaminate infected animal’s coat with shampoo;
also decontaminate kennels or other environments
with quaternary ammonium disinfectants that are
effective in inactivating Giardia cysts.
• Consider vaccinating puppies and kittens at 7 weeks,
with booster 3 weeks later, against Giardia trophozo-
ites1 (controversial).
• Decontaminate hard surfaces with 1% sodium hypo
chlorite, 2% glutaraldehyde, or quaternary ammo-
nium solutions.1
• Keep pets indoors to reduce their exposure to the Figure 9-55 n Giardia cysts concentrated from the feces of a cat by the
organism. zinc sulfate centrifugal flotation technique. Cyst wall, nuclei, axonemes, and
median bodies are apparent in several of the cysts (iodine, ×1100). (From
Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders
Agent Elsevier.)
Giardia is a genus of flagellated protozoan parasite that lives

principally in the upper intestine of vertebrates (Figure 9-54).
Recent classification identifies Giardia intestinalis as the major Geographical Occurrence
species responsible for human infection. Giardia species are
found in most mammals, and while different strains appear to G. intestinalis occurs worldwide in humans and other animals,
have adapted to specific host species, molecular tools for typ- with greater human prevalence in regions with poor sanitation
ing particular isolates are now allowing an examination of how practices and crowding. Reported prevalence in human popu-
much zoonotic transmission is taking place. The current clas- lations ranges from 2% to 4% in developed countries to more
sification includes at least seven distinct assemblages (geno- than 15% in children from developing countries.
types) of G. intestinalis: A and B are found in humans and a
number of other animals, and C through G appear to be more Groups at Risk
host specific.2,3 Giardia organisms exist in two forms, a vegeta-
tive trophozoite form capable of causing illness in the host, and Children appear to become infected more frequently than
a transmissible cyst form that is shed in feces (Figure 9-55). The adults. Particular risk groups include children in day care
cysts measure 7 to 10 microns by 8 to 13 microns and can sur- facilities, day care workers, parents of infected children,
vive up to 2 months in water, where they are resistant to routine individuals living in areas without adequate sanitation or
chlorination. Upon ingestion by a host, the cysts develop into who drink from shallow wells, wilderness travelers who
pathogenic trophozoites that cling to the brush border surface drink unfiltered or untreated water, swimmers who swallow
of the intestinal mucosa and reproduce by fission. water from lakes or ponds, international travelers, and men
who have sex with men.4

In many host species, Giardia infection can produce humoral
immunity after 100 days that may result in self-limiting
infection.5 In the United States, the prevalence of Giardia in
canine kennels has been reported up to 100%.6 Humans and
a wide range of other animals are reservoirs. In many indi-
viduals and species, asymptomatic carriage may occur with
the ability to transmit the infection to others.
Studies of infection prevalence in animals vary greatly:
20% to 35% in puppies, 10% to 15% in kittens, 5% to 90%
in calves, 60% to 80% in lambs, 17% to 32% in foals, and 7%
to 44% in young pigs.7
Figure 9-54 n Wet mount of a fresh fecal sample showing motile tropho-
zoites of Giardia species. Notice the prominent pair of nuclei containing a single Cysts develop in the intestine and are shed into the envi-
karyosome of condensed chromatin, flagella running longitudinally between the
nuclei, and a pair of curved median bodies. The arrangement of the organelles ronment in feces, where they are immediately infective
resembles a wide-eyed face. (From Quesenberry K, Carpenter JW: Ferrets, rabbits (Figure 9-56). Transmission occurs when cysts are ingested
and rodents: clinical medicine and surgery, ed 2, St Louis, 2004, Saunders Elsevier.) through drinking water, direct fecal-oral contamination,
Figure 9-56 n Life cycle, giardiasis. Cysts are resistant forms and are responsible for transmission of giardiasis.
Both cysts and trophozoites can be found in the feces (diagnostic stages). 1, The cysts are hardy and can survive sev-
eral months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral
route (hands or fomites). 2, In the small intestine, excystation releases trophozoites (each cyst produces two tropho-
zoites). 3, Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel
where they can be free or attached to the mucosa by a ventral sucking disk. 4, Encystation occurs as the parasites
transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces. 5, Because the cysts are
infectious when passed in the feces or shortly afterward, person-to-person transmission is possible. While animals are
infected with Giardia, their importance as a reservoir is unclear. (From Centers for Disease Control and Prevention:
Giardiasis. http://www.dpd.cdc.gov/dpdx/HTML/Giardiasis.htm. Accessed September 13, 2008.)
foodborne exposure, or contact with contaminated objects cytes and are thus not shed continuously. Reproduction takes
leading to ingestion. Infected drinking water is thought to place by binary fission and cysts are produced to continue
be the major form of transmission. The infective dose is the life cycle.
low, with a median infective dose (ID50) of 10 cysts. Fecal Circumstantial evidence, such as finding similar geno-
excretion is high—an infected human can secrete 900 mil- types in both children and household dogs, suggests that
lion cysts per day.8 transmission between pets and people takes place.9,10 Case
Once the cysts are ingested, they develop into trophozoites control studies have shown increased odds for infection
in the small intestine. The trophozoites remain there and, if among pet owners and people reporting contact with farm
they cause disease, they do so without invading the mucosa. animals.11 Transmission in animals, as in humans, occurs
They have a sucking disk by which they attach to the entero- through ingestion of cysts.

Because the Giardia cyst can persist for months in the
environment, the status of water supplies is a critical envi-
ronmental factor in sporadic and epidemic outbreaks of
giardiasis in both humans and animals. Inadequate filtration
of drinking water supplies has been associated with major
outbreaks. The degree of contamination of municipal water
supplies and shallow wells with animal and human feces is
also important. On farms, contamination of water sources
could spread infection among animals.
Dogs shedding cysts in feces can contaminate environ-
ments such as a lawn or public park for months,12–14 leading
to risks to children who play around soil. Similarly, livestock
housing facilities and grazing areas can become contami-
nated with Giardia cysts, leading to infection risk for animals Figure 9-57 n Giardia lamblia in a reptile. (From Mader DR: Reptile
and farmers. Even marine shellfish are capable of being con- medicine and surgery, ed 2, St Louis, 2006, Saunders Elsevier. Photograph
taminated with Giardia cysts, suggesting a foodborne infec- courtesy F.L. Frye.)
tion risk to humans.15
and Salmonella, viral gastroenteritis, and other protozoa
Disease in Humans including Cryptosporidium and Cyclospora, and underlying
disease such as celiac sprue. Diagnosis is typically by direct
Giardia infection in humans is usually asymptomatic or microscopic visualization of trophozoites or Giardia cysts
mild enough to escape diagnosis. Most cases are self-limited, in the feces. Repeated fecal analysis may be necessary. ELISA
yet significant acute and chronic infection can occur. Acute and IFA tests for antigen are also commercially available. It
infection can produce bloating, abdominal pain, explosive should be noted that demonstration of cysts alone in feces
diarrhea, with pale, frothy, steatorrheic feces often mixed does not prove Giardia is the cause of a diarrheal episode
with mucus, but not blood. Symptoms may be continuous because many Giardia infections are asymptomatic. In ques-
or intermittent (with bouts of constipation). tionable cases, a duodenal aspirate, string test, or biopsy may
In chronic infections, there can be bloating, abdominal be performed to detect trophozoites.18
pain, flatulence, steatorrhea, lactose intolerance, and weight Animal diagnosis involves testing for Giardia trophozoites
loss. In children this can lead to failure to thrive and develop- in direct unstained fecal smears to look for motile trophozo-
mental delays.16 Rarely, infection can lead to reactive arthritis. ites or using Lugol’s iodine to help distinguish the cysts and
trophozoites (Figure 9-57).19 A zinc sulfur concentration test
Disease in Animals (ZCST) is a fecal flotation method for cysts and is considered a
more sensitive test than a newer, fecal ELISA. A direct IFA test
In dogs and cats, the disease is often subclinical. Young ani- may be more sensitive for detecting low numbers of cysts.20
mals are more likely to show signs of infection and present
with frothy diarrhea that may be foul smelling. Calves, lambs,
Treatment
foals, and caged birds (cockatiels, parrots) may also develop
diarrhea due to Giardia. Table 9-31 provides a comparison of Acute giardiasis is treated with supportive care includ-
clinical manifestations of giardiasis. ing rehydration. Antibiotics are indicated for symptomatic
patients. Table 9-32 provides treatment information for giar-
Diagnosis diasis in humans and other animals.
All drugs for Giardia treatment are extralabel in ani-
In humans, the differential diagnosis includes other causes of mals. However, a number of drugs are effective. In addition
chronic diarrhea, including bacteria such as Campylobacter to antibiotic treatment, an animal’s coat should be washed
Table 9-31 n Giardiasis: Comparative Clinical Presentations in Humans and Other Animals
Species Risk Factors Incubation Period Clinical Manifestations
Humans Children, day care centers, areas of 3-25 days17 Asymptomatic or acute diarrhea with
poor sanitation, international travel, bloating, chronic diarrhea with
backpackers, pet ownership, farm malabsorption, weight loss
animal contact
Dogs, cats, calves, Crowding, contaminated environments 5-14 days Often subclinical
rodents, reptiles
Young animals at increased risk of Weight loss, intermittent diarrhea; chronic
clinical disease infection can lead to debilitation
5. O’Handley RM. Passive immunity and serological immune response in

Table 9-32 n Antibiotic Treatment of Giardia dairy calves associated with natural Giardia duodenalis infections. Vet
Infection in Humans and Other Parasitol. 2003;113(2):89.
6. Kirkpatrick CE. Enteric protozoal infections. In: Greene CE, ed. Infectious
Animals diseases of the dog and cat. Philadelphia: WB Saunders; 1990.
7. Xiao L. Giardia infection in farm animals. Parasitol Today. 1994;
Species Primary Treatment Alternative Treatment 10(11):436.
Humans Tinidazole 2 gm PO × 1 Metronidazole 250 mg and animals: vol. III: chlamydioses, parasitoses. 3rd ed. Washington, DC:
or nitazoxanide 500 PO tid × 5 days Pan American Health Organization; 2003.
mg PO bid × 3 days 9. Volotao AC, Costa-Macedo LM, Haddad FS, et al. Genotyping of Giardia
If pregnant:
duodenalis from human and animal samples from Brazil using beta-
paromomycin 500 mg
giardin gene: a phylogenetic analysis. Acta Trop. 2007;102(1):10.
4×/day × 7 days21
10. Inpankaew T, Traub R, Thompson RC, et al. Canine zoonoses in Bangkok
Dogs, cats22 Fenbendazole 50 mg/kg Albendazole 25 mg/ temples. Southeast Asian J Trop Med Public Health. 2007;38(2):247.
PO q24h × 3-5 days; kg PO q12h for 11. Warburton AR, Jones PH, Bruce J. Zoonotic transmission of giardiasis:
a second 5-day course 2 days; a second a case control study. Commun Dis Rep CDR Rev. 1994;4(3):R32.
may be necessary 5-day course may be 12. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
necessary Station, NJ: Merck; 2005.
13. Grimason AM, Smith HV, Parker JF, et al. Occurrence of Giardia sp.
Cattle Fenbendazole 5-10 Albendazole 20 mg/kg cysts and Cryptosporidium sp. oocysts in faeces from public parks in the
mg/kg PO × 3 days 1 PO once daily for west of Scotland. Epidemiol Infect. 1993;110(3):641.
3 days 14. Graczyk TK, Fayer R, Trout JM, et al. Giardia sp. cysts and infectious
Cryptosporidium parvum oocysts in the feces of migratory Canada geese
(Branta canadensis). Appl Environ Microbiol. 1998;64(7):2736.
15. Robertson LJ. The potential for marine bivalve shellfish to act as trans-
mission vehicles for outbreaks of protozoan infections in humans: a
with an antiseptic shampoo solution to eliminate cysts. review. Int J Food Microbiol. 2007;120(3):201.
Vaccines19 have been developed for dogs and cats, but their 16. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
use is controversial. handbook for primary care. Philadelphia: Mosby Elsevier; 2006.
17. Heymann DL, ed. Control of communicable diseases manual. 19th ed.
References 18. Mandell GE, Bennett JE, Dolin R. Principles and practice of infectious dis-
eases. 6th ed. Philadelphia: Churchill Livingstone Elsevier; 2005.
1. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases 19. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
of companion animals. Ames, IA: The Center for Food Security and Public panion canine and feline infectious disease and parasitology. Ames, IA:
Health, Iowa State University College of Veterinary Medicine; 2008. Blackwell; 2006.
2. Trout JM, Santín M, Greiner E, et al. Prevalence and genotypes 20. Mekaru SR, Marks SL, Felley AJ, et al. Comparison of direct immu-
of Giardia duodenalis in post-weaned dairy calves. Vet Parasitol. nofluorescence, immunoassays, and fecal flotation for detection of
2005;130(3–4):177. Cryptosporidium spp. and Giardia spp. in naturally exposed cats in 4
3. Fayer R, Santín M, Trout JM, et al. Prevalence of species and genotypes Northern California animal shelters. J Vet Intern Med. 2007;21(5):959.
of Cryptosporidium found in 1–2 year old dairy cattle in the eastern 21. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to antimi-
United States. Vet Parasitol. 2006;135(2):105. crobial therapy, 2009 39th ed. Sperryville, VA: Antimicrobial Therapy; 2009.
4. Esfandiari A, Swartz J, Teklehaimanot S. Clustering of giardiasis among 22. Tilley LP, Francis WK. Blackwell’s five-minute veterinary consult: canine
AIDS patients in Los Angeles County. Cell Mol Biol. 1997;43(7):1077. and feline. 4th ed. Ames, IA: Blackwell; 2008.
HANTAVIRUS INFECTIONS
Peter M. Rabinowitz and Lisa A. Conti for rodent infestation or contact that can result in hantavi-
rus risk to humans. Limiting contact between humans and
Hantavirus pulmonary syndrome (ICD-10 A), hemorrhagic rodents (including wild species and laboratory animals) can
fever with nephropathy (ICD-10 A) reduce the risk of infection. However, these interventions are
unlikely to prevent sporadic transmission with serious fatal
Other names in humans: hantavirus (cardio-) pulmonary outcomes.
syndrome (HPS); Four-corners’ disease; in western Europe,
nephropathia epidemica; in parts of eastern Europe and Asia, Key Points for Clinicians and Public Health
hemorrhagic fever with renal syndrome (Korean hemorrhagic Professionals
fever); also many local names
Other names in animals: none
• Provide descriptive epidemiology of cases in the health
Clinical syndromes of hantavirus infection, including han- district.
tavirus pulmonary syndrome (HPS) and hemorrhagic fever • Educate the public about measures to reduce risk,
with nephropathy, are thought at present to be principally including the following:
human diseases. However, the presence of domestic animals  Controlling rodents and their fleas near dwellings
in, and wildlife around, a household can increase the risk (flea control should precede rodent control to
Box 9-4 CDC “Seal up, Trap up, Clean Up” Veterinary Clinicians
Recommendations for Reducing Rodent • Counsel clients about pet-feeding practices that reduce
Infestation and Risk of HPS
the risk of rodent infestation.
• Dogs and cats are not known to be infected with han-
• Seal rodent entry holes or gaps with steel wool, lath metal, or
caulk.
taviruses, but these pets may bring infected rodents
• Trap rats and mice using appropriate snap trap. into contact with people.
• Clean up rodent food sources and nesting sites. • Train veterinary personnel in biosafety measures to
• Keep woodpiles and compost heaps away from house. reduce risk from infected rodents.
• Take precautions when cleaning rodent-infected areas:
 Use cross-ventilation when entering a previously
unventilated enclosed room or dwelling before cleanup.
Agent
 Use rubber, latex, vinyl, or nitrile gloves. Hantaviruses are trisegmented, negative-sense RNA viruses
 Do not stir up dust by vacuuming, sweeping, or any other in the Bunyaviridae family. Unlike other bunyaviruses, which
means. Instead, thoroughly wet contaminated areas with
are arthropod borne, hantaviruses are rodent borne. A num-
a bleach solution or household disinfectant. Hypochlorite
(bleach) solution: Mix 11⁄2 cups of household bleach in
ber of species cause human disease, and new hantaviruses
1 gallon of water. Once everything is wet, take up contami- and their rodent hosts continue to be described. Like other
nated materials with damp towel and then mop or sponge segmented RNA viruses, hantaviruses appear capable of reas-
the area with bleach solution or household disinfectant. sortment when dual infections of target cells occurs, which
• Spray dead rodents with disinfectant and then double-bag could lead to the emergence of novel strains.5
along with all cleaning materials and dispose of bag in an
appropriate waste disposal system.
• Remove gloves and thoroughly wash hands with soap and Geographical Occurrence
water (or waterless alcohol-based hand rubs when soap is not In the New World, hantaviruses are found from Canada to
available and hands are not visibly soiled).
Argentina. In North America, Sin Nombre, New York-1,
From “Prevent Rodent Infestations” at http://www.cdc.gov/rodents/prevent_rodents/ Bayou, and Black Creek Canal hantaviruses have been asso-
index.htm. ciated with HPS.6 In South America, HPS caused by Andes
virus may be particularly pathogenic for humans, and rare
occurrence of human-human transmission of infection has
prevent fleas from seeking new hosts): Box 9-4 lists been linked to this virus in Argentina.7,8 Old World mem-
steps for rodent proofing homes bers of the family, including Seoul virus, Hantaan virus, and
 Avoiding camping near rodent burrows Dobrava-Belgrade virus, cause hantavirus hemorrhagic fever
 Avoiding handling wild rodents1 with renal syndrome.9 Another Old World virus, Pumaala
• Provide exposure risk reduction guidance to workers virus, causes a somewhat milder disease generally referred to
with occupational risk (see below). as nephropathia epidemica. Pumaala virus is the predominant
hantavirus in western and central Europe, whereas Hantaan
Human Health Clinicians and Dobrava-Belgrade viruses are found in eastern Europe.
Hantaan virus is the major pathogen in Asia and has also
• Report disease to public health authorities using the been detected in Africa.
case definition (All About Hantaviruses): http://www.
cdc.gov/ncidod/diseases/hanta/hps/noframes/phys/
Groups at Risk
casedefn.htm.
• Ensure that workers in affected areas who are fre- In the United States, groups at increased risk for hantavirus
quently exposed to rodents or who are involved in infection are those with rodent contact, including persons
cleanup of rodent-infested areas are informed of their living in endemic areas such as the Southwest, forestry work-
occupational risk and have a baseline medical screen- ers, farm workers, construction workers engaged in renova-
ing, including respirator fit testing. They should use tion, wildlife biologists and zoologists, and laboratory animal
protective equipment—including either half-face handlers. Although the risk to such groups is low overall, it
or supplied air respirators with N100 or P100 filters may be higher in areas of endemic foci.2
(Color Plate 9-30)—and gloves while handling rodents
or traps containing rodents; they also should disinfect
gloves after use.2,3
• If fever or respiratory symptoms develop in a worker Rodents and, in a few instances, insectivores (shrews) are the
within 45 days of the last potential exposure, he or she reservoir host of hantaviruses, and each hantavirus species
should immediately seek medical attention and inform is associated primarily with a single rodent or insectivore
the health care provider of the potential occupational species.10 Hantavirus infection within individual rodents
risk of hantavirus infection. The provider should con- of a reservoir species is believed to occur horizontally, with
tact local public health authorities promptly if hanta- males frequently infected at higher prevalence than females.4
virus-associated illness is suspected. A blood sample Lifelong persistence of infection with sporadic shedding of
should be submitted to the state health department for virus has been demonstrated for multiple species. HPS is
hantavirus antibody testing.4 associated with rodents of the subfamily Sigmodontinae.
Infected human being
(Rare)
Bite
Infected rodent Susceptible human being
Feces, saliva, urine Inhalation (or ingestion or wound

contact) of aerosolized excreta
Contaminated environment
Environmental Food sources around

Climate factors
factors: dwellings, rodent density
Figure 9-58 n Transmission of hantavirus infection.
The principal reservoir for hantavirus in the United States is

Disease in Humans
the deer mouse (Peromyscus maniculatus, Color Plate 9-31);
other rodents carriers are the cotton rat (Sigmodon hispi-
dus), the rice rat (Oryzomys palustris), and the white-footed
Hantavirus Pulmonary Syndrome
mouse (Peromyscus leucopus). Seoul viruses are carried by
rats (Rattus species).11 Although most of these reservoir spe- HPS is a life-threatening disease that begins with a nonspecific
cies are usually found in more rural areas, they are capa- prodrome of fever, chills, and myalgia, leading to hypotension
ble of infesting buildings in periurban zones near forested and pulmonary edema with accompanying respiratory distress
areas.12 and shock. The incubation period is 1 to 4 weeks.
Radiographs may reveal diffuse alveolar infiltrates
(Figure 9-59). Mechanical ventilation is often necessary.
Mode of Transmission and Life Cycle Complications may include disseminated intravascular
coagulation, myocardial dysfunction, and cardiac arrhyth-
The spread of virus to humans is believed to occur primarily
mias. The case fatality rate may reach 40%. In parts of South
through inhalation of aerosol of dried feces, saliva, or urine
America, however, milder forms of the disease may occur.17
from infected rodents (Figure 9-58). Bites from infected
rodents or contact with their feces, saliva, or urine with bro-
ken skin, mucous membranes, or through ingestion are other Hantavirus Hemorrhagic Fever with Nephropathy
possible transmission pathways. (Hemorrhagic Fever With Renal Syndrome)
Person-to-person transmission has been reported only
This is a disease of variable severity, with a number of differ-
for Andes virus, which has been isolated from human
ent clinical stages.11
saliva13; this transmission required close personal contact in
an enclosed space (bus).8

Contamination of the environment by urine, saliva, and feces
of infected rodents is the principal driver of transmission.
Under certain conditions, the virus can persist for prolonged
periods (several months) in the environment.14
Environmental factors that increase the density of rodents
around human habitation are critical to human risk. These
factors include abundance of food sources (unsecured food
in kitchens, seeds from bird feeders, pet/livestock food).
A combination of mild winters and increased rainfall related
to El Niño cycles has also been associated with increased
rodent abundance.15
Figure 9-59 n Pulmonary infiltrates in hantavirus pulmonary syndrome.
Spatial risk mapping in the American Southwest has iden- (From Centers for Disease Control and Prevention: Severe hantavirus pulmonary
tified areas of increased hantaviral transmission related to syndrome. http://www.bt.cdc.gov/agent/plague/trainingmodule/3/12hantavirus.
elevation and precipitation.16 htm. Accessed October 2008.)
1. The febrile or toxic stage is characterized by the abrupt References

onset of fever, chills, and headache that may be accom-
1. Center for Disease Control and Prevention. Prevent rodents: index: CDC
panied by photophobia and other symptoms. rodent control. http://www.cdc.gov/rodents/prevent_rodents/index.htm.
2. The hypotensive phase may involve clinical shock and Accessed May 8, 2008.
death. 2. Fulhorst CF, Milazzo ML, Armstrong LR, et al. Hantavirus and arena-
3. The oliguric (renal) phase follows the hypotensive virus antibodies in persons with occupational rodent exposure. Emerg
phase and includes declining renal function and urine Infect Dis. 2007;13(4):532.
3. Mills JN. Regulation of rodent-borne viruses in the natural host: impli-
output. Hemorrhagic complications may occur. cations for human disease. Arch Virol. 2005;45(suppl 19).
4. The diuretic phase is characterized by improved urine 4. Mills JN, Corneli A, Young JC, et al. Hantavirus pulmonary syn-
output and clinical condition. drome—United States: updated recommendations for risk reduction,
5. The convalescent phase may include long-term abnor- Centers for Disease Control and Prevention. MMWR Recomm Rep.
2002;51(RR-9):1.
malities of renal function, including renal acidosis and 5. Rodriguez LL, Owens JH, Peters CJ, et al. Genetic reassortment
renal insufficiency. among viruses causing hantavirus pulmonary syndrome. Virology.
1998;242:99.
6. Monroe MC, Morzunov SP, Johnson AM, et al. Genetic diversity and
distribution of Peromyscus-borne hantaviruses in North America. Emerg
Disease in Animals Infect Dis. 1999;5:75.
Rodents appear to have subclinical infection with hantavi- 7. Wells RM, Sosa Estani S, Yadon ZE, et al. An unusual hantavirus
outbreak in southern Argentina: person-to-person transmission?
ruses. Serological studies in the United States have failed to Hantavirus Pulmonary Syndrome Study Group for Patagonia. Emerg
demonstrate significant rates of subclinical infection in dogs Infect Dis. 1997;3(2):171.
or cats.18 8. Martinez VP, Bellomo C, San Juan J, et al. Person-to-person transmis-
sion of Andes virus. Emerg Infect Dis. 2005;11(12):1848.
9. Acha PN, Szyfres B. Zoonoses and communicable diseases common to
man and animals: vol. II: chlamydioses, rickettsioses, and viroses. 3rd ed.
Diagnosis Washington, DC: Pan American Health Organization; 2003.
10. Arai S, Bennett SN, Sumibcay L, et al. Phylogenetically distinct hantavi-
The differential diagnosis includes legionella, plague, tulare- ruses in the masked shrew (Sorex cinereus) and dusky shrew (Sorex mon-
mia, Q fever, leptospirosis, Goodpasture’s syndrome (anti- ticulus) in the United States. Am J Trop Med Hyg. 2008;78:348.
glomerular basement antibody disease), and drug-induced 11. Heymann DL. Control of communicable diseases manual. 18th ed.
noncardiac edema. Typical hematologic findings of hanta- 12. Abu Sin M, Stark K, van Treeck U, et al. Risk factors for hantavirus
virus infection include immature neutrophils (bandemia), infection in Germany, 2005. Emerg Infect Dis. 2007;13(9):1364.
atypical lymphocytosis, and thrombocytopenia.19 An ELISA 13. Pettersson L, Klingström J, Hardestam J, et al. Hantavirus RNA in saliva
IgM test is available, and immunohistochemistry can be used from patients with hemorrhagic fever with renal syndrome. Emerg Infect
for retrospective diagnosis. Dis. 2008;14(3):406.
14. Clement J, Maes P, Ducoffre G, et al. Hantaviruses: underestimated
respiratory viruses? Clin Infect Dis. 2008;46(3):477.
Treatment 15. Miedzinski L. Community-acquired pneumonia: new facets of an
old disease—hantavirus pulmonary syndrome. Resp Care Clin N Am.
There is no specific treatment for HPS. Treatment is support- 2005;11(1):45.
16. Eisen RJ, Glass GE, Eisen L, et al. A spatial model of shared risk for
ive. Clinicians need to have a high suspicion for the disease plague and hantavirus pulmonary syndrome in the southwestern United
because patients require early transfer to an intensive care States. Am J Trop Med Hyg. 2007;77(6):999.
unit. Mechanical ventilation and support of blood pressure 17. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
with pressor agents may be necessary. Extracorporeal mem- handbook for primary care. Philadelphia: Mosby Elsevier; 2005.
brane oxygenation has reportedly provided clinical benefit 18. Malecki TM, Jillson GP, Thilsted JP, et al. Serologic survey for hanta-
virus infection in domestic animals and coyotes from New Mexico and
in some cases. northeastern Arizona. J Am Vet Med Assoc. 1998;212(7):970.
Hantavirus hemorrhagic fever with nephropathy is also 19. Center for Disease Control and Prevention (CDC). Hantavirus pul-
treated with supportive measures, including dialysis if neces- monary syndrome—five states, 2006. MMWR Morb Mortal Wkly Rep.
sary. Ribavirin has been used in some cases.17 2006;55(22):627.
HOOKWORM INFECTION
Peter M. Rabinowitz and Lisa A. Conti Hookworms of the genus Ancylostoma are common para-
sites that can cause serious infections in dogs and cats and
Cutaneous larva migrans (ICD-10 B76.9) Disease due to usually milder illness in humans. The classic manifesta-
Ancylostoma caninum or Ancylostoma braziliense (B76.0) tion of A. caninum and A. braziliense infection in humans
is a dermatitis resulting from the larvae burrowing under
Other names in humans: ancylostomiasis, creeping eruption, the skin, known as creeping eruption or cutaneous larva
ground itch, dew itch, sandworm, cutaneous larva migrans migrans. Preventive veterinary care and healthy public
policies about pet sanitation can reduce the risk of human
Other names in animals: ancylostomiasis disease.
barefoot on contaminated beaches or soils. Other risk

groups include gardeners, workers who have to crawl into
Professionals
contaminated crawl spaces under buildings, and travelers to
tropical regions.
• Restrict dogs and cats from beaches and other recre-
ational areas or require cleanup of all animal feces. Hosts, Reservoir Species, Vectors
• Promote strategic deworming of all pets. Dogs are the principal reservoir for A. caninum. A. braziliense
• Educate the public about risk of unprotected contact occurs in cats and dogs. A survey of feral cats in Florida found
with sand and soil (e.g., need to wear shoes while walk- 33% infected with A. braziliense. A. braziliense also is found in
ing on beach, using a waterproof barrier to damp soils wild felids. It is thought that infection in rodents (paratenic
when working under a house). hosts) may also play a role in disease transmission.2
• Recommend rodent control as rodents are paratenic
hosts (intermediate hosts are not needed for parasite
development). Mode of Transmission and Life Cycle
Dogs and cats become infected through ingestion of larvae,
Human Health Clinicians skin penetration of larvae or from transmission in milk or
colostrum of infected bitches (dogs) (Figure 9-60). In pup-
• Counsel patients in endemic areas and travelers to pies and kittens, the larvae migrate through the bloodstream
endemic areas about the risks of unprotected skin and lymphatics to the lungs, where they are coughed up and
contact to soil and sand. swallowed and mature in the small intestine. Approximately
• Counsel patients about handwashing after handling 15 to 20 days after infection, the mature worms produce
potentially contaminated soil, washing vegetables and eggs.3 In older cats and dogs, the life cycle is arrested in
fruit. the larval stage, but such larvae may become reactivated
if adult worms are removed from the intestine or during
Veterinary Clinicians pregnancy.
After an infected animal sheds eggs into the environment
• Provide strategic deworming to dogs and cats. in feces, the eggs complete embryonation, hatch, and larvae
• Counsel clients to keep dogs on leash and properly begin to develop through a series of stages. The process of
dispose of feces, discourage contact with wildlife, keep developing into infective larvae takes 7 to 10 days in moist,
cats indoors. warm soil.4
• Treat pregnant bitches prophylactically. Larvae infect humans through contact with skin, usu-
• Decontaminate soil and lawns with sodium borate. ally of the foot. This produces a characteristic dermatitis
(ground itch). The larvae of A. caninum and A. braziliense
Agent burrow under the skin but eventually die. In the pro-
cess they produce the lesions of cutaneous larva migrans.
Hookworms are nematode worms (Color Plate 9-32). Larvae of A. ceylanicum, however, pass through the lym-
Although a number of hookworm species occur in humans phatics and bloodstream into the lungs, ascend up the
and other animals, A. canium (dog hookworm) and A. bra- trachea where they are swallowed (similar to infection
ziliense are the species associated with human disease in the in dogs and cats), and reach the small intestine, where
United States. A. braziliense is considered the most common they attach to the wall and develop to maturity in 3 to
cause of cutaneous larva migrans.1 A related species, A. cey- 4 weeks.4
lanicum, has historically been confused with A. braziliense.2
The adult A. caninum worms are 12 to 15 cm in length; the
other species are somewhat smaller. Environmental Risk Factors
Temperature, humidity, and soil type are important fac-
Geographical Occurrence tors determining how well the hookworm eggs hatch and
Because the larvae prefer warm, humid environmental con- develop into infective larvae. In general, these organisms
ditions, hookworm infection is more common worldwide in prefer moist, warm climates and moist, sandy soils. In
tropical and subtropical regions. A. caninum is more widely moist, warm conditions the third-stage (infective) lar-
distributed than A. braziliense or A. ceylanicum. In the United vae can survive up to 3 weeks.3 Pet sanitation policies in
States, infection with A. caninum and A. braziliense occurs beaches, parks, and other public places can affect the risk
mostly in the southeast states along the Gulf of Mexico. of human infection.
A. ceylanicum is found in tropical regions.
Disease in Humans
Groups at Risk
Human infection with A. caninum or A. braziliense causes
Exposure to contaminated soil and sand is a major risk fac- a linear dermatitis that appears within days to weeks after
tor; therefore human cases occur among bathers who walk infection (Color Plate 9-33). The rash is usually accom-
Susceptible Predation Rodents

dog or cat (paratenic hosts)
Ingestion of Susceptible human
larvae, skin contact being: cutaneous
Lactation with larvae larva migrans
Skin contact (A. caninum,
(dogs) with larvae A. braziliense);
Eggs shed rarely invasive
in feces disease
Infected puppy or kitten
Eggs hatch in soil, Skin contact with
(larvae develop
develop into larvae larvae, ingestion
into adult worms)
Environmental Drivers: Climate Pet sanitation policies

Figure 9-60 n Life cycle of hookworm infection.
panied by intense itching, erythema, and edema. Vesicles

Diagnosis
may appear. Secondary infection may occur. The infection
may last weeks or months. Laboratory findings can include Cutaneous larva migrans in humans is diagnosed clinically
eosinophilia and increased IgE levels. by the characteristic linear, slow-moving rash and a history
Rarely, cases of intestinal infection with A. caninum of exposure to potentially contaminated soils. Biopsy may
have occurred. In such cases, larvae migrate deeper and show an eosinophilic infiltrate but usually does not reveal the
may reach the intestines causing eosinophilic enteri- organism and therefore is not generally indicated to establish
tis. Loeffler’s syndrome (eosinophilia, asthma, migra- the diagnosis.7 In animals, eggs can be identified in feces by
tory pulmonary infiltrates, fever, and urticaria) has been fecal flotation (Figure 9-61).6
described.5
Disease in Animals
In young animals, hookworm infection can be an acute dis-
ease process with significant blood loss and sudden death.
Black, tarry stools may occur. Laboratory tests show anemia
that may be accompanied by eosinophilia. The fourth larval
stage and adult worms cause a chronic anemia and enteritis.
The lung migration phase of the life cycle can rarely cause a
dry cough.6 Because animals may repopulate the bowel with
larvae dormant in tissues, infection may continue for months
or years. Dogs previously sensitized to Ancylostoma may man-
ifest “hookworm dermatitis” at sites of percutaneous larval
penetration (Color Plate 9-34). Table 9-33 shows the compar-
ative clinical presentation of hookworm infection in humans Figure 9-61 n Hookworm ova. (From Centers for Disease Control and
and other animals. Prevention Public Health Image Library, Atlanta, Ga.)
Table 9-33 n Hookworm Infection: Comparative Clinical Presentations in Humans and Other Animals
Humans Unprotected skin contact Days to weeks Linear skin eruption with Eosinophilia
with soil, sand pruritus, erythema, edema
Rarely: Loeffler’s syndrome,
eosinophilic enteritis
Dogs Puppies at increased risk of Varies with the Anemia, acute or chronic; Anemia, iron deficiency
severe disease number of parasites weight loss; tarry stools;
Eggs in feces
sudden death
Cats More severe signs in kittens Usually subclinical Anemia (rare), eggs in feces
Treatment Table 9-34 n Treatment of Hookworm Infections

in Humans and Other Animals
Treatment in Humans Primary Alternative

Species Treatment Treatment
Many human cases of cutaneous larva migrans are self-lim-
ited and do not require medical intervention. However, in Humans: Ivermectin 200 mg Albendazole
symptomatic and persistent infection, anthelmintic therapy cutaneous PO qd × 1-2 days 200 mg PO bid ×
is warranted. Topical thiabendazole cream may be effective.7 larva migrans 3 days8
Table 9-34 lists choices of oral anthelmintic agents, which are Dogs
associated with a high cure rate. Adults and Fenbendazole 50 mg/ Milbemycin oxime
larvae kg PO × 3 days 0.5 mg/kg PO
once, repeat
Treatment in Animals monthly
Acute illness in dogs and cats is treated with an antihelmintic, Adulticide Pyrantel pamoate Praziquantel/
15 mg/kg PO once, pyrantel/febantel
as well as supportive care such as blood transfusions. In dogs, repeat in 14 days PO or milbemycin
adult larvae treatment is sometimes given during the third oxime 1, repeat in
trimester of pregnancy to reduce transmission to offspring. 14 days
Pups should be treated at 2 weeks, then every 2 weeks until Ivermectin 6 mcg/
weaned. kg/pyrantel PO
In cats, the queen is given a dewormer before breeding once, repeat every
and after littering. Kittens can begin treatment with an adul- month
ticide dewormer by 4 weeks of age.7 Table 9-34 outlines anti- Dichlorvos 11 mg/kg
helmintic therapy for hookworm infection. PO once, repeat in
14 days
Cats
References
Adults and Milbemycin oxime Praziquantel/pyrantel
1. Georgiev VS. Parasitic infections. Treatment and developmental thera- larvae 2 mg/kg PO q30 PO once, repeat in
peutics. 1. Necatoriasis. Curr Pharma Des. 1999;5(7):545. days 14 days
2. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man Adulticide Pyrantel pamoate Dichlorvos 11 mg/
and animals: vol. 3: Parasitosis. 3rd ed. Washington, DC: Pan American 20-30 mg/kg PO, kg PO once, repeat
Health Organization; 2001. repeat in 14 days in 14 days
3. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse (extralabel)
5. Schaub NA, Perruchoud AP, Buechner SA. Cutaneous larva migrans 7. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
associated with Loffler’s syndrome. Dermatology. 2002;205(2):207. diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005.
6. Barr SC, Bowman DD. 5-Minute veterinary consult clinical companion 8. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to anti-
canine and feline infectious disease and parasitology. Ames, IA: Wiley- microbial therapy. 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
Blackwell; 2006. 2009.
INFLUENZA
Carina Blackmore and Peter M. Rabinowitz in the United States.2 Outbreaks typically occur in the winter
months in temperate climates, although they may begin in
Influenza (ICD-9-CM 487.1) late autumn and sometimes persist to late spring months. In
recent seasons, two and sometimes three different influenza
Other names in humans: flu, seasonal flu viruses (two type A subtypes, one type B) have co-circulated.
Influenza pandemics can occur when a new influenza
Other names in animals: avian flu, bird flu, fowl plague, fowl virus emerges to which the overall population lacks immu-
pest, swine flu, canine flu nity, typically to a new hemagglutinin subtype (Figure 9-62).
The emergence of a pandemic influenza strain has been
Influenza in humans is an acute, usually self-limited febrile associated with reassortment of gene segments between
respiratory illness caused by influenza virus infections. human and animal strains. Characteristic traits of pan-
Bacterial pneumonia is a common complication in persons demics include concurrent, widespread outbreaks of influ-
older than 65 years. Influenza viruses have caused human epi- enza throughout the world, sometimes outside the usual
demics and, much less commonly, pandemics (worldwide epi- influenza season, with high attack rates in all age groups.1
demics) for at least several hundred years,1 and influenza is still Pandemics are usually associated with substantial increases
one of the most important causes of morbidity and mortality in mortality.
Gene segment Key Points for Clinicians and Public Health

Viral -RNA Professionals
envelope -Nucleoprotein
Neuraminidase -Polymerase
proteins
Hemagglutinin Public Health Professionals
• Educate the public and human health care providers
M1 protein about the importance of good cough etiquette (e.g.,
coughing into your elbow), handwashing practices,
and seasonal influenza immunizations for their at-risk
patients and for themselves.
• Encourage older individuals to get the pneumococcal
(Streptococcus pneumoniae) vaccine.
• Educate human health care providers and veterinary
clinicians about groups at risk for influenza and its
complications, as well as signs and symptoms of the
disease in different age groups.
• Educate travelers to countries where avian influenza
is circulating about the risk of infection from contact
with poultry and environments contaminated with
poultry feces and secretions and uncooked poultry,
and advise them to seek medical care immediately if
signs (e.g., fever, cough) appear.
M2 • Instruct health care workers with influenza-like illness
Protein not to provide direct patient care.
• Be aware of pandemic influenza (panflu) planning in
your area (http://www.pandemicflu.gov/).
Figure 9-62 n Schematic model of an influenza A virus. (From Mandell

GL, Bennett JE, Dolin R (eds): Principles and practice of infectious diseases, ed Human Health Clinicians
6, Philadelphia, 2005, Churchill Livingstone Elsevier.)
• Consider testing patients in whom influenza develops
early or late in the influenza season, those with unusu-
ally severe clinical symptoms, a history of potential
Influenza viruses affect a number of different species, exposure to avian or swine influenza, or who are can-
including birds, swine, horses, and dogs, but animal-to- didates for antiviral treatment.
human transmission has been documented only for birds • Advise symptomatic individuals to avoid caring for
and swine. Humans may transmit human influenza virus sick or immunocompromised individuals.
to pet ferrets and swine.3 The epizootic of H5N1 high • Educate ill patients about the importance of covering
pathogenicity avian influenza in domestic and wild birds their cough, keeping their distance from others, and
in Asia, Europe, and Africa has focused increased attention washing their hands.
on the potential of influenza viruses to cross species barri- • Be aware of CDC guidance for detection and testing of
ers and cause human disease, although this is still consid- avian influenza infections in returning travelers. See
ered a rare event and the H5N1 epizootic has not, to date, Travelers’ Health; http://wwwn.cdc.gov/travel/content
produced a pandemic virus. Dogs and cats have become AvianFluPassengerChecks.aspx.
naturally and experimentally infected with avian influ- • Report influenza cases to state or local health depart-
enza viruses but have not as yet been shown to transmit ment if required in state.
the infection to humans. A swine influenza A H1N1 virus • Recommend influenza vaccinations of high-risk
that emerged in Mexico in the spring of 2009 has further groups. The Advisory Committee on Immunization
underscored the zoonotic nature of this disease. Human Practices (ACIP) recommends annual influenza vacci-
cases were identified worldwide within 1 week after the nations for the following groups5:
cause of the outbreak had been identified. As of October  All persons who want to reduce the risk of becom-
25, 2009, the World Health Organization had confirmed ing ill with influenza or of transmitting influenza to
more than 440,000 humans infected with the pandemic others
H1N1 virus and 5700 deaths worldwide (http://www.  All children aged 6 months to 18 years
who.int/csr/don/2009_10_30/en/index.html). Human-to-  All persons aged 50 years and older
animal transmission of the virus has also caused outbreaks  Women who will be pregnant during the influenza
in swine and turkeys (http://www.fao.org/news/story/en/ season
item/29532/icode/).4 H1N1 influenza infection has also  Adults who have chronic pulmonary (including
been documented in ferrets and a cat (http://www.usda. asthma), cardiovascular (except hypertension),
gov/documents/FINAL_RESULTS_2009_PANDEMIC_ renal, hepatic, hematological, or metabolic disor-
H1NI_INFLUENZA_CHT.pdf). ders (including diabetes mellitus)
 Adults who have immunosuppression (including ing 0.2 mL of the product. Approximately 0.1 mL (i.e.,
immunosuppression caused by medications or by half of the total sprayer contents) is sprayed into one
human immunodeficiency virus of the nostrils and the second half of the vaccine dose
 Adults who have any condition (e.g., cognitive dys- is administered into the other nostril.
function, spinal cord injuries, seizure disorders, or • Clinicians should strongly consider seasonal influenza
other neuromuscular disorders) that can compromise vaccination for poultry and swine workers.6
respiratory function or the handling of respiratory • CDC guidance for detection, testing, and treatment of
secretions or that can increase the risk for aspiration patients infected with the pandemic H1N1 virus and
 Residents of nursing homes and other long-term recommendations for vaccination of people at risk for
care facilities infection with the novel virus strain can be found at:
 Health care personnel (Figure 9-63) http://www.cdc.gov/H1N1FLU.
 Healthy household contacts and caregivers of chil-
dren younger than 5 years and adults 50 years and Veterinary Clinicians
older, with particular emphasis on vaccinating con-
tacts of children younger than 6 months • Contact state veterinarian and public health depart-
 Healthy household contacts and caregivers of per- ment to report suspected or confirmed cases of animal
sons with medical conditions that put them at influenza.
higher risk for severe complications from influenza • Wear appropriate PPE when examining animals with
• Two vaccines, a trivalent inactivated influenza vaccine suspected influenza infection. This includes gloves and
(TIV) and a live, attenuated intranasal vaccine (LAIV) surgical masks—if a highly pathogenic avian influ-
are approved by the Food and Drug Administration enza, swine influenza, or human influenza strain is
(FDA). The TIV is approved for use in people 6 suspected, an N-95 respirator should be used.
months of age or older. The primary series for chil- • Test and isolate sick animals.
dren younger than 8 years consists of 2 doses admin- • Use appropriate infection control measures in the
istered 1 month apart. Individuals who only received practice (hospital and clinic) to avoid environmental
1 dose in their first year of vaccination should receive contamination and nosocomial spread of the virus.7
2 doses in the following year. The TIV is injected into • Educate the animal owner regarding zoonotic risk
the deltoid muscle of older children and adults. Infants (where applicable) and need for adequate PPE and
and young children without adequate deltoid muscle handwashing. Offer direct communication with fam-
mass should be vaccinated in the anterolateral aspect ily physician.
of the thigh. The LAIV is made from a weakened virus • Counsel ferret owners that these pets are susceptible to
and can cause mild illness in some individuals (runny several human influenza strains.
nose, headache, sore throat, or cough). It is approved • Be aware of the USDA’s National Highly Pathogenic
in healthy people (without underlying health problems Avian Influenza (HPAI) Response Plan. Should HPAI
predisposing them to complications from influenza) be identified in the United States, a team of federal
between 2 and 49 years who are not pregnant. Two and state officials will be deployed to the area to
doses of LAIV administered at least 6 weeks apart are assess the scope of disease and the resources needed
recommended for 2- to 8-year-old children who are to confine it.
receiving an influenza vaccine for the first time. If the • Veterinarians and veterinary staff should receive
child receives only 1 dose in the first year, 2 doses are annual seasonal influenza vaccinations.
recommended the following year. The intranasal vac- • If an outbreak of HPAI is identified in wild birds, con-
cine comes in a prefilled, single-use sprayer contain- sider diagnosis in domestic birds or bird predators
with clinical signs and potential virus exposure.
• Influenza virus vaccines are available for swine, dogs,
horses, and domestic birds. Several inactivated whole-
virus swine influenza vaccines are currently on the
market. The vaccines help reduce the severity of dis-
ease in pigs but do not provide complete protection
against infection. Many in the swine industry use
autogenous vaccines produced against the strain cir-
culating in their herd. Animals are usually vaccinated
during the late nursing–early weaning stage to prevent
influenza outbreaks in the growth/early finishing ani-
mals. Breeding herds are often vaccinated as well.
• All horses in contact with other equines should be vac-
cinated against equine influenza. Three types of equine
influenza virus vaccines are available.8 Inactivated vac-
cines and canary pox vector vaccines are administered
Figure 9-63 n Health care professional receiving an intramuscular vac-
intramuscularly. The initial series consists of 2 doses of
cination. (From Centers for Disease Control and Prevention Public Health vaccines given 3 to 6 weeks apart followed by boosters
Image Library, Atlanta, Ga.) every 6 months. Annual influenza vaccine boosters
may be sufficient for horses at low risk of exposure

once they have been primed with 3 doses of vaccine
over a 7-month period. The third vaccine type, modi-
fied live cold-adapted vaccines, is administered intra-
nasally. One priming dose is recommended followed
by boosters every 6 months. The intranasal vaccines are
licensed for nonpregnant horses older than 11 months.
Inactivated vaccines are licensed for horses older than
6 months, and canary pox virus vaccines are safe for
foals 4 months of age or older.
• Vaccination of poultry against avian influenza is not
routine because most poultry in developed countries,
including the United States, are grown in commercial
settings that are free from avian influenza. Vaccines
have been used in specific high-risk situations target-
ing a known hemagglutinin subtype of avian influenza
virus, such as in outdoor-reared turkeys in the upper
Midwest United States when in contact with avian
influenza–infected migratory ducks, or for turkeys in
areas of high swine concentration. Avian influenza Figure 9-64 n Electron micrograph of influenza viruses. (From Centers
vaccination requires approval of the state veterinarian, for Disease Control and Prevention Public Health Image Library, Atlanta, Ga.)
and with H5 and H7 avian influenza, the approval of
the USDA. Most licensed vaccines are inactivated whole
avian influenza virus in oil-emulsified adjuvant, which influenza A viruses recognized to date have possessed H1,
requires individual bird handling and subcutaneous or H2, or H3 and N1 or N2 glycoproteins. Influenza A (H1N1)
intramuscular injection. One fowl poxvirus recombi- and A (H3N2) have been circulating worldwide in human
nant containing an influenza H5 hemagglutinin gene populations since 1977. Influenza B, which occurs only in
insert is licensed for emergency use. The vaccines pro- humans and seals, is also responsible for significant human
tect against clinical disease but HPAI viruses can circu- morbidity globally each year.5 Influenza C is rarely recog-
late undetected in a vaccinated flock. Serological tests nized in comparison to A and B viruses but can cause focal
cannot distinguish between an antibody response to human epidemics.
the vaccine and a natural infection.3 New seasonal influenza viruses evolve from point muta-
tions (antigenic drift) in the surface glycoproteins, particu-
Agent larly the H, which frequently happens during viral replication.
Gene segment reassortment among influenza A viruses can
Influenza viruses (Family Orthomyxoviridae) are enveloped, also occur. If these reassortments involve human and ani-
segmented, negative-stranded RNA viruses covered with mal influenza viruses, they may lead to significant antigenic
two surface glycoproteins (Figure 9-64).1 They are divided changes (antigenic shifts) that can result in the emergence of
into three distinct types (A, B, and C) on the basis of their a novel virus subtype (Figure 9-65).
M and nucleocapsid proteins.9 Influenza A viruses are further Influenza viruses exhibit various degrees of host adaptation
divided into subtypes based on the antigenic characteristics with easy transmission between individuals within the same
of their hemagglutinin (H) and neuraminidase (N) surface species, and greater difficulty of infection and unsustainable
glycoproteins. Each virus carries one H and one N glycopro- transmission to unrelated host species.11,12 The basis of this host
tein type (see Figure 9-63). Sixteen hemagglutinin subtypes or species adaptation is unclear, but the presence of the proper
(H1 through H16) and 9 neuraminidase (N1 through N9) constellation of gene segments is critical and may include
have been identified from avian hosts.10 Seasonal human specific hemagglutinin binding to receptors on host cells,
1918 1947 1957 1968 1977
H1N1 (A0) (A) H1N1
H2N2 H2N2
H3N8 H3N2
1880 1890 1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000
Figure 9-65 n Recent pandemics of influenza. The duration of circulation of viruses of various subtypes is
shown by the boxes. The nature of influenza epidemics before 1918 is known only by serological means. (From
Mandell GL, Bennett JE, Dolin R (eds): Principles and practice of infectious diseases, ed 6, Philadelphia, 2005,
Churchill Livingstone Elsevier.)
especially respiratory cells, and their differential distribu-

tion; cleavability of hemagglutinin protein; presence or
absence of glycosylation sites on the hemagglutinin; length
of neuraminidase protein and its affinity for the sialic acids;
and ability of polymerase complex to function within the
host cell.13
Strains of avian influenza virus are classified as low patho-
genic (LP) or high pathogenic (HP) based on their lethality
in chickens.14 Currently HPAI H5N1 is circulating in Asia,
Europe, and Africa. However, other highly pathogenic strains
have caused outbreaks in the recent past, including H7N7,
H7N3, and H5N2. All HPAI viruses have been H5 and H7,
but most H5 and H7 viruses are of low pathogenicity.
Worldwide.
Groups at Risk
Several population groups are at high risk for complica-
tions of seasonal influenza, including people who are 50
years old or older and people with chronic health problems,
such as cardiovascular disease, renal and metabolic disor-
ders (including diabetes), and respiratory disorders (includ-
ing asthma). Other high-risk groups include women who
are pregnant during the flu season, children and adolescents
who are receiving long-term aspirin therapy, and children
younger than 5 years.15 Severe influenza disease is also often
seen in individuals with immunosuppressive disorders such
as cancer or HIV/AIDS.5
Individuals performing activities involving close contact
with animals, such as slaughtering animals and defeathering
birds, have been reported to be at increased risk for avian and
swine influenza.16-18

Figure 9-66 n Lateral (A) and ventrodorsal (B) radiographs of a fer-
Avian influenza viruses are maintained in nature by wild ret with bacterial pneumonia as a complication of influenza. (From
birds. The viruses have been isolated from more than 100 Quesenberry K, Carpenter JW: Ferrets, rabbits and rodents: clinical medicine
and surgery, ed 2, St Louis, 2004, Saunders Elsevier.)
bird species in 13 genera; however, the most important avian
influenza reservoir hosts belong to the Anseriformes (ducks,
geese, and swans) and the Charadriiformes (gulls, terns, Mode of Transmission and Life Cycle
and shorebirds) groups.19 More virus isolations have been
reported from Mallards (Anas platyrhynchos) than any other Human influenza is usually spread from person to person
bird species. Certain influenza virus strains have adapted to in close contact through large-particle respiratory drop-
genetically distinct horse, swine, poultry, dog, and human let and short-distance small-particle aerosol transmission
viruses and are self-sustaining in those species.19-21 Incidental (coughs, sneezing) (Figure 9-67). Indirect spread via contact
hosts or sporadic infections have been reported in mink, fer- with surfaces contaminated with respiratory droplets is also
rets (Figure 9-66), stone marten, domestic cats, large felids a possible transmission mode, and there is evidence that the
(tigers and leopards), and sea mammals.19,22 virus can persist for 1 to 2 days on some surfaces.5
Swine are susceptible to both human and avian virus In swine, the virus is found in respiratory secretions and
strains and are hypothesized to be able to serve as viral mixing spreads by aerosolization and by direct pig-to-pig contact.24
vessels where human and avian gene segments may reassort.1 Birds can shed high concentrations of influenza virus in feces,
The 2009 H1N1 swine influenza virus is a novel reassortant and fecal/oral spread is believed to be an important route of
of two (parent) swine influenza viruses. It also contains genes virus transmission in wild birds.19 Infected birds can also shed
of avian and human influenza virus origin incorporated into influenza virus in their saliva and nasal secretions. Poultry can
one of the parent viruses at an earlier time.23 However, reas- become infected when they have direct contact with infected
sortment in swine may not be a requirement for emergence birds or indirectly through contact with contaminated sur-
of a pandemic strain if the avian strain can produce infection faces (such as equipment or cages) or feed or water. Aerosol
in a human host. transmission may also be possible over short distances.25
Cats and vomiting are other common influenza manifestations

among children. Young children may be less likely than other
Other Mammals Human beings
influenza cases to present with fever and cough.5 The incuba-
Wild birds
tion period is short (1 to 4 days) and the morbidity period
generally lasts 3 to 7 days. Lassitude and cough may persist
Horses Human beings for 2 weeks or more.26 Adults may be infectious the day before
Wild birds through day 5 after disease onset. Young children may shed
virus several days before and after symptom onset.5
Complications of influenza are common. Patients may
Horses Poultry Swine develop primary viral pneumonia, viral or secondary bac-
terial sinusitis and otitis, or pneumonia and experience
exacerbations of underlying medical conditions such as
Dogs Dogs Poultry Swine pulmonary or cardiac disease. Influenza virus infection also
has been uncommonly associated with encephalopathy,
Transmission route transverse myelitis, myositis, myocarditis, pericarditis, and
Reye syndrome.5
Potential transmission route Humans can on rare occasions become infected with
Figure 9-67 n Life cycle of influenza.
avian27 or swine19,28 influenza viruses. Symptoms range from
a mild conjunctivitis or upper respiratory tract disease to
pneumonia, acute respiratory distress, and death. Further
Touching surfaces contaminated with avian influenza human-to-human transmission of these animal influenza
virus in respiratory droplets and handling infected birds viruses has been reported but is uncommon.
or bird manure are hypothesized risk factors for human
infection with avian influenza, possibly through contami-
nated-hand–to–mucous membrane contact or inhalation Disease in Animals
of contaminated dust particles or aerosols generated during Avian influenza (AI) viruses are classified into low pathoge-
cleaning, slaughtering, defeathering, and other activities.16,18 nicity (LP) and high pathogenicity (HP) based on specific
Swine influenza transmission appears to occur during close criteria related to their ability to produce high mortality rate
direct or indirect human contact with infected swine.17 in chickens or have a hemagglutinin protein cleavage site
sequence compatible with previous HPAI virus.29 Most AI
Environmental Risk Factors strains are LP and generally cause no or few clinical signs in
poultry. Typical clinical signs associated with LPAI reflect an
As stated previously, it is believed that contaminated environ- upper respiratory tract disease or reproductive disease in hens
ments such as surfaces, aerosols, and water may play a role (i.e., drops in egg production with abnormal eggs). However,
in animal-to-animal influenza transmission and may also some H5 and H7 LPAI viruses have mutated into HPAI
be important in human-to-human and animal-to-human viruses in the field. Signs of HPAI include high mortality rate;
transmission, although the significance of such environmen- sudden death without premonitory clinical signs; lethargy;
tal spread in each circumstance is not well understood. severe decrease in egg production; facial edema with swollen
Human crowding, such as in nursing homes, is associated eyelids, comb, wattles, and hocks; purple discoloration of the
with an increased rate of human outbreaks. As in animals, a wattles, combs, and legs; upper respiratory tract signs; inco-
high density of birds or swine in a production facility or a ordination; and diarrhea.30 Turkeys are susceptible to certain
live animal market, as well as mixing of waterfowl, poultry, strains of H1 and H3 swine influenza viruses.31,32
and other animal species including swine in a single facil- Swine influenza A H1N1 and H3N2 viruses are endemic
ity, may facilitate the spread of virus between animals. Farms in swine populations in the United States.33 Clinical signs of
that have ponds or other water bodies where wild waterfowl influenza in pigs include fever, coughing, nasal and/or ocular
can come in contact with domestic animals may also consti- discharge, dyspnea, and depression. Reproductive problems
tute an environmental risk. Whether the seasonal pattern of are seen in both males and females. Milk production may
influenza is related to other environmental variables such as also be reduced. The morbidity period is usually 5 to 7 days.
temperature and humidity remains unclear. Morbidity can reach 100%. Mortality rates are low, usually
between 1% and 3%; however, secondary bacterial infections
may develop and increase mortality.25
Disease in Humans
Influenza A viruses H3N8 and H7N7 cause equine influ-
Influenza virus infections can affect all age groups, although enza in horses and other equids. The incubation period is gen-
the highest infection rates are seen among infants and chil- erally 1 to 3 days. Incubation periods as long as 7 days have
dren. Upper and lower respiratory tract complications been reported. Clinical signs include fever; a harsh, dry cough;
occur across age groups, but hospitalizations and deaths and serous to mucopurulent nasal discharge. In partially
from infection are more common in people older than 65 immune or vaccinated animals, one or more of these signs
years. may be absent. Other typical signs include depression, mus-
Uncomplicated influenza typically has a quick onset of cle soreness, anorexia, and enlarged submandibular lymph
fever, myalgia, headache, malaise, sore throat, and nonproduc- nodes. Young foals lacking maternal antibody protection
tive cough. Rhinitis may also be present. Otitis media, nausea, are susceptible to a fatal viral pneumonia. Horses can also
develop a potentially fatal secondary bacterial pneumonia, dogs and causes outbreaks of respiratory disease. Most
pleuropneumonia, and myocarditis.8,34 animals develop a mild cough, purulent nasal discharge, and
Infected horses may shed virus over an extended period start- low-grade fever.21 Dogs can also develop a more severe dis-
ing during the incubation period and ending a week or more after ease with high fever and pneumonia. Between 5% and 10%
apparent recovery. Peak viral shedding is thought to occur dur- of ill dogs die from the illness.21,35
ing the first 24 to 48 hours when the animal is febrile.8 The virus Avian influenza can cause fatal infection in domestic and
is spread via aerosolized respiratory droplets and fomites with an large cats. Reported signs of HPAI H5N1 in felids include
attack rate that can approach 100% in susceptible populations. fever, panting, nervousness, and depression.36 Table 9-35
Canine influenza was first recognized in 2004. An equine shows comparative clinical presentations in humans and other
influenza virus A H3N8 strain has apparently adapted to animals.
Table 9-35 n Influenza: Comparative Clinical Presentations in Humans and Other Animals
Incubation
Humans Close contact with 1-4 days Fever, myalgia, headache, malaise, DFA, RT-PCR, EIA, viral cultures,
infected person, bird, or swine sore throat, nonproductive cough and rapid diagnostic tests such
and rhinitis, otitis media, nausea and as immunochromatographic
vomiting in children; complications assays, paired sera taken 2-4
include primary viral pneumonia, weeks apart
secondary bacterial sinusitis,
otitis, or pneumonia, exacerbated
underlying medical conditions such
as pulmonary or cardiac disease
Birds Direct contact with secretions 1-5 days LPAI: No or few clinical signs, RRT-PCR and serological
or feces from infected birds, including inappetence, mild screening tests, virus isolation,
contaminated feed, water, respiratory signs (nasal discharge, sequencing, and chicken
equipment, or clothing coughing, sneezing), and pathogenicity test needed for
decreased egg production confirmation of HPAI; serology
by ELISA and AGID are used
for monitoring
Movement of people and birds HPAI: Sudden death; lethargy; Histopathology findings with
decreased egg production, soft- HPAI include hemorrhaging
shelled or misshapen eggs; facial and necrosis of multiple
edema with swollen eyelids, organs19
comb, wattles, and hocks; purple
discoloration of the wattles, combs,
and legs; incoordination; and diarrhea
Swine Contact with nasal secretions or <24 hours Fever; coughing; nasal and/or ocular Lung or nasal tissues can be
aerosol; airborne spread of virus discharge; dyspnea and depression evaluated for the presence of
can occur between farms under Reproductive problems such as live or inactivated virus using
certain circumstances reduced viability of sperm, first- and immunohistochemistry, DFAs,
second- trimester abortions, delayed antigen-capture ELISA, cell
return to estrus, and decreased culture, or PCR
viability of piglets; milk production Tests for detecting H1N1 or H3N2
may also be reduced antibodies include the HI, ELISA,
immunodiffusion, and IFA
Horses Aerosolized respiratory secretions; 1-3 days Clinical signs include fever; a harsh, dry Viral antigen can be detected
contaminated equipment, cough; and serous to mucopurulent from nasopharyngeal swabs,
brushes, or rugs nasal discharge; other typical signs and tracheal and nasal wash
include depression, muscle soreness, samples using virus isolation,
anorexia, enlarged regional lymph RT-PCR, nested RT-PCR, and
notes, colic, edema of the extremities ELISA
and scrotum, viral pneumonia in Paired acute and convalescent
young foals; secondary bacterial serum samples can be
pneumonia, pleuritis, and interstitial submitted for HI testing
myocarditis
Dogs Contact with aerosolized 2-5 days Moist or dry cough, purulent nasal Paired sera taken 2-3 weeks
respiratory secretions and discharge, fever, pneumonia apart, virus detection from nasal
contaminated objects swabs by PCR or viral culture37
Cats Predation on diseased birds 2-5 days Fever, dyspnea, depression, Paired sera, pharyngeal swabs36
conjunctivitis
AGID, Agar gel immunodiffusion; DFA, direct immunofluorescent antibody; ELISA, enzyme-linked immunosorbent assay; HI, hemagglutination-inhibition; IFA, immunofluo-
rescent antibody; RT-PCR, reverse transcriptase polymerase chain reaction; EIA, enzyme immunoassay; RRT-PCR, real-time reverse transcriptase polymerase chain reaction.
ratory secretions in horses, swine, and dogs the first few days
Diagnosis
after disease onset. Optimal specimens include nasal secre-
tions and lung tissue from swine, nasopharyngeal swabs from
Diagnosis in Humans horses, nasal swabs from dogs, and oropharyngeal swabs
from birds. Serological testing is another valuable diagnos-
The differential diagnosis for human influenza includes other
tic tool in animals. Acute and convalescent samples taken 2
respiratory pathogens, including Mycoplasma pneumoniae,
weeks apart are needed.
adenovirus, respiratory syncytial virus, rhinovirus, parain-
In poultry, samples of oropharyngeal and cloacal swabs
fluenza viruses, and Legionella species infection.26 Studies
are preferred for diagnosis. In the United States, matrix gene
have estimated that 80% to 90% of healthy adults presenting
real-time reverse transcriptase polymerase chain reaction
with an acute onset of fever and a cough, the most common
(RRT-PCR) is used to identify influenza A virus and all posi-
presentation of influenza, in areas with confirmed influenza
tives are further tested by H5 and H7 specific RRT-PCR. The
activity have the disease. Young children and older adults are
hemagglutinin proteolytic cleavage site is sequenced for all
less likely to present with these symptoms. Infants may pres-
H5 or H7 RRT-PCR+ samples to determine LP or HP. The
ent with high fevers. A septicemia-like disease, cough, and
avian influenza virus detection is confirmed by virus isola-
fever are seen in 64% of children younger than 5 years, and
tion in 9- to 11-day embryonating chicken eggs. All influenza
fewer than one in three nonhospitalized patients 60 years or
A viruses are subtyped by hemagglutination-inhibition (HI)
older present with typical influenza signs.5
and neuraminidase-inhibition (NI) tests and pathotyped by
Laboratory confirmation of disease is important.
in vivo chicken pathogenicity testing. Serological monitor-
Specimens should be collected the first few days after onset
ing of poultry is done using commercial ELISA and agar gel
of symptoms or no more than a week after disease onset in
immunodiffusion (AGID) tests for influenza A, and positives
young children. The most common diagnostic tests currently
are subtyped by HI and NI tests.
used in clinics, doctors’ offices, and hospitals are rapid influ-
enza tests using immunochromatography. These tests require
no reagent additions or wash steps, usually detect both influ-
Treatment
enza A and B, and use respiratory tract specimens specified in
the manufacturers’ instructions.38 Results are available within
30 minutes. The accuracy of these tests depends on the sensi- Treatment in Humans
tivity and specificity of the assay, the amount of virus in the
Four antiviral medications—amantadine, rimantadine, osel-
sample, and the specimen type used. Infants and young chil-
tamivir (Tamiflu), and zanamivir (Relenza)—are approved
dren shed the highest viral titers, and these tests perform best
by FDA for influenza treatment.39 The first two are not cur-
in this patient group. The rapid tests typically have greater
rently recommended because of the widespread presence
than 90% specificity and an average 70% sensitivity for
of antiviral resistance in influenza A (H3N2) viruses and
detecting influenza. False-positive results are more common
lack of activity against influenza B. The latter two drugs are
when the prevalence of influenza is low; false-negative results
neuraminidase inhibitors with activity against both influ-
are more likely to occur when disease prevalence is high.
enza A and B viruses. Early treatment reduces illness severity
Additional diagnostic tests available in hospital and other
and risk of complications leading to antibiotic use. In hos-
clinical laboratories include viral cultures, direct immunoflu-
pitalized adults, oseltamivir treatment appears to reduce the
orescence antibody (DFA) on clinical specimens, reverse tran-
likelihood of influenza-related mortality. Antiviral resistance
scriptase polymerase chain reaction (RT-PCR), and enzyme
also occurs to the neuraminidase inhibitors, and during the
immunoassay (EIA). The ideal specimen depends on the test
2007-08 Northern Hemisphere season, community circula-
used but may include nasopharyngeal and nasal swabs or aspi-
tion of oseltamivir-resistant H1N1 viruses was noted for the
rates, nasal and bronchial washes, throat swabs, or sputum
first time.
collected within the first 4 days of illness. Results from anti-
Treatment should be started as soon as possible after dis-
gen tests such as DFA or EIA should be available within a few
ease onset. Oseltamivir is approved for treatment of people
hours of arrival at the laboratory. Conventional viral cultures
1 year of age and older. Zanamivir is approved for treat-
can take between 2 and 10 days, whereas rapid centrifugation
ment of people 7 years of age and older. Both drugs can
cultures followed by IFA staining are reported at 1 and 2 days.
also be used as chemoprophylaxis with a disease prevention
RT-PCR assays are currently confined to reference laboratories
efficacy ranging from 70% to 90%. Zanamivir is not recom-
and some large tertiary care hospitals, and where available are
mended for persons with underlying airways disease (e.g.,
performed no more than once a day. Influenza virus infection
asthma or chronic obstructive pulmonary disease). Table
can be confirmed by serology as well. Paired acute and conva-
9-36 outlines treatment guidelines for symptomatic disease
lescent sera taken 2 to 4 weeks apart are needed.5
in humans.
Serological and rapid tests for human influenza A may
not recognize avian influenza viruses (such as influenza A
H5N1).
Treatment in Animals
Diagnosis in Animals Treatment of influenza in horses, dogs, and pigs is gener-

ally supportive. Antivirals as listed above for humans are not
Animal influenza is diagnosed based on clinical signs and approved for treatment of animal infections, in part due to
laboratory test results. Antigen can be recovered from respi- concern about development of drug resistance.
Table 9-36 n Treatment Guidelines for Symptomatic Influenza Disease in Humans
Age Group (yr)
Antiviral Agent 1-6 7-9 10-12 13-64 ≥65
Zanamivir* Treatment, influenza N/A† 10 mg (2 inhalations)

A and B twice daily
Chemoprophylaxis, Ages 1-4 N/A Ages 5-9 10 mg (2 10 mg (2 inhalations)
influenza A and B inhalations) once daily once daily
Oseltamivir Treatment,‡ influenza Dose varies by 75 mg twice
A and B child’s weight§ daily
Chemoprophylaxis, Dose varies by 75 mg/day
influenza A and B child’s weight||
Note: Zanamivir is manufactured by GlaxoSmithKline (Relenza—inhaled powder). Zanamivir is approved for treatment of persons 7 years and older and approved for chemo-
prophylaxis of persons 5 years and older. Oseltamivir is manufactured by Roche Pharmaceuticals (Tamiflu—tablet). Oseltamivir is approved for treatment or chemoprophylaxis
of persons 1 year and older. No antiviral medications are approved for treatment or chemoprophylaxis of influenza among children younger than 1 year. This information is based
on data published by the CDC (http://www.cdc.gov/h1n1flu/recommendations.htm).
*Zanamivir is administrated through oral inhalation by using a plastic device included in the medication package. Patients will benefit from instruction and demonstration of the
correct use of the device. Zanamivir is not recommended for those persons with underlying airway disease.
†Not applicable.
‡A reduction in the dose of oseltamivir is recommended for persons with creatinine clearance less than 30 mL/min.
§The treatment dosing recommendation for children weighing 15 kg or less is 30 mg twice a day; for children weighing more than 15 kg and up to 23 kg, the dose is 45 mg twice a day;
for children weighing >15-23 kg, the dose is 45 mg twice a day; for children weighing >23-40 kg, the dose is 60 mg twice a day; and for children >40 kg, the dose is 75 mg twice a day.
||The chemoprophylaxis dosing recommendation for children weighing 15 kg or less is 30 mg once a day; for children weighing >15-23 kg, the dose is 45 mg once a day; for children
weighing >23-40 kg, the dose is 60 mg once a day; and for children >40 kg, the dose is 75 mg once a day. From http://www.cdc.gov/flu/professionals/antivirals/dosage.htm#table.
References 17. Gray GC, McCarthy T, Capuano AW, et al. Swine workers and swine
influenza virus infections. Emerg Infect Dis. 2007;13(12):1871.
1. Treanor JT. Influenza Virus. In: Mandell GL, Bennett JE, Dolin R, eds. 18. Rabinowitz P, Perdue M, Mumford E. Contact variables for exposure
Principles and practice of infectious diseases. 5th ed. Churchill Livingstone; to avian influenza H5N1 virus at the human-animal interface. Zoonoses
2000:1823–1849. Public Health. March 26, 2009.
2. Centers for Disease Control and Prevention. Key Facts about Seasonal 19. Stallknecht DE, Nagy E, Hunter B, et al. Avian influenza. In: Thomas
Influenza (Flu). http://www.cdc.gov/flu/keyfacts.htm. Accessed May 14, 2009. NJ, Hunter DB, Atkinson CT, eds. Infectious diseases of wild birds. Wiley-
3. Thacker E, Janke B. Swine influenza virus: zoonotic potential and vac- Blackwell; 2007:108–130.
cination strategies for the control of avian and swine influenza. J Infect 20. Song D, Kong B, Lee C, et al. Transmission of avian influenza virus
Dis. 2008;197:S19–S24. (H3N2) to dogs. Emerg Infect Dis. 2008;14(5):741.
4. Government of Saskatchewan. Influenza H1N1. http://www.agriculture. 21. Payungporn S, Crawford PC, Kouo TS, et al. Influenza A virus
gov.sk.ca/H1N1_Influenza. Accessed May 14, 2009. (H3N8) in dogs with respiratory disease, Florida. Emerg Infect Dis.
5. Fiore AE, Shay DK, Broder K, et al. Prevention and control of seasonal 2008;14(6):902.
influenza with vaccines: recommendations of the Advisory Committee on 22. U.S. Geological Survey. Avian influenza. http://www.nwhc.usgs.gov/dis-
lummunization Practices (ACIP) 2009. MMWR. 2009;581-52 Available ease_information/avian_influenza/index.jsp.
at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr58e0724a1.htm. 23. Dawood FS, Jain S, et al. Emergence of a novel swine-origin influenza
6. Gray GC, Baker WS. The importance of including swine and poul- A (H1N1) virus in humans. N Eng J Med. 2009;361.
try workers in influenza vaccination programs. Clin Pharmacol Ther. 24. Merck Veterinary Manual. Swine influenza. http://www.merckvetman-
2007;82(6):638–641. ual.com/mvm/index.jsp?cfile=htm/bc/121407.htm. Accessed November
7. Elchos BL, Scheftel JM, et al. Compendium of veterinary standard pre- 1, 2009.
cautions for zoonotic disease prevention in veterinary personnel. J Am 25. Merck Veterinary Manual. Avian influenza: introduction. http://www.
Vet Med Assoc. 2008;233(3):415–432. merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/206200.htm.
8. American Association of Equine Practitioners Influenza virus vaccination Accessed November 1, 2009.
guidelines. http://www.aaep.org/equine_influenza.htm. Accessed November 26. Centers for Disease Control and Prevention. Influenza symptoms and
1, 2009. laboratory diagnostic procedures. http://www.cdc.gov/flu/professionals/
9. Knipe DM, Howley DM, eds. Fields virology. 5th ed. Philadelphia: diagnosis/labprocedures.htm. Accessed November 1, 2009.
Lippincott Williams & Wilkins; 2007. 27. Centers for Disease Control and Prevention. Avian influenza A virus
10. Capua I, Marangon S. Control of avian influenza in poultry. Emerg infections of humans. http://www.cdc.gov/flu/avian/gen-info/avian-flu-
Infect Dis. 2006;12(9):1319. humans.htm. Accessed November 1, 2009.
11. Gabriel G, Dauber B, Wolff T, et al. The viral polymerase mediates adap- 28. Center for Food Safety and Public Health. Influenza. http://www.cfsph.
tation of an avian influenza virus to a mammalian host. Proc Natl Acad iastate.edu/Factsheets/pdfs/influenza.pdf. Accessed November 1, 2009.
Sci U S A. 2005;102(51):18590. 29. World Organization for Animal Health. Avian influenza. In Terrestrial
12. Smith GJ, Naipospos TS, Nguyen TD, et al. Evolution and adaptation Animal Health Code, Article 2.7.12.1, Paris. Available at: http://www.oie.
of H5N1 influenza virus in avian and human hosts in Indonesia and int/eng/normes/mcode/en_chapitre_2.7.12.htm.
Vietnam. Virology. 2006;350(2):258. 30. Swayne DL, Halvorson DA. Influenza. In: Saif YM, ed. Diseases of poul-
13. Mubareka S, Palese P. The biology of a changing virus. In: Rappuoli R, Del try. 11th ed. Aimes, IA: Iowa State University Press; 2003:135–161.
Giudice G, eds. Influenza vaccines of the future. SpringerLink; 2008:9–30. 31. Choi YK, Lee JH, Erickson G, et al. H3N2 influenza virus transmission from
14. World Health Organization: Avian influenza. http://www.oie.int/eng/ swine to turkeys, United States. Emerg Infect Dis. 2004;10(12):2156.
normes/mmanual/2008/pdf/2.03.04_AI.pdf. Accessed November 1, 2009. 32. Wright SM, Kawaoka Y, Sharp GB, et al. Interspecies transmission and
15. Centers for Disease Control and Prevention. Influenza vaccine: a sum- reassortment of influenza A viruses in pigs and turkeys in the United
mary for clinicians. http://www.cdc.gov/flu/professionals/vaccination/ States. Am J Epidemiol. 1992;136(4):488.
vax-summary.htm. Accessed November 1, 2009. 33. Reference deleted in proofs.
16. Dinh PN, Long HT, Tien NTK, et al. Risk factors for human infec- 34. Merck Veterinary Manual. Equine influenza. http://www.mer-
tion with avian influenza A H5N1, Vietnam, 2004. Emerg Infect Dis. ckvetmanual.com/mvm/index.jsp?cfile=htm/bc/121303.
2006;12(12):1841. htm&word=equine%2cinfluenza. Accessed November 1, 2009.
35. American Veterinary Medical Association. Influenza updates from the 38. Centers of Disease Control and Prevention. Rapid diagnostic testing for
AVMA. http://www.avma.org/public_health/influenza/canine_bgnd. influenza. http://www.cdc.gov/flu/professionals/diagnosis/rapidclin.htm.
asp. Accessed November 1, 2009. Accessed November 1, 2009.
36. Marschall J, Hartmann K. Avian influenza A H5N1 infections in cats. 39. Centers of Disease Control and Prevention. Recommended daily dosage
J Feline Med Surg. 2008;10(4):359–365. of seasonal influenza antiviral medications for treatment and chemopro-
37. Cornell University College of Veterinary Medicine. Canine influ- phylaxis—United States. http://www.cdc.gov/flu/professionals/antivi-
enza virus. http://www.diaglab.vet.cornell.edu/issues/civ.asp. Accessed rals/dosage.htm#table. Accessed November 1, 2009.
November 1, 2009.
LEISHMANIASIS
Peter M. Rabinowitz and Lisa A. Conti • Conduct an immediate investigation of a human or

veterinary case to determine whether it is related to
Cutaneous leishmaniasis (ICD-10 B55.1, B55.2) travel or local transmission.
• In endemic areas, develop a strategy with vector special-
Other names in humans: Aleppo ulcer, Baghdad or Delhi boil, ists for vector control based on local ecology and trans-
Oriental sore, Espundia, uta, chiclero ulcer mission patterns. Interventions may include targeted
spraying in suspected sand fly habitat, including around
Visceral leishmaniasis (ICD-10 B55.0) doorways of dwellings (if residential transmission sus-
pected), stone walls, animal houses, and garbage dumps.
Other names in humans: kala-azar • In endemic areas where dogs are serving as a reservoir,
work with animal control authorities on effective strat-
Other names in animals: canine visceral leishmaniasis egies including use of insecticide-impregnated collars.
Culling of dog populations has not been proven effec-
Leishmaniasis caused by infection with protozoans in the tive in some areas.2
genus Leishmania causes millions of infections each year • Ensure that travelers to endemic areas take steps to avoid
around the world. The infection takes two basic forms: cuta- sand fly bites. Use insect repellent and permethrin-
neous and visceral, but disease syndromes may overlap. The impregnated bed nets and protective clothing.2
severity of human infection ranges from mild skin lesions to
severe disfiguring facial involvement or systemic disease with Human Health Clinicians
organ failure and death. This zoonotic disease is transmitted
by insect vectors, usually of the phlebotomine sand fly fam- • Consider the diagnosis in all patients with a history of
ily. Leishmaniasis has been transmitted directly from dog to recent travel or residence in an endemic area.
dog in the United States. Worldwide risk of leishmaniasis is • Immediately report disease to public health
increasing in both humans and animals. Factors responsible authorities.
may include the transboundary movement of humans and • Counsel travelers to endemic areas about risk reduc-
animals, global climate change affecting the distribution of tion in terms of avoiding sand fly bites (see above).
vectors, the HIV epidemic,1 and increasing contact of humans
with wilderness areas where the disease is endemic. In addi- Veterinary Clinicians
tion to being a disease of travelers returning to the United
States, there is an expanding focus of human cases of leishma- • Consider the diagnosis in dogs in the United States,
niasis in Texas, as well as an ongoing outbreak of canine vis- especially foxhounds, who present with constitutional
ceral leishmaniasis in foxhounds in the eastern United States. signs.
The complex interrelationships of leishmaniasis infection in • Consider the diagnosis in equids with nonhealing
animals and humans demand ongoing cooperation between cutaneous lesions on the head.
animal and human health professionals to detect new cases • Counsel clients not to let cats and dogs roam outside
and better control this challenging disease. and to provide insect repellent for horses in endemic
areas.
• Increase index of suspicion of leishmaniasis in animals
Key Points for Clinicians and Public Health with a travel history to the Mideast, tropics, or sub-
Professionals tropics or with previous blood transfusion.
• Be aware that autochthonous transmission of visceral
Public Health Professionals canine leishmaniasis has occurred in the United States
in the absence of insect vectors.3
• Characterize the risk in the community, including • Vaccine trial work shows promise for use in endemic
whether the sand fly vector is present and if there is areas.4
evidence of transmission to humans or domestic • Treat infected dogs using the CDC protocol through
animals. the state public health veterinarian. Canine leishma-
• Educate human health providers that infection could niasis may be reportable to your state health or agri-
be spread through shared needles. culture department.
by L. major is spread by bites of the sand fly Phlebotomus

Agent
papatasis.5 A major reservoir is gerbils (Meriones unguic-
At least 20 species in the genus Leishmania are pathogenic ulatus). Hyraxes (Procavia capensis) are another mamma-
in humans, and are found in a range of mammalian reser- lian host. Although dogs can be infected, they do not always
voirs and vectors. Leishmania are obligate intracellular pro- serve as a competent reservoir for cutaneous leishmaniasis.
tozoan parasites, with virulence and types of disease varying A human-to-human transmission cycle of cutaneous leish-
between the strains.5 Visceral leishmaniasis is caused by L. maniasis in the Old World due to L. tropica is spread by
donovani, L. infantum, and L. chagasi. In the United States, L. P. sergenti.
mexicana is the cause of cutaneous leishmaniasis in Texas. In Lutzomyia species sand flies spread visceral leishmania-
Latin America, L. braziliensis causes a more aggressive form sis in the New World, whereas L. donovani is spread person
of cutaneous leishmaniasis.6 to person in the Indian subcontinent and Eastern Africa by
a number of sand fly species. Dogs and wild canids (foxes
and jackals) are the principal animal reservoir for visceral
leishmaniasis.5
Leishmaniasis occurs in 88 countries, mainly in the trop-
ics and subtropics, with varying patterns of disease and Mode of Transmission and Life Cycle
ecological relationships (the disease has not been reported
in Australia and Oceania). In the United States, most cases Transmission is largely vector-borne through bites of the
are seen in travelers and their pets returning from endemic female phlebotomine sand fly injecting the infective, flagel-
regions. There is a small focus of cases of cutaneous leishma- lated promastigote forms into the skin of a vertebrate host
niasis in Texas that appears to be extending northward.6 (Figure 9-68). The parasite then transforms into the non-
Cutaneous leishmaniasis due to L. braziliensis and L. flagellated amastigote (Color Plate 9-35) and multiplies
mexicana complexes occurs in Latin American countries within macrophages throughout the host’s reticuloendothe-
with the exception of Chile and Uruguay. In the Eastern lial system. The vector cycle is complete with sand fly infec-
Hemisphere, cutaneous leishmaniasis is caused by L. tropica, tion from the vertebrate host, where the organisms multiply
L. major, and L. aethiopica; hotspots include the Indian sub- extracellularly in the sand fly gut over 8 to 20 days to produce
continent, China, southwestern Asia including Afghanistan infectious promastigotes (see Figure 9-68).5
and Iran, the Mediterranean region, and sub-Saharan Africa Once infected, a mammalian host appears to retain the
including Sudan. ability to be infectious to others even after treatment. The
In the New World, visceral leishmaniasis in humans is agent may remain dormant in the host animal for years, and
due to infection with L. infantum and L. chagasi and is found then infection can recur when immune status declines, such as
across Central and South America. In the Old World, L. don- in HIV infection, malnutrition, or administration of immu-
ovani is the principal cause of visceral leishmaniasis, which nosuppressive drugs for organ transplants or other condi-
occurs in mostly rural areas of India, Bangladesh, China, tions. Chronically infected individuals, even after receiving
Nepal, Pakistan, southern regions of the former Soviet treatment, can serve as a reservoir for further infection of
Union, the Middle East and Mediterranean, and sub-Saha- sand fly vectors. In addition to vector-borne transmission,
ran and East Africa.2 person-to-person transmission has been reported through
In the United States, L. infantum seroprevalence studies of blood transfusions and the sharing of needles between IV
dog kennels have identified positive results in 21 states. drug users.
In an outbreak of canine visceral leishmaniasis among
U.S. foxhounds, transmission occurred dog to dog (but not
Groups at Risk
dog to person) through direct contact with blood and secre-
Groups at increased risk for leishmaniasis include individu- tions and transplacentally from an infected bitch to her pups.
als who encounter the sand fly vector, including forest work- There is no evidence of vector transmission to dogs in the
ers and rural residents. In areas where visceral leishmaniasis United States, and sand flies are not found in many of the
is endemic and the sand fly vector is found, dog ownership regions where dogs are infected.8 However, in areas where
can be a risk factor for infection.7 both visceral leishmaniais in dogs and sand flies occur, there
is a potential risk of future episodes of vector-borne trans-
mission from dogs to humans.
The vectors and reservoir hosts of leishmaniasis are Environmental Risk Factors
diverse and vary in part by geographical region and agent.
Phlebotomine sand flies are most active dusk through dawn Key environmental factors include the population of res-
and difficult to see as they are about one third of the size of ervoir hosts and the population of vectors. Sand fly popu-
a mosquito. lations may increase with availability of breeding sites and
In the Americas, New World cutaneous leishmaniasis has humid areas around ponds or in tree holes. Factors that
zoonotic transmission through bites of a number of sand fly increase contact between humans and vectors and reser-
species; mammalian hosts include small rodents and larger voirs have been tied to outbreaks, including deforestation
mammals. In Texas, the burrowing wood rat (Neotoma and encroachment of human habitation into forested areas.
micropus) is the apparent reservoir for cutaneous leishma- Climate change appears to be playing a role in the extension
niasis. Zoonotic Old World cutaneous leishmaniasis caused of the ranges of some vectors and animal reservoirs.
Figure 9-68 n Life cycle of Leishmania species, the causal agents of leishmaniasis. (From Centers for Disease
Control and Prevention Public Health Image Library, Atlanta, Ga. Courtesy Alexander J. da Silva and Melanie Moser.)
Leishmaniasis recidivans caused by L. tropica occurs in Iran

Disease in Humans
and other parts of central Asia. The tuberculoid lesions tend
Table 9-37 provides clinical presentations of leishmaniasis. to involve the face, spreading outward and often relapsing. It
also tends to be a chronic infection lasting for decades.9
Mucocutaneous leishmaniasis due to L. braziliensis or
Cutaneous Leishmaniasis
related species can develop in individuals years after the
Each year cutaneous leishmaniasis occurs in approximately lesions of cutaneous leishmaniasis have healed. The symp-
1.5 million people worldwide. Cutaneous involvement of toms may begin with nasal stuffiness but progress to respi-
leishmaniasis infection can take a number of forms, depend- ratory and swallowing difficulties as tissue destruction
ing on the species involved and the immune status of the involves the nose, mouth, and laryngopharyngeal regions
host. (Color Plate 9-37).
Simple cutaneous leishmaniasis often begins with a small
macule at the site of the fly bite that progresses to a papule. Visceral Leishmaniasis
The papule enlarges over time and may ulcerate.9 In many
cases, the lesions resolve spontaneously over a period of Visceral leishmaniasis (kala-azar), occurring in about a
months or years (Color Plate 9-36). half million people each year, is usually due to infection
Diffuse cutaneous leishmaniasis tends not to ulcerate but with either L. donovani or L. infantum. This disease is char-
instead spreads gradually through the skin, causing chronic acterized by systemic signs such as fever and weight loss.
nodular lesions especially on the face and extremities. It may Hepatosplenomegaly, pancytopenia, and increased gamma-
be a lifelong infection. globulins can occur. Lymphadenopathy and abnormal liver
Atypical cutaneous leishmaniasis in Central America function test results are common. In India, hyperpigmentation
caused by L. infantum or L. chagasi is characterized by is part of the clinical syndrome. Although many cases resolve
cheloid-type lesions without ulceration.2 spontaneously, malnutrition and immunocompromised
Table 9-37 n Leishmaniasis: Clinical Presentations in Humans and Other Animals
Humans
Simple cutaneous Exposure to sand At least a week, may be Macule progressing to Biopsy of lesion may
leishmaniasis flies, malnutrition, many months2 papule with ulceration demonstrate intracellular
immunosuppression, amastigotes; positive
Diffuse cutaneous proximity to reservoir At least a week,2may be Nodular lesions spreading
leishmaniasis many months slowly on face and leishmanin skin test
habitat
extremities
Leishmaniasis recidivans Develops over months Relapsing lesions on face
to years with central healing
Mucocutaneous Tissue destruction of nose,
leishmaniasis oropharynx
Visceral leishmaniasis Typically 2-6 months, Weight loss, fever, Anemia, leukopenia,
range 10 days to years2 hepatosplenomegaly thrombocytopenia,
elevated liver function
tests, biopsy may show
amastigotes
Dogs Exposure to sand flies, 3 months to years May be subclinical; Proteinuria, elevated liver
crowding, receipt hyperkeratosis, function tests
of blood products chapping, weight loss, Tissue biopsy and culture
from infected donors, anorexia, fever, visceral
parturition (?) involvement including
renal failure
Cats, Horses Exposure to sand flies 3 months to years Skin nodules on head Biopsy may reveal
organisms
condition predispose patients to more severe disease and the occur in up to a third of affected dogs. Epistaxis, muscle atro-
risk of fatal complications. A post–kala-azar cutaneous leish- phy, and seizures can also occur (Color Plate 9-38). The skin
maniasis can occur in recovered individuals. These lesions lesions tend to present as hyperkeratosis and chapping over
can be a reservoir for continued transmission through sand the head, muzzle, and footpads. These lesions can ulcerate.
fly bites. Renal failure is the most common cause of death and is pre-
ceded by nausea and vomiting. Laboratory findings include
hyperproteinemia, proteinuria, and elevated liver function
Disease in Animals
test results.10
Dogs tend to develop systemic, visceral, and cutaneous Infection in cats and horses is less common than in dogs
involvement (Figures 9-69 and 9-70). Weight loss, anorexia and principally involves the skin, typically presenting with
and fever are common. Splenomegaly and lymphadenopathy nodules on the ears (Color Plate 9-39 and Figure 9-71).10
Figure 9-69 n Canine leishmaniasis showing exfoliative dermatitis and Figure 9-70 n Dog with characteristic features of leishmaniasis. Note
scaling on face. (From Greene CE: Infectious diseases of the dog and cat, ed 3, cachexia, muscle atrophy, and excessive scaling. (From Greene CE: Infectious
St Louis, 2006, Saunders Elsevier.) diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier.)
Figure 9-71 n Leishmaniasis. A, Nonhealing ulcer on muzzle. B, Macrophage containing numerous amastig-
otes (Leishman-Donovan bodies). (From Scott DW, Miller WH Jr: Equine dermatology, St Louis, 2003, Saunders
Elsevier. A, Courtesy A. Sales; B, Courtesy T. French.)
Visceral leishmaniasis in endemic areas can be con-

Diagnosis
fused with other causes of fever, chronic weight loss, and
The differential diagnosis of cutaneous leishmaniasis in splenomegaly such as malaria and schistosomiasis. The
humans can be broad and includes sporotrichosis, cutane- diagnosis can be made by isolating amastigotes from mac-
ous tuberculosis or atypical mycobacterial infection, blasto- rophages in a bone marrow biopsy or a splenic biopsy. The
mycosis, sarcoidosis, syphilis, and neoplasia. latter is considered more sensitive but involves a risk of
The presence of suggestive lesions in the setting of a hemorrhage.9
potential contact such as history of travel to an endemic area In animals, a skin biopsy can reveal the presence of
should lead one to consider the diagnosis. Definitive diag- intracellular organisms. Serology with IFA or ELISA is
nosis is often accomplished by a biopsy of the lesion with available but cross-reactions with Trypanosoma cruzi can
tissue identification of amastigotes or culture of promas- occur. Biopsies of skin, spleen, bone marrow, or lymph
tigotes.9 The leishmanin skin test result is often positive nodes can be cultured; smears of these samples may reveal
in simple cutaneous leishmaniasis. PCR techniques are in the organism.10 A PCR test is available at some academic
development.11 institutions.12
Table 9-38 n Treatment of Leishmaniasis Infection in Humans and Other Animals
Humans (Adult)
Cutaneous: New Sodium stibogluconate (Pentostam) (available Amphotericin B 1 mg/kg IV qod × 20 doses or liposomal
World* through CDC) or meglumine antimoniate amphotericin 3 mg/kg/day × 6 days (simple cutaneous)
20 mg/kg IV/IM/day in 2 divided doses or 3 weeks (mucocutaneous) or miltefosine 2.5 mg/kg
× 28 days14 PO qd × 28 days14
Cutaneous: Old Stibogluconate or meglumine 20 mg/kg/day
World* IV × 10 days14
Visceral* Liposomal amphotericin 3 mg/kg/day IV once Stibogluconate or meglumine 20 mg/kg/day IV once daily
daily days 1-5, then day 14 and 2114 × 28 days or miltefosine 2.5 mg/kg PO qd × 28 days14
WHO regimen: 10 mg/kg IV on 2 consecutive
days14
Dogs Sodium stibogluconate (Pentostam) 30-50 mg/ Allopurinol 10 mg/kg PO q8h × 3-24 months (long-
kg IV/SC q24h × 30 days (available through term maintenance), works best when combined with
CDC) amphotericin B 0.25-0.5 mg/kg IV q48h until total
cumulative dose of 5-10 mg/kg
Cats Pinnectomy Meglumine antimoniate 5 mg/kg SC with 10 mg/kg
ketoconazole PO, 4-wk course followed by no therapy for
10 days, repeated three times (used successfully to treat
cutaneous lesions in one cat)15
Horses Observation for lesion resolution, pinnectomy
*Management complex; resistance varies by region; infectious disease consultation recommended.

endemic areas of France: double-blind randomised efficacy field trial.

Treatment Vaccine. 2007;25(21):4223.
5. Desjeux P. Leishmaniasis: current situation and new perspectives. Comp
Treatment in humans may involve an often prolonged course Immunol Microbiol Infect Dis. 2004;27(5):305.
of treatment with a variety of agents. The medical manage- 6. Wright NA, Davis LE, Aftergut KS, et al. Cutaneous leishmaniasis
ment of leishmaniasis is complicated and drug resistance in Texas: a northern spread of endemic areas. J Am Acad Dermatol.
varies by region; therefore infectious disease consultation is 2008;58(4):650.
7. Miró G, Cardoso L, Pennisi MG, et al. Canine leishmaniasis—new con-
advisable. Table 9-38 outlines some currently recommended cepts and insights on an expanding zoonosis: part two. Trends Parasitol.
therapeutic regimens.14 2008;24(8):371.
In dogs, no drug has been consistently curative. Relapses 8. Duprey ZH, Steurer FJ, Rooney JA, et al. Canine visceral leishmaniasis,
and the repeated need for treatment are common, although United States and Canada, 2000–2003. Emerg Infect Dis. 2006;12(3):440.
9. Mandell GE, Bennett JE, Dolin R. Principles and practice of infectious dis-
maintenance therapy can reduce parasitemia and reduce the eases. 6th ed. Philadelphia: Churchill Livingstone; 2000.
likelihood of transmission.10 10. Barr SC, Bowman DD. The 5-minute veterinary consult clinical compan-
ion canine and feline infectious disease and parasitology. Blackwell; 2006.
11. Weigle KA, Labrada LA, Lozano C, et al. PCR-based diagnosis of acute
References and chronic cutaneous leishmaniasis caused by Leishmania (Viannia).
J Clin Microbiol. 2002;40(2):601.
1. World Health Organization. Leishmaniais and HIV coinfection. http:// 12. North Carolina State College of Veterinary Medicine Veterinary
www.who.int/leishmaniasis/burden/hiv_coinfection/burden_hiv_coin- Teaching Hospital. Tick borne diagnostic laboratory. http://www.cvm.
fection/en/index.html. Accessed August 23, 2008. ncsu.edu/vth/ticklab.html. Accessed August 23, 2008.
2. Heymann DL. Control of communicable diseases manual. 19th ed. 13. Sundar S, Jha TK, Thakur CP, et al. Oral miltefosine for Indian visceral
Washington DC: American Public Health Association; 2008. leishmaniasis. Trans R Soc Trop Med Hyg. 2006;100(suppl 1):S26.
3. Schantz PM, Steurer FJ, Duprey ZH, et al. Autochthonous vis- 14. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
ceral leishmaniasis in dogs in North America. J Am Vet Med Assoc. microbial therapy 2009. 39th ed. Antimicrobial Therapy 2009.
2005;226(8):1316. 15. Greene CE. Infectious diseases of the dog and cat. 3rd ed. St Louis:
4. Lemesre JM, Holzmuller P, Gonçalves RB, et al. Long-lasting protection Saunders Elsevier; 2006.
against canine visceral leishmaniasis using the LiESAp-MDP vaccine in
LEPTOSPIROSIS
Peter M. Rabinowitz and Lisa A. Conti • Educate the public on modes of transmissions (e.g., do
not allow animals to drink from contaminated water
Leptospirosis ictohemorrhagica (ICD-10 A27.0), Other forms bodies, maintain good hygiene at kennels and in live-
of leptospirosis (A27.8) stock birthing areas, control rodents).
• Support rodent control efforts in the community.
Other names in humans: Weil’s disease, mud fever, swamp • Educate local veterinary and human health clinicians
fever, rice field fever, swineherd disease in endemic areas about prevention strategies targeted
to groups at risk.
Other names in animals: redwater of calves, moon blindness • Educate occupational health providers regarding risk
(ophthalmia periodica) of horses, Stuttgart disease, canicola groups and how to recognize signs and symptoms of
disease in dogs disease.
• Ensure that workers at risk are using appropriate PPE.
Although leptospirosis is considered a rare disease in the • Disinfect with 1% sodium hypochlorite, 70% ethanol,
United States, it is one of the most prevalent and impor- glutaraldehyde, detergents and acid. The organism is
tant zoonotic diseases worldwide.1 The epidemiology of this killed by pasteurization and moist heat (121° C for 15
emerging infection appears to be changing due to climate and minutes).2
manmade alterations in the environment. Contamination of
water supplies by infected animals is a major source of human Human Health Clinicians
exposure, underscoring the importance of waterborne infec-
tious disease risks. The occurrence of leptospirosis in dogs and • Screen patients for occupational, recreational, hous-
wildlife living near human habitation and the fact that it is ing, and animal (pet and livestock) exposures.
capable of causing both serious disease and outbreaks among • Treat and report cases to health department if report-
groups with high-risk exposure argue for greater awareness of able in state.
this disease among human and animal health professionals. • Counsel patients on measures to reduce risk of trans-
mission to other humans (direct transmission is rare
but possible; e.g., during sexual intercourse and breast-
Key Points for Clinicians and Public Health feeding) and from animals (e.g., hygiene regarding
Professionals urine, reduce rodent exposure).
• Ask patients/family members about any observed ill-
Public Health Professionals ness in pets or other nearby animals; communicate with
veterinary professionals animal cases are suspected.
• Provide descriptive epidemiology of the disease in ani- • Counsel immunocompromised patients about risks
mal and human populations. from animal and environmental contact.
• No human vaccine is available in the United States.

• Exposure prophylaxis: In evaluating an individual who
has been exposed to leptospirosis through occupational
or environmental contact, consider antibiotics for pro-
phylaxis. A systematic review concluded that prophylac-
tic treatment with doxycycline 200 mg PO weekly for
individuals at high risk of exposure (such as individuals
training in jungle conditions during the rainy season)
was superior to placebo in preventing cases of infection.
(evidence-based recommendation: strength B).3
• Segregate and treat infected animals.
• Vaccinate at-risk dogs and cattle and pigs. Vaccination
does not protect against the carrier state. Annual vac- Figure 9-72 n Scanning electron micrograph of Leptospira interrogans
showing helical structure and curved (hooked) ends (original magnifica-
cination in closed herds, semiannual vaccination in tion ×60,000). (From Mandell GL, Bennett JE, Dolin R (eds): Principles
open herds.4 and practice of infectious diseases, ed 6, Philadelphia, 2005, Churchill
• Counsel owners and veterinary staff about ways to Livingstone Elsevier. Courtesy of Rob Weyant, Centers for Disease Control
reduce zoonotic risks (precautions with animal urine and Prevention, Atlanta, Ga.)
and other body fluids) and symptoms of disease in
humans, advise them to contact medical providers if
suspect human cases.
• If veterinary staff experiences occupational exposure
to infected animal, consult occupational or infectious Groups at Risk
disease provider regarding follow-up and possible Leptospirosis is an important occupational disease risk for
antibiotic prophylaxis. farmers, dairy and abattoir (slaughterhouse) workers, butch-
• If treating an infected pet, counsel family members ers, hunters, dog handlers, veterinarians, and other veteri-
regarding zoonotic risk and to contact their health nary health providers who have direct contact with animals.
care provider for further advice. Consider directly Workers with exposure to contaminated water, such as
contacting the medical care provider, especially when military personnel, rice farmers, fishing industry workers,
immunocompromised patients are in the household plumbers, and sewer workers, are also at risk.
or otherwise in contact with an animal case. Recreational exposure to contaminated water leads to
• Report animal cases to appropriate animal health infection in campers, sportsmen, freshwater bathers, and
authority if indicated in state. travelers returning from highly endemic countries. Urban
slum dwellers with rodent exposure are another risk group
Agent and infection has been reported in children who handled
infected puppies.5 In the United States, recent reported cases
Leptospirosis is caused by gram-negative spirochete bacteria have occurred among cleanup workers at a Hawaiian univer-
in the genus Leptospira. Based on molecular analysis, there sity campus where a stream had flooded,8 a returning traveler
are believed to be at least 13 different species of Leptospira who had explored caves in Malaysia,9 an inner-city hospital
and more than 250 serovars.5 These species and serovars patient who had recently swum in a creek,10 and triathletes
vary widely in pathogenicity. Leptospires can be cultured in and community dwellers who had swum in and ingested
polysorbate-albumin media (Figure 9-72).5 water from a contaminated lake.11
HIV-infected and other immunocompromised patients
Geographical Occurrence are at risk of severe disease.12
Leptospirosis is considered an emerging infectious disease
and one of the most common global zoonoses1; it is found Hosts, Reservoir Species, Vectors
worldwide except in the polar regions. It is highly prevalent
in tropical countries with areas of high rainfall and alka- Hosts who exhibit clinical infection with leptospirosis
line soils.6 The CDC has removed leptospirosis from the include humans, dogs (where the incidence is reported to be
list of nationally reportable diseases, and estimates that 1 to increasing),13 horses, cattle,14 sheep, and swine. Leptospira
200 cases are identified yearly in the United States (50% species appear to exist subclinically in a large number of
of cases occur in Hawaii).7 However, recent outbreaks and wildlife species, including rats and other rodents, rac-
sporadic cases in the United States suggest that leptospiro- coons, opossums, reptiles, and frogs. However, in some
sis remains underdiagnosed and underreported in animals wildlife species, such as sea lions, periodic epidemics of
and humans, and that many U.S. health care providers are clinical disease can occur.15 In the northeastern United
unfamiliar with the epidemiology and clinical presentation States and Canada increasing rates of infection among res-
of this disease, which is capable of causing severe morbidity ervoir hosts, such as skunks, raccoons, and squirrels, that
and (rarely) death. are common in suburban settings has been reported.16
soils and alkaline freshwater, rodent infestation, and sub-

urban encroachment on wildlife habitat. A case control
Leptospira enter the body through breaks in the skin or con- study of dogs found that seropositive dogs were more likely
tact with mucous membranes (Figure 9-73). Humans are to live in periurban environments.18 Inner-city house-
commonly infected by exposure to water, moist soil, or food holds with cats have been associated with a decreased risk
contaminated by urine or secretions, or by direct contact of leptospirosis, possibly through a reduction in rodent
with infected animals. Venereal transmission occurs in swine exposure.19
and has been suspected in humans.17 Eating infected rodents
or other animals can result in infection through mucous
membrane contact. Direct person-to-person transmission Disease in Humans
has been reported between soldiers working in close proxim-
ity in swampy areas, and in relation to breastfeeding.6 Leptospirosis in humans has protean manifestations,
depending in part on the infecting serovar. Infection leads
to a systemic vasculitis. The majority of human infections
Environmental Risk Factors are mild and self-limited; however, in approximately 10% of
Outbreaks in humans and animals have been linked to cases, severe and even fatal illness can develop. The two main
heavy rains resulting in flooding, moist soils, and stand- severe forms of the disease are Weil’s disease (a triad of jaun-
ing water. Other environmental risk factors include alkaline dice, acute renal failure, and bleeding) and severe pulmonary
hemorrhagic syndrome (SPHS) (Table 9-39).
After the bacteria enter the body, there is an incubation
period of approximately 10 days, followed by the abrupt
onset of the leptospiremic phase or febrile phase, which can
last 4 to 9 days. In addition to fever, conjunctival suffusion,
Infected Predation, direct contact
animal or uveitis, myalgias, and a pretibial rash can be seen. A conva-
with urine or other secretions Susceptible
human lescent (leptospiruric or immune) phase follows. During this
being with host period, which often lasts several weeks or longer, secondary
leptospiruria transmission may occur through excretion of the leptospires
in urine. Aseptic meningitis is a common occurrence during
Exposed skin, mucous this phase of illness.5 Figure 9-74 shows the biphasic nature
membranes, cuts of the illness.
Water, soil, food Weil’s disease may develop during the immune phase
contaminated or progress directly from the acute phase of infection.
by infected urine
Prominent features include renal failure caused by nephri-
tis, hepatic dysfunction, and thrombocytopenia with hemor-
rhagic complications.
In some cases, hemorrhagic pneumonitis and severe
Environmental factors: respiratory distress leading to circulatory collapse can occur
Heavy rainfall, flooding
without hepatic or renal failure. Mortality is high in severe
Figure 9-73 n Life cycle of leptospirosis. cases of Weil’s disease and SPHS (Color Plate 9-40).
Table 9-39 n Leptospirosis: Comparative Clinical Presentations in Humans and Other Animals
Humans Exposure to fresh water, 10 days (2-30)22 Acute onset of uveitis, conjunctival Leukocytosis, liver,
flooding, contact with suffusion, myalgias, fever, renal renal function test
animals failure, jaundice abnormalities
Dogs Rural/suburban exposure 4-12 days4 Acute renal failure, fever, depression, Leukocytosis, renal
to wildlife, peridomestic lethargy, uveitis and liver function
rodents, contaminated test abnormalities,
water proteinuria, hematuria
Sheep Rare, exposure to infected Lambs with more severe disease,
animals of other species fever, anorexia
Horses Exposure to contaminated 2-8 months for Most asymptomatic6
urine, water, soil chronic symptoms Uveitis (moon blindness), abortions
Cattle Calves: fever anorexia, dyspnea,4
Adults: abortion, stillbirth,
hemoglobinuria
Pigs Abortions, stillbirth
Approximate time scale: Week 1 Week 2 Week 3 Week 4 Months-years Years

Incubation period Acute Convalescent
stage stage
Uveitis
2–20 days ? interstitial nephritis
Inoculation
Fever
Leptospires present in:
Blood
CSF Reservoir host
Urine Convalescent shedder
Antibody titers
Normal response
High
Low Titers decline at

Early treatment varying rates
Delayed
“Negative” Anamnestic
Laboratory investigations
Blood
Culture CSF
Urine
Serology 1 2 3 4 5
Phases Leptospiremia
Leptospiruria and immunity
Figure 9-74 n Biphasic nature of leptospirosis. The serology numbers refer to specimens taken at different
phases of illness to either diagnose acute illness or document chronic or past infection. (From Mandell GL, Bennett
JE, Dolin R (eds): Principles and practice of infectious diseases, ed 6, Philadelphia, 2005, Churchill Livingstone
Elsevier. Adapted from Turner LH: Leptospirosis, Br Med J 1:231, and reproduced from Levett PN: Leptospirosis,
Clin Microbiol Rev 14:296, 2001, with permission of ASM Press.)
illness. Most laboratory diagnosis of human leptospirosis is

Disease in Animals
currently based on serology using the microagglutination test
Although many cases of leptospirosis in dogs are subclini- (MAT) or ELISAs. Antibodies develop after about 1 week of
cal and chronic, dogs can develop acute disease with fever, illness. The MAT has a high specificity for specific serovars.
anorexia, jaundice, vomiting, and hematuria. Other fea- However, it may lead to underdiagnosis if a person is infected
tures of infection can include injected mucous membranes, with an unusual serovar not well covered by the standard test.
uveitis, and cough.20 The most common serious complica- Serial serology titers are required to document seroconver-
tions in dogs appear to be acute renal failure, vasculitis, and sion—a fourfold increase in titer is considered evidence of
hepatic dysfunction.21 The disease is much rarer in cats, but recent infection.6 The use of PCR techniques for diagnosing
similar clinical features to dog leptospirosis may be seen.20 human leptospirosis has been reported.23
Cattle and other livestock including sheep, pigs, and In animals, the MAT and ELISA are also used; paired sera
horses can develop either acute or chronic forms of infec- are preferred. Diagnosis can be affected by a history of immu-
tion. The acute form is more common in young animals and nization, and the results of serology must be interpreted with
can include fever or respiratory involvement. Adult livestock caution in vaccinated animals. A milk ELISA can be used on
are more likely to develop the chronic form of the disease a single cow or for bulk tank sampling.
and manifest infection as abortion or stillbirth.
The disease is often subclinical in wild animals including
Exposure Prophylaxis
rodents. Seals and sea lions may have depression, fever, and
abortion. A study of antibiotic prophylaxis for soldiers during jungle
military training showed a protective benefit of doxycycline, 200
Diagnosis mg/week, in preventing infection with leptospirosis.24 Therefore
individuals with high-risk exposures for short periods can con-
The differential diagnosis in humans includes acute causes of sider such prophylaxis. However, the efficacy of prophylaxis in
fever and jaundice such as hepatitis and malaria. Leptospirosis other situations, such as after exposure, remains unclear.
should be suspected in a patient who presents with exposure
risk factors and fever, uveitis/conjunctival suffusion, and
Treatment
abnormal liver and renal function test results. Leptospires can
be cultured from blood and cerebrospinal fluid (CSF) during Antibiotic treatment in people and animals is not always
the acute phase of illness and in urine after the first week of curative but should be started as early in the course of disease
8. Gaynor K, Katz AR, Park SY, et al. Leptospirosis on Oahu: an outbreak

Table 9-40 n Leptospirosis Treatment in Humans associated with flooding of a university campus. Am J Trop Med Hyg.
and Other Animals 2007;76(5):882.
9. Mortimer RB. Leptospirosis in a caver returned from Sarawak, Malaysia.
Species Primary Treatment Alternative Wilderness Environ Med. 2005;16(3):129.
10. Shaukat A, Pohlel K, Rubin Z, et al. Case of Weil’s disease in an inner-
city hospital in the USA. J Gastroenterol Hepatol. 2004;19(10):1221.
Humans Penicillin G 1.5 million Doxycycline 100 mg 11. Morgan J, Bornstein SL, Karpati AM, et al. Leptospirosis Working
units IV q6h or IV/PO q12h or Group, Outbreak of leptospirosis among triathlon participants and
ceftriaxone 1 gm ampicillin 0.5-1 gm community residents in Springfield, Illinois, 1998. Clin Infect Dis.
q24h × 7 days IV q6h27 2002;34(12):1593.
Dogs Doxycycline 5 mg/ Penicillin G 25,000- 12. Jones S, Kim T. Fulminant leptospirosis in a patient with human immu-
kg q12h PO/IV × 14 40,000 units/ nodeficiency virus infection: case report and review of the literature.
days kg q12h IM/SC/ Clin Infect Dis. 2001;33(5):e31.
IV × 14 days or 13. Ward MP, Glickman LT, Guptill LE. Prevalence of and risk factors for
ampicillin 22 leptospirosis among dogs in the United States and Canada: 677 cases
mg/kg PO/IV/SC (1970–1998). J Am Vet Med Assoc. 2002;220(1):53.
q6-8h × 14 days 14. Talpada MD, Garvey N, Sprowls R, et al. Prevalence of leptospiral infec-
or amoxicillin tion in Texas cattle: implications for transmission to humans. Vector
22 mg/kg q8-12h Borne Zoonotic Dis. 2003;3(3):141.
PO × 14 days20 15. Lloyd-Smith JO, Greig DJ, Hietala S, et al. Cyclical changes in seroprev-
alence of leptospirosis in California sea lions: endemic and epidemic
Swine Tetracycline 800 gm/ton disease in one host species. BMC Infect Dis. 2007;7:125.
of feed × 8-11 days26 16. Barry M, Wisnewski AV, Matthias MA, et al. Suburban leptospirosis:
Cattle Tetracycline 40 mg/kg Amoxicillin 15 mg/kg atypical lymphocytosis and gamma-delta T cell response. Clin Infect Dis.
IM qd × 3-5 days, 1 or 2 (q48h) 2006;43(10):1304.
oxytetracycline4,26 doses26 17. Harrison NA, Fitzgerald WR. Leptospirosis—can it be a sexually trans-
mitted disease? Postgrad Med J. 1988;64(748):163.
18. Ward MP, Guptill LF, Wu CC. Evaluation of environmental risk fac-
tors for leptospirosis in dogs: 36 cases (1997–2002). J Am Vet Med Assoc.
as possible because of a possible benefit (Table 9-40). 2004;225(1):72.
19. Childs JE, Schwartz BS, Ksiazek TG, et al. Risk factors associated with
Recommended agents include penicillin G, doxycycline, cef- antibodies to leptospires in inner-city residents of Baltimore: a protec-
triaxone, and amoxicillin. The serovar may affect the efficacy tive role for cats. Am J Public Health. 1992;82(4):597.
of the selected antibiotic. Supportive care may be indicated, 20. Barr SC, Bowman DD. 5-Minute veterinary consult clinical companion
and hemodialysis is correlated with improved prognosis in canine and feline infectious disease and parasitology. Ames, IA: Wiley-
severe acute renal failure cases.25 Blackwell; 2006.
21. Langston CE, Heuter KJ. Leptospirosis: a re-emerging zoonotic disease.
Vet Clin North Am Small Anim Pract. 2003;33(4):791.
References 22. Heymann DL. Control of communicable diseases manual. 19th ed.
1. Bharti AR, Nally JE, Ricaldi JN, et al. Peru-United States Leptospirosis 23. Roczek A, Forster C, Raschel H, et al. Severe course of rat bite-
Consortium. Leptospirosis: a zoonotic disease of global importance. associated Weil’s disease in a patient diagnosed with a new Leptospira-
Lancet Infect Dis. 2003;3(12):757. specific real-time quantitative LUX-PCR. J Med Microbiol. 2008;
2. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases 57(Pt 5):658.
of companion animals. Ames, IA: The Center for Food Security and Public 24. Sehgal SC, Sugunan AP, Murhekar MV, et al. Randomized controlled
Health, Iowa State University College of Veterinary Medicine; 2008. trial of doxycycline prophylaxis against leptospirosis in an endemic area.
3. Guidugli F, Castro AA, Atallah AN. Antibiotics for preventing lep- Int J Antimicrob Agents. 2000;13(4):249.
tospirosis. Cochrane Database Syst Rev. 2000;4. 25. Adin CA, Cowgill LD. Treatment and outcome of dogs with leptospiro-
4. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed.Whitehouse sis: 36 cases. http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve
Station, NJ: Merck; 2005. &db=PubMed&list_uids=10668536&dopt=AbstractPlus). Accessed
5. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious February 18, 2008.
diseases. 6th ed. Philadelphia: Churchill Livingstone Elsevier; 2005. 26. Giguere S. Antimicrobial therapy in veterinary medicine. http://books.google.
6. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man com/books?id=lxmyfSave4IC&pg=PA388&lpg=PA388&dq=leptospirosis+
and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington, DC: treatment+veterinary&source=web&ots=ekP7_-1Ete&sig=uzSH8exIoc9dU
Pan American Health Organization; 2001. AJCAkYTHe2t-2I. Accessed February 18, 2008.
7. Centers for Disease Control and Prevention. Disease listing, leptospirosis, 27. Gilbert DN, Moellering RC, Ellopoulos GM, et al. Sanford guide to
technical information. http://www.cdc.gov/Ncidod/dbmd/diseaseinfo/ antimicrobial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial
leptospirosis_t.htm. Accessed December 5, 2007. Therapy; 2009.
LYME DISEASE
Peter M. Rabinowitz and Lisa A. Conti Lyme disease is caused by a bacterial spirochete, Borrelia
burgdorferi, and is the most commonly reported arthropod-
Lyme Disease (ICD-10 A69.2) borne human infection in the United States.1 Lyme disease
presents opportunity for collaboration between human and
Other names in humans: Lyme borreliosis animal health practitioners. The increased environmental
exposure of dogs to ticks, as well as the availability of routine
Other names in animals: Lyme borreliosis, Lyme arthritis in-house screening tests, has provided critical evidence of
the geographical incidence and prevalence of the infection in • Counsel patients to avoid tick exposure and use appro-
dogs that serves as a sentinel for human Lyme disease infec- priate tick repellents.
tion risk.2 Although ticks are considered the principal vector • Inquire about occupational risk factors for infection,
for transmission of Borrelia species to humans and animals, and ensure that workers at risk are taking precautions.
there have been occasional published reports of the potential • Understand that Lyme disease screening tests may pro-
for transmission through blood, milk, placenta, or urine, but vide false-positive or false-negative results and may
none of these alternative transmission routs has been con- require a confirmatory analysis at a reference labora-
firmed by unambiguous culture results.3 In addition to dogs, tory such as the CDC.
Lyme disease has been reported in cats, horses, cattle, and • Become aware of Lyme disease prevalence through dis-
goats. Tick avoidance and tick control are important preven- cussions with public health authorities.
tion measures for both humans and domestic animals. The • Ask patients about pet ownership generally. For those
risk of Lyme disease to humans and other animals is related with pets who live in Lyme endemic areas or who may
to landscape change and human advancement on the habitat visit endemic areas, ask if they have discussed Lyme
of local deer and rodent populations that maintain the vec- disease risk with their veterinarian.
tor tick Ixodes scapularis (formerly known as I. dammini). • Judiciously use antibiotics; antibiotics may not be indi-
Therefore development of recommendations that focus on cated as a prophylaxis for (nonengorged) tick bite alone.
environmental factors associated with Lyme disease could • No vaccine for Lyme disease is currently commercially
decrease infection risk and benefit both humans and com- available for humans.
panion animals.
Professionals • Educate clients and hospital team members about how
to appropriately remove ticks. Have pet owners remove
Public Health Professionals ticks as soon as possible, ideally before attachment.
Conduct daily tick checks on dogs, preferably when
• Provide descriptive epidemiologic analysis of this coming in from outdoors, with particular attention to
reportable disease and assessment of local Lyme dis- the head, ears, and warm fold areas (e.g., between toes,
ease risk for the health district. groin). Frequent brushing removes unattached ticks
• Educate the public to: from pets that may be transferred to humans.
 Avoid tick-infested areas, but if not possible, wear • In endemic areas, consider screening dogs with a Lyme
appropriate clothing (long sleeves, long pants, tuck C6 antibody test to diagnose subclinical dogs. Among
pants legs into socks, and light-colored clothing to infected dogs, 90% to 95% may be subclinical or have
visualize ticks). Wash clothes with hot water.4 vague clinical signs that go unnoticed by owners.3,6
 Use CDC-recommended tick repellents such as • Educate clients to treat dogs and cats preventatively
DEET, picaridin, or alternatives on clothes or bare with topical tick control.
skin following label instructions. • Consider vaccinating dogs that are at risk and in
 Do frequent tick checks to remove even tiny imma- endemic areas annually against Lyme disease with an
ture-stage ticks (“seed” ticks). Inspect children at OspA Lyme vaccine (controversial).3,6
least once daily for ticks. When in heavily infested
areas inspect children every 3 to 4 hours.
 Use appropriate technique to remove ticks. Wear Agent
gloves or grasp tick with tweezers as close to the Lyme disease is caused by a number of species of gram-nega-
skin as possible and pull gently (do not use a match, tive, spirochete bacteria belonging to the genus Borrelia (Figure
petroleum products, or nail polish). Follow up by 9-75). Borrelia species that cause Lyme disease are grouped
cleaning the area, applying antibiotic topical on tick under the name Borrelia burgdorferi sensu lato. In the United
bite site, and washing hands.5 States, the predominant genotype associated with Lyme dis-
 Implement integrated pest management techniques ease is Borrelia burgdorferi sensu stricto. This genotype also
including landscape management (see Box 9-3). causes Lyme disease in Eurasia, as do B. afzelii, B. garinii, and
Counsel pet owners to discuss Lyme disease preven- B. japonica (Japan). Among these genotypes, there is consid-
tion strategies with their veterinarian. erable genetic diversity.7 Borrelia are slow-growing bacteria
• Work with local agencies to control deer and rodent (Figure 9-76) that require special culture medium and gen-
populations. erally are difficult to culture from blood and tissue biopsies.8
• Work with local planning agencies on smart growth to The organisms are sensitive to heat and ultraviolet light and
avoid fractionating forested areas. do not survive long outside the body. Effective disinfectants
include 1% sodium hypochlorite and 70% ethanol.9

• Report Lyme disease cases to public health authori-
ties using the case definition; see http://www.cdc.gov/ Initially recognized in the Northeastern United States,
ncphi/disss/nndss/casedef/lyme_disease_2008.htm. specifically in Lyme, Connecticut, in 1975, Lyme disease
2 m
A B
Figure 9-75 n A, Transmission electron micrograph of B. burgdorferi showing periplasmic flagella that have
been released from the confines of the outer membrane secondary to specimen preparation (phosphotungstic acid,
×7100). B, Scanning microscopic view of B. burgdorferi (×15,000). (From Greene CE: Infectious diseases of the dog
and cat, ed 3, St Louis, 2006, Saunders Elsevier. Courtesy R. Straubinger, University of Leipzig, Leipzig, Germany.)
A B
Figure 9-76 n A, Transmission electron microscopic (×12,000) and B, scanning electron microscopic (×12,000)
appearance of cystic form of B. burgdorferi, a defense mechanism of organism for survival under adverse conditions
such as antimicrobial therapy or host immune defenses. (From Greene CE: Infectious diseases of the dog and cat,
ed 3, St Louis, 2006, Saunders Elsevier. Courtesy R. Straubinger, University of Leipzig.)
has now been reported in almost every state and in 1984.11,12 Geographical foci of higher infection risk are
Canada, although the tick vectors have a more restricted found along the East Coast, Wisconsin, Minnesota, and
distribution. The distribution of Lyme disease in the parts of California and Oregon (Figure 9-77), particu-
United States is concentrated, with 12 states accounting larly in peridomestic areas. Areas of endemic Lyme dis-
for about 95% of reported human cases.10 Clinical ill- ease activity have been reported in Europe, Russia, China,
ness from B. burgdorferi was first documented in dogs in and Japan.8
Reported cases of Lyme Disease – United States, 2007
Figure 9-78 n The black-legged tick Ixodes scapularis (formerly I. dam-

One dot placed randomly within county mini), one of the vectors for transmitting Lyme disease. This tick is very
of residence for each reported case small and can easily go unnoticed when fixed to the skin in an unengorged
state. (From Habif TP: Clinical dermatology: a color guide to diagnosis and
Figure 9-77 n Distribution of Lyme disease cases in the United States therapy, ed 4, St Louis, 2004, Mosby Elsevier.)
(2007). (From Centers for Disease Control and Prevention: Lyme disease statis-
tics. http://www.cdc.gov/ncidod/dvbid/lyme/ld_Incidence.htm.)
maintain adult tick populations by serving as hosts for the
adult ticks. Birds may introduce I. scapularis into previously
Groups at Risk nonendemic areas.13 Adult male ticks tend to remain on deer,
whereas adult females will engorge after mating to drop off
The risk of Lyme disease varies among regions and is gener- and lay about 2000 eggs in the spring.
ally correlated to the abundance of host ticks that can carry Humans and domestic animals are accidental hosts for
the disease agent. Individuals at most risk for infection are B. burgdorferi. Dogs have an increased risk of Lyme disease
those living in endemic areas of high vector tick density, with exposure in endemic areas relative to humans, and this risk
a large proportion of the ticks infected, and that are engaged can be highly focal with seroprevalence rates as high as 50%
in activities with increased time and exposure to vector to 90% in endemic areas, providing sentinel information
ticks.13 Behavioral factors including frequent outdoor activi- for humans.10 Cats appear to have significant exposure risks
ties such as hunting, camping, and hiking most likely play an as well; a seroprevalence study in Connecticut found more
important role in disease susceptibility.14 Higher numbers of than 45% of cats showed evidence of infection with B. burg-
cases have been reported in children aged 5 to 14 years and dorferi, as well as a significant amount of coinfection with
adults aged 35 to 60.15 Anaplasma phagocytophilum; yet most cats did not show
clinical signs.17
Principal tick vectors include the black-legged (or deer tick)
Ixodes scapularis (formerly I. dammini) in the Northeastern The life cycle of B. burgdorferi is related to the 2-year life
and upper Midwestern United States (Figures 9-78 and 9-79), cycle of the hard Ixodes tick vector. Ixodes ticks pass through
and I. pacificus (western black-legged tick) in the Western larval, nymphal, and adult forms (Figure 9-81). To mature
United States, as well as I. ricinus (Europe) and I. persulcatus from one form to another, they must consume a blood meal.
(Asia).13 Often, a tick carrying the B. burgdorferi spirochete Eggs are laid in the spring and the larvae hatch in the sum-
is also coinfected with other pathogens including Anaplasma mer. As they feed on the blood of vertebrates, the larvae can
and Babesia. Ixodid ticks attach quickly and feed to repletion become infected with B. burgdorferi. After feeding, the larvae
without changing hosts. become less active and mature into nymphs by the following
Wild rodents, including the white-footed mouse spring.18 The majority of human cases occur in the spring
(Peromyscus leucopus) in the Eastern seaboard (Figure 9-80), and summer as a result of bites by nymphs that are active and
and the dusky-footed wood rat (Neotoma fuscipes) and kan- seeking a blood meal to allow them to develop into adults.8
garoo rats (Dipodomys californicus) in the West, serve as Once they have fed, the nymphs develop into adults. The
disease reservoirs for Lyme disease, remaining persistently adult female lays eggs the following spring to continue the
infected and capable of infecting naïve ticks. In the West, cycle. With every feeding, it is possible for a tick to become
the life cycle is more complex; the spirochete is maintained reinfected with B. burgdorferi and also coinfected with other
in an independent enzootic cycle involving I. spinipalpis as pathogens such as Babesia and Anaplasma.
the arthropod vector.13 Lizards may function as reservoirs in When an infected nymphal or adult tick initially bites an
some parts of the United States or be a “dilution host,” reduc- animal, it appears that it must remain attached and feed for
ing the vector infection prevalence in other areas.16 about 24 hours for upregulation of spirochete outer surface
In the United States, the white-tailed deer (Odocoileus protein C (OSP C) and transmission of organisms to take
virginianus) is the preferred host for I. scapularis and helps place. Peak transmission occurs after about 48 hours.3,19
1 inch
Blacklegged Tick (Ixodes scapularis)
Adult Adult
female male Nymph Larva
Lone Star Tick (Amblyomma americanum)
Dog Tick (Dermacentor variabilis)
Figure 9-79 n Relative sizes of these tick species. Only the black-legged ticks are known to transmit Lyme dis-
ease. (From Centers for Disease Control and Prevention: Lyme disease transmission. http://www.cdc.gov/ncidod/
dvbid/lyme/ld_transmission.htm.)

The relation of environmental factors to the risk of Lyme
disease is complex but it appears that landscape modification
in the United States related to suburbanization of the human
population is playing a significant role. As suburban devel-
opments and other human built environments encroach into
land that was previously forest habitat, they produce “frag-
mentation” of forests (Figure 9-82). This breaking up of for-
ested area into patches interspersed with human residential
development has caused an increase in deer populations by
providing ideal vegetative habitat (including ornamental
shrubs for deer to eat) and reduced pressure of being hunted
and predators. It also appears to favor increases in popu-
lations of peridomestic Peromyscus, which are important
Figure 9-80 n White-footed mouse, Peromyscus leucopus, a wild hosts for Ixodes ticks and for B. burgdorferi. Such forest frag-
rodent reservoir host of ticks, which are known to carry the bacteria mentation has been shown to be related to tick abundance
Borrelia burgdorferi, responsible for Lyme disease. During their larval and infection rates.20 However, individual human behavior
stage, Ixodidae, or “hard ticks,” feed on small mammals, particularly the
white-footed mouse, which serves as the primary reservoir for B. burg-
appears to play an important role in determining human
dorferi. (From Centers for Disease Control and Prevention Public Health risk, including time spent outdoors and use of protective
Image Library, Atlanta, Ga.) repellents and clothing.
Figure 9-81 n Life cycle, Lyme disease. (Modified from Centers for Disease Control and Prevention: Lyme dis-
ease transmission. http://www.cdc.gov/ncidod/dvbid/lyme/ld_transmission.htm.)
Another environmental factor is climate and climate change. examined whether environmental modifications can reduce
Warmer winters may result in increased tick abundance dur- such risk. Area-wide acaricide use reduces tick populations,
ing the following spring and summer.21 Because the environ- but many communities are reluctant to use wide-scale pesti-
ment appears to play a role in Lyme disease risk, studies have cides. However, targeting small areas of high human exposure,
Figure 9-82 n Suburban development and other human built environments encroach into land that was pre-
viously forest habitat. (From Centers for Disease Control and Prevention: Learn about Lyme disease. http://www.
cdc.gov/ncidod/dvbid/lyme/index.htm.
such as residential yards, has been highly effective in reduc-

ing nymphal tick density.22 Treating host animals with acari-
cides, such as the “four poster” method of treating deer with
acaricide at feeding stations, has reduced tick populations,
but the distribution of bait designed to reduce tick feeding on
rodents is less effective. By eliminating the deer population,
the maintenance host of ticks, the risk of Lyme disease has
been nearly eliminated in an island setting.23,24 Integrated pest
management can be effective to aid in tick control, including
landscape modification around dwellings (see “Key Points for
Clinicians and Public Health Professionals”).
Disease in Humans
In many of the reported cases, the disease begins with early
localized infection, consisting of fever and a characteristic Figure 9-83 n Inflammation involving knee joint in Lyme disease. (From
skin rash (erythema migrans [EM]) that often starts with a Yanoff M, Duker JS: Ophthalmology, ed 3, St Louis, 2004, Mosby Elsevier.
Adapted with permission of the American Academy of Ophthalmology:
red macule or papule at the site of the tick bite that expands Basic and clinical science course, San Francisco, American Academy of
into a circular rash. The rash may develop central clearing, Ophthalmology, 1998-1999.)
producing a bull’s-eye appearance (Color Plate 9-41). The
bacterium is sometimes cultured from the leading edge of
the rash. Accompanying symptoms may include fatigue,
fever, headache, anorexia, arthralgias, myalgias, and lymph-
adenopathy. Southern tick-associated rash illness (STARI),
a differential in the early diagnosis of Lyme disease, mani-
fests with a similar EM rash (Color Plate 9-42), mild clinical
signs, and absence of antibodies to B. burgdorferi. STARI may
be associated with B. lonestari rather than B. burgdorferi and
transmitted by the lone star tick, A. americanum (see http://
www.cdc.gov/ncidod/dvbid/stari/index.htm).
Days to weeks after the onset of the rash, early disseminated
infection may develop, with more severe systemic symptoms.
Multiple EM lesions may appear during this phase, as well
as borrelial lymphocytomas—blue-red nodules on the ear-
lobes or nipples. Early disseminated infection can involve the
nervous system with the development of chronic symptoms
including seventh nerve (Bell’s) palsy or facial paralysis, men-
ingitis, motor or sensory peripheral neuropathy, and encephal-
opathy. Cardiac involvement may occur with atrioventricular
block. If infection remains untreated, late-stage disease can
develop months to years after initial infection, with arthritis
of the knees or other weight-bearing joints (Figure 9-83). In
late-stage disease, the skin can develop acrodermatitis chronica
atrophicans, erythematous plaques and nodules on the extrem-
ities. Other complications include encephalopathy and keratitis
(Figure 9-84).25 Previous infection does not confer immunity.
Disease in Animals Figure 9-84 n T2-weighted magnetic resonance imaging scan in a patient
with Lyme disease reveals areas of increased signal intensity in the cerebral
Most dogs do not manifest clinical signs after exposure to white matter. (From Mandell GL, Bennett JE, Dolin R: Principles and practice
of infectious diseases, ed 6, New York, 2005, Churchill Livingstone Elsevier.)
B. burgdorferi or have vague signs that go unnoticed by the
owner. Dogs have not been reported to have the bull’s-eye rash.
Approximately 5% of seropositive dogs develop clinical Lyme be related in part to immune complex deposition, can prog-
disease.6,26 Clinical signs may not appear for 2 to 6 months ress to a fatal acute oliguric or anuric renal failure.6,26 Some
after infection and may include lameness, fever, anorexia, have questioned whether the nephropathy could be related to
myalgia, lethargy, lymphadenopathy, cardiac arrhythmias coinfections with other agents. Coinfection with other tick-
(rarely), neurological signs, and ocular manifestations (Color borne diseases is common, either transmitted by the same
Plates 9-43 and 9-44).3,6 Dogs have also been reported with tick vector (A. phagocytophilum, Babesia microti, or Bartonella
Lyme arthropathy, a recurrent arthritis with lameness par- species) or other tick vectors (Ehrlichia species and Rickettsia
ticularly in the tarsal and carpal joints (Figure 9-85). Lyme rickettsii).3,6 Previous infection with B. burgdorferi does not
nephropathy, a chronic protein-losing nephropathy that may appear to confer immunity.
Diagnosis
In humans who present with a classic EM rash (described as
5 cm or greater to differentiate it from a hypersensitivity reac-
tion) and a history of a tick bite or tick exposure in a Lyme-
endemic area, serological confirmation may not be necessary.
However, a search should be performed for possible coinfec-
tion with agents such as Anaplasma and Babesia. When the
rash is not present but Lyme disease is suspected and pre-
test probability is 20% or greater, serological testing using a
two-step method is recommended. This consists of a screen-
ing ELISA test followed by a confirmatory Western blot if the
ELISA is indeterminate or positive. If less than 4 weeks has
elapsed since the onset of infection, both IgG and IgM should
be tested; if more than 4 weeks have elapsed, only IgG should
Figure 9-85 n Experimentally induced borrelial arthritis in the thoracic be tested. The two-step method is considered to have high
limb of beagle dog. Fever and shifting leg lameness develop 60 to 90 days
after inoculation. Lameness occurs earliest and is most severe in the limb specificity and a low risk of false-positive diagnosis.31,32
closest to the inoculation site. (From Greene CE: Infectious diseases of the In animals, a rapid antibody test has been developed to
dog and cat, ed 3, St Louis, 2006, Saunders Elsevier. Courtesy R. Straubinger, detect antibodies against the C6 B. burgdorferi protein and
University of Leipzig.) correlates well with the Western blot immunoassay.33 This
test detects only antibodies against antigen acquired through
natural exposures, and therefore will not yield positive
Cats appear to be largely asymptomatic but can rarely results in vaccinated animals.6 In dogs, testing validates expo-
develop arthritis.27 sure to the B. burgdorferi organism but not clinical illness.
Serosurveys using ELISA antibody screening have Supporting evidence for a diagnosis of Lyme disease is based
reported seroprevalence rates in horses greater than 80% on history of exposure to B. burgdorferi through exposure
in endemic areas.28 Although a wide range of clinical con- to Ixodes ticks in an endemic area, clinical signs, positive C6
ditions have been associated with Lyme infection in horses, peptide and/or Western blot antibody test results, ruling out
clinical infection is considered to be extremely rare and other differential diagnoses, and response to antibiotics.6
poorly understood.29 EM lesions have been experimentally Controversy exists in the veterinary literature about whether
caused by infecting rabbits with B. burgdorferi. Table 9-41 healthy dogs should be routinely screened for B. burgdorferi
provides a comparison of Lyme disease clinical presentations antibodies.6 Limitations to serological testing include a long
in humans and other animals. incubation period, presence of subclinical infections, cross-
Table 9-41 n Lyme Disease: Comparative Clinical Presentations in Humans and Other Animals
Humans Tick exposures Days to weeks Early localized form: EM skin Positive serology, direct
lesion, fever immunofluorescence, rarely
Early disseminated infection: isolation from skin biopsy
paralysis of facial muscles,
meningitis, numbness in arms
or legs
Late-stage infection: arthritis,
cardiac pathology, neuropathy
Dogs Tick exposures 2-5 months in Often subclinical C6 Borrelia burgdorferi ELISA (both
experimentally qualitative and quantitative) and
Younger dogs appear to Arthritis, anorexia, and depression,
infected dogs30 Western blot antibody test
be more susceptible than cardiac disease, nephritis,
older dogs, coinfection lymphadenopathy 27
Antibodies generally can
with other agents be detected 3-5 wk after
experimental infection in dogs6
Cats Tick exposures 4-6 weeks Usually subclinical; fever, arthritis C6 B. burgdorferi ELISA and
may occur Western blot antibody test
Horses Tick exposures Weeks to months Fever, lameness, Bell’s palsy Antibodies generally take
4-6 wk to develop in horses;
immunoblots may not become
positive until 10-12 wk in
horses, skin biopsy
ELISA, Enzyme-linked immunosorbent assay; EM, erythema migrans.

reactions with other spirochetes, and persistence of antibody should be directed toward the affected organ system. Dogs do
titers for months. A positive serological result in the presence or not appear to develop natural immunity to infection nor do
absence of clinical signs should alert the clinician to also search they develop long-term immunity after vaccination. Therefore
for coinfections commonly associated with B. burgdorferi after the full course of antibiotic treatment, subsequent expo-
exposure, including Anaplasma, Babesia, Ehrlichia, Rickettsia, sure to B. burgdorferi can result in reinfection.
Bartonella, Leptospira, Mycoplasma, and Neorickettsia.6,10 In the United States there are currently four vaccines for
Clinically normal dogs with positive serological findings dogs that stimulate antibody production against a single
should have follow-up by a veterinarian with semiannual or outer surface protein A (OSP A) located on the bacterium
annual health examinations, be monitored for proteinuria, and when it is attached to the tick’s gut.6 This prevents infection
the owner should be alerted to contact the veterinarian if any because the vaccinated dog’s OSP A antibodies move with
clinical signs of Lyme disease develop. the blood to the tick’s gut and bind to the bacteria, thus pre-
venting the bacteria from upregulating OSP C and moving
to the saliva to infect the dog.34
Treatment
Management of B. burgdorferi infection in humans and ani- References
mals involves the use of antibiotics for treatment of disease.
Prophylaxis with oral doxycycline may be offered to adults or 1. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment,
treatment, and prevention of Lyme disease, human granulocytic ana-
children if a tick bite is due to an adult or nymphal I. scapu- plasmosis, and babesiosis: clinical practice guidelines by the Infectious
laris tick that has been attached for at least 24 hours, less than Diseases Society of America. Clin Infect Dis. 2006;43(9):1089.
72 hours has elapsed since removal of the tick, and the use of 2. Duncan AW, Correa MT, Levine JF, et al. The dog as a sentinel for
doxycycline is not contraindicated (doxycycline 200 mg PO human infection: prevalence of Borrelia burgdorferi C6 antibodies in
for 1 dose; children 8 and older, 4 mg/kg).1 Following a tick dogs from southeastern and mid-Atlantic states. Vector Borne Zoonotic
Dis. 2004;4(3):221.
bite, regardless of whether prophylaxis is given, individuals 3. Greene CE, Straubinger RK. Borreliosis. In: Green CE, ed. Infectious dis-
should be monitored for any signs of disease such as devel- eases of the dog and cat. 3rd ed. St Louis: Saunders Elsevier; 2006.
opment of a fever or an EM rash. 4. Centers for Disease Control and Prevention. Lyme disease prevention
The use of antibiotics for disease treatment depends on and control: protect yourself from tick bites. http://www.cdc.gov/ncidod/
dvbid/lyme/Prevention/ld_Prevention_Avoid.htm. Accessed September
the stage of disease. Table 9-42 outlines recommended anti- 28, 2008.
biotics regimens outlined by the Infectious Diseases Society 5. Placerville Veterinary Clinic. Tick removal tools. http://placervillevet.
of America (IDSA). The use of macrolides should be reserved com/ticktools.htm. Accessed February 28, 2009.
for persons who are unable to tolerate tetracyclines, penicil- 6. Littmann MP, Goldstein RE, Labato MA, et al. ACVIM small animal
lins, or cephalosporins because their efficacy may be lower. consensus statement on Lyme disease in dogs: diagnosis, treatment, and
prevention. J Vet Intern Med. 2006;20(2):422.
Recommended antibiotic regimens for animals with clinical 7. Bunikis J, Garpmo U, Tsao J, et al. Sequence typing reveals extensive
manifestations of Lyme disease are also shown in Table 9-42. strain diversity of the Lyme borreliosis agents Borrelia burgdorferi in North
More specific supportive and symptomatic medical treatment America and Borrelia afzelii in Europe. Microbiology. 2004;150(Pt 6):1741.
Table 9-42 n Antibiotic Treatment of Lyme Disease in Humans and Other Animals
Humans (based on IDSA

guidelines1)
Oral regimens: Adults: amoxicillin 500 mg PO tid, doxycycline Adults and children: consider selected
100 mg PO bid, or cefuroxime axetil 500 mg macrolide if unable to tolerate penicillins,
Early localized disease, isolated PO bid cephalosporins, or tetracyclines
fifth nerve palsy, carditis (if only
first-degree block), or arthritis Children: amoxicillin 50 mg/kg/day (maximum Monitor closely for resolution of clinical
without neurological signs 500 mg/dose) divided q8h, doxycycline if ≥8 yr manifestations
4 mg/kg/day divided bid (maximum 100 mg/dose),
or cefuroxime 30 mg/kg/day (maximum
500 mg/dose) divided bid
Parenteral regimens: Lyme Adults: ceftriaxone 2 gm IV qd Adults: cefotaxime 2 gm, IV 8h or penicillin G
meningitis, other acute Children: ceftriaxone 50-75 mg/d IV 18-24 million units/day divided q4h IV
neurological manifestations, (maximum 2 gm) Children: cefotaxime 150-200 mg/kg/day
carditis IV divided tid or qid, maximum 6 gm/day
or penicillin G 200,000-400,000 units/kg/
day, maximum 18-24 million units/day
divided into doses q4h
Pregnant women Same as nonpregnant but avoid doxycycline
Dogs Doxycycline 5 mg/kg PO q24h × 28 days6 Amoxicillin 20 mg/kg PO q8-12h × 28 days27
Horses Doxycycline 10-20 mg/kg PO q12h35 Tetracycline 6.6 mg/kg IV qd36
IDSA, Infectious Diseases Society of America.

8. Heymann DL, ed. Control of communicable diseases manual. 19th 22. Curran KL, Fish D, Piesman J. Reduction of nymphal Ixodes dammini
ed.Washington, DC, American Public Health Association; 2008. (Acari: Ixodidae) in a residential suburban landscape by area applica-
9. Center for Food Security and Public Health, Iowa State University. Lyme tion of insecticides. J Med Entomol. 1993;30(1):107.
disease. http://www.cfsph.iastate.edu/Factsheets/pdfs/lyme_disease.pdf. 23. Rand PW, Lubelczyk C, Holman MS, et al. Abundance of Ixodes scapularis
Accessed November 2008. (Acari: Ixodidae) after the complete removal of deer from an isolated off-
10. Littman MP. Canine borreliosis. Vet Clin North Am Small Anim Pract. shore island, endemic for Lyme disease. J Med Entomol. 2004;41(4):779.
2003;33(4):827. 24. Piesman J. Strategies for reducing the risk of Lyme borreliosis in North
11. Lissman BA, Bosler EM, Camay H, et al. Spirochete associated arthritis America. Int J Med Microbiol. 2006;296(suppl 40):17.
(Lyme disease) in a dog. J Am Vet Med Assoc. 1984;185(2):219. 25. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
12. Kornblatt AN, Urband PH, Steere AC. Arthritis caused by Borrelia burg- handbook for primary care. St Louis: Mosby Elsevier; 2005.
dorferi in dogs. J Am Vet Med Assoc. 1985;186(9):960. 26. Chou J, Wunschmann A, Hodzic E, et al. Detection of Borrelia burgdor-
13. Fritz CL, Kjemtrup AM. Lyme borreliosis. J Am Vet Med Assoc. feri DNA in tissues from dogs with presumptive Lyme borreliosis. J Am
2003;223(9):1262. Vet Med Assoc. 2006;229(8):1260.
14. Connally NP, Ginsberg HS, Mather TN. Assessing peridomestic 27. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
entomological factors as predictors for Lyme disease. J Vector Ecol. panion: canine and feline infectious diseases and parasitology. Ames, IA:
2006;31(2):364. Blackwell; 2006.
15. Centers for Disease Control and Prevention. Lyme disease—United 28. Magnarelli L, Fikrig E. Detection of antibodies to Borrelia burgdorferi
States, 2003–2005. MMWR. 2007;56(23):573. in naturally infected horses in the USA by enzyme-linked immuno-
16. Giery ST, Ostfeld RS. The role of lizards in the ecology of Lyme dis- sorbent assay using whole-cell and recombinant antigens. Res Vet Sci.
ease in two endemic zones of the Northeastern United States. J Parasitol. 2005;79(2):99.
2007;93(3):511. 29. Butler CM, Houwers DJ, Jongejan F, et al. Borrelia burgdorferi infections
17. Magnarelli LA, Bushmich SL, IJdo JW, et al. Seroprevalence of antibod- with special reference to horses. A review. Vet Q. 2005;27(4):146.
ies against Borrelia burgdorferi and Anaplasma phagocytophilum in cats. 30. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases
Am J Vet Res. 2005;66(11):1895. of companion animals. Ames, IA: The Center for Food Security and Public
18. Centers for Disease Control and Prevention. Lyme disease transmission. Health, Iowa State University College of Veterinary Medicine; 2008.
http://www.cdc.gov/ncidod/dvbid/Lyme/ld_transmission.htm. Accessed 31. DePietropaolo DL, Powers JH, Gill JM, et al. Diagnosis of Lyme disease.
February 28, 2009. Am Fam Physician. 2005;72(2):297.
19. Schwan TG. Temporal regulations of the outer surface proteins of 32. Centers for Disease Control and Prevention. Notice to readers: caution
the Lyme-disease spirochaete Borrelia burgdorferi. Biochem Soc Trans. regarding testing for Lyme disease. MMWR. 2005;54(5):25.
2003;31(1):108. 33. IDEXX Laboratories. Lyme Quant C6Test. http://www.idexx.com/ani-
20. Brownstein JS, Skelly DK, Holford TR, et al. Forest fragmentation malhealth/laboratory/c6/. Accessed May 7, 2008.
predicts local scale heterogeneity of Lyme disease risk. Oecologia. 34. Goldstein RE, Karyn Gavzer K. Lyme disease: what clients need to know.
2005;146(3):469. Clinician’s Brief. 2008;(suppl) April 1.
21. Bennet L, Halling A, Berglund J. Increased incidence of Lyme borrelio- 35. Gilger B. Equine ophthalmology. St Louis: Saunders Elsevier; 2005.
sis in southern Sweden following mild winters and during warm, humid 36. Sellon DC, Long M. Equine infectious diseases. St Louis: Saunders
summers. Euro J Clin Microbiol Infect Dis. 2006;25(7):426. Elsevier; 2007.
LYMPHOCYTIC CHORIOMENINGITIS
Lynda U. Odofin defects in children. In addition, because of recent outbreaks

in organ transplant patients,7-9 LCM is a reportable disease in
(ICD-9 049.0 Non-arthropod–borne lymphocytic chorio- some U.S. states; such states require physicians to report the
meningitis (ICD-9 049.0), Unspecified non-arthropod–borne disease to local health authorities.
viral diseases of central nervous system (ICD-9 049.9), Viral
encephalitis NOS (ICD-10 A87.2) Key Points for Clinicians and Public Health
Professionals
Other names in humans: none
Other names in animals: none Public Health Professionals

Lymphocytic choriomeningitis (LCM) is a rodent-borne viral • Recommend that LCM be reportable in all states.
infection that may cause substantial neurological disease,1,2 • Provide descriptive epidemiologic analysis of disease
especially in immunocompromised individuals. Like other in the community.
members of the Arenadiviridae family, the causative agent, • Investigate new cases of disease to determine the source
lymphocytic choriomeningitis virus (LCMV), uses rodents as of infection. Search home, place of employment, and
reservoirs.3 Although the common house mouse, Mus muscu- immediate surroundings for presence of house mice.
lus, is the natural host and principal reservoir of LCMV,4 wild, Test rodents, including pets found on such premises,
pet, and laboratory rodents (rats, guinea pigs, hamsters) can for virus.
be infected also. Infected mice can shed the virus through- • Trace the source of infected pets. Work with pet stores
out their lives4; infected females transmit the virus to their to ensure all rodents sold are LCMV free.
offspring, which may become asymptomatic persistent viral • Recommend rodent-proofing homes:
shedders.5 Human infection is through contact with infected  Seal rodent entry holes or gaps with steel wool, metal
pet rodents or infected wild mice or their droppings. Infected lath, or caulk.
rodents often do not show any signs of illness.6 LCMV is an  Trap rats and mice using appropriate snap trap.
emerging neuroteratogen, known to cause diverse congenital  Clean rodent food sources and nesting sites.
 Take precautions when cleaning rodent-infected areas: • Consider the diagnosis in patients (especially children)
 Use cross-ventilation when entering a previously presenting with ocular scars regardless of no history
unventilated enclosed room or dwelling before of LCM. There have been reports from Europe about
cleanup. such cases.
 Use rubber, latex, vinyl, or nitrile gloves. • Report suspicion of disease immediately to public
 Do not stir up dust by vacuuming, sweeping, health authorities. LCM is reportable in some U.S.
or any other means. Instead, thoroughly wet states.
contaminated areas with a bleach solution or • Discourage immunocompromised individuals, preg-
household disinfectant. Hypochlorite (bleach) nant women, and families with children younger
solution: mix 11⁄2 cups of household bleach in 1 than 5 years from owning rodent pets. Also educate
gallon of water. Once everything is wet, take up these individuals and parents about the consequences
contaminated materials with damp towel and of owning pet rodents.11 Consider routine testing of
then mop or sponge the area with bleach solu- exposed pregnant women for the virus.
tion or household disinfectant. • If caring for occupational groups at risk, ensure that
 Spray dead rodents with disinfectant and then they are educated about symptoms of the disease,
double-bag along with all cleaning materials and potential routes of transmission, use of adequate pro-
dispose of bag in an appropriate waste disposal tective equipment, and that efforts are taken to reduce
system. the risk of infection.
 Remove gloves and thoroughly wash hands with • Educate patients on reduction of environmental expo-
soap and water (or waterless alcohol-based hand sure risk through the elimination of wild rodents. Seal
rubs when soap is not available and hands are not up rodent entry holes or gaps with steel wool, metal
visibly soiled). lath, or caulk.
• Counsel people about appropriate rodent pet handling • Trap rats and mice by using an appropriate snap trap.
and care: Clean up rodent food sources and nesting sites and take
 Wash hands with soap and water after handling precautions when cleaning rodent-infected areas.11
pet rodents; use waterless alcohol-based hand rubs • Promote proper handwashing after pet handling, and
when soap is not available. educate patients on providing a clean environment for
 Keep rodent cages clean and free of soiled bedding. pet rodents, such as supplying fresh bedding, food, and
 Clean the cage in a well-ventilated area or outside. water on a regular basis. Clean cages outdoors or in
 Wash hands thoroughly with soap and water after well-ventilated areas.11
cleaning up pet droppings. Closely supervise young • Provide an information sheet on LCM prevention and
children, especially those younger than 5 years, control for at risk patients; a CDC information sheet
when cleaning cages, and make sure they wash their is available at http://www.cdc.gov/ncidod/dvrd/spb/
hands immediately after handling rodents and ro- mnpages/dispages/lcmv.htm.
dent caging or bedding.
 Do not kiss pet rodents or hold them close to the
face. Veterinary Clinicians
• Recommend that testing for LCMV should be included • Advise clients to consult their physicians if an infected
in the screening protocols for potential organ donors. rodent is seen or if they are considering acquiring a
rodent as a pet.
Human Health Clinicians • Although the length of LCMV infection in pets varies,
it has been shown that hamsters (subfamily Cricetinae)
• Ensure that potentially exposed immunocompro- can transmit the virus for at least 8 months. Thus it is
mised persons and pregnant women are given imme- advisable to euthanize infected rodents.
diate medical attention, and advise such individuals to • Although LCMV is not reported in animals, it is advis-
avoid contact with rodents and rodent droppings and able to report increased incidence of cases to the local
to rodent-proof their homes. health authorities. Disease in animals may serve as an
• As part of the history, patients with aseptic meningitis early warning of environmental exposure risk and pos-
and encephalitis should be asked about contact with sible human outbreaks.
rodents or rodent droppings.10 • Screening pet rodents is not recommended as serolog-
• Consider the diagnosis in all patients with rodent ical testing on rodents can be inaccurate and results
contact, such as pet owners, laboratory workers, and misleading; however, hygienic practices (handwashing,
people from endemic areas. Work closely with respec- cage sanitation) should be followed.12
tive state health department to discuss forwarding of
samples on patients with disease suggestive of LCM
Agent
to state laboratories or CDC for testing. (Testing for
LCMV infection in asymptomatic persons is not LCMV is an enveloped single-stranded RNA virus belong-
necessary.) ing to the family Arenaviridae. The virus is serologically
• Consider LCMV infection in organ transplant recipi- related to Lassa, Machupo, Junin, Guaranito, and Sabia
ents with unexplained fever, hepatitis, or multisystem viruses5 and has been referred to as the prototypic member
organ failure.10 of the family. Along with Lassa and Lassa-related viruses,
LCMV forms the Old World group of the Arenaviridae.13

Groups at Risk
Because of its unique properties, the LCMV model has been
used to make important contributions to the fields of virol- In general, people who are in contact with rodents are at risk
ogy and immunology14 and further understanding of viral- from LCMV infection; these include laboratory workers who
immune interactions. For instance, a specific glycoprotein routinely work with LCMV and laboratory mice and other
(GP1), which is expressed on the envelope of LCMV,15 rodents, farmers who are in frequent contact with wild mice,
mediates attachment of the virus, thereby initiating infec- homeowners with mouse infestations, veterinarians who
tion; thus mutations in this protein have the potential to handle sick hamsters and other rodents, pet-store keepers,
alter viral targeting and influence the course of disease.14 and pet rodent owners. Immunocompromised individuals,
The immune system plays a major role in the outcome of children younger than 5 years, and fetuses are particularly
human LCMV infection, ranging from no disease in healthy vulnerable to LCMV, which usually lead to severe infection
individuals to severe neurological disease in immunocom- in these subpopulations.
promised individuals. Recently LCMV infection has been associated with organ
transplants.8,9 Transmissions of virus between donors and
Geographical Occurrence recipients have been documented in the United States and
other parts of the world. In one of these cases, the donor had
LCMV is found worldwide and is endemic in wild mice. The recently acquired a pet hamster.22
virus has the greatest geographical range potential of any
arenavirus and may occur on all land masses where the genus
Mus has been introduced, including all continents except
Antarctica.7,16 The CDC estimates 5% of the U.S. wild mouse LCMV has a highly restrictive host range; the house mouse
population is infected with LCMV, although epidemiologi- (M. musculus) is the natural host and reservoir. Once infected,
cal studies have documented a prevalence ranging from 3% house mice often become lifelong shedders of the virus.
to 21% in various U.S. locations.11 An overall prevalence Infection has also been reported in other rodents such as
rate of 9% (43/468) was determined in wild mice captured wood mice (Apodemus sylvaticus) and yellow-necked field
in various sites, including residential and park locations in mice (A. flavicollis).23 Pet hamsters and guinea pigs are not
Baltimore, Maryland.13 known to be natural reservoirs for LCM, but pet rodents can
In general, human infection, with the exception of those become infected if they have contact with wild house mice
associated with hamsters,13 tends to reflect the distribution in a breeding facility, pet store, or home. The golden hamster
of house mice.17-19 Several serological studies conducted in (Mesocricetus auratus) has become an important linkage host
urban areas have shown that the prevalence of LCMV infec- for LCMV transmission in humans and has been the source of
tion among humans ranges from 2% to 5%.11 In Baltimore, recent outbreaks in the United States and abroad.24-27
LCMV antibodies were found in 4.7% of 1149 inner-city
residents tested,6,20 and 49% of these reported house mice
within their residence.21
The true incidence of LCM is unknown because many Infected house mice play a major role in maintaining the life
cases go unreported owing to the self-limiting effect in cycle of LCMV, thereby ensuring its persistence in nature
healthy individuals and lack of recognition by physicians. (Figure 9-86). Wild mice are usually infected in utero, thereby
Infected female
wild rodent
In utero transmission
Direct and indirect (fomite) contact with Human being (pet

Persistently infected
infected rodent excreta and body fluids owners, laboratory workers,
wild rodent
(urine, feces, saliva, blood) veterinarians, farmers)
Direct contact Inhalation
Ingestion
Susceptible pet rodent
(hamsters, guinea pigs) In utero
transmission
Human fetus Organ recipients

Infected pet rodent (congenital
(hamsters, guinea pigs) disease such as
hydrocephalus,
microcephaly,
chorioretinitis)
Figure 9-86 n Transmission cycle of lymphocytic choriomeningitis virus.

becoming chronically or persistently infected. The virus is usually vomiting. Other symptoms that appear less frequently include
excreted in urine, saliva, and feces of infected mice; transmission sore throat; cough; arthritis; pain in the chest, testicles, and
to humans occurs through the oral and respiratory contact with parotid gland; and rarely a rash. Most people recover after this
virus-contaminated excreta, food, or dust or through the con- phase. However, some may proceed to the second phase of the
tamination of skin lesions and cuts. Fomites such as bedding disease consisting of symptoms of meningitis or characteris-
materials and other articles contaminated by infected rodents tics of encephalitis. The course of the disease is usually short,
can put nearby humans at infection risk. rarely fatal (about 1% mortality rate), and the prognosis is
Human-to-human transmission occurs vertically between usually good, although convalescence with fatigue and vaso-
infected mother and fetus and horizontally from organ motor instability may be prolonged. An association between
transplant between infected donors and recipients. Many of LCMV infection and myocarditis has been suggested.
the women who gave birth to children with congenital LCM Immunosuppressed patients such as organ recipients may
had a known exposure to wild mice or sick hamsters during develop fatal hemorrhagic fever; of 11 organ recipients descri
pregnancy.28 bed in three LCM clusters, 10 died of multisystem organ failure,
with LCMV-associated hepatitis the prominent feature.10
Congenital LCMV infection first was recognized in Europe
half a century ago.24,29-31 The first U.S. cases were reported in
Most of the human LCMV infection is usually associated 199330,31 and were characterized by severe brain and retinal
with contact with infected rodents (wild and pet rodents); injury.15,32-35 Infection of the fetus during the early stages of
thus the virus persistence in the environment is dependent on pregnancy may lead to developmental deficits that are per-
the infection rate of mice and frequency of contact between manent; congenital LCM can be manifested in a variety of
infected rodents and humans. For instance, during the fall neurological signs such as microcephaly, chorioretinitis,
there appear to be more mice in residential areas and even hydrocephalus, seizures, and hypertonia (Figure 9-87). These
commercial areas such as restaurants because the mice look signs are usually evident within 48 hours of birth. Diverse
for warmer places to spend the winter. This enables more clinical signs have been recorded among 20 children diag-
contact with nearby pet rodents (hamsters, guinea pigs) and nosed with congenital LCMV infection.36 LCMV was diag-
even humans. nosed in these children at birth with follow-up of 11 years.
Clinical signs covered a wide spectrum of neurological dis-
ease, but chorioretinitis was the only common presenting
Disease in Humans
sign. In addition, the study suggested that the variability of
The immune response plays a major role in determining the the disease was related to the gestational timing of infection.
manifestation and progression of clinical symptoms following The most common laboratory abnormalities are leukope-
LCMV infection. Thus infection in healthy people usually goes nia and thrombocytopenia in the first phase of disease with a
unnoticed and the virus is readily cleared. The onset of symp- mild elevation in liver enzymes in the serum. After the onset
toms in ill individuals occur 8 to 15 days after exposure and of neurological disease, an increase in protein levels and the
is characterized by a biphasic febrile illness. The initial phase, number of white blood cells or a decrease in the glucose lev-
which may last as long as a week, typically begins with any els in the CSF is usually observed. No chronic state has been
or all of the following flulike symptoms: fever, malaise, lack reported in humans, who usually clear the virus after the
of appetite, muscle aches, retroorbital headache, nausea, and acute phase of the disease.
Figure 9-87 n Computed tomography at 5 months of an infant with profound developmental delay and chori-
oretinitis due to intrauterine lymphocytic choriomeningitis virus infection. The scan shows microencephaly, lissen-
cephaly, and calcifications that are periventricular, intracerebral, and over the convexities of the brain. (From Long
SS, Pickering LK, Prober CG: Principles and practice of pediatric infectious diseases, ed 3, Philadelphia, 2008, Saunders
Elsevier. Courtesy G.L. Rodgers and S.S. Long, St. Christopher’s Hospital for Children, Philadelphia, Pa.)
other aseptic meningitides and viral encephalitides, such as

Disease in Animals
those caused by enteroviruses, the arthropod-borne togavi-
Wild mice infected with LCMV in utero or at an early age ruses, or herpes simplex virus. Drug-induced meningitis is
develop a persistent subclinical infection and likely shed the also a differential. In the case of congenital LCM, valid differ-
virus for life. In naturally infected colonies of wild mice, the ential diagnoses include TORCH infections (toxoplasmosis,
proportion of mice with persistent infection increases over rubella, cytomegalovirus, herpes, and syphilis), parvovi-
time and at 4 years almost all the animals will be shedding rus, and enterovirus. Confirmatory diagnosis usually is by
virus.37 Although most rodents with LCMV infection are sub- virus isolation in blood or CSF, by PCR, or identification of
clinical, there have been reports of illness in infected ham- anti-LCMV IgM and IgG by ELISA or complement fixation.
sters characterized by a wasting disease that may run a long Detection of rising antibody titers in paired sera by IFA, and
course (ranging from several weeks to months). Early signs LCMV antigens by immunohistochemistry in liver biopsy or
include loss of activity, loss of appetite, and rough coat. Later at autopsy also are considered diagnostic.
the animal may show signs of weight loss, hunched posture, In rodents, confirmatory diagnosis is by viral isolation via
inflammation of the eye lids (blepharitis), clonic convul- inoculation in guinea pigs or LCM-free mice, complement
sions, and eventually death. The effects of LCMV have been fixation, and fluorescent antibody (Table 9-43).
studied in laboratory mice and mimic the disease in humans.
Mice exposed to the virus at an older age are more likely to
Treatment
develop clinical disease. Gross lesions include necrosis of the
liver and lymphoid tissue. LCMV infection has been docu- Early diagnosis is the key to successful treatment of LCM.
mented in other animals such as dogs and monkeys; how- Treatment is mainly supportive and involves use of antiin-
ever, this is rare and has been consistently associated with flammatory drugs. As for other cases of aseptic meningitis,
contact to infected rodents. suggested treatment regimens include intravenous fluids and
analgesics.38
Treatment in animals is normally not advocated because
Diagnosis they could develop a chronic state and continue to shed the
virus, thereby posing a risk for other animals and humans.
In humans, the early stage of disease could be confused with In general, by the time clinical signs are seen the prognosis
the flu, and at latter stages it must be differentiated from is poor.
Table 9-43 n Lymphocytic Choriomeningitis: Clinical Presentations in Humans and Other Animals
Humans Rodent exposure, 8-13 days; 15-21 Adults: flulike symptoms, Early stages of disease: isolation of
immunocompromised days until myalgia, retroorbital headache, virus from blood or CSF by PCR
meningeal orchitis, parotiditis, arthritis, or intracerebral inoculation of
symptoms myocarditis, muscle ache, acute LCM-free mice (3-5 weeks old)
appear5 hydrocephalus, occasional rash5 or by cell culture5
In rare cases, muscle weakness, Demonstration of anti-LCMV IgM
paralysis, body sensation and IgG in serum or CSF by
changes ELISA or complement fixation;
Newborns/infants (0-<2 yr): Also demonstration of rising
hydrocephalus, chorioretinitis, titers by IFA in paired sera
seizures, irritability, Liver biopsy and multiple
microcephaly, blistered skin, autopsy specimen stained
hypertonia, hypotonia, light positive for LCMV antigens by
perception, blindness, spastic immunohistochemistry
quadriparesis, quadriplegia,
hearing loss, cognitive deficits
Children (2-11 yr): same as in
infants, and ataxia, spastic
diplegia
Lethargy, anorexia, fever, shock,
Organ Infected organ donor 2-4 wk after hepatitis, multisystem organ
recipients transplant failure
Rodents Exposure to infected Varies (several Weight loss, ocular and nasal Virus isolation by inoculation
(hamsters, animals weeks to discharge, hunched posture, of LCM-free mice or guinea
guinea pigs, months) inflammation of the eyelids, pigs, complement fixation,
mice) clonic convulsions and fluorescent antibody on
serum; immunofluorescence
test on liver tissue
CSF, Cerebrospinal fluid; LCM, lymphocytic choriomeningitis; LCMV, lymphocytic choriomeningitis virus.
References 20. Childs JE, Glass GE, Ksiazek TG, et al. Human-rodent contact and infec-
tion with lymphocytic choriomeningitis and Seoul viruses in an inner-
1. Jahrling PB, Peters CJ. Lymphocytic choriomeningitis virus. A neglected city population. Am J Trop Med Hyg. 1991;44(2):117.
pathogen of man. Arch Pathol Lab Med. 1992;116(5):486. 21. Childs JE, Glass GE, LeDuc JW. Rodent sightings and contacts in an
2. Peters CJ. Lymphocytic choriomeningitis virus—an old enemy up to inner-city population of Baltimore, Maryland, USA. Bull Soc Vector
new tricks. N Engl J Med. 2006;354(21):2208. Ecol. 1991;16(2):245.
3. Rowe WP, Murphy FA, Bergold GH, et al. Arenoviruses: proposed name 22. Amman BR, Pavlin BI, Albariño CG, et al. Pet rodents and fatal lym-
for a newly defined virus group. J Virol. 1970;5(5):651. phocytic choriomeningitis in transplant patients. Emerg Infect Dis.
4. Buchmeier M, Zajac A. Lymphocytic chiromeningitis virus. In: Ahmed 2007;13(5):719.
R, Chen I, eds. Persistent viral infections. New York: Wiley; 1999. 23. Lehmann-Grube F. Lymphocytic choriomeningitis virus, Virology mono-
5. Heymann DL, ed. Control of communicable diseases manual. 19th graphs. 10. Wein and New York: Springer-Verlag; 1971.
ed.Washington, DC: American Public Health Association; 2008. 24. Ackermann R, Stille W, Blumenthal W, et al. Syrian hamsters as vectors
6. College of Veterinary Medicine. University of Minnesota: lymphocytic of lymphocytic choriomeningitis [in German]. Dtsch Med Wochenschr.
choriomeningitis virus (LCMV). www.cvm.umn.edu Accessed August 1972;97(45):1725.
20, 2008. 25. Biggar RJ, Woodall JP, Walter PD, et al. Lymphocytic choriomeningitis
7. Enria D, Mills JN, Flick R, et al. Arenavirus infections. In: Guerrant RL, outbreak associated with pet hamsters. Fifty-seven cases from New York
Walker DH, Weller PF, eds. Tropical infectious diseases: principles, patho- State. JAMA. 1975;232(5):494.
gens, and practice. 2nd ed. Philadelphia: Churchill Livingstone Elsevier; 26. Deibel R, Woodall JP, Decher WJ, et al. Lymphocytic choriomeningi-
2006. tis virus in man. Serologic evidence of association with pet hamsters.
8. Fischer SA, Graham MB, Kuehnert MJ, et al. Transmission of lympho- JAMA. 1975;232(5):501.
cytic choriomeningitis virus by organ transplantation. N Engl J Med. 27. Hirsch MS, Moellering Jr RC, Pope HG, et al. Lymphocytic-choriomeningitis-
2006;354(21):2235. virus infection traced to a pet hamster. N Engl J Med. 1974;291(12):610.
9. Palacios G, Druce J, Du L, et al. A new arenavirus in a cluster of fatal 28. Wright R, Johnson D, Neumann M, et al. Congenital lymphocytic cho-
transplant-associated diseases. N Engl J Med. 2008;358(10):991. riomeningitis virus syndrome: a disease that mimics congenital toxoplas-
10. Centers for Disease Control and Prevention. Lymphocytic choriomen- mosis or cytomegalovirus infection. Pediatrics. 1997;100(1):e9.
ingitis virus transmitted through solid organ transplantation—Massa- 29. Komrower GM, Williams BL, Stones PB. Lymphocytic choriomen-
chusetts, 2008. MMWR. 2008;57(29):799. ingitis in the newborn. Probable transplacental infection. Lancet.
11. Centers for Disease Control and Prevention. Lymphocytic choriomen- 1955;268(6866):697.
ingitis. http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/lcmv/ 30. Barton LL, Budd SC, Morfitt WS, et al. Congenital lympho-
qa.htm. Accessed on August 27, 2008. cytic choriomeningitis virus infection in twins. Pediatr Infect Dis J.
12. Centers for Disease Control and Prevention. Interim guidance for min- 1993;12(11):942.
imizing risk for human lymphocytic choriomeningitis virus infection 31. Larsen PD, Chartrand SA, Tomashek KM, et al. Hydrocephalus compli-
associated with rodents. MMWR. 2005;54(30):747. cating lymphocytic choriomeningitis virus infection. Pediatr Infect Dis J.
13. Childs JE, Glass GE, Korch GW, et al. Lymphocytic choriomeningitis 1993;12(6):528.
virus infection and house mouse (Mus musculus) distribution in urban 32. Barton LL, Mets MB, Beauchamp CL. Lymphocytic choriomeningitis
Baltimore. Am J Trop Med Hyg. 1992;47(1):27. virus: emerging fetal teratogen. Am J Obstet Gynecol. 2002;187(6):1715.
14. Kang SS, McGavern DB. Lymphocytic choriomeningitis infection of the 33. Barton LL, Peters CJ, Ksiazek TG. Lymphocytic choriomeningitis virus:
central nervous system. Front Biosci. 2008;13:4529. an unrecognized teratogenic pathogen. Emerg Infect Dis. 1995;1(4):152.
15. Wright KE, Spiro RC, Burns JW, et al. Post-translational processing 34. Enders G, Varho-Gobel M, Lohler J, et al. Congenital lymphocytic cho-
of the glycoproteins of lymphocytic choriomeningitis virus. Virology. riomeningitis virus infection: an underdiagnosed disease. Pediatr Infect
1990;177(1):175. Dis J. 1999;18(7):652.
16. Sage RD. Wild mice. In: Foster HL, Small JD, Fox J, eds. The mouse 35. Mets MB, Barton LL, Khan AS, et al. Lymphocytic choriomeningi-
in biomedical research, vol I: history, genetics, and wild mice. New York: tis virus: an underdiagnosed cause of congenital chorioretinitis. Am J
Academic Press; 1981. Ophthalmol. 2000;130(2):209.
17. Armstrong C, Sweet L. Lymphocytic choriomeningitis. Report of two 36. Bonthius DJ, Perlman S. Congenital viral infections of the brain: lessons
cases, with recovery of the virus from gray mice (Mus musculus) trapped learned from lymphocytic choriomeningitis virus in the neonatal rat.
in the two infected households. Public Health Rep. 1939;54:673. PLoS Pathog. 2007;3(11):e149.
18. Blumenthal W, Ackermann R, Scheid W. Distribution of the lympho- 37. Acha PN, Szyfres B. Zoonoses and communicable diseases common to
cytic choriomeningitis virus in an endemic area [in German]. Dtsch Med man and animals, vol. II: chlamydioses, rickettsioses and viroses. 3rd ed.
Wochenschr. 1968;93(19):944. Washington, DC: Pan American Health Organization; 2003.
19. Smithard EHR, Macrae AD. Lymphocytic choriomeningitis; associated 38. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to antimi-
human and mouse infections. Br Med J. 1951;1(4718):1298. crobial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy; 2009.
METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS INFECTION

Peter M. Rabinowitz and Lisa A. Conti c ommonly causes skin and soft tissue infections, invasive
strains of MRSA have been associated with necrotizing
Staphylococcal infection, unspecified (ICD -10 A49.0) pneumonia, sepsis, and necrotizing fasciitis, even in previ-
ously healthy persons.1 This community-acquired MRSA
Other names in humans: MRSA (CA-MRSA) has also been found in companion animals2-13
and livestock,14-17 and there is evidence of transmission
Other names in animals: MRSA between animals and humans.4,8,12,15,18-26 Concern has been
expressed in the media about the emergence of a new
In recent years, methicillin-resistant Staphylococcus aureus “superbug” in people and animals. The picture is complex
(MRSA), long considered a nosocomial infection of hos- and evolving, reinforcing the need for close cooperation
pitalized patients, has emerged as a significant pathogen and communication between human and veterinary health
in the community setting. Although S. aureus most professionals.
Key Points for Public Health Professionals • Isolate and screen all suspected cases. Isolate confirmed
and Clinicians cases.
• Consider the role of household pets and other ani-
mal contacts in situations where MRSA transmission
Public Health Professionals appears to be ongoing in a household. Recommend
testing of pets in situations where the entire household
• Provide descriptive epidemiology of infection in is being tested. Animal results should be reported to
human and animal populations. the physician with pet owner consent.
• Educate the public on prevention strategies, such as • Ensure that adequate hand hygiene procedures and
not sharing towels, clothes, or razors; frequent hand- a high standard of environmental cleaning and dis-
washing (the Healthcare Infection Control Practices infection are in place for staff in veterinary hospitals,
Advisory Committee has specific guidance), bandag- and isolation procedures are used for suspected MRSA
ing wounds, and disinfecting surfaces27 (disinfectants cases.
include 1% sodium hypochlorite, glutaraldehyde, and • Consider screening of veterinary personnel32 during
iodone/alcohol combinations28); and the occurrence extreme circumstances (i.e., when there is epidemio-
of carrier states.29 logical evidence of personnel-borne transmission and
• Educate local veterinary and human health clinicians transmission persists after improvement in infection
in risk areas and during high-risk periods about groups control practices are made). Note: The prevalence of
at risk and symptoms of disease. MRSA colonization is higher in general among veteri-
• Educate health providers regarding risk groups and nary personnel than the general population4,20,23,33 and
how to recognize clusters of patients. veterinary staff can be exposed at any time. A negative
• Ensure that workers at risk are using appropriate screening result does not ensure that the person’s test
handwashing and PPE, as well as isolation of suspected result will be negative the following day. A positive
cases. result also does not mean the person is involved in
• Encourage community members to be immunized transmission, and there is no indication to restrict the
against seasonal influenza as MRSA pneumonia can duties of a veterinary worker in whom MRSA has been
occur when healthy persons get influenza. colonized.
• Encourage and facilitate communication among phy-
sicians, veterinarians, and public health personnel.
Agent
• Ensure that positive aspects of animal contact are
not ignored when assessing risk of zoonotic MRSA The S. aureus bacterium is a gram-positive coccus that is
transmission.30 coagulase positive and exists as a commensal organism in
humans and many animal species, typically carried in the
Human Health Clinicians nasopharynx. The resistance of S. aureus to β-lactam anti-
biotics (penicillins and cephalosporins) including methicil-
• Be alert to the possibility of MRSA when diagnosing lin is due to the production of a penicillin-binding protein
and treating soft tissue infections. (PBP2a) encoded by the mecA gene, which is carried on a
• Treat and report cases to health department if report- transposable genetic element called the staphylococcal cas-
able in state. sette chromosome mec (SCCmec). There are at least five dif-
• Ensure that adequate hand hygiene practices are used ferent SCCmec types (I-V) and several subtypes.34 The
with all patients and isolation procedures are used for PBP2a protein is expressed in the cell wall and has a low
suspected MRSA cases.31 affinity for β-lactam antibiotic binding. Some MRSA also
• Counsel patients in whom MRSA has been colonized have membrane-bound protein pumps to remove antibiot-
regarding measures to reduce risk of transmission to ics. Although strains of S. aureus that are resistant to methi-
other humans and animals (bandage wounds, avoid cillin have been identified for many years, some recent clones
direct contact). circulating in humans since 2000 include genes coding for
• Query patients about animal contact. Ask patients/ Panton-Valentine leukocidin (PVL), a membrane toxin that
family members about any observed illness in pets. appears to be related to virulence (Figure 9-88).29 The bacte-
• Consider the role of household pets and other ani- ria are stable in the environment for 17 hours in sunlight, 46
mal contacts in situations where MRSA transmission hours on glass, less than 7 days on floors, 42 days in carcasses
appears to be ongoing in a household.30 Recommend and organs, and 60 days in meat products.35
testing of pets only in situations where the entire
household is being tested. All animal testing should
be directed by the attending veterinarian, with results
reported to the physician with pet owner consent. S. aureus is a major human pathogen that is found world-
wide. It appears to have a predominantly human reservoir
Veterinary Clinicians and can be isolated from the nares of about 30% of healthy
adults.36 MRSA has emerged in developing countries, where
• Ensure that the clinical laboratory processing bacterial it remains common.37 In some parts of the United States, the
cultures is able to identify S. aureus and MRSA in clini- majority of community isolates of S. aureus from ill patients
cal specimens. are now MRSA.38
human populations from pigs and cattle.4 A study in a

small animal hospital found 9% of the dogs were MRSA
carriers, whereas almost 18% of the staff was infected.5
Among S. aureus isolates from sick animals in veterinary
teaching hospitals, 14% were MRSA.46 Among healthy
dogs and cats in the general population, MRSA prevalence
has been reported at 1% to 3%, although there was a high
rate of infection with methicillin-resistant coagulase-neg-
ative Staphylococcus (MRCoNS).14 The epidemiology in
pigs may be different. A relatively high prevalence of nasal
carriage of MRSA has been reported47 in agreement with
previous studies showing transmission between pigs and
farmers.14
MRSA infections associated with pigs and calves have
emerged as a significant concern in Europe. Studies have
identified pig or calf contact as significant risk factors for
both colonization or infection with a specific MRSA strain,
Figure 9-88 n Magnified (×20,000), this scanning electron micrograph called ST398, which has been found in pigs in Europe, Asia,
depicts a grouping of MRSA bacteria. (From Centers for Disease Control and North America.15-17,42 Astoundingly high rates of colo-
and Prevention Public Health Image Library, Atlanta, Ga. Photo Courtesy nization have been identified in pig and cattle farmers.15,16,25
Janice Carr.) There is concern that this strain is now causing infections
beyond direct human contacts and that farm animals
may be an important reservoir of this strain for human
infections.25,48,49
Groups at Risk
The major risk factor for MRSA infection continues to be Mode of Transmission
contact with the health care system, such as a recent hospi-
The risk of transmission between humans and other animals
talization, nursing home stay, or surgery.39 Studies of hos-
may vary by species and type of MRSA (Figure 9-89). One
pital personnel have found MRSA in nasal carriages in 6%
study found evidence of MRSA transmission between dogs
of persons sampled.1 For cases that arise in the community,
and veterinary workers.50 Equine-human zoonotic transmis-
reported risk factors include age younger than 2 years, low
sion has been fairly clearly established.12
socioeconomic status, participation in contact sports, injec-
The mode of transmission in the community is thought
tion drug use, men who have sex with men, military per-
to be primarily by hands that become contaminated by con-
sonnel, inmates of correctional facilities, veterinarians, pet
tact with colonized or infected body sites of other individuals
owners, and pig farmers.40
or fomites contaminated with body fluids containing MRSA.
Other factors contributing to transmission include skin-to-
Hosts, Reservoir Species, Vectors skin contact, crowded conditions, and poor hygiene.51 Risk
factors for acquisition of MRSA are likely to include certain
Although humans are considered the primary host for S.
antimicrobial use in veterinary medicine.
aureus infection, S. aureus is clearly a commensal of many
other species. In addition to skin and soft tissue infection,
pneumonia, and other pathologic conditions, asymptomatic
nasal carriage rates of 30% or greater have been reported.
Previous surveys have indicated that human nasal carriage MRSA can persist on environmental surfaces and has been
rates of MRSA are much lower than for S. aureus in general, cultured from surfaces in veterinary hospitals.4 Despite find-
but this may be changing.41 ing MRSA on various environmental surfaces, evidence
In animals, S. aureus is not as common a pathogen as of surfaces as a source of infection is weak; direct contact
other Staphylococcus species such as S. pseudintermedius with humans or animals is a much more likely route of
(previously referred to as S. intermedius).7 However, recent transmission.
studies have found significant carriage rates of MRSA in
dogs and cats from almost all body sites tested (wounds,
abscesses, and chronic pyodermas). Other animals that
carry MRSA include horses, pigs, elephants, rabbits, cat-
tle, and birds.4,12,14-15,17,21,42,43 Strain-typed MRSA infections Infected
human
found in dogs and cats are typically indistinguishable from being or Susceptible
predominant human strains.3,6,8,44,45 To date, studies have other Direct contact with infected host
shown transmission of MRSA from people to animals animal wound or secretions, contact
and animals to people, but it is not clear whether animals with contaminated
environmental surface
are a significant reservoir for people. However, evidence
suggests that several new MRSA strains may have entered Figure 9-89 n Life cycle, MRSA infection.
Disease in Humans Table 9-45 n MRSA Treatment in Humans and

Other Animals
S. aureus typically causes skin and soft tissue infection,
including furunculosis, folliculitis, and cellulitis. The more Primary
invasive strains of MRSA have been associated with necro- Species Treatment Alternative
tizing pneumonia and necrotizing fasciitis (Color Plate
9-45). Sepsis can occur with any strain. Often the first sign Humans (health care– Vancomycin Teicoplanin,
of infection is a small pustule or area of redness. This can associated) daptomycin,
linezolid,
rapidly progress to a localized abscess or a more generalized dalbavancin,
infection (Color Plate 9-46). TMP-SMX (test
susceptibility first)
Disease in Animals Human (community TMP-SMX double Doxycycline or

acquired): abscess, strength minocycline or
Infection in animals, while often subclinical, can be associ- immunocompetent, clindamycin
afebrile (outpatient
ated with a wide range of opportunistic infections, ranging care)
from skin and soft tissue infections to pneumonia and sep-
sis (Color Plate 9-47). S. aureus causes mastitis in cows, and Abscess with fever TMP-SMX double Clindamycin or
(outpatient care) strength ± doxycycline
milk is a recognized source of S. aureus infection (but not rifampin
MRSA). Surveys of dairy products have detected MRSA in
Pneumonia Vancomycin IV Linezolid IV
milk and cheese.52 Table 9-44 provides comparative clinical
presentations in humans and other animals. Bacteremia, Vancomycin IV Daptomycin IV53
endocarditis, septic
Dogs Chloramphenicol
Diagnosis 33 mg/kg tid
In humans and animals, the cornerstone of diagnosis is cul- Cats Chloramphenicol
ture with appropriate sensitivities. Genotyping can provide 50 mg/kg bid
information about strain type but does not provide any Horses Based on
guidance regarding clinical management. For rapid diagno- susceptibility
testing
sis in human patients, a Gram stain showing gram-positive
cocci in clusters is suggestive of S. aureus infection. This does Cattle Based on
not apply in animals where other Staphylococcus organisms susceptibility
testing
are common.
Some veterinary laboratories may not perform the stud- D-test, Double-disk diffusion; quino/dalfo, quinupristin/dalfopristin; TMP-SMX,
ies necessary to identify a case of staphylococcal infection as trimethoprim-sulfamethoxazole.
S. aureus or MRSA because traditionally S. pseudintermedius
has been a more important pathogen. or D-test should be performed before using this agent.53
Antimicrobial therapy should be based on antibiogram as well
Treatment as patient (e.g., age, renal function) and infection factors (e.g.,
location, organic debris, drug penetration). In most cases,
Table 9-45 outlines treatment guidelines in humans and other MRSA isolates are susceptible to a variety of antimicrobials,
animals. Since clindamycin resistance occurs in some cases, a and commonly used antimicrobials such as chloramphenicol
test for inducible resistance “double D” (double disk diffusion) may be used. Trimethoprim-sulfamethoxazole is often useful;
Table 9-44 n Methicillin-Resistant Staphylococcus Aureus: Comparative Clinical Presentations in Humans

and Other Animals
Species Risk Factors for all Species Clinical Manifestations Laboratory Findings
Humans Contact with a colonized or Soft tissue infection, pneumonia Gram stain showing gram-positive cocci
infected person or animal; in clusters, culture and sensitivity,
Dogs Soft tissue infection
nosocomial contact; poor PFGE, spa typing, latex agglutination
Cats hygiene Soft tissue infection for PBP2a
Horses Soft tissue infection, joint infections,
pleuropneumonia
Cattle Mastitis
Pigs Subclinical carriage, rare skin
infections
PBP2a, Penicillin-binding protein 2a; PFGE, pulsed-field gel electrophoresis.

however, adverse effects (keratoconjunctivitis sicca, arthrop- 20. Hanselman B, Kruth S, Rousseau J, et al. Methicillin-resistant
athy) must be considered. Aminoglycosides are often effec- Staphylococcus aureus colonization in veterinary personnel. Emerg Infect
Dis. 2006;12:1933.
tive but must be administered parenterally. Some isolates may 21. Juhász-Kaszanyitzky E, Jánosi S, Somogyi P, et al. MRSA transmission
appear susceptible to fluoroquinolones in vitro, but this class between cows and humans. Emerg Infect Dis. 2007;13:630.
of drugs should not be used because in vivo response is typi- 22. Manian FA. Asymptomatic nasal carriage of mupirocin-resistant,
cally poor and resistance develops quickly. methicillin-resistant Staphylococcus aureus (MRSA) in a pet dog asso-
ciated with MRSA infection in household contacts. Clin Infect Dis.
There is currently controversy about the use of drugs in a 2003;36:e26.
veterinary setting that are important in human medicine (i.e., 23. Moodley A, Nightingale EC, Stegger M, et al. High risk for nasal carriage
vancomycin, linezolid). Although veterinarians have the ability of methicillin-resistant Staphylococcus aureus among Danish veterinary
to use such drugs in an extra-label fashion, ethical issues about practitioners. Scand J Work Environ Health. 2008;34:151.
the use of these critically important human drugs should be 24. van Duijkeren E, Wolfhagen MJ, Heck ME, et al. Transmission of a
Panton-Valentine leukocidin-positive, methicillin-resistant Staphylococcus
considered, and if used, they should only be used in extreme aureus strain between humans and a dog. J Clin Microbiol. 2005;43:6209.
circumstances when no other options exist and the infection 25. van Rijen MM, Van Keulen PH, Kluytmans JA, et al. Increase in a Dutch
cannot be treated topically or in some other manner. hospital of methicillin-resistant Staphylococcus aureus related to animal
farming. Clin Infect Dis. 2008;46:261.
26. Wulf M, van Nes A, Eikelenboom-Boskamp A, et al. Methicillin-
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ORF
Natasha Rabinowitz, Matthew S. Alkaitis, Lisa Conti, • Encourage barrier protection such as the use of non-
and Peter Rabinowitz porous gloves when handling infected or recently vac-
cinated animals in addition to handwashing.
Other orthopox infections (ICD-10 B08.0) • Encourage animal owners and exhibitors to carefully
monitor their animals and promptly quarantine those
Other names in humans: ecthyma contagiosum, contagious that present lesions or were recently vaccinated.5
ecthyma virus, contagious pustular dermatitis virus, conta-
gious pustular stomatitis, giant orf
Other names in animals: cutaneous ecthyma, scabby mouth
• Consider the diagnosis in humans compared with
disease, sore mouth disease, ovine pustular dermatitis
other life-threatening conditions such as cutaneous
anthrax.
Infection with orf virus is primarily a disease of sheep and
• Counsel at-risk workers regarding the importance of
goats that can significantly affect husbandry operations.
protecting open wounds, using nonporous gloves, and
Transmission of the disease to humans was first recognized in
handwashing when caring for infected or recently vac-
the 1930s1-3 and remains an occupational risk to those who
cinated sheep and goats5-7 and to use caution when
handle these animals, particularly immunocompromised
handling the animal vaccine.
individuals. It is also a hazard in public settings such as pet-
• Counsel immunocompromised individuals or those
ting zoos and county fairs. Recent outbreaks in the United
with chronic skin disorders to avoid contact with
States have underscored the importance of differentiating orf
potentially infected animals.
virus infection from life-threatening or other rare diseases in
• No human vaccine is available.
humans and from other economically significant diseases in
animals such as foot and mouth disease (FMD).
• Consider orf in the differential diagnosis of vesicular
Professionals
lesions, including foot and mouth disease.
• Counsel farmers to remove thistle and harsh brush
from grazing areas, which can reduce skin trauma to
the mouth and muzzle area necessary for transmission
• Provide descriptive epidemiology for the community. of the virus.6
• Educate local veterinary and human health clinicians • Counsel animal owners to refrain from bringing
in risk areas and during high-risk periods about groups infected or recently vaccinated animals to public events
at risk and the signs and symptoms of disease. or shows.
• Educate the public, especially parents, on ways to pre- • Advise PPE and sharps injury prevention for veteri-
vent general transmission of infection on farms and nary staff and farm workers during vaccination and
petting zoos. care of infected animals.
• Encourage handwashing after handling animals. • Ensure that veterinarians and veterinary staff can rec-
• Provide animal owners and exhibitors with the ognize signs of occupational infection and seek care.
Compendium of Measures to Prevent Disease Associated • Report disease to veterinary/agriculture and public
with Animals in Public Settings.4 health authorities as well as occupational health care
• Work with local agricultural authorities to exclude providers caring for at-risk workers.
potentially infected animals from fairs, exhibitions, and • Live, nonattenuated orf virus vaccines are commercially
other locations where cross-infection could occur. available.5 Preparations can also be made from scabs of
previously infected animals. Both types are potentially family Poxviridae with a double-stranded DNA genome
infectious to humans who handle the vaccine, experi- of approximately 140 kb.12 It can be visualized by electron
ence a sharps injury during vaccine administration, or microscopy of negatively stained samples and appears as a
have contact with the vaccine site or recently vaccinated cylinder of roughly 260 × 160 nm with a crisscross pattern
animals.5 Orf virus vaccines are intended to produce characteristic of poxviruses.7,13 Several other related parapox
controlled infection in flocks and will ultimately seed viruses cause zoonotic infections. Paravaccinia virus (also
the environment with virus-containing scabs.6 Thus known as pseudo-cowpox) infect the teats of cattle and cause
vaccination should be used only in previously infected nodular lesions on the hands of dairy workers (milker’s
flocks.8,9 The immunity conferred by current vaccines is nodule).12 Other zoonotic parapox virus infections include
not lifelong and failures have been reported.5 The 2001 bovine papular stomatitis and seal pox.14
USDA National Animal Health Monitoring System
(NAHMS) sheep survey reported that 5% of sheep Geographical Occurrence
operations vaccinated replacement or breeding ewes
and 14% vaccinated nursing lambs.10 In counseling ani- Orf virus is found worldwide with a higher prevalence in
mal owners who are considering vaccinating their live- countries with extensive sheep and goat populations.6-8
stock, veterinary clinicians should: According to the 2001 national USDA NAHMS survey, 40%
 Encourage the vaccination of lambs at ≈1 month of of U.S. sheep operations reported cases of orf infection
age and a second vaccination at 2 to 3 months for within the past 3 years.10 Human cases in recent years have
at-risk lambs.11 been reported in Illinois, Tennessee, Missouri, New York, and
 Provide proper precaution to prevent outbreaks California.5,6 The incidence of human cases reflects the prev-
and transmission to humans associated with alence of infection in sheep and goat populations. However,
vaccine use. cases in humans are probably underreported because those
 Discourage the use of vaccines in flocks that have at risk are often familiar with the disease, recognize that it is
not previously been infected. self-limiting, and choose not to seek medical attention.1,2,16,17
The fact that many laboratories lack the diagnostic capability
for orf virus testing may further contribute to underreport-
Agent
ing of the disease.6
Orf is caused by Parapoxvirus ovis, also known as orf virus
(Figure 9-90). It is a highly epitheliotropic poxvirus of the Groups at Risk
Orf virus is an occupational risk to those who handle sheep
and goats, including farmers, shepherds, veterinarians,
butchers, and abattoir workers.2,16 Wildlife researchers
with contact with wild sheep and goat species are also at
risk. These groups are especially at risk during the primary
lambing season (spring and summer) because young ani-
mals are more susceptible to infection.1,5,12 Those handling
orf vaccines or recently vaccinated flocks are at greater risk
of developing an infection.1,5,6 Children may be at greater
risk in both occupational (e.g., family farm) or recreational
(e.g., petting zoo4) settings because common childhood
behaviors such as nuzzling animals can lead to significant
skin contact or bites.5 Furthermore, children may be less
likely to wash their hands or use gloves than adults.5 Orf has
been reported in conjunction with religious holidays during
which families customarily slaughter a sheep or cow.12,16,17
Contact with wildlife such as deer can also result in trans-
mission to humans.18 Patients with chronic skin disorders
such as eczema are at increased risk for contracting orf
infection.5 Immunocompromised individuals are at risk for
more severe disease.6

Small ruminants including sheep and goats are the predomi-
nant species affected, although infection has been reported
in gazelles, musk oxen, alpacas, camels, deer, reindeer, and
dogs.7,19,20 Wild bighorn sheep (Ovis canadensis) and other
Figure 9-90 n Negative-stained transmission electron micrograph
image depicted the ultrastructural details of an orf virus, a member of the wild sheep and goats can be infected. Certain breeds such
genus Parapoxvirus. (From Centers for Disease Control and Prevention as Boer goats are particularly susceptible to infection.8,19
Public Health Image Library, Atlanta, Ga. Photo courtesy A. Likos.) Humans are accidental hosts.
Infected or Symptoms of infection progress through several stages, each

recently Direct or indirect contact Susceptible lasting approximately a week.2
vaccinated ovines and The maculopapular stage begins with isolated or multi-
ovines and caprines ple erythematous macules and papules appearing at the site
caprines
of contact that may be pruritic. The target stage features the
Infectious scabs development of vesiculonodules characterized by a white
Direct or indirect contact
Contact with soil ring enclosing a red center (Color Plate 9-48). This is fol-
lowed by an acute stage with an erythematous nodule with
weeping, bleeding, and eventual crusting.
Contact with soil Contaminated In immunocompetent patients, the infection is usu-
Human being
environment ally self-limited with full healing without scarring over a
6-week period.5,6,13,16 Bacterial superinfection of the lesions
may occur.7,13 Other reported complications include pain,
Figure 9-91 n Life cycle of orf virus. fever, malaise, erythema multiforme, blindness from ocu-
lar involvement, lymphangitis, and autoimmune pemphi-
gus with bullous eruptions.1,13,17,22-24 Immunocompromised
patients are at greater risk for these complications, in addi-
tion to progressive or recurring “giant” lesions.5,6,8,13 Infection
with orf confers immunity, but reinfection has been reported,
Orf virus is transmitted via direct contact with broken although it is typically less severe.1
skin or mucous membranes (Figure 9-91). Skin trauma is
considered a predisposing factor in both animals9,19,21 and
humans.5,6,9 Modes of transmission between animals include Disease in Animals
contact with infected animals or fomites such as bedding, Although animals of any age are susceptible, the disease is
feed, stalls fences, and trailers.7,8 Because young animals are seen primary in animals younger than 1 year because adult
particularly susceptible due to their developing immune sys- animals are typically immune as a result of previous con-
tems, outbreaks often occur during the principal lambing tact.5 Outbreaks among livestock tend to occur in spring and
season.1,5 Suckling can lead to lesions on the mother’s teats summer.
and cause her to withhold feeding, leading to the spread of Lesions occur primarily on the muzzle, nostrils, ears,
the disease to non-mother adults or to humans via tube- or lips, eyelids, lower legs, buccal mucosa, or teats, especially
bottle-feeding practices.5 when nursing.2 Boer goats may develop suppurative arthri-
Transmission from animals to humans can be facilitated tis, chronic fibrinous pneumonia, and premature thymic
by either minor (thistle pricks, torn cuticle) or severe (ani- involution.19 No loss of appetite or difficulty in nursing
mal bite) skin trauma.5,6 Other human activities that can lead was reported in lambs infected with buccal cavity lesions.21
to infection include shearing, petting, and handling infected Recovery occurs within a month. Some animals may require
equipment.8 Orf virus can persist in wool and hides for over feeding assistance. Animals can be infected more than once
a month after the resolution of lesions, putting butchers, during their lifetime, but infections occur far apart and
abattoir workers, and shearers at risk.7,22 Orf virus vaccine young animals present with the most severe cases.8 Table
is a live, nonattenuated preparation that has been known 9-46 shows comparative clinical presentations in humans
to cause outbreaks among sheep and human handlers.6,7 and other animals.
Human-to-human transmission of orf infection has yet to
be reported.
Diagnosis
Infected animals can shed virus-containing scabs that persist Diagnosis in Humans
in animal housing and other inanimate objects such as har-
The diagnosis of orf in humans can be made clinically
nesses, and pastures.7,8,12 This environmental contamination
based on a history of exposure to sheep or goats and the
can lead to indirect infection of other animals and humans.
presence of characteristic skin lesions. The differential
Although the virus is susceptible to ultraviolet rays, it is resis-
diagnosis includes a number of potentially life-threaten-
tant to desiccation, temperature drops, and other environ-
ing infections, including cutaneous anthrax,5 tularemia,
mental stressors and can survive in the soil and on surfaces
and erysipeloid.5,6 Other similar conditions include milk-
for months.7,13,22
er’s nodule, cowpox, pyogenic granuloma, and skin can-
cer.3,17 Clues to the clinical diagnosis include a history of
Disease in Humans exposure to sheep, goats, deer, and alpacas in petting zoos,
farms, or other settings such as fairs, especially if animals
Initial signs of infection appear at the site of skin penetra- were recently vaccinated or have skin lesions. Laboratory
tion after a 2- to 3-day incubation period. Lesions can reach diagnostic techniques include PCR, electron microscopic
3 cm in diameter and typically occur on the hands or fore- histopathological analysis, and viral isolation, but these
arms, although infection of the face has also been reported.2 tests are not widely available.
Table 9-46 n Orf Virus: Comparative Clinical Presentations in Humans and Other Animals
Incubation
Humans Direct contact with infected 3-7 days Maculopapular eruption PCR, EM, viral isolation
animals; contact with soil progressing to weeping nodule
and objects contaminated by
animals, vaccine exposure
Sheep, goats, Contact with infected or 2-3 days Papules, vesicles, pustules on the PCR, EM, viral isolation
alpaca, camels, recently vaccinated animals or lips, mouth, nostrils, eyelids,
deer contaminated environments ears, extremities
EM, Electron microscopy; PCR, polymerase chain reaction.
Diagnosis in Animals 7. Acha PN, Szyfres B. Zoonoses and communicable diseases common to
man and animals, vol. II: chlamydioses, rickettsioses and viroses. 3rd ed.
Lesions in animals can resemble foot and mouth disease Washington, DC: Pan American Health Organization; 2003.
because both diseases can present as erythematous, ulcerated 8. Centers for Disease Control and Prevention. Frequently asked questions
about sore mouth (orf virus). http://www.cdc.gov/ncidod/dvrd/orf_virus.
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foot and mouth disease is the proliferative nature of the 9. Büttner M, Rziha HJ. Parapoxviruses: from the lesion to the viral
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Inspection Service, Veterinary Services, National Animal Monitoring
System. Sheep 2001, part II: reference of sheep health in the United States,
Treatment 2001. Fort Collins: USDA; 2003.
11. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
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In animals, repellent should be applied to avoid develop- Dermatol. 2002;12:183.
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report of a human case from the United Arab Emirates and review of the
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therapeutics. Pediatr Infect Dis J. 2007;26:740. J Med Virol. 2001;64:543.
6. Centers for Disease Control and Prevention. Orf virus infection in
humans—New York, Illinois, California, and Tennessee, 2004–2005.
MMWR. 2006;55:65.
PLAGUE

Box 9-5 Steps for Rodent-Proofing Homes
Plague (ICD-10 A20)
• Seal rodent entry holes or gaps with steel wool, lath metal, or
caulk.
Other names in humans: bubonic plague, pneumonic plague,
• Trap rats and mice using appropriate snap trap.
septicemic plague, black death • Clean up rodent food sources and nesting sites.
• Keep wood piles and compost heaps away from the house.
Other names in animals: feline plague, rodent plague, syl- • Take precautions when cleaning rodent-infected areas:
vatic plague  Use cross-ventilation when entering a previously unventilated
enclosed room or dwelling before to cleanup.
Yersinia pestis, the agent of plague in humans and other  Use rubber, latex, vinyl, or nitrile gloves.
animals, has caused some of the largest epidemics in his-  Do not stir up dust by vacuuming, sweeping, or any other
tory. Plague continues to be an important and potentially means. Instead, thoroughly wet contaminated areas with
fatal zoonotic disease, with 1 to 40 reported cases each year a bleach solution or household disinfectant. Hypochlorite
(bleach) solution: mix 11⁄2 cups of household bleach in
in the United States associated with rodent and flea contact
1 gallon of water. Once everything is wet, take up contaminated
and occasionally contact with sick cats.1 Worldwide, several materials with damp towel and then mop or sponge the area
thousand cases are reported yearly to the World Health with bleach solution or household disinfectant.
Organization. Y. pestis is a category A potential biological  Spray dead rodents with disinfectant and then double-bag
warfare agent. Despite its fearsome reputation and sensi- along with all cleaning materials and dispose of bag in an
tivity to prompt antibiotic treatment, delays in diagnosis appropriate waste disposal system.
of plague in both humans and animals are frequent, often  Remove gloves and thoroughly wash hands with soap and
with tragic consequences. There is a continuing need for water (or waterless alcohol-based hand rubs when soap is not
heightened awareness of the disease, especially in enzootic available and hands are not visibly soiled).
areas.
• Ensure that workers with occupational risk for Y. pestis

Key Points for Clinicians and Public Health infection receive adequate surveillance and reduction
Professionals of exposure risk through exposure controls and pro-
tective equipment.
• A plague vaccine is being developed.
• Provide descriptive epidemiology of the disease in Human Health Clinicians
the health district. Use of GIS risk mapping has been
• Consider the diagnosis in all patients with recent travel
helpful in determining areas of high risk for endemic
or residence in an enzootic area, with occupational
plague.2
exposure (such as veterinarians or wildlife workers),
• Educate the public about measures to reduce risk,
history of handling rodents, rabbits, or flea bites, as
including the following:
well as the possibility of deliberate use.
 Control rodents and their fleas near dwellings (flea
• Report disease immediately to public health authori-
control should precede rodent control to prevent
ties using the CDC case definition (see http://www.cdc.
fleas from seeking new hosts); Box 9-5 lists steps for
gov/ncphi/disss/nndss/casedef/plague_current.htm).
rodent-proofing homes.
CDC, Fort Collins, is a WHO Collaborating Center for
 Avoid camping near rodent burrows.
Reference and Research on Plague Control, and reports
 Avoid handling wild rodents (plague in the United
all human plague cases in the United States to the WHO.
States is strongly associated with ground-dwelling
• Ensure patients are hospitalized with drainage and
sciurid rodents, such as various species of prairie
secretion precautions (bubonic plague) and main-
dogs and their fleas).
tain droplet precautions until 48 hours of appropriate
 Use flea control on cats and dogs.
antibiotic treatment has been completed with clinical
 Prevent pets from hunting.1
improvement (including defervescence).
• Conduct an immediate investigation of human, cat,
• Counsel patients in endemic areas with rodent expo-
or dog cases; consider the possibility of deliberate use
sure or with cats or dogs in risk reduction measures,
(biological warfare).
including regular use of flea control (see above).
• Ensure flea control in an outbreak situation before ini-
tiating rodent control measures.
• Ensure that persons with exposure to cases of pneu- Veterinary Clinicians
monic plague or other high-risk exposures (including
exposures to cats with plague) are receiving antibiotic • Consider the diagnosis in any sick cat from an enzo-
prophylaxis (see below) and are maintained under sur- otic area with fever, lymphadenopathy, and abscesses
veillance for 7 days. on the head and neck or progressive respiratory signs
accompanied by other systemic signs. The submandib- October, when temperatures favor transmission from the fleas
ular lymph node is the most common site of lymph- and potential human and rodent interactions are higher.5
adenopathy due to the inoculation of the oral mucosa
from ingestion of plague-infected rodents. Hosts, Reservoir Species, Vectors
• Train veterinary personnel in biosafety measures such
as masks and gloves when working with potentially Worldwide, an important reservoir for Y. pestis is domestic rats
infected animals. N-95 respirators are recommended.3 (R. rattus and R. norvegicus), especially in urban settings. In the
• Treat animals at the veterinary hospital for 48 to 72 United States, however, wild rodents are the principal reservoir
hours and observe clinical improvement (including species, including ground squirrels, rock squirrels, and prairie
defervescence) before allowing animal to be treated at dogs.9 In many of these species, susceptible individuals develop
home. This will ensure that owners will not be exposed the disease and significant die-offs among colonies of some spe-
to infectious saliva and other secretions when handling cies of prairie dogs are well documented (Color Plate 9-50).10
or treating their pet. Black-footed ferrets, an endangered species, can become infected
• Isolate and control fleas on suspected cases while treat- from preying on prairie dogs.4 Risk of exposure to fleas infected
ing with antibiotics. by Y. pestis is elevated in areas adjacent to rodent colonies experi-
• Follow local and state reporting regulations; contact encing widespread mortality, and these die-offs provide a warn-
local health department immediately regarding sus- ing of infection risk to humans and domestic animals.
pected animal cases. Fleas are the principal vector of plague. Urban plague has
• Recommend keeping cats indoors. been linked to exposure to the oriental rat flea Xenopsylla
• Counsel clients not to let cats and dogs roam outside cheopis (Color Plate 9-51), which commonly infests Rattus
or otherwise come in contact with wildlife in endemic species. Fleas, once infected, may remain infectious for a
areas, and to treat monthly to control and prevent flea year or longer.11 Both male and female fleas can transmit
infestations. the infection. Wild rodent fleas vary by species in their abil-
• Store animal food in rodent-proof containers. ity to be effective vectors. Cat fleas (Ctenocephalides felis)
• A plague vaccine for use in endangered black-footed are considered poor vectors for plague.3,11 The human flea
ferrets has been developed and used.4 (Pulex irritans) may spread the infection between humans in
situations of crowding and poor sanitation.11
Agent
Y. pestis is a gram-negative, bipolar staining, nonmotile bacil-
lus that is a member of the family of Enterobacteraciae.5 The Plague is spread through flea bites, direct contact with an
CDC classifies Y. pestis to be a category A biological warfare infected animal, and by inhalation of infectious aerosols
agent due to its ability to be produced and disseminated in (Figure 9-92).12,13 Fleas that have ingested a blood meal from
quantities sufficient to affect large populations and its high an infected host can then infect another animal through a bite.
case fatality rate among untreated persons. It is believed that
deliberate use of the agent would be in an aerosol form.6
Inhalation of
Geographical Occurrence droplets
Humans from Humans
Plague occurs in localized areas on most continents, with coughing
most cases being reported in less-industrialized countries patients
(Color Plate 9-49). Some cases in developing countries are
related to rats and their fleas in urban areas (urban plague). In Bites of Direct Inhalation of
the United States, most cases occur in rural areas west of the rodent handling of respiratory
fleas animal secretions
Mississippi, where the disease exists in wild (ground-dwell- tissues (cats)
ing) rodent reservoirs (sylvatic plague)—New Mexico, Idaho,
Colorado, Nevada, Oregon, Texas, Arizona, California, Utah,
Washington, and Wyoming. Mapping of rodent habitat in the Animal reservoirs:
Southwestern United States has successfully identified areas Rats, ground squirrels, prairie
of increased human risk related to conifer forests and amount dogs, field mice, bobcats, cats,
rabbits, chipmunks, camels
of precipitation. Much of the area of increased plague risk in
the Southwest overlaps with risk areas for hantaviral infec-
tion, another rodent-borne disease.7
Ingestion of contaminated
Groups at Risk animal tissues
Groups at increased risk for Y. pestis infection include hunt- Bites of fleas
ers, veterinarians, mammalogists, campers, hikers, Native
Americans, owners of cats allowed to roam free, and rural Figure 9-92 n Transmission of plague. The wide arrows indicate common
residents in enzootic areas. A significant number of cat-asso- modes of transmission, the medium arrows indicate occasional modes of
transmission, and the thin arrow indicates a rare kind of transmission. (From
ciated human cases have occurred among veterinarians and Mandell GL (ed): Mandell, Douglas, and Bennett's principles and practice of
veterinary assistants.3,8 Most U.S. cases occur between May and infectious diseases, ed 7, Philadelphia, 2010, Churchill Livingstone Elsevier.)
The usual source of human infection is a bite from an Cats are known to be susceptible to plague and can exhibit
infected flea or direct handling of an infected animal car- bubonic, pneumonic, or septicemic forms of the disease.
cass. Dogs and cats may bring fleas into a home where they Bubonic plague of the head and neck is the most common
can bite humans. Infected cats with pneumonic plague are form in cats following bites from infected flea or consump-
a source of respiratory spread to humans. Person-to-person tion of infected rodents (Color Plate 9-54).15 Secondary sep-
transmission through infectious aerosols occurs when there ticemic or pneumonic plague can also develop in cats; this
is respiratory involvement but has not been documented in form has led to primary pneumonic plague infection of
the United States since 1924. humans in close contact with such cats (Figure 9-93). Signs
in cats include fever, malaise, cough, and buboes. Without
treatment, feline plague can be fatal in a substantial propor-
tion of cases. Wild felids such as bobcats and mountain lions
The bacterium does not appear to survive long outside a are also susceptible to plague.
mammal host. It can be destroyed by sunlight and drying.14 Although dogs are less likely to develop clinical illness
Environmental factors influencing the risk of plague include than cats, signs of infection have been documented in three
those driving increases in rodent populations. Human habi- naturally infected dogs in New Mexico (Color Plate 9-55).16
tation encroachment into wildlife habitat is an environmen- Clinical signs included fever, lethargy, submandibular
tal driver of infection risk, because it leads to contact between lymphadenitis, a purulent intermandibular lesion, oral cavity
wild rodent reservoirs of the infection and their fleas and lesions, and cough. In dogs, antibodies to plague appear by
peridomestic rodents. Dogs and cats may contribute to this day 8, peak by day 21, and decline by day 100 after exposure.
wildlife-human contact by bringing fleas into dwellings. This characteristic, combined with their relative resistance to
clinical illness, makes dogs potentially useful as sentinels for
plague risk in enzootic areas.
Disease in Humans
Table 9-47 summarizes the clinical presentations of plague
There are several forms of human plague infection: in humans and other animals.
• Bubonic plague usually results from a flea bite or direct
contact with an infected animal. There can be a local reac-
tion at the site of the bite. After 2 to 6 days, fever, weak- Diagnosis
ness, and malaise develop with lymphadenopathy. The The differential diagnosis of bubonic plague in humans
swollen, extremely tender lymph nodes (buboes) typi- includes other causes of acute lymphadenopathy, including
cally occur most commonly in the groin, neck (rarely), bartonellosis (cat-scratch disease), staphylococcal abscess,
or axilla and are often unilateral (Color Plate 9-52). tuberculosis, and lymphogranuloma venereum. The rapid
Bacteremia is common. Without treatment, bubonic onset and associated symptoms should help the clinician
plague can progress to sepsis, shock, and death. make the diagnosis. Pneumonic plague can resemble other
• Primary septicemic plague may develop without rapidly progressive pneumonias. A history of exposure to
buboes. This form has a higher fatality rate than fleas, rodents, sick cats, or wild carnivores can be help-
bubonic plague, possibly because of delays in diagno- ful, as well as any information of recent outbreaks among
sis. Hypotension and disseminated intravascular coag- animals or humans where the person lives or has recently
ulation can occur with shock and organ failure (Color traveled.
Plate 9-53). Samples of blood and wound drainage should be sent for
• Pneumonic plague may result from secondary spread to culture and chest x-rays films should be obtained. A national
the lungs of bubonic plague or from primary infection network of laboratories has been established for rapid
caused by contact with a human or cat with respira-
tory involvement. Most cases of primary pneumonic
plague in the United States are currently related to
exposure to infected cats.8 Pneumonic plague is highly
fatal and can lead to further horizontal transmission to
close contacts through respiratory spread.
• Pharyngeal plague also results from respiratory infec-
tion and is characterized by sore throat, pharyngitis,
and local lymphadenopathy.
• Meningeal plague is rare but may be a complication of
bubonic plague.5
Disease in Animals
Although certain subpopulations of the rodent hosts of the
disease are apparently resistant to developing clinical infec-
tion, other individuals are susceptible, so that high mortality
Figure 9-93 n Thoracic radiograph of a cat with pneumonic plague.
rates can occur. In these latter groups, such as prairie dogs, (From Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006,
monitoring acute mortality can help predict plague activity Saunders Elsevier. Courtesy Dennis Macy, Colorado State University, Fort
in an area. Collins.)
Table 9-47 n Plague: Comparative Clinical Presentations in Humans and Other Animals
Humans
Bubonic plague Flea bite, contact with 2-7 days Fever, lymphadenopathy Elevated WBC count, abnormal
Septicemic plague infected animal liver function tests, culture of
Fever, hypotension, DIC blood, DFA of LN aspirate
Pneumonic plague Infectious aerosol 1-4 days1 Cough, hemoptysis, fever Abnormal coagulation studies
Pharyngeal plague Sore throat, pharyngitis, cervical Pulmonary infiltrates on x-ray
lymphadenopathy
Plague meningitis Can result from Meningeal signs WBCs in CSF
bubonic plague
Cats
Bubonic plague Flea bites, ingestion of 2-7 days Lymphadenopathy with cellulitis Culture of blood, lymph node
(pneumonia may rodent on head and neck, abscess biopsy or aspirate, DFA of LN
accompany) formation, drainage, fever, aspirate
depression, dehydration, Serology HI (may persist more
anorexia, oral ulcers than a year in surviving animals)
Septicemic plague Fever, depression, vomiting
Pneumonic plague Inhalation of infectious Fever, cough, bloody sputum3
aerosol
Dogs Flea bites 7-10 days17 Often subclinical, mild fever, Serology HI
depression
Rodents, Rabbits Flea bites Days May be subclinical in a minority
of cases
Death
CSF, Cerebrospinal fluid; DIC, disseminated intravascular coagulation; DFA, direct immunofluorescence antibody; HI, hemagglutination inhibition; LN, lymph node; WBC,
white blood cell.
iagnosis of plague, and consultation should be obtained

d large and fluctuant they may require incision and drainage.
regarding the appropriate testing facility to process speci- Supportive care with intravenous fluids and close hemody-
mens. In bubonic plague, the bubo can be aspirated and sent namic monitoring is necessary for most patients.
for Gram stain, Wayson stain, DFA, and culture.5 PCR tests Persons with close contact with a patient or animal with
may be available. Diagnosis can be confirmed by serology pneumonic plague or other potential exposures (bite from a
obtained acutely and after several weeks showing a fourfold cat with potentially infectious saliva, bubo drainage in an open
rise in titer, a single titer greater than 1:128,18 or by positive wound, and so on) should receive antibiotic prophylaxis and
bacteriophage testing from a culture isolate. surveillance for symptoms for 7 days after exposure ceases.
In animals, culture and DFA of tissues antibody serology
testing are the mainstays of diagnosis. Diagnostic samples Treatment in Animals
can include wound drainage, lymph node aspirates, blood,
and necropsy specimens biopsy of liver, lung, spleen, or bone Infected cats should be hospitalized, isolated, and have
marrow. If there is evidence of respiratory involvement, a immediate flea treatment with imidacloprid or pyrethrin.
pharyngeal swab can be performed. Specimens should be Antibiotics should be begun immediately and intravenous
kept chilled.3 fluids and other supportive measures used aggressively. Cats
with the pneumonic form of the disease should be con-
sidered for euthanasia if adequate infection control is not
Treatment available in a veterinary hospital because of the infectious
nature of the respiratory droplets and the high fatality rate
of primary pneumonic plague.17 Table 9-48 lists recommen-
Treatment in Humans dations for antibiotic treatment of plague in humans and
Treatment in human beings with antibiotics should be begun animals.
as soon as the diagnosis is suspected. Patients should be
hospitalized in an intensive care unit with wound drainage References
and droplet precautions until 48 hours of appropriate anti-
biotics with clinical improvement (including defervescence). 1. Heymann DL, ed. Control of communicable diseases manual. 19th ed.
Although streptomycin has the greatest proven efficacy, it is 2. Eisen RJ, Reynolds PJ, Ettestad P, et al. Residence-linked human plague
not widely available in the United States, and gentamicin or in New Mexico: a habitat-suitability model. Am J Trop Med Hyg.
doxycycline may be used (Table 9-48).19 If buboes become 2007;77(1):121.
5. Mandell GL, Bennett JE, Dolin R. Principles and practice of infectious

Table 9-48 n Treatment of Plague Infection in diseases. 6th ed. Philadelphia: Churchill Livingstone Elsevier; 2005.
Humans and Other Animals 6. Centers for Disease Control and Prevention. Biological and chem-
ical terrorism: strategic plan for preparedness and response.
Primary Alternative Recommendations of the CDC Strategic Planning Workgroup.
Species Treatment Treatment MMWR. 2000;49:1.
7. Eisen RJ, Glass GE, Eisen L, et al. A spatial model of shared risk for
plague and hantavirus pulmonary syndrome in the southwestern United
Humans (adult) Gentamicin Doxycycline 200 mg States. Am J Trop Med Hyg. 2007;77(6):999.
5 mg/kg × 1, then 100 mg 8. Gage KL, Dennis DT, Orloski KA, et al. Cases of human plague
IV q24h or PO or IV or associated with exposure to infected domestic cats. Clin Infect Dis.
streptomycin ciprofloxacin 500 2000;30:893.
15 mg/kg gm mg PO bid, or 400 9. Centers for Disease Control and Prevention. Plague fact sheet. http://
IV bid mg IV q12h, or www.cdc.gov/ncidod/dvbid/plague/facts.htm.
gentamicin plus 10. Cully Jr JF, Barnes AM, Quan TJ, et al. Dynamics of plague in a
doxycycline Gunnison’s prairie dog colony complex from New Mexico. J Wildlife
Prophylaxis (close Doxycycline 100 Ciprofloxacin 500 Dis. 1997;33:706.
contact with mg PO bid × 7 mg PO bid × 7 11. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
infected animal days20 days20 and animals, vol. I: bacterioses and mycoses. 3rd ed. Washington, DC:
or human) Pan American Health Organization; 2003.
12. Webb CT, Brooks CP, Gage KL, et al. Classic flea-borne transmission
Cats Immediate flea does not drive plague epizootics in prairie dogs. Proc Natl Acad Sci USA.
treatment 2006;103(16):6236.
Imidacloprid 13. Wilder AP, Eisen RJ, Bearden SW, et al. Oropsylla hirsuta (Siphonaptera:
Bubonic form Tetracycline 25 mg/ Doxycycline Ceratophyllidae) can support plague epizootics in black-tailed prairie
kg PO q8h × 10 dogs (Cynomys ludovicianus) by early-phase transmission of Yersinia
days; parenteral pestis. Vector Borne Zoonotic Dis. 2008;8(3):359.
7.5 mg/kg q12h 14. Colville J, Berryhill D. Handbook of zoonoses: identification and preven-
Chloramphenicol tion. St Louis: Mosby Elsevier; 2007.
30-50 mg/kg PO 15. Eidson M, Thilsted JP, Rollag OJ. Clinical, clinicopathologic, and patho-
q8h21 logic features of plague in cats: 119 cases (1977–1988). J Am Vet Med
Assoc. 1991;199(9):1191.
Pneumonic Euthanasia if 16. Orloski KA, Eidson M. Yersinia pestis infection in three dogs. J Am Vet
form infection control Med Assoc. 1995;207:316.
is inadequate 17. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
Dogs Flea treatment panion: canine and feline infectious diseases and parasitology. Ames, IA:
Antibiotic treatment Blackwell; 2006.
generally not 18. St. Louis University School of Public Health: Institute for Biosecurity.
necessary Bioterrorism agent fact sheet: plague/Yersinia pestis. http://bioterrorism.
slu.edu/bt/quick/plague01.pdf.
19. Boulanger L, Ettestad P, Fogarty J, et al. Gentamicin and tetracyclines
for the treatment of human plague: a review of 75 cases in New Mexico,
3. Centers for Disease Control and Prevention. Emergency preparedness 1985–1999. Clin Infect Dis. 2004;38(5):663.
and response: plague: veterinary issues: dogs and ungulates. http://www. 20. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
bt.cdc.gov/agent/plague/trainingmodule/7/04.asp. microbial therapy. 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
4. Rocke TE, Mencher J, Smith SR, et al. Recombinant F1-V fusion protein 2009.
protects black-footed ferrets (Mustelae nigripes) against virulent Yersinia 21. Tilley LP, Smith FWK. Blackwell’s five-minute veterinary consult: canine
pestis infection. J Zoo Wildl Med. 2004;35:142. and feline. 4th ed. Ames, IA: Blackwell; 2008.
Q FEVER
Peter M. Rabinowitz and Lisa A. Conti ersistence has been considered a potential bioterrorism agent.
p
The true impact of Q fever as a zoonotic disease is probably
Q fever (ICD-10 A78) underrecognized because of the nonspecific nature of the ill-
ness in many cases.
Other names in humans: query fever, coxiellosis, abattoir
fever, Australian Q fever, nine-mile fever, quadrilateral fever,
Balkan influenza1
Professionals
Other names in animals: coxiellosis
Q fever is a disease caused by Coxiella burnetii that has a reservoir
in a number of animal species. It is spread to humans by direct • Human disease is reportable to public health
contact, most commonly through inhalation of organisms but authorities.
also possibly through ingestion or other intake routes. It causes • In the event of a case report, determine whether others
potentially serious disease in a proportion of people infected, are at risk and whether there is an ongoing risk of expo-
and because of its high infectiveness and environmental sure (consider bioterrorism potential of this agent).
• Recommend cleaning sources of contaminated soils

and dusts from the environment (understanding that
the organism is highly resistant to chemical and physi-
cal agents) and disinfection with 0.05% hypochlorite,
5% peroxide, or 1:100 Lysol solution.2
• Educate the public, veterinarians, and human health cli-
nicians about risk factors for transmission; organisms
localize in reproductive and mammary tissues and can be
also be shed in urine and feces and spread by ticks (viable
organisms have been recovered from tick feces after 19
months and after 42 months in milk at 4° to 6°C).2
• Support the maintenance of milk pasteurization to
prevent infection in the general population.
Figure 9-94 n Electron photomicrograph of Coxiella burnetii–infected
Human Health Clinicians caprine placenta. (From Songer JG, Post KW: Veterinary microbiology: bac-
terial and fungal agents of animal disease, St Louis, 2005, Saunders Elsevier.
• Report human disease to public health authorities. Courtesy Raymond E. Reed.)
http://www.cdc.gov/ncphi/disss/nndss/casedef/q_
fever_2008.htm.
• Consider diagnosis in high-risk individuals such as
persons with occupational exposure. Francisella, and Rickettsiella) (Figure 9-94). The organism is
• Consider in the differential diagnosis of patients pre- highly infectious, with an infective dose of 1 to 10 organ-
senting with culture-negative endocarditis. isms.3 It exists in two different antigenic phases, and the
• Provide occupational preventive services to high-risk human antibody response generated to each antigen phase
individuals, including counseling on PPE and bio- can be used to assess progression of infection. Phase II anti-
safety, as well as consideration of vaccine. Persons with bodies are more predominant in humans experiencing acute
valvular heart disease should not work in laboratory infection, whereas phase I antibodies are proportionately
settings with C. burnetii. more common in chronic disease states, such as endocardi-
• Vaccine: a vaccine has been developed for high-risk tis.4 There are also at least two different morphologic forms
individuals in Australia but is limited to those at high of the bacteria; one is large and bacilliform, another is small
risk of exposure and who have no demonstrated sensi- and coccoid. The small, high-density form (small cell vari-
tivity to Q fever antigen.3 The vaccine is not currently ant [SCV]) has some resemblance to a spore in terms of its
available in the United States either commercially or hardiness; it is highly resistant to environmental degradation
through an investigational new drug permit. and therefore plays an important role in transmission.
• Person-to-person transmission is rare but has been
reported through sexual contact and to health care staff Geographical Occurrence
during obstetrical procedures on infected patients.
C. burnetii occurs worldwide. It is probably more prevalent
than recognized owing to the often subclinical nature of
disease in humans and animals and the difficulty with labo-
• Instruct owners and any others in contact with infected ratory diagnosis. In 2000, cases were reported in California,
animals to immediately seek medical advice. Colorado, Idaho, Kansas, Minnesota, Nebraska, Nevada,
• Segregate parturient animals and destroy (burn or Oregon, and Utah.
bury) placentas and other reproductive discharges to
reduce transmission. Groups at Risk
• Ensure veterinary staff follow proper biosafety proce-
dures, including around parturient animals. Q fever often occurs as an occupational disease. Workers at
• Isolate infected animals and implement airborne trans- risk include slaughterhouse workers; veterinarians and vet-
mission precautions for staff. erinary staff; farmers; researchers working with pregnant
• Ensure that ruminants used for research purposes are animals, especially sheep; and workers in diagnostic labora-
free of C. burnetii through serological testing. tories where the organism may be cultured. However, even
• A vaccine for livestock has been developed and shown to casual contact with farm environments or farm animals can
reduce infection in calves and reduce shedding in previ- lead to infection. Also, because the agent may be spread on
ously infected animals. However, the vaccine is not cur- dust, persons living near high-risk areas may be at risk for
rently commercially available in the United States. infection through windborne spread.
Although it is less commonly reported among chil-
dren than adults, Q fever does occur in children, especially
Agent
among those exposed to farm animals and farm environ-
Q fever is caused by Coxiella burnetii, a gram-negative ments for even brief amounts of time.5 Children can also be
obligate intracellular, coccobacillus organism in the gamma infected by drinking raw milk, although they are typically
subdivision of Protobacteria (along with Legionella, asymptomatic.
Exposure to parturient cats has caused outbreaks in Infected host

Inhalation of aerosol
Nonimmune
humans in the past among pet owners and their families.6 containing bacteria,
animal contaminated dairy foods human being
Hosts, Reservoir Species, Vectors Inhalation of aerosol

containing bacteria
Animals are the natural reservoir for C. burnetii. It is found Inhalation of
worldwide in sheep (Figure 9-95), cattle, goats, birds, dogs, organism, Tick-borne Environment
ingestion transmission
and cats. Serological evidence of past exposure has also been of tissue
(dusts)
shown in a variety of wild mammals. In the United States,
seroprevalence studies have shown antibodies in more than
Infected host animal
40% of sheep, 16% of goats, and 3% of cattle.7 A study in (definitive host)
Colorado found that more than 8% of female cats studied
had evidence of C. burnetii in uterine tissue, raising the issue
of risk to owners during birthing. A study in Asian cats found
seroprevalence rates of up to 41% in stray cats and 14% in Environmental factors: Proximity to farms Proximity to forests
pet cats.8 However, the risk of pet-to-human transmission
Figure 9-96 n Life cycle, Q fever infection.
may be low, as an Austrian seroprevalence study did not
find that pet ownership was a risk factor for seropositivity
to C. burnetii.9 The agent can be found in a number of species of ticks,
but tickborne transmission is believed to be more important
in wildlife populations than in domestic animal or human
Mode of Transmission and Life Cycle infection.1 However, the patterns of C. burnetii infection in
Animals infected with C. burnetii shed high concentra- wildlife remain poorly understood.
tions of the organism in birth products and milk, as well as
lower concentrations in feces and urine (Figure 9-96). The Environmental Risk Factors
organism can be tickborne in animal-to-animal transmis-
sion, but transmission from animals to humans is thought Coxiella can persist for months in the environment. The SCV
to result mostly from inhalation of droplets and/or aero- form of the bacteria that is shed in feces and other body flu-
sols containing organisms from infected placental tissue, ids is similar in some ways to a spore and quite resistant to
other parturient tissues, and dusts containing dried body disinfectants and temperature extremes. Therefore infectious
fluids. The organism is found commonly in raw milk with particles can persist in fomites and dusts, and aerosol trans-
reported prevalence of >94%.10 Milk pasteurization has been mission has occurred over long distances through windborne
designed specifically to destroy this heat-resistant organ- spread.1 Proximity to farms is a risk factor for infection, as
ism. Foodborne transmission to humans may occur rarely wind patterns appear to play a role in environmental trans-
through unpasteurized milk. Transmission in domestic ani- mission by dispersing infectious aerosols over wide areas.11
mals is thought, as in humans, to occur mostly through Although the role of wildlife is not well understood, living
inhalation of infectious aerosols or ingestion of contami- near forested areas has been found to be a risk factor for
nated tissue. suburban dwellers.12
Figure 9-95 n Infected sheep have been associated with outbreaks of Q fever in humans. (From Centers for
Disease Control and Prevention Public Health Image Library, Atlanta, Ga. Courtesy Edwin P. Ewing, Jr.)
Table 9-49 n Q Fever Infection: Comparative Clinical Presentations in Humans and Other Animals
Humans High-risk occupation 2-3 weeks (acute form) Fever, malaise, chills, sweats, Serology, stained tissue
headache; hepatomegaly, (blood culture from
abortion, placentitis endocarditis patients
typically negative)
Elderly, debilitated, Months to years (chronic Chest pain
underlying valvular infection)
disease
Dogs Tick exposure, contact with Fever, neurological PCR in some laboratories,
farm animals syndrome with vasculitis, serology (ELISA), and
including lethargy, complement fixation
anorexia, ataxia, seizures
Cats Tick exposure, contact with Anorexia, lethargy, fever,
farm animals abortion
Cattle, sheep, Inhalation of infectious Anorexia, abortion
goats aerosols
ELISA, Enzyme-linked immunosorbent assay; PCR, polymerase chain reaction.
greater than 1:128 suggest acute infection.11 A PCR test has

Disease in Humans
been developed to aid in diagnosis.14 In chronic infection,
Q fever can present with acute or chronic symptoms (Table high levels of phase I antibody titers (IgG >1:800) are seen,
9-49). Some cases in humans are asymptomatic or consist of and phase I antibody titers are usually greater than phase II
sufficiently nonspecific symptoms, which results in missed titers. Blood cultures appear sterile because of the need for
diagnoses. After an incubation period of several weeks, the dis- intracellular cultivation. Although cell culture and embryo-
ease in its acute form often presents with fever, malaise, chills, nated egg methods exist to culture the organism from blood,
weakness, headache, and sweats. Pneumonia is a predomi- laboratory workers are at risk of infection through such pro-
nant feature, although pulmonary symptoms may be absent cedures, which should not be attempted outside a specialized
even though pneumonitis may be seen on radiographs (Figure laboratory experienced in handling the C. burnetii organism.
9-97).4 Chronic symptoms may develop over months to years. The CDC can provide assistance in isolation. C. burnetii is
Chronic infection may include granulomatous hepatitis, men- considered a “select agent,” so handling of live organisms in
ingitis, and osteomyelitis. The most serious form of chronic a laboratory setting is restricted. On biopsy tissue, immunos-
infection is bacterial endocarditis, which occurs particularly in tains and electron microscopy can be diagnostic for the C.
persons with underlying valvular disease (Color Plate 9-56). burnetii organism.4
Infection in children can often be asymptomatic but can also Serological testing is also used in animals. A fourfold
present acutely, with encephalitis and neurological symp- increase in IgG over a 4-week period is diagnostic.16 Tissue
toms.13 In convalescent individuals, a postinfectious fatigue (aborted fetus, placenta) can be submitted for immuno-
syndrome (fever fatigue syndrome) has been described.4 histochemical testing. The organism can be isolated from
blood in specialized test laboratories (New Mexico Department
of Agriculture, Veterinary Diagnostic Services).16
Disease in Animals
Animals typically do not manifest clinical signs with the excep-
tion of reproductive disease, especially abortion, infertility, Treatment
and retained placenta (see Table 9-49; Color Plate 9-57).
Because infection often goes unrecognized in animals human Acute Q fever is treated with doxycycline as a first-line
illness may serve as sentinel events, indicating the presence of agent. Chronic infection, including infective endocarditis in
infection in a domestic animal population.14 humans resulting from Q fever, is treated with a combination
of antibiotics for an extended time (18 months to 3 years).
Although information on the efficacy of treatment in
Diagnosis animals is limited, prophylactic treatment of endemic herds
(or asymptomatic pets) with tetracyclines may reduce the
The diagnosis in humans is usually made by serology. A rise zoonotic potential (rather than eliminate infection).17
in titers is seen in acute infection. Because the prevalence of Other control measures include segregating pregnant ani-
antibody positivity in certain populations is relatively high, it mals indoors and burying or burning infected reproduc-
is necessary to examine paired serological titers. Laboratories tive tissue wastes.7 Table 9-50 provides antibiotic treatment
interpreting serological results need to use caution; misdiag- information for Q fever infection in humans and other
nosis has resulted from improper interpretation.15 IgM levels animals.
Figure 9-97 n Radiographic manifestations of Q fever pneumonia. All four patients are members of one family
who developed Q fever after exposure to the infected products of feline conception. Their cat gave birth to kittens in
their house. A, Multiple rounded opacities. B, Left upper lobe opacity. C, Pleural-based opacity involving the right
upper lobe. D, Right lower lobe opacity. In an endemic area A is characteristic of cat-related Q fever pneumonia,
and C is suggestive of this diagnosis. However, B and D are not at all distinctive and could be due to any pulmo-
nary pathogen. (From Mandell GL, Bennett JE, Dolin R [eds]: Principles and practice of infectious diseases, ed 6,
Philadelphia, 2005, Churchill Livingstone Elsevier.)
References Public Health, Iowa State University College of Veterinary Medicine;

2008.
1. Acha PN, Szyfres B. Zoonoses and communicable diseases common to 3. U.S. Department of Health and Human Services, Centers for Disease
man and animals, vol. II: chlamydioses, rickettsioses and viroses. 3rd ed. Control and Prevention, National Institutes of Health. Biosafety in
Washington, DC: Pan American Health Organization; 2003. microbiological and biomedical laboratories. 4th ed. Washington, DC: US
2. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic dis- Government Printing Office. Available at http://www.cdc.gov/od/ohs/
eases of companion animals. Ames, IA: The Center for Food Security and biosfty/bmbl4/bmbl4toc.htm, Accessed February 14, 2009.

Table 9-50 n Antibiotic Treatment of Q Fever Washington, DC: American Public Health Association; 2008.
Infection in Humans and Other 5. Barralet JH, Parker NR. Q fever in children: an emerging public health
issue in Queensland. Med J Aust. 2004;180(11):596.
Animals 6. Pinsky RL, Fishbein DB, Greene CR, et al. An outbreak of cat-associated
Q fever in the United States. J Infect Dis. 1991;164(1):202.
Species Primary Treatment Alternative Treatment 7. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
Humans: acute Doxycycline 100 mg Erythromycin 8. Komiya T, Sadamasu K, Kang MI, et al. Seroprevalence of Coxiella bur-
disease bid netii infections among cats in different living environments. J Vet Med
Sci. 2003;65(9):1047.
Chronic Ciprofloxacin or Fluoroquinolone PLUS
9. Skerget M, Wenisch C, Daxboeck F, et al. Cat or dog ownership and
disease doxycycline PLUS doxycycline × 3 yr
seroprevalence of ehrlichiosis, Q fever, and cat-scratch disease. Emerg
rifampin
Infect Dis. 2003;9(10):1337.
Endocarditis Doxycycline 100 mg Pregnancy: need 10. Kim SG, Kim EH, Lafferty CJ, et al. Coxiella burnetii in bulk tank milk
PO bid PLUS long-term TMP- samples, United States. Emerg Infect Dis. 2005;11:619.
hydroxychloroquine SMX18 11. Tissot-Dupont H, Amadei MA, Nezri M, et al. A pedagogical farm as a
600 mg qd × source of Q fever in a French city. Eur J Epidemiol. 2005;20(11):957.
1-3 yr18 12. Gardon J, Heraud JM, Laventure S, et al. Suburban transmission of
Q fever in French Guiana: evidence of a wild reservoir. J Infect Dis.
Acute disease Doxycycline Erythromycin 2001;184(3):278.
Chronic Ciprofloxacin or Fluoroquinolone PLUS 13. Ravid S, Shahar E, Genizi J, et al. Acute Q fever in children presenting
disease doxycycline Doxycycline × 3 yr with encephalitis. Pediatr Neurol. 2008;38(1):44.
14. Cutler SJ, Bouzid M, Cutler RR. Q fever. J Infect. 2007;54(4):313.
Dogs Tetracycline 22 mg/kg Doxycycline 20 mg/ 15. Conti LA, Belcuore TR, Nicholson WL, et al. Pseudoepidemic of Q fever at
PO q8h × 2-6 wk kg PO q12h × 1wk an animal research facility. Vector Borne Zoonotic Dis. 2004;4(4):343.
Enrofloxacin 10 mg/kg 16. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
PO q12h × 1 wk16 panion: canine and feline infectious diseases and parasitology. Ames, IA:
Blackwell; 2006.
Cats Tetracycline 10–20 Doxycycline 17. American Veterinary Medical Association. Backgrounder: Q fever.
mg/kg PO q8-12h × 5-10 mg/kg PO http://www.avma.org/public_health/biosecurity/qfever_bgnd.asp. Accessed
2-3 wk q12-24h × 2-4 wk February 14, 2009.
Cattle, sheep, Tetracycline7 18. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
goats microbial therapy. 2008. 38th ed. Sperryville, VA: Antimicrobial Therapy;
2008.
RABIES
Peter M. Rabinowitz and Lisa A. Conti Rabies can therefore serve as a model for improved com-
munication and cooperation among public health, animal
Rabies (ICD-10 A82) health, and human health professionals.
Other names in humans: lyssa, hydrophobia Key Points for Clinicians and Public Health
Professionals
Other names in animals: rage
Rabies is one of the most feared zoonotic diseases because Public Health Professionals
it almost invariably causes fatal human encephalitis. Despite
the availability of an effective vaccine for humans and • Provide rabies control and prevention guidance to
domestic animals, rabies continues to be a global public the public, veterinarians, and human health clinicians
health problem. The first World Rabies Day by the Alliance (see World Rabies Day education bank, http://www.
for Rabies Control took place in September 2007, drawing worldrabiesday.org/EN/Education-Bank/english.
attention to the need for human health and animal health html). Risk reduction measures include:
professionals to work together to reduce this disease threat.1  Animal bite avoidance, especially with children
This is intended to be an annual event.  Keeping cats indoors and monitoring dogs when
Human rabies is relatively rare in North America, but outside
exposure to potentially rabid wild or feral animals occurs  Avoidance of feeding or handling wildlife or un-
frequently. Owner noncompliance with rabies vaccina- known cats and dogs
tion protocols of their pets, especially cats, can be a source  Appropriate exclusion of bats from buildings
of exposure as well. Managing and preventing such expo- • Analyze and report trends from compulsory reports of
sures requires an understanding by human health and ani- animal and human rabies.
mal health professionals of the status of rabies infection in • Advise the public that any bite wound or potential expo-
local wildlife and domestic animal populations, the judicious sure to rabies should be thoroughly washed with soap and
use of vaccination strategies, and animal control measures. water, and the bite reported to local health authorities.
• Work with local human and veterinary medical pro- pretravel rabies immunization. In evaluating travelers
viders and animals control officials in the management returning from rabies-endemic countries, obtain history
of potential rabies exposures. of any animal exposures (see Chapter 10).
• Support the preexposure vaccination of high-risk
individuals. Veterinary Clinicians
• Explore methods of control of viral transmission in
wildlife population (such as oral vaccine). • Be familiar with the most recent National Association
• Discourage ownership of pet wildlife or wild/domestic of State Public Health Veterinarians Compendium on
hybrids. Animal Rabies Prevention and Control (http://www.
• Support appropriate vaccination requirements and nasphv.org/Documents/RabiesCompendium.pdf).
policies to reduce translocation and importation of • Ensure dogs, cats, ferrets, and appropriate livestock (e.g.,
potentially rabid animals. horses) are currently vaccinated against rabies following
• Support scientific research on which to base public the label use of the vaccine.2 There is no parenteral vac-
health policy. cine approved for use in wolf hybrids or pet wildlife.
• Provide access to appropriately trained laboratorians • Report adverse vaccine reactions, including rabies in
to diagnose the disease. a vaccinated animal to the USDA, APHIS, Center for
Veterinary Biologics at http://www.aphis.usda.gov/
animal_health/vet_biologics/vb_adverse_event.shtml.
• Work with public health officials in observing a healthy
• In evaluating any patient with an animal bite, take an dog, cat, or ferret that has bitten a human for signs of
accurate history of the species involved and circum- illness within 10 days from the time of a bite. If no ill-
stances of the bite incident (see Figure 9-105). ness occurs, the person has not been exposed to rabies
• Coordinate with public health and animal control from that animal.
authorities as PEP may not be required if the animal • Consider assisting public health officials by providing
is able to be tested, or the dog, cat, or ferret is available appropriate animal isolation and observation for clini-
for observation. Certain monkey bites may need to be cal sign of rabies:
evaluated for herpes B exposure potential.  If a currently vaccinated dog, cat, or ferret is exposed
• Prevention of the development of clinical disease to a known or suspect rabid animal, it should be re-
through the use of preexposure and postexposure vac- vaccinated, confined, and observed for 45 days.
cination strategies is the mainstay of preventing rabies  If the dog, cat, or ferret is not currently vaccinated,
deaths in humans. Become familiar with Human Rabies it should be isolated and observed for clinical signs
Prevention—United States, 2008: Recommendations of the of rabies for 6 months (vaccinated 1 month before
Advisory Committee on Immunization Practices (ACIP) release).
(http://www.cdc.gov/mmwr/preview/mmwrhtml/ • Consider assisting public health officials by providing
rr57e507a1.htm). Ensure that candidates for PEP are animal decapitation services for rabies testing.
rapidly evaluated and treated appropriately. Note that • Consider rabies in the differential diagnosis of any dog,
persons previously vaccinated with the human dip- cat, ferret, horse, or livestock with behavioral changes
loid cell vaccine (HDCV) or purified chick embryo or exhibiting unexplained neurological signs.
cell (PCEC) vaccine should not receive human rabies • Contact public health authorities immediately with
immunoglobulin (HRIG). suspected animal case of rabies.
• Report bite incident or use of PEP if required in the • Disinfect any cage and housing of a rabid animal with
state. soap solutions, 1% sodium hypochlorite, 2% glutar-
• Report suspected human cases of rabies to pub- aldehyde, iodine solutions, or quaternary ammonium
lic health authorities (consider using the Wisconsin compounds.3
protocol for rabies treatment: http://www.mcw.edu/ • Support the PEP of staff at high risk for rabies
FileLibrary/Groups/Pediatrics/InfectiousDiseases/ exposure.
Milwaukee_rabies_protocol2_1.pdf).
• Coordinate with state health authorities for collection Agent
of proper human diagnostic samples for rabies testing
at CDC laboratories (http://www.cdc.gov/rabies/ Rabies is caused by a number of related rhabdoviruses,
statehealthdept.html). which are bullet-shaped RNA viruses belonging to the genus
• Provide preexposure vaccinations to high-risk work- Lyssavirus. Lyssa viruses are unique among rhabdoviruses in
ers including veterinarians and staff working with their ability to replicate in a host animal’s CNS.4 Different
rabies vector species and laboratory workers in facili- strains of rabies virus are adapted to particular animal spe-
ties handling rabies vaccine. For persons previously cies and can have spillover to other species. Rabies viruses
unvaccinated against rabies, initial preexposure can affect any mammal.
vaccination consists of a regimen of three 1-mL
doses of HDCV or PCEC vaccines administered Geographical Occurrence
intramuscularly.
• Counsel travelers to rabies-endemic countries about the Rabies viruses occur worldwide on all continents except
risk from exposure to dogs and other animals. Consider Antarctica and Australia but in varying degrees of prevalence.
Reliable data on the prevalence in many countries are not

available. Certain Pacific and Caribbean islands, including
Hawaii, are considered to be free of the virus.5 The WHO has Animals are the natural reservoir for rabies viruses. Although
estimated that 55,000 fatal cases occur in humans annually, all mammals are considered susceptible to infection, only car-
with the greatest disease burden in Asia (31,000 deaths), fol- nivores and bats are capable of maintaining the viral reservoir
lowed by Africa (24,000 deaths).6 (Figure 9-98).4 Worldwide, domestic and wild canids and other
carnivores are the principal reservoir species for rabies virus.
Groups at Risk In the United States, dog rabies strain has now been eliminated
largely as a result of aggressive vaccination and animal control
The majority of human cases occur in countries where rabies efforts. However, the disease is now most frequently reported
is endemic in the dog population. Travelers to such areas are among wild mammals with identifiable virus variants circu-
therefore one group at risk of exposure and infection. lating in bats, raccoons, skunks, and foxes (Table 9-51). These
Occupational groups at risk include veterinarians, wild- variants can affect other mammals including humans, cats, and
life rehabilitators, wildlife management workers, zoologists, dogs.4,7 The disease is generally not reported in small rodents
animal quarantine workers, animal control officers, and lab- (e.g., squirrels, hamsters, gerbils, mice, or rats), lagomorphs
oratory workers. (rabbits), or marsupials (opossums).
Children may be at increased risk because of their behav- Unlike many other zoonotic diseases, animals are not
ior of contacting wild and domestic animals. Once exposed, believed to be subclinical carriers. Bats, canines, and other
immunocompromised individuals may be at increased risk animals that develop rabies and are capable of spreading
of contracting infection. infection to other animals typically die of the disease within
Unvaccinated dogs and cats with exposure to wild ani- a short time.8
mals, particularly raccoons, bats, foxes, and skunks, are at In the United States and Europe, oral rabies vaccine pro-
increased risk of rabies exposure and infection. grams are used to contain and eliminate the virus from
ANIMAL RABIES CASES BY GEOGRAPHIC REGION FOR 1998 (n=32,342)
Asia
n=7258
42 1
8
Europe
n=6108
85
10
10
13 50
USA and Canada 17

n=8333
2 1
43 Africa
6 n=4365
Bat 12 42 Racoon 4 4
16
30
50
Americas not including 26
Skunk
USA and Canada
n=6160
3
10
29 58 Dog Ruminant Cat
Fox Mongoose Other
Figure 9-98 n Animal rabies cases by geographic region for 1998. A total of 32,342 cases are displayed.
According to World Health Organization sources in the 34th World Survey, which was based on data from 110
countries reporting from 193 members, wildlife rabies predominates in some regions, such as the United States
and Canada, and dogs remain a significant reservoir in many other countries. Values shown are percentages.
(Note: Rabies has been diagnosed among bats in Australia, but these cases are not represented here.) (From Cohen
J, Powderly WG: Infectious diseases, ed 2, Philadelphia, 2004, Mosby Elsevier.)
Humans are usually exposed through a bite from a rabid

Table 9-51 n Reported Animal Cases of Rabies in
animal. Not all humans bitten by rabid animals become
the United States (1998-2002) infected, even in the absence of prophylactic immuniza-
Average No.
tion. The likelihood of transmission depends in part on the
of Cases amount of virus in the saliva. Therefore very minor bites
Animal* (1998-2002) Geographical Focus† and bites through clothing may be less likely to transmit
infection.8 Transmission by contact of saliva with mucous
Raccoon 2962 Eastern United States membranes and conjunctiva is possible but less common
Skunk 2257 California, upper and lower than bite-related transmission. Both humoral and cell-
Midwest, eastern United mediated immunity appear to play an important role in
States susceptibility to infection. Immunocompromised individu-
Bat 1175 Entire United States, except als are therefore at higher risk of infection from exposure to
Hawaii a rabid animal.
Fox 443 Alaska, Texas, southwestern Aerosol transmission has been reported in humans
United States entering caves frequented by bats and in laboratory settings,
Cat 276 Entire United States, except but this route of exposure is considered rare. Human infec-
Hawaii tion through ingestion of infected meat or milk has not been
Cattle 106 Entire United States, except reported.8 Person-to-person transmission has rarely been
Hawaii reported through corneal or organ donation.10
Dog 105 Entire United States, except
Transmission between animals results from direct contact
Hawaii such as bites. Dogs and other infected animals are infectious
for several days (as long as 13 days has been reported with
Horse or mule 62 Entire United States, except
Hawaii some rabies virus strains) before symptoms appear and then
continue to shed virus in saliva until death; the total period
Mongoose 58 Puerto Rico
of infectiousness may vary among species.8
Woodchuck 50 Eastern United States
Bobcat 30 Entire United States, except Environmental Risk Factors
Hawaii
Sheep or goat 9 Entire United States, except Worldwide, factors affecting the density of dog populations
Hawaii have been drivers of rabies infection risk. Increasing urban-
Other wild 24 Entire United States, except ization has brought migrants from rural areas to live closer
animal Hawaii together, often in extreme poverty, with accompanying dogs
Other domestic 3 Entire United States, except
and other domestic animals that are inadequately immu-
animal Hawaii nized against rabies.
In countries such as the United States where wildlife popu
*All mammals are considered susceptible to rabies, and incidental (or spillover) lations are reservoirs, key factors include translocation of
infection from wild animal reservoirs may occur in any species.
†Rabies may occur in an exposed animal in any location; the geographical foci listed
animals from a rabies-endemic area to one that has been free
here are based on current epidemiological trends. No cases of rabies have been of rabies. For example, the epizootic of rabies in raccoons
reported in Hawaii or in American Samoa, the Commonwealth of the Northern along the Eastern Seaboard of the United States occurred in
Mariana Islands, Guam, or the U.S. Virgin Islands.
From Rupprecht CE, Gibbons RV: Clinical practice. Prophylaxis against rabies, N part because of the transportation of rabid raccoons across
Engl J Med 351(25):2626-35, 2004. state lines to be released for hunting purposes. Another fac-
tor is the increasing contact between wildlife such as bats,
raccoons, skunks, and coyotes related to encroachment of
r accoon, skunk, fox, and coyote populations.9 In parts of suburban housing developments on wildlife habitat (Figure
the developing world, especially Asia and Africa, the disease 9-101). Cats could play a potential role in increasing contact
remains endemic in the domestic dog populations and con- between rabid wildlife and human populations.
stitutes a risk to travelers to rabies endemic countries (see
Chapter 10). In Latin America, vaccination campaigns have
Disease in Humans
drastically reduced cases of rabies in domestic animals and
humans, but canine and wildlife rabies (including vampire After exposure to rabies the disease has an incubation period
bats) remains a risk. that varies from weeks to months (usually 20 to 90 days),8
but the incubation period has been reported to be as long
Mode of Transmission and Life Cycle as several years.11 The distance from the exposure site to the
head and neck helps determine the length of time until the
The rabies virus enters the body by a bite, an open wound, onset of symptoms (Table 9-52).
or by contact with mucous membranes and replicates near Early symptoms include anxiety, headache, fever, and mal-
the site of exposure (Figures 9-99 and 9-100). It then travels aise. There may be pain, irritation, and other sensory changes
slowly through sensory and motor nerves to the CNS, where around the bite. The patient often becomes excitable with sensi-
it causes encephalitis. Finally, it spreads centrifugally to the tivity to light and sound and demonstrates aerophobia (fear of
salivary glands and other organs through peripheral nerves. flying)12 as well as pupil dilation and increased salivation. Over
Blood, urine, and feces are not considered infectious. a short period (2 to 6 days), the disease progresses inexorably
PATHOGENESIS OF RABIES
INFECTION INCUBATION DISEASE
Incubation period
20–90 days
Route of
infection Salivary gland
Broken skin Centripetal retrograde

Intact mucosa axonal transport
Rabies encephalomyelitis
of virus to CNS
(Respiratory
Intracellular viral replication Clinical effects:
tract)
Inclusion (Negri) body behavioral
Corneal
formation changes,
transplant
hydrophobia,
Trans-synaptic spread
paralysis, electro
Neurotransmitter functions encephalo-graphic
altered changes
Neuronal dysfunction
Centrifugal axonal transport
Virus may replicate in Extracellular virus appears

muscle at bite site. Virus produced in salivary glands
Viral binding at nerve Dissemination also to lungs, heart, adrenal
endings especially at motor
end plates and lacrimal glands, skin and skeletal muscle
Figure 9-99 n Pathogenesis of rabies. (From Cohen J, Powderly WG: Infectious diseases, ed 2, Philadelphia, 2004,
Mosby Elsevier.)
to weakness; paralysis, including spasm of the swallowing by trying to help the animal swallow. The paralysis spreads
muscles, leading to inability to swallow even liquids; and fear to the extremities, leading to generalized paralysis and death
of water (hydrophobia). Delirium and seizures can follow, as (Figures 9-103 and 9-104).
well as generalized paralysis, with death usually to the result of
respiratory arrest. Management of Rabies Exposures in Humans
In the United States, most autochthonous human rabies
cases have been identified as bat rabies variants among peo- Management of potential rabies exposure consists of three
ple who did not recognize their exposure or who did not seek components: (1) wound first aid, (2) risk assessment, and (3)
postexposure treatment. administration of PEP if indicated.
Disease in Animals First-Aid

The incubation period appears to vary among species (see Any bite or scratch from a potentially infected animal should
Table 9-52) but usually last weeks to months. Once clinical be cleaned immediately with soap and water and irrigated
signs develop, there are two major manifestations of rabies copiously with water and/or a dilute solution of povidone-
infection in animals, termed furious rabies and dumb (par- iodine and water. A tetanus booster should be administered
alytic) rabies. Either or both forms may occur during the if more than 10 years have elapsed since the last vaccination
course of infection in a single infected animal. (see Chapter 10).
Furious rabies is characterized by agitation, aggression
(including unprovoked biting attacks on other animals, Risk Assessment
humans, and itself), sexual stimulation and priapism, roam-
ing behavior, excess salivation and drooling, and abnormal Risk assessment and decisions regarding PEP are crucial
vocalizations (Figure 9-102). Convulsions often develop. steps in the management of rabies exposures. This requires
Dumb rabies is marked by lethargy and paralysis. The the clinician to gather an accurate history of the exposure,
muscle paralysis begins in the head and neck, with difficulty including the following information that should be included
swallowing that may lead a dog owner to become exposed in the clinical chart:
Spillover
Susceptible Infected wild Infected Susceptible

wild animal animal dog or cat dog or cat
Virus enters
wound or
Sylvatic rabies Urban rabies
by mucous
membranes
Susceptible
human being
Movement Suburbanization, Urbanization,

Environmental factors:
of animals loss of habitat vaccination policies
Figure 9-100 n Rabies transmission.
• Whether a bite or scratch occurred or whether the cir-

cumstances suggest an unrecognized exposure (such as
a bat found in a room where someone was sleeping)
• If the animals is a domestic animal, record of immuni-
zation and name/contact information of veterinarian
caring for animal
Using this information, the clinician can then assess the
risk of rabies transmission and the need for PEP. Public
health officials can be consulted to assist in determining the
need for rabies PEP.
Figure 9-105 shows an algorithm for making this decision.
The risk assessment process often requires close cooperation
among the treating clinician, the public health department,
animal control or veterinarian evaluating the animal, and
the public health or other laboratory performing tests on the
brain of the animal (if available).
Figure 9-101 n The brown bat Eptesicus fuscus ranges from southern
Canada through North and Central America to extreme northern South
America. (From Centers for Disease Control and Prevention Public Health Postexposure Prophylaxis
Image Library, Atlanta, Ga. Courtesy Ivan Kuzmin.)
If the biting animal is tested for rabies or is a dog, cat, or ferret
that can be monitored for 10 days, PEP is not necessary unless
• Current location of animal, and whether animal con- the animal shows clinical signs and subsequent test results are
trol or other authority is aware of incident and is going positive for rabies. However, if it is determined that PEP is
to quarantine/observe or euthanize the animal (in indicated, it should be initiated as soon as possible after rabies
which case PEP can be reserved unless the test results exposure. The CDC posts updated recommendations for PEP
for rabies are positive) on its Web site.14 PEP should be started even if a prolonged time
• Type of exposure (e.g., bite to exposed skin, bite through has elapsed since exposure because the incubation of human
clothing, scratch, lick, contact with intact skin only) rabies can be many months. Table 9-53 lists the vaccines and
• The exact location of all bites or scratches antibody preparations available in the United States.
• When exposure occurred For persons who have never been vaccinated against rabies,
• Rabies immunization history of the individual PEP should include administration of both passive antibody
• Whether the individual is immunocompromised (rabies immune globulin) and vaccine. For previously unvac-
• The species of animal involved, if known cinated persons, the vaccine regimen consists of HDCV or
• Whether the animal showed any signs of illness PCECV, 1.0 mL IM (deltoid area), one each on days 0, 3, 7, and
(including the signs of rabies listed in Table 9-52) 14. The deltoid area should be used in adults and the anterior
Table 9-52 n Rabies Infection: Comparative Clinical Presentations in Humans and Other Animals
Signs that May Increase Risk of

Species Risk Factors Incubation Period Clinical Manifestations Human Exposure
Humans Handling rabies vector Usually 2-12 weeks, Prodrome: malaise, fever,
species but can be years pain or pruritus at the site
of bite
Increasing agitation, anxiety,
confusion, difficulty
swallowing
Hyperexcitability or paralysis
Death within 2-10 days of onset
of clinical signs
Dogs Unvaccinated, allowed Usually 10-60 days8
unsupervised outdoors
Cats Unvaccinated, allowed Furious rabies more common
All species:
unsupervised outdoors than paralytic form8
Furious rabies: Irritable,
Bats Reservoir species Variable attacking, biting, scratching, Flying in daytime, resting
swallow objects, chewing, on ground, attacking
salivation animals, fighting, roosting
in buildings, carried into the
Dumb (paralytic) rabies:
house by pet
Paralysis of throat and masseter
Raccoons Reservoir species Variable muscles, inability to swallow, Loss of fear of humans,
profuse salivation, paralysis aggression, active during
extending to rest of body13 the day
Skunks Reservoir species Variable Phonation may be altered or Abnormal aggression (such as
animal may exhibit signs of attacking a porcupine)
choking
Cattle Unvaccinated 25-150 days Cessation of lactation,
Rabies-endemic area abnormal bellowing, signs
of choking
Horses Unvaccinated 14-60 days Rolling on ground, resembling
Rabies-endemic area colic
Figure 9-102 n Dog with rabies. Note open jaw and visible tongue Figure 9-103 n A 4-year-old Holstein was first noticed to be abnormal
with excessive salivary secretions resulting from the inability to swallow. when she buckled on both hind limbs coming into the parlor. Within 2 hours,
(From Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, she was recumbent, would not eat, and began bellowing. Cerebrospinal fluid
Saunders Elsevier. Courtesy Centers for Disease Control and Prevention, had a lymphocytic pleocytosis. She tested positive for rabies. (From Divers
Atlanta, Ga.) T: Rebhun’s diseases of dairy cattle, ed 2, St Louis, 2008, Saunders Elsevier.)
thigh can be used in children. The gluteal area should not be

used for rabies immunization. Hema rabies immune globu-
lin (HRIG, 20 international units/kg body weight) should be
given just once, at the beginning of antirabies prophylaxis, and
infiltrated directly around the wound site if possible.
Do not administer HRIG to a person who previously
received any of the rabies vaccinations from Table 9-53 either
for preexposure or postexposure purposes. Previously immu-
nized individuals should receive only vaccine (HDCV or
PCECV, 1.0 mL IM [deltoid area]), one each on days 0 and 3
after exposure.
Management of Rabies Exposure in Animals

Vaccinated dogs, cats, ferrets, and livestock that have been
Figure 9-104 n Dog with dumb rabies, manifested as depression, leth- exposed to a known or suspected rabid animal should be revac-
argy, and a seemingly overly tame disposition. Domesticated animals with cinated and observed in the home or farm for 45 days for signs
dumb rabies may become increasingly depressed and try to hide in isolated of rabies.15 If an unvaccinated dog, cat, ferret, or livestock ani-
places, whereas wild animals seem to lose their fear of humans, often appear-
ing unusually friendly. (From Centers for Disease Control and Prevention mal is bitten by a rabid or potentially rabid animal, it should be
Public Health Image Library, Atlanta, Ga.) euthanized or maintained in strict quarantine and monitored
Figure 9-105 n Decision tree for rabies postexposure prophylaxis. (Modified from Rupprecht CE, Gibbons
RV: Clinical practice. Prophylaxis against rabies, N Engl J Med 351[25]:2626-35, 2004.)
Table 9-53 n Rabies Vaccines and Immunoglobulin Available in the United States
Type Name Route Indications
Human diploid cell vaccine Imovax Rabies Intramuscular Preexposure or postexposure

(HDCV)
Purified Chick Embryo Cell RabAvert Intramuscular Preexposure or postexposure
Vaccine (PCEC)
Human rabies immune Imogam Rabies-HT Local infusion at wound site, with Postexposure
globulin additional amount IM at site
distant from vaccine
Human rabies immune HyperRAB TM S/D Local infusion at wound site, with Postexposure
globulin additional amount IM at site
distant from vaccine
From Centers for Disease Control and Prevention: Rabies post-exposure. http://www.cdc.gov/rabies/exposure/postexposure.html.
closely for signs of rabies for 6 months. Quarantine should be plished with disinfectants such as a 1% solution of house-
under the supervision of local animal control or public health hold bleach.2
authorities at an approved boarding site. If the animal victim
is a valuable specimen (e.g., zoo animal), contact public health
professionals to determine possible management. References
1. Alliance for Rabies Control. World Rabies Day. http://www.worldrabiesday.
org. Accessed August 23, 2008.
Diagnosis 2. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
panion: canine and feline infectious disease and parasitology. Ames, IA:
The diagnosis in humans can be made by biopsy of the skin Blackwell; 2006.
at the nape of the neck (at the hairline) and by using DFA 3. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases
staining of frozen skin sections. Serology is also used to of companion animals. Ames, IA: The Center for Food Security and Public
detect viral neutralizing antibody in serum and CSF,12 and Health, Iowa State University College of Veterinary Medicine; 2008.
a PCR test is available to detect Lyssavirus RNA. Clinicians 4. Nel LH, Markotter W. Lyssaviruses. Crit Rev Microbiol. 2007;
33(4):301.
must work with their state public health officials to submit 5. Kansas State University College of Veterinarian Medicine: Kansas State
specimens to the CDC laboratory. Veterinary Diagnostic Laboratory: Rabies Laboratory. Rabies serol-
In animals, the brain of euthanized animals is examined ogy and animal transport to rabies-free areas. http://www.vet.ksu.edu/
using DFA staining (Color Plate 9-58).2 A rapid immuno- depts/dmp/service/rabies/table.htm. Accessed August 23, 2008.
6. World Health Organization. Fact sheets: rabies. http://www.who.int/
histochemical test has recently been developed and provides mediacentre/factsheets/fs099/en/. Accessed August 23, 2008.
high sensitivity and specificity.16 7. Rupprecht CE, Gibbons RV. Clinical practice. Prophylaxis against
rabies. N Engl J Med. 2004;351(25):2626.
8. Acha PN, Szyfres B Zoonoses and communicable diseases common to
Treatment man and animals, vol. II: chlamydioses, rickettsioses, and viroses. 3rd ed.
Washington, DC: Pan American Health Organization; 2003.
9. Slate D, Rupprecht CE, Rooney JA, et al. Status of oral rabies vac-
Treatment in Humans cination in wild carnivores in the United States. Virus Res. 2005;
111(1):68.
Although a number of aggressive attempts to treat symp- 10. Srinivasan A, Burton EC, Kuehnert MJ, et al. Rabies in transplant
tomatic rabies infection with antiviral therapy have reported recipients investigation team. Transmission of rabies virus from
an organ donor to four transplant recipients. N Engl J Med. 2005;
survival success in an isolated case (see Milwaukee Protocol 352(11):1103.
at http://www.chw.org/display/PPF/DocID/33223/router. 11. Smith JS, Fishbein DB, Rupprecht CE, et al. Unexplained rabies in three
asp),17 clinical rabies infection in humans remains an immigrants in the United States: a virologic investigation. N Engl J Med.
almost invariably fatal disease, with the principal treatment 1991;324(4):205.
supportive intensive care. 12. Heymann DL, ed. Control of communicable diseases manual. 19th ed.
Therefore prevention of the development of clinical dis- 13. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
ease through the use of preexposure and postexposure vac- Station, NJ: Merck; 2005.
cination strategies is the mainstay of preventing rabies 14. Centers for Disease Control and Prevention. Rabies post-exposure. http://
deaths in humans. (See Human Rabies Prevention—United www.cdc.gov/rabies/exposure/postexposure.html. Accessed August 23,
2008.
States, 2008 Recommendations of the Advisory Committee 15. Centers for Disease Control and Prevention. Human Rabies Prevention—
on Immunization Practices (ACIP) at http://www.cdc.gov/ United States, 2008: Recommendations of the Advisory Committee on
mmwr/preview/mmwrhtml/rr57e507a1.htm.) Immunization Practices. MMWR. 2008;57(RR-3):1.
16. Lembo T, Niezgoda M, Velasco-Villa A, et al. Evaluation of a direct,
rapid immunohistochemical test for rabies diagnosis. Emerg Infect Dis.
Treatment in Animals 2006;12(2):310.
17. Hemachudha T, Wilde H. Survival after treatment of rabies. N Engl J
Treatment is not attempted in animals. Rabid animals are Med. 2005;8; 353(10):1068.
euthanized. Disinfection of the cage area should be accom-
ROCKY MOUNTAIN SPOTTED FEVER AND OTHER RICKETTSIAL INFECTIONS
Peter M. Rabinowitz and Lisa A. Conti tuck pants legs into socks, and wear light-colored
clothing to visualize ticks). Wash clothes with hot
Rocky Mountain spotted fever (ICD-10 A77.0) water.6
 Use CDC-recommended tick repellents such as
Other names in humans: North American tick typhus, DEET or permethrin (apply to clothes, not skin). Be
New World spotted fever, tickborne typhus fever, São Paolo sure to follow label instructions before using any re-
fever pellent.
 Do frequent tick checks to remove even tiny imma-
Other names in animals: none ture-stage ticks. Inspect children at least once daily
for ticks. When in heavily infested areas, inspect
Rocky Mountain spotted fever (RMSF) and other named dis- children every 3 to 4 hours.
eases caused by Rickettsia rickettsii, refer to a severe tickborne  Use appropriate technique to remove ticks, such
infection occurring in the Americas that is one of the dead- as a tick removal "spoon," or wear gloves or grasp
liest known infectious diseases. In the preantibiotic era, case tick with tweezers as close to the skin as possible
fatality was as high as 75%. Currently in the United States, and pull gently. Applying matches, diesel fuel, nail
the mortality rate is approximately 20% for untreated cases polish, or petroleum jelly on the tick is not rec-
and 5% for treated cases,1 with frequent long-term seque- ommended and could lead to additional exposure
lae in survivors including limb amputation and neurological to infectious material from the tick.7
signs such as deafness.2 RMSF causes similarly severe dis-  Disinfect tick bites with household 70% isopropyl
ease in dogs. The number of cases reported each year has alcohol or 2% iodine solution. Follow up by clean-
increased since 2001, and there is evidence of expansion of ing the area, applying antibiotic topical on the tick
host range and tick vector species. At the same time, RMSF bite site, and washing hands.
probably remains underdiagnosed and underreported by  Implement integrated pest management techniques
both human health care providers and veterinarians. The including landscape management (see Box 9-3) to
diagnosis can be difficult because many patients present with reduce tick exposures.
nonspecific signs and may not have the classic triad of fever, • Advocate for tick prevention in dogs to reduce human
rash, and tick bite. Estimation of RMSF mortality indicates exposure of the infection.
that national surveillance for the disease misses some 60% of
fatal cases.3 In numerous instances, there have been temporal Human Health Clinicians
relationships between RMSF cases in dogs and human infec-
tion in members of the same households, demonstrating that • Instruct patients on tick exposure prevention (see above).
dogs can serve as sentinels for human environmental infec- • Consider the diagnosis in all patients with animal con-
tion risk.4 Tragically, lack of communication between veteri- tact and/or travel to endemic countries.
narians and human health care providers has contributed to • Report suspicion of disease immediately to public health
delays in diagnosis, sometimes with fatal consequences. In authorities. See http://www.cdc.gov/ncidod/dvrd/rmsf/
other cases, however, detection of RMSF in dogs has alerted Case_Rep_Fm.pdf for the CDC case report form.
human health care providers to initiate timely treatment of
an infected person.5 In addition to tick bites, a risk factor for Veterinary Clinicians
human infection is exposure to infectious tick feces, tissues,
or fluids when removing ticks from dogs. RMSF is therefore • Recommend preventive acaricide treatment for pets.
a grim reminder to human and animal health profession- • Notify health care professional if cases are diagnosed in
als of the importance of considering the diagnosis, sharing dogs. Such cases could both pose a risk to humans and
information about animal and human cases, and educating serve as a sentinel warning of environmental exposure
patients and clients about proper measures to prevent tick- risk.
borne disease.
Agent
Key Points for Clinicians and Public Health The causative agent of RMSF, Rickettsia rickettsii, is a mem-
Professionals ber of a family of closely related spotted fever Rickettsiae that
are found worldwide. Rickettsiae are obligate intracellular
Public Health Professionals coccobacilli with one of the smallest bacterial genomes.8
Because of a history of laboratory-acquired infections,
• Characterize the risk of rickettsial disease in the many of which have proven fatal,9 handling of R. rickettsii
community. cultures requires biosafety level 3 containment. Because this
• Educate the public to prevent tick exposure through bacterium was added to the select agent list, only approved
the following measures: laboratories can maintain cultured R. rickettsii.
 Avoid tick-infested areas, but if not possible, wear Table 9-54 shows diseases caused by Rickettsiae in the
appropriate clothing (long sleeves, long pants, spotted fever group. Several of these agents in addition to
Table 9-54 n RMSF: Diseases Worldwide Caused by Rickettsiae of the Spotted Fever Group
Agent Disease Geographical Distribution
Rickettsia rickettsii Rocky Mountain spotted fever North Central and South America
Rickettsia conorii Mediterranean spotted fever, boutonneuse Europe, Asia, Africa, India, Israel, Sicily, Russia
fever, Israeli spotted fever, Astrakhan fever,
Indian tick typhus
Rickettsia parkeri10 American boutonneuse fever11 United States, possibly South America
Rickettsia akari Rickettsialpox Worldwide
Rickettsia sibirica Siberian tick typhus, North Asian tick typhus Siberia, People’s Republic of China, Mongolia,
Europe
Rickettsia australis Queensland tick typhus Australia
Rickettsia honei Flinders Island spotted fever, Thai tick typhus Australia, South Eastern Asia
Rickettsia africae African tick-bite fever Sub-Saharan Africa, Caribbean
Rickettsia japonica Japanese or Oriental spotted fever Japan
Rickettsia felis Cat-flea rickettsiosis, flea-borne typhus Worldwide
Rickettsia slovaca Necrosis, erythema, lymphadenopathy Europe
Rickettsia heilongjiangensis Mild spotted fever China, Asian region of Russia
Adapted from Centers for Disease Control and Prevention: Rocky Mountain spotted fever: epidemiology. http://www.cdc.gov/ncidod/dvrd/rmsf/Epidemiology.htm.
R. rickettsii are found in the United States. Rickettsia akari cultures because infection can occur by accidental paren-
causes rickettsialpox, a disease transmitted from mice to teral exposure or through aerosols.
humans via mites that causes a vesicular skin rash, fever,
and adenopathy and has been reported in urban dwellers Hosts, Reservoir Species, Vectors
in the eastern United States.12 Rickettsia parkeri can cause
a mild form of spotted fever with eschar formation at the Ixodid (hard) ticks are both a disease reservoir and the vec-
site of a tick bite.10,13 Rickettsia felis is transmitted by cat tors for RMSF, although R. rickettsii appears to cause mor-
fleas to other animals, including humans, and is one of the tality in ticks. At present, the two principal tick species
causes of flea-borne (murine) typhus, a mild rickettsial associated with RMSF in the United States are the American
disease.12 dog tick (Dermacentor variabilis) (Figure 9-106) found east
of the Great Plains, and the Rocky Mountain wood tick
(Dermacentor andersoni) (Figure 9-107) found between the
Geographical Occurrence Cascade and Rocky Mountains of the west.
Despite its name, human cases of RMSF occur throughout
the United States with higher incidence in the south Atlantic
and western-central regions (Color Plate 9-59).12 Even in
endemic areas, infection rates of ticks with R. rickettsii are
low. Outside the United States, RMSF occurs throughout the
Western Hemisphere, with cases reported from Canada to
Brazil and Argentina.
Groups at Risk
Since 1920, the disease has gone through three major
cycles of emergence and has been increasing in incidence
since 2000.The reasons for this are unclear.14 The major-
ity of reported cases in the United States occur in children
younger than 15 years with a peak incidence between ages
5 and 9 years. This is believed to be due to behaviors that
expose children to ticks.15 Living near dogs carrying ticks Figure 9-106 n American dog tick (Dermacentor variabilis). (From
is a reported risk factor. Laboratory workers are at risk and Centers for Disease Control and Prevention: Rocky Mountain spotted fever:
should use caution when handling infected material and natural history. http://www.cdc.gov/ncidod/dvrd/rmsf/natural_hx.htm.)
Figure 9-107 n Rocky Mountain wood tick (Dermacentor andersoni). (From Centers for Disease Control
and Prevention: Rocky Mountain spotted fever: natural history. http://www.cdc.gov/ncidod/dvrd/rmsf/
natural_hx.htm.)
Immature ticks of these two species feed predominantly

on small rodents in rural and suburban environments,
including the rice rat, golden mouse, white-footed mouse,
and pine vole.16 The brown dog tick (Rhipicephalus san-
guineus), by contrast, feeds mainly on dogs and has been
associated with recent human infections in the southwestern
United States and is the principal vector of RMSF in Mexico
(Figure 9-108).17 In South America, the major tick vector is
Amblyomma cajennense.
In addition to ticks, dogs and rodents can also serve as
disease reservoirs for RMSF as well as infected hosts that may
develop clinical disease.18

Once infected with R. rickettsii, many ticks die.14 Those that
survive remain infected for life, and female ticks can pass
the infection to their offspring through transovarial trans-
mission. The ticks have a three-stage life cycle from larva to
nymph and adult (Figure 9-109). To progress from one stage
to another, the tick must have a blood meal; all three stages
feed on vertebrates and can transmit infection. During blood
meals, R. rickettsii in the salivary gland of an infected tick
can be injected into the dermis of the host animal, resulting
in transmission. If an uninfected tick feeds on an infected
host animal, the tick can become infected with the organ-
ism. For tick-to-human transmission to occur, the tick must
be attached for at least 6 hours and may remain attached for
days to weeks.
In addition to tick bites, humans can become infected
by exposure to tick feces, tissues, or fluids by removing and
Figure 9-108 n Brown dog tick (Rhipicephalus sanguineus), an emerg-
crushing an infected tick, allowing secretions to contact cuts ing vector of Rocky Mountain spotted fever. (From Centers for Disease
or broken skin.8 The rickettsial organism can also be spread Control and Prevention Public Health Image Library, Atlanta, Ga. Courtesy
human to human by blood transfusion.19 James Gathany and William Nicholson.)

Environmental factors driving the emergence of RMSF are
poorly understood and are thought to vary with the ecology
of the different tick reservoir species. In areas where D. vari-
abilis is the principal tick reservoir, the environmental risk
of RMSF has been estimated based on the density of small
mammals in a particular area that serve as hosts for the tick.16
Seasonality and climate play a strong role in human infection
risk, with most cases in the United States reported between
April and December when the adult ticks are more active.15
Transovarial Eggs
Disease in Humans
Adult
In the early stage of RMSF, symptoms can be nonspecific,
including fever, myalgias, and headache. Only 3% to 18% of
Larva patients present at their first medical visit with the classic
triad of fever, rash, and a history of a tick bite.20 Therefore
the disease should be suspected even if one of these signs is
absent. Abdominal pain, nausea, and vomiting can be promi-
nent features. The rash of RMSF occurs eventually in most
cases and is often a maculopapular eruption with central
petechiae that typically begins in the extremities around the
Nymph wrists and ankles and spreads centripetally toward the trunk
Rodents (Figure 9-110). In many, but not all, cases the rash involves
the palms and soles (Color Plate 9-60).8 Elderly and dark-
skinned patients may have no visible rash (Rocky Mountain
Figure 9-109 n Relations of tick and hosts in RMSF transmission.
spotless fever).
(From Songer JG, Post KW: Veterinary microbiology: bacterial and fungal Thrombocytopenia, elevated liver function test results, and
agents of animal disease, St Louis, 2005, Saunders Elsevier.) hyponatremia are often seen. Nearly half of patients experience
Figure 9-110 n A, Exanthem of Rocky Mountain spotted fever. B, Close-up view. (From McGinley-Smith DE,
Tsao SS: Dermatoses from ticks, J Am Acad Dermatol 49:363, 2003.)
hemorrhages from vasculitis rather than low platelets. In

severe cases, renal failure, pulmonary edema, and respira-
tory distress develop. The development of neurological signs,
including meningismus, neurological deficits, deafness, and
photophobia, is associated with a poor prognosis. Death can
occur between 8 and 15 days after the onset of symptoms
if antibiotic treatment has not been started early enough in
the course of the disease.8 Survivors of severe cases may have
deafness, other neurological deficits, and gangrene of the
extremities.2 Male gender, advanced age, chronic alcoholism,
African American race, and glucose-6-phosphate dehydro-
genase deficiency have been associated with a greater risk of
fulminant disease.1
Figure 9-111 n Weimaraner with chronic glaucoma in the left eye second-
Disease in Animals ary to bilateral uveitis from Rickettsia rickettsii infection. Buphthalmia is pres-
ent in the left eye, with corneal edema. (From Dziezyc J, Millichamp NJ: Color
Dogs are often infected in endemic areas, with reported sero- atlas of canine and feline ophthalmology, St Louis, 2005, Saunders Elsevier.)
prevalence rates ranging from 4% to 63%, some of which
could be due to cross-reactivity with other Rickettsiae in the
spotted fever group.18 Infection causes a systemic vasculitis
with signs resembling some of those in humans. Within sev- Diagnosis
eral days of tick attachment, dogs may develop fever, leth-
argy, lameness, and anorexia. Other signs can include edema The differential diagnosis of RMSF in humans includes a
of the scrotum, face, ears, or extremities; epistaxis and other large number of other acute febrile illnesses, including viral
bleeding problems, including ecchymoses and petechiae; respiratory tract infection, gastroenteritis, other tickborne
respiratory distress; ataxia, conjunctivitis; and eye pain diseases including ehrlichiosis (which causes fever but no
(Figure 9-111 and Color Plate 9-61). Neurological disease is rash), thrombocytopenic purpura, and mononucleosis.
seen in about a third of cases.21 Cases can be mild or severe Clinicians must maintain a high level of suspicion for infec-
with fatality as a result of arrhythmias, shock, and dissemi- tion in endemic areas. Clues to the diagnosis include pres-
nated intravascular coagulation. The vasculitis can result in ence of fever and rash, exposure to ticks, and occurrence of
gangrene of the extremities in severely affected dogs. The RMSF in other humans or dogs in the household or area.
case fatality rate can be as high as 10%. In recovered animals, Findings of thrombocytopenia, hyponatremia, and ele-
immunity appears to be lifelong.19 vated transaminase values support the diagnosis. Physicians
RMSF has rarely been reported in cats, which are believed should never delay treatment waiting for laboratory con-
to be much less susceptible to infection than dogs.19 The firmation. Immunohistochemistry can offer timely diag-
organisms have been isolated from opossums, rabbits, nosis but is not widely available. A PCR test is available in
chipmunks, squirrels, rats, and mice, which seem to have some centers but is not 100% sensitive. Diagnostic serol-
inapparent infection. Table 9-55 summarizes the clinical pre- ogy can be done but is mostly useful for retrospective diag-
sentation of RMSF in humans and other animals. nosis of cases. Therefore the burden falls on clinicians to
Table 9-55 n RMSF: Clinical Presentations in Humans and Other Animals
Humans Children: Exposures to ticks, 2-14 days Early symptoms often Thrombocytopenia, elevated
dogs with ticks nonspecific; fever, myalgias, liver function tests,
Elderly, African American, G6PD abdominal pain, nausea, hyponatremia
deficiency at risk for severe centripetal rash PCR, immunohistochemistry,
sequelae Neurological signs, hemorrhage, positive serological titers for
respiratory and renal failure confirmation
Fourfold rise in titer IFA, ELISA
Dogs Tick exposure, mtost often in 2-14 days19 Fever, anorexia, lethargy, Thrombocytopenia
<3 years swelling, epistaxis, Positive serology: fourfold
conjunctivitis, respiratory rise in titer by IFA, ELISA,
distress, ataxia, ecchymoses, latex agglutination
petechiae, shock immunofluorescence
PCR if available
G6PD, Glucose-6 phosphate dehydrogenase.

3. Paddock CD, Holman RC, Krebs JW, et al. Assessing the magnitude of
Table 9-56 n Antibiotic Treatment of RMSF in fatal Rocky Mountain spotted fever in the United States: comparison of
Humans and Other Animals two national data sources. Am J Trop Med Hyg. 2002;67(4):349.
4. Elchos BN, Goddard J. Implications of presumptive fatal Rocky
Species Primary Treatment Alternative Treatment Mountain spotted fever in two dogs and their owner. J Am Vet Med
Assoc. 2003;223(10):1450–1452, 1433.
5. Paddock CD, Brenner O, Vaid C, et al. Short report: concurrent Rocky
Humans Doxycycline 100 mg Mountain spotted fever in a dog and its owner. Am J Trop Med Hyg.
PO/IV bid × 7 days 2002;66(2):197.
or 2 days after 6. Centers for Disease Control and Prevention. Lyme disease prevention:
normalization of protect yourself from tick bites. http://www.cdc.gov/ncidod/dvbid/lyme/
temperature22 Prevention/ld_Prevention_Avoid.htm. Accessed September 28, 2008.
Dogs23 Doxycycline 10 mg/kg PO Enrofloxacin 3 mg/kg PO, 7. Needham GR. Evaluation of five popular methods for tick removal.
or IV q12h × 10 days SC q12h × 10 days19 Pediatrics. 1985;75(6):997.
8. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005.
9. Pike RM. Laboratory-associated infections: summary and analysis of
3921 cases. Health Lab Sci. 1976;13(2):105.
suspect the diagnosis and initiate antibiotics often on clin- 10. Paddock CD, Sumner JW, Comer JA, et al. Rickettsia parkeri: a newly
ical grounds. recognized cause of spotted fever rickettsiosis in the United States. Clin
In dogs, the disease can be confused with canine ehrli- Infect Dis. 2004;38(6):805.
chiosis, which responds to the same treatment. The scrotal 11. Goddard J. American boutonneuse fever: a new spotted fever rickettsio-
sis. Infect Med. 2004;21:207.
edema may resemble that seen in brucellosis. Helpful labo- 12. Heymann DL, ed. Control of communicable diseases manual. 18th ed.
ratory diagnostic findings in dogs include thrombocytope- Washington, DC: American Public Health Association; 2004.
nia and serology using immunofluorescence (micro-IF or 13. Whitman TJ, Richards AL, Paddock CD, et al. Rickettsia parkeri infec-
direct), ELISA, or latex agglutination. PCR is available in tion after tick bite, Virginia. Emerg Infect Dis. 2007;13(2):334.
14. Dumler JS, Walker DH. Rocky Mountain spotted fever—changing ecol-
some centers.19 ogy and persisting virulence. N Engl J Med. 2005;353(6):551.
15. Centers for Disease Control and Prevention. Rocky Mountain spot-
ted fever: epidemiology. http://www.cdc.gov/ncidod/dvrd/rmsf/
Treatment Epidemiology.htm. Accessed August 2, 2008.
The treatment of choice for RMSF in adults and children is 16. Kollars Jr TM. Interspecific differences between small mammals as hosts
of immature Dermacentor variabilis (Acari: Ixodidae) and a model for
doxycycline (Table 9-56).1 In pregnant women, the benefit detection of high risk areas of Rocky Mountain spotted fever. J Parasitol.
may also outweigh the risk, but an infectious disease spe- 1996;82(5):707.
cialist and/or the patient’s obstetrician should be consulted. 17. Demma LJ, Traeger MS, Nicholson WL, et al. Rocky Mountain spot-
Antibiotic treatment should never be delayed while await- ted fever from an unexpected tick vector in Arizona. N Engl J Med.
2005;353(6):587.
ing results of diagnostic testing, because delay in treatment 18. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
can lead to fatal outcomes.20 Patients may require support- Station, NJ: Merck; 2005.
ive care in intensive care settings if necessary if complica- 19. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
tions develop. Treatment in dogs usually involves inpatient panion: canine and feline infectious diseases and parasitology. Ames, IA:
care with early administration of antibiotics and supportive Blackwell; 2006.
20. Centers for Disease Control and Prevention. Consequences of delayed
treatment with intravenous fluids and blood transfusion if diagnosis of Rocky Mountain spotted fever in children—West Virginia,
necessary. Michigan, Tennessee, and Oklahoma. MMWR. 2000;49(39):885.
21. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic dis-
eases of companion animals. Ames, IA: The Center for Food Security and
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of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrli- microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
chioses, and anaplasmosis—United States: a practical guide for physi- 2009.
cians and other health-care and public health professionals. MMWR. 23. Langston C. Postexposure management and treatment of anthrax in
2006;55(RR-4):1. dogs—Executive Councils of the American Academy of Veterinary
2. Archibald LK, Sexton DJ. Long-term sequelae of Rocky Mountain spot- Pharmacology and Therapeutics and the American College of Veterinary
ted fever. Clin Infect Dis. 1995;20(5):1122. Clinical Pharmacology. AAPS Journal. 2005;07(02):E272.
RIFT VALLEY FEVER*
Tracy DuVernoy Key Points for Clinicians and Public Health

Professionals
Rift Valley fever (ICD–9 066.3)
Other names in humans: none • Be alert to the possibility of RVF introduction into
the Western hemisphere and the subsequent spread by
mosquito vectors.
Other names in animals: enzootic hepatitis • The irregular interval between RVF epizootics/epidem-
ics adds to the challenge of preventing and controlling
Rift Valley fever (RVF) is a zoonotic arboviral disease that this virus. Consider increased use of techniques such as
primarily affects ruminant livestock (cattle, sheep, and goats) satellite remote sensing to predict global outbreaks of
and camels, but the disease can also occur in humans. Cattle, RVF. Environmental criteria in west and south Africa
sheep, and goats appear to be particularly susceptible to may require further evaluation to determine the valid-
infection. Animal infection is characterized by acute hepatic ity and applicability of remote sensing imagery in these
necrosis; increased abortions among pregnant animals; and areas.
high mortality rates in young, neonatal livestock populations. • Ensure that populations that work with livestock in
Most human infections are asymptomatic or may present as endemic areas use proper precautions when butcher-
an uncomplicated influenza-like illness. However, a small ing and processing meat.
percentage of human infections may result in significant • Use of mosquito control techniques may be highly
neurological illness, retinitis, hepatitis, or hemorrhage pro- effective in either preventing the introduction of the
gressing to death. RVF virus could potentially be introduced virus in domestic animal populations by killing imma-
into the United States by an infected person or animal, espe- ture stages of vectors3 or control of adults during epi-
cially during their viremic phase, or by an infected vector. zootic/epidemic conditions.
Although RVF is currently found in Africa and the Arabian
Peninsula, the virus has the potential to become established
in other geographical areas owing to the abundant range Human Health Clinicians
of competent vectors capable of transmitting infection, the
high level of viremia that develops in both infected animals • Generally, the risk of infection in travelers is low.
and humans that allows sustainability of the virus, and the However, travelers to RVF-affected areas during an
ability of the virus to adapt to different ecological conditions. epizootic or epidemic should take appropriate pre-
However, for the virus to become established in the United cautions, such as using bed nets during sleep periods,
States, climatic conditions must be favorable to ensure sur- using mosquito repellents, and avoiding contact with
vivability of the mosquito vector, and appropriate numbers infected livestock.
of livestock are necessary for adequate amplification of the • Due to the zoonotic nature of this virus, it is critical
virus. A recent publication evaluated potential pathways of that individuals take appropriate precautions when
RVF introduction into the United States and concluded that (1) performing necropsies on suspect animals, (2)
air transportation of a viremic civilian or mechanical trans- performing laboratory procedures, (3) assisting with
portation via aircraft or ship of an RVF-infected vector were livestock parturitions, (4) butchering possibly infected
likely pathways for introduction of RVF virus into the United animals, or (5) performing other procedures that may
States.1 Therefore it is essential that communication among place them at high risk of exposure to RVF virus.
animal and human health officials be coordinated to detect • Report any suspected case of RVF to the appropriate
this potentially devastating zoonotic infectious disease. local and state public health authorities. RVF cases sus-
Fortunately, a multiagency working group has been formed pected or confirmed in active duty U.S. military per-
to discuss a research agenda, modeling efforts, and surveil- sonnel are reportable to their respective services per
lance and response capabilities, among other activities, to the Tri-Service Reportable Events guidelines.4
develop a comprehensive national RVF prevention and • Use appropriate precautions especially when handling
response plan.2 acute-phase blood products from suspect patients.
• No commercially available preventive vaccine exists
for use in humans. An experimental inactivated vac-
cine has been used to protect laboratory and veterinary
workers at high risk of RVF infection.
*The opinions and assertions contained in this chapter are the private views
of the author and are not to be construed as official or reflecting true views
of the Department of the Army or the Department of Defense, to whom the Veterinary Clinicians
author was contracted during the writing of this chapter.
The author is grateful for the contributions of Dr. Kenneth Linthicum to • Consider RVF infection with increased abortions in
this section. ruminants; high mortality rates in neonatal and young
lambs, kids, and calves; and human illness particularly S (small), M (medium), and L (large)—that is readily inac-
after heavy rains. tivated by a pH below 6.8, lipid solvents, or strong solutions
• In the United States, RVF is a foreign animal disease; of sodium hypochlorite.7 There is only one serotype of RVF
therefore for any suspected case of RVF, it is critical to virus. However, there are three distinct lineages: Egyptian,
promptly notify the appropriate state and federal vet- West African, and Central East-African.8
erinary regulatory authorities.
• Ensure that appropriate PPE is worn when performing Geographical Occurrence
a necropsy on a suspect animal, when treating an ill
suspect case, or when assisting with reproductive pro- RVF is a disease that occurs primarily in Africa and the
cedures. At a minimum, consider wearing a mask (to Arabian Peninsula. RVF was first identified in 1930 in Merino
help avoid aerosols), gloves, and goggles. sheep along the shores of Lake Naivasha in the Rift Valley
• Before submitting any specimens for diagnostic pur- of Kenya9 when a total of 3500 lambs and 1200 ewes died
poses, contact the appropriate reference laboratory5 to of acute hepatic necrosis after a period of excessive rainfall.
inquire about shipping requirements, diagnostic capa- Herdsmen who managed the flocks on the farm also com-
bilities, and required specimens for submission. plained of fever and arthralgia.9 Animal epizootics, along
• Animal disease prevention in enzootic areas may be with human epidemics, have occurred periodically since
accomplished by vaccination of susceptible livestock. The then, primarily in sub-Saharan Africa. Significant RVF out-
administration to small ruminants of one dose of a live breaks were reported in 1950-1951 (South Africa); 1997-1998
attenuated virus vaccine (Smithburn strain) may confer (Kenya, Tanzania, Somalia); 2006-2007 (Kenya, Tanzania,
long-term immunity and will minimize animal disease Somalia); 2007 (Sudan), and recently in 2008 (South Africa,
before the onset of an epizootic. However, live vaccine Madagascar). The 1997-1998 outbreak in east Africa was the
use may induce abortions or fetal abnormalities in preg- largest to date in terms of human disease, with approximately
nant animals. For disease prevention in pregnant rumi- 89,000 human cases and 478 fatalities.10 During the past three
nants in nonzoonotic areas, an initial dose and booster decades, human and animal disease has also been confirmed
dose of a formalin-inactivated vaccine may be adminis- in western Africa and Egypt, associated with the construction
tered to cattle, sheep, and goats; annual revaccination is of dams and subsequent flooding or irrigation projects that
required. In addition, animal movement control is essen- favor mosquito production. In 1977-1978 an outbreak that
tial to prevent introduction of infected animals into new affected both humans and animals was confirmed in Egypt,
geographical locations that can support maintenance of the first time the virus had been identified outside sub-Saha-
the virus. ran Africa.11 A second occurrence of RVF occurred in Egypt
in 1993. In 2000, RVF infection was reported in southern
Saudi Arabia and northern Yemen along the Red Sea, the first
Agent
time this virus was confirmed outside the African continent.
RVF is a mosquito-borne virus of the genus Phlebovirus in The appearance of the virus in this new geographical location
the family Bunyaviridae6 (Figure 9-112). Vector transmis- was likely due to the importation of viremic livestock from
sion may occur by mechanical or biological means. It is a eastern Africa into the Arabian Peninsula.12 In Saudi Arabia,
single-stranded enveloped RNA virus with three segments— 882 human cases were reported that resulted in 124 deaths,13
and Yemen reported 1087 suspected case patients and 121
deaths.14 Abortions in small ruminants and increased mortal-
ity in young susceptible livestock were reported concurrent
with human illness.
Groups at Risk
Human groups at increased risk of RVF infection include
veterinarians, abattoir workers, livestock herdsmen, and
virology laboratorians as a result of occupational exposures.
During epidemics, the general human population is at risk
as a result of direct contact with infected livestock or animal
products (including unpasteurized milk) or exposure to
mosquito vectors. During epidemics, the risk of infection to
travelers, soldiers, relief workers, or other individuals may be
high if exposed to infected mosquitoes or to infected ani-
mals, their blood, or infected tissues.
Within animal populations, newborn ruminants (sheep,
goats, and cattle) are particularly susceptible to RVF virus,
resulting in a fatal infection; followed by pregnant rumi-
nants; and then young sheep and cattle. Adult ruminants are
Figure 9-112 n This transmission electron micrograph depicts a highly
magnified view of a tissue that had been infected with RVF virus. (From
less susceptible to infection; however, exotic breeds are more
Centers for Disease Control and Prevention Public Health Image Library, susceptible and exhibit more pathology. Horses and swine
Atlanta, Ga. Courtesy F.A. Murphy and J. Dalrymple.) are even less susceptible.
Human
beings
Butchering, other Butchering, other
direct contact, direct contact,
ingestion, inhalation ingestion, inhalation
Aedes
mosquitoes Domestic
Wildlife(?)
ruminants
Transovarial
transmission
Environmental Rainfall, Vector Animal Trade,

Figure 9-113 n Female Aedes mosquito in the process of acquiring a factors: flooding density density movement
blood meal from her human host. (From Centers for Disease Control and of animals
Prevention Public Health Image Library, Atlanta, Ga. Courtesy Frank Hadley
Collins, University of Notre Dame). Figure 9-114 n Transmission and life cycle of Rift Valley fever infection,
including the ecological drivers for outbreaks.

Many different species of mosquitoes are involved in the trans-
mission of RVF; the virus has been isolated from more than
30 species among six genera of mosquitoes (Figure 9-113).15
Additionally, RVF virus has been isolated from flies and
Culicoides, biting midges. However, a few arthropod species
play key roles in the transmission during epidemics/epizoot-
ics and during the period between these disease-occurring
events. The reservoir of RVF in sub-Saharan Africa is thought
to be Aedes mosquitoes (Ae. vexans, Ae. mcintoshi, and Ae.
dalzieli primarily) that can transovarially transmit RVF virus
to their drought-resistant eggs,16 thereby allowing the virus to
remain dormant and survive for long periods in soil depres-
sions pending significant rainfall.17 This vertical transmission
is critical in maintaining RVF in endemic/enzootic areas.
The natural reservoir of RVF virus is currently unknown.
The role of wildlife in the perpetuation, maintenance, and
circulation of virus during the interepizootic period is also
not clearly understood.18 Experimentally, rhesus macaques19
and inbred laboratory mice20 have been shown to demon-
strate clinical signs of disease once infected with RVF virus.

Once appropriate levels of rainfall occur and land depres-
sions fill with water, dormant RVF-infected Aedes mosquito
eggs hatch and adults emerge (Figure 9-114) and, acting as
primary vectors, feed on susceptible livestock (Figure 9-115).
Infected livestock amplify the virus, developing significant
viremias—up to 108.0 plaque-forming units (PFUs)/mL1— Figure 9-115 n Epidemiological investigation in Saudi Arabia that had
and contribute to epizootic maintenance, circulation, and been initiated as a response to a Rift Valley fever outbreak in the region.
spread of the virus via secondary vectors (Culex mosquitoes) These goats were penned in a village that was within the geographical param-
eters of the investigation. (From Centers for Disease Control and Prevention
that feed on livestock and perpetuate the infection. Intense Public Health Image Library, Atlanta, Ga. Courtesy Abbigail Tumpey.)
virus activity may last for 6 to 12 weeks.21
Human infection can occur after a bite from an infected
mosquito or by mechanical transmission from other insects. on infected animals. In this way, RVF can be considered an
However, most infections occur as a result of direct or indirect occupational disease of individuals who work with livestock
exposure to infected blood, tissues, or body fluids of infected (see Chapter 12). Infection occurs by way of inoculation or
animals; by the butchering or slaughtering of infected ani- aerosolization and inhalation of virus. Infection may also
mals; or by performing veterinary or obstetrical procedures occur subsequent to consuming unpasteurized milk from
infected animals. Direct human-to-human horizontal trans- have used satellite imagery remote sensing to create pre-
mission has not been documented; however, two recent arti- dictive risk maps for RVF outbreaks. This remote sensing
cles describe case reports of vertical transmission of RVF approach incorporates measures such as the normalized dif-
infection from pregnant mother to fetus.22,23 Direct animal- ference vegetation index (an indicator of recent rainfall and
to-animal transmission has not been reported. green vegetation), sea surface temperature, and rainfall.26 In
October 2006, this technology assessed such environmen-
tal conditions and accurately forecasted an outbreak of RVF
in Kenya before an actual confirmed outbreak in December
Epizootics and epidemics occur at irregular internals (rang- 2006. Figure 9-116 shows an example of an environmental
ing from 3 to 15 years)21,24 and typically follow significant risk map for RVF produced by NASA.
rainfall that floods areas of sub-Saharan eastern and south- The outbreak in Egypt along the Nile Delta in 1977-1978
ern Africa, subsequently hatching dormant floodwater Aedes was a concern because the virus had not been previously
mosquito eggs.25 However, in more arid areas of Africa, the identified north of the Sahara Desert. However, conditions
interval may approach every 15 to 35 years. The frequency that favored an outbreak included construction of the Aswan
depends on rainfall and other climatic conditions that favor High Dam and flooding of the Nile River delta24 and a con-
large vector populations, susceptible animal species popula- current large outbreak in East Africa. Another incident fol-
tions, and the existence or introduction of virus in the geo- lowing a change to the environment occurred in western
graphical area. For these reasons, satellite imagery may offer Africa in Mauritania and Senegal in 1987. One year after
an early warning of environmental conditions that favor dis- the construction of the Diama Dam and subsequent flood-
ease occurrence, allowing a few months’ lead time to mitigate ing of the Senegal River basin, an outbreak of RVF affected
disease impacts in both animals and humans. The National both humans and other animals.24,27 Despite the linkages
Aeronautical and Space Agency (NASA) and other agencies between recent flooding and rainfall to many RVF outbreaks,
RVF Potential December 2006
30
15
−15
RVF risk areas
RVF endemic regions

−30
−15 0 15 30 45 60
DoD-GEIS NASA/GSFC
WRAIR GIMMS
Figure 9-116 n Risk map for Rift Valley fever based on normalized difference vegetation index (NVDI, an
indicator of green vegetation). (From U.S. Department of Defense, Global Emerging Infections Surveillance and
Response System: Rift Valley fever (RVF): monthly updates: state of climate and environmental conditions. http://
www.geis.fhp.osd.mil/GEIS/SurveillanceActivities/RVFWeb/monthlypages/0612.htm.)
not all follow this pattern because some outbreaks appear adult cattle and small ruminants is often subclinical; however,
to be related to the trade and movement of infected viremic some animals may develop fever, anorexia, bloody diarrhea,
domestic animals across borders.11,12,24 and a mucopurulent nasal discharge. Adult camels do not
demonstrate clinical signs of illness; however, they do abort.
The mortality rate in adult livestock may range from 10%
Disease in Humans in cattle to 20% in sheep. Infection and disease in domestic
animals causes considerable economic losses because of the
In humans, the incubation period of RVF is 2 to 6 days; RVF significant number of abortions, the high rate of mortality
produces an influenza-like illness with fever, headache, arth- in young ruminants, and the disruption in trade and exports
ralgia, and myalgia.28 Viremic titers are high after infection that are associated with epizootics.
and can persist for more than 1 week. Recovery is usually Although some species of wildlife have detectable anti-
complete; however, complications or a more serious form of body levels against RVF, such infections are generally sub-
the disease can manifest as three different syndromes. clinical. One recent publication reported that of 16 different
wildlife species sampled during 1999-2006 in Kenya, seven
Retinitis had detectable neutralizing antibodies against RVF. These
data suggest that native wildlife are indeed infected with
Between 0.5% and 2% of human RVF infections result in
RVF30; however, additional studies are needed to determine
retinitis; onset occurs 1 to 3 weeks after the initial symptoms.
their role as reservoirs or amplifiers of the virus. Table 9-57
The disease may resolve within 10 to 12 weeks; however, per-
shows the comparative presentation of disease in humans
manent vision loss may occur in 1% to 10% of those with
and other animals.
this syndrome. Death is uncommon in those infected with
the ocular form of RVF.
Diagnosis
Meningoencephalitis In humans, RVF should be suspected in the differential diag-
Meningoencephalitis occurs in 1% of those infected with nosis when the following conditions are observed: influ-
RVF, generally 1 to 4 weeks subsequent to the initial symp- enza-like illness, retinitis, and/or meningoencephalitis and
toms. Patients may report an intense headache, photopho- hemorrhagic fever in individuals with livestock contact, espe-
bia, memory loss, and confusion; convulsions and coma may cially in the setting of high mosquito vectors associated with
ensue. The death rate is low; however, neurological sequelae recent flooding or after significant rainfall. Cases of abortion
are common in individuals with this form of RFV infection. in ruminants also support the diagnosis in humans. Recent
human infection is determined by serology to detect IgM
antibodies by ELISA; by virus isolation during the acute, vire-
Hemorrhagic Fever mic phase; or by RT-PCR to detect viral antigen.28
Fewer than 1% of those infected have hemorrhagic fever, In animals, the differential diagnoses for a “storm” of abor-
which typically develops 2 to 4 days after illness onset; jaun- tions in pregnant ruminants and a high mortality rate among
dice is generally observed first. Additional hepatic involvement young/neonatal ruminants includes a number of diseases such
manifests as hemorrhage, hematemesis, melena, ecchymoses, as brucellosis, ovine enzootic abortion, Nairobi sheep disease,
and persistent bleeding from other sites. Death occurs 3 to 6 rinderpest, peste de petit ruminants, vibriosis, ephemeral
days after onset of these symptoms; the case fatality rate may fever, Wesselsbron disease, trichomonas, and heartwater. To
approach 50%. detect RVF infection in animals, heparinized blood may be
The overall case fatality rate of RVF infection in humans analyzed for virus isolation, especially during the acute phase
typically ranges from 0.5% to 1.0%. However, during a recent when virus levels are elevated. Acute and convalescent sera
outbreak in Kenya, the case fatality rate was 29% among 404 can be used to detect a rise in antibody levels by ELISA or
confirmed or probable cases during a 3-month period from hemagglutination inhibition; antibody is present within 6 to
November 30, 2006, to January 25, 2007.29 The high case 7 days after infection.31 Tissue specimens may also be submit-
fatality rate was likely due to severe illness and the hemor- ted for virus isolation as long as they are not formalinized.
rhagic fever presentation of many of those infected. Electron microscopy may be used to detect viral particles in
tissue specimens or RT-PCR can be used to detect viral anti-
gen. For histopathological review, the best necropsy samples
Disease in Animals
to submit in 10% buffered formalin include the spleen, liver,
RVF causes morbidity and mortality in many different live- and brain (particularly from aborted fetuses).
stock species. In Africa, exotic livestock breeds are more suscep-
tible to infection than indigenous breeds such as Bos indicus.21
Treatment
In pregnant ungulates, abortion is the most common clini-
cal sign. Abortion may occur at any time during the gestation Asymptomatic human infections typically do not warrant
period and the rate may approach 100% in infected pregnant treatment. For individuals with more significant illness,
ewes. In newborn lambs, kids, and calves after an incubation treatment is supportive. Although there are no specific anti-
period as short as 12 hours, the most prevalent clinical sign is virals that are effective once symptoms occur, antivirals such
death, preceded by fever. Mortality rates can approach close to as ribavirin and interferon-alpha have shown some promise
100% in some species. Older animals may demonstrate weak- in treatment trials involving nonhuman primates. There is
ness, anorexia, listlessness, and a nasal discharge. Infection in no treatment available for infected animals.
Table 9-57 n Clinical Presentation of Rift Valley Fever in Humans and Other Animals
Incubation
Species Risk Factors Period Clinical Manifestations Diagnostic Findings
Humans Direct or indirect contact 2-6 days Asymptomatic or mild IgM serology (ELISA),
with infected livestock/ influenza-like illness RT-PCR, virus isolation
products, aerosolization More severe disease
via slaughtering, (<2% of cases): retinitis,
mosquito bites meningoencephalitis, or
hemorrhagic fever
Neonatal Exposure to infected 12 hours- Fever, anorexia, weakness, Virus isolation, RT-PCR,
and young mosquitoes 3 days listlessness, diarrhea, histopathology
domestic mucopurulent nasal discharge,
ruminants high mortality rate
Adult domestic 1-3 days Abortions ELISA to detect IgG and
ruminants Subclinical in nonpregnant animals; IgM, virus isolation,
however, some develop fever, RT-PCR
anorexia, ptyalism, diarrhea
Wild ruminants Unknown Subclinical; however, may abort Serological evidence of
(African buffalo) antibodies
References 14. Centers for Disease Control and Prevention. Outbreak of Rift Valley
fever—Yemen, August-October 2000. MMWR. 2000;49(47):1065.
1. Kasari TR, Carr DA, Lynn TV, et al. Evaluation of pathways for release 15. House JA, Turell MJ, Mebus CA. Rift Valley fever: present status and
of Rift Valley fever virus into domestic ruminant livestock, ruminant risk to the Western hemisphere. Ann N Y Acad Sci. 1992;653:233.
wildlife, and human populations in the continental United States. J Am 16. Peters CJ, Linthicum KJ. Rift Valley Fever. In: Beran GW, Steele JH, eds.
Vet Med Assoc. 2008;232(4):514. Handbook of zoonoses. 2nd ed. Boca Raton, FL: CRC Press; 1994.
2. Britch SC, Linthicum KJ. Rift Valley Fever Working Group: Developing 17. Linthicum KJ, Davies FG, Kairo A, et al. Rift Valley fever virus (family
a research agenda and a comprehensive national prevention and Bunyaviridae, genus Phlebovirus). Isolations from Diptera collected dur-
response plan for Rift Valley fever in the United States. Emerg Infect Dis. ing an inter-epizootic period in Kenya. J Hyg (Lond). 1985;95(1):197.
http://www.cdc.gov/eid/content/13/8/e1.htm. Accessed July 2, 2008. 18. LaBeaud AD, Muchiri EM, Ndzovu M, et al. Interepidemic Rift
3. Linthicum KJ, Logan TM, Thande PC, et al. Efficacy of a sustained Valley fever virus seropositivity, northeastern Kenya. Emerg Infect Dis.
release methoprene formulation on vectors of Rift Valley fever in field 2008;14(8):1240.
studies in Kenya. J Am Mosq Control Assoc. 1989;5(4):603. 19. Peters CJ, Jones D, Trotter R, et al. Experimental Rift Valley fever in rhe-
4. Armed Forces Health Surveillance Center. Tri-Service reportable sus macaques. Arch Virol. 1988;99(1–2):31.
events: guidelines and case definitions, June 2009. http://www.afhsc. 20. Ritter M, Bouloy M, Vialat P, et al. Resistance to Rift Valley fever virus
mil/Documents/TriService_CaseDefDocs/June09/TriServeGuide.pdf. in Rattus norvegicus: genetic variability within certain “inbred” strains. J
Accessed October 31, 2009. Gen Virol. 2000;81(Pt 11):2683.
5. Davies FG, Martin V. Recognizing Rift Valley fever (FAO Animal Health 21. Geering WA, Davies FG. Preparation of Rift Valley fever contingency
Manual 17). Rome: Food and Agriculture Organization of the United plans (FAO Animal Health Manual 15). Rome: Food and Agriculture
Nations; 2003. Organization of the United Nations; 2002.
6. Mahy BWJ, ter Meulen V. Topley & Wilson’s microbiology and microbial 22. Adam I, Karsany MS. Case report: Rift Valley fever with vertical trans-
infections, Virology. 10th ed. London: Hodder Arnold/American Society mission in a pregnant Sudanese woman. J Med Virol. 2008;80(5):929.
of Microbiology Press. 23. Arishi HM, Aqeel AY, Al Hazmi MM. Vertical transmission of fatal Rift
7. Metwally S. Rift Valley fever. In: Brown C, Torres A, eds. Foreign animal Valley fever in a newborn. Ann Trop Paediatr. 2006;26(3):251.
diseases. 7th ed. Boca Raton, FL: Boca Publications Group, 2008. 24. Gerdes GH. Rift Valley fever. Rev Sci Tech. 2004;23:613.
8. Sall AA, de A Zanotto PM, Vialat P, et al. Origin of 1997–98 Rift Valley 25. Davies FG, Linthicum KJ, James AD. Rainfall and epizootic Rift Valley
fever outbreak in East Africa. Lancet. 1998;352(9140):1596. fever. B World Health Org. 1985;63(5):941.
9. Daubney R, Hudson JR, Garnham PC. Enzootic hepatitis or Rift Valley 26. Linthicum KJ, Anyamba A, Tucker CJ, et al. Climate and satellite
fever: an undescribed virus disease of sheep, cattle and man from East indicators to forecast Rift Valley fever epidemics in Kenya. Science.
Africa. J Pathol Bacteriol. 1931;34:545. 1999;285(5426):397.
10. Centers for Disease Control and Prevention. Rift Valley fever—East 27. Flick R, Bouloy M. Rift Valley fever virus. Curr Mol Med. 2005;5(8):827.
Africa, 1997–1998. MMWR. 1998;47(13):261. 28. World Health Organization. Rift Valley fever fact sheet. Wkly Epidemiol
11. Gad AM, Feinsod FM, Allam IH, et al. A possible route for the introduc- Rec. 2008;83(2):17.
tion of Rift Valley fever virus into Egypt during 1977. J Trop Med Hyg. 29. Centers for Disease Control and Prevention. Rift Valley fever out-
1986;89(5):233. break—Kenya, November 2006–January 2007. MMWR. 2007;56(4):73.
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SALMONELLOSIS

Box 9-6 Recommendations for Preventing
Transmission of Salmonella from
Salmonellosis (ICD-10 A02) Reptiles and Amphibians to Humans
Other names in humans: Salmonella infection
• Pet store owners, health care providers, and veterinarians
should provide information to owners and potential purchasers
Other names in animals: salmonellosis, songbird fever, fowl of reptiles and amphibians about the risks for and prevention
typhoid of salmonellosis from these pets.
• Persons at increased risk for infection or serious complications
The genus Salmonella was named after Dr. Daniel Salmon, a from salmonellosis (e.g., children younger than 5 years and
noted veterinary pathologist. As an infectious disease challenge, immunocompromised persons) should avoid contact with
it epitomizes the importance of human health and animal reptiles and amphibians and any items that have been in
health clinicians working collaboratively. It is one of the most contact with reptiles and amphibians.
common causes of infectious diarrhea and gastroenteritis. At • Reptiles and amphibians should not be allowed in
the same time, its true importance is probably underestimated; households that include children younger than 5 years or
it is thought that fewer than 1% of cases in industrialized coun- immunocompromised persons. A family expecting a child
should remove any pet reptile from the home before the infant
tries, and even fewer in developing countries, are reported.
arrives.
• Reptiles and amphibians should not be allowed in child care
Key Points for Clinicians and Public Health centers.
Professionals • Persons always should wash their hands thoroughly with soap
and water after handling reptiles and amphibians or their cages.
• Reptiles and amphibians should not be allowed to roam freely
Public Health Professionals throughout a home or living area.
• Educate clinicians that Salmonella infection is report- • Pet reptiles and amphibians should be kept out of kitchens and
other food-preparation areas. Kitchen sinks should not be used
able to public health authorities.
to bathe reptiles and amphibians or to wash their dishes, cages,
• Educate the public about the risk to children and oth- or aquariums. If bathtubs are used for these purposes, they
ers of Salmonella poisoning from food. should be cleaned thoroughly and disinfected with bleach.
• Use good kitchen hygiene; be particularly careful with • Reptiles and amphibians in public settings (e.g., zoos and
foods prepared for children, the elderly, or immuno- exhibits) should be kept from direct or indirect contact with
compromized individuals. patrons except in designated animal-contact areas equipped
• Thoroughly wash raw vegetables and fruits. with adequate handwashing facilities. Food and drink should
• Do not eat foods made with raw eggs or unpasteurized not be allowed in animal contact areas.
milk products. From Centers for Disease Control and Prevention: Diseases from reptiles. http://www.
• Cook poultry, ground beef, and eggs thoroughly. cdc.gov/healthypets/animals/reptiles.htm. Accessed January 16, 2009.
• Breastfeeding prevents salmonellosis and many other
health problems in infants.1
• Counsel pregnant women to remove any reptiles kept
• Educate the public, veterinarians, and human health
as pets in the house.4
clinicians on CDC guidelines for prevention of rep-
• Counsel immunocompromised patients, young chil-
tile and other animal associated salmonellosis; such
dren, older adults, and patients with sickle cell anemia to
educational messages have proven effective2 (Box 9-6;
avoid contact with puppies and kittens that have diar-
see also http://www.cdc.gov/healthypets/spotlight_an_
rhea and with any reptiles, baby chicks, or ducklings.
turtles.htm).3
• Ensure that local petting zoos and other areas where
the public has contact with animals have policies and Veterinary Clinicians
procedures for reduction of infection risk such as • Counsel pet owners not to feed dogs and cats raw meat
handwashing stations. diets and to wash hands after handling animals, feces,
• Ensure that local pet stores are not selling small and animal food treats.
turtles. • Counsel owners to practice good sanitation of cages,
• Disinfect with 1% sodium hypochlorite, 70% ethanol, runs, feed and water dishes; proper storage of feed and
2% glutaraldehyde, or iodine solutions. feed utensils; reduce overcrowding situations; isolate
and screen for illness in new animals.
Human Health Clinicians • Ensure that appropriate infection control proce-
dures are being followed by staff in veterinary care
• The disease is reportable to public health authorities. facilities.
• Ask about a history of pet and other animal contact in • Counsel clients that immunocompromised individu-
all patients presenting with gastroenteritis and other als, infants, and older adults should avoid contact with
Salmonella infections. reptiles, baby chicks, and ducklings.
• Counsel owners who want to give antibiotics prophy- and are potentially zoonotic. β-Lactamase–mediated anti-
lactically to their pets that that practice is ill advised microbial resistance is common. Antibiotic resistance in
due to the possibility of selecting for antibiotic-resis- Salmonella species has been linked to the use of antibiotics
tant strains. in animal agriculture.6
• Be aware of CDC recommendations about reptiles and
pets; see http://www.cdc.gov/healthypets/spotlight_ Geographical Occurrence
an_turtles.htm.
• Counsel reptile owners on proper handwashing after Salmonella occur commonly worldwide in both animals and
pet handling and not bathing reptiles in bathtubs or humans. S. Enteritidis is the most common species, followed
sinks (Figure 9-117).5 by S. typhimurium.
Agent Groups at Risk

Salmonella are gram-negative, facultative anaerobic rod- Young children appear to be at increased risk of significant
shaped bacteria belonging to the family Enterobacteriaceae infection. Playing in sandboxes has been linked to risk in
that colonize the small intestine. There are thousands of dis- children.7 Older adults and immunocompromised individ-
tinct serovars, many adapted to particular animal species. In uals are also considered high-risk groups. Individuals with
humans, the most common agents are S. typhimurium and HIV infection are at risk of recurrent septicemia. Patients
S. Enteritidis. Salmonella Typhi, the causative agent of typhoid with sickle cell disease can develop focal infections such as
fever, and S. Enteritidis serotype Paratyphi are found only osteomyelitis. Other risk factors include achlorhydria, ant-
in humans. Most Salmonella serovars have animal reservoirs acid treatment, antibiotic therapy, and malnutrition.
Figure 9-117 n Association of Reptilian and Amphibian Veterinarians Salmonella brochure. Clients must be warned of potential risks of reptile owner-
ship. (From Mader DR: Reptile medicine and surgery, ed 2, St Louis, 2006, Saunders Elsevier.)
Ownership of reptiles and other pets (including rodents) treats have been found to be contaminated and pose a risk to
is a risk factor for infection (Figures 9-118 and 9-119). An pets and their owners.
estimated 4% of the U.S. population owns reptiles, and a
FoodNet study estimated that 6% of reported salmonello-
sis cases in the United States were attributable to reptile and Hosts, Reservoir Species, Vectors
amphibian ownership.8
Animals are the natural reservoir for all Salmonella species
Salmonellosis can also be an occupational disease. An
except S. Typhi and S. Paratyphi. A wide range of species may
outbreak occurred among 45 workers in companion ani-
be asymptomatic carriers of Salmonella, including dogs, cats,
mal veterinary medical facilities, and lack of proper biosafety
birds (including poultry), cattle, swine, horses, reptiles and
precautions was considered the cause.9 Other cases have
amphibians, wildlife (including rodents), carnivores, and
occurred among veterinary pathologists performing necrop-
even crustaceans. Poultry are considered one of the principal
sies,10 workers producing poultry vaccines,11 and workers
reservoirs for Salmonella organisms and have harbored hun-
exposed to raw meat.7
dreds of different serovars.
Newborns and debilitated animals are at risk of more
Prevalence rates of subclinical infection in dogs is between
severe disease. Crowding, boarding, mixing, and malnutri-
1% and 35%.13 A recent survey found infection rates as high
tion are stressors that predispose many animals to infection.
as 50% in group-housed cats.14 Infected migrating songbirds
Group housing is associated with higher rates of infection
can result in epidemics in bird-hunting cats.
in cats. Feeding dogs and cats raw meat has been found to
Reptiles have rates of subclinical infection as high as 90%
increase the risk of infection.12 Dry pet food and pig ear dog
and pose a significant risk of transmission to pet owners and
animal handlers in zoos and pet stores. The sale or distri-
bution of small turtles has been illegal in the United States
since 1975 because children were more likely to treat smaller
turtles as toys and put them in their mouths.15 However, pet
turtles continue to be sold illegally and have caused recent
outbreaks of salmonella infection.

Salmonella is considered primarily a foodborne disease, usu-
ally of animal origin. Food or water that is contaminated
with feces from an infected animal is then ingested by a
susceptible human host (Figure 9-120). Person-to-person
spread can occur by the fecal-oral route or by food handlers
who are shedding organisms and contaminate ready-to-eat
food items.
Figure 9-118 n Young boy holding a box turtle. Turtles and other rep- Infection can occur sporadically or in large outbreaks
tiles and amphibians are sources of Salmonella infection, which is potentially
dangerous to children. (From Centers for Disease Control and Prevention
involving thousands of individuals with a common expo-
Public Health Image Library, Atlanta, Ga. Photo courtesy James Gathany.) sure.16 Contaminated peanut butter and peanut paste was
the source of a multistate outbreak of S. Typhimurium infec-
tion for people and pets through contamination of processed
foods and pet treats.17
An outbreak in humans and dogs in the United States and
Canada was linked to contaminated raw food pet treats; pre-
sumably the owners did not wash their hands adequately after
handling the treats.18 Coprophagia and scavenging spreads
the bacteria. Zoonotic transmission can also occur by direct
contact with the feces of an infected animal. Animals with
acute illness shed copious numbers of Salmonella in feces.
Ingestion of food or
Infected host Nonimmune host
water contaminated
animal animal (including
by feces, direct
(definitive host) human being)
contact with feces
Figure 9-119 n A young child appropriately washing his hands after Environmental Antibiotic Seasonality,
handling a turtle, which could have been contaminated with Salmonella. factors: use temperature
(From Centers for Disease Control and Prevention Public Health Image
Library, Atlanta, Ga. Photo courtesy James Gathany.) Figure 9-120 n The life cycle of salmonellosis.
arthritis, endocarditis, meningitis, and pneumonia. Patients

with sickle cell anemia are more susceptible to some of these
Salmonella can persist for months in food, feces, soil, and conditions.21
water given appropriate environmental conditions. The bac- In patients with AIDS and other immunocompromised
teria are resistant to dehydration and salinity. Survival in individuals, bacteremia is common and often includes severe
composted manure is as short as a week, and pasteurization complications including localized infections, fulminant diar-
kills Salmonella organisms.19 Seasonality appears to affect the rhea, and death.
occurrence of disease, with more cases reported in the spring
and summer.20 Disease in Animals
In adult cattle, sheep, pigs, and horses the disease takes three
Disease in Humans
forms: subclinical carriage, mild clinical disease, or acute
Human infection with non-typhi Salmonella can take a onset of fever and diarrhea, often with dehydration, abdomi-
number of forms, including gastroenteritis, bacteremia and nal pain, and sometimes bacteremia and death (Color Plates
vascular infection, localized infection, and chronic carrier 9-62 to 9-64). Abortion may be the presenting sign of infec-
state (Figure 9-121).21 Gastroenteritis in an immunocom- tion. Malabsorption and pneumonia may be part of the clin-
petent adult often manifests as self-limited diarrhea. The ical syndrome. Newborn calves, lambs, piglets, and foals are
incubation period is 6 to 72 hours. The principal symptoms more likely to develop septicemia (Figure 9-122). Outbreaks
are acute onset of diarrhea, often accompanied by nausea, occur on farms, often precipitated by crowding, stress, calv-
abdominal pain, headache, fever, myalgias, vomiting, and ing, and mixing in feedlots.19 Outbreaks also occur in equine
malaise. Dehydration, sometimes severe, may occur, espe- hospitals.19
cially among the young and elderly. In most cases, symptoms In dogs and cats, the disease is often subclinical. In pup-
resolve within 3 to 7 days. Diarrhea lasting longer than 10 pies, kittens, or adults stressed by hospitalization, boarding, or
days should suggest another diagnosis. However, convales- concurrent disease, acute diarrhea with fever and septicemia
cent patients may shed bacteria for weeks or months, and a can occur. Complications can include development of chronic
chronic carrier state can occur in adults.21 infection and recurrence of disease under stressful conditions.
Certain strains of Salmonella are particularly patho- In caged birds, clinical salmonellosis is rare but may be
genic in humans, such as S. choleraesuis and S. dublin, seen in immunocompromised or stressed animals (song-
which can cause prolonged bacteremia, invasive disease, bird fever) (Color Plate 9-65). Although poultry often do not
and death.6,22 However, other Salmonella serotypes can also manifest disease, two serovars adapted to poultry, S. Pullorum
cause bacteremia, which can be accompanied by endovas- and S. Gallinarum, cause serious losses on farms worldwide.
cular infection. Pullorum disease causes anorexia and diarrhea in chicks and
Localized infection can occur in 5% to 10% of cases of has a high mortality rate. Fowl typhoid due to S. Gallinarum
bacteremia. Specific infections include osteomyelitis, septic is a disease of adult birds (Figure 9-123).
Reptiles can shed Salmonella without clinical signs;
however they may develop abscesses (Figure 9-124). Infection
in wildlife is common, and clinical cases have been seen even
Non-typhoid Salmonella gastroenteritis in manatees and beluga whales.19 Table 9-58 provides clin-
ical presentations of salmonellosis in humans and other
Non-typhoid animals.
Salmonella
Lysosome
Enterocytes
IL-8 and other

mediators
Neutrophils
attraction and
migration
Figure 9-122 n One day’s death toll of neonatal calves from a dairy farm
Figure 9-121 n Pathogenesis of Salmonella gastroenteritis. (Adapted with high mortality rates in cattle of all ages during an epidemic caused by
from Kliegman RM, Behrman RE, Jenson HB et al: Nelson textbook of pedi- a highly virulent Salmonella typhimurium strain. (From Divers TJ, Peek SF:
atrics, ed 18, Philadelphia, 2007, Saunders Elsevier.) Rebhun’s diseases of dairy cattle, ed 2, St Louis, 2008, Saunders Elsevier.)
Figure 9-123 n Avian salpingitis as a result of Salmonella infection.

(From Songer JG, Post KW: Veterinary microbiology: bacterial and fun-
gal agents of animal disease, St Louis, 2005, Saunders Elsevier. Courtesy
Raymond E. Reed.)
Diagnosis
Gastroenteritis in humans due to Salmonella can resem-
ble other bacterial, viral, and protozoal forms of diar-
Figure 9-124 n Salmonella species dermatitis in an Eastern Indigo
rhea. The incubation period and the presence of fever and snake (Drymarchon cooperi, top) and green iguana (Iguana iguana, bot-
often bloody stools can help narrow the differential diag- tom). (From Mader DR: Reptile medicine and surgery, ed 2, St Louis, 2006,
nosis, and definitive diagnosis is made by bacterial culture Saunders Elsevier. Photograph courtesy D. Mader.)
Table 9-58 n Salmonella Infection: Comparative Clinical Presentations in Humans and Other Animals
Incubation
Humans
(S. Typhimurium,
S. Enteritidis, others)
Gastroenteritis Contaminated food, 6-72 hours Diarrhea, often with mucus Fecal leukocytes, organisms
immunocompromised status, or blood; abdominal seen on Gram stain, dark-
children at increased risk, cramping, fever field, or phase-contrast
prior antibiotic treatment, microscopy of feces, stool
contact with animals culture
Bacteremia HIV/AIDS, other immuno Fever, localized infection Blood culture, culture of
compromised status, sickle cell (bone, joint vascular, localized infection
anemia, older age CNS, other)
Dogs, cats Puppies and kittens at increased 3 days19 Acute diarrhea with Leukopenia with left
risk; raw meat diets; recent septicemia, pneumonia, shift, fecal culture, fecal
hospitalization, concurrent abortion, chronic febrile leukocytes, blood culture
disease/immunocompromised illness, conjunctivitis (cats)
status, pregnant dogs
Cattle, sheep, swine, Young animals at increased Variable, 6-24 Acute septicemia in Leukopenia (horses)
horses risk, crowding, malnutrition, hours in newborns19
mixing, stress, rodents, horses Acute or subacute enteritis in
Infected feed, contact with adults and young animals
sick animals with fever, watery diarrhea,
decreased milk production,
abdominal pain, abortion
Chronic enteritis (pigs and
cattle)
Caged birds Clinical disease with stress,
immunocompromised status
Poultry Chicks at increased risk for < 2 weeks Anorexia, diarrhea, death Serology for S. Pullorum,
S. Pullorum S. Gallinarum
CNS, Central nervous system.

Table 9-59 n Antibiotic Treatment of Salmonella Infection in Humans and Other Animals
Humans (gastroenteritis) Ciprofloxacin 500 mg PO BID × 5-7 days (14 days if Azithromycin 1 gm PO once, then 500 mg
immunocompromised status)23 PO q24h × 6 days
Dogs, cats (neonate, geriatric, or Follow culture and sensitivity results: trimethoprim- Enrofloxacin 5 mg/kg PO or SC q12h × 7
debilitated animal) sulfamethoxazole 15 mg/kg PO or SC q12h, days25 (avoid in neonates, pregnant or
chloramphenicol dogs 50 mg/kg PO, IV, IM, or SC growing animals)
q8h; cats 50 mg/kg PO, IV, IM, SC q12h24
Amoxicillin 10-20 mg/kg PO q8h × 10 days
(use trimethoprim-sulfamethoxazole and
chloramphenicol with caution in neonates and
pregnant animals)
Cattle, sheep, swine, horses Septicemia: broad-spectrum antibiotics initially, Ampicillin, fluoroquinolones, third-
consider trimethoprim-sulfamethoxazole generation cephalosporins; check local
antimicrobial resistance patterns19
of feces, blood, or other localized infections (such as joint References

fluid or CSF) from ill individuals. Serology is not useful in
1. Centers for Disease Control and Prevention. Division of Foodborne,
humans. Bacterial and Mycotic Diseases: Salmonellosis: general information. http://
In animals, fecal analysis and culture are used to diag- www.cdc.gov/nczved/dfbmd/disease_listing/salmonellosis_gi.html.
nose infection. In poultry, serology is used to identify and Accessed August 15, 2008.
eliminate flocks that have carriers of S. pullorum and S. 2. de Jong B, Andersson Y, Ekdahl K. Effect of regulation and education on
gallinarum. reptile-associated salmonellosis. Emerg Infect Dis. 2005;11(3):398.
3. Centers for Disease Control and Prevention. Reptile-associated salmo-
nellosis—selected states, 1998–2002. MMWR. 2003;52(49):1206.
Treatment 4. Milstone AM, Agwu AG, Angulo FJ. Alerting pregnant women to the
risk of reptile-associated salmonellosis. Obstet Gynecol. 2006;107(2 Pt
2):516.
Treatment in Humans 5. Bender JB, Minicucci L. Diseases pets and people share. Minn Med.
2007;90(4):43.
The mainstay of treatment for enteritis caused by Salmonella 6. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
and animals, vol. I: bacterioses and mycoses. 3rd ed. Washington, DC:
in immunocompetent adults is fluid and electrolyte replace- Pan American Health Organization; 2003.
ment. Mild and asymptomatic infection does not require 7. Doorduyn Y, Van Den Brandhof WE, Van Duynhoven YT, et al. Risk
antibiotic treatment. Indications for the use of antibiotics factors for Salmonella enteritidis and typhimurium (DT104 and non-
include age younger than 1 year or older than 50 years, com- DT104) infections in The Netherlands: predominant roles for raw eggs
promised immune status, and presence of vascular grafts or in Enteritidis and sandboxes in typhimurium infections. Epidemiol Infect.
2006;134(3):617.
prosthetic joints. 8. Mermin J, Hutwagner L, Vugia D, et al. Reptiles, amphibians, and
When antibiotics are used, their use should be guided by human Salmonella infection: a population-based, case-control study.
the culture and sensitivity results because some Salmonella Clin Infect Dis. 2004;38(suppl 3):S253.
organisms are resistant to ciprofloxacin and other antibi- 9. Wright JG, Tengelsen LA, Smith KE, et al. Multidrug-resistant
Salmonella typhimurium in four animal facilities. Emerg Infect Dis.
otics. Evidence of localized infection is an indication for 2005;11(8):1235.
longer courses of treatment. Antimicrobial treatment may 10. Bemis DA, Craig LE, Dunn JR. Salmonella transmission through splash
also prolong the carrier state, which may affect the ability of exposure during a bovine necropsy. Foodborne Pathog Dis. 2007;4(3):387.
some food workers to return to work. 11. Centers for Disease Control and Prevention. Salmonella serotype enter-
itidis infections among workers producing poultry vaccine—Maine,
November–December 2006. MMWR. 2007;56(34):877.
12. Stiver SL, Frazier KS, Mauel MJ, et al. Septicemic salmonellosis in two
Treatment in Animals cats fed a raw-meat diet. J Am Anim Hosp Assoc. 2003;39(6):538.
13. Finley R, Ribble C, Aramini J, et al. The risk of salmonellae shedding by
Subclinical carriage in animals is not treated with antibiot- dogs fed Salmonella-contaminated commercial raw food diets. Can Vet
ics. If an adult dog or cat has uncomplicated gastroenteri- J. 2007;48(1):69.
tis, it also can be treated without antibiotics with isolation, 14. van Immerseel F, Pasmans F, De Buck J, et al. Cats as a risk for trans-
supportive care, and gastrointestinal protectants. Infected mission of antimicrobial drug-resistant Salmonella. Emerg Infect Dis.
2004;10(12):2169.
neonates, aged, and immunocompromised animals are 15. Centers for Disease Control and Prevention. Reptiles and Salmonella. http://
candidates for isolation, possible plasma transfusions, sup- www.cdc.gov/Features/ReptilesSalmonella. Accessed August 15, 2008.
portive care, and glucocorticoid (for endotoxic shock) and 16. Centers for Disease Control and Prevention. Salmonella. http://www.
antibiotic therapy. Fecal cultures should be monitored on cdc.gov/nczved/dfbmd/disease_listing/salmonellosis_gi.html. Accessed
a monthly basis to determine whether an animal is a car- August 15, 2008.
17. Centers for Disease Control and Prevention (CDC). Multistate out-
rier. Table 9-59 shows recommend antibiotics for treatment break of Salmonella infections associated with peanut butter and pea-
of Salmonella infection in humans and other animals when nut butter-containing products—United States, 2008–2009. MMWR.
antibiotic treatment is appropriate. 2009;58(4):85.
18. Centers for Disease Control and Prevention. Human salmonellosis 22. Jones TF, Ingram LA, Cieslak PR. Salmonellosis outcomes differ sub-
associated with animal-derived pet treats—United States and Canada, stantially by serotype. J Infect Dis. 2008;198(1):109.
2005. MMWR. 2006;55(25):702. 23. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
19. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
Station, NJ: Merck; 2005. 2009.
20. Oloya J, Theis M, Doetkott D, et al. Evaluation of Salmonella occur- 24. Tilley LP, Smith FWK. Blackwell’s five-minute veterinary consult: canine
rence in domestic animals and humans in North Dakota (2000–2005). and feline. 3rd ed. Ames, IA: Blackwell; 2004.
Foodborne Pathog Dis. 2007;4(4):551. 25. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
21. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious panion: canine and feline infectious diseases and parasitology. Ames, IA:
diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005. Blackwell; 2006.
SCABIES
Russell W. Currier and Roger I. Ceilley • Educate veterinarians about the zoonotic potential
of scabies and other mites and encourage voluntary
Sarcoptic itch (ICD-10 B86) Other acariasis (ICD-10 B88.0) reporting of cases of sarcoptic mange in animals.
Other names in humans: sarcoptic itch, acariasis, crusted

scabies, Norwegian scabies, pseudoscabies, cavalryman’s itch, Human Health Clinicians
pig-handler’s itch • Disease usually not reportable but public health author-
ities should be notified in outbreak settings such as
Other names in animals: sarcoptic mange, cutaneous among institutionalized persons and day care centers.
acariasis • In evaluating cases of pruritic skin rash, consider pos-
sibility of zoonotic transmission of scabies or other
Scabies is a skin infestation caused by the mite Sarcoptes mites (pseudoscabies); ask about contact with animals
scabiei. Reports of scabies in humans date back to antiquity, or fomites that could contain mites. Consider consult-
and it was the first infectious disease linked to a specific etiol- ing a veterinarian.
ogy with the use of a microscope. In 1834 the mite was con- • Immunocompromised patients may present with
clusively demonstrated on a young female patient in a Paris heavier scabies mite burdens, requiring extended treat-
clinic, establishing the association between the mite and its ment regimens.
dermatological manifestations.1 This little-appreciated his- • Delusions of parasitosis can be an underlying condi-
torical event represented the first etiological diagnosis in tion in the absence of scabies or following diagnosis
medicine. In human medicine, scabies continues to cause and treatment of actual infestations.
both sporadic cases and outbreaks in industrial countries,
and immunocompromised persons can experience severe
infection. Dogs and many other animals also experience sig- Veterinary Clinicians
nificant infections with variants of S. scabiei that are adapted • Counsel owners of a pet with scabies about the risk
to particular host species. With close contact such as occupa- of human transmission and that it could be self-limit-
tional exposure, transmission of animal scabies variants from ing or persistent, requiring treatment after the pet has
animals to humans can occur. Although such zoonotic infes- been treated.
tations (pseudoscabies) are usually self-limited, they under- • Advise health care providers and public health profes-
score the importance of communication between human sionals about the risk to humans of animal scabies and
and animal health professionals about cases of skin rashes other mite infestations.
occurring concurrently in humans and animals. This section • Companion animals should be carefully screened for
focuses on scabies, but there are a number of other mite spe- scabies and other mite infestations.
cies that infest animals and are capable of causing self-lim- • Animal scabies may be reportable to agriculture/pub-
ited skin infections in humans that may be misdiagnosed or lic health authorities if history is linked with a pet store
missed by medical providers. or facility that permits contact with animals in public
settings (e.g., petting zoo).
• Some states require reporting of sarcoptic mange in
sheep and cattle.
Professionals
Public Health Professionals Agent

• Be alert for outbreaks of skin disease caused by scabies Sarcoptes scabiei is a species of mite in the family Sarcoptidae
in situations of human crowding. that lives parasitically on or in the skin of mammals. Adult
• Consider zoonotic mite infestation as a cause of out- mites are 0.3 to 0.5 mm long and roughly circular with
breaks of skin rashes in the community; consult with four pairs of legs (Figure 9-125). Variants of S. scabiei are
local veterinarians. found in a variety of animal species but are taxonomically
Figure 9-126 n Feline scabies. Microscopic image of Notoedres cati

mite from a skin scraping as seen with a ×10 objective. (From Medleau L,
Hnilica KA: Small animal dermatology: a color atlas and therapeutic guide,
ed 2, St Louis, 2006, Saunders Elsevier. Courtesy G. Norsworthy.)
Figure 9-125 n Ventral view of a cleared and mounted Sarcoptes sca-

biei mite. (From Centers for Disease Control and Prevention Public Health
Image Library, Atlanta, Ga.)
specific, it is capable of infecting humans as well, causing a
papular skin rash or an external otitis.6
Notoedres cati (feline scabies) is a rare but highly conta-
i ndistinguishable between human and animal species. For gious disease of cats that can also infect humans,7 causing
example, scabies in dogs is caused by S. scabiei var canis.2 In a pruritic rash within hours without visible skin burrows
addition to S. scabiei, a number of other mites that infest ani- (Figure 9-126 and Color Plate 9-66).
mals are able to also cause skin rashes in humans. Table 9-60
lists some of these mite species with zoonotic potential. Geographical Occurrence
Dermanyssus gallinae, the red poultry mite, is a noctur-
nal blood-sucking mite that is the most common mite found Scabies is a global problem with widespread distribution
in pigeons. Close contact with poultry, wild birds, or nest- in human populations of all ages. It is also found in animal
ing material can lead to human infection, which presents as populations worldwide. Outbreaks of often fatal sarcoptic
a nonspecific dermatitis that is intensely pruritic and often mange in animals have occurred in wildlife populations such
misdiagnosed.3,4 as foxes, leading to fluctuations in population size.
Cheyletiella species, the walking dandruff mite, may be
present as a subclinical infection in dogs and cats but can Groups at Risk
cause an erythematous, papular rash in humans in contact
with infected animals. The papules are usually on the arms, Human scabies can occur in outbreaks among institutional-
trunk, and buttocks and develop into yellow crusted lesions ized patients8 or in other situations of crowding such as refu-
that can be intensely pruritic. Rarely, bullous eruptions and gee camps. The presence of immunocompromised patients
systemic reactions have been reported.5,6 in such settings may facilitate transmission, and immuno-
Otodectes cynotis is a common mite found in the ears of compromised individuals are at risk of more severe infec-
dogs and cats, where it causes local irritation. It can migrate tion. Sexual contact is another major risk factor for disease
to other parts of the pet’s body, and because it is not host transmission.
Persons at risk for zoonotic transmission of scabies include
farmers, veterinarians, wildlife rehabilitators, and pet owners
Table 9-60 n Mites With Zoonotic Potential who have close contact with potentially infected animals.
In industrialized nations, scabies often presents as a sex-
Mite Species Name Host Species ually transmitted parasitic infection with secondary trans-
mission to household members, especially children, who are
Sarcoptes scabiei Scabies Humans, dogs, cattle, easily infected when parents or caretakers are infested.9
foxes, horses, pigs Patients with HIV-AIDS and other immunocompromis-
Dermanyssus gallinae Red poultry Chickens, pigeons, ing states are easily infected and sustain heavy mite burdens
mite other birds leading to crusted or hyperkeratotic scabies.10
Cheyletiella species Fur mite, Cat, dog, rabbit, small In animal populations, contact with infected animals is
walking mammals the major risk factor for scabies infection. Puppies, espe-
dandruff mite cially those from a pound or animal shelter or whelped in
Otodectes cynotis Ear mite Dogs, cats a large breeding kennel, may be at increased risk. Dogs that
Notoedres cati Feline scabies Cats are allowed to roam freely and contact wildlife or other dogs,
including at dog parks, may be at higher risk of infestation.6
specific animal populations. Species affected include dogs,

cattle, sheep, pigs, horses, and foxes. Variants adapted to one
species may infect another species, but in such instances sus-
tained transmission does not occur.
The S. scabiei mite is not considered a vector for other
infectious agents, although cases of infestation may become
superinfected with Staphylococcus, Streptococcus, or other
bacteria.

Scabies is transmitted through sustained direct skin-to-
skin contact12 during activities such as sexual contact,
holding infants and animals, or while performing hands-
on care. Casual contact such as handshaking is unlikely to
lead to transmission. Sustained person-to-person and other
intraspecies transmission requires adult female mites. After
impregnation, the female burrows quickly into the epider-
mis of the host animal, forming a tunnel in the stratum cor-
neum at the boundary with the stratum granulosum (Figure
9-128). Two to three large eggs are laid daily and these hatch
in 4-6 days, giving rise to nymphal mites that molt to adult
forms. Eggs develop into adult mites within 10 to 14 days.
Because many variants of the scabies mite cannot live
long outside the body, indirect transmission via fomites is
generally less important than direct transmission. However,
in the case of crusted (hyperkeratotic) scabies, infected indi-
viduals have enormous quantities of mites on their person
Figure 9-127 n Hyperkeratosis caused by Sarcoptes scabiei in the fox and shed mites on clothing, bed linen, and even furniture.13
(×22). The mites (arrows) are found in the deeper layers of the greatly thick-
ened epidermis. (From Bowman DD: Georgis’ parasitology for veterinarians,
These mites can persist for days on particles of sloughed epi-
ed 9, St Louis, 2009, Saunders Elsevier.) dermis. In such situations, contact with fomites can easily
lead to further disease transmission.
When an animal strain of S. scabiei infects a human, the
Debilitated animals may be at increased risk of severe cases mite is able to penetrate the skin and rapidly cause a pru-
of sarcoptic mange. ritic rash but is unable to successfully reproduce and persist.
Wildlife also can sustain scabies; foxes are particularly The result is the self-limited condition termed pseudoscabies.
susceptible to heavy mite infestations (Figure 9-127). In one Reverse zoonotic transmission can also occur.
case report, a wild red fox (Vulpes vulpes) infected a wildlife
rehabilitator and a veterinarian who were treating the ani-
mal, as well as several dogs residing near a golf course where
the affected fox was originally found.11 Mites in the environment are highly susceptible to tempera-
ture and humidity conditions and rarely survive beyond 2 to
Hosts, Reservoir Species, Vectors 3 days. Higher ambient temperatures lead to lower survival
times.7 Environmental conditions that predispose human
Only one distinct genus and species of S. scabiei exists but to scabies transmission include crowding and institutional-
variants are somewhat host adapted to humans and various ization. Similarly, environments with animal crowding and
Direct contact Infected human being

Infected animal (rare)
Direct Direct
contact contact
Fomites in environment
Susceptible animal Susceptible human being
(especially crusted scabies)
Environmental factors: Crowding, temperature, dog-wildlife contact

Figure 9-128 n Scabies transmission.
extensive animal-to-animal contact, such as animal shel- Elderly patients such as residents of long-term care facili-
ters, breeding colonies, dog parks, and crowded kennels, may ties frequently have extensive lesions on the shoulders and
encourage animal-to-animal transmission of scabies. Areas upper back as well as the usual areas noted. Secondary ecze-
where wildlife such as foxes contact domestic animals also matization or thickening of the skin is common in this pop-
represent environmental risks. ulation, as well as low-grade bacterial infections such as
Staphylococus aureus and Streptococcus pyogenes. Although
these cases are fairly easy to diagnose, they also are more
Disease in Humans
challenging to treat.
Scabies in humans is manifested about 20 to 35 days after Crusted or hyperkeratotic (Norwegian) scabies occurs
transmission and results in pruritus that is particularly evi- usually in immunocompromised patients and has a distinc-
dent in the evening hours while the affected person is trying tive appearance of grey-green crustiness on the hands and
to sleep. This hypersensitivity is incompletely understood and feet, occasionally elbows and arms. Pruritus may be absent.
results from some metabolite of the mites. Skin lesions com- This condition is also easy to diagnose but very difficult to
monly appear on the webbing of the fingers, genitalia, breasts, treat. Color Plate 9-68 shows a patient with crusted scabies.
flexor surface of the wrists, elbows, and later the abdomen. In cases of pseudoscabies, intense pruritus and an erythema-
The burrow or track is diagnostic (Color Plate 9-67) but is not tous rash are often present, but burrows may be absent.
always visible. More commonly papules and vesicles are the
most typical skin lesions. Feet and legs are commonly affected Disease in Animals
areas in children. Rarely do lesions appear on the face and
neck except in infants and immunocompromised patients, in The presentation of disease in animals is variable as shown
whom face and neck lesions are more common. in Table 9-61. The hallmark of animal scabies is pruritus
Table 9-61 n Clinical Presentation of Scabies in Humans and Other Animals

Sarcoptes scabiei Incubation
Species Variant Risk Factors Period Clinical Manifestations Diagnostic Findings
Humans
Scabies Variant hominis Crowding 2-6 weeks Papular rash, vesicles, Skin scraping may
(1-4 days if pruritus reveal mites
previously
infested)18
Crusted scabies Variant hominis Immunocompromised 2-6 weeks18 Diffuse crusting lesions, Skin scraping reveals
status, fomites pruritus may be absent high mite burden
Pseudoscabies Animal variants Direct contact with 2-6 weeks18 Self-limited rash, Skin scraping often
(zoonotic) infected animal pruritus negative
Dogs Variant canis Kennels, animal shelters, 2-6 weeks18 Pruritic papules with Skin scraping, fecal
dog parks, contact thick crusts; abdomen, flotation may reveal
with infected wildlife; chest, ears, elbows, mites or eggs;
puppies at increased risk and legs affected; ELISA antibody test
alopecia minimal early can show specific
in disease with more antibodies7
hair loss later
Cattle Variant bovis Rare in United States; 2-6 weeks18 Head, neck, shoulders
contact with infected with later spread to
animals entire body
Lesions on nonwooly
Sheep Variant ovis Rare in United States; 2-6 weeks18 skin
contact with infected
animals
Goat Variant caprae Rare in United States 2-6 weeks18 Generalized
hyperkeratosis Skin scrapings
showing either
Horses Variant equi Rare in United States; 2-6 weeks18 Intense pruritus mites, eggs, or
contact with infected Head, neck, shoulders scybala
animals affected; alopecia
and crusting; later
lichenified with skin
folds
Pigs Variant suis Contact with infected 2 to 11 weeks Generalized pruritus;
animals or bedding crusting of luminal
surface of ears
Foxes Variant vulpes Contact with infected 2-6 weeks18 Diffuse alopecia,
animal or bedding crusting, wasting
that may not represent location of mites; this is also true for
humans (Figures 9-129 and 9-130). Generally longer dura-
tion infestations result in thickening of skin with secondary
bacterial infections.7
In clinical veterinary practice, sarcoptic mange is a com-
mon presentation in dogs. The infestation has no age, breed,
or sex predilection, occurs with no seasonality, and presents
as an intensely pruritic, papular crusting dermatosis affect-
ing the periocular skin, pinnal margins, elbows, and hocks,
which may later progress to more generalized involvement,
especially of the ventral areas (Figure 9-131). There may
be very little to moderate hair loss in contradistinction to
demodicosis (eyelash mites) or red mange, which shows little
pruritus and extensive alopecia.
Figure 9-131 n Canine scabies. Generalized alopecia and crusts affect-
In horses, sarcoptic mange is the most severe type of ing a pruritic puppy. The alopecic ear pinnae are characteristic of scabies.
mange, with intensely pruritic lesions on the head, neck, and (From Medleau L, Hnilica KA: Small animal dermatology: a color atlas and
shoulders. Swine historically have suffered extensive involve- therapeutic guide, ed 2, St Louis, 2006, Saunders Elsevier.)
ment, calling for routine mass treatment of most herds. Modern

antihelmintic treatment of swine with broad-spectrum para-
siticides has successfully eliminated this problem. Foxes may
develop severe sarcoptic mange that can be fatal.
Diagnosis
Skin scrapings are the most common and reliable method
to demonstrate the presence of mites, eggs, and scybala (dis-
crete fecal pellets) in both humans and other animals. This
procedure is as simple as it is essential and could be per-
formed by technicians, nursing staff, physicians, and veteri-
narians. Standard references14 call for applying mineral oil
(some clinicians prefer to use type B microscopic immersion
oil because it is more viscous and easier to work with) to
Figure 9-129 n Sarcoptic mange in a guinea pig caused by Trixacarus a lesion or placing oil on a sterile scalpel blade (disposable
caviae. (From Quesenberry K, Carpenter JW: Ferrets, rabbits, and rodents:
clinical medicine and surgery, ed 2, St Louis, 2004, Saunders Elsevier.) #10 or #20), which is held at a right angle to the skin sur-
face and used to scrape the area in a manner to remove vis-
ible skin debris until the superficial skin or stratum corneum
is removed, leaving the scraped area pink but not neces-
sarily hemorrhaging. The material adhering to the blade
from two to three postage stamp–sized areas is then trans-
ferred to a microscope slide, diluted with more oil if neces-
sary, with a cover slip applied after using it to scrape excess
oil adhering to the scalpel blade, and the wet mount speci-
men is examined under ×4 and ×10 low power. The slide
should be methodically examined as follows: Sweep left to
right, move down one field, and right to left until the entire
slide area is examined for mites (adults, nymphs, or larval
mites) or distinctive eggs and the smaller scybala (fecal pel-
lets that are numerous and distinct brown-gold/orange in
color). Occasionally some skin lesions may be due to the
Demodex folliculorum mite (eyelash mite) that has wide-
spread distribution in human populations. These distinctive
cigar-shaped mites have an elongated tail structure, whereas
Sarcoptes mites have a distinctive turtle-like shape with four
Figure 9-130 n Chamois with clinical scabies. The typical lesions pairs of legs (Figure 9-132).
begin at the head and neck and then spread over the back. (From Fowler
M, Miller RE: Zoo and wild animal medicine current therapy, ed 6, St Louis, The scraping procedure not only enables diagnosis within
2008, Saunders Elsevier. Courtesy T. Steineck, Research Institute of Wildlife minutes, but also helps to classify patients for mite load.
Ecology, VMU, Vienna.) A human patient’s scraping with only a mite or two prob-
red, raised, pruritic lesions and evidence of secondary

eczematization. Although these lesions are not specifi-
cally crusted scabies, these cases are classified as “atypical
crusted scabies” or “aggressive scabies” and require more
intense treatment and oversight.15
In dogs and humans, skin scrapings may not always pro-
duce mites or their effects but call for thorough attempts at
recovery nonetheless. After scraping and in the absence of
mites, a diagnosis can be made based on exclusion of other
diseases, epidemiological links, clinical impression (degree
of pruritus, history, distribution pattern), and response to
treatment.
Other techniques for diagnosis include epidermal shave
biopsy, needle biopsy, and burrow ink test. In the latter tech-
Figure 9-132 n Scabies organism in a wet mount preparation. (From nique, a blue or black felt-tip pen is rubbed over the lesions
Mandell GL, Bennett JE, Dolin R (eds): Principles and practice of infectious
diseases, ed 6, Philadelphia, 2005, Churchill Livingstone Elsevier.)
and then ink is removed with an alcohol pledget and the
blue or black ink dye is pulled into the burrow by capillary
action and is diagnostic. A solution of tetracycline can also
be applied and examined under a Wood’s light.
ably is not highly infectious for others (average of 10 adult
female mites on a patient) and needs only minimal treat- Treatment
ment and simple contact precautions for a brief period of
a day or two. However, patients with crusted or hyperk-
eratotic scabies demonstrate an extraordinary number of Treatment in Humans
mites on each slide. Patients, especially the elderly with
a history of extensive home care or long-term care resi- Table 9-62 outlines treatment guidelines with various scabi-
dency, may have a large number of mites from skin with cides. Treatment is preceded with a bath or shower in water
Table 9-62 n Treatment of Scabies in Humans and Other Animals
Humans
Scabies Permethrin 5% cream, apply entire skin chin to Ivermectin 200 mcg/kg PO once, second
toes, leave on 8-14 hr, repeat in 1 wk (safe in dose after 14 days or Crotamiton 10%
children >2 months) cream, apply × 24 hr, rinse and reapply
× 24 hr17
Immunocompromised, crusted Permethrin 5% as above day 1, then 6% sulfur Ivermectin 200 mcg/kg PO on days 1 and
(Norwegian) scabies in petrolatum daily days 2-7, repeat × several 14 PLUS permethrin 5% cream on days
weeks 1 and 1416
Pseudoscabies (zoonotic mite No treatment may be necessary; veterinary
transmission) consultation for treatment of animal contacts
Dogs Lime sulfur dip for young dogs, several dips 5 days Ivermectin 200 mcg/kg PO or SC, for 2
apart treatments 2 weeks apart (contraindicated
Selamectin 6 mg/kg topically; repeated twice in Collies and Collie crosses)
at 1-month interval7
Cattle Toxaphene, coumaphos, phosnet, Injectable avermectins except dairy cattle
lime sulfur dip (dairy cattle)
Sheep, Goat Injectable ivermectin Doramectin or moxidectin
Horses Organophosphate insecticide or lime-sulfur Ivermectin or moxidectin 200 mcg/kg PO ×
solution by spraying, sponging, or dipping; several treatments 2-3 weeks apart
repeat at 12- to 14-day intervals at least 3-4
times7
Pigs Ivermectin 300 mcg/kg SC, repeat in 2 weeks Lindane, malathion, or chlordane sprays7
or doramectin 300 mcg/kg IM
Foxes Ivermectin 200 mcg/kg PO or SC, for 2
treatments 2 weeks apart
of tepid temperature. Patients should clip fingernails and toe- handled by individuals with diabetes or applied to patients
nails, remove rings and bracelets, and wash the area under nails with diabetes.
with a hand brush or toothbrush. Apply the scabicide accord- Systemic therapy is an attractive alternative and includes
ing to directions behind the ears and from the neck down, extralabel use of macrocyclic lactones—for example, ivermec-
paying particular attention to the hands (especially between tin (Ivomec; Merial Animal Health), milbemycin (Interceptor;
fingers), the umbilical area, groin, the buttocks, and feet (espe- Novartis Animal Health), moxidectin (Cydectin; Fort Dodge
cially between the toes). The medication should be left on for Animal Health), and selamectin (Revolution; Pfizer Animal
the prescribed number of hours and then thoroughly rinsed Health) that are licensed for treatment of canine sarcoptic
off with tepid soapy water (bath or shower). At the conclusion mange. Ivermectin should not be used in Collies or sheep
of therapy, intimate articles of clothing and bed linens should dogs and their crosses. Consult product literature for safe
be laundered in hot water and dried on the hot cycle. Patients and proper administration.16
should be counseled that 24 hours after therapy, they no longer It would be prudent to also treat all dogs known to have
are infectious but may still experience itching for a few weeks contact with an affected animal. Concurrent environmental
afterward. Family members should be treated even if asymp- treatment of bedding, grooming equipment, and the gen-
tomatic. The majority of patients respond to one treatment, eral areas of habitation with an ascaricidal spray (e.g., one
and although there is a lack of well-controlled studies docu- containing permethrin) is recommended to prevent possible
menting that two applications are better than one, treatment reinfestation.
is usually repeated, especially if there is microscopic and/or
morphologic evidence of treatment failure. Patients in institu-
tional settings may have a higher mite burden and require one
to two additional treatments. References
Scabies in immunocompromised individuals (crusted or
Norwegian scabies) generally requires much more intense 1. Friedman R. The story of scabies. Medical Life. 1934;41(8):381.
scabicidal treatment. Keratolytic agents (salicylic acid or 2. Champion RH, Burton JL, Burns DA, et al., eds. Rook/Wilkinson/Ebling
textbook of dermatology. 6th ed. Malden MA: Blackwell; 1998.
alpha-hydroxy acid products) can be used to soften tissue, 3. Cafiero MA, Camarda A, Circella E, et al. Pseudoscabies caused by
permitting better penetration of topicals, coupled with fre- Dermanyssus gallinae in Italian city dwellers: a new setting for an old
quent reassessment and longer periods of contact isolation. dermatitis. J Eur Acad Dermatol Venereol. 2008;22(11):1382.
Bedding and personal effects initially need special handling. 4. Rosen S, Yeruham I, Braverman Y. Dermatitis in humans associated with
the mites Pyemotes tritici, Dermanyssus gallinae, Ornithonyssus bacoti
Such patients have heavy mite burdens and need multiple and Androlaelaps casalis in Israel. Med Vet Entomol. 2002;16(4):442.
applications of topical treatments. 5. Dobrosavljevic DD, Popovic ND, Radovanovic SS. Systemic mani-
Treatment of pseudoscabies due to zoonotic mite trans- festations of Cheyletiella infestation in man. Int J Dermatol. 2007;
mission often relies on treatment of the infected animal 46(4):397.
and disinfection of the environment. Consultation with a 6. Moriello KA. Zoonotic skin diseases of dogs and cats. Anim Health Res
Rev. 2003;4(2):157.
veterinarian is recommended if zoonotic transmission is 7. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse
suspected. Station, NJ: Merck; 2005.
8. Arlian LG. Biology, host relations, and epidemiology of Sarcoptes scabiei.
Ann Rev Entomol. 1989;34:139.
Treatment in Animals 9. Green MS. Epidemiology of scabies. Epidemiol Rev. 1989;11:126.
10. DePaoli RT, Marks VJ. Crusted (Norwegian) scabies: treatment of nail
Treatments for animals are summarized in Table 9-62. involvement. J Am Acad Dermatol. 1987;17(1):136.
Requirements vary with species and age of the animal. It is 11. Rabinowitz PM, Gordon Z. Outfoxing a rash: clinical example of
wise to follow label directions owing to risk of toxicity. It is human-wildlife interaction. EcoHealth. 2004;1:404.
important to counsel animal handlers about risk of human 12. Mellanby K. Scabies in 1976. R Soc Health J. 1977;97(1):32.
13. Carslaw RW, Dobson RM, Hood AJK, et al. Mites in the environment of
transmission. Norwegian scabies. Br J Dermatol. 1975;92(3):333.
Treatment may be approached topically or systemically. 14. Muller G, Jacobs PH, Moore NE. Scraping for human scabies: a better
Topical treatments include a 2.5% lime sulfur dip (Lym Dip; method for positive preparations. Arch Dermatol. 1973;107(1):70.
DVM Pharmaceutical, Inc.) that is licensed for weekly use 15. Lerche NW, Currier RW, Juranek DD, et al. Atypical crusted
“Norwegian” scabies: report of nosocomial transmission in a commu-
with a wide margin of safety. Disadvantages include foul nity hospital and an approach to control. Cutis. 1993;31(6):637.
odor and staining of light-colored coats. Amitraz (Mitaban; 16. van den Hoek JA, et al. A persistent problem with scabies in and outside
Pharmacia & Upjohn Animal Health) is an alternative and a nursing home in Amsterdam: indications for resistance to lindane and
is applied as a 0.025% sponge-on solution at 2-week inter- ivermectin. Eurosurveillance. 2008;13(48).
vals. Amitraz should not be used on Chihuahuas, in pregnant 17. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
bitches, or puppies younger than 3 months. Clipping hair of 2009.
dogs with long coats and/or dense hair coats is recommended. 18. Heymann DL, ed. Control of communicable diseases manual. 19th ed.
Amitraz vapors can induce hyperglycemia; it should not be Washington, DC: American Public Health Association; 2008.
TOXOCARA INFESTATION
Peter M. Rabinowitz and Lisa A. Conti • Counsel pet owners about the proper disposal of animal
feces and handwashing.
Visceral larva migrans (ICD-10 B83.0) • See the CDC manual about toxocariasis for veterinari-
ans that reviews specific prevention and treatment mea-
Other names in humans: roundworm infection, ocular larva sures4; available online at http://www.cdc.gov/ncidod/
migrans, Toxocara infection) dpd/parasites/ascaris/prevention.htm.
• Recommend keeping cats indoors.
Other names in animals: roundworm infection, ascariasis
Agent
Infection with roundworms of the genus Toxocara is prob-
ably one of the most common infections associated with Toxocara canis and T. cati are ascarid roundworms (nematodes)
ownership of cats and dogs. Puppies and kittens often have that are large (10 to 12 cm long) and live in the small intes-
symptomatic infections. Visceral or ocular larval migrans tine of carnivorous mammals but also migrate into tissues and
can occur in people. Seroprevalence studies suggest 5% to cause extraintestinal pathology (Figure 9-133). T. canis is rec-
30% of children may be infected.1,2 ognized more widely in both animals and humans than T. cati

Professionals

• Provide descriptive epidemiology of the likely preva-
lence in animal and human populations.
• Educate the public on modes of transmission and ways
to prevent infection:
 Control stray dogs and cats.
 Encourage dog and cat owners to have their ani-
mals regularly dewormed by a veterinarian.
 Encourage basic handwashing awareness.
 Discourage keeping raccoons as pets.
 Cover sandboxes when not in use.
• Promote local measures to require that dog and cat
feces are picked up by owners and do not contaminate
local soils and play areas.
• Educate the local veterinary and human health clini-
cians in risk areas and during high-risk periods about
groups at risk and the signs and symptoms of disease.

• Teach parents, especially pet owners, of the danger of
contamination and exposure of areas by feces from
untreated dogs and cats.
• Teach parents to not allow geophagia.
• Teach patients to always wash hands after handling soil
and before eating.3
• Encourage patients with dogs and cats to ensure ade-
quate veterinary treatment for worm infection. It is espe-
cially important for pregnant dogs and cats and young
puppies and kittens to be dewormed. If a human health
clinician inquires about this, it might raise awareness.
• No human vaccine is available.
Veterinary Clinicians Figure 9-133 n Adults of Toxocara canis. The male measures 6 cm and
the female measures 9 cm in length. (From Long SS, Pickering LK, Prober
• Ensure pet owners bring animals for strategic deworm- CG: Principles and practice of pediatric infectious diseases, ed 3, Edinburgh,
ing and prompt parasite treatment. 2008, Churchill Livingstone Elsevier.)
and causes more serious infections in dogs.5 Toxascaris leonina highest attack rates as a result of direct contact with dogs
is seen in adult dogs and cats and is less well recognized as a and cats and/or soil contaminated by infective eggs. Children
zoonotic agent. The raccoon roundworm, Baylisascaris procyo- with pica (inappropriate ingestion of soil and other sub-
nis, results in rare but serious disease in humans. stances related to nutritional deficiencies) are considered at
increased risk.
Toxocara infections occur worldwide, with human sero-
prevalence rates varying widely (from 0 to more than 80%) Humans, dogs, cats, and wild carnivores can develop clinical
among populations.3 A recent CDC study estimated the sero- manifestations. Humans are a terminal host, meaning that
prevalence rate in the United States at 14%.6 In one study, the roundworms cannot reproduce and carry on their life
more than 30% of dogs younger than 6 months sampled cycle. Rodents are paratenic hosts.7
across the United States were shedding T. canis eggs, whereas
rates of feline infection with T. cati have been reported to Mode of Transmission and Life Cycle
exceed 25%.
In both animals and humans, infection often begins by swal-
lowing of infective, embryonated eggs. Because the eggs take
Groups at Risk
up to two weeks to embryonate, the source of eggs is usually
Although roundworms can occur in adults, disease in chil- contaminated soil or food rather than direct contact with an
dren is most frequently reported. A recent CDC seropreva- infected animal.8 These eggs then hatch, the larvae penetrate
lence study found increased risk among children and youth the intestinal mucosa, and then migrate through the liver
younger than 20 years. Children are believed to have the and bloodstream to the lungs (Figure 9-134). In humans,
Larvae migrate to various

organs where their
Circulation development is arrested
Larvae
released
in intestine In pregnant and lactating dogs, the
larvae can be reactivated and cause:
- intestinal infection in the mother
- infection of the offspring
Dogs > 5 weeks (by transplacental and
(non-pregnant) transmammary transmission)
Circulation → Lungs → Bronchial

Larvae released tree → Esophagus
in intestine
Human (and other

paratenic hosts) In heavy infections, larvae Adults in lumen
can passed in feces of intestine
Dogs < 5 weeks
Eggs passed in feces

Eggs ingested
External Environment
i
Embryonated Eggs
egg with larva
i  Infective stage
Enviromental factors: Soil contamination, pet sanitation policies

Figure 9-134 n Life cycle of Toxocara canis and Toxocara cati, the causal agents of toxocariasis. (Adapted from
Centers for Disease Control and Prevention Public Health Image Library, Atlanta, Ga.)
they may then pass to other tissues as well, causing granu- Visceral larva migrans is seen particularly among pre-
lomatous lesions in the lungs and abdominal organs (visceral school children. Signs and symptoms include fever, weight
larva migrans) or the eye (ocular larva migrans).3 If infective loss, wheezing, cough, abdominal pain, skin rashes, and
eggs are swallowed by a puppy, the larvae hatch and migrate hepatosplenomegaly. Laboratory findings include leukocy-
as above; but once in the lungs, the larvae are often coughed tosis and eosinophilia.
up and swallowed to then mature into adult worms in the Ocular larva migrans may develop as long as 10 years after
animal’s small intestine. These adult worms then produce infection with T. canis and is usually seen among older chil-
eggs, which are shed in the puppy’s feces, and also can cause dren who present with unilateral vision loss. Findings on
abdominal distention and obstruction. examination can include a subretinal mass, leukocoria, cata-
Transplacental transmission occurs when a pregnant racts, and retinal scarring (Color Plate 9-69).8 When motile
bitch transmits infective larvae directly to the developing larvae are trapped in the eye, a diffuse unilateral subacute
fetus. Larvae that migrate to the mammary gland can also be neuroretinitis can occur.9
passed to puppies during nursing.5
Cats are thought to be infected by eating tissue contain- Disease in Animals
ing larvae of other infected animals, especially rodents.7
Transplacental passage of T. canis is not thought to occur in T. canis infection in dogs usually produces more severe signs
cats, but transmammary transmission has been reported.4 in puppies than in older dogs. In puppies infected in utero,
a parasitic pneumonia may develop with a resultant high
mortality rate. Development of a large parasitic load in the
intestine may lead to abdominal distention, colic, anorexia,
Because the eggs of Toxocara species can survive for years in vomiting, rough hair coat, diarrhea, cachexia, coughing,
soils,7 the degree of environmental contamination of play- and sometimes death. Neurological involvement may occur
grounds, sandboxes, and other locations frequented by chil- including twitching and seizures. Eosinophilia is often seen.
dren is a significant environmental risk factor. In surveys Cats generally have less severe disease than dogs. A pot-
in the United States, the United Kingdom, and Japan, 30% bellied appearance, diarrhea, and vomiting may develop.
of playground soil samples and 75% of sampled sandboxes Eosinophilia is common.7
contained potentially infectious eggs.3 Table 9-63 compares the clinical presentations of toxocar-
iasis in humans and other animals.
Disease in Humans
Toxocara infection in humans is usually asymptomatic. When Diagnosis
disease develops, it is often chronic and mild and related to
hypersensitivity response to larval invasion of tissues. The In humans, clues to the diagnosis of visceral larva migrans
two main forms of disease are visceral larva migrans and include a history of exposure to contaminated soils or foods,
ocular larva migrans. the appearance of typical signs and symptoms, eosinophilia,
Table 9-63 n Toxocariasis: Clinical Presentations in Humans and Other Animals
Humans: visceral larva Preschool age: ingestion Weeks to months (the Abdominal pain, fever, Leukocytosis,
migrans of contaminated soils disease is self-limited hepatosplenomegaly, eosinophilia, anti-
or food but the larvae may rash, wheezing Toxocara antibodies
remain dormant in
tissues for years)
Humans: ocular larva Children Up to 10 years Unilateral vision loss,
migrans retinal scarring/
subretinal mass on
examination
Dogs (usually Toxocara Prenatal exposure, Weeks Parasitic pneumonia, Eosinophilia, leukocytosis,
canis) nursing, ingestion of respiratory difficulty, eggs in feces
contaminated soils death
Abdominal infection:
abdominal distention,
vomiting, diarrhea
Cats (usually T. cati) Ingestion of soils Weeks Abdominal distention, Eosinophilia, leukocytosis,
containing eggs, vomiting, diarrhea eggs in feces
nursing or eating
animal tissue
containing larvae
and antibodies to Toxocara. Enzyme immunoassay with

Treatment
Toxocara excretory-secretory antigens is the preferred sero-
logical test.8 However, it may lead to underdiagnosis if a
person is infected with an unusual serovar not well covered Treatment in Humans
by the standard test. Serial serology titers are required to
Antihelmintic treatment is directed toward relief of symp-
document seroconversion; a fourfold increase in titer is
toms. Because infection is generally asymptomatic in
considered evidence of recent infection.10
humans, treatment is sometimes withheld. In cases of severe
Ocular migrans is diagnosed clinically. Antibody titers to
organ involvement, steroids may be indicated in addition to
Toxocara species may be elevated in aqueous and vitreous
antihelmintics. Table 9-64 outlines treatment guidelines in
fluid compared with serum levels, which may aid in diagno-
humans and other animals.
sis. The differential diagnosis includes other causes of retinal
masses, including retinoblastoma.9
In animals, the detection of eggs in feces through a fecal Treatment in Animals
flotation test is diagnostic (Figure 9-135). The spherical, pit-
In dogs and cats, infection is usually treated aggressively with
ted eggs of T. canis and T. cati can be distinguished from the
a number of antihelmintic agents. Because transplacental
smooth, ovoid eggs of T. leonine, which has less zoonotic
infection does not occur with T. cati, cats are usually treated
potential.5
as kittens.
Strategic deworming against roundworms (and hook-
worms) includes deworming the pregnant dog; treating pup-
pies and kittens beginning at 2 weeks of age, then every 2 weeks
through weaning (6 to 8 weeks); and then treating monthly
until the pet is 6 months old. Nursing dogs and queens should
be treated with their litters. Older animals can be monitored
through at least annual fecal examinations. Many pups and
T
kittens are not brought to the veterinarian until they are 6 to 8
weeks, so owners of pregnant animals need to work with their
veterinarians to ensure earlier deworming.
H References
H 1. Ellis Jr GS, Pakalnis VS, Worley G, et al. Toxocara canis infestation.
Clinical and epidemiological associations with seropositivity in kinder-
garten children. Ophthalmology. 1986;93(8):1032.
2. Marmor M, Glickman L, Shofer F, et al. Toxocara canis infection of
children: epidemiological and neuropsychologic findings. Am J Public
Health. 1987;77(5):554.
Figure 9-135 n Photomicrograph of a fecal flotation analysis from a dog Washington, DC: American Public Health Association; 2008.
demonstrating characteristic ova from hookworms (H) and Toxocara canis (T). 4. Centers for Disease Control and Prevention. CDC guidelines for veter-
(Magnification ×400.) (From Willard MD: Disorders of the intestinal tract. In inarians: prevention of zoonotic transmission of hookworm and ascarid
Nelson RW, Couto CG (eds): Small animal internal medicine, ed 4, St Louis, infection of dogs and cats. http://www.cdc.gov/ncidod/dpd/parasites/
2009, Mosby Elsevier. Courtesy Tom Craig, Texas A & M University.) ascaris/prevention.pdf. Accessed February 7, 2008.
Table 9-64 n Toxocariasis Treatment in Humans and Other Animals
Humans: visceral larva migrans Albendazole 400 mg PO BID × 5 days Mebendazole 100-200 mg PO bid × 5
days11
Humans: ocular migrans First 4 weeks of symptoms: prednisone 30-60 mg PO qd, PLUS subtenon triamcinolone
40 mg/week × 2 weeks11
Dogs: treatment in pregnancy Fenbendazole 50 mg/kg PO q24h from day Ivermectin 1 mg/kg PO q24 on days 20 and
40 of gestation to 2 weeks after birth 42, or 0.5 mg/kg PO on days 38, 41, 44,
Milbemycin oxime 0.5 mg/kg PO and 477
Pyrantel pamoate 5-10 mg/kg PO
Dogs: pups at 2 weeks of age then every Pyrantel pamoate 5mg/kg PO Praziquantel/pyrantel/febantel (praziquantel
2 weeks until 8 weeks, then monthly Fenbendazole 50 mg/kg PO q24h × 3 days 5-12 mg/kg) PO once
thereafter Milbemycin oxime 0.5 mg/kg PO
Cats Fenbendazole 50 mg/kg PO q24h × 3 days Selamectin 6/mg/kg topically
Pyrantel pamoate 5 mg/kg PO
5. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse 9. Mandell GE, Bennett JE, Dolin R, eds. Principles and practice of infectious
Station, NJ: Merck; 2005. diseases. 6th ed. Philadelphia: Churchill Livingstone Elsevier; 2005.
6. Won K, Kruszon-Moran D, Schantz P, et al. National seroprevalence 10. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
and risk factors for zoonotic Toxocara spp. infection. Am J Trop Med and animals: vol. 1: bacterioses and mycoses. 3rd ed. Washington, DC:
Hyg. 2008;79(4):552. Pan American Health Organization;
7. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com- 11. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
panion: canine and feline infectious diseases and parasitology. Ames, IA: microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
Blackwell; 2006. 2009.
8. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
handbook for primary care. St Louis: Mosby Elsevier; 2005.
TOXOPLASMOSIS
Toxoplasmosis (ICD-10 B58) Congenital toxoplasmosis (P37.1)
Other names in humans: Toxoplasma infection
Other names in animals: Toxoplasma infection
Toxoplasmosis is a common zoonotic infection in nearly all

mammals and some birds caused by the obligate, intracellu-
lar organism Toxoplasma gondii. Cats are the definitive host,
shedding oocysts in their feces. Toxoplasmosis can cause
severe and fatal disease in fetuses and immunocompro-
mised patients. Ingestion of oocysts following contact with
cat feces or contaminated soil is a pathway for human infec- Figure 9-136 n A pregnant woman in the process of washing a batch of
tion. However, a number of human infections are believed assorted produce before the preparation of a salad. Note that the food prepara-
to result from eating raw or undercooked meat containing tion area around the sink is also kept clean and free of unclean kitchen imple-
infectious cysts.1 Toxoplasmosis is a disease that underscores ments either inside or outside the sink. (From Centers for Disease Control and
the importance of communication between veterinarians Prevention Public Health Image Library, Atlanta, Ga. Courtesy James Gathany.)
and human health clinicians; studies have found that many
physicians provide inappropriate advice to their pregnant
patients regarding the risk of disease from cats. • Educate local veterinary and human health clinicians
about the signs and symptoms of the disease.
• Work with local animal control agencies to encourage
control of stray cat populations.
Professionals

• Educate patients (particularly seronegative pregnant
• Educate the public on reducing risk of infection by: patients and immunocompromised patients) about
 Proper food handling (fruits and vegetables thor- risk reduction (avoidance). With such measures, preg-
oughly washed or peeled) and cooking (145° F for nant and immunocompromised individuals should
beef or lamb; 160° F for pork, ground meat, or wild not have to give up a cat.
game; 180° F for poultry). • No human vaccine is available.
 Appropriate kitchen hygiene (washing items in hot
soapy water after they come in contact with raw meats Veterinary Clinicians
or unwashed fruits and vegetables) (Figure 9-136).
 Appropriate hand hygiene: washing hands after • Counsel pet owners about the following additional
handling raw meats, soil, or sand. preventive steps:
 Pregnant women and immunocompromised per-  Do not feed bones, viscera, unpasteurized milk (espe-
sons should wear gloves when handling soil, sand, cially goat’s milk), or raw or undercooked meat to cats.
and avoid handling soil. They should avoid han-  Wash your hands after handling cats and cat litter.
dling cat feces by having someone else change the  Dispose of cat litter on a daily basis to reduce the
cat litter or by wearing gloves to do so. They should risk of exposure to infectious oocysts.
not have to give up their cat (Figure 9-137).  Disinfect cat litter box with boiling water on a
 Keeping sandboxes covered and vegetable gardens weekly basis.
fenced.  Keep cats indoors.
Figure 9-138 n Histopathology of active toxoplasmosis of myo-

cardium. Numerous tachyzoites of Toxoplasma gondii are visible within
a pseudocyst in a myocyte. (From Centers for Disease Control and
Prevention Public Health Image Library, Atlanta, Ga. Courtesy Edwin P.
Ewing, Jr.)
11.0% (95% CL 9.5%, 12.4%).3 Higher rates have been reported

in other parts of the world, including European countries where
undercooked meat consumption is common, and sub-Saharan
Africa where extensive contact with cats can occur.1
Groups at Risk
Analysis of NHANES data has suggested that individuals in
occupations with soil contact, lower educational level, living
Figure 9-137 n A pregnant woman is about to pet her cat while her hus- in crowded conditions, and foreign-born individuals are at
band is in the process of changing the cat’s litter so that the woman can avoid
contact with possible pathogens such as Toxoplasma gondii, the etiologic increased risk.1 Other studies have reported increased risk
agent responsible for the disease toxoplasmosis. (From Centers for Disease with cat ownership, soil contact, eating unwashed vegetables,
Control and Prevention Public Health Image Library, Atlanta, Ga. Courtesy and eating undercooked or raw meat. In a number of studies,
James Gathany.) however, current ownership of a cat has not been associated
with increased risk of seropositivity.1 Fetuses and immuno-
compromised persons are particularly vulnerable to severe
• Counsel owners that healthy seropositive cats are lit- sequelae from infection.
tle danger to owners. Seronegative cats that have the
potential to become infected and shed oocysts are Hosts, Reservoir Species, Vectors
more of a human risk.
• A modified live vaccine is available in Europe and New Cats and other felids are the only hosts in which T. gondii
Zealand for sheep. can reproduce sexually. Infection is most commonly seen
in intermediate hosts such as humans, sheep, goats, swine,
dogs, and horses, although most mammals and some birds
Agent
are infected. Game animals such as deer can be infected with
Toxoplasma gondii is a protozoan that has three infectious tissue cysts, posing a risk for human consumption.
stages: oocysts (shed in the feces, containing sporozoites), Mechanical vectors include contaminated vegetables and
tachyzoites (rapidly multiplying form found in tissues), and other food products, soil, and sand.
bradyzoites (slowly multiplying form found in tissues; Figure
9-138).2 In addition, tissue cysts (found in muscle or CNS Mode of Transmission and Life Cycle
tissue) contain dormant bradyzoites.
When naïve cats ingest viable Toxoplasma organisms, the
parasite is able to reproduce in the cat’s intestinal lining and
results in the shedding of immature oocysts in the feces. After
The disease is found worldwide. The U.S. National Health and a period of 2 to 3 weeks, the cat develops immunity and no
Nutrition Examination Survey (NHANES 1999-2004) found longer sheds oocysts. The immature oocysts shed in cat feces
an age-adjusted T. gondii seroprevalence among persons 6 to 49 are not immediately infectious but take 1 to 5 days to sporulate
years old of 10.8% (95% confidence limits [CL] 9.6%, 11.9%), into mature oocysts with viable sporozoites (Figure 9-139).
and a rate among women of childbearing age (15 to 44 years) of These infectious oocysts can persist in the environment for
Figure 9-139 n Life cycle of toxoplasmosis. (From Centers for Disease Control and Prevention Public Health
Image Library, Atlanta, Ga. Courtesy Alexander J. DaSilva and Melanie Mosher.)
several months. If they are ingested by an intermediate host to contact with cat feces or contaminated soil or fomites, and
either directly or through contaminated soil, they begin to congenital infection. The relative importance of these differ-
asexually multiply in the host’s intestinal epithelium and pro- ent routes of transmission is poorly understood and prob-
duce tachyzoites. The tachyzoites disseminate in the interme- ably varies by geographical region. A survey of more than
diate host’s bloodstream and lymph system both freely and 6000 commercial samples of beef, chicken, and pork from
intracellularly within monocytes and macrophages.4 After retail stores in the United States found a low incidence of
several weeks of rapid multiplication, the intermediate host infectious cysts, with viable T. gondii detected only in sam-
may develop immunity. Once the host is immune, the life ples of pork.6 Transplacental transmission occurs during
cycle shifts to the production of bradyzoites, which multiply active infection of the mother with the tachyzoite phase. The
less rapidly and tend to form tissue cysts in brain, myocardial, risk of transmission from an infected pregnant woman to
and nervous tissue where they may persist for life. her fetus is considered lower in early pregnancy (although
If an intermediate host ingests raw or undercooked meat the consequences to the fetus are greater) than in subsequent
containing these cysts, the bradyzoites may be released and weeks.7 Other transmission pathways include organ trans-
develop into tachyzoites. The first time cats are infected, the plants and blood transfusions.
parasite’s life cycle is completed when some of the bradyzoites
initiate a sexual cycle to produce unsporulated oocysts that Environmental Risk Factors
are shed in the feces for 1 to 2 weeks. Cats are typically resis-
tant to reinfection.5 A number of factors, such as humidity and temperature,
The primary routes of toxoplasmosis transmission to determine how long it takes for immature oocysts to develop
humans are the ingestion of raw or undercooked meat that into mature infectious oocysts and how long such oocysts
contains viable cysts, the ingestion of infectious oocysts due can persist in soil and water and on environmental surfaces.
Disease in Humans
Most cases of toxoplasmosis in immunocompetent children
and adults are asymptomatic. Symptoms, when they occur,
are usually self-limited and can include significant cervical
or other lymphadenopathy and fever with atypical lympho-
cytosis. Rarer complications can include toxoplasmic chori-
oretinitis, myocarditis, and myositis. The incidence of ocular
toxoplasmosis in immunocompetent persons is believed to
be more common than previously thought, and toxoplas-
mosis is one of the most common causes of uveitis in the
general population, leading to vision loss in some cases.8,9
Encephalitis and even death can occur but are rare in immu-
nocompetent hosts.9
In immunocompromised patients, toxoplasmosis often
produces severe disease, including encephalitis and cerebral
abscesses (Figure 9-140), pneumonitis, chorioretinitis (Color
Plate 9-70), and myocarditis with a high mortality rate if
the disease is not treated in a timely fashion. Symptoms of
encephalitis can include confusion, seizures, sensorimotor
deficits, and ataxia.10 Infection in immunocompromised
humans may be the result of reactivation of latent infec-
tion but can also result from acute infection. Organ trans-
plants can be a source of infection in immunocompromised
persons.9
One of the most significant complications of human
toxoplasmosis infection occurs when a pregnant woman is
in the acute phase of the illness (tachyzoite phase) and the
organism passes to a fetus, resulting in congenital infection.
Congenital toxoplasmosis can present as mild to severe dis-
ease, with complications including hydrops fetalis, perinatal
death, prematurity, decreased birth weight, retinal scarring,
and a classical triad of chorioretinitis, hydrocephalus, and
cerebral calcifications (Figure 9-141). Although more than
half of infected newborns are considered normal shortly
after birth, most will develop ocular and/or other complica-
tions if not treated.11
Disease in Animals
Evidence of past infections in cats and many other animal
species is common, but clinical cases are rarely recognized
because most infections are subclinical (Figure 9-142). In
cats, the disease is most commonly seen in congenitally
infected kittens, leading to stillbirth, neonatal fever, respira-
tory distress, uveitis, and neurological involvement (Color
Plate 9-71).12 It is also seen in immunocompromised animals
with lethargy, fever, neurological signs, or generalized retini-
tis (Color Plate 9-72).
Dogs, especially puppies, may develop acute signs of infec-
tion including fever, respiratory signs (Color Plate 9-73), and
diarrhea. Immunosuppressed older dogs may manifest neu-
rological involvement (Figure 9-143).
In sheep, goats, and swine, toxoplasmosis can cause abor-
tion and neonatal mortality (Figure 9-144). Birds, including Figure 9-140 n MRI images of Toxoplasma abscess in the right thala-
mus with extensive surrounding vasogenic edema and irregular peripheral
poultry, are commonly infected but generally do not mani- enhancement. A, Axial T2-weighted and (B) gadolinium-enhanced T1-
fest clinical signs. Table 9-65 compares clinical presentations weighted images. (From Adam A, Dixon AK (eds): Grainger & Allison’s diag-
of toxoplasmosis in humans and other animals. nostic radiology, ed 5, Edinburgh, 2008, Churchill Livingstone Elsevier.)
Figure 9-141 n Congenital toxoplasmosis with hydrocephalus. (Courtesy

Peter Rabinowitz.)
Figure 9-143 n Lipemia retinalis in a Dachshund with toxoplasmosis.

Lipemia retinalis makes blood vessels look pink (red blood with white lipid
added). There are multifocal gray opacities indicative of active chorioretini-
tis. (From Dziezyc J, Millichamp NJ: Color atlas of canine and feline ophthal-
mology, St Louis, 2005, Saunders Elsevier.)
Figure 9-142 n Photomicrograph of Toxoplasma gondii tachyzoites from

the lungs of a cat with acute toxoplasmosis. The extracellular tachyzoites are
crescent shaped with a centrally placed nucleus. They are approximately 6
microns in length (bronchoalveolar lavage fluid, Wright stain). (From Hawkins
EC: Diagnostic tests for the lower respiratory tract. In Nelson RW, Couto CG
(eds): Small animal internal medicine, ed 4, St Louis, 2009, Mosby Elsevier.) Figure 9-144 n Ovine protozoal placentitis, toxoplasmosis, abortion,
placenta, sheep. The cotyledons have hundreds of white foci of necrosis, a
lesion that is characteristic of Toxoplasma gondii–induced abortion in sheep
and goats. (From McGavin MD, Zachary JF: Pathologic basis of veterinary
Diagnosis disease, ed 4, St Louis, 2007, Mosby Elsevier. Courtesy Ontario Veterinary
College, University of Guelph.)
In humans, the cornerstone of diagnosis is serology.13 High
titer of anti-Toxoplasma IgM suggests an acute infection
(IgM titers can persist for 18 months), whereas IgG anti-
bodies may indicate past infection. Elevated IgM titers can
Treatment
be verified at a Toxoplasma reference laboratory such as the
CDC or Toxoplasmosis Serology Lab (Palo Alto Medical Treatment in immunocompetent humans is usually not
Foundation Research Institute).5 When congenital toxoplas- indicated because of the mild and self-limited nature of
mosis is suspected, diagnostic studies include maternal sero- the disease. If significant organ involvement occurs or in
conversion detected via the immunosorbent agglutination particular clinical situations such as immunocompromise,
assay (ISAGA), fetal ultrasound findings, and amniocentesis pregnancy, and congenital infection, antimicrobial treatment
with PCR detection of T. gondii. is necessary (Table 9-66). In addition to antimicrobials, pred-
In animals, the serological testing for IgG, IgM, and anti- nisone is added to the treatment regimens for congenital tox-
gen with follow-up tests in 3 weeks helps differentiate acute oplasmosis, chorioretinitis, and toxoplasma meningitis. The
from chronic infection. The IgM antibodies rise 2 weeks recommended treatment regimens are complex, and consul-
after infection and may persist for a maximum of 3 months. tation with an infectious disease specialist is advisable.
A fourfold increase in IgG titers between samples is also sug- Antibiotics can be used in animals but they may not clear
gestive of a recent infection.12 infection.
Table 9-65 n Toxoplasmosis: Comparative Clinical Presentations in Humans and Other Animals
Incubation
Human beings 10-23 days

Immunocompetent Ingestion of raw or Usually asymptomatic in Immunohistochemical
undercooked meat or direct immunocompetent host, staining, PCR, serology (IFA,
exposure to oocysts from or lymphadenopathy, ELISA)
cat feces chorioretinitis can occur
Immunocompromised Reactivation of latent disease Encephalitis, pneumonitis, Abnormal CT, MRI, CSF
or new infection (see chorioretinitis, other findings
above), organ transplants
Congenital Maternal infection Fetal death, prematurity; triad of Maternal seroconversion
chorioretinitis, hydrocephalus, detected via ISAGA; fetal
cerebral calcifications; delayed ultrasound findings,
ocular disease amniocentesis with PCR
detection of Toxoplasma gondii
Cats Hunting, immunodeficiency, 3-21 days Usually subclinical Serology (ELISA, IFA, CF), fecal
congenital Neurological involvement flotation for active infection
Fever, respiratory distress, (oocysts are 10-12 mcm)
ocular involvement
Dogs Ingestion of undercooked Weeks Usually subclinical, varies with As with cats
meat, immunodeficiency, organ system involvement,
congenital including encephalitis, myositis,
hepatitis, and retinitis
Sheep, goats Ingestion of oocysts from Weeks Abortion, neonatal death As with cats
contaminated soil
CF, Complement fixation; CSF, cerebrospinal fluid; CT, computed tomography, ISAGA, immunosorbent agglutination assay; MRI, magnetic resonance imaging.
Table 9-66 n Toxoplasmosis Treatment in Humans14 and Other Animals15
Humans: Immunocompetent
Acute illness with lymphadenopathy No treatment unless severe symptoms or significant organ involvement
Active chorioretinitis, meningitis, Pyrimethamine 200 mg PO on day 1, then 50-75 mg q24h PLUS sulfadiazine 1-1.5 gm
transfusion related PO qid PLUS leukovorin (folinic acid) 5-20 mg 3×/wk, treat 1-2 week beyond resolution
of signs/symptoms; continue leukovorin 1 week after stopping pyrimethamine, PLUS
prednisone 1 mg/kg/day in 2 divided doses for acute inflammation16
Acute infection in pregnancy <18 wk gestation: spiramycin 1 gm PO q8h until delivery if amniotic fluid PCR negative
>18 wk gestation and documented infection: pyramethamine 50 mg PO q12h x 2 days
then 50 mg/day PLUS sulfadiazine 75 mg/kg PO x 1 dose then 50 mg/kg q12h (max.
4 gm/day) PLUS folinic acid 10-21 mg PO daily
Congenital Management complex; consultation with specialist advisable; pyrimethamine PLUS
sulfadiazine PLUS leucovorin16
Patients With AIDS
Cerebral toxoplasmosis Pyrimethamine 200 mg PO, then 75 mg/ Pyrimethamine PLUS folinic acid PLUS
day PO PLUS sulfadiazine 1-1.5 gm PO qd either clindamycin, clarithromycin,
PLUS folinic acid 10-20 mg/day PO × 4-6 azithromycin, or atovaquone16
weeks after signs/symptoms resolve; then
suppressive treatment or TMP-SMX 10/50
mg/kg/day PO/IV divided q12h × 30 days
Suppression after treatment of cerebral Sulfadiazine 500-1000 mg PO 4×/day Clindamycin PLUS pyrimethamine PLUS
toxoplasmosis PLUS pyrimethamine 25-50 mg PO q24h folinic acid or atovaquone16
PLUS folinic acid 10-25 mg PO q24h
Primary prophylaxis: patients with AIDS TMP-SMX DS 1 tab PO q24h or TMP- Dapsone PLUS pyrimethamine PLUS folinic
with CD4 < 100 and positive IgG SMX-SS 1 tab PO q24h acid or atovaquone16
Toxoplasma antibody
Cats Clindamycin 10-12.5 mg/kg PO/IM Trimethoprim-sulfadiazine 15 mg/kg PO/IV
q12h × 2-4 wk q12h × 2 wk
Dogs (Rare) Clindamycin 10-12.5 mg/kg PO/IM Trimethoprim-sulfadiazine 15 mg/kg PO/IV
q12h × 2-4 wk q12h × 2 wk13
TMP-SMX, Trimethoprim-sulfamethoxazole.
References 8. Holland GN. Reconsidering the pathogenesis of ocular toxoplasmosis.

Am J Ophthalmol. 1999;128(4):502.
1. Jones JL, Kruszon-Moran D, Wilson M, et al. Toxoplasma gondii infec- 9. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
tion in the United States: seroprevalence and risk factors. Am J Epidemiol. diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005.
2001;154(4):357. 10. Sax PE, Cohen CJ, Kuritzkes DR. HIV essentials. Royal Oak, MI:
2. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Merck; 2005. Physicians Press; 2007.
3. Jones JL, Kruszon-Moran D, Sanders-Lewis K, et al. Toxoplasma gon- 11. Kliegman RM, Behrman RE, Jenson HB, et al. Nelson textbook of pediat-
dii infection in the United States, 1999–2004, decline from the prior rics. 18th ed. Philadelphia: Saunders Elsevier; 2007.
decade. Am J Trop Med Hyg. 2007;77(3):405. 12. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
4. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man panion: canine and feline infectious diseases and parasitology. Ames, IA:
and animals: vol. III: chlamydioses, parasitoses. 3rd ed. Washington, DC: Blackwell; 2006.
Pan American Health Organization; 2003. 13. Remington JS, Thulliez P, Montoya JG. Recent developments for diag-
5. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases nosis of toxoplasmosis. J Clin Microbiol. 2004;42(3):941.
of companion animals. Ames, IA: The Center for Food Security and Public 14. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
Health, Iowa State University College of Veterinary Medicine; 2008. microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
6. Dubey JP, Hill DE, Jones JL, et al. Prevalence of viable Toxoplasma 2009.
gondii in beef, chicken, and pork from retail meat stores in the United 15. Giguere S, Prescott JF, Baggot JD, et al. Antimicrobial therapy in veteri-
States: risk assessment to consumers. J Parasitol. 2005;91(5):1082. nary medicine. 4th ed. Ames, IA: Blackwell; 2006.
7. Dunn D, Wallon M, Peyron F, et al. Mother-to-child transmis-
sion of toxoplasmosis: risk estimates for clinical counseling. Lancet.
1999;353(9167):1829.
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Peter M. Rabinowitz and Lisa A. Conti lower rates (see “Disease in Humans” section on the follow-
ing page). Chronic wasting disease (CWD), a prion disease
Subacute spongiform encephalopathy, Creutzfeldt-Jakob of wildlife such as deer and elk, is extending its range in the
disease (CJD) (ICD-10 A81.0) United States and Canada. Scrapie, a prion disease of sheep,
continues to affect sheep and goat populations in some
Other names in humans: variant CJD, fatal familial insom- parts of the world. The origin, transmissibility, and ability
nia (FFI), and Gerstmann-Sträussler-Scheinker disease for cross-species infection of these diseases remain poorly
(GSS), prion disease, TSE, kuru understood. Therefore ongoing vigilance for the emergence
of TSE-related disease in humans and other animals by
Other names in animals: bovine spongiform encephalop- human and veterinary clinicians and public health authori-
athy (BSE), mad cow disease, feline spongiform enceph- ties is warranted.
alopathy (FSE), chronic wasting disease of elk and deer
(CWD), transmissible mink encephalopathy (TME), exotic
ungulate encephalopathy, scrapie
Professionals
In 1986, an outbreak of bovine spongiform encephalopathy
(BSE) occurred in the United Kingdom that was eventually
linked to the use of livestock feed containing meat and bone
from animals infected with a prion disease (prion is short • Encourage reporting of human prion disease to public
for proteinaceous infectious particle). Shortly afterward, out- health authorities. CJD is reportable in some states. If
breaks of transmissible spongiform encephalopathies (TSEs) it is not reportable in your region, consider adding it to
were reported in zoo animals and domestic cats that had the list of reportable diseases.
consumed BSE-contaminated meat products. In retrospect, • Ensure safety of the blood supply (leukodepletion,
this unusual occurrence of prion diseases in animals was a screening of donors to exclude those who have resided
sentinel event for human health risk. In 1996, the emergence in high-risk areas).2
in humans of a variant form of Creutzfeldt-Jakob disease • Ensure that steps are being taken to reduce the possi-
(vCJD), a progressive dementia, was attributed to consump- bility of transmission of prion diseases through organ
tion of contaminated beef from BSE-infected cattle. As a transplant and infected surgical instruments; see guide-
result of the implementation of a number of feed bans, such lines at http://www.who.int/csr/resources/publications/
as a prohibition against feeding mammalian protein to any bse/WHO_CDS_CSR_APH_2000_3/en/.
farmed animals in the United Kingdom, the incidence of • In areas where CWD has been reported, educate hunt-
reported cases of both BSE and vCJD has dropped dramati- ers about measures to reduce the risk of exposure to the
cally in recent years. Outbreaks in cats and other animals also CWD agent, including not harvesting deer or elk that
declined related to similar feed bans. appear sick or abnormal; wearing puncture-resistant rub-
Despite the success in controlling BSE and vCJD, prion ber, vinyl, or latex gloves while dressing carcasses; avoid-
diseases continue to be a public health concern. Sporadic ing contact with brain, spinal cord, and lymphoid tissues;
Creutzfeldt-Jakob disease (CJD), which has no known link deboning meat; disinfecting knives, saws, and tables with
to animal prion diseases, occurs worldwide at a case rate of 50% bleach; and having animals tested for CWD.3
approximately 1 case per 1 million persons.1 Other varia- • Investigate clusters of human cases of neurodegenera-
tions of human prion disease are reported worldwide at tive disease.
been detected in neighboring states, as well as in Wisconsin,

Illinois, West Virginia, New York, and in the provinces of
• Report suspected cases of iatrogenic CJD, vCJD, Alberta and Saskatchewan in Canada.
or human CWD cases to local and state health The prevalence of scrapie among sheep in the United
departments. States has been estimated at approximately 0.2%, based on
• Conduct an autopsy on suspected human cases and voluntary surveillance.10 Scrapie is considered eradicated
submit tissues for diagnosis to the National Prion from Australia and New Zealand.
Disease Pathology Surveillance Center; see http:// Transmissible mink encephalopathy (TME), first
www.cjdsurveillance.com/. described in 1947, has occurred sporadically in the United
• Remove or institute enhanced sterilization procedures States, Canada, Finland, Germany, and Russia.
on contaminated surgical or dental instruments from
practice.4,5 Groups at Risk
Groups at increased risk for vCJD include those who resided
in the United Kingdom during the BSE epidemic and con-
• Consider the diagnosis of a TSE in cattle, sheep, cats, sumed beef products. Hunters are at risk of exposure to
and other animals with abnormal behavior and pro- CWD in deer and elk through dressing carcasses and meat
gressive neurological deterioration consistent with consumption. Similarly, persons working with sheep and
prion disease. goat carcasses may have some exposure to the scrapie agent,
• Counsel owners and farmers about federal feed restric- and mink farmers may have exposure to TME. To date, no
tions and proper feeding practices to reduce risk of cases of TSEs related to CWD, FSE, or TME exposure have
disease transmission. been described in humans.11
Agent Hosts, Reservoir Species, Vectors

TSEs are believed to be caused by abnormal forms (PrP ) sc
BSE is a disease of cattle, but concurrent with the BSE out-
of naturally occurring (PrPC) cellular prion proteins.6 These break in the United Kingdom, a similar disease tied to BSE-
misshapen prion proteins are capable of self-replication contaminated feed consumption appeared in other bovids
and transmissibility and form protease-resistant deposits in kept in zoos, including kudu, eland, oryx, gemsbok, bison,
the brains of infected animals. For many years, TSEs were nyala, and Ankole (exotic ungulate encephalopathy).
referred to as slow virus infections because of their transmis- FSE has been found in fewer than 100 domestic cats and
sibility, resistance to filtration, and long latent periods. Most captive felids, including cheetahs, pumas, ocelots, and a tiger.9
pathologic features of prion diseases involve the CNS. TSE CWD occurs in captive and free-ranging Cervidae,
agents, such as the agent of scrapie, are remarkably resis- including mule deer, white-tailed deer, and elk, and has been
tant to disinfection and inactivation by heat, radiation, or detected in a moose.
chemicals,7 although more robust disinfection strategies are Scrapie occurs in sheep and goats.
effective.8 Strains differ between abnormal prions infecting
different species, possibly related to variations in the three- Mode of Transmission and Life Cycle
dimensional protein structure or length and sequence of
the amino acid chain. The BSE agent has been transmitted Transmission of BSE, vCJD, FSE, and TME is believed to be
experimentally, using a variety of techniques and doses, to due to ingestion of contaminated animal products (Figure
other species, including cats, mice, pigs, sheep, goats, cattle, 9-145). Scrapie can be transmitted horizontally in flocks.
mink, macaque monkeys, and marmosets.9 In addition, maternal transmission appears to play a role in
scrapie infection.12 Person-to-person transmission of vCJD
has been reported through contaminated blood products,
possibly due to the persistence of the agent in lymphocytes.
vCJD has been reported mostly in the United Kingdom, with CWD transmission appears related to both direct contact
smaller numbers of cases reported elsewhere in Europe and between animals and indirect contact with contaminated
in Japan. Three cases reported in the United States and one environments.
case reported in Canada are believed to be the result of expo-
sure to the BSE agent overseas. In addition to the United Environmental Risk Factors
Kingdom, BSE has been reported in smaller numbers in
most other European countries and in Japan, Israel, Canada, Transmission of iatrogenic CJD involves contaminated arti-
and the United States. cles such as surgical instruments. For other TSEs, the role
Cases of feline spongiform encephalopathy (FSE) were of environmental contamination is less clear. CWD is spread
reported in captive felids in zoos in the United Kingdom horizontally between deer and elk, and such transmission is
and domestic cats in the United Kingdom and Europe. Cases believed to be due in part to environmental contamination,
have declined greatly since a ban on bovine spleen and CNS leading to ingestion of the agent.3 Research is focusing on the
tissue in cat foods.2 role of saliva in the environmental spread of disease. Scrapie
CWD of deer and elk occurs primarily in an endemic may also be transmitted through pastures contaminated with
area of Colorado and Wyoming. In recent years, CWD has birth products from an infected animal.3
Inoculation (transmission) Disease in Animals

Spontaneous conformational change
Sporadic cases BSE initially presents with subtle locomotive and behavioral
Inherited cases abnormalities that progress over a period of months. Cattle
spend decreased time ruminating and demonstrate increased
PrPc nose licking, sneezing, nose wrinkling, head tossing, and
teeth grinding. An increased startle response can develop, but
PrPc undisturbed animals may develop paresis, ataxia, and fall-
PrPSc ing episodes. Weight loss and decreased lactation can occur.
PrPc Recumbency (downer cow), coma, and death occur weeks to
PrPc
months later (Figure 9-146).
An atypical form of BSE has been reported to be due to
Normal PrP a variant prion causing a disease termed bovine amyloidal
PrPSc PrPc spongiform encephalopathy (BASE). The molecular form of
this new bovine PrPsc resembles that found in a particular
Conformational change, form of human sporadic CJD.6
may require other proteins
Converts PrPc to PrPSc
CWD of elk and deer produces subtle changes in behav-
ior and weight loss (Figure 9-147). A spectrum of symptoms
To form
Aggregates amyloid
including loss of fear of humans, somnolence, and hyper-
PrPSc PrPSc excitability may occur. Late disease manifests with increased
plaques
water consumption, increased salivation, low head carriage,
Figure 9-145 n Prion protein. In prion diseases (spongiform encephal- a fixed stare, and chronic weight loss despite continued feed
opathies), PrP (Pr Pc), a normal neuronal protein, is converted to an abnor- intake.3
mal β-pleated sheet isoform (PrP Sc) through the interaction of PrPSc with FSE produces an increase in aggressive or shy behav-
PrPc. (From McGavin MD, Zachary JF: Pathologic basis of veterinary disease,
ed 4, St Louis, 2007, Mosby Elsevier.) ior, ataxia, and increased sensitivity to sound or touch. On
biopsy of cases, spongiform degeneration of the neuropil of
the brain and spinal cord have been described (Color Plate
9-74).9 Death occurs within 6 to 8 weeks of onset of signs.
Disease in Humans Scrapie also has an insidious onset, with behavioral
changes including increased excitability. Tremors of the head
At least four different prion-related diseases have been and neck (tremblante du mouton) may occur, as can sei-
reported in humans, all chronic and invariably fatal neu- zures. Intense pruritus develops, leading to loss of fleece over
rodegenerative conditions. These include CJD, Gerstmann- body areas (Figure 9-148).
Sträussler-Sheinker syndrome (GSS), fatal familial insomnia TME produces abnormal behavior, including increased
(FFI), and kuru. Of these, CJD is the most common.2 GSS excitability, tremors, circling, and biting. The disease progresses
and FFI are genetically mediated diseases, whereas kuru to death within weeks or months. Table 9-67 compares clinical
transmission has been linked to cannibalism among island- presentations of TSEs in humans and other animals.
ers in the South Pacific.
CJD has three main variants: sporadic CJD (sCJD), iatro-
genic CJD, and variant CJD (vCJD). vCJD is associated with
BSE. Recently a new type of CJD has been described, known
as proteinase-sensitive prionopathy (PSPr).13
Iatrogenic CJD is a rare form of CJD that has been linked
to corneal transplants, growth hormone derived from pitu-
itary extracts, dura matter grafts, and contaminated neuro-
surgical instruments.7
sCJD is characterized by a rapidly progressive dementia with
confusion and often associated movement disorders such as
ataxia and myoclonus. It is typically a disease of older individu-
als (median age, 68 years). In sCJD the electroencephalogram
(EEG) may show periodic high-voltage complexes. Samples of
CSF are acellular with normal glucose but may show elevation
of protein including a protein known as 14-3-3.14
vCJD differs from sCJD in a number of ways, including the
younger age of patients (median age, 28 years), the prominent
symptoms of paresthesias, the lack of specific EEG findings,
specific MRI findings of an increased signal in the posterior
thalamus, and the ready detection of the agent in lymphoid Figure 9-146 n Cattle, such as the one pictured here, affected by BSE
experience progressive degeneration of the nervous system. (From Centers
tissue. Patients with vCJD also have a prolonged clinical for Disease Control and Prevention Public Health Image Library, Atlanta,
course compared with patients with sCJD (median illness Ga. Courtesy U.S. Department of Agriculture Animal and Plant Health
duration of 13 to 14 months vs. 4 to 5 months for sCJD).7 Inspection Service, Washington, DC.)
Figure 9-147 n Clinical chronic wasting disease (CWD) in captive female wapiti (A) and free-ranging male mule
deer (B). The female wapiti had been showing subtle signs of CWD, primarily changes in response to handling and
interaction with herd mates, for more than 6 months before the photo was taken. The wapiti was euthanized about
3 months later after signs progressed, although still not to classic end-stage CWD. The male mule deer showed signs
that included cachexia, piloerection, diminished alertness, and vacant facial expression (all evident in photo), and mild
ataxia also was appreciable when the deer moved. (From Fowler ME: Zoo and wild animal medicine: current therapy, ed
6, St Louis, 2008, Saunders Elsevier. A, Courtesy M.W. Miller; B, courtesy S.W. Miller.)
A B
Figure 9-148 n Spongiform encephalopathy (scrapie), brain, motor neurons, sheep. A, Neuronal cell bodies
contain one or more discrete and/or coalescing clear vacuoles. There are no inflammatory cells in this disease. Similar
spongiosis is evident in the neuropil (hematoxylin-eosin stain). B, Scrapie, experimental, brain, cerebellum, mouse.
The cerebellar granule cells are at the top of the figure. There is notable hypertrophy and proliferation (astrocytosis)
of astrocytes and their fibers (astrogliosis) (black branching fibers). Some of the processes (running diagonally across
the illustration) end, as is normal for astrocytes on the walls of capillaries. Cajal’s gold sublimate stain was used for
astrocytes. (From McGavin MD, Zachary JF: Pathologic basis of veterinary disease, ed 4, St Louis, 2007, Mosby Elsevier.
A, Courtesy D. Gould, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, and M.
McAllister, College of Veterinary Medicine, University of Illinois. B, courtesy W.J. Hadlow.)
referred to a qualified neurologist for definitive diagnosis.15

Diagnosis
MRI findings of ribbons of cortical hyperintensity or basal
The differential diagnosis of CJD in humans includes other ganglia or thalamic hyperintensity can help suggest the
causes of dementia, such as Alzheimer’s disease, Lewy body diagnosis.17
dementia, normal-pressure hydrocephalus, neurosyphi- The disease can be diagnosed by brain biopsy showing
lis, hypothyroidism, HIV-associated dementia, and senile spongiform changes and the presence of the prion protein
dementia. The diagnosis of vCJD should be suspected in PRPsc (Figure 9-149). Other tests include tonsillar biopsy for
any person who has resided in a BSE area who presents with PRPsc as well as CSF testing for the stress protein 14-3-3, which
behavioral abnormalities and sensory complaints accom- is elevated in some patients with CJD, although it occurs in
panied by signs of dementia. Suspected cases should be other conditions as well.18
Table 9-67 n Transmissible Spongiform Encephalopathies: Comparative Clinical Presentations in

Humans and Other Animals
Species/Disease Risk Factors Incubation Period Clinical Manifestations Laboratory Findings
Humans: vCJD Linked to bovine Unknown Younger age than sCJD; MRI increased signal in
spongiform confusion, progressive posterior thalamus
encephalopathy dementia, paresthesias,
Abnormal EEG
ataxia
Elevated CSF 14-3-3 protein
Tonsil biopsy may show PrPSc6
Illness duration 13-14 months
Humans: sCJD Idiopathic Unknown Older individuals; EEG may show periodic
confusion, progressive high-voltage complexes
dementia, ataxia,
myoclonus
Illness duration approximately
6 months15
Cattle: BSE Linked to consumption Months to years Abnormal behavior, ELISA or Western blot
of contaminated feed abnormal movements, analysis on brain tissue,
Other bovids: exotic staring, exaggerated startle with confirmation by
ungulate encephalopathy reflex, falling immunohistochemistry
Cats: FSE Linked to consumption Weeks to months Abnormal behavior, increased Spongiform degeneration
of BSE-infected foods sensitivity to touch of neuropil on biopsy
Mink: transmissible Thought to result from 7-12 months Increased aggression, biting, Neuropil vacuolation on
mink encephalopathy consumption of foods circling brain biopsy9
infected with scrapie or
other TSE agent
Deer, elk: chronic Origin unknown, 1.5-3 years Behavior changes, weight Immunochemistry, ELISA,
wasting disease possibly scrapie loss, staring, low head Western blot of brain
carriage tissue and/or lymph
nodes
Sheep, goats: scrapie Susceptible genotypes16 2-3 years Excitability, tremors, pruritus ELISA or Western blot
with loss of fleece analysis of brain tissue
postmortem or by biopsy
of lymphoid tissue
EEG, Electroencephalogram; MRI, magnetic resonance imaging.
In cattle, BSE is often diagnosed by ELISA or Western

blot analysis on brain tissue with confirmation by
immunohistochemistry.
CWD can be diagnosed by immunohistochemistry,
Western blot, or ELISA on brain and/or lymph nodes.
Scrapie diagnosis is usually by ELISA or Western blot
analysis of brain tissue postmortem, or by biopsy of
lymphoid tissue (retropharyngeal, third eyelid, or rectal
mucosa).
Treatment
At present, CJD and other prion diseases in humans
are fatal neurological diseases without proven effective
therapies. There is ongoing research for development of
vaccines and for potential compounds with anti-prion
Figure 9-149 n Magnified (×100) and stained with hematoxylin-eosin activity.14,19,20,21). Current treatment of affected humans
staining technique, this light photomicrograph of brain tissue reveals the pres-
ence of prominent spongiotic changes in the cortex and loss of neurons in a case is limited to alleviating symptoms and patient comfort.
of variant Creutzfeldt-Jakob disease. (From Centers for Disease Control and Affected animals should be euthanized and removed from
Prevention Public Health Image Library, Atlanta, Ga. Courtesy Teresa Hammett.) the food supply.
References 10. Lynn T, Grannis J, Williams M, et al. An evaluation of scrapie surveil-

lance in the United States. Prev Vet Med. 2007;81(1–3):70.
1. Brown P, McShane LM, Zanusso G, et al. On the question of sporadic 11. Mawhinney S, Pape WJ, Forster JE, et al. Human prion disease and
or atypical bovine spongiform encephalopathy and Creutzfeldt-Jakob relative risk associated with chronic wasting disease. Emerg Infect Dis.
disease. Emerg Infect Dis. 2006;12(12):1816. 2006;12(10):1527.
2. Heymann DL, ed. Control of communicable diseases manual. 19th 12. Konold T, Moore SJ, Bellworthy SJ, et al. Evidence of scrapie transmis-
ed.Washington, DC: American Public Health Association; 2008. sion via milk. BMC Vet Res. 2008;8(4):14.
3. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse 13. Will R, Head M. A new prionopathy. Ann Neurol. 2008;63(6):677.
Station, NJ: Merck; 2005. 14. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
4. Lumley JS. CJD Incidents Panel, Engineering and Scientific Advisory diseases. 6th ed. Philadelphia: Churchill Livingstone Elsevier; 2005.
Committee et al: The impact of Cruetzfeldt-Jacob disease on surgical 15. Beisel CE, Morens DM. Variant Creutzfeldt-Jakob disease and the
practice. Ann R Coll Surg Engl. 2008;90(2):91. acquired and transmissible spongiform encephalopathies. Clin Infect
5. Palacios-Sánchez B, Esparza-Gómez GC, Campo-Trapero J, et al. Dis. 2004;38(5):697.
Implications of prion disease for dentistry: an update. Oral Surg Oral 16. Baylis M, Chihota C, Stevenson E, et al. Risk of scrapie in British sheep
Med Oral Pathol Oral Radiol Endod. 2008;105(3):316. of different prion protein genotype. J Gen Virol. 2004;85(Pt 9):2735.
6. Casalone C, Zanusso G, Acutis P, et al. Identification of a second 17. Wada R, Kucharczyk W. Prion infections of the brain. Neuroimaging
bovine amyloidotic spongiform encephalopathy: molecular similari- Clin N Am. 2008;18(1):183.
ties with sporadic Creutzfeldt-Jakob disease. Proc Natl Acad Sci U S A. 18. Fauci AS, Braunwald E, Kasper DL, et al. Harrison’s principles of internal
2004;101:3065. medicine. 17th ed. New York: McGraw-Hill; 2008.
7. Belay ED, Schonberger LB. The public health impact of prion diseases. 19. Müller-Schiffmann A, Korth C. Vaccine approaches to prevent and treat
Ann Rev Public Health. 2005;26:191. prion infections: progress and challenges. BioDrugs. 2008;22(1):45.
8. Fichet G, Comoy E, Duval C, et al. Novel methods for disinfection of 20. Stewart LA, Rydzewaska LH, Koegh GF, et al. Systematic review of therapeu-
prion-contaminated medical devices. Lancet. 2004;364(9433):521. tic interventions in human prion disease. Neurology. 2008;70(15):1272.
9. Sigurdson CJ, Miller MW. Other animal prion diseases. Br Med Bull. 21. Trevitt CR, Collinge J. A systematic review of prion therapeutics in
2003;66:199. experimental models. Brain. 2006;129(9):2241.
TUBERCULOSIS AND OTHER MYCOBACTERIAL INFECTIONS
Elena Hollender and Peter M. Rabinowitz shown a resurgence of TB in animals among diverse species
such as white-tailed deer,7 bobcats, coyotes, opossums, rac-
Tuberculosis (ICD-10 A15-A19), Non-tuberculous mycobac- coons, and red foxes.8,9
terial disease (ICD-10 A31) Although the public health linkage between TB in humans
and other animals has been recognized for more than a cen-
Other names in humans: TB; atypical mycobacterial infec- tury, the key issue was believed to be human infection with
tion, MAI, MAC, Mycobacterium marinum, leprosy bovine TB through the ingestion of unpasteurized dairy
products. However, recent advances in molecular diagno-
Other names in animals: TB; mycobacteriosis, avian tuberculosis sis have shed light on additional human-animal TB issues
including occupational and reverse zoonotic infection. This
Tuberculosis (TB), an infectious, granulomatous disease, is section discusses TB in humans and other animals. Infection
one of the oldest recognized diseases in humans and animals with non-tuberculous mycobacteria (NTM) is covered in an
and exemplifies the close parallels between human and ani- accompanying summary.
mal health. Mycobacterium tuberculosis complex (MTBC),
which includes M. tuberculosis and M. bovis, has been found
in Egyptian and New World mummies1,2 and recovered from
Professionals
spinal and bone lesions of Iron Age human remains in Britain
and South Siberia.3,4 In animals, there is documentation of
TB in buffalo in China more than 500,000 years ago.5 TB is
believed to have been a key factor in the extinction of mam-
moths and mastodons around 10,000 years ago.5 The control of TB in both humans and other animals relies
Approximately one third of the world’s human population, on similar basic practices and principles:
or about 2 billion people, are infected with TB; active cases of • Identify, test, and treat/manage high-risk populations.
TB in 2006 were reported to exceed 9 million.6 Coinfection • Physically isolate or separate cases from other people
with HIV disease accounts for more than 15 million cases of or animals.
TB infection, and TB is an important cause of HIV-related • Ensure appropriate medical treatment and management
deaths throughout the world. TB has now become the leading of the case and/or livestock and herd management.
cause of death from any infectious disease worldwide, with • Provide case investigation.
mortality from tuberculosis in 2006 of 1.7 million.6  Identify probable routes of transmission, mainly
TB in livestock and wildlife is a worldwide problem and respiratory and gastrointestinal.
has serious socioeconomic ramifications, especially in devel-  Identify close contacts of cases to prevent or con-
oping nations. In the United States, recent surveillance has trol secondary cases, including companion animals
and those at high risk of infection; evaluate close Veterinary Clinicians

contacts for active TB, perform tuberculin skin test-
ing of contacts, treat close contacts if indicated, and • Isolate and screen herd replacements.
work with agriculture officials to cull livestock if • Quarantine infected herds, test and slaughter to erad-
indicated. icate infection, and disinfect facilities where infected
 Address issues of ongoing transmission; identify animals have been housed.
potential human or animal sources of infection, • Report animals with positive test results to agriculture
shared common sources (human or animal con- officials and notify public health authorities.
gregate living facilities, congregate areas of po- • Ensure proper biosafety procedures are followed in the
tential exposure, such as waiting rooms, holding veterinary facility and that staff are aware of signs of
pens), and infected food or water supply (unpas- infection in humans and other animals.
teurized dairy products, especially from endemic • Consider TB in animals living in a household of a
countries). human case of TB or with other close contact with a
• Encourage communication and consultation between human case (if this human information is presented).
human and veterinary public health programs and • Pulmonary or disseminated TB in a companion ani-
awareness of the national and local incidence and prev- mal should suggest the presence of, or close contact
alence of TB in human, domestic animal, and wildlife with, active human TB. Communication with local
populations. public health officials may alert them to the possibility
• Encourage coordination and consultation between of an undiagnosed active TB case or provide valuable
veterinary and human public health programs for con- epidemiological data regarding an already known case.
tact investigation and recommendations for compan- If applicable, contact investigation may be considered
ion or household animals of active human TB cases for both humans and/or other animals.
and human contacts of veterinary TB. • When draining cutaneous lesions or performing a
• In endemic areas, encourage coordination between necropsy on an animal with suspected TB, use protec-
local agricultural and wildlife agencies regarding test- tive equipment including N-95 respirator, gloves, and
ing and control in domestic livestock and wildlife. eye protection.
• Educate the public regarding possible means of trans- • Disinfect surfaces with 1% sodium hypochlorite, 70%
mission of zoonotic TB, such as consumption of unpas- ethanol, or iodine solutions.
teurized milk and dairy products, especially from, or in,
countries with endemic TB.
• Educate hunters of wildlife such as bison, deer, elk and Agent
other Cervidae and feral swine in areas of endemic
zoonotic TB regarding the infection control precau- Mycobacteria are nonmotile, rod-shaped, obligate aerobic
tions, such as gloves and protective clothing to be used bacteria classified as acid-fast because of the impermeability
when dressing and handling meat and disposing of of their thick, waxy coats to certain dyes and stains. There
carcasses. are more than 120 species of mycobacteria, which are gener-
• Educate medical and veterinary health clinicians regard- ally divided into rapidly growing (visible on culture within
ing TB and zoonotic TB, occupational risks factors such 7 days) and slow growing (those requiring longer periods
as zookeepers and exotic animal handlers, the possibility of growth). Most mycobacteria are not considered patho-
of interspecies transmission. See veterinary guidelines genic. The species of greatest pathogenicity to humans and
at http://www.aphis.usda.gov/animal_health/animal_ other animals are those classified as Mycobacterium tuber-
diseases/tuberculosis/ and at http://www.oie.int/eng/ culosis complex (MTBC), the etiologic agents of TB. Of all
normes/mmanual/2008/pdf/2.04.07_BOVINE_TB.pdf. the mycobacteria, only MTBC and M. leprae (the agent of
leprosy) are obligate intracellular organisms; the others live
freely in the environment.
Because of the importance of MTBC as a pathogen to
• Immediately report cases to public health authorities: humans and other animals, other mycobacteria are generally
state and local public health TB programs (for a case referred to as nontuberculous mycobacteria (NTM) or myco-
definition, see http://www.cdc.gov/ncphi/disss/nndss/ bacteria other than tuberculosis (MOTT). However, as they
casedef/tuberculosis_current.htm; a list of state TB are found throughout the environment, they may also be
control offices can be found at http://www.cdc.gov/tb/ referred to as environmental mycobacteria (EM). These NTM
pubs/tboffices.htm). are discussed below in a separate section.
• Ensure that workers in high-risk occupations are using
appropriate biosafety procedures. Mycobacterium Tuberculosis Complex
• If treating a patient with active TB, determine whether
pets are in the household and could have been exposed. MTBC is a highly successful clonal group pathogen of both
If so, recommend veterinary evaluation. humans and other animals that includes the species M. tuber-
• Inquire about occupational risk factors for zoonotic culosis, M. africanum, M. bovis, M. canettii, M. caprae,
TB and ensure that workers at risk (such as zookeep- M. microti, and M. pinnipedii (Table 9-68). In the past, human
ers) are monitored with baseline and yearly tuberculin TB was thought to be caused solely by M. tuberculosis, except
skin tests. for zoonotic cases of M. bovis acquired through contact with
Table 9-68 n MTBC and Common Hosts Hosts, Reservoir Species, Vectors
Species Common Hosts As Table 9-68 shows, different members of the MTBC group
are adapted to different host species, although interspecies
M. africanum Humans and cattle (Africa) transmission can occur. TB in wildlife has become a major
M. bovis Widest host spectrum; humans, problem in many parts of the world, and transmission of
mammalian vertebrates disease is increasingly bidirectional at the livestock-wildlife
interface in industrialized and developing countries. Wildlife
M. canettii Humans (immunocompromised)
reservoirs such as badgers, opossums, ferrets, deer and other
M. caprae Goats, cattle, wild boar, pigs, humans cervids, feral pigs, African buffalo, and bison serve as sylvatic
M. microti Rodents, humans reservoirs and ongoing sources of infection to pastured ani-
(immunocompromised) mals primarily through contamination of water and food
M. pinnipedii Seals sources within their shared environment. The presence of
M. tuberculosis Humans, vertebrates (e.g., cattle, multiple maintenance hosts favors the long-term persistence
primates, elephants) of infection and disease among differing populations.15,16
Conversely, infection in wildlife species such as kudu,
baboons, lions, and hyenas may represent a sporadic spill-
over from a livestock reservoir. Therefore TB in livestock and
unpasteurized dairy products. Similarly, TB in cattle (bovine pastured animals will no longer be able to be eradicated or
TB) was believed to be caused only by M. bovis. However, controlled by traditional livestock control programs that do
recent breakthroughs in molecular analysis and mapping of not take into account the wildlife disease reservoirs. In addi-
the genomic sequence of M. tuberculosis have led to a new tion to the risks of transmission between wildlife and live-
understanding of the pathogenesis, host range, evolution, stock, wildlife TB can pose a zoonotic threat to game hunters
and phenotypic differences within the MTBC, including the who butcher carcasses (respiratory and cutaneous exposure)
discovery of interspecies disease by most members of the and who consume undercooked meat.17,18 In addition, TB in
MTBC, that challenge previous assumptions. peridomestic wildlife such as nonhuman primate popula-
TB was traditionally thought to be a zoonotic disease tions in Asia may pose a risk of direct zoonotic transmission
transferred to humans during the neolithic ages through con- to humans via close contact.
tact between humans and animals domesticated for livestock.
It was therefore believed that M. tuberculosis had evolved Mode of Transmission and Life Cycle
from M. bovis. There is now evidence that all members of the
MTBC evolved from a TB progenitor, M. prototuberculosis, Infection with TB begins when the organism is introduced
estimated to be as old as 3 million years (Color Plate 9-75). into the body, usually by inhaled droplet nuclei containing
In addition, researchers have shown that tubercle bacilli are tubercle bacilli, which when <5 microns reach the pulmo-
able to exchange parts of their genome with other strains, nary alveoli (Figure 9-151). The bacilli are then phagocytized
a process that is crucial to the adaptation of pathogens to by the pulmonary alveolar macrophages and destroyed or
different host species.10,11 contained. The alveolar macrophages are an important part
in the initiation of the host’s immune response to the myco-
bacteria. Antigen of the tubercle bacilli then stimulates the
host’s cellular immune response and the immune cascade is
Mycobacteria of the MTBC group are found worldwide. triggered. Immunologic control or containment of the infec-
Zoonotic TB due to foodborne and occupational exposures tion is achieved through a potent cell-mediated immune
occurs more commonly in developing countries. response beginning with helper T-lymphocytes and, later,
a delayed hypersensitivity response. This immune response
also involves the production of proinflammatory cytokines,
Groups at Risk
especially interferon-gamma (IFN-γ), tumor necrosis factor
Certain occupational groups are at an increased risk of expo- (TNF), and interleukin-1.
sure to TB, including health care workers, exposure livestock The spread of the infection may be halted by the immune
workers, workers in zoos and animal parks, and animal care system at the local lymph node level. However, because cellu-
workers in primate facilities (see Chapter 12). For example, lar immune response usually takes between 4 and 12 weeks to
there has been zoonotic transmission of M. bovis from a be elicited, it may not, or only partially, be stopped there. The
diseased white rhinoceros to seven zookeepers.12 MTBC bacillus may then spread systemically via the regional
Along with zoo workers, zoo animals appear to be at an lymph nodes and lymphatic system and enter the bloodstream
increased risk of potential infection. A multispecies epizootic (primary disease). Hematogenous circulation of the tubercle
transmission of M. tuberculosis occurred in a metropolitan bacilli is generalized but may affect mainly organs and tissues
zoo among Asian elephants, Rocky Mountain goats, a black that are more densely vascularized, such as bone, liver, spleen,
rhinoceros, and humans.13 There has also been documented central nervous system, kidneys, and genital tract, where the
transmission in an exotic animal farm among four elephants bacilli are then targeted by local mononuclear phagocytes.
with M. tuberculosis and 11 of 22 handlers, one of whom These organs, along with lymph nodes, are therefore the most
subsequently had active disease. The isolates for all active common sites of extrapulmonary disease. Studies of tissue
cases were identical.14 from infected asymptomatic individuals have shown viable
M. tuberculosis in primary lesions in the lung and in lesion- linked cluster of six cases identified in the United Kingdom.
free areas of lung and lymph nodes. Although primary lesions Five of the patients had pulmonary TB disease and one had
can occur anywhere in the lung, postprimary disease most TB meningitis24; only one was known to be HIV infected. The
commonly develops in the apical regions.19 The immune index case had a history of occupational exposure and con-
system continues to attempt to isolate the bacillus, forming sumption of unpasteurized milk and cheese both as a young
granulomas or tubercles (Color Plate 9-76) The granuloma adult and recently in a country not free from bovine TB. In
may become thick walled and dense, effectively encapsulating another cluster, human nosocomial transmission of M. bovis
the organism and preventing further spread. The bacilli then among HIV-infected individuals occurred in a Spanish hos-
become latent within the granulomas. These granulomas may pital, resulting in 30 deaths.25 Humans may also serve as a
eventually calcify. source of TB infection for animals, including nonhuman pri-
The major route of transmission for humans (and one mates, cattle, dogs, and macaws.26-31
of the main routes for animals) is through respiratory aero- Animal-to-animal transmission of TB occurs through
solization. When there is active TB in the lungs, the bacillus is respiratory and gastrointestinal routes.32 Respiratory infec-
expelled and aerosolized in the form of droplet nuclei through tion can occur in herds or closely quartered animals through
coughing (or any explosive respiratory action such as singing, pulmonary disease or draining lymphadenopathy. Infection is
shouting, sneezing, or talking). For these droplet nuclei to be also acquired by ingestion of infected meat, sharing of infected
inhaled and reach the alveoli in humans, they must be 3 to 5 water and food sources, grooming, and exposure to secretions.
microns or less in size. In animals, the exact sizes of infecting
droplet nuclei may vary depending on the species. Environmental Risk Factors
Other risk of exposure to infectious aerosols includes
opening an infected chest cavity such as during autopsy, Because a major influence on the aerosol transmission of TB
necropsy, or slaughter of livestock, as well as hosing down in humans and other animals is the closeness and duration
an area where an infected animal has been housed. The effi- of contact with the infected individual, population density
ciency of transmission of TB depends on a number of fac- can be a key environmental factor driving TB transmis-
tors, as shown in Box 9-7.20 sion. Although being outdoors significantly decreases the
The second most common route of transmission is through risk of transmission, the close or sheltered outdoor hous-
the gastrointestinal tract by the ingestion of infected material. ing of animals and humans may decrease that advantage.
Drinking or eating unpasteurized milk products traditionally Contaminated water can be another environmental risk for
has been the principal means by which humans have acquired disease transmission in animals.
zoonotic TB.21 In industrialized countries pasteurization and
strict herd testing and management have made such gastroin- Disease in Humans
testinal transmission rare, but zoonotic TB caused by M. bovis
acquired through ingestion may be seen in immigrants from During primary and latent infection, the person does not
countries with a continuing prevalence of M. bovis infection exhibit signs of disease and is not considered infectious.
in cattle or livestock.22,23 Immunocompetent individuals will develop a balance
Of note are the recent documented human-to-human between host and mycobacteria, and the infection will remain
transmissions of M. bovis, including an epidemiologically latent. However, if there is a breakdown of the host’s immune
function and the infection is no longer able to be effectively
contained, active disease may develop (Figure 9-150).
More than 90% of humans infected with MTBC main-
Box 9-7 Factors Determining Transmission
of Tuberculosis tain control of the infection through immune mechanisms
during their lifetime. These individuals have an approxi-
mately 10% chance of developing active TB disease during
Characteristics of the Source Case their lifetime: 5% within the first few years of infection (pro-
• Concentration of organisms in sputum gressive primary TB disease) and 5% at a later stage in their
• Presence of cavitary disease lives (reactivation TB disease). However, that probability of
• Frequency and strength of cough progressing to active disease is significantly increased in the
Characteristics of the Exposed Individual presence of comorbid conditions that compromise immune
• Previous tuberculosis infection function. Factors associated with this increased risk are out-
• Innate resistance to tuberculosis infection lined in Box 9-8.
• Genetic susceptibility to tuberculosis infection/disease HIV exerts a significant adverse affect on the pathogen-
Characteristics of the Exposure esis of TB. With a suppressed or poorly functioning immune
• Frequency and duration of exposure system, the host will release an immature response to the
• Dilution effect (volume of air containing infectious droplet tubercle bacillus. The decrease in the number and function
nuclei) of T-cell lymphocytes as a result of HIV disease weakens the
• Ventilation (turnover of air in a space) immune reaction and the host cannot, or only poorly, contain
• Exposure to ultraviolet light, including sunlight the TB organisms that are present. There is a greater chance
Virulence of the Infecting Strain of Mycobacterium of rapid progression from infection to disease after recent TB
Tuberculosis Complex infection. There is also a question of whether an individual
Adapted from CDC “Guidelines for preventing the transmission of Mycobacterium
with HIV has an increased chance of infection with TB from
tuberculosis in health-care settings, 2005. http://www.cdc.gov/mmwr/pdf/rr/rr5417.pdf. the loss of innate resistance. People with HIV have an 8% to
Cavities open into the bronchi,

allowing spread of M. tuberculosis
through coughing
Lung
M. tuberculosis Cavity
TB lesion
90-95% 5-10%
of infected of infected
individuals individuals
Reactivation of TB: for example, after

immunosuppression, HIV infection of smoking
Haematogenous spread:
M. tuberculosis DNA
detected in tissues by Progression to cavitary TB
in situ PCR
Figure 9-150 n Phases of infection with tuberculosis. (From Rook GA, Dheda K, Zumla A: Immune responses
to tuberculosis in developing countries: implications for new vaccines, Nat Rev Immunol 5(8):661-7, 2005.)
of T-cell lymphocytes. These T cells are then targeted by the

Box 9-8 Risk Factors for Developing virus, resulting in increased HIV replication. If the tubercu-
Tuberculosis Disease lous infection is initially contained by the immune system,
which then subsequently experiences a significant deteriora-
• Recent TB infection (within past 2 years) tion in the quantity and function of T-helper cells, the bacil-
• HIV infection lus may no longer be contained and the TB reactivates. In
• Chest radiographic findings suggestive of previous TB
addition, the cytokines produced in response to TB infection
• Contact with a recent case of active TB
• Recent immigration from tuberculosis-endemic country within stimulate the production of HIV in vitro.33
5 years of immigration Active TB is usually a slowly progressive disease character-
• Malnutrition ized by systemic symptoms of weight loss, fatigue, anorexia,
• 10% below ideal body weight fevers, chills, night sweats, and wasting. The severe weight
• Alcohol and drug abuse (especially IV drugs) loss and wasting associated with the disease led to its former
• Newborn, infants <2 years name of consumption. When the disease is pulmonary, pre-
• Comorbid medical conditions: senting symptoms may also include a persistent cough (with
 Diabetes or without sputum production), chest pain, and hemoptysis.
 Gastrectomy or jejunoileal bypass (total or partial) Although TB is generally a chronic, debilitating disease, it may
 Silicosis (affects pulmonary macrophage function)
present with an acute, rapidly progressing course. Disease is
 Cancer (especially head and neck tumors)
 Hematologic malignancies (leukemia, lymphoma) generally pulmonary, followed by lymphatic drainage and
 Chronic renal failure local lymphadenopathy, or disseminated (especially in immu-
 Solid organ transplant (chronic immunosuppressive therapy) nocompromised hosts; Color Plate 9-77). Manifestations may
• Immunosuppressive conditions, including: vary depending on the extrapulmonary site of disseminated
 Cancer chemotherapy disease. Central nervous system involvement may present as
 Prolonged treatment with corticosteroids either meningeal or parenchymal disease. Meningitis more
 Treatment with anti-TNFα agents commonly affects the basilar meninges, and the cranial
nerves may also be involved. Parenchymal lesions may be
single or multiple and present as solid tuberculomas or
10% chance per year to progress from infection to active TB. TB abscesses. Symptoms will depend on the location of
The 1-year mortality rate for treated, HIV related TB is 4 the lesion and/or mass effect from surrounding edema
times the rate of non-HIV related TB, around 35%. TB also (Figure 9-151). TB may also present in the spinal vertebrae
worsens HIV disease by inducing stimulation and replication (Pott’s disease) (Figure 9-152).
Disease in Animals
As in humans, TB can be either a chronic or rapidly progres-
sive disease, with the clinical signs varying greatly according
to the species involved. As with humans, it is believed that
many animals infected with MTBC remain in a latent phase,
although the natural history is less well understood.
In cattle, TB is often not apparent, and therefore not diag-
nosed, until terminal stages of the disease; it is often found
only at necropsy or in abattoirs (Color Plate 9-78). This,
unfortunately, allows for a prolonged period of transmission.
The initial presentation, besides cachexia, progressive weak-
ness, and anorexia, may also include cough, lymphadenitis,
and draining sinus tracts, especially around the neck, face,
and chest. In later stages, lymph nodes may be enlarged to
the point of impingement on airways, gastrointestinal (GI)
tract, or blood vessels.34 GI tract involvement may be mani-
fested by diarrhea or constipation. The female genital tract
may be involved. At necropsy, both tuberculous granulomas
and abscesses may be present.
In Cervidae, which include deer, antelope, moose, elk,
and reindeer, TB has been found in both farmed and free-
living animals. The course may be chronic and progres-
sive or acute. The presentation is similar to that found in
Figure 9-151 n A magnetic resonance image of tuberculoma in a child cattle with granulomas, but thin-walled abscesses are also
with culture-positive tuberculous meningitis. The child’s presenting signs common.
and symptoms included fever, altered mental status, and hemiparesis. (From In nonhuman primates, as in humans, there is a broad
Gershon AA, Hotez PJ, Katz S: Krugman’s infectious diseases of children, ed
11, St Louis, 2004, Mosby Elsevier.)
clinical spectrum of disease, including latent TB, chronic
Figure 9-152 n A, Vertebral tuberculosis. B, Tuberculosis of the spine (Pott’s disease). C, Kyphosis is second-
ary to anterior destruction of vertebral bodies resulting in wedging of adjacent vertebrae and loss of disk space
clearly seen by radiography. (From Cohen J, Powderly WG: Infectious diseases, ed 2, Philadelphia, 2004, Mosby
Elsevier. A and B, Courtesy J. Cohen, Brighton, U.K. C, Courtesy A. Wightman.)
primary TB, rapidly progressing and fulminant disease, and mycobacterial interspersed repetitive units (MIRU) or spoli-
reactivation TB.35 Old World species appear to be more sus- gotyping. Genotyping is used to assist TB control programs
ceptible than New World species. in identifying outbreaks and recent transmission in a more
Culture-confirmed cases of TB have been diagnosed in at real-time manner so that appropriate secondary testing and
least 36 elephants in the United States from 1994 to 2006.36 management can be performed sooner. Molecular testing of
It has been reported in captive elephants, primarily Asian, the TB isolate for genetic resistance mutations is beginning
although the potential for transmission to wild elephants to be used.
is increasing. Clinical disease in elephants usually has a Thoracic radiographs may be part, or the initial finding, of
chronic, debilitating presentation. Signs may not be present the clinical presentation of TB in humans and other animals
until the disease is advanced and include weakness, weight (Figures 9-153 and 9-154). Classically, TB is an upper lobe
loss, and coughing, although they may also be specific to the disease, either unilateral or bilateral. Abnormalities typically
organ system involved, such as chronic vaginal discharge or are seen in the apical and posterior segments of the upper lobe
conjunctivitis. or the superior segments of the lower lobe; however, lesions
TB also occurs in domestic and companion animals. Dogs may appear in any part of the lungs. Radiographic abnor-
and cats may present with a typical clinical picture of wasting, malities may present as infiltrates, nodules, cavitary lesions,
anorexia, and progressive decline. If the MTBC was acquired pleural thickening, or a diffuse miliary pattern. Hilar and
through the respiratory tract, signs may also include cough mediastinal lymphadenopathy may be present, with or with-
and shortness of breath; if acquired through the ingestion of out accompanying infiltrates or cavities. Immunosuppressed
infected meat or milk, GI signs may be present. individuals may present with only hilar or mediastinal ade-
nopathy, or the chest radiograph may appear normal.
Diagnosis
Active Disease
The key factor in the diagnosis of active TB is that of clin-
ical suspicion based on the presenting history, signs or
symptoms, chest radiograph, and/or laboratory testing.
Microscopy looks for the presence of acid-fast bacilli (AFB)
on direct smears of clinical specimens. The finding of AFB
indicates the presence of mycobacteria but not the specific
species.
Identification of the mycobacterial species is through culture
or molecular testing such as polymerase chain reaction. A tis-
sue biopsy specimen may show characteristic histological find-
ings, such as granuloma, caseation, necrosis, calcification, and
typical cellular immune response. The presumptive diagnosis Figure 9-153 n Chest radiograph of a patient with pulmonary tubercu-
of TB (mycobacteriosis) may be made on this basis, especially losis. There is extensive parenchymal streaking, predominantly in the upper
fields of the lungs. These changes are typical of chronic bilateral pulmonary
in animals. tuberculosis. Some enlargement of the heart is also evident. (From Male
Cultures may use liquid media, such as the mycobacte- D, Brostoff J, Roth D et al: Immunology, ed 7, Philadelphia, 2006, Mosby
ria growth indicator tube (MGIT, BBL Becton Dickinson Elsevier.)
Microbiology Systems, Cockeysville, Md.) and/or solid
agar media, such as Bactec (Becton-Dickinson Diagnostic
Instrument Systems, Sparks, Md.) Lowenstein-Jensen, or
Middlebrook 7H10. MTBC is a slow-growing organism that
replicates approximately every 24 hours. Growth in liquid
media usually occurs within 1 to 3 weeks, whereas growth on
solid media may be 6 to 8 weeks. Drug susceptibility testing
is performed on isolates of MTBC routinely for isoniazid,
rifampin, pyrazinamide, and ethambutol.
Since the genetic mapping of MTBC, molecular testing
has been used in the diagnosis of TB. Nucleic acid amplifi-
cation (NAA) tests, such as the Mycobacterium tuberculosis
Direct (MTD) test (Gen-Probe, Inc., San Diego, Calif.) are
performed on direct specimen smears based on the pres-
ence of MTBC RNA. The sensitivity and specificity of the
NAA test on a positive AFB smear are greater than 95% and
99.6%, respectively. PCR is a species-specific DNA-based test Figure 9-154 n Lateral thoracic radiograph of a cat with disseminated
M. bovis infection. (From Greene CE: Infectious diseases of the dog and cat,
used to identify MTBC. Further genotyping on positive TB ed 3, St Louis, 2006, Saunders Elsevier. Courtesy D. Gunn-Moore, University
cultures often may be done, usually by one of two methods: of Edinburgh, Scotland.)
Latent Infection infected (e.g., contact investigation) and in the evaluation

of those with signs or symptoms or those who are suspected
The tuberculin skin test (TST) has been the standard of having TB.
screening tool for TB infection in humans and other ani- The TST is administered by subcutaneously injecting a
mals (Figure 9-155). It produces a delayed-type hypersen- preparation of (inactive) mycobacterial antigens. In humans,
sitivity reaction in those with tuberculous infection. It is 0.1 mL of purified protein derivative (PPD) is placed on
useful for determining how many individuals in a group are the inner surface of the forearm. More complete informa-
tion on TB skin test placement, reading, and interpreta-
tion is available at http://www.cdc.gov/TB/pubs/slidesets/
core/html/trans4_slides.htm. The TST is usually read after
48 to 72 hours. The induration (not the erythema) is mea-
sured and should be recorded in millimeters, not simply as
negative or positive. In humans, a positive TST reaction may
be measured for up to 7 days, although a negative reaction
can only be read until 72 hours. The TST, however, has lim-
ited sensitivity and specificity. In humans, there is an overall
false-positive rate of 20% and a false-negative rate of 20%.
False-positive results may be seen in NTM infection, recent
Bacillus Calmette-Guérin (BCG) vaccination, or incorrect
administration. False-negative results may occur in over-
whelming TB disease, anergy, recent TB infection, newborns,
recent live-virus vaccinations, some viral illnesses, incorrect
administration, or waning immune response (usually due to
Figure 9-155 n This technician is in the process of correctly placing age or prolonged time since infection). Because of the pos-
a tuberculin skin test in this recipient’s forearm, which will cause a 6-mm sibility of a waning immune response, in some instances a
to 10-mm wheal (i.e., a raised area of skin surface) to form at the injection two-step TST is performed. In those situations, an initial
site. The tuberculin skin test is used to evaluate people for latent tubercu- TST may serve to stimulate, or boost, subsequent TSTs. A
losis infection. In the United States, this skin test consists of an intradermal
injection of exactly one tenth of a milliliter of tuberculin, which contains 5 two-step TST is therefore currently recommended for base-
tuberculin units. Correct placement of this intradermal injection involves line testing in those who will undergo periodic testing, such
inserting the needle bevel slowly at a 5- to 15-degree angle. The needle bevel as health care workers.37 This helps to differentiate between a
is advanced through the epidermis, the superficial layer of skin, approxi- boosted reaction and one due to recent infection. The criteria
mately 3 mm so that the entire bevel is covered and lies just under the skin
surface. A tense, pale wheal that is 6 mm to 10 mm in diameter appears over
for determining whether a human TST is positive depends
the needle bevel. (From Centers for Disease Control and Prevention Public on the risk group of the individual. Table 9-69 defines the
Health Image Library, Atlanta, Ga. Courtesy Gabrielle Benenson.) size of the induration per risk group.
Table 9-69 n Criteria for Tuberculin Positivity, by Risk Group
Reaction ≥5 mm of Induration Reaction ≥10 mm of Induration Reaction ≥15 mm of Induration
HIV positive status Recent immigrants (i.e., within the past 5 years) Persons with no risk factors for TB
Recent contacts of TB case patients from high-prevalence countries
Fibrotic changes on chest radiograph Injection drug users
consistent with prior TB Residents and employees† of the following high-
Patients with organ transplants and risk congregate settings: prisons and jails, nursing
other immunosuppressed patients homes, and other long-term facilities for the
(receiving the equivalent of 15 mg/day elderly; hospitals and other health care facilities;
of prednisone for ≥1 month)* residential facilities for patients with acquired
AIDS; and homeless shelters
Mycobacteriology laboratory personnel
Persons with the following clinical conditions
that place them at high risk: diabetes mellitus,
chronic renal failure, some hematological
disorders (e.g., leukemias and lymphomas), and
other specific malignancies (e.g., carcinoma
of the head or neck and lung), weight loss of
≥10% of ideal body weight, gastrectomy, and
jejunoileal bypass
Children younger than 4 years or infants, children,
and adolescents exposed to adults at high risk
*Risk of TB in patients treated with corticosteroids increases with higher dose and longer duration.
†For persons who are otherwise at low risk and are tested at the start of employment, a reaction of ≥15 mm induration is considered positive.
From American Thoracic Society (ATS) and the Centers for Disease Control and Prevention (CDC): Targeted tuberculin testing and treatment of latent tuberculosis infection,
MMWR Morb Mortal Wkly Rep 49(RR-6):1–51, 2000.
Recently IFN-γ–releasing assays (IGRAs) are being used in cervids, primates, badgers, camelids, elephants, and other
to detect latent TB infection. Generally these are whole exotic wildlife, among others.40
blood assays that measure and compare the amount of
IFN-γ released by white blood cells in response to anti- Treatment
gens of MTBC. In humans, QuantiFERON-Gold (Cellestic,
Inc., Valencia, Calif.) and T-SPOT.TB (Oxford Immunotec, Primary prevention remains the optimum course of disease
Oxford, U.K.) are examples of assays used.38 control. It has proven extremely difficult, if not impossible,
In other animals, the TST is the only skin test for use to eradicate any public health disease such as TB without an
in cattle prescribed by the World Organisation for Animal effective vaccine. Currently numerous studies are assessing
Health.39 However, there is no standardization of TST vaccines for human and differing veterinary populations to
testing in animals, as individual protocols are established prevent infection.
by each country. In cattle, testing may use M. bovis anti-
gen alone (caudal fold test [CFT], cervical test [CT]) or Treatment in Humans
along with M. avium (comparative cervical test [CCT]).8
Test results are read at 72 hours ± 6 hours. The preferred Treatment of active TB uses a combination of antibiotics for
TST placement sites in animals differs by species and a prolonged period of time. The exact regimen is based on
include the caudal fold in bovids, ear in pigs, and eyelid or modified according to the organism’s susceptibilities. For
in primates. drug-susceptible isolates, treatment usually is with three or
Skin testing in animals produces high rates of false-posi- four drugs (isoniazid [INH], rifampin [RIF], pyrazinamide
tive and false-negative results. These are often from the same [PZA] with or without ethambutol [EMB]) for the first 2 months,
interference: mycobacterial species, such as M. avium or M. then INH and RIF to complete 6 months’ total treatment.
avium subsp. paratuberculosis, overwhelming or advanced Table 9-70 shows drug treatment regimens for pan-susceptible
disease, in the face of comorbidity that prevents an appro- TB.42 Multidrug-resistant tuberculosis (MDR-TB) is resistant
priate immune response, early infection, or improper test to at least INH and RIF, the two best first-line TB medications.
administration. Extensively drug-resistant tuberculosis (XDR-TB) in addition
In cattle, buffalo, bison, and other bovids, several sero- to INH and RIF is also resistant to the best second-line drugs,
logical tests based on M. bovis have been developed and are the fluoroquinolones and an injectable such as kanamycin or
in use, such as SeraLyte-Mbv (PriTest, Redmond, Wash.) capreomycin. The treatment of TB with drug-resistant organ-
and Chembio Bovid TB STAT-PAK (Chembio Diagnostic isms is more complicated and difficult and should be done
Systems, Inc., Medford, NY).36 There are also assays for use by or in consultation with experts. Regimens for resistant TB
Table 9-70 n Drug Regimens for Culture-Positive Pulmonary Tuberculosis Caused by

Drug-Susceptible Organisms
Initial Phase Continuation Phase Range of Rating* (Evidence)†

Total Doses
Interval and Doses‡ Interval and Doses‡,§ (minimal
Regimen Drugs (minimal duration) Regimen Drugs (minimal duration) duration) HIVneg HIVpos
1 INH 7 days/wk for 56 doses 1a INH/RIF 7 days/wk for 126 182-130 A (I) A (II)
(8 wk) or 5 days/wk doses (18 wk) (26 wk)
RIF for 40 doses (8 wk)¶ or 5 days/wk for
PZA 90 doses (18 wk)¶
EMB 1b INH/RIF Twice weekly for 36 92-76 (25 wk) A (I) A (II)¶
doses (18 wk)
1c# INH/RPT Once weekly for 18 74-58 (26 wk) B (I) E (I)
doses (18 wk)
2 INH 7 days/wk for 14 doses 2a INH/RIF Twice weekly for 36 62-58 (26 wk) A (II) B (II)**
(2 wk), then twice doses (18 wk)
RIF weekly for 12 doses
PZA (6 wk) or 2b# INH/RPT Once weekly for 18 44-40 (26 wk) B (I) E (I)
doses (18 wk)
EMB 5 days/wk for 10 doses
(2 wk),¶ then twice
weekly for 12 doses
(6 wk)
3 INH Three times weekly for 3a INH/RIF Three times weekly for 78 (26 wk) B (I) B (II)
24 doses (8 wk) 54 doses (18 wk)
RIF
PZA
EMB
Table 9-70 n Drug Regimens for Culture-Positive Pulmonary Tuberculosis Caused by

Drug-Susceptible Organisms—(Continued)
Initial Phase Continuation Phase Range of Rating* (Evidence)†
Total Doses
Interval and Doses‡ Interval and Doses‡,§ (minimal
Regimen Drugs (minimal duration) Regimen Drugs (minimal duration) duration) HIVneg HIVpos
4 INH 7 days/wk for 56 doses 4a INH/RIF Seven days/wk for 217 273-195 C (I) C (II)
(8 wk) or doses (31 wk) or (39 wk)
RIF
EMB 5 days/wk for 40 doses 5 days/wk for 155
(8 wk)¶ doses (31 wk)¶
4b INH/RIF Twice weekly for 62 118-102 C (I) C (II)
doses (31 wk) (39 wk)
From Blumberg HM, Burman WJ, Chaisson RE et al: American Thoracic Society/Centers for Disease Control and Prevention/Infectious Diseases Society of America: treatment
of tuberculosis, Am J Respir Crit Care Med 167(4):603–62, 2003.
EMB, Ethambutol; INH,isoniazid; PZA, pyrazinamide; RIF, rifampin; RPT, rifapentine.
*Definitions of evidence ratings: A = preferred; B = acceptable alternative; C = offer when A and B cannot be given; E = should never be given.
†Definitions of evidence ratings: I = randomized clinical trial; II = data from clinical trials that were not randomized or were conducted in other populations; III = expert opinion.
‡When directly observed therapy (DOT) is used, drugs may be given 5 days/wk and the necessary number of doses adjusted accordingly. Although there are no studies that com-
pare 5 with 7 daily doses, extensive experience indicates this would be an effective practice.
§Patients with cavitation on initial chest radiograph and positive cultures at completion of 2 months of therapy should receive a 7-month (31-week; either 217 doses [daily] or
62 doses [twice weekly]) continuation phase.
¶Five-day-a-week administration is always given by DOT. Rating for 5 day/wk regimens is AIII.
¶Not recommended for patients with HIV infection with CD4+ cell counts <100 cells/mL.
#Options 1c and 2b should be used only in HIV negative patients who have negative sputum smears at the time of completion of 2 months of therapy and who do not have cavi-
tation on the initial chest radiograph. For patients who start this regimen and are found to have a positive culture from the 2-month specimen, treatment should be extended an
extra 3 months.
generally use a combination of first- and/or second-line drugs Due to a paucity of data, the medication dosing for TB in
for an extended period of time—between 9 and 24 months animals has been based loosely on data from human phar-
depending on the resistance pattern. macokinetic studies and dosages. However, the increased use
Treatment of latent TB infection (LTBI) in humans, of pharmacotherapy for veterinary TB may result in more
previously referred to as prophylaxis, is based on the TST species-specific recommendations. For example, a number
risk groups previously discussed. Because current skin test of pharmacokinetic studies have been done on TB drug lev-
recommendations target high-risk groups, the intent to test els in elephants.41-45 Expert consultation is suggested in the
is generally the intent to treat. The first-line medication for treatment of veterinary TB.
the treatment of LTBI remains INH, currently recommended The first-line TB medications used in animals are the
for 9 months. An alternative treatment is INH for 6 months. same as humans: INH, RIF, EMB, and PZA (which is not
INH regimens may be daily or intermittent. Table 9-71 shows used in the treatment of M. bovis as this organism is usually
recommended regimens for the treatment of LTBI. resistant). Other antituberculous medications also include
quinolones and systemic aminoglycosides. Veterinary quino-
lones used for TB include enrofloxacin and marbofloxacin,
Treatment in Animals
and aminoglycosides include amikacin and streptomycin.
Until recently, the approach to treatment of TB in animals has Nevertheless, much more investigation is needed in the
not included the use of medications to treat until cure, and area of veterinary antituberculous pharmacotherapy.
it is still the rare exception. The overwhelming majority of Companion animals rarely are treated for TB, either
animals with suspected or confirmed TB are culled or eutha- because of the advanced condition of the animal, belief that
nized, such as with cattle. This has been done for several rea- TB cannot be treated, or concerns regarding public health. It
sons: an effort to halt the spread of the disease to other animals is probable that many, if not most, cases of TB in these ani-
or herds and mitigate the economic loss of herd and trade; the mals have gone undiagnosed as a result of a combination of
lack of practical alternatives; the difficulty of testing methods lack of awareness of the disease, lack of information regard-
to distinguish MTBC disease from infection or from nontu- ing diagnostics and testing, and the impression that, regard-
berculous mycobacterial disease; the cost of TB medication less, treatment is not feasible. That TB in companion animals
regimens; problems with drug administration and monitor- is an issue of public health concern has been cited as another
ing; and the inability or unreliability of monitoring response reason for not considering pharmacotherapy. However,
to disease or LTBI treatment. In non-herd situations or where it may be possible in these situations to consider some of
the animal is of significant economic or species value, such as the same principles of TB disease control as used in other
zoo animals and rare or endangered species, pharmacother- human and veterinary settings, such as housing the animal
apy has been used. Treatment of elephants with multidrug separately and/or outdoors while awaiting test results or a
regimens has been documented, including for MDR-TB. response to therapy. Nonetheless, the logistics and feasibility
Table 9-71 n Recommended Drug Regimens for the Treatment of LTBI in Adults
Interval and Rating† (Evidence)‡

Drug Duration Comments* HIV Negative HIV Infected
Isoniazid Daily for 9 In persons with HIV infection, isoniazid may be administered A (II) A (II)
months§|| concurrently with NRTIs, protease inhibitors, or NNRTIs.
Twice weekly DOT must be used with twice-weekly dosing. B (II) B (II)
for 9 months§||
Isoniazid Daily for 6 Not indicated for persons with HIV infection, those with B (I) C (I)
months|| fibrotic lesions on chest radiographs, or children.
Twice weekly DOT must be used with twice-weekly dosing. B (II) C (I)
for 6 months||
Rifampin¶ Daily for 4 Used for persons who are contacts of patients with B (II) B (III)
months isoniazid-resistant, rifampin-susceptible TB.
In persons with HIV infection, most protease inhibitors or
delavirdine should not be administered concurrently with
rifampin. Rifabutin with appropriate dose adjustments
can be used with protease inhibitors (saquinavir should
be augmented with ritonavir) and NNRTIs (except
delavirdine). Clinicians should consult Internet updates for
the latest specific recommendations.
RZ Daily for 2 RZ generally should not be offered for treatment of latent D (II) D (II)
months tuberculosis infection for persons with or without HIV
infection.
Twice weekly for D (III) D (III)
2-3 months
Adapted from CDC: Targeted tuberculin testing and treatment of latent tuberculosis infection, MMWR Morb Mortal Wkly Rep 49(RR-6):1-51, 2000.
*Interactions with human immunodeficiency virus (HIV)-related drugs are updated frequently and are available at http://www.aidsinfo.nih.gov/guidelines.
†Strength of recommendation: A = Both strong evidence of efficacy and substantial clinical benefit support recommendation for use. Should always be offered. B = Moderate
evidence for efficacy or strong evidence for efficacy but only limited clinical benefit supports recommendation for use. Should generally be offered. C = Evidence for efficacy is
insufficient to support a recommendation for or against use, or evidence for efficacy might not outweigh adverse consequences (e.g., drug toxicity, drug interactions) or cost of
the treatment or alternative approaches. Optional. D = Moderate evidence for lack of efficacy or for adverse outcome supports a recommendation against use. Should generally
not be offered. E = Good evidence for lack of efficacy or for adverse outcome support a recommendation against use. Should never be offered.
‡Quality of evidence supporting the recommendation: I = Evidence from at least one properly randomized controlled trial. II = Evidence from at least one well-designed clinical
trial without randomization from cohort or case-controlled analytic studies (preferably from more than one center), from multiple time-series studies, or from dramatic results
from uncontrolled experiments. III. = Evidence from opinions of respected authorities based on clinical experience, descriptive studies, or reports of expert committees.
§Recommended regimen for persons aged <18 years.
||Recommended regimens for pregnant women.
¶The substitution of rifapentine for rifampin is not recommended because rifapentine’s safety and effectiveness have not been established for patients with latent tuberculosis
infection.
NRTIs, Nucleoside reverse-transcriptase inhibitors; NNRTIs, non–nucleoside reverse-transcriptase inhibitors; DOT, directly observed therapy; RZ, rifampin plus pyrazinamide.
of this approach depend on each individual situation, and and surveillance information is limited. The clinical and epi-
discussion with TB experts is advisable. demiological presentation of NTM infection has changed dra-
matically in recent years. This is thought to be due, in part, to
the ability of these organisms to survive and flourish in habitats
Nontuberculous Mycobacteria
shared with humans and other animals, such as drinking water.
NTM are environmental opportunistic pathogens that differ In addition, an increase in the proportion of HIV-infected
from the members of MTBC (and M. leprae) in that they are and other immunosuppressed hosts suggest a continuing and
not obligate pathogens but rather are found in the environ- increasing prevalence of NTM infections in the future. Human
ment and environmental reservoirs that serve as the source risk factors associated with NTM disease include comorbid
of infection.46 Although most NTM do not cause human or lung conditions such as prior TB disease, silicosis, and bron-
animal disease, some may be pathogenic with potential for chiectasis, and host immunosuppression such as HIV infection.
interspecies and zoonotic transmission. Table 9-72 shows With the rise of HIV infection in the 1980s came increasing
common potentially pathogenic mycobacteria, classified reports of disseminated human NTM infections, such as M.
according to growth rate as either rapid growing (less than 1 avium complex (MAC).
week) or slow growing (more than 1 week). The most common sites of NTM disease in humans are
Transmission of NTM is achieved through inhalation or pulmonary, lymphatic, skin, and soft tissue and disseminated
ingestion of water, particulate matter or aerosols, or through disease. Pulmonary disease, commonly from M. avium, M.
trauma.47 NTMs are not generally considered communicable intracellulare, M. kansasii, or M. abscessus, generally pres-
between humans and animals or as zoonotic infections and as ents as a chronic condition with a persistent or varying
such are not reportable diseases. Consequently, epidemiological cough; additionally, there may be fatigue, malaise, sputum
data on the prevalence of NTM disease are not well established production, fever, weight loss, dyspnea, and hemoptysis.
in cervical, submandibular, submaxillary, or preauricular lymph

Table 9-72 n Potentially Pathogenic
nodes. The diagnosis may be made by lymph node biopsy and
Nontuberculous Mycobacteria specimen culture. A negative skin test response (<10 mm) may
Mycobacterial Growth Disease
be helpful. Treatment may depend on the particular species of
Species Classification* Presentation NTM, but localized disease in immunocompetent individuals
may include surgical excision of the lymph node.
M. abscessus Rapid Pulmonary, skin, soft Skin, soft tissue, and bone disease, most commonly caused
tissue, bone by M. fortuitum, M. abscessus, M. chelonae, M. marinum, or
M. avium complex: Slow Pulmonary, M. ulcerans, usually occurs through penetration, such as in
M. avium, lymphadenitis, puncture wounds, traumatic injuries, surgical wounds or
M. intracellulare, gastrointestinal, injection, or skin trauma. For example, tenosynovitis of the
M. paratuberculosis wasting
hand, commonly from M. marinum, may occur in those
M. chelonae Rapid Skin, soft tissue, bone cleaning aquariums (Color Plate 9-79). Chronic infections
M. fortuitum Rapid Skin, soft tissue, bone may occur in tendons, joints, and bones. In addition to anti-
M. kansasii Slow Pulmonary
biotics, surgical intervention may be indicated.
M. ulcerans is the agent causing Buruli’s ulcer, which is an
M. leprae Slow Skin, peripheral nerve increasing cause of morbidity and disability in many parts of
M. malmoense Slow Pulmonary, the world, especially West Africa.49 In animals, natural infec-
lymphadenitis, skin tions with M. ulcerans have been observed in koalas, ringtail
and soft tissue
possums, and an alpaca.50
M. marinum Slow Skin, soft tissue, bone In animals, M. paratuberculosis is the causative agent of
M. scrofulaceum Slow Lymphadenitis, skin Johne’s disease (Figure 9-156). This is a progressive infection
M. xenopi Slow Pulmonary,
affecting ruminants, causing GI symptoms such as diarrhea
lymphadenitis and wasting, and is an important cause of economic losses in
cattle. M. paratuberculosis also has been postulated as a cause
M. ulcerans Slow Skin, soft tissue
(Buruli’s ulcer) of Crohn’s disease in humans.
Avian mycobacteriosis (avian TB) in birds may be
*Rapid = growth <1 week; slow = growth >1 week. caused by several species of NTM, usually of the MAC or
M. genavense, which are environmentally ubiquitous. These
organisms may infect any bird (though uncommon in grey-
In HIV unaffected individuals, pulmonary infections with cheeked parakeets), but is more common in older or immu-
NTM traditionally had been found in older males. However, nosuppressed birds (Color Plate 9-80 and Figure 9-157).
it has been found that bronchiectatic MAC disease may Avian TB usually presents as a chronic disease involving
also present in older, thin females without prior pulmo- the GI tract and liver; signs include wasting despite a good
nary disease (Lady Windermere syndrome), sometimes in appetite and loose droppings. Primary respiratory signs are
the presence of pectus excavatum, mitral valve prolapse, or uncommon. Rarely, tubercles may be seen on the face and
scoliosis.48 oral cavity of infected birds.51 The diagnosis of avian TB
In HIV-infected individuals, NTM disease usually mani- usually has been made by culture of the organism, although
fests when the host’s CD4/T-lymphocyte cell counts are less adequate culture specimens may be difficult to obtain. The
than 50 cells/mL and often presents as a disseminated, mul-
tiorgan infection, commonly from M. avium. Acquisition
of the NTM is usually through the GI or respiratory tracts;
symptoms are nonspecific and include fever, night sweats,
weight loss, anorexia, and diarrhea. Disseminated disease has
also been reported with M. intracellulare, M. simiae, M. mari-
num, M. xenopi, and M. abscessus.
The diagnosis of pulmonary NTM disease is based on a
combination of clinical and laboratory criteria48:
1. Symptoms and findings on imaging studies (chest
radiograph or high-resolution CT scan) consistent
with the diagnosis,
2. Exclusion of other conditions with a similar presenta-
tion, such as TB, and
3. Either multiple positive sputum cultures of the NTM spe-
cies, a positive culture from a bronchial wash or lavage,
or a biopsy specimen with typical histological features Figure 9-156 n Granulomatous enteritis, Johne’s disease (Mycobacte
and a positive culture result from either the biopsy speci- rium avium spp. paratuberculosis) in a cow. There is chronic wasting and
men or sputum. diarrhea in this 18-month-old heifer. The age at which this cow showed clin-
ical signs is not typical of the disease. Signs usually occur 2 or more years
Lymphatic disease is the most common NTM presentation after initial infection. (From McGavin MD, Zachary JF: Pathologic basis of
in children and rarely affects immunocompetent adults. The veterinary disease, ed 4, St Louis, 2007, Mosby Elsevier. Courtesy College of
majority of cases are due to MAC, and sites are usually unilateral Veterinary Medicine, Cornell University.)
M. leprae is the causative agent of leprosy (Hansen’s dis-

ease) in humans, a chronic, granulomatous disease primar-
ily affecting the skin and peripheral nerves. Leprosy has also
been reported in wild armadillos and nonhuman primates.
M. lepraemurium is the etiologic agent of murine leprosy, a
disease primarily affecting the skin and viscera of rats and
mice.54
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TULAREMIA
Peter M. Rabinowitz and Lisa A. Conti t errorism agent as well as a zoonotic pathogen with
potential to cause significant health effects in human and
Tularemia (ICD-10 A21) animal populations.
Other names in humans: rabbit fever, Francis disease, deer-fly Key Points for Clinicians and Public Health
fever, Ohara’s disease, market men’s disease Professionals
Other names in animals: rabbit fever, deerfly fever
Francisella tularensis causes an acute febrile illness in
humans and other animals that can be fatal. The inci- • Provide epidemiological analysis of this reportable
dence of tularemia has decreased in the United States disease.
since the first half of the twentieth century.1 However, • Educate the public to avoid tick, fly, and mosquito bites
sporadic outbreaks continue to occur, and the disease by using appropriate clothing and repellents.
has emerged in regions where it previously had not been • Educate hunters to use puncture-resistant gloves when
recognized. Moreover, its widespread occurrence in wild- skinning or handling game, especially rabbits, and to
life and arthropod vectors, its ability to persist in water cook wild meat thoroughly.
and soils, and its high infectiousness for both humans and • The CDC recommends that laboratory personnel
domestic animals make it both a high-priority biological be alerted when tularemia is suspected. Diagnostic
procedures involving tularemia should be performed disinfected with 1% hypochlorite, 70% ethanol, glutaralde-
in at least biosafety level 2 conditions. Examining sus- hyde, or formaldehyde or inactivated by moist heat (121° C
pected cultures should be done in a biological safety for at least 15 minutes) and dry heat (160-170° C for at least
cabinet. Procedures that could produce aerosols or 1 hour).7
droplets require biosafety level 3 conditions.2
• Disinfect with 1% sodium hypochlorite, 70% ethanol, Geographical Occurrence
and glutaraldehyde.
• Consider the possibility of bioterrorism in the event of Tularemia is a disease of the Northern Hemisphere.
a cluster of unexplained cases. Historically, the highest prevalence has been recorded in the
United States and Russia. However, in both countries the
prevalence has declined significantly since World War II. In
the United States, the incidence peaked in 1939 with 2291
• Report disease to public health authorities using the reported cases; in recent decades the average number of U.S.
case definition; see http://www.cdc.gov/ncphi/disss/ cases has been less than 200 annually.1 Most cases occur in the
nndss/casedef/tularemia_current.htm. south-central and western states, including Missouri, Alaska,
• Consider the diagnosis in persons presenting Oklahoma, South Dakota, Tennessee, Kansas, Colorado,
with acute onset of fever and exposure to ticks or Illinois, Utah, and Montana.8 The two major pathogenic
animals. strains vary in their geographical distribution. F. subspecies
• Inquire about occupational risk factors for infection tularensis is primarily confined to North America, although
and ensure that workers at risk take precautions. isolation of strains resembling F. tularensis subspecies tula-
• Ensure that any laboratory workers handling strains of rensis has recently been reported in Europe.9 F. tularensis
tularemia virulent to humans are using biosafety level holarctica is also found in North America but to a lesser
3 precautions.3 extent. By contrast, it is the predominant strain in Europe
• Provide PEP following aerosol exposure. and Northern Asia. A third strain, F. tularensis subspecies
• A vaccine for tularemia is under review by the FDA but mediasiatica, is found in central Asia.
is not currently available in the United States.4
Groups at Risk
Veterinary Clinicians In the United States, higher attack rates occur in children
• In many states tularemia in horses is a reportable aged 5 to 9 years and individuals 75 years or older. Native
disease to the state veterinarian. Disease in cats and Americans/Alaskan natives have an incidence of 0.5 per
dogs may be reportable to public health authorities. 100,000, 10 times the rate in whites (0.04/100,000). It is
• In endemic areas, counsel owners to neuter cats to pre- thought that the higher rates in children reflect exposure risk
vent roaming and keep cats indoors. due to tick and other insect bites, whereas the increased risk
• Treat dogs, cats, and horses for ectoparasites. in Native Americans may be related to increased exposure.
• Ensure policies are in place to isolate suspected cases High rates of infection in ticks and dogs have been found in
and for veterinary staff to use protective equipment reservations reporting human outbreaks.1
and extreme care in handling infected animals, car- Other risk groups include farmers, landscapers (espe-
casses, or tissues. cially those engaged in mowing lawns10), and hunters who
• Treat early if tularemia is suspected; otherwise, prognosis may encounter carcasses of infected rabbits or other animals.
is poor. Cat ownership has been reported as a risk factor for infection
in areas experiencing outbreaks.11 Veterinarians and wildlife
rehabilitators may be at risk through handling sick animals.
Agent Laboratory workers are also at risk because of the infectious-
Francisella tularensis is a small, gram-negative intracellular ness of the organism.
coccobacillus. Two major subspecies are recognized with dif-
ferent biochemical and pathological characteristics: F. tula- Hosts, Reservoir Species, Vectors
rensis tularensis and F. tularensis holarctica. F. tularensis
subspecies tularensis (Jellison type A) is considered to have Tularemia is found in more than 250 species of mammal,
higher virulence, with human case fatality rates between 5% birds, reptiles, and fish.8 Aquatic animals have developed tula-
and 15% without treatment and a median lethal dose (LD50) remia after being immersed in contaminated water Different
in rabbits of 1 to 10 organisms. F. tularensis subspecies hol- species vary in their susceptibility to the disease. In the
arctica (Jellison type B) has a lower infectivity (LD50 >106 United States, cottontail rabbits (Sylvilagus species) as well as
organisms in rabbits) and rarely causes human fatalities.5 jackrabbits, beaver, moles, squirrels, muskrat, meadow voles,
Recently type A isolates in the United States have been fur- and sheep are prone to the disease, which is often fatal.
ther divided, using molecular techniques, into type A-East Cats are at increased risk because of their predatory
and type A-West, with type A-West less virulent than either habits. A serological survey found evidence of past infection
type A-East or type B.6 Viable organisms can be found for in 24% of cats tested in Connecticut and New York, suggest-
months in fomites or the carcasses or hides of infected ani- ing that the disease in cats may be more common than often
mals and years in frozen infected meat. The organism can be recognized.12
Tularemia is found in a number of vector species, includ- host causes the oculoglandular form of the disease. Ingestion
ing several species of tick, deer flies, mites, lice, midges, fleas, of contaminated meat or water can cause a typhoidal form of
bedbugs, and mosquitoes. Vector-transmitted infections are the disease characterized by fever and nonspecific GI symp-
believed to account for the majority of human and other toms, including diarrhea.13
animal cases in the United States. Recognized vectors in the Although rare, there are cases of humans developing
United States include the wood tick (Dermacentor andersoni), infection from contact with infected cats and dogs. Exposure
dog tick (D. variabilis), lone star tick (Amblystoma america- risk factors include cat bites14 and being licked by an infected
num), and the deer fly (Chrysops discalis).8 Flies can carry dog.15
Francisella for 2 weeks and ticks may be infected throughout
their lifespan. Environmental Risk Factors
F. tularensis can survive for months in water and sediment.
A number of human outbreaks have occurred next to bodies
Animal-to-animal and animal-to-human transmission of of water, including one associated with crayfish fishing.16
tularemia appears to take place through a variety of mecha- In an outbreak of pneumonic tularemia in Martha’s
nisms, including direct inoculation through a bite from an Vineyard, skunks and raccoons were found to frequently be
infected arthropod vector, a bite or scratch or conjunctival seroreactive, raising the possibility of peridomestic environ-
contact from an infected animal, inhalation of aerosols con- mental contamination by feces; however, this has not been
taining organisms, and ingestion of contaminated food or confirmed as the source of illness.17 Another environmental
water (Figure 9-158). Human-to-human transmission has factor is the changing conditions that can lead to increases
not been reported. The mode of transmission helps deter- in rodent populations; outbreaks have been associated with
mine the clinical form of the disease. increases in populations of rodents. Intentional introduction
In the United States, the most common form of the of game animals such as hares into new geographical areas
disease is the ulceroglandular type, which develops after a for hunting has lead to outbreaks in Spain, where it had not
vector bite (usually a tick or fly) and consists of an ulcer at been previously reported.18
the site of the bite with associated lymphadenopathy and
fever. Direct handling of infected carcasses (especially rab- Disease in Humans
bits) can also result in this form of infection. Less commonly,
the inhalation of organisms results in primary pneumonic Tularemia causes an acute febrile disease that usually begins
tularemia. Contact with mucous membranes of a susceptible 3 to 5 days after exposure. Although most cases are charac-
LIFE CYCLES OF FRANCISELLA TULARENSIS
Deer flies Mosquitoes
Voles
Lagomorphs
a Water/soil b Water/soil
Ticks Ticks
Voles
Lagomorphs
Figure 9-158 n Life cycles of Francisella tularensis. (From Cohen J, Powderly WG: Infectious diseases, ed 2,
Philadelphia, 2004, Mosby Elsevier.)
Cats can develop an acute febrile syndrome caused by tula-

remia that can be fatal (Color Plate 9-83). Ulceroglandular
disease in cats has also been reported.20 Dogs appear to be
more resistant and likely to develop asymptomatic infection.
However, fever, anorexia, and lethargy have been reported in
a dog that ate an infected rabbit.21
Horses can develop a febrile infection associated with
impaired coordination and depression.22 Cattle appear to be
resistant. Table 9-73 compares clinical presentations of tula-
remia in humans and other animals.
Diagnosis
Diagnosis in humans is usually based on clinical signs and
confirmed by serological studies showing at least a four-
Figure 9-159 n This Vermont muskrat trapper contracted tularemia, fold rise in titer that occurs 2 weeks after the onset of illness.
which manifested as a cutaneous lesion on his left lateral forehead. (From
Centers for Disease Control and Prevention Public Health Image Library, A direct immunofluorescence test and/or PCR test may be
Atlanta, Ga.) available for rapid diagnosis.
Culture of body fluids should be performed only in refer-
ence laboratories because of risk of infection to laboratory
personnel. Lymph nodes should not be biopsied unless anti-
terized by the abrupt onset of fever, chills, fatigue, myalgia, biotics have already been started because of the risk of induc-
headache, and nausea, several distinct forms of the disease ing bacteremia.5
are related to the mode of transmission and the virulence of In other animals, a direct antibody or IFA assay (Color
the organism. Infection caused F. tularensis subspecies tula- Plate 9-84) is considered the most rapid and accurate means
rensis may progress to septicemia, with disseminated intra- of diagnosis15; an immunohistochemical analysis for forma-
vascular coagulation, acute respiratory distress syndrome, lin-fixed tissue has also been developed. Serology is used if
CNS involvement, and multiorgan failure. Disease related to the animal survives, with a fourfold titer difference between
F. tularensis subspecies holarctica is more likely to produce acute and convalescent titers confirming infection. Culture
mild symptoms with a low case fatality rate. of the bacterium can be performed but poses a health risk for
Most cases (87%)19 present as ulceroglandular tularemia, laboratory personnel.
resulting from insect bites or direct contact with an infected
carcass (Figure 9-159 and Color Plate 9-81). One of the first
symptoms is lymphadenopathy localized in the area where Treatment
the bite or scratch occurred. A painful papule develops either
simultaneously or within several days at the site of the ini- Antibiotics are the mainstay of therapy. Isolation of patients
tial skin entry. This papule then ulcerates, taking several and prophylactic treatment of contacts of human patient are
weeks to heal.5 The lymphadenopathy may also suppurate not necessary because human-to-human transmission has not
and become ulcerative (Color Plate 9-82). Rarely, if there is been observed. For individuals who have had high-risk expo-
contact with conjunctival membranes, oculoglandular tula- sures to infected animals or other sources of the organism,
remia develops, with purulent conjunctivitis and lymphade- prophylactic antibiotics are indicated as shown in Table 9-74.
nopathy. Glandular tularemia resembles the ulceroglandular (Note: tetracycline and chloramphenicol are bacteriostatic
form but without skin lesions.19 and have been associated with relapses in humans).
Primary pneumonic tularemia results from inhalation of Little is known about effective treatment regimens in
infected aerosols and manifests as pneumonitis and bron- animals because the disease is often fatal before treatment
chiolitis, which may lead to respiratory failure. Pneumonic begins. However, recommended antibiotic regimens are
tularemia may also develop as a complication of other forms shown in Table 9-74. An important part of animal treat-
and is associated with a higher mortality rate.19 ment is isolation of the animal and protection of veterinary
The typhoidal form of tularemia is considered rare, is staff, including wearing of gowns, gloves, and face masks,
caused by ingestion of contaminated food or water, and may including eye protection, when handling a suspected
be difficult to diagnose. Symptoms can include fever, gas- case.15
troenteritis, septicemia, and pneumonia. Ingestion may also
lead to oropharyngeal tularemia with throat pain, prominent
pharyngitis, oral ulcers, and enlargement of cervical lymph References
nodes. 1. Centers for Disease Control and Prevention. Tularemia—United States,
1990–2000. MMWR. 2002;51(9):182.
2. Centers for Disease Control and Prevention: Abstract of Dennis DT,
Disease in Animals Inglesby TV, Henderson DA, et al. Consensus statement: tularemia as
a biological weapon: medical and public health management. JAMA.
Susceptibility to F. tularensis infection varies among animal 2001;285(21):2763.
species. Rabbits and many rodents develop fatal disease. 3. Titball RW, Sjostedt A, Pavelka Jr MS, et al. Biosafety and selectable
Sheep also have high mortality rates. markers. Ann N Y Acad Sci. 2007;1105:405.
Table 9-73 n Tularemia: Comparative Clinical Presentations in Humans and Other Animals
Incubation
Humans Children, Native Americans, Usually 3-5 days Fever, lymphadenopathy, fatigue, Positive serology, direct
hunters, landscapers, (range, 1-14)5 pneumonia immunofluorescence
others with wildlife
Ulceroglandular form: ulcer at site
contact
of entry
Glandular form
Primary pneumonic form
Oropharyngeal form
Typhoidal form
Cats, dogs Outdoor/hunting cats 2-7 days15 Fever, anorexia, lethargy, Pan leukopenia,
lymphadenopathy, leukocytosis, elevated
Tick and other insect bites hepatosplenomegaly liver function tests
Dogs more resistant than Ulcers in mouth, pseudomembrane DFA of tissues, serology,
cats on tongue15 blood culture
Mucous membranes icteric
Sheep Tick exposures 1-10 days 8
Fever, septicemia, rigid gait,
diarrhea, urination, respiratory
distress, death22
Swine Tick exposures 1-10 days8 Adults fairly resistant: fever, shortness
of breath, depression22
Young animals: lack of coordination,
depression, anorexia, neurological
signs
Rabbits Very susceptible 1-10 days8 Depression, anorexia, ataxia,
roughened coat, tendency to
huddle, weakness, fever, ulcers,
abscesses at site of infection,
dyspnea, swelling of regional
lymph nodes, sudden death
Usually not recognized until dead or
dying
Horses Tick exposure (rare) 1-10 days8 Lack of coordination, fever,
depression, dyspnea
DFA, Direct immunofluorescence antibody.
Table 9-74 n Antibiotic Treatment of Tularemia Infection in Humans and Other Animals
Humans (adult)
Inhalational Streptomycin 15 mg/kg IV bid or gentamicin 5 mg/ Doxycycline 100 mg PO or IV bid × 14-21 days or
kg IV qd × 10 days ciprofloxacin 400 mg IV (or 750 mg PO) bid ×
14-21 days24
Typhoidal Gentamicin or tobramycin 5 mg/kg/day divided q8h Add chloramphenicol if evidence of meningitis24
IV × 7-14 days
Postexposure prophylaxis: Doxycycline 100 mg PO bid × 14 days Ciprofloxacin 500 mg PO bid × 14 days
adult
Cats, dogs (early Amoxicillin 20 mg/kg IM or SC q12h or PO q8h PLUS Enrofloxacin 10-15 mg/kg PO, IM, IV, or SC q12h15
treatment is critical) gentamicin 4.4 mg/kg IM or SC q12h once, then
q24h thereafter until clinical response or until 7 days
Sheep Streptomycin or gentamicin Chloramphenicol 25 mg/kg IV qid or
tetracyclines8
4. Centers for Disease Control and Prevention. Key facts about tularemia. 15. Barr SC, Bowman DD. The 5-minute veterinary consult clinical com-
http://www.cdc.gov/ncidod/dvbid/tularemia.htm. panion: canine and feline infectious diseases and parasitology. Ames, IA:
5. Heymann DL, ed. Control of communicable diseases manual. 19th ed. Blackwell; 2006.
Washington, DC: American Public Health Association; 2008. 16. Anda P, Segura del Pozo J, Diaz Garcia JM, et al. Waterborne out-
6. Staples JE, Kubota KA, Chalcraft LG, et al. Epidemiologic and molecu- break of tularemia associated with crayfish fishing. Emerg Infect Dis.
lar analysis of human tularemia, United States, 1964–2004. Emerg Infect 2001;7(suppl 3):575.
Dis. 2006;12(7):1113. 17. Matyas BT, Nieder HS, Telford SR 3rd. Pneumonic tularemia on
7. Center for Food Security and Public Health, Iowa State University. Martha’s Vineyard: clinical, epidemiologic, and ecological characteris-
Tularemia. http://www.cfsph.iastate.edu/Factsheets/pdfs/Tularemia.pdf. tics. Ann N Y Acad Sci. 2007;1105:351.
Accessed April 6, 2009. 18. Andres Puertas C, Mateos Baruque ML, Buron Lobo I, et al. Epidemic outbreak
8. Kahn CM, Line S, eds. The Merck veterinary manual. 9th ed. Whitehouse of tularemia in Palencia [in Spanish]. Rev Clin Esp. 1999;199(11):711.
Station, NJ: Merck; 2005. 19. Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious
9. Gurycova D. First isolation of Francisella tularensis subsp. tularensis in diseases. 6th ed. New York: Churchill Livingstone Elsevier; 2005.
Europe. Eur J Epidemiol. 1998;14(8):797. 20. Valentine BA, DeBey BM, Sonn RJ, et al. Localized cutaneous infection
10. Feldman KA, Stiles-Enos D, Julian K, et al. Tularemia on Martha’s with Francisella tularensis resembling ulceroglandular tularemia in a cat.
Vineyard: seroprevalence and occupational risk. Emerg Infect Dis. 2003; J Vet Diagn Invest. 2004;16(1):83.
9(3):350. 21. Meinkoth KR, Morton RJ, Meinkoth JH. Naturally occurring tularemia
11. Eliasson H, Lindback J, Nuorti JP, et al. The 2000 tularemia outbreak: in a dog. J Am Vet Med Assoc. 2004;225(4):545–547 538.
a case-control study of risk factors in disease-endemic and emergent 22. Acha PN, Szyfres B. Zoonoses and communicable diseases common to man
areas, Sweden. Emerg Infect Dis. 2002;8(9):956. and animals: vol. I: bacterioses and mycoses. 3rd ed. Washington, DC:
12. Magnarelli L, Levy S, Koski R. Detection of antibodies to Francisella Pan American Health Organization; 2001.
tularensis in cats. Res Vet Sci. 2007;82(1):22. 23. Kwan-Gett TS, Kemp C, Kovarik C. Infectious and tropical diseases: a
13. Greco D, Allegrini G, Tizzi T, et al. A waterborne tularemia outbreak. handbook for primary care. St Louis: Mosby Elsevier; 2005.
Eur J Epidemiol. 1987;3(1):35. 24. Gilbert DN, Moellering RC, Eliopoulos GM, et al. Sanford guide to anti-
14. Arav-Boger R. Cat-bite tularemia in a seventeen-year-old girl treated microbial therapy 2009. 39th ed. Sperryville, VA: Antimicrobial Therapy;
with ciprofloxacin. Pediatr Infect Dis J. 2000;19(6):583. 2009.
WEST NILE VIRUS AND OTHER ARBOVIRUS INFECTIONS
Carina Blackmore guidances discussed below are relevant for prevention of

and control of them all. They are also relevant for poten-
West Nile virus infection (ICD-10 A92.3) tially emerging zoonotic arboviruses such as Rift Valley
Fever virus.
Other names in humans: West Nile fever, West Nile meningi-
tis, West Nile encephalitis, West Nile poliomyelitis
Professionals
Other names in animals: West Nile virus infection
West Nile virus (WNV) was first isolated from a febrile

woman in Uganda in 1937.1 The first human disease out-
break occurred 20 years later in Israel. The virus was first • Recommend to the public:
detected in the Americas in 1999 by a veterinary pathologist  Do not go outdoors at dusk and dawn when mos-
when a flavivirus was identified as the cause of an appar- quitoes are most active.
ent zoonotic encephalitis outbreak in humans and corvid  Empty containers and drain stagnant waters where
birds (e.g., crows and jays) in Queens, New York. WNV has mosquitoes lay their eggs.
since become the most important cause of mosquito-borne  Install or repair window and door screens.
disease in North America. It spread across the 48 continen-  Dress so skin is covered with clothing.
tal United States in 6 years, and more than 27,000 human  Stock ornamental ponds with mosquito-eating fish.
cases and 25,000 horse cases of WNV disease were reported  Maintain pools.
during the period 1999 to 2007. Outbreaks of human or  Protect bare skin and clothing with a mosquito repel-
equine WNV encephalitis have also occurred in southern lent. Make certain the repellent is used according to
Europe, Israel, the Democratic Republic of the Congo, and its label. Do not use repellents over cuts, wounds, or
Russia. WNV is an example of a disease where tracking sen- irritated skin. Do not use repellent under clothing.
tinel cases in birds,2 horses, dogs,3 and other animals, as • DEET (N,N-diethyl-3-methylbenzamide)4 and picari-
well as WNV positive pools of mosquitoes, has proved use- din5 are effective repellents registered for skin appli-
ful for efforts aimed at early detection and prevention of cation by the EPA. Depending on the duration of
human cases. protection desired, products containing 4.75% DEET
Several zoonotic arthropod-borne (arboviral) diseases provide roughly 90 minutes’ effectiveness; products
are known to circulate within the United States, including containing 23.8% DEET provide an average of 5 hours
St. Louis encephalitis (SLE), Eastern equine encephalitis of protection.6
(EEE), La Crosse encephalitis (LAC) and Western equine • Among plant-based repellents registered with the
encephalitis (WEE). These arboviruses may have different EPA, oil of lemon eucalyptus provides longer-lasting
vector and vertebrate hosts than WNV but many of the protection than others, with an efficacy similar to a
repellent with low concentrations of DEET. Repellents provides the following guidance on WNV vaccination
can be reapplied according to the manufacturer’s of horses7: Primary vaccination of previously unvacci-
instructions. nated horses with either the inactivated or canary pox
• Sunscreen and insect repellent can be applied simul- vector vaccine involves administration of 2 doses of
taneously. However, it is not recommended to use a vaccine 4 to 6 weeks apart followed by revaccination at
product combining sunscreen and repellents as sun- a 12-month interval. Label instructions for the modi-
screen often needs to be applied more frequently and fied live chimera vaccine recommend a single injection
repeated application may increase the toxic effects of followed by a 12-month revaccination interval. More
the repellent. frequent boosters may be warranted for juvenile (<5
• Permethrin, a pyrethroid product, is an effective repel- years) or geriatric (>15 years) horses. Although the
lent registered for application on clothing, camping licensed WNV vaccines are currently not labeled for
gear, or mosquito nets. administration to pregnant mares, many veterinary
• Safety precautions when using repellents on children: practitioners do administer them to pregnant mares.
 Keep repellents out of the reach of children. Booster vaccination of pregnant mares 4 to 6 weeks
 Do not allow young children to apply insect repel- before foaling provides passive, colostral protection to
lent to themselves; have an adult do it for them. their foals. To avoid interference from colostral anti-
 Apply the repellent to your own hands and then rub bodies, primary vaccination of foals from vaccinated
them on the child. Avoid children’s eyes and mouth mares should be started at 4 to 6 months of age. Foals
and use it sparingly around their ears. should receive a third dose in the spring of the year
 Do not apply repellent to children’s hands as children following their birth. Foals of unvaccinated mares
may tend to put their hands in their mouths. should ideally receive two doses of vaccine before the
 Wash treated skin with soap and water after return- mosquito-borne disease season starting at 3 months
ing indoors and wash treated clothing. of age. The modified live flavivirus chimera vaccine is
 The American Academy of Pediatrics does not rec- labeled for foals 5 months or older. A single dose should
ommend repellents be used on children younger be administered followed by a second dose at 10 to 12
than 2 months. Instead, they recommend the use of months of age (before the next WNV season).
mosquito netting over infant carriers. Oil of lemon • Prevent dogs and cats from eating birds and other wildlife.
eucalyptus products should not be used on children • Maintain barrier precautions when performing
younger than 3 years. necropsies, particularly on birds.
• Determine and implement the most appropriate • Related flaviviruses are destroyed by 1% sodium
surveillance methods for WNV risk in your region, hypochlorite, 2% glutaraldehyde, and 70% ethanol.8
considering possible use of mosquito, bird, or mam-
mal sentinel information, as well as climate tracking Agent
(Color Plates 9-85 and 9-86).
WNV is part of the Flaviviridae family in the genus Flavivirus
(Figure 9-160). Flaviviruses are small (40 to 60 nm), lipid-
enveloped RNA viruses containing a single positive-strand
• In suspected cases, submit serum and/or CSF for WNV genomic RNA. The lipid surface contains the viral enve-
antibody testing. lope (E) and membrane (M) “spike” proteins. WNV and
• Monitor public health surveillance on human WNV SLE virus are closely related and both are members of the
disease in the local area, including surveillance of sen-
tinel animals, to estimate current human health risk.
• Counsel all patients, especially adults older than
50 years and families with infants, to avoid being bitten
by mosquitoes, including the appropriate use of repel-
lents and mosquito netting.
• Report cases to the health department if required in
the state per recommended case definition.
• Advise horse owners on how to prevent equine WNV
disease. Horses should be protected from mosquito
bites. This can be done by eliminating mosquito breed-
ing sites, providing screened housing, and applying
insect repellents.
• Vaccinate horses against WNV disease. There are three
licensed WNV vaccines currently available: an inacti-
vated whole virus vaccine, a live recombinant canary
pox vector vaccine, and a modified live chimera vac- Figure 9-160 n Electron microscopy of the West Nile virus. (From
cine. The American Association of Equine Practitioners Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.)
Japanese encephalitis antigenic serocomplex.1 More distantly West Nile Virus Transmission Cycle
related mosquito-borne flaviviruses in the Americas include West
yellow fever and Dengue virus. Nile
virus
Mosquito vector
Geographical Occurrence West
Nile West Nile
WNV was first identified in Uganda in 1937. It is now virus virus Incidental
infection
endemic in parts of Africa, Europe, Australia, and Asia as well
as North, Central, and South America.9,10
Bird
Incidental infection
reservoir
Groups at Risk hosts
WNV is transmitted by mosquito bite, and persons in all age

groups are at risk of infection. In areas where WNV is hyper-
endemic, it is a mild, common childhood illness.11 In indus-
trialized temperate areas the incidence of neuroinvasive Figure 9-162 n West Nile virus transmission cycle. (From Centers for
Disease Control and Prevention: Flowchart: West Nile virus transmission cycle.
WNV disease and death increases in those who are immuno- http://www.cdc.gov/ncidod/dvbid/westnile/cycle.htm.)
suppressed or 50 years and older.11,12 The risk for WNV men-
ingitis and encephalitis is also slightly higher among males
than females.
Virus amplification and transmission are favored by warm
Hosts, Reservoir Species, Vectors temperatures, and the peak virus activity occurs in the late
WNV is a mosquito-borne virus. The enzootic cycle involves summer months. Different vectors prefer different breeding
transmission of the virus among infected Culex mosqui- habitats. The Culex pipiens species breed in stagnant pools
toes and wild birds (Figure 9-161). Many bird species can of groundwater, artificial containers, catch basins, or sewage
become infected by WNV, although only a small propor- seepage. They prefer to breed in highly organic (polluted)
tion are likely to be important reservoir hosts. Passerine water. Culex tarsalis, the most important WNV vector in the
birds (crows, jays, finches, grackles, sparrows) are thought western United States, tolerates a wide range of habitats but
to play a role in the WNV transmission cycle. They are prefers permanent or semipermanent seepage areas and sur-
common, widespread, and develop a high and prolonged face pools associated with irrigated pastures. Culex nigripal-
viremia,13 all important features for a vertebrate reservoir pus, a principle WNV vector in the Southeast, is a floodwater
host. Humans, horses, and other mammals are incidental mosquito.
hosts of the virus.
Disease in Humans
Mode of Transmission and Life Cycle Most individuals infected with WNV (80%) remain asymp-
tomatic.17 The clinical presentation ranges from a mild non-
WNV is maintained in nature by mosquitoes and wild birds
neuroinvasive fever illness to encephalitis, coma, and death
(Figure 9-162). The overwintering mechanisms of the virus
(Table 9-75). It is estimated that fewer than 1% of infected
are not fully understood; however, overwintering adult
persons develop severe neurological disease. Typical symp-
mosquitoes are thought to play a role.14 Human and other
toms of West Nile fever include fatigue, fever, headache, and
mammals are incidental hosts of the virus. Non-mosquito-
muscle weakness. Half of the persons interviewed in a survey
borne transmission such as transplacental infection, breast-
among West Nile fever patients in Chicago also had difficulty
feeding, blood transfusion, and organ transplantation have
concentrating.18 More severe clinical syndromes include
also been documented.15 Fecal-oral transmission has been
aseptic meningitis, myelitis, polyradiculitis, and encephalitis.
reported among animals including alligators, cats, some rap-
Patients often present with a prodrome of fever, headache,
tors, hamsters, and golden crows.16
and other nonspecific symptoms. Many develop movement
disorders such as severe tremors and parkinsonism.19
Disease in Animals
Horses infected with WNV may develop fever, depression or
apprehension, stupor, behavioral changes, intermittent lame-
ness, ataxia, caudal paralysis, droopy lip, teeth grinding, muscle
twitching, tremors, difficulty rising, recumbency, convulsions,
and death.20,21 In one study, approximately 33% of horses with
clinical signs of WNV infection died from the disease.
Figure 9-161 n Culex mosquito. (From Florida Medical Entomology Clinical signs of WNV infection in birds vary greatly
Laboratory, Michelle Cutwa-Francis, photographer.) among species. Many avian species develop clinically
Table 9-75 n West Nile Virus Infection: Comparative Clinical Presentations in Humans and
Other Animals
Humans Mosquito exposure, age, 3-14 days18 Fever, headache, muscle CSF: Specific WNV IgM
immunosuppression after pain, weakness, fatigue, antibodies, lymphocytic
organ transplantation, and ocular pain, malaise, pleocytosis, elevated protein,
male gender are risk factors anorexia, maculopapular or normal glucose
for severe illness19 morbilliform rash on neck, Blood: Specific WNV IgM or
Other risk factors include trunk, and extremities 5-12 IgM and IgG antibodies in
receiving blood transfusions days after onset18,19 serum
or organ donations, and Neuroinvasive disease: ataxia Peripheral blood total
occupational exposure and extrapyramidal signs, leukocyte count normal
Infants may become infected optic neuritis, seizures, or elevated, anemia, and
by maternal infection during tremor, myoclonus, lymphocytopenia
pregnancy or breastfeeding parkinsonism and altered Brain magnetic resonance
mental status12,27 imaging results often normal
Rash, polyradiculitis, and acute Signal abnormalities may be
asymmetric poliomyelitis like detected in the basal ganglia,
flaccid paralysis are seen in a thalamus, and brainstem of
small number of patients.19,28 patients with encephalitis
and in the anterior spinal
cord in patients with flaccid
paralysis19
Virus detection in CSF or
tissues is also possible
Horses Mosquito exposure 3-15 days Fever, depression or Fourfold rise in WNV serum
apprehension, stupor, antibody, positive IgM ELISA
behavioral changes, antibody test in serum or CSF
intermittent lameness, Antigen detection in brain
knuckling over at tissue using viral culture, PCR,
the metacarpo- or or immunohistochemistry
metatarsophalangeal
joints, ataxia, caudal
paralysis, droopy lip, teeth
grinding, muscle twitching,
fasciculations and tremors,
difficulty rising, recumbency,
convulsions, blindness, and
colic or death16,20,21
Birds Mosquito exposure Unknown Signs of WNV neurological WNV detection in brain, heart,
disease include sudden onset kidney or liver tissue
Possible contact with other of mild ataxia, abnormal Fourfold rise in WNV antibody
birds or their excretions head posture, circling, titer
Possible exposure from reclining, quadriparesis, and Rapid screening tests on oral
predation on other infected tremors; nystagmus, seizures, or cloacal swabs, swabs of
birds/mammals disorientation, signs of organ tissue, or feather pulp
depression, anorexia, weight
loss, impaired vision, and
sudden death may also be
present.16,23
Dogs, cats Allowed to roam outdoors, Unknown22 Usually asymptomatic, fever, Serology, PCR
stray animals lethargy reported in cats,
encephalitis, arthritis,
myocarditis in dogs
CSF, Cerebrospinal fluid.
i napparent infections, whereas others become severely ill orrhaging liver and spleen, myocardial degeneration
and succumb to the virus. Signs of WNV neurological dis- and inflammation, pericardial lesions, pancreatitis, and
ease include sudden onset of mild ataxia, abnormal head chronic adrenalitis.
posture, circling, reclination, quadriparesis, and tremors. Dogs and cats appear to be relatively resistant to WNV
Nystagmus, seizures, disorientation, signs of depression, and generally develop subclinical disease after exposure.
weight loss, impaired vision, and sudden death may also Acute encephalitis, polyarthritis, and myocarditis have been
be present.9,23 Birds shed virus orally and in their feces, reported in dogs.22 Fever and lethargy have been reported in
and bird-to-bird transmission has been reported.9,24 Gross cats. In addition, WNV has been isolated from the brain of a
pathology often includes an enlarged, necrotic, and hem- cat with neurological disease.25
Outbreaks of WNV disease with high mortality rates have ncidod/dvbid/westnile/qa/insect_repellent.htm. Accessed September
been seen among farm-raised alligators. The virus appears 8, 2008.
7. American Association of Equine Practitioners. West Nile virus. http://
to spread via fecal-oral transmission in the alligator pens www.aaep.org/wnv.htm. Accessed September 8, 2008.
(Color Plates 9-87 and 9-88). 8. Dvorak G, Rovid-Spickler A, Roth JA, et al. Handbook for zoonotic diseases
WNV infection has also been documented in bats, a of companion animals. Ames, IA: The Center for Food Security and Public
skunk, and a few rodent species. Health, Iowa State University College of Veterinary Medicine; 2008.
9. Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann
Intern Med. 2002;137(3):173.
Diagnosis 10. Diaz LA, Komar N, Visintin A, et al. West Nile virus in birds, Argentina.
Emerg Infect Dis. 2008;14(4):689.
Serological tests used to diagnose WNV infection include 11. Campbell GL, Marfin AA, Lanciotti RS, et al. West Nile virus. Lancet
ELISA and antigen (IgM and IgG) capture ELISA, hemag- Infect Dis. 2002;2(9):519.
12. Centers for Disease Control and Prevention. West Nile virus: clinical
glutination inhibition, plaque reduction neutralization, description. www.cdc.gov/ncidod/dvbid/westnile/clinicians/clindesc.
and virus neutralization. Virus can also be identified in htm. Accessed September 8, 2008.
the CNS and other tissues using virus isolation, PCR, and 13. Komar N, Langevin S, Hinten S, et al. Experimental infection of North
immunohistochemistry. American birds with the New York 1999 strain of West Nile virus. Emerg
Infect Dis. 2003;9(3):311.
For surveillance of WNV in dead birds, public health 14. Nasci RS, Savage HM, White DJ, et al. West Nile virus in overwin-
and partner agencies have used the VecTest antigen-capture tering Culex mosquitoes, New York City, 2000. Emerg Infect Dis.
assay (Medical Analysis Systems, Camarillo, Calif.),29 Rapid 2001;7(4):742.
Analyte Measurement Platform (RAMP) assay (Response 15. Hayes EB, Komar N, Nasci RS, et al. Epidemiology and transmission
Biomedical Corp, Burnaby, British Columbia, Canada),30 dynamics of West Nile virus disease. Emerg Infect Dis. 2005;11(8):1167.
16. Trevejo RT, Eidson M. West Nile virus. J Am Vet Med Assoc.
and real-time RT-PCR. 2008;232(9):1302.
17. Mostashari F, Bunning ML, Kitsutani PT, et al. Epidemic West Nile
encephalitis, New York, 1999: results of a household-based seroepide-
Treatment miological survey. Lancet. 2001;358:261.
18. Watson JT, Pertel PE, Jones RC, et al. Clinical characteristics and func-
There is no specific treatment for WNV infection in either tional outcomes of West Nile fever. Ann Intern Med. 2004;141(5):360.
humans or animals. In more severe human cases, intensive 19. Hayes EB, Seyvar JJ, Zaki SR, et al. Virology, pathology and clini-
supportive care is indicated, such as hospitalization, intravenous cal manifestations of West Nile virus disease. Emerg Infect Dis.
2005;11(8):1174.
fluids, airway management, respiratory support (ventilator), 20. Schuler LA, Khaitsa ML, Dyer NW, et al. Evaluation of an outbreak
prevention of secondary infections (pneumonia, urinary tract, of West Nile virus infection in horses: 569 cases. J Am Vet Med Assoc.
etc.), and good nursing care. Research trials are under way to 2002;225(7):1084.
identify effective antiviral treatment and vaccines. 21. Ward MP, Levy M, Thacker HL, et al. Investigation of an outbreak of
Nonspecific immunoglobulin and plasmapheresis should encephalomyelitis caused by West Nile virus in 136 horses. J Am Vet
Med Assoc. 2002;225(7):84.
be considered for patients with Guillain-Barré syndrome. 22. Austgen LE, Bowen RA, Bunning ML, et al. Experimental infection of
The treatment is not indicated for patients with paralysis due dogs and cats with West Nile virus. Emerg Infect Dis. 2004;10(1):82.
to damage of anterior horn cells.28 23. D’Agostino JJ, Isaza R. Clinical signs and results of specific diagnos-
tic testing among captive birds housed at zoological institutions and
infected with West Nile virus. J Am Vet Med Assoc. 2004;224(10):1640.
References 24. McLean RG, Ubico SR. Arboviruses in birds. In: Thomas NJ, Hunter DB,
Atkinson CT, eds. Infectious diseases of wild birds. Ames, IA: Blackwell;
1. Hayes CG. West Nile virus: Uganda, 1937, to New York City, 1999. Ann 2007.
N Y Acad Sci. 2001;951:25. 25. Komar N. West Nile virus: epidemiology and ecology in North America.
2. Komar N. West Nile virus surveillance using sentinel birds. Ann N Y Adv Virus Res. 2003;61:185.
Acad Sci. 2001;951:58. 26. Deubel V, Fiette L, Gounon P, et al. Variations in biological features of
3. Resnick MP, Grunenwald P, Blackmar D, et al. Juvenile dogs as poten- West Nile viruses. Ann N Y Sci. 2001;951:195.
tial sentinels for West Nile virus surveillance. Zoonoses Public Health. 27. Sejvar JJ, Haddad MB, Tierney BC, et al. Neurologic manifesta-
2008;55(8–10):443. tions and outcome of West Nile virus infection. J Am Med Assoc.
4. US Environmental Protection Agency. The insect repellent DEET. 2003;390(4):511.
http://www.epa.gov/pesticides/factsheets/chemicals/deet.htm. Accessed 28. Sejvar JJ, Leis AA, Stokic DS, et al. Acute flaccid paralysis and West Nile
September 8, 2008. virus infection. Emerg Infect Dis. 2003;9(7):788.
5. US Environmental Protection Agency. New pesticide fact sheet: pica- 29. Stone WB, Okoniewski JC, Therrien JE, et al. VecTest as diagnostic and
ridin. http://www.epa.gov/opprd001/factsheets/picaridin.pdf. Accessed surveillance tool for West Nile virus in dead birds. Emerg Infect Dis.
September 8, 2008. 2004;10(12):2175.
6. Centers for Disease Control and Prevention. West Nile virus: ques- 30. Stone WB, Therrien JE, Benson R, et al. Assays to detect West Nile virus
tions and answers: insect repellent use and safety. http://www.cdc.gov/ in dead birds. Emerg Infect Dis. 2004;11(11):1770.
Infectious Disease
Scenarios 10
TRAVEL AND ANIMAL CONTACT Human Health Clinicians

• When providing pretravel screening and counseling,
The U.S. Department of Commerce estimates that at least inquire about whether the person is traveling with
30 to 40 million Americans visit other countries each year.1 pets and provide counseling about health risks from
Some of these travelers contract diseases while overseas and animal contacts while traveling. See the CDC’s “Your
may return home still symptomatic. Some of these travel- Survival Guide to Safe and Healthy Travel,” available
related diseases are zoonoses resulting from contact with online at http://wwwn.cdc.gov/travel/contentSurvival
domestic or wild animals. Guide.aspx.
Many international travelers restrict their stays to hotels • If a patient is planning to travel with a pet, advise him
in urban or other well-developed areas that involve reduced or her to consult a veterinarian for pretravel risk assess-
risk of animal contact. Yet the growing popularity of eco- ment and preventive care.
tourism, religious pilgrimages, wildlife safaris, and other • When evaluating the returning traveler with illness,
forms of adventure travel may increase the chances of travel- inquire about animal contacts as well as the health of
ers contracting an animal-related infectious disease during any pets that have accompanied the traveler or that the
their trips. Animal contacts are possible even in cities and traveler has acquired overseas.
elsewhere on the beaten path; for example, high levels of
pet allergens have been found in vacation hotels in some
countries.1 Veterinary Clinicians
Animal travel across borders is increasing as well. In 2006, • Provide appropriate pretravel risk assessment and
more than 287,000 dogs were estimated to have entered the vaccination of pets and documentation of animal
United States from foreign countries (including Mexico and health status.
Canada), 25% of which were unvaccinated.2 Many of these • Counsel owner about signs of illness to monitor in his
dogs were imports, accompanying their owners. The increas- or her pet and quarantine regulations.
ing popularity of traveling with one’s pet may result in a wide • In the evaluation of an ill animal after travel, consider
range of exposure risks for both the pet and owner. In addi- risks of imported diseases.
tion, some individuals may acquire a pet overseas and return • Advise clients regarding the health risks of adopting a pet
home with it. overseas (e.g., documented cases of rabies, leishmaniasis,
and leptospirosis have been reported in imported pets).
Professionals
TRAVEL MEDICINE
Travel medicine is a medical discipline that deals with pre-

vention of infectious diseases during international travel as
• Consider recent foreign travel in human beings or well as the personal safety of travelers and the avoidance of
other animals as a risk factor for unexplained cases or environmental risks during travel.3 Medical providers who
outbreaks of infectious disease in the community. care for human beings traveling to other countries need to
• Collaborate with agriculture officials on the regulation be aware of the principles of travel medicine and be able
of animal movement of public health importance. to perform the functions of pretravel risk assessment and
299
verlooked during such visits. Table 10-2 summarizes these

o
Table 10-1 n Elements of Travel Medicine
risks and provides the basics of counseling on risk reduction
Practice for particular animal contact situations.
HUMAN HEALTH RISKS OF ANIMAL CONTACT

WHILE TRAVELING
Injuries From Animals

Animal bites and other animal-related injuries can be a
significant hazard during travel (Color Plate 10-1). Although
an attack from a wild animal, including snakes, crocodiles,
large felids, and elephants, can cause dramatic injuries, falls
from horseback or attacks by bulls or other large domestic
animals can also maim and kill (Figures 10-1 and 10-2; Color
Plates 10-2 and 10-3). A review of animal-associated injuries
reported to the GeoSentinel Surveillance Network found that
dog bites were the most common animal-associated injury
to travelers, followed by bites from monkeys and cats. Three-
quarters of the exposures occurred in countries where rabies
is endemic, with the majority occurring in Asia. Fifty percent
of bitten travelers had a travel duration of 1 month or less, and
traveling for tourism was associated with an increased risk of
an animal injury. Males were more likely to receive a dog bite,
whereas monkey exposures were more common for females.
Children were also at increased risk of exposure.4 Despite the
risk of rabies from such exposures (fatal cases of human rabies
have occurred in U.S. travelers from dog bites received during
international travel5), a study of returning travelers with ani-
mal injuries found that most had not had pretravel rabies vac-
cine6 and two thirds of persons with injuries did not receive
postexposure prophylaxis (which may not be routinely avail-
able in some countries). Rabies vaccine should be considered
for all travel to rabies-endemic countries, especially for chil-
dren, although a minimum travel duration of 6 weeks in an
endemic area is recommended by some experts as an indi-
From Hill DR, Ericsson CD, Pearson RD et al: The practice of travel medicine:
guidelines by the Infectious Diseases Society of America, Clin Infect Dis
cation for vaccine. The strength of that recommendation
43:1499, 2006. should be influenced by the availability of medical care and
*Permanent records should be maintained. rabies immunization products locally.
†
Advice should be given both verbally and in writing.
Other reported diseases related to bite and scratch expo-
sures in travelers include bacterial infection from Pasteurella
reventive counseling, vaccination, and posttravel evaluation
p or other agents, rat-bite fever from rodents (see Animal and
of illness. A complete discussion of the many travel-related Human Bites below), and Bartonella infection from cats, the
health risks is beyond the scope of this book. However, Table most common animal-associated infection reported in the
10-1 shows the key elements of travel medicine practice. GeoSentinel study.
Veterinary providers who care for animals that are either Exposure to nonhuman primates can occur during travel;
traveling internationally or arriving from another country also monkey temples are a popular tourist site in Asia. Simian
need to be aware of the principles of travel medicine and be able foamy virus infection has been reported in a visitor to a
to perform similar functions of pretravel risk assessment and monkey temple.7 Bites from Old World monkeys also carry
counseling, vaccination, and posttravel assessment on animals. a risk of herpes B infection that can cause fatal disease in
human beings (see Animal and Human Bites later in this
chapter). Herpes B infections in human beings have been
PRETRAVEL RISK ASSESSMENT AND ANIMAL mostly observed in occupational settings (see Chapter 12),
CONTACT COUNSELING and to date no known cases have been reported in travelers.8
Travelers should never try to pet, handle, or feed unfamil-
In a pretravel risk assessment, clinicians consider both the iar animals, domestic or wild, particularly in areas of endemic
medical status of the traveler as well as the infectious and rabies. Because children are at greatest risk of animal bites,
other environmental risks related to the countries they including severe injuries, and may be less likely to report a
plan to visit and the activities they plan to undertake (see bite incident,8 they need to be counseled to avoid petting or
Table 10-1). Risks of travel-related animal contact may be handling dogs, cats, or other animals and should be supervised
Chapter 10 n Infectious Disease Scenarios 301
Table 10-2 n Prevention of Human Health Risks Associated With Travel and Animal Contact
Activity Types of Contact Pathogens Preventive Steps
Bites, scratches from direct Contact with dogs, cats, Pasteurella, rabies virus, Avoid animal contact in rabies-
contact with animal monkeys Bartonella, other endemic countries, supervise
children around animals
Simian immunodeficiency Consider pretravel rabies vaccine
viruses, herpes B for visits to rabies-endemic
countries
Avoid contact with monkeys
Wash wound immediately and
seek medical care immediately
if bitten or scratched
Farm visits, agricultural Contact with goats, sheep, Q fever, brucellosis, E. coli, Avoid close contact with animals
tourism cattle, poultry, hogs, Nipah, avian influenza, or confined spaces with dust,
contaminated dusts anthrax handwashing after contact
Religious pilgrimages, festivals Slaughter and consumption of Anthrax (cattle, camels, goats) Avoid contact with slaughter
(e.g., Hajj/Eid al-Adha, Lunar animals Avian influenza (poultry) activities
New Year) Avoid live animal markets, bird
farms; avoid contact with sick
or dead birds
Handwashing
Live animal markets Slaughter of animals; fecal Avian influenza, SARS, E. coli, Avoid visiting live animal markets
contamination of surfaces, air other
Safaris, wilderness travel Mosquito-borne infections Malaria, yellow fever, dengue, Use DEET and/or Picaridin insect
Chikungunya fever repellents; other mosquito,
tick, and fly precautions
Tickborne infections Rickettsial infection (scrub
typhus), tick paralysis
Fly-borne Trypanosomiasis, leishmaniasis
Rodent-infested buildings Hantavirus Avoid rodent areas (see Chapter
9)
Infected fresh water Leptospirosis, E. coli, other Avoid swimming in or drinking
pathogens untreated fresh water
Exposures to bats or bat guano Rabies, other viral pathogens, Use caution visiting caves and
histoplasmosis sleeping outdoors to avoid
bats and bat guano
Local delicacies, bushmeat Undercooked meat, raw milk Campylobacter, Salmonella, Avoid uncooked meats, fish,
bovine tuberculosis, brucellosis, raw/unpasteurized dairy
listeriosis, anthrax products, soft cheeses
Primate meat Simian viruses, Ebola Avoid bushmeat consumption
Bear Trichinella
Raw fish, shellfish Cholera, hepatitis,
gnathostomiasis,
paragonimiasis, rat lungworm
Souvenirs Animal skins drums Anthrax Avoid purchasing unprocessed
animal hide souvenirs
Beaches, sandboxes Walking barefoot, swimming Hookworm infection, tungiasis, Do not walk barefoot on
marine envenomations beaches, use caution when
swimming
Travel with pet Pet can come in contact with Zoonotic infections Use of pet insecticide, periodic
local domestic and wildlife Allergy from pet deworming of pet, avoid
species, may also develop feeding uncooked meat,
vector-borne disease and/or do not allow pet to roam
toxic exposures free outdoors, pretravel and
posttravel vet visits (see Boxes
10-2 and 10-3)
Figure 10-1 n Wound from bison goring. (From Auerbach PS: Wilderness
Figure 10-3 n Farm contact may expose the traveler to diseases
medicine, ed 5, Philadelphia, 2007, Mosby Elsevier. Photo courtesy Karen
such as Q fever and brucellosis. (From Centers for Disease Control and
Hansen.)
Prevention Public Health Image Library, Atlanta, Ga. Photo courtesy
Edwin P. Ewing Jr.)
aerosols.10 Travel to a farm in Guyana was associated with

a cluster of human cases of Q fever, presumably from con-
tact with a parturient goat and dog on a farm.11 If the farm
contains poultry, risks include exposure to Chlamydophila,
Campylobacter, Salmonella, and avian influenza virus.
Brucellosis is another potential farm-related exposure, either
through direct contact with animals or consumption of
unpasteurized dairy products. Brucellosis has been termed a
“travel-associated foodborne zoonosis” in Germany, where a
recent rise in cases has been traced to consumption of unpas-
teurized cheese from brucellosis-endemic countries.12 In a
series of brucellosis cases in San Diego, travel to Mexico was
a risk factor for infection.13
Figure 10-2 n African elephant bluff-charges the photographer. (From
Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.
Photo courtesy Cary Breidenthal.) Festivals Involving Animal Contact
An increasing amount of international travel is related to
around animals at all times. If an exposure occurs, clean the religious and cultural festivals. Each year several million
wound thoroughly and immediately seek medical care for pos- Muslims participate in the Hajj pilgrimage to Mecca.
sible rabies postexposure prophylaxis (see Chapter 9). Tetanus Although local agricultural authorities have taken steps to
prophylaxis is also indicated if the traveler is not up to date reduce animal contact risks to pilgrims,14 the end of the
with tetanus vaccination. In the case of an Old World monkey Hajj is marked by the festival of Eid al-Adha, which may
bite, medical care should be sought as soon as possible for pro- involve increased exposure to animal slaughtering activities.
phylactic treatment against herpes B infection. For example, a suspected outbreak of anthrax was linked to
Envenomations from snakes, scorpions, and spiders rep- slaughter and distribution of infected meat from a camel
resent another animal-associated injury risk to travelers; during the festival.15
medical care should be sought immediately. The treatment of Similarly, the Lunar New Year festivals in Asia often involve
snakebites and other venomous animal bites usually depends increased slaughtering and consumption of poultry, with
on the species of animal responsible (see Chapter 8). an attendant increased risk of avian influenza. The CDC has
issued travel advisories for U.S. travelers visiting Asia during
Farm Visits the Lunar New Year festival. These recommendations include
handwashing; avoidance of bird farms or live bird markets; not
Agricultural tourism is the experience of visiting a working touching live or dead birds, including chickens, ducks, and wild
farm or related operation for enjoyment and is a growing birds, even if they do not seem sick; and not touching surfaces
type of tourism both nationally and internationally (Figure contaminated with bird feces, blood, or other body fluids.16
10-3).9 Specialized tour operators offer package tours to farms
in a number of countries. During such visits tourists may
Live Animal Markets
come in contact with both farm animals and contaminated
soils and dusts that may contain infectious pathogens. Q At any time of year visits to live animal markets, present in many
fever is considered to be underdiagnosed in travelers, who cities and villages in a large number of countries, carry a risk
can acquire it by exposure to farm animals or contaminated of infection with zoonotic agents. In such markets numerous
s pecies of wildlife and domestic animals may be housed in with bat droppings or sustain bat bites. In addition to rabies
close proximity, creating an increased opportunity for disease risk, bats are reservoirs for a wide range of other viral patho-
transmission. Color Plate 10-4 shows a typical scene from a gens, including other lyssa viruses, Nipah virus, SARS-like
live animal market in Asia. Human infection with the H5N1 coronavirus, and Marburg virus.25 Exposure to aerosolized
avian influenza virus has been linked to visits to live bird bat guano has also been associated with the development of
markets, even for individuals who denied direct contact with acute pulmonary histoplasmosis in travelers.26
sick or healthy-appearing poultry.17 Avian influenza has been
found on surfaces and dusts in such markets, and exposure may Local Delicacies Involving Animal Products and
occur by touching contaminated surfaces as well as breathing Bushmeat Consumption
contaminated dusts. Severe acute respiratory syndrome (SARS)
is another infection linked to live animal markets in Asia. Many local delicacies that travelers encounter may involve
Travelers wishing to reduce risk of zoonotic diseases while trav- animal products from domestic or wild animals. Meat and
eling should avoid visiting live animal markets, especially if a dairy products may be served raw or undercooked and
country is experiencing an outbreak of highly pathogenic avian may be a source for zoonotic infections such as brucello-
influenza.18 A current list of countries is maintained at http:// sis, trichinosis, and salmonellosis in returning travelers.27
www.cdc.gov/flu/avian/outbreaks/current.htm. Raw chicken sashimi from an island in Japan is known to be
contaminated with Campylobacter. However, local residents
do not appear to become ill, suggesting a role for acquired
Safaris and Wilderness Travel
protective immunity that a traveler would presumably not
Wilderness travel overseas increases the risk of exposure enjoy.28 Travelers to Southeast Asia and Africa have become
to a number of pathogens as well as injuries from snakes, infected with parasites, including Paragonimus, trematodes
crocodiles, and other wildlife. Visitors on safari to game parks Clonorchis sinensis or Haplorchis pumilio, and gnathostomes.
in Africa have become infected with African tick fever and Paragonimiasis is acquired by eating raw freshwater crabs or
other rickettsial infections that may have a reservoir in the crayfish. Gnathostomiasis is a nematode infection acquired
local wildlife populations.19 Although most forms of malaria, by ingestion of various intermediate hosts in addition to
one of the most common causes of fever in returning travel- fish.29,30 Eating unwashed produce and undercooked foods
ers, are not zoonotic, certain monkey malaria species such as such as mollusks in some countries poses risks of numerous
Plasmodium knowlesi have been described in human beings infectious diseases, including viral hepatitis, bacterial enteri-
and may be underdiagnosed.20 Other zoonotic arthropod- tis, and eosinophilic meningitis from rat lungworm.31 There
borne infections such as trypanosomiasis, yellow fever, is increasing awareness of the infectious risks of improperly
and Chikungunya fever have been reported in safari and cooked poultry products. Such practices have been linked
wilderness travelers.21,22 Sleeping in huts and shelters that to cases of avian influenza.32 Bovine tuberculosis transmis-
may also be home to local rodent populations can increase sion to human beings can involve consumption of uncooked
risk of infection with hantaviruses and various hemorrhagic meat as well as raw milk (see Chapter 9).33
fevers, including Lassa fever.23 Swimming in fresh water in Bushmeat (wild game killed for food) is an important source
areas frequented by wildlife has led to outbreaks of lep- of animal protein for communities in many parts of the world.
tospirosis in adventure travelers.24 Wilderness travelers may It has been estimated that in Central Africa alone more than
be exposed to bats when visiting caves or sleeping outside in 1 billion kilograms of meat from wild animals are consumed
areas frequented by bats, where they could come in contact each year (Figure 10-4).34 Table 10-3 shows the diversity of
Figure 10-4 n South African market with bushmeat for sale. (From Fowler ME: Zoo and wild animal medicine: current therapy, ed 6, St Louis, 2008,
Saunders Elsevier. Photo courtesy R. A. Cook.)
Table 10-3 n Protected and Unprotected Species Sold in Village and Urban Bushmeat Markets in
Northeastern Democratic Republic of Congo During Peacetime and Wartime*
Village (Kiliwa) Market Day Sales Urban (Dungu) Market Day Sales
Taxon† Peace (kg) War (kg) P Peace (kg) War (kg) P
Protected Species
Elephant, Loxodonta africana 0.0 ± 0.0 0.0 ± 0.0 NS 23.5 ± 1.5 120.3 ± 10.3 <.05
Hippo, Hippopotamus amphibius 0.0 ± 0.0 0.0 ± 0.0 NS 9.3 ± 0.6 48.0 ± 4.2 <.05
Buffalo, Syncerus caffer 0.1 ± 0.1 0.0 ± 0.0 NS 19.6 ± 1.2 98.2 ± 8.4 <.05
Bongo, Tragelaphus euryceros 0.0 ± 0.0 0.0 ± 0.0 NS 0.5 ± 0.1 2.2 ± 0.5 <.05
Large antelope, multiple species‡ 0.2 ± 0.1 0.3 ± 0.3 NS 3.7 ± 0.3 23.7 ± 2.1 <.05
Pigs, multiple species§ 0.4 ± 0.1 0.4 ± 0.2 NS 5.6 ± 0.3 9.5 ± 1.1 <.05
Chimpanzee, Pan troglodytes 0.0 ± 0.0 0.0 ± 0.0 NS 0.6 ± 0.1 0.5 ± 0.2 NS
Aardvark, Orycteropus afer 0.1 ± 0.1 0.0 ± 0.0 NS 0.7 ± 0.1 0.8 ± 0.2 NS
All protected species 0.8 ± 0.2 0.8 ± 0.4 NS 63.6 ± 3.7 303.1 ± 25.5 <.05
Unprotected Species
Duikers, multiple species|| 1.0 ± 0.2 1.7 ± 0.7 NS 16.7 ± 0.5 15.7 ± 0.9 NS
Monkeys, multiple species¶ 1.5 ± 0.3 1.8 ± 0.6 NS 8.7 ± 0.3 8.4 ± 0.5 NS
Crested porcupine, Hystrix cristata 0.2 ± 0.1 0.2 ± 0.1 NS 1.0 ± 0.0 1.0 ± 0.1 NS
Uganda grass hare, Poelagus marjorita 0.3 ± 0.1 0.7 ± 0.3 NS 2.5 ± 0.1 2.6 ± 0.1 NS
Cane rat, Thryonomys swinderianus 0.2 ± 0.1 0.1 ± 0.1 NS 0.7 ± 0.0 0.7 ± 0.0 NS
All unprotected species 3.1 ± 0.6 4.5 ± 1.5 NS 29.7 ± 0.8 28.3 ± 1.4 NS
From De Merode E, Cowlishaw G: Species protection, the changing informal economy, and the politics of access to the bushmeat trade in the Democratic Republic of Congo,
Conserv Biol 20:1262, 2006.
*Mean and standard error of kilograms of fresh meat sold per market day. Tests for statistical significance (P) indicate whether the difference between peacetime and wartime is
significant (P < .05) or not significant (NS). Sample sizes (market days) in peacetime and wartime are 96 and 341 for the rural markets and 336 and 120 for the urban markets,
respectively. To calculate daily sales (incorporating both market days and nonmarket days), multiply all rural figures by 0.29 (i.e., 2 market days/week) and multiply all urban
figures by 2.71 (i.e., 19 market days/weeks).
†Taxa are grouped according to protected and unprotected status, although all species are protected within the boundaries of Garamba National Park and ordered by decreas-
ing body size within these groups. Where several species are incorporated into a single taxon, the median species weight is used, with all body size data taken from Rowcliffe
JM, de Merode E, Cowlishaw G: Do wildlife laws work? Species protection and the application of a prey choice model to poaching decisions, Proc Biol Sci 271:2631-2636, 2004.
Where a taxon is composed of multiple species, allocation of that taxon to either one of these groups depends on the relative proportion of protected and unprotected species;
if at least half of the species is protected, the taxon is placed in the protected group. Taxonomy follows Kingdon J: The Kingdon field guide to African mammals, San Francisco,
1997, Academic Press.
‡Hartebeest (Alcelaphus buselaphus), kob (Kobus kob), waterbuck (Kobus ellipsiprymnus), bohor reedbuck (Redunca redunca), bushbuck (Tragelaphus scriptus), and sitatunga
(Tragelaphus spekii). Hartebeest, waterbuck, and sitatunga are protected.
§Giant forest hog (Hylochoerus meinertzhageni), common warthog (Phacochoerus africanus), and red river hog (Potamochoerus porcus). Giant forest hog and red river hog are
protected.
||Bay duiker (Cephalophus dorsalis), red-flanked duiker (Cephalophus rufilatus), blue duiker (Cephalophus monticola), and bush duiker (Sylvicapra grimmia). None of these spe-
cies is protected.
¶Agile mangabey (Cercocebus agilis), tantalus monkey (Cercopithecus [aethiops] tantalus), red-tailed monkey (Cercopithecus [cephus] ascanius), patas monkey (Cercopithecus
[erythrocebus] patas), Dent’s monkey (Cercopithecus [mona] denti), de Brazza’s monkey (Cercopithecus neglectus), guereza colobus (Colobus guereza), and olive baboon (Papio
anubis). None of these species is protected.
species that may end up being sold for human consumption, for acquiring zoonotic hookworm infection (cutaneous larva
especially during times of civil unrest.35 Emerging pathogens migrans, also known as creeping eruption (see Chapter 9 and
linked to bushmeat consumption include simian immuno- Color Plate 9-33).37 Another beach-related zoonosis is tungia-
deficiency viruses, anthrax, and hemorrhagic fever viruses.36 sis, a skin infestation caused by the sand flea Tunga penetrans
Although the risk of infection from bushmeat exposure may (jiggers). Walking barefoot on beaches also carries risks of
be greatest to persons who butcher carcasses, travelers to areas stings from jellyfish and other marine organisms (see Chapter
where bushmeat is an important part of local diets may be at 8). Sandboxes and play areas are another source of contact for
risk if they consume improperly cooked bushmeat. hookworms, roundworms (Toxocara), and Toxoplasma.
Beaches and Sandboxes Souvenirs

Travelers should avoid going barefoot on beaches frequented Persons purchasing souvenirs while traveling should be aware
by animals. Many beaches that travelers visit during interna- that improperly processed hides used for drums and other
tional vacations are frequented by dogs and cats. Walking bare- souvenirs may be a source of exposure for cutaneous anthrax
foot on beaches contaminated with their feces is a risk factor (see Chapter 9).38 However, this risk is considered to be low.
of 21 persons, the euthanasia of a contact animal, and legal

POSTTRAVEL ASSESSMENT action against the travelers.44 In 2007, a puppy rescued from
an animal shelter in India by a veterinarian who brought the
In the returning traveler with illness, a careful history of animal into the United States at 11 weeks of age was found
animal-related exposures should be obtained in addition to to be positive for rabies by the Alaska Department of Health
the standard questions (Box 10-1). If the response to any of and Social Services.45 Such introduction of rabies from ani-
these questions is affirmative, further evaluation is warranted. mal travel can involve foreign rabies virus variants. As a
result, the CDC is considering strengthening federal regula-
tions regarding the importation of companion animals.2
TRAVELING WITH A PET AND OTHER ANIMAL Vector-borne diseases are a documented risk to traveling
TRAVEL MEDICINE ISSUES dogs. For example, leishmaniasis has been reported in dogs
traveling in high-incidence countries, leading to the intro-
Traveling with pets is becoming increasingly popular. There duction of disease upon returning home.
are a number of reasons why people travel with a pet. These
include emotional, economic, gene transfer, and seeking spe-
cialized veterinary care.39 Emotional reasons include com- Other Risks Associated With Traveling Animals
panionship, treating an animal as a member of the family,
and reluctance to leave an animal behind. Economic factors Animals may cause allergic reactions if they come into con-
can include the cost of arranging care for the animal while tact with sensitized travelers or airline, train, or other trans-
traveling. Gene transfer involves activities such as taking a portation personnel. Animals with allergy may also be
pedigreed animal to another location to breed with another exposed to a variety of allergens during travel.
animal. Finally, owners may take an ill animal to another Toxic risks to traveling animals include contaminated pet
location for specialized veterinary care.39 food,46 water, pesticides, and accidental ingestion of rodenti-
Veterinarians should go through similar steps as their cides (see Chapter 8).
human health counterparts in evaluating animals that are Animals risk physical injury from being shipped in con-
traveling. These include pretravel risk assessment and owner tainers or otherwise restrained, heat stress and cold expo-
counseling, vaccines and other preventive care as necessary, sures, and fights with other animals. Other potential stressors
and evaluation of returning and newly imported animals include unfamiliar surroundings, disruption of circadian
after travel. schedules, noise, and other noxious stimuli.
Infectious Disease Risks and Pets That Travel Logistics

Many of the infectious disease risks to traveling compan- Travelers wishing to travel with pets will need to identify
ion animals are shared with human beings. Even travel to the logistic requirements for transporting and housing the
different regions in the same country can expose an animal animal during travel. Airlines may vary in their rules regard-
to new health risks. Pets that travel also face potential expo- ing whether an animal can be carried in a pet container that
sure to animal diseases that are not zoonotic in nature, such can be placed under a seat, or whether all animals need to
as canine parvovirus, canine viral hepatitis, and feline pan- be placed in cargo. There have been instances of companion
leukopenia virus. animals dying from heat and cold stress and other trauma
Particular zoonoses associated with dog travel include while being shipped in cargo, and owners should be aware
rabies, leishmaniasis, and roundworm infection.40-43 A case of the risks to animals undergoing air travel.47 There may be
of a rabid puppy imported illegally from Morocco to France restrictions on the number of animals allowed. Rental car
by a traveling couple resulted in the prophylactic treatment companies, trains, buses, and hotels may also have restric-
tive policies about pets. These policies should be clarified in
advance of travel.
Box 10-1 Evaluation of the Returning Traveler
Regarding Animal-Related Risks
Documentation and Regulation of Animal Travel
• Were you in the vicinity of live animals, either on a farm, and Importation
in a house, or in a market? If so, what types of animals and
Animals that travel often need documentation of vaccina-
environments? Did you touch any animals or notice any
sickness in the animals? tion status, tick or other prophylactic treatments, and a state-
• Were you bitten, scratched, or licked by dogs, cats, monkeys, or ment from a veterinarian that they are free of communicable
other animals? disease and able to travel safely. Such documentation may be
• Did you eat uncooked or undercooked meat, fish, or shellfish? necessary for the animal to enter another country. Owners
• Did you consume bushmeat? should contact the embassies of countries they plan to visit
• Did you eat or drink unpasteurized dairy products? to go through the required entry processes as well as deter-
• Did you walk barefoot on beaches or swim in fresh water? mine the U.S. clearance processes upon return.48 Policies of
• Did you travel in the wilderness? some countries may require an animal to be quarantined or
• Did you visit caves or sleep outdoors in areas frequented by destroyed without proper documentation. Additional infor-
bats?
mation is available at http://www.aphis.usda.gov/import_
• Did you receive bites from ticks, flies, or mosquitoes?
export/animals/animal_exports.shtml.
Many countries limit movement of dogs and other importation of pet birds from countries where highly patho-
a nimals based on rabies status. Dogs and cats generally can- genic avian influenza H5N1 is present in poultry. To import
not pass from a rabies-endemic country to a rabies-free a pet bird of non-U.S. origin, the importer or owner must
country without a process of quarantine and/or vaccina- obtain a USDA import permit,51 have a certificate of health
tion documentation. Table 10-4 lists countries reporting no from a veterinarian in the exporting country, and allow the
indigenous rabies in 2005. bird to be quarantined for 30 days in a USDA animal import
A number of federal agencies are involved with regulation center at the owner’s expense. Pet birds arriving from Canada
of animals entering the United States. The CDC regulates are not required to be quarantined.52 Entry into the United
the importation into the United States of dogs, cats, turtles, States of birds that are covered by endangered species conven-
bats, monkeys, and other animals as well as animal products tions is regulated by the U.S. Fish and Wildlife Service.
capable of causing human disease (see http://wwwn.cdc.gov/ The CDC periodically issues embargoes on specific ani-
travel/yellowBookCh7-AnimalImport.aspx).48 Pets taken out mals associated with disease risk, including civets (SARS),
of the United States are subject to the same regulations when birds from specific countries (avian influenza), and African
returning to the country as are newly imported animals. The rodents (monkeypox).
U.S. Department of Agriculture (USDA) regulates a number CDC regulations do not apply to horses not known to be
of species being imported based on their disease risk to plants carrying diseases infectious to human beings, but the USDA
and animals of agricultural concern. may regulate horse import due to risks of diseases of agricul-
No single agency regulates entry of dogs into the United tural importance such as screwworm.
States. Although the CDC does not require a general certifi- Importation of fish into the United States is not regulated
cate of health for dogs, dogs with evidence of illness may not by the CDC, but U.S. Fish and Wildlife Service regulations
be allowed entry. Documentation of rabies vaccination at may apply.
least 30 days before entry is required, although dogs younger Finally, importation of certain animals and animal prod-
than 3 months and dogs without proof of rabies vaccination ucts is regulated by other federal agencies such as the U.S.
may be allowed to enter if the owner completes a confinement Customs Service.53
agreement and certifies the animal will be vaccinated and If animals are traveling, they should have a veterinary
kept confined at least 30 days after vaccination. Unvaccinated evaluation for pretravel risk assessment and administration
dogs from countries considered rabies free (see Table 10-4) of necessary vaccines and other preventive treatments. Box
may also be allowed entry.49 In addition to CDC regulations, 10-2 outlines the elements of such a visit.
the USDA regulates the importation of dogs potentially car- The veterinarian should determine whether travel is med-
rying diseases of agricultural importance, including screw- ically advisable for the animal. Travel is riskier for immuno-
worms or some Taenia species of tapeworm.2 compromised animals, including young animals and animals
For cats, a general certificate of health is not required to with underlying illness. Certain species, such as snakes, may
enter the United States, but some states and air carriers may not be allowed entry by other countries. Animals with behav-
require such documentation. Rabies vaccination is also not ioral problems may attack other animals or people or present
required, but some states may require proof of rabies vaccine other travel risks.
documentation. All pet cats entering Hawaii and Guam are The veterinarian should ensure that animals with ongo-
subject to local quarantine requirements.49 ing illnesses have an adequate supply of medications and that
Importation of birds is regulated by the USDA Animal and plans for emergency veterinary medical care while traveling
Plant Health Inspection Service.50 The USDA currently restricts are discussed with the owner.
Table 10-4 n Countries and Political Units Reporting No Indigenous Cases of Rabies During 2005*
Region Countries
Africa Cape Verde, Libya, Mauritius, Réunion, São Tome and Principe, Seychelles
Americas North: Bermuda, St. Pierre et Miquelon
Caribbean: Antigua and Barbuda, Aruba, Bahamas, Barbados, Cayman Islands, Dominica, Guadeloupe, Jamaica,
Martinique, Montserrat, Netherlands Antilles, Saint Kitts (Saint Christopher) and Nevis, Saint Lucia, Saint Martin,
Saint Vincent and Grenadines, Turks and Caicos, Virgin Islands (U.K. and U.S.)
South: Uruguay
Asia Hong Kong, Japan, Kuwait, Lebanon, Malaysia (Sabah), Qatar, Singapore, United Arab Emirates
Europe Austria, Belgium, Cyprus, Czech Republic†, Denmark†, Finland, France†, Gibraltar, Greece, Iceland, Ireland, Isle of
Man, Italy, Luxemburg, Netherlands†, Norway, Portugal, Spain† (except Ceuta/Melilla), Sweden, Switzerland,
United Kingdom†
Oceania‡ Australia†, Northern Mariana Islands, Cook Islands, Fiji, French Polynesia, Guam, Hawaii, Kiribati, Micronesia, New
Caledonia, New Zealand, Palau, Papua New Guinea, Samoa, Vanuatu
*Bat rabies may exist in some areas that are reportedly free of rabies in other animals.
†Bat lyssa viruses are known to exist in these areas that are reportedly free of rabies in other animals.
‡Most of Pacific Oceania is reportedly rabies free.
From Centers for Disease Control and Prevention: CDC health information for international travel 2008: prevention of specific infectious diseases: rabies. http://wwwn.cdc.gov/
travel/yellowBookCh4-Rabies.aspx#653.
References
Box 10-2 Pretravel Risk Assessment Checklist for
Pet 1. Office of Travel & Tourism Industries. U.S. citizen air traffic to over
seas regions, Canada and Mexico. 2007. http://tinet.ita.doc.gov/view/m-
Health and Appropriateness of Animal 2007-O-001/index.html. Accessed February 28, 2008.
2. McQuiston JH, Wilson T, Harris S, et al. Importation of dogs into the
• Determine whether travel is medically appropriate for pet United States: risks from rabies and other zoonotic diseases. Zoonoses
(consider species, medical conditions, age). and Public Health. 2008;55(8–10):421–426.
• If the pet has an ongoing medical condition, ensure adequate 3. Hill DR, Ericsson CD, Pearson RD, et al. Infectious Diseases Society of
supply of medication. America: The practice of travel medicine: guidelines by the Infectious
Diseases Society of America. Clin Infect Dis. 2006;43(12):1499–1539.
Vaccination and Preventive Medications 4. Gautret P, Schwartz E, Shaw M, et al. GeoSentinel Surveillance Network
• Ensure current rabies and other core vaccinations are up to Animal-associated injuries and related diseases among returned trav-
date and that owner has documentation. elers: a review of the GeoSentinel Surveillance Network. Vaccine.
• Consider the following preventable diseases that could be 2007;25(14):2656–2663.
acquired during travel39: 5. Schmiedel S, Panning M, Lohse A, et al. Case report on fatal human
• Dogs rabies infection in Hamburg, Germany, March 2007. Euro Surveill.
2007;12(5):E070531.5.
Canine distemper
6. Gautret P, Shaw M, Gazin P, et al. Rabies postexposure prophylaxis in
Canine parvovirus returned injured travelers from France, Australia, and New Zealand: a
Canine hepatitis retrospective study. Travel Med. 2008;15(1):25–30.
Canine parainfluenza 7. Jones-Engel L, Engel GA, Schillaci MA, et al. Primate-to-human retrovi-
Rabies ral transmission in Asia. Emerg Infect Dis. 2005;11(7):1028–1035.
Bordetella 8. Centers for Disease Control and Prevention. CDC health information for
• Cats international travel 2008: animal associated hazards. http://wwwn.cdc.
Feline panleukopenia virus gov/travel/yellowBookCh6-Animal.aspx. Accessed October 16, 2008.
Feline calicivirus 9. Lobo R, Small Farm Center, University of California-Davis. Helpful
agricultural tourism (agritourism) definitions. http://www.sfc.ucdavis.
Feline herpesvirus
edu/agritourism/definition.html. Accessed May 29, 2008.
Rabies 10. Terheggen U, Leggat PA. Clinical manifestations of Q fever in adults and
• Perform routine deworming, provide heartworm prophylaxis children. Travel Med Infect Dis. 2007;5(3):159–164.
• Provide flea and tick treatment and prevention (topical or 11. Baret M, Klement E, Dos Santos G, et al. Coxiella burnetii pneumopa-
systemic acaricides) thy on return from French Guiana [in French]. Bulletin de la Societe de
Pathologie Exotique. 93(5):325–327, 2000.
12. Dahouk SA, Neubauer H, Hensel A, et al. Changing epidemiol-
Evaluation of Illness in an Animal After Travel ogy of human brucellosis, Germany, 1962–2005. Emerg Infect Dis.
2007;13(12):1895–1900.
Animals imported into the United States are required to 13. Troy SB, Rickman LS, Davis CE. Brucellosis in San Diego: epidemiology
be healthy. However, if illness develops, evaluation should and species-related differences in acute clinical presentations. Medicine.
2005;84(3):174–187.
involve the steps outlined in Box 10-3. If infectious condi- 14. Ahmed QA, Arabi YM, Memish ZA. Health risks at the Hajj. Lancet.
tions are identified, the possibility of zoonotic transmission 2006;367(9515):1008–1015.
to the animal’s owner should be considered, and there should 15. International Society for Infectious Diseases: Dengue/DHF update 2008.
be rapid communication to either a human health care pro- http://promedmail.org.
vider, public health department, or both. 16. Centers for Disease Control and Prevention. In the news: keeping your
self safe from bird flu: an important message for people traveling to Asia to
Further steps should be based on the results of this pre- celebrate the Lunar New Year. 2008. http://wwwn.cdc.gov/travel/content
liminary evaluation. AvianFluLunarNewYear08.aspx. Accessed February 28, 2008.
17. Yu H, Feng Z, Zhang X, et al. Avian influenza H5N1 study group.
Human influenza A (H5N1) cases, urban areas of People’s Republic of
Box 10-3 Evaluation of an Ill Pet After Travel China, 2005–2006. Emerg Infect Dis. 2007;13(7):1061–1064.
18. Hurtado TR. Human influenza A (H5N1): a brief review and recom-
mendations for travelers. Wilderness Environ Med. 2006;17(4):276–281.
• Did the animal go through a quarantine process before 19. Buchau AS, Wurthner JU, Reifenberger J, et al. Fever, episcleritis,
reentering the country? epistaxis, and rash after safari holiday in Swaziland. Arch Dermatol.
• Is there documentation of rabies vaccination status, and did the 2006;142(10):1365–1366.
animal travel to or originate from a rabies-endemic country? 20. Ng OT, Ooi EE, Lee CC, et al. Naturally acquired human Plasmodium
• Is the animal otherwise up to date on necessary vaccinations knowlesi infection, Singapore. Emerg Infect Dis. 2008;14(5):814–816.
and preventive treatment (see Box 10-2)? 21. Jelinek T, Bisoffi Z, Bonazzi L, et al. European Network on Imported
• Were there other endemic disease risks in the countries visited, Infectious Disease Surveillance. Cluster of African trypanosomiasis in trav-
elers to Tanzanian national parks. Emerg Infect Dis. 2002; 8(6): 634–635.
including leishmaniasis and other parasitic infections?
22. Centers for Disease Control and Prevention. Chikungunya fever diag-
• Has illness been noticed in any other animals that were in nosed among international travelers—United States, 2005–2006.
contact with this one? MMWR Morb Mortal Wkly Rep. 2006;55(38):1040–1042.
• Did the animal visit farms or wilderness areas or have other 23. Castillo C, Nicklas C, Mardones J, et al. Andes hantavirus as possible
contact with animals, including sick animals? cause of disease in travellers to South America. Travel Med Infect Dis.
• What kind of diet was the animal on during travel? Did it 2007;5(1):30–34.
consume raw meat? 24. Centers for Disease Control and Prevention. Outbreak of acute febrile
• Is there any evidence of infection with endoparasites and/or illness among participants in EcoChallenge Sabah 2000-Malaysia, 2000.
ectoparasites? JAMA. 2000;284(13):1646.
25. Wong S, Lau S, Woo P, et al. Bats as a continuing source of emerging
• Are there reports of illness in the owner or other human beings
infections in humans. Rev Med Virol. 2007;17(2):67–91.
that accompanied the pet that could be related to travel? (This 26. de Vries PJ, Koolen MG, Mulder MM, et al. Acute pulmonary histoplas-
could provide clues regarding shared exposure risks.) mosis from Ghana. Travel Med Infect Dis. 2006;4(5):286–289.
27. Dore K, Buxton J, Henry B, et al. Multi-provincial Salmonella Typhimu 41. Barr F, British Small Animal Veterinary Association Scientific
rium case-control study steering committee. Risk factors for Salmonella Committee. Checklist of infections that may be imported into the UK
typhimurium DT104 and non-DT104 infection: a Canadian multi- by the travelling pet. J Small Anim Pract. 2001;42(2):95–97.
provincial case-control study. Epidemiol Infect. 2004;132(3):485–493. 42. Teske E, van Knapen F, Beijer EG, et al. Risk of infection with Leishmania
28. Moore JE, Matsuda M. Consumption of raw chicken sashimi, Kyushu spp. in the canine population in The Netherlands. Acta Vet Scand.
Island, Japan—risk of campylobacteriosis or not. Travel Med Infect Dis. 2002;43(4):195–201.
2007;5(1):64–65. 43. Impact of pet travel on animal and public health. Vet Rec.
29. Del Giudice P, Cua E, Le Fichoux Y, et al. Gnathostomiasis: an emerg- 2008;162(14):429–430.
ing parasitic disease [in French]? Ann Dermatol Venereol. 2005;132(12 44. Galperine T, Neau D, Moiton MP, et al. The risk of rabies in France
Pt 1):983–985. and the illegal importation of animals from rabid endemic countries [in
30. Hale DC, Blumberg L, Frean J. Case report: gnathostomiasis in two trav- French]. Presse Med. 2004;33(12 Pt 1):791–792.
elers to Zambia. Am J Trop Med Hyg. 2003;68(6):707–709. 45. Castrodale L, Walker V, Baldwin J, et al. Rabies in a puppy imported
31. Weir E. Travel warning: eosinophilic meningitis caused by rat lung- from India to the USA March 2007. Zoonoses and Public Health.
worm. CMAJ. 2002;166(9):1184. 2008;55(8–10):427–430.
32. Centers for Disease Control and Prevention. Guidelines and recommen 46. Brown CA, Jeong KS, Poppenga RH, et al. Outbreaks of renal failure
dations: interim guidance about avian influenza (H5N1) for U.S. citizens associated with melamine and cyanuric acid in dogs and cats in 2004
living abroad. http://wwwn.cdc.gov/travel/contentAvianFluAmericans and 2007. J Vet Diagn Invest. 2007;19(5):525–531.
Abroad.aspx. Accessed February 28, 2008. 47. Humane Society of the United States. Tips for safe pet air travel. http://
33. Etter E, Donado P, Jori F, et al. Risk analysis and bovine tuberculosis, a www.hsus.org/pets/pet_care/caring_for_pets_when_you_travel/travel-
re-emerging zoonosis. Ann N Y Acad Sci. 2006;1081:61–73. ing_by_air_with_pets/. Accessed October 21, 2008.
34. Karesh WB, Cook RA. The human-animal link. Foreign Affairs. 48. Centers for Disease Control and Prevention. Importation of pets, other
2005;84:38–50. animals, and animal products into the United States. http://www.cdc.gov/
35. De Merode E, Cowlishaw G. Species protection, the changing infor- ncidod/dq/animal/index.htm. Accessed February 28, 2008.
mal economy, and the politics of access to the bushmeat trade in the 49. Centers for Disease Control and Prevention. Bringing an animal into
Democratic Republic of Congo. Conserv Biol. 2006;20(4):1262–1271. the United States. http://www.cdc.gov/ncidod/dq/animal/dogs.htm.
36. Wolfe ND, Daszak P, Kilpatrick AM, et al. Bushmeat hunting, defor- Accessed October 21, 2008.
estation, and prediction of zoonoses emergence. Emerg Infect Dis. 50. U.S. Department of Agriculture. Pet travel: tips, facts, and scam informa
2005;11(12):1822–1827. tion—for you and your pet. http://www.aphis.usda.gov/animal_welfare/
37. van Nispen tot Pannerden C, van Gompel F, Rijnders BJ, et al. An itchy pet_travel/content/wp_c_pet_travel_tips.shtml. Accessed May 29, 2008.
holiday. Neth J Med. 2007;65(5):188–190. 51. U.S. Department of Agriculture. Animal health permits. http://www.
38. Centers for Disease Control and Prevention. Anthrax Q&A: anthrax and aphis.usda.gov/permits/index.shtml. Accessed October 15, 2008.
animal hides. http://www.bt.cdc.gov/agent/anthrax/faq/pelt.asp. Accessed 52. U.S. Department of Agriculture. Animal and animal product import:
March 29, 2008. non-US origin pet birds. http://www.aphis.usda.gov/import_export/ani-
39. Leggat PA, Speare R. Travel with pets. J Travel Med. 2000;7:325–329. mals/nonus_pet_bird.shtml. Accessed October 10, 2008.
40. Deplazes P, Staebler S, Gottstein B. Travel medicine of parasitic dis- 53. U.S. Customs Service. Pets and wildlife. http://www.cbp.gov/linkhandler/
eases in the dog [in German]. Schweiz Arch Tierheilkd. 2006;148(9): cgov/newsroom/publications/travel/pets_wild.ctt/pets.pdf. Accessed May
447–461. 29, 2008.
EXOTIC AND WILDLIFE PETS
Animal and human health clinicians need to understand the of State and Territorial Epidemiologists (CSTE) to do
scope of the exotic and wildlife pet trade, the related health the following:
risks, and ways to reduce such risks. Driven by popular  Develop comprehensive federal regulations with
demand, trade in live animals for pets has been increasing enforcement that provide oversight to the private
both in the United States and worldwide.1 More than 200 ownership of exotic and wild animals.
million animals, representing thousands of individual  Develop and maintain a list of approved species for
species, are estimated to be legally imported into the United interstate distribution and importation.
States from more than 160 countries. The majority of these  Limit ports of entry.
imports were for the pet and aquarium trade.2 The number  Improve regulation and inspection of exotic animal
of animals illegally imported each year is unknown but is breeders, dealers, auctions, swap meets, Internet
also believed to be considerable.3 As a result, the United sales, pet outlets, and animal imports.
States is the world’s largest importer of live animals.2 At the  Develop a system to track imported and captive-
same time, many potential pet owners are unaware of the bred exotic animals in the pet trade.
health risks of such nontraditional pets.4 • Support the USDA and local agencies to ensure that
individuals and events selling or bartering exotic
Key Points for Clinicians and Public Health animals, including pet stores, are properly licensed and
Professionals that exotic, wild, and imported animals are screened
for known zoonoses, quarantined and observed for
signs of disease, and have limited opportunities for
Public Health Professionals ecological release into the nonnative environment.
• Educate the public and health care providers about
• Support efforts of the National Association of State the risks of ownership and contact with wildlife and
Public Health Veterinarians (NASPHV) and Council exotic pets, including zoonotic infections, injury, and
(depending on species) envenomation. Discourage

exotic or wild pet ownership among immunocompro- SCOPE OF THE PROBLEM
mised persons and families with children younger than
5 years. Discourage contact with mammals at high risk Much of the pet trade involves traditional pets, species that
of transmitting rabies (e.g., bats, raccoons, skunks, have been bred and maintained over multiple generations
foxes, and coyotes). for human companionship and have acknowledged popu-
• Ensure that local pet stores, pet swap meets, petting larity as pets. Examples include dogs, cats, and horses. Caged
zoos, schools, and other venues with human-animal birds such as parakeets and canaries and pocket pets such as
contact are aware of the recommendations of the gerbils and hamsters are also popular and are bred for the
NASPHV for reducing risk of transmission in such set- pet trade. Another large segment of the pet trade involves
tings, including adequate handwashing facilities, sepa- tropical fish, which have generally been associated with fewer
ration of animal and nonanimal areas, and avoidance zoonotic diseases than other animals.
of high-risk species.5 Much of the remainder of the pet trade, however, is in
• If a human health clinician reports a zoonotic disease nontraditional pets, or species that are not domesticated
associated with an exotic or wildlife pet, coordinate a and are captured from the wild or captive-bred to meet an
response with agricultural and wildlife veterinarians. increasing demand for unusual pets. Nontraditional pets
• Form interdisciplinary networks and working groups include exotic species that are nonnative to the local ecosys-
to address exotic and wild animal pet issues that arise tem and native wildlife, which are local wildlife species. The
locally and regionally. Groups should consist of vet- number of wild animals, including reptiles and amphibians,
erinarians, public health professionals, wildlife agen- captured in the United States for the pet trade each year is not
cies and rehabilitators, zoologic park staff, university precisely known but appears to be in the range of millions of
representatives, physicians, and environmental health animals.7 This segment of the pet trade is extremely lucra-
professionals. tive and mainly uses the Internet, specialty newsletters, swap
meets, auctions, and private sales rather than pet shops. Such
settings are largely unregulated and lack disease prevention
Human Health Clinicians and control methods such as quarantine or veterinary care
and may contribute to species reduction. Currently, 22 states
• Ask patients about ownership and contact with exotic ban or regulate certain exotic pets.
or wild animals. If they report such contact, list the spe- Reptiles such as turtles and iguanas are popular pets
cies, origin, and types of interactions. Consider con- (Figure 10-5). However, as subclinical carriers of Salmonella,
sulting the patient’s veterinarian about the health risks they have been the source of many human illnesses.8 A 1975
(zoonotic and injury potential) of particular species. FDA ban on the sale of turtles with a carapace less than 4
• Discourage acquisition, contact with, and main- inches is estimated to have prevented more than 100,000
tenance of exotic and wildlife pets, particularly for infections.
families with children or immunocompromised The importation, trade, and ownership of wild-caught
persons. and exotic animals for pets enhances the risk of dissemi-
• If patients report ownership of venomous animals, nation and transmission of novel, rare (hantavirus, rabies,
ensure they are aware of the steps to take if enveno- lymphocytic choriomeningitis virus), emerging, and exotic
mation occurs and that local emergency treatment
(such as appropriate antivenin) is available locally (see
Chapter 8).
• If zoonotic disease is suspected or identified in a per-
son in contact with exotic or wild animals (pets, rec-
reational or occupational exposure) or works in a pet
shop or other animal handling facility, notify the local
and state public health department.
• Support efforts of state and national agencies to regu-
late or license ownership of exotic or wild pets.
• Counsel clients to refrain from owning wild-caught
animals, about disease transmission routes, and the
risks of ownership and contact with wildlife and exotic
animals as pets.6
• Assist prospective pet owners in appropriate pet
selection.
• Counsel owners on techniques to avoid high-risk Figure 10-5 n Green iguana. (From Mitchell M, Tully TN Jr: Manual of
contact with exotic or wild animals. exotic pet practice, St Louis, 2008, Saunders Elsevier.)
(Ebola, monkeypox, Nipah virus) pathogens. Human beings,

domestic animals, and native wildlife are at risk.9 Serious
injuries are also a risk when handling wild or exotic animals
because captivity and human companionship do not change
natural behaviors or tame these animals. Many nonhuman
primate pets have all their teeth removed but can still injure
handlers.10
In addition to the zoonotic disease risk, some exotic and
native wildlife species kept as pets are venomous and pose
envenomation risks to other animals and pet owners (see
Chapter 8).11 Exotic venomous reptiles may produce venom
for which antivenin may be not widely available.
INFECTIONS LINKED TO EXOTIC AND

WILDLIFE PETS Figure 10-6 n African hedgehog (Atelerix albiventris). (From Mitchell M,
Tully TN Jr: Manual of exotic pet practice, St Louis, 2008, Saunders Elsevier.)
Not surprisingly, the international trade in animals and
the use of wildlife as pets have been linked to a number of
zoonoses and other animal diseases. Table 10-5 shows doc- since 1991 because of concern about possible importation of
umented examples of exotic and wildlife pets and diseases foot and mouth disease.23 Other exotic animals linked to sal-
associated with them. Clearly the potential exists for injuries monellosis include a komodo dragon at a zoo that infected
(trauma, envenomation), infections (viruses, bacteria, par- 65 persons, mainly children, with contact to a temporary
asites, fungi) and allergies, although not specifically docu- barrier around the exhibit.24
mented in the literature as a pet encounter. Spurred and leopard tortoises imported to Florida from
These cases of reported disease illustrate the complex- Africa have been found to be infested with ticks of the genus
ity of the issues surrounding nontraditional pets. The 1994 Amblyomma, which can be a vector for heartwater, a seri-
outbreak of Salmonella associated with African pygmy ous livestock disease caused by the bacterium Cowdria rumi
hedgehogs (Figure 10-6) involved captive-bred animals. nantium.25 As a result, these African tortoises are currently
Importation of hedgehogs from Africa had been banned banned in the United States. More recently, African vipers
have been diagnosed with severe and even fatal tickborne
disease related to a Cowdria-like organism.26
Table 10-5 n Reported Infections Related The 2003 multistate outbreak of monkeypox has received
to Nontraditional Pets significant scientific and media attention and has a number
of instructive points about imported zoonotic pathogens of
Nontraditional Pet wildlife. The outbreak was traced to the importation of wild-
Species Associated Disease Affected Species
caught giant Gambian pouched rats (Cricetomys gambi
Hedgehogs (Atelerix Salmonellosis, Human beings
anus; Figure 10-7) and other rodents that had been recently
albiventris)12 dermatophytes, imported from Africa for the pet trade.
herpesvirus, Some of these exotic rodents were carriers of the
yersiniosis, monkeypox virus. When housed in dealer facilities, they
mycobacteriosis
Leopard tortoises Heartwater (found Cattle
(Geochelone in Amblyomma
pardalis)13 ticks on tortoises)
Various reptiles and Salmonellosis Human beings
amphibians14–16
Gambian rat Monkeypox Human beings,
(Cricetomys spp.) prairie dogs
Prairie dogs Tularemia, Human beings
(Cynomys spp.)17,18 monkeypox
Southern flying Leptospirosis Human beings
squirrel (Glaucomys
volans)19
Marmosets (Callithrix Rabies Human beings
jacchus)20
Macaque monkeys Herpes B Human beings
(Macaca spp.)21
Egyptian rousette Lagos bat lyssa virus Human beings
bat (Rousettus
egyptiacus)22 Figure 10-7 n Gambian pouched rat. (From Wikipedia, http://en.wikipedia.
org/wiki/Gambian_Pouch_Rat.)
were caged close to a susceptible native wildlife animal spe- zoonoses present challenges to health care providers and
cies, black-tailed prairie dogs (Cynomys ludovicianus). These public health professionals. It appears that reduction of the
prairie dogs then were sold as pets, and in the process 71 rate of introduced pathogens can only be achieved by every-
human beings, including pet owners, pet store workers, dis- one at every level working on some aspect of the prevention
tributors, and veterinarians, contracted infection through
contact with sick animals or their secretions (Figure 10-8).27-29
Figure 10-9 shows the complex web of contact and distribu-
tion that resulted in human cases. The outbreak did not pro-
duce human fatalities but clearly showed the potential for a
novel pathogen to cause outbreaks in the United States as a
result of the global pet trade.
Examples of native wildlife used as pets and infecting
their owners include a wild-caught prairie dog transmitting
tularemia to an owner.18 In Brazil, a new rabies virus variant
was identified in human cases associated with pet marmosets
(Callithrix jacchus).20
CONTROL EFFORTS
The magnitude and diversity of animal species being main- Figure 10-8 n Monkeypox. (From the Centers for Disease Control and
tained as pets and the ongoing potential for novel and rare Prevention, Atlanta, Ga.)
Rodent shipment from Accra, Ghana

4/9/03
WI
4/9/03 NJ Human cases:
TX-1**
TX-2 * RS, BP 17 confirmed
50 Gambian giant rats (GR)
GR TS, SM 22 probable/
53 rope squirrels (RS) IL
2 brushtail porcupines (BP) suspect
Human cases:
47 tree squirrels (TS) 4/11/03 TX-3 42 PD 8 confirmed
100 striped mice (SM) RS, SM traced 4 probable/
510 dormice (DM) 4/1 DM suspect IN
6/0 Human cases:
3 14 PD
†
4/21/03 7 confirmed
4/17/03 IA IL-1 traced
9 probable/
GR, DM GR, DM 24 PD suspect
traced
200 prairie dogs (PD)
at facility
TX-4 TX-5 1 PD
DM DM traced
4/26/03 MO
1 PD
Human cases:
traced
4/2
TX-6 2 confirmed
*
8/0
TS, SM
11 PD SC
3
DM TX-9
3 No human
8/0 DM traced
TX-7 TX-8 4/2 cases
4/29
DM DM /03 MI
TX-10 No human
DM KS
5/1
5/12/03 cases
Human cases:
8/0
1 confirmed
3
IL-2
Japan DM 6/1/03
DM
MN 6/5/03 WI
* Date of shipment unknown.
** Identified as distributor C in MMWR 2003;52:561-4. DM DM
† Identified as distributor D in MMWR 2003;52:561-4.
Identified as distributor B in MMWR 2003;52:561-4.
Includes two persons who were employees at IL-1.
Figure 10-9 n Movement of imported African rodents to animal distributors and distribution of prairie dogs from an animal distributor associated with
human cases of monkeypox in 11 states (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, New Jersey, South Carolina, Texas, and Wisconsin) as
of July 8, 2003. Japan is included among the locations having received shipment of rodents implicated in this outbreak. (This does not include one probable
human case from Ohio.) (From Centers for Disease Control and Prevention: Update: multistate outbreak of monkeypox—Illinois, Indiana, Kansas, Missouri,
Ohio, and Wisconsin, 2003, MMWR Morb Mortal Wkly Rep 52:642, 2003.)
and control—from local awareness of the problem to policy rodents, and animal products capable of causing human
changes on a national or international level that restrict the disease,32 only a small number of species (including the
trade in live animals.2 NASPHV has joined with CSTE in African rodents linked to the importation of monkeypox)
developing position statements requesting a federal inter- are currently banned. In addition, most of the animals that
agency work group to address the risks posed by the exotic are imported, with the exception of avian species, are nei-
animal trade (see Developing Importation and Importation ther quarantined nor tested for infectious disease agents
Restrictions on Exotic and Native Wildlife with Potential before entering the country.
Adverse Impact on Public Health, available online at http:// NASPHV has developed guidelines titled “Compendium
www.cste.org/PS/2003pdfs/03-ID-13%20-%20FINAL. of Measures to Prevent Disease Associated with Animals in
pdf).30 In particular, NASPHV has called for the creation Public Settings” to prevent spread of infections at public set-
of an “approved species” list to reduce the threat of disease tings where animal contact could take place, including animal
importation, more extensive inspection and quarantine of displays, petting zoos, animal swap meets, pet stores, zoolog-
imported animals, and tracking of animals that have been ical institutions, nature parks, circuses, carnivals, farm tours,
imported. The AVMA is also on record discouraging exotic livestock-birthing exhibits, county or state fairs, schools, and
animals and wildlife as pets.31 Although CDC regulations wildlife photo opportunities.5 Key recommendations of these
govern the importation of dogs, cats, turtles with a cara- guidelines, as well as other recently published recommenda-
pace of less than 4 inches, monkeys, bats, civets, birds from tions to reduce the risk of diseases related to nontraditional
countries with H5N1 influenza, several species of African pets, are shown in Box 10-4.
Box 10-4 Guidelines for Prevention of Human Diseases From Nontraditional Pets at Home and Exposure
to Animals in Public Settings
Adapted from Pickering LK, Marano N, Bocchini JA et al: Committee on infectious diseases: exposure to nontraditional pets at home and to animals in public settings: risks to
children, Pediatrics 122:876, 2008.
References 18. Avashia SB, Petersen JM, Lindley CM, et al. First reported prairie
dog-to-human tularemia transmission, Texas, 2002. Emerg Infect Dis.
1. Rosen T, Jablon J. Infectious threats from exotic pets: dermatological 2004;10(3):483–486.
implications. Dermatol Clin. 2003;21(2):229–236. 19. Chomel BB. Wildlife zoonoses. Michigan Veterinary Medical Association.
2. Jenkins PT, Genovese K, Ruffler H. Broken screens: the regulation of live http://www.michvma.org/documents/MVC%20Proceedings/Chomel.
animal importation in the United States. Washington DC: Defenders of pdf.
Wildlife; 2007. 20. Favoretto SR, de Mattos CC, Morais NB, et al. Rabies in mar-
3. Karesh WB, Cook RA, Bennett EL, et al. Wildlife trade and global dis- mosets (Callithrix jacchus), Ceara, Brazil. Emerg Infect Dis.
ease emergence. Emerg Infect Dis. 2005;11(7):1000–1002. 2001;7(6):1062–1065.
4. Pickering LK, Marano N, Bocchini JA, et al. Committee on Infectious 21. Ostrowski SR, Leslie MJ, Parrott T, et al. B-virus from pet macaque
Diseases: Exposure to nontraditional pets at home and to animals in monkeys: an emerging threat in the United States? Emerg Infect Dis.
public settings: risks to children. Pediatrics. 2008;122(4):876–886. 1998;4(1):117–121.
5. National Association of State Public Health Veterinarians. Compendium 22. Chomel BB, Belotto A, Meslin FX. Wildlife, exotic pets, and emerging
of measures to prevent disease associated with animals in public set- zoonoses. Emerg Infect Dis. 2007;13(1):6–11.
tings, 2007. MMWR Recomm Rep. 2007;56(RR-5):1–14. 23. Centers for Disease Control and Prevention. African pygmy hedgehog–
6. Kuehn BM. Wildlife pets create ethical, practical challenges for veteri- associated salmonellosis—Washington, 1994. MMWR. 1995;44(24):
narians. J Am Vet Med Assoc. 2004;225(2):171–173. 462–463.
7. Reaser JK, Clark Jr EE, Meyers NM. All creatures great and minute: a 24. Friedman CR, Torigian C, Shillam PJ, et al. An outbreak of salmo-
public policy primer for companion animal zoonoses. Zoonoses Public nellosis among children attending a reptile exhibit at a zoo. J Pediatr.
Health. 2008;55(8–10):385–401. 1998;132:802–807.
8. Centers for Disease Control and Prevention. Reptile-associated salmo- 25. Burridge MJ, Simmons LA, Allan SA. Introduction of potential heart-
nellosis—selected states, 1998–2002. MMWR Morb Mortal Wkly Rep. water vectors and other exotic ticks into Florida on imported reptiles.
2003;52(49):1206–1209. J Parasitol. 2000;86(4):700–704.
9. Marano N, Arguin PM, Pappaioanou M. Impact of globalization 26. Kiel JL, Alarcon RM, Parker JE, et al. Emerging tick-borne disease in
and animal trade on infectious disease ecology. Emerg Infect Dis. African vipers caused by a Cowdria-like organism. Ann N Y Acad Sci.
2007;13(12):1807–1809. 2006;1081:434–442.
10. Johnson-Delaney CA. Safety issues in the exotic pet practice. Vet Clin 27. Reynolds MG, Davidson WB, Curns AT, et al. Spectrum of infection
North Am: Exot Anim Pract. 2005;8(3):515–524, vii. and risk factors for human monkeypox, United States, 2003. Emerg
11. Peterson ME. Toxic exotics. Vet Clin North Am: Exot Anim Pract. Infect Dis. 2007;13(9):1332–1339.
2008;11(2):375–387, vii–viii. 28. Croft DR, Sotir MJ, Williams CJ, et al. Occupational risks dur-
12. Riley PY, Chomel BB. Hedgehog zoonoses. Emerg Infect Dis. 2005;11(1):1–5. ing a monkeypox outbreak, Wisconsin, 2003. Emerg Infect Dis.
13. Burridge MJ, Simmons LA, Simbi BH, et al. Evidence of Cowdria rumi 2007;13(8):1150–1157.
nantium infection (heartwater) in Amblyomma sparsum ticks found on 29. Centers for Disease Control and Prevention. Update: multistate outbreak
tortoises imported into Florida. J Parasitol. 2000;86(5):1135–1136. of monkeypox-Illinois, Indiana, Kansas, Missouri, Ohio, and Wisconsin,
14. Nagano N, Oana S, Nagano Y, et al. A severe Salmonella enterica sero- 2003. MMWR Morb Mortal Wkly Rep. 2003;52(27):642–646.
type Paratyphi B infection in a child related to a pet turtle, Trachemys 30. National Association of State Public Health Veterinarians. Council of
scripta elegans. Jpn J Infect Dis. 2006;9(2):132–134. State and Territorial Epidemiologists: Joint statement: developing impor
15. Schroter M, Roggentin P, Hofmann J, et al. Pet snakes as a reservoir tation and exportation restrictions on exotic and native wildlife with
for Salmonella enterica subsp. diarizonae (serogroup IIIb): a prospective potential adverse impact on public health, 2003. http://www.cste.org/
study. Appl Environ Microbiol. 2004;70(1):613–615. PS/2003pdfs/03-ID-13%20-%20FINAL.pdf. Accessed August 30, 2008.
16. Greene S, Yartel A, Moriarty K, et al. Salmonella kingabwa infec- 31. American Veterinary Medical Association. Birds, exotics and wild
tions and lizard contact, United States, 2005. Emerg Infect Dis. animals. http://www.avma.org/careforanimals/animatedjourneys/petse-
2007;13(4):661–662. lection/birds.asp.
17. Guarner J, Johnson BJ, Paddock CD, et al. Veterinary Monkeypox Virus 32. Centers for Disease Control and Prevention. Global migration and
Working Group: Monkeypox transmission and pathogenesis in prairie quarantine. http://www.cdc.gov/ncidod/dq/animal/index.htm. Accessed
dogs. Emerg Infect Dis. 2004;10(3):426–431. October 23, 2009.
IMMUNOCOMPROMISED INDIVIDUALS
Available evidence continues to suggest that the psycho- • Stress general hygiene principles, including handwash-
social support value of companion animals, particularly ing, and ensure proper food preparation and safe water
for the elderly or infirm,1–3 outweighs the risk of acquir- supplies.
ing a serious infection from such animals. Nevertheless,
issues regarding hygiene and common sense practices Human Health Clinicians
must be addressed to support a healthy human-animal
bond, especially among immunocompromised people or • Understand the risks and considerable benefits of
pets. companion animal ownership among immunocom-
promised persons.
• Ensure that a thorough history is taken to best man-
age the patient’s potential exposure to zoonotic
Professionals
disease.
• Be aware of the Guidelines for Preventing
Opportunistic Infections among HIV-Infected
Persons: Recommendations of the US Public
• Provide public health guidance to reduce Health Service and the Infectious Diseases Society
opportunistic infections among immunocompro- of America (http://www.annals.org/cgi/content/
mised persons. full/137/5_Part_2/435).
• With an immunocompromised patient’s permission, commonly, as a result of a secondary or acquired factor such
consider coordinating preventive interventions with as debilitation, immunosuppressive chemotherapy (Figure
the patient’s veterinarian. 10-10), human immunodeficiency virus (HIV) in human
• Counsel immunocompromised patients with occupa- beings, or feline leukemia virus (FeLV) in cats (Table 10-6).
tional exposure to animals about zoonotic infection
risk and risk reduction measures.
• Provide consultation about zoonotic disease risk
reduction.
• Provide guidance on maintaining the health of immu-
nocompromised animal patients, including a healthy
environment.
• Maintain confidentiality of information regarding
immunocompromised persons.
ETIOLOGY OF IMMUNOSUPPRESSION
Millions of people and companion animals in this country

Figure 10-10 n Alopecia in a 7-year-old Schnauzer undergoing doxo-
are living with less than a robust immune system. rubicin and dacarbazine chemotherapy. (From Couto CG: Complications of
Immunosuppression can result from a number of etiologies, cancer chemotherapy. In Nelson RW, Couto CG (eds): Small animal internal
either from a primary or genetic malfunction (rare) or, more medicine, ed 4, St Louis, 2009, Mosby Elsevier.)
Table 10-6 n Etiologies of Immunocompromise in Human Beings and Other Animals
Examples (Breed Predilection)
Common to All Species

Chemicals Immunosuppressive medication (e.g., corticosteroids, cyclosporin, 6-mercaptopurine, methotrexate,
azathioprine), mercury, PCBs
Radiation Radiation therapy, excess radiation exposure
Neoplasia Leukemia, other cancers
Other causes Severe malnutrition, chronic diabetes, renal/hepatic/splenic failure, prematurity, advancing age
Human Beings
Primary (genetic) X-linked agammaglobulinemia, X-linked hyper-IgM syndrome, Wiskott-Aldrich syndrome, Ataxia
telangiectasia, chronic granulomatous disease, SCID
Infections HIV, other severe infections
Dogs
Primary (genetic)4 X-linked severe combined immunodeficiency (Basset Hounds, Cardigan Welsh Corgis)
Severe combined immunodeficiency disease (Jack Russell terriers)
IgA deficiency (Beagles, German Shepherd dogs, Chinese Shar-Peis, English Cocker Spaniels, Irish Wolfhounds)5
IgM deficiency (Doberman Pinschers)
Thymic hypoplasia (dwarfed Weimaraners)
Cyclic hematopoiesis (gray Collies)
Leukocyte adhesion deficiency (Irish Setters)
Complimentary deficiency (Brittany Spaniels)
Bactericidal defect (Doberman Pinschers)
Transient hypogammaglobulinemia (Samoyeds)
Chemicals Organophosphate toxicity6
Cats
Primary (genetic) Chediak-Higashi syndrome (Persian cats)
Infectious FIV/FeLV
Horses
Primary (genetic) SCID (Arabians)
PCBs, Polychlorinated biphenyls; Ig, immunoglobulin; SCID, severe combined immune deficiency.
In general, defects in humoral immunity (B-cell lines)

can lead to increased susceptibility to bacterial infections; HUMAN HEALTH CARE PROVIDERS
cell-mediated immunity (T-cell lines) defects to viral, fungal,
or protozoal infections; and defects of phagocytosis or the Pet-owning human health care providers must be vigi-
complement system to disseminated infections. lant regarding nosocomial zoonoses, particularly if they are
working with immunocompromised patients. In one situ-
ation, a common yeast pathogen of canine otitis externa
IMPACT OF IMMUNODEFICIENCY STATES ON (Figure 10-11) was introduced into a neonatal intensive care
ANIMAL-HUMAN DISEASE TRANSMISSION unit by a dog-owning health care worker, causing coloniza-
tion in infants, some resulting in serious infections.13,14 In
A large proportion of American households include pets,7 another case, a cat on a geriatric ward was the likely suspect
and pet ownership among immunocompromised per- of staphylococcal infections (see Chapter 5).15
sons is common. For example, studies of patients with HIV
infection have reported rates of pet ownership similar to that
of the general population, with approximately half owning
or living with pets.8 In addition, on a global level, the HIV/ GENERAL GUIDELINES FOR THE
AIDS pandemic has created large populations of individu- PREVENTION OF ZOONOTIC DISEASE IN
als with compromised immune systems, many of whom may IMMUNOCOMPROMISED PATIENTS
also be exposed to zoonotic diseases.9,10 Human and veter-
inary clinicians are quite likely to encounter situations in Guidance From Both Human Health and
which they may provide appropriate guidance for reducing Veterinary Health Care Providers
animal sources of infectious diseases for human beings and Hand and food hygiene is vital (Figures 10-12 and
vice versa by educating themselves and staff to provide the 10-13). Pets are not likely to be the most common source
best available information. of zoonotic disease infection. More likely, contact with
There are at least three possible effects of human immu- raw or undercooked meat or from an environmental infec-
nodeficiency on animal-human disease transmission: tious source is implicated in transmission. Unequivocally,
1. An immunocompromised host is more susceptible to immunocompromised individuals should avoid raw meat
infection with opportunistic disease. and eggs and unpasteurized dairy products. For example,
2. An immunocompromised host may transmit opportu- although cats are the definitive host for Toxoplasma gondii,
nistic disease to others. undercooked meat (less than 165° F) and inadequately
3. A disease may be more severe in an immunocompromised washed, contaminated fruits and vegetables are likely the
host (e.g., toxoplasmosis, which causes asymptomatic or source for infection. See USDA food safety fact sheets:
mild disease in most immunocompetent patients but can http://www.fsis.usda.gov/Factsheets/Keep_Food_Safe_
cause severe and even fatal systemic disease in immuno- Food_Safety_Basics/index.asp and http://www.fsis.usda.
compromised individuals). gov/Factsheets/At_Risk_&_Underserved_Fact_Sheets/
index.asp.
The knowledge level among immunocompromised Serologic or fecal evaluation of healthy cats for Toxo
persons and their health care providers about the risk of plasma infection is not recommended. Oocysts are shed
acquiring infections from pets could be increased with an transiently and are easily missed, and serologic evaluation
appropriate educational strategy. In one study in which does not predict cats shedding oocysts. Instead, prevention
more than 400 patients with AIDS were interviewed—half
of whom owned pets—only about 10% who were living
with pets were given any information about zoonotic dis-
eases from their health care provider, and one quarter of this
information was incorrect or misunderstood (e.g., “fleas can
give you rabies” or “cats can give you AIDS”).8 Because pet
ownership is as common (and understanding of zoonoses as
uncommon) among persons living with HIV as in the general
population, human health care providers must be prepared
to discuss with immunocompromised patients the risks of
living with pets. Overly conservative approaches, including
physician recommendations for their patients to relinquish
pets, have largely been unheeded as owners often have strong
bonds with their animals.11 Armed with complete and accu-
rate information, patients and their care providers can weigh
these risks against the often substantial benefits of love,
touch, social support, and companionship that accrue to pet
owners. Zoonotic disease prevention is a shared responsibil-
Figure 10-11 n Otitis externa in a dog. Brown, waxy exudate with
ity among human, veterinary, and public health professionals. a secondary yeast infection associated with an underlying allergy. (From
Improving communication among these persons will enhance Medleau L, Hnilica KA: Small animal dermatology: a color atlas and therapeutic
zoonotic disease prevention.12 guide, ed 2, St Louis, 2006, Saunders Elsevier.)
Figure 10-14 n Have an immunocompetent person clean the litterbox.

(From Bunch SE: The exocrine pancreas. In Nelson RW, Couto CG (eds):
Figure 10-12 n Handwashing is critical to disease prevention. (From Small animal internal medicine, ed 3, St Louis, 2003, Mosby Elsevier.)
Atlanta, Ga. Photo courtesy Kelly Thomas.)
• Review guidance to reducing exposure to selected oppor-
tunistic diseases among persons with HIV (see http://
www.cdc.gov/mmwr/preview/mmwrhtml/rr5108a1.htm).
• Encourage questions about healthy living with companion
animals and discourage kissing or face-to-face contact.
• Pet vaccines, including live attenuated strains, should be
recommended and given as needed; they are not believed
to present a human health hazard.17
Occupational or Recreational Risk Reduction

• Avoid contact with wild animals to reduce the risk of
enteric disease, such as acquiring Cryptosporidium from
wild birds.
• NEVER touch the feces of any animal.
• Avoid farm animals and petting zoos to decrease exposure
to Escherichia coli in ruminants, Bordetella bronchiseptica
Figure 10-13 n Pregnant women and immunosuppressed patients can in swine, and Salmonella in chicks and ducks.
be at greater risk in acquiring foodborne illness and need to take additional • Occupational health care workers working with high-risk
precautions when handling raw food products. Cook meat, poultry, and personnel such as veterinarians, veterinary staff, zookeep-
eggs thoroughly. Using a thermometer to measure the internal temperature
of meat is a good way to be sure that it is cooked sufficiently to kill bacte- ers, and pet shop workers should counsel immunocom-
ria. For example, ground beef should be cooked to an internal temperature promised workers about the risk of occupational of
of 160 ° F. Eggs should be cooked until the yolk is firm. (From Centers for zoonotic disease infection and possible work restrictions
Disease Control and Prevention Public Health Image Library. Photo cour- to reduce risk for those with significant impairment of
tesy James Gathany.)
immunity.
of transmission of Toxoplasma directly from cats should

focus on the following husbandry recommendations: Animal Selection Recommendations
• Avoid contact with feces (have an immunocompetent • Select healthy, well-mannered dogs or cats 6 months or
person clean the litterbox or fecal accidents, or wear gloves older to decrease the likelihood of exposure to enteric
followed by washing hands) (Figure 10-14). diseases and Bartonella from kittens.
• Pets should not be given prophylactic antibiotics with- • Avoid petting or handling free-roaming animals; when
out clinical signs of infection. For example, Salmonella selecting a pet, choose one with a documented veterinary
carriage in reptiles cannot be eliminated. Use of antibio health history and current vaccinations.
tics for this purpose has been unsuccessful and may favor • Avoid exotic or wild animals to reduce the likelihood
development of antibiotic-resistant bacteria.16 of exposure to emerging infections (i.e., monkeypox in
• Any bite or wound from an animal should be flushed rodents) and known diseases such as herpes B infection
with copious amounts of soap and water and a health care from macaque monkeys and Salmonella from reptiles
provider should be contacted for wound management, (Figure 10-15).
including assessment for appropriate antibiotics, tetanus, Cockatoos, like pigeons, may shed Cryptococcus in their
and possible rabies postexposure prophylaxis (see Animal feces. Transmission of this infection from a cockatoo to its
and Human Bites later in this chapter). owner who was chronically immunocompromised because
Figure 10-17 n Pet rodents have been implicated in fatal LCMV infec-
tion in human beings. (From Sheldon CC, Sonsthagen T, Topel JA: Animal
Figure 10-15 n Immunocompromised persons should avoid selecting restraint for veterinary professionals, St Louis, 2006, Mosby Elsevier.)
reptiles as pets, such as this frilled dragon (Chlamydosaurus kingii). (From
Mader DR: Reptile medicine and surgery, ed 2, St Louis, 2006, Saunders
Elsevier.) • Keep pets indoors or leashed on walks to decrease the
likelihood of engagement with other animals.
of a renal transplant has occurred.18 Therefore some authors • Because of occasional cases of Bordetella bronchiseptica
have recommended that immunocompromised patients not among immunocompromised persons,21,22 avoid expos-
own cockatoos (Figure 10-16).19 ing dogs or owners to situations in which dogs are con-
A fatal outbreak of lymphocytic choriomeningitis virus gregated, such as boarding kennels, grooming parlors,
(LCMV) in solid-organ transplant recipients was traced back off-leash dog parks, or dog shows.
to a pet hamster acquired by the organ donor 17 days before • Do not allow pets to hunt, scavenge, or eat feces to reduce
donation (Figure 10-17). The prevalence of this virus in the likelihood of exposure to enteric infections.
rodent populations has led to recommendations that immu- • Do not feed pets raw meat or egg diets or provide unpas-
nocompromised individuals (as well as pregnant women) teurized dairy products to limit exposure to enteric
should avoid owning pet rodents or having contact with wild infections.
or pet rodents.20 • Do not allow your pet to drink from the toilet.
Have a veterinarian conduct a physical examination and • Keep animals and litterboxes out of food preparation
fecal analysis on a new pet. areas.
• Avoid exposure to pet urine, feces, and saliva (don’t allow
your pet to lick your face or open lesions).
ANIMAL HUSBANDRY GUIDANCE • Have a nonimmunocompromised household member
• Seek veterinary care early in the course of clinical disease remove a pet’s solid waste and dispose daily by flushing
of pets to limit chances for zoonotic disease exposure. down a toilet or discarding in the garbage or in a compost
area (not to be spread on fruits or vegetables).
• Avoid animals with diarrhea. Have an immunocompe-
tent household member clean soiled areas in the house
of organic debris, followed by a 1:10 household bleach
solution.
• Avoid rough play with the pet that could result in being
bitten or scratched; keep pet’s nails trimmed short.
• Remove and dispose of bird cage linings daily and use
“wet” cleaning for the cage and utensils on a weekly basis.
Wear gloves when handling items that are contaminated
with bird droppings.
• Have a helper clean the fish tank (Figure 10-18) or wear
disposable gloves during such activities, followed by
washing hands thoroughly by rubbing hands together
vigorously for 15 to 20 seconds with running water and
soap.
• If assistance is required to care for your pet, con-
Figure 10-16 n Nodular cutaneous cryptococcosis in an HIV-positive
tact local volunteer groups who may be willing to
cockatoo owner. (From Rosen T, Jablon J: Infectious threats from exotic provide exercise, food, or foster care (e.g., during
pets: dermatological implications, Derm Clin 21:229, 2003.) hospitalization).
Figure 10-18 n Types of fish tanks. (From Mitchell M, Tully TN Jr: Manual of exotic pet practice, St Louis, 2008, Saunders.)
about zoonotic disease diagnosis, control, and preven-

U.S. PUBLIC HEALTH SERVICE GUIDELINES FOR tion. Veterinarians should also emphasize among their staff
PERSONSAWHO ARE HIV POSITIVE B
the need for strict confidentiality regarding any personal
information an animal owner happens to disclose about
Although any zoonotic disease that occurs in immunocom- his or her own medical status (it is not recommended, for
petent individuals can also affect immunocompromised example, to document human medical information in the
patients, the U.S. Public Health Service has highlighted a veterinary record).
number of animal agents that pose a significant risk to HIV-
infected persons. These include causes of enteritis (espe-
cially Campylobacter, Salmonella, and Cryptosporidium), and Care for Pets of Immunocompromised Owners
Bartonella, Toxoplasma, Histoplasma, and Mycobacterium
• Neuter pets.
marinum.
• Provide strict adherence to strategic deworming protocols
The evidence-based recommendations of the U.S. Public
and maintenance of appropriate vaccinations.
Health Service and the Infectious Diseases Society of America
• Be prepared to discuss end-of-life planning for the pet’s con-
are listed in Table 10-7.
tinued care (http://www.hsus.org/pets/pet_care/guidelines_
Although these guidelines recommend that human health
for_finding_a_responsible_home_for_a_pet.html).
care providers counsel their immunocompromised patients
about zoonotic disease risk reduction, surveys of physicians
have indicated that many believe that veterinarians are best Care for Immunodeficient Animals
equipped to provide such counseling and should therefore
be involved in patient education of immunocompromised • Do not administer modified live virus vaccines.
individuals.12 Some authorities have stated that veterinarians • Manage secondary and opportunistic infections (Color
are more qualified than physicians to advise pet owners and Plate 10-5).
persons in high-risk professions about zoonotic risks.23 • Provide supportive care.
Guidance for Owners of Immunodeficient

PUBLIC HEALTH ROLE OF THE Animals
VETERINARIAN: SAFER PET OWNERSHIP FOR
IMMUNOCOMPROMISED PERSONS AND CARE • Animals with primary immunodeficiency disorders
OF IMMUNOCOMPROMISED PETS should not be bred.
• Cats with FIV or FeLV can spread the viruses to other
In the veterinary setting, pet owners may be more will- cats, typically by bite wounds or close contact (FeLV)
ing to request information regarding safer pet ownership (Color Plate 10-6). Therefore separate household con-
for immunocompromised persons if there are, for exam- tacts that are FIV/FeLV negative. (All cats with unknown
ple, posters and handouts encouraging such client educa- FIV/FeLV status with a bite wound should be tested for
tion or information in practice newsletters. Veterinarians these viruses at the time of presentation and again 60
can address high-risk persons during general discussions days later.)
Table 10-7 n Guidelines for Preventing Opportunistic Infections Among HIV-Infected Persons
Strength of
Topic Recommendation Recommendation*
General Pet-Related Recommendations

Health care providers should advise HIV-infected persons of the potential risk of pet ownership DIII
but should not routinely advise HIV patients to part with their pets.
Seek veterinary care when pet develops diarrhea. BIII
Animals with diarrhea (and animals <6 months old) should be examined and stool tested for BIII
Cryptosporidium, Salmonella, and Campylobacter.
When obtaining a new pet, avoid animals <6 months (1 year for cats) and animals with CIII
diarrhea. Avoid stray animals.
Wash hands after handling pet, including before eating, and avoid contact with pet feces. BIII
Supervise handwashing in HIV-positive children.
Avoid contact with reptiles (e.g., snakes, lizards, iguanas, turtles) as well as chicks and ducklings BIII
to reduce salmonellosis risk.
Use gloves when cleaning aquarium to reduce risk of Mycobacterium marinum infection. CIII
Avoid contact with exotic pets (e.g., nonhuman primates). BII
Avoid exposure to calves and lambs and premises where calves and lambs are raised. BII
Cat ownership Discuss with HIV patient and caretakers that cat ownership increases risk of Bartonella and CIII
enteric infections.
Patients acquiring a cat should adopt or purchase cat >1 year old and in good health; avoid BII
acquiring a stray cat.
Toxoplasmosis Wash hands after working in a garden; wash all fruits and vegetables and ensure that raw BIII
meats are handled separately from raw food. Clean cat litterbox daily, preferably by HIV-
negative, nonpregnant person (use gloves and wash hands afterwards), keep cat indoors, do
not allow cat to hunt, do not feed cat undercooked meat.
Testing cats for toxoplasmosis EII (not
recommended)
Bartonella Declawing of cat not usually advised. Avoid activities resulting in bites or scratches. BII
infection
Wash bites or scratches promptly. CIII
Do not allow cats to lick wounds. BIII
Flea control for cats. CIII
Testing cat for Bartonella. DII (not
recommended)
Occupational Occupations with animal contact may pose risk for cryptosporidiosis, toxoplasmosis,
exposures salmonellosis, campylobacteriosis, or Bartonella, but data are insufficient to recommend
against patients with HIV working in such settings.
Follow recommendations and protocols for protective equipment and clothing. BII
Avoid contact with young farm animals, specifically those with diarrhea, to reduce BIII
cryptosporidiosis infection.
Handwashing after gardening or soil contact to reduce risk of cryptosporidiosis and toxoplasmosis. CIII
In areas endemic for histoplasmosis, avoid risk activities including soil contact, cleaning chicken
coops, disturbing soil beneath bird roosts, demolishing buildings, or cave exploring.
Birds Screening healthy birds for Cryptococcus neoformans, Mycobacterium avium, or Histoplasma DIII
capsulatum is not recommended.
Adapted from Kaplan JE, Masur H, Holmes KK: Guidelines for preventing opportunistic infections among HIV-infected persons—2002. Recommendations of the U.S. Public
Health Service and the Infectious Diseases Society of America, MMWR Recomm Rep 51(RR-8):1, 2002.
*System used to rate the strength of recommendations and quality of supporting evidence is as follows:
Rating strength of recommendation
A, Both strong evidence for efficacy and substantial clinical benefit support recommendation for use; should always be offered.
B, Moderate evidence for efficacy or strong evidence for efficacy but only limited clinical benefit; supports recommendation for use; should usually be offered.
C, Evidence for efficacy is insufficient to support a recommendation for or against use, or evidence for efficacy might not outweigh adverse consequences (e.g., drug toxicity, drug
interactions) or cost of the chemoprophylaxis or alternative approaches; use is optional.
D, Moderate evidence for lack of efficacy or for adverse outcome supports a recommendation against use; should usually not be offered.
E, Good evidence for lack of efficacy or for adverse outcome supports a recommendation against use; should never be offered.
Rating quality of evidence supporting the recommendation
I, Evidence from ≥1 correctly randomized, controlled trials.
II, Evidence from ≥1 well-designed clinical trials without randomization, from cohort or case-controlled analytic studies (preferably from more than one center), or from multiple
time-series studies, or dramatic results from uncontrolled experiments.
III, Evidence from opinions of respected authorities based on clinical experience, descriptive studies, or reports of consulting committees.
• Keep these animals indoors; do not allow pets to hunt, cat in for evaluation and zoonotic disease prevention if diar
scavenge, or consume raw meat or egg diets or unpasteur- rhea or signs of respiratory disease developed.
ized dairy products.
• Wash hands before and after handling the pet. References
• Provide appropriate endoparasite and ectoparasite
control. 1. Raina P, Waltner-Toews D, Bonnett B, et al. Influence of compan-
• Avoid exposure to other ill animals. ion animals on the physical and psychological health of older peo-
ple: an analysis of a one-year longitudinal study. J Am Geriatr Soc.
1999;47(3):323–329.
2. Castelli P, Hart LA, Zasloff RL. Companion cats and the social support
CASE STUDIES systems of men with AIDS. Psychol Rep. 2001;89(1):177–187.
3. Siegel JM, Angulo FJ, Detels R, et al. AIDS diagnosis and depression
in the Multicenter AIDS Cohort Study: the ameliorating impact of pet
Case Study 1 ownership. AIDS Care. 1999;11:157–170.
4. Tilley LP, Smith FWK. Blackwell’s five-minute veterinary consult: canine
A public health veterinarian working as an AIDS surveillance and feline. 3rd ed. Ames, IA: Blackwell; 2004.
coordinator received a number of questions for which the 5. Day MJ. Immunodeficiency disease in the dog. In: World Small Animal
human-animal bond was never more poignant. Indeed, one Veterinary Association World Congress Proceedings. 2004. http://www.
vin.com/proceedings/Proceedings.plx?CID=WSAVA2004&PID=8598
was from a gentleman who was recently diagnosed with AIDS &O=Generic. Accessed May 3, 2009.
and who owned a 4-year-old neutered male Golden Retriever. 6. Sykora B, Tomsikova A. Kaposi’s sarcoma in dog with acquired immu-
His family practitioner, concerned about any increased risk for nodeficiency after phosphate poisoning. Folia Microbiol (Praha).
opportunistic infections, advised him to find another home for 1998;43(5):543–544.
7. American Veterinary Medical Association. Market research statistics:
his beloved pet. This man was heartbroken, trying to gather U.S. pet ownership—2007. http://www.avma.org/reference/marketstats/
as much information as possible about what specifically he ownership.asp.
would face if he ignored his doctor’s advice. Fortunately, with 8. Conti L, Lieb S, Liberti T, et al. Pet ownership among persons with
his permission, the veterinarian was able to contact his physi AIDS in three Florida counties. Am J Public Health. 1995;85(11):
cian to discuss the relatively low risk as well as the benefits of 1559–1561.
9. Etter E, Donado P, Jori F, et al. Risk analysis and bovine tuberculosis, a
owning a healthy pet (one that was receiving regular veteri re-emerging zoonosis. Ann N Y Acad Sci. 2006;1081:61–73.
nary care) and encouraged the doctor to continue to contact 10. Feldman RL, Nickell K. Avian influenza: potential impact on sub-
public health practitioners for information as well as this pet Saharan military populations with high rates of human immuno-
owner’s veterinarian (with permission) about the animal’s deficiency virus/acquired immunodeficiency syndrome. Mil Med.
2007;172(7):753–758.
preventive health care. Additionally, this pet owner happened 11. Angulo FJ, Glaser CA, Juranek DD, et al. Caring for pets of immu-
to live in an area with an active volunteer organization that nocompromised persons. J Am Vet Med Assoc. 1994;205(12):
assisted with walking and feeding pets of persons living with 1711–1718.
AIDS. Armed with these resources, the patient was able to 12. Grant S, Olsen CW. Preventing zoonotic diseases in immunocompro-
maintain a healthy pet. mised persons: the role of physicians and veterinarians. Emerg Infect Dis.
1999;5(1):159–163.
13. Chang HJ, Miller HL, Watkins N, et al. An epidemic of Malassezia
pachydermatis in an intensive care nursery associated with colonization
Case Study 2 of health care workers’ pet dogs. N Engl J Med. 1998;338(11):706–711.
A public health veterinarian who was also a relief clinical veter 14. Morris DO. Malassezia pachydermatis carriage in dog owners. Emerg
Infect Dis. 2005;11(1):83–88.
inarian was presented with a 7-year-old neutered female cat for 15. Marcus LC, Marcus E. Nosocomial zoonoses. N Engl J Med.
toxoplasmosis serologic testing and (reluctant) possible eutha 1998;338(11):757–759.
nasia of the cat. The cat’s owner was the spouse of a cancer 16. Bradley T, Angulo FJ, Raiti P. Association of Reptilian and Amphibian
patient and was concerned that the spouse was on immunosup Veterinarians guidelines for reducing risk of transmission of Salmonella
spp. from reptiles to humans. J Am Vet Med Assoc. 1998;213:51–52.
pressive chemotherapy and therefore at great risk for toxoplas 17. Hemsworth S, Pizer B. Pet ownership in immunocompromised
mosis from their pet. The veterinarian explained the life cycle children—a review of the literature and survey of existing guidelines.
of toxoplasmosis, the epidemiology in people and cats, and that Eur J Oncol Nurs. 2006;10(2):117–127.
if the serology was positive it could actually be protective. The 18. Nosanchuk JD, Shoham S, Fries BC, et al. Evidence of zoonotic trans-
owner declined both serologic testing and euthanasia because mission of Cryptococcus neoformans from a pet cockatoo to an immuno-
compromised patient. Ann Intern Med. 2000;132(3):205–208.
the cat had never hunted in its lifetime, was indoors only, and 19. Rosen T, Jablon J. Infectious threats from exotic pets: dermatological
was fed an exclusively commercial diet. There was no evidence implications. Dermatol Clin. 2003;21(2):229–236.
of mice or rats in the house, decreasing the cat’s likelihood of 20. Amman BR, Pavlin BI, Albarino CG, et al. Pet rodents and fatal lym-
exposure to the parasite. However, the spouse enjoyed garden phocytic choriomeningitis in transplant patients. Emerg Infect Dis.
2007;13(5):719–725.
ing—a much greater potential for exposure to toxoplasmosis. 21. Berkowitz DM, Bechara RI, Wolfenden LL. An unusual cause of
Fortunately the patient always wore gloves when doing so and cough and dyspnea in an immunocompromised patient. Chest.
thoroughly washed afterwards. The veterinarian and the cat 2007;131(5):1599–1602.
owner discussed additional toxoplasmosis exposure reduction, 22. Trevejo RT, Barr MC, Robinson RA. Important emerging bacte-
including proper handling of raw meats and washing raw foods. rial zoonotic infections affecting the immunocompromised. Vet Res.
2005;36:493–506.
The veterinarian and cat owner agreed that the owner would 23. Nowotny N, Deutz A. Preventing zoonotic diseases in immunocompro-
be the person cleaning the litterbox, schedule overall wellness mised persons: the role of physicians and veterinarians. Emerg Infect Dis.
examinations of the cat every 6 months, and would bring the 2000;6(2):208.
Animal and Human Bites
Each year in the United States several million per- and treatment of animals bitten by other animals is similar
sons are bitten by animals. Although up to 80% of bites to that for animal bites in human beings.
may never be reported, more than 300,000 emergency The optimal prevention and treatment of animal bites
department visits occur each year for dog bites alone.1 require good communication among veterinary, human
Approximately half of reported animal bite v ictims are health, and public health professionals. Often the veterinar-
children. Dogs are responsible for the majority of reported ian (and sometimes a zoologist) must provide critical infor-
animal bite injuries to human beings in the United mation about the animal source of the bite, such as rabies
States, followed by cats and rodents.2 Bites from human risk status, whereas the public health professional may
beings are rarer. With the increasing popularity of exotic become involved in issues such as rabies prophylaxis and
pets, patients may present to emergency departments animal quarantine. As discussed in Chapter 12, animal bites
with bites from a wide range of species. In addition to are a major occupational risk of veterinarians, their staff,
trauma, infection (Color Plate 10-7) and envenoma- and other animal workers. This section covers key aspects of
tion (see Chapter 8) can be major concerns with animal management and prevention of animal bites as well as bites
bites. Animal bites can also result in allergy and anaphy- by human beings.
laxis, which might be immediate or delayed (e.g., ana-
phylaxis has been reported after rodent bites and horse
bites, even when the patient had a history of only mild Key Points for Clinicians and Public Health
allergic symptoms in the past3,4). In addition, the v ictim Professionals
and/or animal owner might experience psychological
trauma associated with either the bite incident itself or
the consequent decisions that must be made regarding
the biting animal. Animal (especially dog) bite fatalities • Be aware of rabies risk in the community and be avail-
in human beings are uncommon but occur at the rate of able for consultation with clinicians on postexposure
1 to 2 dozen each year in the United States.5 prophylaxis.
Animal bites are common in companion animals and • Provide public education to avoid feeding or handling
livestock as well (Figure 10-19), and fatalities in animals can wild or stray animals.
occur if they are not systematically reported. The initial care • Support community animal control efforts.
• Educate families to never leave a child alone with an
animal.
• Be aware of educational resources for animal bite preven-
tion, such as:
• Humane Society of the U.S. (HSUS): http://www.hsus.
org/pets/pet_care/dog_care/stay_dog_bite_free/index.
html
• CDC: http://www.cdc.gov/ncipc/duip/biteprevention.
htm (Box 10-5)
• AVMA: http://www.avma.org/press/publichealth/dog-
bite/messpoints.asp.
• US Postal Service: http://www.usps.com/communica-
tions/community/dogbite.htm.
A
• Provide information on bite prevention to patients with
animals and families with children.
• Counsel pregnant women and immunocompromised
persons to avoid contact with rodents.
• Counsel patients on first-aid procedures to be taken in
the event of a bite injury and to seek medical care for all
bites.
• In caring for animal bite injuries, take a complete history
regarding the animal, circumstances of the bite, history of
B allergies, and rabies and tetanus risk. Documentation that
includes a drawing or photograph of the wound may be
Figure 10-19 n A, This goat was attacked by dogs. Note bite wound helpful because of legal implications.
on the ventral neck area. B, At postmortem, the skin has been removed to
show the extensiveness of the injury; note tracheal defects and muscle lacer-
• Systematically evaluate the need for antibiotic, rabies, and
ations. (From Fubini SL, Ducharme N: Farm animal surgery, St Louis, 2004, tetanus prophylaxis, consulting with veterinary and pub-
Saunders Elsevier. Courtesy John King, Cornell University.) lic health professionals as necessary.
Box 10-5 CDC Recommendations for Dog-Bite Prevention
Things to Consider Before You Get a Dog • Immediately seek professional advice (e.g., from veterinarians,
• Consult a professional (e.g., veterinarian, animal behaviorist, or animal behaviorists, or responsible breeders) if the dog
responsible breeder) to learn about suitable breeds of dogs for develops aggressive or undesirable behaviors.
your household.
• Dogs with histories of aggression are inappropriate in households Preventing Dog Bites
with children. • Teach children basic safety around dogs and review regularly.
• Be sensitive to cues that a child is fearful or apprehensive about • Do not approach an unfamiliar dog.
a dog and, if so, delay acquiring a dog. • Do not run from a dog and scream.
• Spend time with a dog before buying or adopting it. Use • Remain motionless (e.g., “be still like a tree”) when approached
caution when bringing a dog into the home with an infant or by an unfamiliar dog.
toddler. • If knocked over by a dog, roll into a ball and lie still (e.g., “be
• Spay or neuter virtually all dogs (this frequently reduces aggressive still like a log”).
tendencies). • Do not play with a dog unless supervised by an adult.
• Never leave infants or young children alone with any dog. • Immediately report stray dogs or dogs displaying unusual
• Do not play aggressive games with your dog (e.g., wrestling). behavior to an adult.
• Properly socialize and train any dog entering the • Avoid direct eye contact with a dog.
household. Teach the dog submissive behaviors (e.g., • Do not disturb a dog who is sleeping, eating, or caring for puppies.
rolling over to expose abdomen and relinquishing food • Do not pet a dog without allowing it to see and sniff you first.
without growling). • If bitten, immediately report the bite to an adult.
From Centers for Disease Control and Prevention: Dog bite prevention. http://www.cdc.gov/ncipc/duip/biteprevention.htm.
• Consider allergic, envenomation, and posttraumatic stress

complications of an animal bite. MANAGEMENT OF ANIMAL BITE INJURY IN
• Consider whether other family members or other human HUMAN BEINGS
beings are at risk.
• Consult public health officials regarding the need for Prevention
rabies postexposure prophylaxis in particular bite
situations. Many animal bites can be prevented through avoidance
of high-risk situations. Table 10-8 lists some risk factors
for human animal bites from dogs and cats. These include
Veterinary Clinicians factors affecting animal aggressiveness, characteristics of
• Counsel pet owners to appropriately socialize and train bitten human beings, and characteristics of injury events.
pets to be well mannered. Risk factors for animal aggressiveness include female gender
• Counsel clients and staff on proper handling precautions in cats and male gender (especially unneutered) in dogs as
to minimize the risk of animal bites to human beings (see well as particular dog breeds. Human victims of dog bites
Box 10-5). tend to be younger than victims of cat bites. Bite injuries are
• Counsel clients and staff on proper first-aid to minimize often associated with particular types of aggressive behavior
the risk of animal bite infection. in the biting animal. These include dominance aggression,
• When dealing with animal behavioral problems such in which an animal assert its social dominance over another
as aggression, fears, and phobias, assess risk of bites animal (such as a child) that it perceives as being weaker
to human beings and whether modifications to the (e.g., members of a wolf pack) and possessive aggression, in
animal environment or handling practices are indicated which an animal attacks to prevent an object such as a toy or
or whether animal should be euthanized. food being taken away.
• Assist human health care providers in indentifying Education about reduction of animal bite risk can be
specific zoonotic disease risks from particular animal incorporated into preventive health care counseling by both
species. human health clinicians and veterinarians. Dog bite pre-
• Neuter pets and practice preventative medicine (e.g., vention recommendations by the CDC are summarized in
ensure all dogs, cats, and ferrets are current with rabies Box 10-5. Other preventive steps include avoiding feeding or
vaccination). handling wild or stray animals (see Exotic and Wildlife Pets
• Counsel cat owners to keep their pets indoors and in this chapter), and keeping companion animals indoors
dog owners to disallow their pets to hunt or garbage except for daily, accompanied exercise.
feed.
• Provide booster rabies vaccine to pets with animal bite
History
wounds from known or suspected rabid animals and
work with local public health officials concerning man- The clinician caring for a human victim of an animal bite
agement for potential rabies exposure. should determine and document in the chart how, where, and
• Test pet cats with bite wounds for FeLV/FIV at time of when the bite occurred; the species and distinguishing char-
presentation and again 6 months later.6 acteristics of the animal; whether the bite was provoked or
Table 10-8 n Epidemiologic Characteristics Associated With Dog- and Cat-Related Bites or Scratches
Characteristics of Cats and Dogs Exhibiting Aggression
Cats Dogs
Age Insufficient data <5 years (49%)

Sex Female (67%) Male (70%-79%)
Ownership status Stray (57%) Owned (a significant number of these aggressive dogs
live in a household with at least one child)
Reproductive status Insufficient data Intact (not neutered)
Size Insufficient data Large dogs (>50 lb)
Breed Insufficient data Total annual number of bites: mixed breed and German
Shepherds
Bite rates: German Shepherds and Chow-Chows
Highest rate of severe or fatal bites: Staffordshire Terriers
(pit bulls), German Shepherds, Chow-Chows
Characteristics of People Injured by Cats and Dogs
Age 25-34 years <20 years, with significant occurrence in those 5-9 years
Sex Females (59%) Males (62%)
Relationship to animal Victim does not own cat Victim is family member or acquaintance to the owners.
Dog owners are most frequently bitten by dogs but
not necessarily their own dogs (family’s dog, 30%;
neighbor’s dog, 50%)
Characteristic of the Injury Event (Common Scenario)
Kinds of aggression Fear-related aggression, play aggression, Dominance aggression, possessive aggression, fear-
redirected aggression, “biting and petting related aggression, protective/territorial aggression,
syndrome” punishment-induced aggression, pain-elicited
aggression
Time of year May through August (warm weather) May through August (warm weather)
Time of day 9:00 am to noon Late afternoon
Other factors If the cat is owned, 50% of the victims are the Unusually high incidence of bites by chained dogs who
owners are restrained on their own property
Typical wound 80% of all bites require medical attention 20%-60% of all bites require medical attention
characteristics
50% of all wounds become infected Insufficient data on number of wounds that become
infected
29% of all cat-bite victims return to doctor 5% of all dog-bite victims return to doctor after initial
after initial visit because of complications visit because of complications
Wounds consist of scratches (70%); punctures Wounds consist primarily of puncture and tears to
(27%) and tears (3%) to finger (21%), arm extremities (76%) and to face (15%). 70% fatal injuries
(18%), foot or leg (8%), face or neck (7%); to children <9 years. Highest death rate to neonates
and multiple body locations (3%) (<1 month old). Death rates of neonates 295/100
million; for children 1-11 months, 47/100 million.
Location of Bite Wounds (% Bites)
Face, scalp, or neck 2 16
Trunk 0 2
Shoulder, arm, or forearm 23 12
Hand 63 50
Thigh or leg 9 16
Feet 3 4
From Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier.
unprovoked; whether the animal is available for observation; For human beings bitten by an animal, it may be worth-
its current location; and relevant veterinary information while to draw a diagram or take a photograph of the wound
about the animal, including rabies vaccination status or any because many animal bites result in litigation. Children
other known illnesses. bitten on the neck or head should have cervical immobiliza-
It is also necessary to determine the date of the human tion until cervical fractures can be ruled out by radiological
patient’s most recent tetanus vaccination and any history of studies.7
medical conditions placing them at increased risk of infec-
tion, such as immunocompromised conditions (e.g., HIV), Wound Culture
cancer, diabetes, splenectomy, or immunosuppressive drugs.
A history of prosthetic joints or heart valves is also an impor- For fresh bite wounds, routine cultures are not necessary.
tant risk factor for complications in human beings.1 The However, if a wound later shows signs of infection such as
human patient should be asked about any allergies to animals redness, swelling, or discharge, cultures for both aerobic and
or medications. Finally, for both human beings and compan- anaerobic bacteria should be obtained (Figure 10-20).
ion animals, if considering rabies postexposure prophylaxis,
determine whether the patient has previously received rabies Initial Wound Care, Irrigation, and Debridement
vaccination, including where and when.
Table 10-9 lists risk factors for animal bite infections. If First-aid for an animal bite should involve control of
these risk factors are present, antibiotic prophylaxis appears bleeding and initial cleansing. Bleeding should be con-
reasonable. If none of these risk factors is present, antibio trolled with local pressure. Adequate cleaning and irriga-
tics may be withheld in many cases and the wound rechecked tion of a bite wound is critical to its management. Initial
in 48 hours. cleaning can be done immediately after the bite with
soap and water. As soon as possible, copious irrigation of
the wound with saline solution with an 18- or 19-gauge
Physical Examination
needle or catheter tip and large syringe should be per-
A careful head-to-toe physical examination should be performed. Many bite wounds involve damage to tissue at
formed looking for other signs of trauma. The wound should the wound edges. Therefore wound tissue that appears
be carefully explored to assess damage to deeper structures, devitalized or necrotic should be carefully debrided.1 In
including joints and bones. A detailed neurovascular exami- human patients, significant bites to the hand may require
nation should be performed to assess damage to nerves and reconstructive surgery, and a detailed examination for
blood vessels. possible injury to tendons, nerves, and other deeper
tissues is warranted. A hand surgeon may need to be
consulted, especially if there is any evidence of infection.
Table 10-9 n Risk Factors for Animal Bite If there are significant facial lacerations, a plastic surgeon
Infection consultation is appropriate.
High-risk species Cat

Nonhuman primate Radiographs
Reptile
Rat, other rodent If there is concern about involvement of joints and other
Rabies vector species (raccoons, bats, bony structures, including facial bones and the skull, take
skunks, foxes) radiographs (Figure 10-21) and obtain orthopedic consulta-
Animal appearing sick tion for possible surgical intervention.
Human being
Severity and Hands, feet, wrist, neck, genital area
location of bite Joints, bones
Severe bites (involving large area, deep
tissue structures, multiple bites)
Puncture wounds
Necrotic or poorly vascularized tissue
Wounds where primary closure has been
performed
Host factors Immunocompromising medical conditions
(e.g., HIV infection, FIV/FeLV infection,
cancer chemotherapy, diabetes,
steroids and other immunosuppressive
medications, malnutrition, alcoholism,
asplenia)
Prosthetic joints or heart valves
Infants or elderly
Other Delays (more than several hours) in
cleaning wound and seeking care
High degree of contamination (extensive Figure 10-20 n Cat-bite abscess of the wrist with presentation for care
contact with animal saliva or other delayed 1 month after injury. Pasteurella multocida was isolated in pure
infectious material) culture. (From Long SS, Pickering LK, Prober CG: Principles and practice of
pediatric infectious diseases, ed 3, Philadelphia, 2008, Saunders Elsevier.)
individuals and those with asplenia or compromising

medical conditions should receive prophylactic antibi-
otics for most animal bites. Table 10-10 provides recom-
mendations for empiric antibiotic dosing for animal bites
to human beings.
Dog bites usually do not become infected. Reported infec-
tion rates range from 5% to 15%.10 Cat bites often involve deep
puncture wounds that are prone to infection. Infection rates
from cat bites may be as high as 80%.11 The choice of anti-
microbial prophylaxis for cat bites and high-risk dog bites
should cover Pasteurella, Streptococcus, and Staphylococcus.
A 5- to 7-day course of antibiotics should be administered.
Ferret bites are increasing in frequency with their popularity
as pets and their tendency to bite. Little is known about their
microbial flora. Pig bites are considered to carry a high risk for
infection.12
Alligators and related species tend to inflict severe
Figure 10-21 n Radiograph of finger after a bite by a captive sub- bites and have polymicrobial flora that can lead to
adult Gila monster (Heloderma suspectum) after touching the lizard’s
tail. It took approximately 40 seconds to pry the reptile off with tongs. infection.13 Many snake bites do not become infected.7
Immediately after, the patient complained of “10 out of 10” pain. Shortly Two controlled trials of prophylactic antibiotics for pit
after, he developed swelling and redness extending to his mid-forearm, as viper envenomation did not show a clinical benefit.14,15
well as nausea and vomiting. A tooth was retained in the wound for more Nevertheless, snake bites should be monitored for poten-
than 2 months before it was spontaneously expelled. (From Auerbach PS:
Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier. Courtesy
tial infection.16 Iguana bites can be severe and infection
Sean Bush.) has been reported.17
Human bites to another human are considered
high-risk bites for infection. In addition to bacterial
Wound Closure pathogens (see Table 10-10), risk of infection with blood-
borne pathogens such as HIV and hepatitis B should be
Whether to close an animal bite wound with sutures or considered.
other technique is controversial. Considerations include
risk factors for infection and cosmetic impact of the injury.
Dog bites to the face rarely become infected and are often Vaccinations
closed to reduce the possibility of disfiguring scars. Wounds
that are at high risk of infection (e.g., from a high-risk spe- Rabies Postexposure Prophylaxis
cies, in a high-risk area such as the hand, or in an immuno- The risk of rabies should be assessed in every animal
compromised patient), are more than 24 hours old, or that bite situation in a human or pet, with rabies postexpo-
are already infected generally should not be closed. Low- sure prophylaxis (PEP) for high-risk bites provided. 18
risk wounds can be closed, after thorough irrigation, with However, studies have shown that rabies PEP is often
sutures, staples, or other techniques and observed closely for given inappropriately by clinicians treating bites in
signs of infection.8 emergency care settings, such as when the biting animal
is low risk or available for observation or testing (see
Antibiotic Prophylaxis and Therapy Chapter 9).19 The biting animal should be captured and
monitored for 10 days for signs of rabies if it is a dog,
Whether prophylactic antibiotics are indicated for an ani- cat, or ferret; for 14 days if livestock; or euthanized and
mal bite is also controversial, and data regarding the bites tested if a rabies vector species (e.g., bat, raccoon, skunk,
of many species are limited. A Cochrane review of anti- fox) or other wild carnivore such as a river otter (Figure
biotic prophylaxis in uncomplicated dog and cat bites 10-22). If animal rabies testing is positive or if the ani-
found no clear evidence of benefit.9 Clinical decision mal is not available for observation or testing and is a
making regarding antibiotic prophylaxis involves assess- high-risk rabies species, PEP should be provided to the
ing the risk of infection. Risk factors include the species patient.
responsible for the bite, any information about the health
of the animal, the severity and location of the bite, and
Tetanus
whether the patient is immunocompromised or has other
conditions that increase the risk of infection. High-risk Tetanus status should be determined in all human bite
bites include crush injuries that involve devascularized patients. A booster should be provided for a low-risk bite if
tissue and puncture wounds, hand involvement, signifi- the patient was not vaccinated within the past 10 years and
cant edema, possible involvement of joints or bones, and for a high-risk bite if the patient was not vaccinated within
proximity to genitalia or prosthetic joints nearby. Patients the past 5 years. If there is not a history of at least 3 teta-
with very high-risk bites or evidence of tenosynovitis or nus vaccinations in the past (for an adult), tetanus immune
deep infection should be admitted for parenteral antibi- globulin should also be given. Table 10-11 details these
otics and hospital observation. Immunocompromised recommendations.
Table 10-10 n Pathogens Complicating Animal Bites to Human Beings and Recommended Empiric
Therapy
Empiric Antibiotic Therapy
Species Reported Pathogens Primary Alternative
Dogs Usually polymicrobial, mixed aerobic and Amoxicillin-clavulanate Clindamycin 300 mg PO qid +
anaerobic organisms1 875/125 mg bid or fluoroquinolone (adults) or
Aerobic bacteria: Pasteurella (P. canis, P. 500/125 mg PO tid30 Clinda + Trimethoprim sulfa
multocida multocida, P. multocida septica), (children)30
Streptococcus spp. (S. immitis, S. mutans,
S. pyogenes), Staphylococcus (S aureus, S.
epidermidis, S. intermedius7), Moraxella,
Corynebacteria, Bergeyella zoohelcum,
Capnocytophaga spp.
Anaerobes: Fusobacterium, Bacteroides,
Porphyromonas, Prevotella1
Cats Often polymicrobial, mixed aerobic and Amoxicillin-clavulanate Cefuroxime axetil 0.5 gm
anaerobic organisms31 875/125 mg bid or PO q12 h or doxycycline
Aerobic bacteria: Pasteurella multocida 500/125 mg PO tid30; 100 mg PO bid; do not use
multocida, P. multocida septica, Streptococcus itraconazole cephalexin30
spp. (S. mitis, S. mutans), Staphylococcus (S.
epidermidis, S. warneri, S. aureus), Moraxella,
Corynebacteria, Bergeyella zoohelcum, Bacillus,
Capnocytophaga spp.
Anaerobes: Fusobacterium, Bacteroides,
Porphyromonas, Prevotella1
Sporothrix schenckii
Human beings Streptococcus viridans, Staphylococcus Early: amoxicillin-clavulanate Cefoxitin 2 g IV q8 h, or
epidermidis, Corynebacterium, 875/125 mg bid ×5 days ticarcillin-clavulanate 3.1 g
Staphylococcus aureus, Eikenella, Bacteroides, Infected: ampicillin/sulbactam IV q6 h or piperacillin-
Peptostreptococcus 1.5 g IV q6 h tazobactam 3.375 g IV q6 h
or 4-hour infusion 3.375 g
q8 h (x-rays for clenched fist
injuries)30
Ferrets Not well documented; consider rabies risk As for cat and dog bites32
Horses Pasteurella caballi , S. aureus, Neisseria, and
38
As for dog
other anaerobic gram-negative bacilli33
Sheep Actinobacillus, others33 As for dog
Rats Streptobacillus moniliformis (North America, Amoxicillin-clavulanate Doxycycline 100 mg PO bid
Europe), Spirillum minus (Asia), Leptospira 875/125 mg bid30
Pigs Polymicrobial: gram-positive cocci, gram- Amoxicillin-clavulanate Third-generation
negative bacilli, anaerobes, Pasteurella spp.30 875/125 mg bid30; some cephalosporin or ticarcillin-
recommend adding clavulanate or ampicillin-
ciprofloxacin34 sulbactam or imipenem30
Rabbits Pasturella multocida35 (rabies has been As for dog and cat
reported29)
Nonhuman primates Consider risk for herpes B virus (Herpes simiae) Valacyclovir Acyclovir26
(e.g., macaque)
Hamsters Francisella tularensis,36 Pasteurella spp. See rat
Reptiles (e.g., Pseudomonas aeruginosa, Proteus, Clostridium, Ceftriaxone (infected
iguanas, snakes, Bacteroides fragilis, Salmonella groups IIIa and wounds)30
alligators) IIIb,13,37 Serratia marescens17
Bats, raccoons, Staphylococcus and Streptococcus spp. (skin Amoxicillin-clavulanate Doxycycline 100 mg PO bid30
skunks, foxes flora) 875/125 mg bid or
500/125 mg PO tid30
Rabies virus Assess for rabies postexposure
prophylaxis
Seal Marine Mycoplasma (sealpox; see Chapter 12) Tetracycline ×4 weeks30
Figure 10-22 n Victim of river otter attack. (From Auerbach PS:

Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier. Photo cour-
tesy Jill Hanna.) Figure 10-23 n A toddler with facial cellulitis from Pasteurella multo
cida after a dog bite. (From Long SS, Pickering LK, Prober CG: Principles and
practice of pediatric infectious diseases, ed 3, Philadelphia, 2008, Saunders
Elsevier. Courtesy J. H. Brien.)
SPECIFIC BITE INFECTIONS
Clinicians should be familiar with a number of specific bite-

associated infections. bitten by peridomestic rodents. With the popularity of rats
as pets and the use of rats in laboratories, cases now occur
Pasteurella Infection in pet store employees, pet owners, and laboratory animal
workers. The disease causes a rash (Color Plate 10-8) that
Pasteurella multocida is the most common agent isolated from may be petechial, hemorrhagic, or purpuric, as well as fever,
infected dog and cat wounds (Figure 10-23). It causes cellulitis and systemic symptoms including arthralgias. Without
and can cause bacteremia with sepsis, meningitis, and hem- treatment, the case fatality rate can be 10%. Most domes-
orrhagic complications. Pasteurella wound infections tend tic and wild rats carry the causative agent, S. moniliformis,
to develop rapidly, producing swelling, redness, tenderness, in their oral flora. Up to an estimated 10% of rat bites can
and discharge at the wound area within 12 to 24 hours after become infected.21 Patients with rat bites need to be coun-
the bite.20 Tenosynovitis and osteomyelitis can develop and seled about the signs and seriousness of this disease, and
should be aggressively treated with parenteral antibiotics. prophylactic antibiotics should be considered for infection-
prone bites.
S. moniliformis in guinea pigs causes cervical lymphadeni-
Rat-Bite Fever
tis or granulomatous pneumonia; in mice, purulent lesions
Rat-bite fever from Streptobacillus moniliformis in human and acute septicemia; and endocarditis or septic arthritis in
beings was traditionally a disease of inner-city children nonhuman primates.
Table 10-11 n Indications for Tetanus Prophylaxis in Wounds
Clean, Minor Wound All Other Wounds*
History of Absorbed Tetanus Toxoid

(Doses) Tdap or Td† TIG Tdap or Td† TIG
Unknown or <3 Yes No Yes Yes

≥3 No‡ No No§ No
From Kretsinger K, Broder KR, Cortese MM et al: Preventing tetanus, diphtheria, and pertussis among adults: use of tetanus toxoid, reduced diphtheria toxoid and acellular per-
tussis vaccine recommendations of the Advisory Committee on Immunization Practices (ACIP) and recommendation of ACIP, supported by the Healthcare Infection Control
Practices Advisory Committee (HICPAC), for use of Tdap among health-care personnel, MMWR Recomm Rep 55(RR-17):1, 2006.
*Such as, but not limited to, wounds contaminated with dirt, feces, soil, and saliva; puncture wounds; avulsions; and wounds resulting from missiles, crushing, burns, and
frostbite.
†Tdap is preferred to Td for adults who have never received Tdap. Td is preferred to TT for adults who received Tdap previously or when Tdap is not available. If TT and TIG
are used, tetanus toxoid absorbed rather than tetanus toxoid for booster use only (fluid vaccine) should be used.
‡Yes, if ≥10 years since the last tetanus toxoid–containing vaccine dose.
§Yes, if ≥5 years since the last tetanus toxoid–containing vaccine dose.
Capnocytophaga Infection Sporotrichosis

Capnocytophaga canimorsus is found in dog and cat saliva Sporotrichosis is a fungal disease (Color Plate 10-9) that
(especially the former). In asplenic and immunocompromised can produce ulcerating skin nodules and systemic infec-
human beings, it can produce septicemia with meningitis, tion (rare). It is usually acquired from contact with plants
endocarditis, and eye involvement.22 Serious infections have or soil but has been reported in association with cat bites
also been reported in persons with no apparent risk factors.23 and scratches (with an outbreak of more than 1000 cats
The first known animal with a Capnocytophaga-infected dog and 500 persons in Brazil27) and after a squirrel bite.28
bite wound, a pet rabbit, was successfully treated.24 Veterinarians are at increased risk of occupational infec-
tion. Sporothrix schenckii has also been reported in horse
and dog lesions.
Herpes B Infection
Herpes B infection causes an often fatal viral meningo- Cat-Scratch Fever
encephalitis that can be transmitted to human beings
from Old World monkeys of the genus Macaca (Figure Bartonella infection can be transmitted by cat bites and
10-24; see Chapter 12). 25 Although there have been no scratches (see Chapter 9).
controlled trials of prophylaxis, the B Virus Working
Group recommends antiviral prophylaxis for high-risk
bites (or other exposures) from these monkeys. The
recommended prophylactic regimen is 1 g valacyclovir MANAGEMENT OF BITES IN ANIMALS
three times a day for adults, excluding pregnant women.
An alternative regimen is 800 mg acyclovir five times a As in human beings, immunocompromised conditions
day. Prophylaxis should begin as soon as possible after (such as FIV/FeLV in feline patients) predispose an animal
exposure. If signs of herpes B infection appear, sys- to bite-related infection. Pet dogs, cats, and ferrets that are
temic treatment with antivirals and hospitalization are bitten by potentially or known rabid animals should be
necessary. 26 managed according to their rabies vaccination status. If
they are currently vaccinated, a booster vaccine should be
immediately administered and the pet should be observed
Lymphocytic Choriomeningitis for 45 days for signs of rabies. If the pet is unvaccinated, it
LCMV can be present in the saliva of rodents, especially should be euthanized or held in strict isolation for 180 days
mice, and can pose a risk after a bite (see Chapter 9). Fetal and provided a rabies vaccine 1 month before release from
complications can occur in pregnant women and severe quarantine. Certain domestic animals such as rabbits are at
disease in immunocompromised persons. Therefore pregnant risk of wildlife rabies if caged outside or allowed to roam
women and immunocompromised individuals should avoid outside.29
rodent exposure. Table 10-12 provides recommended antibiotic therapy
for animal bite infections in dogs and cats. Depending on
the severity of the bite, other treatment modalities, including
physical therapy, may be required for rehabilitation of the
animal (Figure 10-25).
Figure 10-24 n A lower lip ulceration in a rhesus monkey caused by

herpes B virus infection. (From Mandell GL, Bennett JE, Dolin R: Principles Figure 10-25 n Cat relaxing on ball after surgery to repair dog bite
and practice of infectious diseases, ed 6, New York, 2005, Churchill Livingstone wound. (From Gaynor JS, Muir WW 3d: Handbook of veterinary pain
Elsevier.) management, ed 2, St Louis, 2008, Mosby Elsevier.)
Table 10-12 n Recommended Therapy for Bite Infections in Cats and Dogs
Drug Species Dose (mg/kg) Route Interval (hr) Antibacterial Spectrum
Amoxicillin-clavulanate D 10-20 PO 8 Most gram-positive and gram-negative

aerobes and anaerobes; first-choice
D 13.75 PO 12 drug for most bite wounds
C 10-20 PO 12
Ampicillin (amoxicillin) B 22 PO 8 Some gram-positive and gram-negative
aerobes
B 11-22 SC, IV 6–8
Ticarcillin D 20-50 IV 6–8 Gram-positive and gram-negative
aerobes and anaerobes
Cefotaxime B 15-30 IV, IM, SC 6–8 Sepsis from bite wounds caused by
gram-negative aerobes or anaerobes
Doxycycline D 5 PO, IV 12 Some aerobes and anaerobes;
mycoplasmas
Clindamycin B 5-11 PO 8–12 Gram-positive aerobes and anaerobes
Enrofloxacin D 5 PO, SC 12–24 Gram-negative aerobes
Difloxacin D 5-10 PO 24 Gram-negative aerobes
Orbifloxacin D 2.5-7.5 PO 24 Gram-negative aerobes
Marbofloxacin D 2-4 PO 24 Gram-negative aerobes
Azithromycin D 20 PO 24 Gram-positive aerobes; mycoplasmas
and mycobacteria
Chloramphenicol D 25-50 PO, IV, IM, SC 8 Some anaerobes; variable with gram-
positive and gram-negative aerobes
Metronidazole B 10 PO, IV 8 Anaerobes
From Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier.
D, Dog; C, cat; B, dog and cat; PO, by mouth; SC, subcutaneous; IV, intravenous; IM, intramuscular.
References 13. Hertner G. Caiman bite. Wilderness Environ Med. 2006;

17(4):267–270.
1. Taplitz RA. Managing bite wounds. Currently recommended antibiot- 14. Kerrigan KR, Mertz BL, Nelson SJ, et al. Antibiotic prophylaxis for
ics for treatment and prophylaxis. Postgrad Med. 2004;116(2):49–52, pit viper envenomation: prospective, controlled trial. World J Surg.
55–56, 59. 1997;21(4):369–372.
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2008;19(1):7–14. 16. Wu CH, Hu WH, Hung DZ, et al. Snakebite complicated with Vibrio
3. Guida G, Nebiolo F, Heffler E, et al. Anaphylaxis after a horse bite. vulnificus infection. Vet Hum Toxicol. 2001;43(5):283–285.
Allergy. 2005;60(8):1088–1089. 17. Hsieh S, Babl FE. Serratia marcescens cellulitis following an iguana bite.
4. Lim DL, Chan RM, Wen H, et al. Anaphylaxis after ham- Clin Infect Dis. 1999;28(5):1181–1182.
ster bites—identification of a novel allergen. Clin Exp Allergy. 18. Manning SE, Rupprecht CE, Fishbein D, et al. Advisory Committee on
2004;34(7):1122–1123. Immunization Practices Centers for Disease Control and Prevention:
5. Garth AP, Harris NS. Bites, animal. http://www.emedicine.com/emerg/ Human rabies prevention—United States, 2008: recommendations of
topic60.htm. Accessed April 16, 2009. the Advisory Committee on Immunization Practices. MMWR Recomm
6. Journal of the American Veterinary Medical Association. 2001 Feline Rep. 2008;57(RR-3):1–28.
practitioners recommend new FIV and FeLV testing guidelines, initi 19. Conti LA, Wiersma S, Hopkins R. Evaluation of state-provided rabies
ate public awareness campaign. http://www.avma.org/onlnews/javma/ post-exposure prophylaxis (PEP), Florida, July-September 1997 and
apr01/s041501g.asp. Accessed April 16, 2009. July-September 1998. Southern Med J. 2002;95(2):225–230.
7. Morgan M. Hospital management of animal and human bites. J Hosp 20. Kristinsson G. Pasteurella multocida infections. Pediatr Rev. 2007;28(12):
Infect. 2005;61(1):1–10. 472–473.
8. Auerbach PS. Wilderness medicine. 5th ed. Philadelphia: Mosby Elsevier; 21. Elliott SP. Rat bite fever and Streptobacillus moniliformis. Clin Microbiol
2007. Rev. 2007;20(1):13–22.
9. Medeiros IM, Saconato H. Antibiotic prophylaxis for mammalian bites. 22. Jolivet-Gougeon A, Sixou J-L, Tamanai-Shacoori Z, et al. Antimicrobial
Cochrane Database Syst Rev. 2001;(2):CD001738. treatment of Capnocytophaga infections. Int J Antimicrob Agents.
10. Moran GJ, Talan DA, Abrahamian FM. Antimicrobial prophylaxis for 2007;29(4):367–373.
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11.Louisiana State University School of Veterinary Medicine. What you 24. van Duijkeren E, van Mourik C, Broekhuizen M, et al. First documented
should know about animal bites. http://www.vetmed.lsu.edu/animal_ Capnocytophaga canimorsus infection in a species other than humans.
bites.htm. Vet Microbiol. 2006;118(1–2):148–150.
12. Barnham M. Pig bite injuries and infection: report of seven human 25. Andersen E. B virus—the risks in monkey business. AAOHN Journal.
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Group. Recommendations for prevention of and therapy for expo- Med. 1998;16(3):425–427.
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28. Saravanakumar PS, Eslami P, Zar FA. Lymphocutaneous sporotrichosis 35. Silberfein EJ, Lin PH, Bush RL, et al. Aortic endograft infection
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29. Eidson M, Matthews SD, Willsey AL, et al. Rabies virus infection in a 36. Centers for Disease Control and Prevention (CDC). Tularemia
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Foodborne Illness
11
The Centers for Disease Control and Prevention (CDC) esti- health and animal health practice and require increased
mates that each year in the United Sates 76 million persons cooperation and communication across disciplines. This
experience foodborne illness, leading to 300,000 hospital- chapter presents a systems approach to foodborne illness
izations and 5000 deaths. Although most of these cases are at different levels of the food chain and outlines principles
attributable to infectious etiologies, exposure to foodborne of the evaluation and management of foodborne illness in
toxins occurs as well.1 Companion animals are also believed human beings and other animals.
to commonly experience foodborne illness, with signs including
acute gastritis or diarrhea, although the actual incidence of
animal foodborne illness is not known.
Professionals
In the United States the Foodborne Diseases Active
Surveillance Network of the CDC (FoodNet) performs
active surveillance for nine pathogens in selected states
(Campylobacter, Cryptosporidium, Cyclospora, Listeria,
Salmonella, Shiga toxin–producing Escherichia coli [STEC] • Educate farmers, retailers, and consumers about food
O157, Shigella, Vibrio, and Yersinia). Clinicians can access safety at all stages of the food production chain (see
recent reports at http://www.cdc.gov/FoodNet/reports. National Food Safety Programs at http://www.food-
htm. Despite ongoing prevention efforts on the part of safety.gov).
both public health and agricultural health authorities, the • Support preventive strategies such as hazard analysis
rates of Campylobacter, Listeria, Salmonella, Shigella, STEC and critical control point process principles.
O157, Vibrio, and Yersinia infections do not appear to have • Support food sustainability measures.
declined in recent years, whereas the rate of cryptosporidi- • Ensure that local farms and retailers comply with food
osis has increased. The rate of Salmonella infection was the safety guidelines.
furthest from public health goals. It is clear that controlling • Consider cases of disease in food industry workers
or eliminating foodborne illness will require comprehensive as potential sentinel events for inadequate preventive
efforts from farm to fork.2 The production of safe, healthy measures.
food for the expanding world population has increased the • Support uniform standards and practices across fed-
complexity and globalization of the process. There are multi- eral, state, and local levels.
ple potential interactions between human and animal health • Educate human health and veterinary care providers
at a number of steps of the food chain (Table 11-1). regarding the detection and reporting of foodborne
Dog and cat food sales were close to $17 billion in the illness in human beings and animals.
United States in 2008 (Figure 11-1).3 Although many human
health care providers may be unaware of the magnitude of
the pet food industry, the human health relevance of food-
borne illness in companion animals is becoming more evi- • Consider foodborne illness in all patients presenting
dent. Human outbreaks of salmonellosis have been linked with gastrointestinal symptoms or unexplained fever.
to contact with contaminated pet food. Similarly, the out- Take adequate history of food-related exposures.
break of melamine contamination in human infant formula • In evaluating a patient with suspected foodborne ill-
in China was presaged by an outbreak of disease in cats and ness, ask whether other human beings or animals in
dogs traced to a similar melamine contamination of pet food the vicinity are also sick.
imported from the same country. • Report suspected cases of foodborne illness to the
Clearly, then, food safety and foodborne illness are issues health department.
that human health and animal health care providers can- • If diagnosing foodborne illness in a farm worker or
not ignore. They cross any artificial barriers between human food industry worker, provide that information to the
331
Table 11-1 n Risks Along the Food Chain

Level Risks to Animals Risks to Human Beings Preventive Steps
Animal feed, manure, and Direct poisoning or infection, Occupational exposure through Limit use of antibiotics,
other animal waste for antibiotic resistance handling of feed or manure hormones, and pesticide
plant crops treatments in feed; use
appropriate water source;
safely handle of livestock
wastes
Farm and field Infection in animals, Occupational exposure to Farm management,
animal-animal transmission infected animal, animal-human veterinary surveillance,
transmission traceback, occupational
surveillance
Harvest and processing NA Occupational exposure to Personal protection,
infected animal; animal- pasteurization, refrigeration,
human transmission through occupational surveillance of
butchering, handling processor workers
Retail NA Occupational exposure to Personal protection
infected meat handling, live
animal market exposures
Consumer Pet food contaminated with Meat and dairy products Home and food safety
infectious or toxic agents or contaminated with infectious or practices and recalls;
low-level antibiotic; hormone toxic agents; low-level antibiotic; clinicians and public health:
exposures hormone exposures; vegetables, detect and investigate
grains, or fruit contaminated sentinel events, traceback
with pathogens or chemicals
NA, Not applicable.
local health department to consider whether other two concepts are interrelated. Animal feed may include both
workers or animals may be at risk. plant and animal products, and plant fertilizer may contain
• Counsel patients about food safety in the home for livestock manure and other animal wastes.7 At this stage of
human beings and companion animals (Box 11-1). the production chain, the health risks are primarily to the
food animals, with some risk also to agricultural workers
• In evaluating an animal with suspected foodborne
illness, ask whether other animals or nearby human
beings are also sick.
• Consider contacting the local or state health depart-
ment regarding suspected cases of foodborne illness in
animals.
• Counsel clients about food safety in the home for
companion animals and human beings (see Box 11-1).
RISKS ALONG THE FOOD CHAIN
Foodborne risks and food safety can be thought of concep-

tually in terms of a chain of production from animal feed or
plant fertilizer to consumer.4,5 At each stage in the chain there
are certain risks for both human beings and other animals. At
each stage are also opportunities for prevention and control.
The Center for Veterinary Medicine of the Food and Drug
Administration (FDA) has recommended applying hazard
analysis and critical control point (HACCP) principles to the
food manufacturing processes to detect and reduce risks.6
Animal Feed and Plant Fertilizer

The first stage of food production involves supplying safe Figure 11-1 n Bipedal posture used to request food. (From Beaver BV:
feed for food animals and safe fertilizer for plant crops. The Feline behavior, ed 2, St Louis, 2003, Saunders Elsevier.)
Chapter 11 n Foodborne Illness 333
Box 11-1 Food Safety in the Home for Human

Beings and Animals28
The core four practices:

1. Clean: Wash hands and surfaces often.
2. Separate: Do not cross-contaminate!
3. Cook: Cook to proper temperature.
4. Chill: Refrigerate promptly.
Other human-animal food safety points:
• Wash hands after handling pets, pet food, and food and water
bowls.
• Do not wash pet food or water dishes in the sink or dishwasher
where human dishes are washed.
• Do not feed pets raw meat or unpasteurized milk products.
Figure 11-2 n Open-mouth breathing in a 5-year-old cow. (From Divers

directly handling animal feed and fertilizer. Risks to animals TJ, Peek SF: Rebhun’s diseases of dairy cattle, ed 2, St Louis, 2008, Saunders
include both toxic and infectious agents. Examples of toxic Elsevier.)
exposures have included dioxin contamination in pigs8 and
poultry; exposure of cattle to the fire retardant PBB (poly- known as silo filler’s disease. This is also a risk for livestock
brominated biphenyl) through inadvertent contamination housed near silage; outbreaks of respiratory disease and death
of feed; and heavy metal poisoning from cadmium, lead, in cattle from silo gases have been reported (Figure 11-2),
or mercury contamination of fertilizers applied to crops potentially providing warning to human beings of the toxic
and pastures.9 Infectious agents threatening the human and risk (see Chapter 12).14
animal food supply include bovine spongiform encephalopa- A number of measures can be implemented to prevent
thy, which appeared in cattle and other animals after being disease at the level of feed and manure production. In the
fed meat and bone meal prepared from animals infected case of bovine spongiform encephalopathy, banning the use
with transmissible spongiform encephalopathy (TSE) (see of animal protein for cattle feed effectively reduced the inci-
Chapter 9). This risk has been greatly reduced through ani- dence of new cases of the disease. Similarly, weighing the risks
mal feeding bans. Less clear cut are the risks from the use of and benefits of feed additives that include hormones and
antibiotics and hormones in animal feed. Such additives may antibiotics is an ongoing assessment process between agri-
be used to reduce infection and increase meat or dairy prod- cultural and public health agencies. Inspections of animal
uct production (growth promoters).10 There is evidence that feed can further improve the safety at this stage.
these practices can increase the development of antibiotic- On a clinical level, surveillance for sentinel disease in both
resistant pathogens.11 However, most animals treated with farm animals by veterinarians and workers handling feed
such agents show no ill effects and may have increased meat and manure by occupational medicine professionals can
and dairy product output. detect emerging problems at this stage of the food produc-
Not all animals who have ingested either toxicants or tion chain.
infectious agents show evidence of disease and therefore
may pass the risks along the food production chain. A patho- Farm and Field
gen that has proved difficult to control is Salmonella, many
strains of which are adapted to a wide number of animal In the farm environment, animal-animal, animal-human,
hosts (see Chapter 9). There is evidence that Salmonella may and human-animal transmission of infectious agents can
enter the food supply chain through rendered animal protein occur. In addition to the feed and manure exposures listed,
used as animal feed.6 environmental exposures (e.g., water, mosquitoes, and other
Occupational exposure to animal feed and manure fertil- vectors) and contact with wildlife can introduce pathogens
izers can result in disease in agricultural workers and persons into the food chain if meat is consumed raw or undercooked
engaged in small-scale (backyard) food production. Manure or if dairy products are unpasteurized. For example, a recent
used as fertilizer on fields may come from animals who shed multistate outbreak of salmonellosis in Serrano peppers was
pathogens in their feces. Such contaminated feces can then traced to contaminated irrigation water in Mexico.15 Rift
be a risk to workers. For example, contact with infected Valley fever is an example of a vector-borne disease in which
chicken manure for use in a backyard garden has been linked infected cattle can then pose an occupational risk to abattoir
to a fatal human case of avian influenza.12 Commercial (slaughterhouse) workers.
farm workers who have direct contact with infected human At this stage of the food production chain, preventive care
or animal wastes used as fertilizer on crops may also be at by veterinarians is crucial to improved herd health and also
risk of infection.13 Another hazard of animal feed to work- improved public health for both workers and future con-
ers is allergic and other reactions to grain, which can include sumers. Early detection, prevention, and treatment of disease
“farmer’s lung,” grain mite allergy, and endotoxin exposure in herds are key. Agricultural extension services and other
(see Chapters 7 and 12). Stored silage can be a source of toxic veterinary preventive services can encourage improved bio
nitrogen dioxide. This gas forms nitric acid when in contact security in farming methods that reduce potential for disease
with the respiratory mucosa and creates acute lung damage, outbreaks.
Harvest and Processing and fruit (e.g., raspberries with Cryptosporidium)23 have been
contaminated with pathogens from animal manure, there is
When animals are slaughtered and processed for human some risk of retail workers becoming sickened by handling
and pet consumption, any pathogens that have entered the such produce.
food chain can be spread to contaminate other carcasses and A special case of retail exposure is the live animal mar-
pose a risk to abattoir workers and butchers. Meat inspec- ket, many of which exist even in developed countries such
tion at this point often may involve both veterinary and as the United States. In these markets animals of different
agricultural professionals as well as public health inspec- species are often housed in the same or immediately adja-
tors. Occupational medicine professionals and other human cent cages, allowing pathogen spread among species and to
health clinicians can play an important role in providing human beings. In addition, contamination of such markets
medical surveillance of abattoir workers and detecting sen- with feces, feathers, and other animal waste can be an indi-
tinel cases of disease that have implications for both animal rect source of exposure for market workers (as well as con-
and human health. sumers visiting the markets). Animal slaughter taking place
Although most processing of animal meat in industrial- in such markets exposes workers to the same pathogens faced
ized countries occurs in specialized facilities with infection by workers in abattoirs but with less potential for biosecurity
control policies and adequate refrigeration, food animals in measures.
other countries are slaughtered in backyards or households, Agricultural agencies have an important role to play in
farmyards, or open air markets. In these settings biosecurity such markets by veterinary surveillance of live animals and
is low, meat inspection and refrigeration are often not avail- animal products. Workers in such markets should also receive
able, and the potential for infection consequently is greater. ongoing medical surveillance for infectious diseases as well
In addition, hunting for subsistence bushmeat consump- as training in risk reduction measures. The occurrence of a
tion as well as hunting of deer, waterfowl, and other game zoonotic disease in a market worker is sometimes an impor-
often involves both slaughter and dressing of the wild animal tant sentinel health event indicating the presence of risk for
carcass in a field or other improvised location. Such activities, diseases such as avian influenza. Unfortunately, such workers
even in developed countries, may take place without avail- may not be included in ongoing preventive programs.
ability of running water or the use of gloves or other types
of personal protection. Transmission of simian viruses has Consumer
been documented in bushmeat hunters,16 and toxoplasmosis,
tularemia, and brucellosis have been reported in U.S. hunters By the time that food is prepared and served for consump-
who field-dressed their carcasses without personal protection in the home or restaurant, it has ideally been monitored
tion. In these informal settings there is generally no process all along the food production chain to reduce the chance of
of organized inspection or medical surveillance of at-risk causing illness. The fact that outbreaks tied to residential
individuals. Recently there has been a call for improved sur- and restaurant food consumption continue to occur makes
veillance of bushmeat hunters17 to detect emerging patho- it clear that food may contain pathogens as well as certain
gens and other foodborne diseases that could trigger disease toxicants. For example, in 2007, 9% of sampled chicken
outbreaks in human beings. Occupational medicine sur- broilers, 17% of ground turkey, and 26% of ground chicken
veillance of farmers and workers in processing facilities and samples were positive for Salmonella.24 The USDA Food
marketing retail chains can help detect sentinel health events Safety and Inspection Service (FSIS), through its Pathogen
in human beings (e.g., a Q fever or brucellosis outbreak),18 Reduction: Hazard Analysis and Critical Control Point (PR/
indicating the presence of the disease in the livestock as well HACCP) rule, has set a priority of reducing the prevalence of
and a likely problem with food safety (see Chapter 12). Salmonella in broiler chicken carcasses.
To reduce the possibility of disease transmission, dairies Pet foods also can contain significant contamination. This
generally use pasteurization methods on waste milk fed to can pose a risk to both the pet as well as the owner who handles
calves. Although milk pasteurization for human consump- the food. For example, a multistate outbreak of Salmonella was
tion occurs at the farm level in farms that produce milk traced to dry dog food.25 Outbreaks in North America have
and milk products, most U.S. dairies ship milk for human also been tied to pet treats, including pig ears and dried beef.26
consumption to processing plants, where it is pasteurized Salmonella-contaminated pet food has also been shown to
and then shipped to distributors.19 Pasteurization prac- persist as a contaminant on the surface of dog feed bowls, pos-
tices may vary between farms and regions. Although there ing an ongoing environmental infection risk.27
is a consumer market for unpasteurized dairy products, Because food entering the home must therefore be
which are considered by some to be more “natural,” such assumed to possibly contain foodborne pathogens, food
products have resulted in a number of foodborne illness safety measures in the home are critical (Figure 11-3). These
outbreaks.20,21 also need to involve pet food and pet food dish handling.
A number of Web sites provide guidelines to consum
ers regarding safe food handling and preparation, includ-
Retail
ing http://www.foodsafety.gov, http://www.fightbac.org,
In the retail sector, handling of meat carries a risk of patho- and http://www.cdc.gov/healthypets. The Partnership for
gen exposure similar to that faced by workers in abattoirs, Food Safety’s Fight Bac program to reduce risk of bacte
although exposures tend to be lower and reported disease rial contamination of foods includes four basic steps: clean,
cases are fewer. If vegetables (e.g., peppers contaminated separate, cook, and chill.28 These four steps are explained
with Salmonella and spinach contaminated with E. coli)22 in Box 11-1.
Botulism
Botulism is caused by seven different toxins (types A-G) pro-
duced by Clostridium botulinum, an anaerobic spore-forming
bacteria. The bacteria are found in soil as well as the digestive
tract of a wide range of mammals, fish, and birds. Foodborne
illness can occur when spores germinate in carcasses and
decaying vegetation and the bacteria begin producing toxin,
which is then ingested. Alternatively, ingesting spores could
lead to intestinal toxin production—or wound infection can
occur, leading to bacterial growth and toxin production. The
toxin causes muscle paralysis, which can result in respiratory
failure. Most botulism in animals is due to type C, whereas
type A is more common in human beings. Cattle become
sick from eating contaminated feed (Figure 11-4). Massive
die-offs can occur in waterfowl. Dogs are relatively resistant
but can occasionally develop weakness.39
Clostridial Food Poisoning

Clostridium perfringens is a gram-positive sporogenic bacil-
lus that produces extracellular toxins. There are several
types of C. perfringens (A-F). C. perfringens type A is found
in soil and as normal flora in the gastrointestinal tract of
human beings and other animals. When allowed to grow in
Figure 11-3 n A pregnant woman washing an apple to avoid acquir- food that is not adequately cooked or refrigerated, C. per-
ing a possible foodborne illness. (From Centers for Disease Control and fringens type A produces an alpha toxin that can cause acute
Prevention Public Health Image Library, Atlanta, Ga. Photo courtesy James foodborne illness in human beings marked by diarrhea and
Gathany.) abdominal discomfort. Clostridial food poisoning from
type A toxin is not well described in animals, but types B,
Clinicians have an important role to play in the detec- C, D, and E can cause infection and hemorrhagic enteritis
tion of outbreaks of foodborne disease. Detection of such in calves, sheep, pigs, and other livestock.36 There is some
disease can lead to improved treatment outcomes for the evidence that C. perfringens infection can cause diarrhea
animals and human beings, link to other reported cases, and in dogs and cats.35,45 C. perfringens type A is being increas-
allow for traceback to discover the source of common-source ingly recognized as a cause of necrotizing enteritis in
outbreaks. chickens.46
Listeriosis
SPECIFIC FOODBORNE ILLNESSES
Listeria monocytogenes is a gram-positive coccobacillus
Because of public health interventions of sewage treatment, bacterium found in soil and the intestines of a wide range
water disinfection, and milk pasteurization, previously com- of animals, including mammals, birds, fish, and insects.
mon foodborne illnesses such as typhoid fever, cholera, and Contaminated food, including pasteurized dairy products,
bovine tuberculosis are rarely reported in the United States. undercooked meat, and drinking water, can be a source of
However, vigilance must be maintained as emerging pathogens infection for human beings. Human infection during preg-
are now recognized as causing foodborne illness (e.g., Vibrio nancy can cause miscarriages, stillbirth, and neonatal sepsis.
vulnificus, E. coli) O157:H7, and Cyclospora cayetanensis).29 Older and immunocompromised individuals can develop
Clinicians should always maintain a heightened aware- meningitis and other complications. It also can cause enceph-
ness of foodborne illness in both human beings and other alitis, vomiting, septicemia, and neonatal death in ruminants
animals. A key point is that susceptibility to particular food- (Figure 11-5).36
borne illnesses varies significantly between species. For some
conditions such as staphylococcal food poisoning, it is not Staphylococcal Food Poisoning
clear that animals are susceptible. Therefore it is unlikely
that both human beings and animals would be affected in an Staphylococcus aureus is a gram-positive bacterium that is
outbreak. In other situations, such as melamine contamina- part of the microbial flora of the skin, nose, and throat in a
tion of food, both animals and human beings have shown wide range of animals, including human beings (see Chapter 9).
susceptibility and outbreaks in animals have provided warn- When food is contaminated with a toxin-producing strain
ing about human risk. Table 11-2 lists the clinical presenta- of S. aureus, a toxin is produced that is heat resistant and
tion of a number of specific agents in human beings and can cause the rapid onset of nausea, vomiting, cramping, and
other animals. Several of these agents are covered in Chapters diarrhea. Animals do not appear to be susceptible to staphy-
8 and 9. Others are described in the following paragraphs. lococcal food poisoning.39
336
Table 11-2 n Presentation and Management of Selected Foodborne Illnesses in Human Beings and Other Animals
Incubation Period
Agent (Human Beings)1 Human Beings Dogs Cats Other Animals Principles of Treatment
Bacteria
Campylobacter jejuni 2-5 days Diarrhea, cramps, fever Diarrhea, usually mild, possibly with mucus or Calves: diarrhea with Supportive care,
(neurologic sequelae blood (enteritis is more common in young blood and mucus, antibiotics in severe
may occur) animals) fever cases
Chick hatchlings: acute
enteritis and death
Clostridium botulinum 12-72 hours Usually type A, B, or Rare; usually type Type C reported after Waterfowl and Supportive treatment,
(botulism toxin)30 E: vomiting, diarrhea, C, possibly type eating contaminated other bird die-offs gastric lavage,
cranial nerve signs D (after eating bird or fish carcasses31 (especially type Botulinum antitoxin
(diplopia, blurred contaminated bird C; also A or E): given early
vision), muscle or fish carcasses): paralysis, drowning
weakness cranial nerve Horses: type C and B
involvement, Cattle: type C and D:
weakness weakness, drooling,
incoordination
Clostridium perfringens 8-16 hours Watery diarrhea, Clostridial food poisoning not well described; Calves, lambs: Food poisoning in human
(preformed toxin)32 abdominal pain (toxin infection possible33-35 hemorrhagic beings: supportive care
produced by type A enteritis (types B, C, Treat animals with clinical
growing in food) D, and E)36 signs
Chickens: necrotic
enteritis (types A
and C)
Escherichia coli O157:H7 1-8 days Severe diarrhea, Acute enteritis, Cattle, sheep, goats, Supportive care, monitor
possibly bloody; idiopathic cutaneous pigs, deer, poultry hematologic and renal
vomiting, abdominal vasculopathy of do not have clinical status
pain; hemolytic Greyhounds signs
uremic syndrome may
develop
Enterotoxigenic E. coli 1-3 days Watery diarrhea, Supportive care,
cramps, vomiting antibiotics often not
needed
Listeria 9-48 hours (invasive Neonatal sepsis, Rare: generalized Not reported Septicemia, abortion, Antibiotics
disease after 2-6 miscarriage, stillbirth, neurologic signs37; encephalitis, mastitis
weeks) meningitis tonsillitis reported38 in ruminants
Salmonella 1-3 days Diarrhea, fever, Malaise, fever, diarrhea, Fever without Pregnant, young, and Supportive care,
vomiting abortion diarrhea, abortion lactating animals are antibiotics for
most susceptible sepsis and S.
typhi, S. paratyphi,
extraintestinal infection
NSAIDs to decrease the
effects of endotoxemia
Staphylococcus aureus 1-6 hours Vomiting, nausea, Animals do not appear to be susceptible to staphylococcal food Supportive care
(toxin) cramps; possible poisoning39
diarrhea and fever
Yersinia enterocolitica 24-48 hours Abdominal pain Subclinical infection Supportive care,
(yersiniosis) (pseudoappendicitis), antibiotics for invasive
fever, diarrhea, disease
vomiting
Parasites
Taeniasis 8-12 weeks Abdominal discomfort, Animals resistant to infection with adult parasite40
bloating, anal
discomfort
Cryptosporidium 2-10 days Watery diarrhea, cramps, Usually subclinical Calves 1-3 weeks old Supportive care,
nausea most susceptible; antibiotics for severe
diarrhea, weight loss cases; hyperimmune
bovine colostrum in
calves
Giardia 1-2 weeks Diarrhea, cramps, Puppies, kittens, calves, and lambs may have diarrhea, poor haircoat, Antibiotics fenbendazole,
bloating flatulence, weight loss albendazole,
metronidazole
Toxoplasma 5-32 days Flulike illness, Generalized infection Usually subclinical Abortion in sheep, Supportive care
lymphadenopathy, in puppies and hogs, and goats; and antibiotics in
severe disease in immunocompromised fever and dysphagia pregnancy and
immunocompromised dogs, fever, weight immunocompromised
individuals loss, diarrhea, individuals (antibiotics
encephalitis do not destroy
bradyzoites or eliminate
infection)
Trichinella 1-2 days for initial signs Variable; possible fever, Mild vomiting, diarrhea Mild vomiting, diarrhea42 Antibiotics mebendazole
and symptoms muscle pain, eye or albendazole in
swelling, diarrhea41 human beings;
mebendazole or
fenbendazole in dogs42
Toxicants
Chapter 11
Lead (see Chapter 8) Acute or chronic Abdominal pain, Vomiting, anorexia Removal from exposure,
weakness chelation in severe
cases
Melamine and other Renal failure in infants Renal toxicity43
protein additives fed contaminated
n
formula
Foodborne Illness
Vomitoxin Minutes to hours Headache, nausea, Vomiting, anorexia44 Cows, sheep, pigs: Supportive care
vomiting fever, abortion44
NSAIDs, Nonsteroidal antiinflammatory drugs.
337
gastroenteritis to septicemia and abdominal pain that can

mimic appendicitis. Yersinia appears to only rarely cause
disease in animals; enteritis has been reported in a number
of species.36
Taeniasis/Cysticercosis
Cestode tapeworms Taenia solium (pork tapeworm) and
T. saginata (beef tapeworm) cause a unique foodborne ill-
ness in that human beings are the definitive host for these
parasites. Infected human beings with adult tapeworms
in their intestine may have few symptoms but can release
gravid proglottids in feces, which then release eggs. If
human beings have defecated in pastures or other areas
frequented by swine or cattle, the animals can become
Figure 11-4 n An adult cow with generalized weakness from botulism. infected through ingestion of the tapeworm eggs. When
She was one of several that became affected when a new grass silage that had
not been properly fermented was fed. The cow was recumbent for nearly
ingested by animals, the tapeworms form larval cysts
30 days but recovered with supportive care. (From Divers TJ, Peek SF: (cysticerci) in tissues. Human beings can become infected
Rebhun’s diseases of dairy cattle, ed 2, St Louis, 2008, Saunders Elsevier.) by eating undercooked pork or beef (Figure 11-6).
Veterinary inspection in slaughterhouses can reduce the
risk of human infection.
Yersiniosis
Symptoms in human beings include abdominal pain,
Yersinia enterocolitica is a gram-negative rod that is classi- nausea and bloating, and anal discomfort. Infection with
fied in the same genus as the agent of plague (Yersinia pestis; T. solium is more common in developing countries where
see Chapter 9). Many animals carry Yersinia in their intes- human beings live closely with swine, and is rare in developed
tinal flora and shed bacteria in their feces. Human beings countries where intensive swine rearing prevents access of
can become infected by ingesting contaminated water or swine to human feces. Infection with T. saginata from under-
food. Often the source of infection is not clear, but pigs are cooked beef is more widely distributed.
believed to be the reservoir for many human infections. Cysticercosis infection in human beings occurs when
Occupational groups such as butchers may be at increased human beings ingest viable eggs of T. solium that have been
risk. Yersinia infection in human beings can range from mild shed in human feces (Figure 11-7). The most serious compli-
cation of human infection is neurocysticercosis. Symptoms
include headache, psychiatric disturbances, and seizures.
Ocular involvement and painful muscle cysts can also
occur.40 Cysticercosis infection in pigs is usually subclinical.
Dogs will occasionally manifest signs of neurocysticercosis
that can resemble rabies.40
Trichinellosis
Trichinellosis is a foodborne disease caused by parasitic
roundworms of the genus Trichinella, including T. spiralis
(found in pigs and rodents; Figure 11-8), T. murelli (found
in wild game), and T. nativa (found in bears, foxes, wolves,
walrus, and other cold-climate mammals).39 Most human
cases are from consumption of undercooked meat. Infection
can produce muscle swelling, pain, and headache. In severe
cases encephalitis can develop. Although pigs and many
other animals show no signs of infection, dogs and cats may
show vomiting, diarrhea and, in rare cases, muscle stiffness
and muscle pain.42
The fact that the encysted larval form can be detected by
microscopic inspection of muscle tissue allowed nineteenth-
century researchers to link trichinellosis to the consumption
of pork and the development of veterinary control over the
slaughter of animals for food consumption.47
Control measures include education of consumers about not
eating raw meat, inspection of both domestic meat and relevant
Figure 11-5 n Vomiting and depression were the most noticeable clinical wild game meat such as wild boar, prohibitions on feeding ani-
signs in this adult cow with listeriosis. (From Divers TJ, Peek SF: Rebhun’s mal carcasses or raw waste to swine, and prevention of contact
diseases of dairy cattle, ed 2, St Louis, 2008, Saunders Elsevier.) between domestic swine and infected rodents or wildlife.48
Figure 11-6 n Life cycle of Taeniasis (pork and beef tapeworm) infection. (From Centers for Disease Control
and Prevention, Laboratory of Parasites of Public Health Concern, Atlanta, Ga.)
Vomitoxin as whether the diarrhea is bloody or contains mucus (a

sign of large-bowel disease). The clinician should inquire
Vomitoxin (deoxynivalenol) is a trichothecene mycotoxin about any other symptoms, including neurologic signs.
found in moldy grain. Because it is heat stable, it will persist A detailed food and exposure history should be obtained,
even after cooking. It is a widespread contaminant in grain including whether the patient has visited farms, petting
supply and is particularly associated with fungal infection zoos, what type of pets are owned (especially asking about
in the field. It can cause vomiting and anorexia in animals, reptiles, puppies, kittens, ducklings, and any animals with
including cattle, hogs, dogs, and cats. Its effects on human diarrhea), any current health problems, consumption
beings are not well understood but are believed to include of unpasteurized dairy products, recent travel, day care
nausea and vomiting. center exposures, camping trips or other exposure to
untreated water, attendance at events where food was
served, and whether any persons with similar exposures
EVALUATION OF SUSPECTED FOODBORNE also have symptoms.
ILLNESS
Physical Examination
History
Determine the degree of dehydration and whether hospi-
In taking a history from a patient with suspected food- talization for intravenous hydration is indicated. Particular
borne illness, it is important to determine when symptoms attention should be paid to the abdominal exam and whether
began, the particular constellation of symptoms, and a surgical consult should be obtained.
whether any other human beings or animals in the vicin-
ity are experiencing illness. The reported time interval
Laboratory Tests
between exposure and illness onset, as well as the pattern
of symptoms, can help the clinician sort through the When foodborne illness is suspected in human beings, appro-
differential diagnosis. priate lab testing supports the diagnosis, yet hospitals and
The presence or absence and the volume of vomiting, laboratories may vary in their testing protocols. If the patient
diarrhea, and hematuria should be determined, as well is immunocompromised or has fever, bloody diarrhea, severe
Figure 11-7 n Lifecycle of cysticercosis. (From Centers for Disease Control and Prevention, Laboratory of
Parasites of Public Health Concern, Atlanta, Ga.)
abdominal pain, or severe or persistent illness, or if fecal leu- If a particular food is suspected to be the cause of illness,
kocytes are present, fecal cultures are indicated.49 Many labo- samples should also be obtained and submitted for culture
ratories limit fecal culture screening to Salmonella, Shigella, (and possible toxic analysis). The public health department
and Campylobacter species. If infection with Vibrio, Yersinia, should be able to assist with such analysis.
or E. coli O157:H7 is suspected, it may be necessary to contact
the laboratory to arrange special culture media or incubation.
If diarrhea is chronic or does not respond to antimicrobial EVALUATION OF SUSPECTED FOODBORNE
therapy or there is a suggestive history of travel or other risk ILLNESS IN ANIMALS
factors (such as immunocompromised status or an ongoing
outbreak), fecal examination should include testing for para- The veterinarian evaluating an animal with suspected
sitic infection. foodborne illness should ask the caretaker about routine
Blood cultures should be obtained if septicemia is sus- foods eaten (including animal treats and food “toys”) and
pected. Samples of vomitus may be obtained in particular whether unusual foods have been eaten recently. Whether a
cases, such as suspected toxic ingestion. cat or dog is allowed to roam outside and could have eaten
REPORTING OF FOODBORNE ILLNESS
Because foodborne illnesses occurring in a human or animal

can signal a problem with food safety affecting potentially
large populations, it is essential that cases be reported in a
timely manner to the appropriate public health author-
ity. Infection with Salmonella, Shigella, E. coli O157:H7,
other Shiga toxin–producing E. coli, hemolytic uremic syn-
drome (HUS), and hepatitis A are reportable almost every-
where in the United States. Infection with other pathogens
may also be reportable.50 The CDC’s Foodborne Disease
Outbreak Response and Surveillance Team conducts national
surveillance for outbreaks and assists states in investigations.
A number of national and international reporting mecha-
nisms are in place in addition to the FoodNet system previ-
ously described. Many foodborne pathogens are reportable
to local and state health departments (see Chapter 13). The
GeoSentinel system of the International Society of Travel
Medicine, in cooperation with the CDC, reports on illnesses
occurring in travelers, including foodborne illness. The
World Health Organization is working to strengthen the
Figure 11-8 n Trichinella spiralis cyst in a fresh squash preparation of
capacity of its member states in the surveillance and control
pork muscle (magnification ×160). (From Bowman DD: Georgi’s parasitol- of major foodborne diseases.
ogy for veterinarians, ed 8, 2003, St Louis, Saunders Elsevier.) Private veterinary practitioners can become certified
through a voluntary accreditation program with the USDA to
control exported animal diseases from entering another state
garbage, an animal carcass, or a source of toxins such as or country.51 The certification of animals for national and
mushrooms should also be determined. A history of any international movement is one important part of veterinary
other animals or nearby human beings with clinical illness accreditation. Accredited veterinarians work cooperatively
should also be obtained. In addition to asking about signs with federal veterinarians and state animal health officials
of diarrhea, anorexia, and vomiting, the veterinarian should and are the backbone of many U.S. regulatory programs for
also inquire about muscle weakness and spasms, which could livestock and poultry diseases. All veterinarians are required
indicate neurologic involvement. to report animal cases of disease of agricultural impor-
tance that are notifiable or foreign to the state veterinarian
Physical Examination or USDA veterinarian. This information is then compiled at
the national level through the USDA National Animal Health
The physical examination should always include a careful Policy and Programs staff or through the National Animal
abdominal exam to palpate for masses, distension, and ten- Health Reporting System maintained by the USDA.52 Many
derness, which could indicate obstruction. states also require selected diseases in animals to be reported
to the public health system to prevent human disease from
Laboratory Tests occurring (see Chapter 13). The World Organization for
Animal Health (OIE) tracks reports of disease outbreaks in
As with the evaluation of human beings, the choice of labo- animals with trade and food safety implications. OIE mem-
ratory testing depends on the clinical scenario. Feces can be ber countries are required to report to the OIE the status of
submitted for bacterial culture as well as for parasites if sus- OIE reportable diseases in their country and on events that
pected. A fecal enterotoxin assay by enzyme-linked immuno- may require immediate reporting. Veterinarians diagnosing
sorbent assay is available.42 In particular situations, samples animals with suspected disease that could pose a risk to other
of food, blood, or vomitus may be submitted for analysis. animals or people should contact their state veterinarian,
state public health veterinarian, or USDA veterinarian.
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23. Smith HV, Caccio SM, Cook N, et al. Cryptosporidium and Giardia as Adv Parasitol. 2006;63:367–439.
foodborne zoonoses. Vet Parasitol. 2007;149(1–2):29–40. 48. Gamble HR, Bessonov AS, Cuperlovic K, et al. International Commission
24. United States Department of Agriculture Food Safety and Inspection on Trichinellosis: recommendations on methods for the control of
Service. Progress report on Salmonella testing of raw meat and poultry Trichinella in domestic and wild animals intended for human consump-
products, 1998–2007, 2008 http://www.fsis.usda.gov/science/progress_ tion. Vet Parasitol. 2000;93(3–4):393–408.
report_salmonella_testing/index.asp. Accessed April 20, 2009. 49. American Medical Association, et al. Diagnosis and management of
25. Centers for Disease Control and Prevention. Multistate outbreak of human foodborne illnesses: a primer for physicians. MMWR Recomm Rep.
Salmonella infections caused by contaminated dry dog food—United 2001;50(RR-2):1–69.
States, 2006–2007. MMWR Morb Mortal Wkly Rep. 2008;57(19):521–524. 50. Centers for Disease Control and Prevention. Reporting a foodborne
26. Centers for Disease Control and Prevention. Human salmonellosis asso- illness—healthcare professionals. http://www.cdc.gov/foodborneout-
ciated with animal-derived pet treats-United States and Canada, 2005. breaks/reporting_professionals.htm. Accessed July 14, 2008.
MMWR. 2006;55:702–705. 51. United States Department of Agriculture. Animal and Plant Health
27. Weese JS, Rousseau J. Survival of Salmonella Copenhagen in food bowls fol- Inspection Service: Veterinary accreditation. http://www.aphis.usda.gov/
lowing contamination with experimentally inoculated raw meat: effects of animal_health/vet_accreditation. Accessed July 14, 2008.
time, cleaning, and disinfection. Canadian Veterinary J. 2006;47(9):887–889. 52. United States Department of Agriculture. Animal and Plant Health
28. Partnership for Food Safety Education. Safe food handling. http://www. Inspection Service: Animal health monitoring and surveillance. http://
fightbac.org/content/view/6/11/. Accessed July 14, 2008. www.aphis.usda.gov/vs/ceah/ncahs/nahrs. Accessed July 14, 2008.
Occupational Health of
Animal Workers 12
Ben Hur P. Mobo, Peter M. Rabinowitz, Lisa A. Conti, and Oyebode A. Taiwo
Some of the most intensive human-animal interactions occur animals in public settings to ensure that the guidelines of
in the occupational setting. Animal workers may encounter the National Association of Public Health Veterinarians
hundreds to thousands of animals each day, which increases (NAPHV) for Animals in Public Settings (http://www.
the risk of exposure to biological, physical, and chemical haz- nasphv.org/Documents/AnimalsInPublicSettings.pdf)
ards. In recent years a number of emerging infectious diseases are being followed. This will help protect both the
have first appeared—as deadly outbreaks among workers public and workers in such settings.
with animal exposures. In addition to zoonotic disease risks,
high rates of allergic disease, physical injuries, and psycho- Human Health Care Providers
logical stress have also been reported in animal handlers.
Many animal workers in both developing and developed • Ask patients whether they work with animals. If they
countries are not enrolled in formal occupational safety and do, assess their occupational risks.
health programs or may receive medical care from human • If asked to provide medical services (such as a pre-
health care providers who are not familiar with the occupa- placement physical) for a worker with animal contact,
tional risks these workers face. consider contacting the veterinarian responsible for
Veterinarians have a special role to play in the development the health of the animals in the workplace to discuss
of occupational safety and health strategies for animal work- specific occupational risks.
ers because they are intimately familiar with animal diseases • When evaluating a worker with an animal-related expo-
and the necessary procedures involved in animal care and sure (e.g., bite, scratch, mucous membrane contact),
handling. Therefore improving occupational health and safety ensure that all potential zoonotic pathogens are being
among animal workers represents a global health challenge considered in the risk assessment and that prophylac-
that will require increased communication and cooperation tic medication is started as necessary if indicated.
between human health and animal health care providers. • When evaluating animal workers with acute or chronic
This chapter outlines the occupational health hazards illnesses, including asthma, dermatitis, and other aller-
that animal workers encounter, presents a One Health team gic conditions, determine whether work exposures
approach to worker health and safety that involves both could play a causative role.
human and animal health professionals, and suggests pre- • If contracting to provide occupational health services to
ventive health programs for particular worker groups. a group of workers with animal contact, employ a team
approach to preventive care. The team should ideally
include the veterinarian providing care to the animals as
well as experts in exposure reduction such as an infec-
tion control/biosafety specialist and/or an industrial
Professionals
hygienist. This team approach will help ensure that rel-
evant health risks in the workplace are being identified
and addressed with adequate preventive services, includ-
ing engineering controls, training, vaccination, postex-
• Identify occupational groups in the community that posure protocols, and surveillance.
have significant exposures to animals and work to • Counsel immunocompromised and pregnant workers
educate them, local medical providers, and veterinary about particular risks of animal handling.
providers to ensure they receive appropriate preventive • Safeguard the confidentiality of any medical informa-
health services. tion about animal workers, including medical records
• Work with local petting zoos, county fairs, pet stores, and any information regarding immunocompromising
and other organizations involved in human contact with conditions.
343
The components of an occupational health approach are

simple and adaptable to a wide range of work settings. They
• If managing a clinical practice, ensure that policies and involve identification and control of hazardous exposures,
procedures are in place so that veterinary staff receive medical services such as careful screening of workers at base-
adequate preventive health services. line, vaccination, surveillance of workers’ health, identifica-
• If providing veterinary services to a facility such as a tion of sentinel health events, and management of necessary
zoo, animal shelter, research laboratory, or pet store, work restrictions and work-related problems. Although such
advise management about the need for adequate pre- preventive services may be viewed by some employers as an
ventive health services for the animal workers. unnecessary expenditure of resources, they can be cost effec-
• Help inform human health care providers in the tive in the long run by preventing potentially compensable
community who will be performing preplacement and work-related illness and injury and promoting worker well-
follow-up examinations of workers about the occupa- being. Box 12-1 illustrates this approach.
tional health risks and needs of animal workers.
• Respect the confidentiality of any medical informa-
tion about animal workers, including medical records OCCUPATIONAL HEALTH TEAM
and any information regarding immunocompromised
individuals. Because of the diversity of the hazards encountered by animal
workers, providing effective occupational health services to
such workers is best accomplished through a team approach.
TYPES OF ANIMAL WORKERS Such a team can include a medical provider to provide
screening and management of medical problems, a veteri-
More than 2 million people in the United States are engaged narian who is familiar with zoonotic disease risks, industrial
in a wide range of occupational activities that involve hygienists to identify and evaluate hazardous exposures and
animals.1 These include approximately 750,000 persons help devise engineering and work practice controls to reduce
involved with livestock confinement; 500,000 involved with them, and biosafety/infection control specialists to focus on
dairy farming2; 200,000 workers employed in animal care zoonotic disease transmission risks. Figure 12-1 diagrams
and services as kennel attendants, groomers, stable hands, the ideal components of an occupational health team that
zoo keepers, and animal trainers3; and 125,000 research- provides preventive health care to animal workers.
ers and animal handlers involved with laboratory animal Actively involving a designated human health care pro-
research.4 Globally, as much as 49% of the world’s popula- vider in an occupational health approach for animal work-
tion is estimated to be involved in agriculture, which often ers also has many advantages. Such involvement can lead to
involves animal husbandry and animal-associated health the medical provider becoming more knowledgeable about
risks.5 Some of these workers are formally employed in full- the specific health risks faced by animal workers. Ongoing
time positions in animal-related care and may receive pre- communication between the medical provider and the vet-
ventive health services (such as described in this chapter) erinarian helps ensure that injured workers are properly
through their workplace. However, many individuals who managed, workers at increased risk of illness (e.g., immuno-
work part-time or full-time with animals may receive lit- compromised persons) and injury are adequately counseled,
tle or no preventive health services related to their work and preventable hazards in the workplace are identified and
exposures. For example, staff at pet swap meets, pet store addressed.
employees, volunteers at zoos and county fair animal exhib- Veterinarians can play key roles in an occupational health
its, wildlife rehabilitators, wildlife biologists, volunteer ani- team. The veterinarian is the source of knowledge about rel-
mal rescue workers, individuals engaged in home slaughter evant animal diseases and the necessary procedures of ani-
of animals for family consumption, and subsistence (bush- mal handling and typically has regular contact with the
meat) hunters may all face significant “occupational” health animals, the workplace, and the animal workers. In animal
risks related to their contact with animals, yet may never research facilities, the veterinarian is often the administrative
receive preplacement examinations, prophylactic vaccina-
tions, or follow-up surveillance examinations to prevent or
detect work-related disease. If they do see a medical pro-
vider for care of a work-related injury or illness, that medi- BOX 12-1 Components of Occupational Health
cal provider may not be aware of the range of health risks Approach to Workplace Health Hazards
these workers face, and therefore the treatment or recom-
mendations for prevention may not be optimal. • Hazard identification
• Hazard control using hierarchy of controls
• Preplacement screening of workers
OCCUPATIONAL HEALTH APPROACH • Preventive vaccines and training
• Medical surveillance
The majority of occupational health services in the United • Acute injury/illness management; identification of sentinel
States are provided by family physicians and other clinicians health events
without specialized training.6 However, when using a team • Management of work restriction, job modification, and return
to work
approach these individuals can learn to provide adequate
• Confidential management of records and medical information
occupational health services to animal workers.
Chapter 12 n Occupational Health of Animal Workers 345
Human health
Veterinarian
care provider
Animals Sentinel
Animal
Work practices health event
Work worker
(illness or injury)
environment
Industrial Infection control/

hygienist biosafety specialist
Figure 12-1 n Occupational health team for animal workers.
s upervisor of the animal care workers. In veterinary hos- Biological Hazards

pitals the veterinarian may be both the chief clinician and
Allergens
the practice director. For wildlife rehabilitation facilities,
animal shelters, zoos, and many other settings, the consult- As discussed in Chapter 7, many animal proteins are poten-
ing veterinarian may be the principal point of contact with tial allergens in human beings. Although guinea pigs, mice,
the medical providers as well as the chief source of medical rats, and cats are common causes of allergy, virtually any
information about occupational health and safety hazards of species, including primates, larger domestic animals (such as
the workplace. The veterinarian may be the health profes- horses and cattle), and reptiles can also pose an allergic risk
sional who is most familiar to the workers and with whom to workers.7,8 Exposure to insects such as roaches, flies, and
the workers have established a trusting relationship. The vet- mites as well as insect parts, shellfish (e.g., snow crabs, king
erinarian may also be in regular contact with the employer or crab, lobster, shrimp, scallops), and fish species (e.g., salmon,
worksite supervisor and be able to advocate for the provision trout, pilchard, anchovy, hake) has also been associated with
of occupational health services for the workers. For all these allergic reactions.9 Other animal-related sources of allergens
reasons the veterinarian may be the most appropriate pro- in the workplace include molds and thermophilic bacteria
fessional to assemble and help lead the occupational health that infect animal foods (including hay and prepared animal
team as well as ensure that the services provided to workers food) and cause asthma, rhinitis, dermatitis, and hypersensi-
are appropriate for the work setting. tivity pneumonitis.10
Industrial hygienists have training in the identification In addition to animal allergens, other allergen expo-
and engineering control of a wide range of workplace sures for animal workers may include latex gloves, allergenic
hazards, including chemical, physical, and biological agents. chemicals such as disinfecting agents (e.g., glutaraldehyde),
Consultation from such individuals can help an occupational other cleaning agents and detergents, and organic dusts (e.g.,
health team design safe strategies for the handling of hazard- red cedar shavings used as animal bedding).
ous chemicals such as cleaning agents and anesthetic gases, Not surprisingly, allergic reactions are a well-recognized
control of noise, and methods to reduce dust exposures that health problem among animal workers.11 In some set-
can cause allergy and infection. tings almost half of animal workers have been reported
Infection control and biosafety specialists are profes- to develop allergy-related symptoms such as rhinitis,
sionals who specialize in the prevention of infectious dis- conjunctivitis, asthma, contact urticaria, and other types of
ease transmissions in workplaces and other settings. They allergic dermatitis.1,4,12,13 Risk factors for developing aller-
can play a consulting role in the occupational health team gic responses to antigens include the intensity and duration
by identifying specific infectious disease hazards and help- of exposure to specific antigens4,13 and a history of atopy
ing design strategies to reduce both animal-animal and (allergic predisposition).14 Allergic exposures can pose a
animal-human transmission of disease. This may involve difficult problem for sensitized workers because even low
the design of ventilation systems and work policies such as levels of exposure to an allergen may provoke a response
disposal of infectious waste and use of personal protective in a previously sensitized individual. In addition, personal
equipment. protective equipment may not adequately protect them
from further allergic reactions.
HAZARD IDENTIFICATION Zoonotic Pathogens

Animal workers face a wide number of potential occupa- As described in Chapter 9, a large number zoonotic patho-
tional health hazards that can be classified as biological, gens can pose a hazard to animal workers, who generally
chemical, physical, or psychosocial. These hazards and their have increased exposures to zoonotic diseases compared
control are listed in Table 12-1. with the general public. Many of these individual zoonotic
TABLE 12-1 n Occupational Hazards Encountered by Animal Workers and Relevant Hierarchy of
Control Strategies
Administrative/ Work Personal Protective

Hazard Elimination Substitution Engineering Controls Practice Controls Equipment
Biological
Allergens, Eliminate Work with Adequate ventilation Avoid wearing street Masks/respirators,
endotoxin particular different in work areas; clothes while working gloves, gowns to
allergenic species/ reduce dust with animals1; perform reduce allergen
source gender with generation; clean animal manipulations in exposure
less allergenic frequently; reduce safety hood if possible;
potential; animal density job modification or
substitute restriction for sensitized
bedding employees
material that is
less allergenic
or dusty
Zoonoses41 Vaccinate or Work with Nonporous surfaces; Written infection control Gloves, sleeves
otherwise different appropriate use plan; hand hygiene; when handling
eliminate disease species with of disinfectants; bite and other injury fluids, infected
in animals less zoonotic separation of prevention; worker animals, necropsy,
(preventive potential patient areas from vaccination; restrict dental procedures,
veterinary care) staff break areas; eating and drinking in resuscitation,
physical isolation care areas; consider job obstetrics, diagnostic
of sick animals; modification/restriction specimens, tick
disposal containers for immunocompromised removal
for infectious or pregnant workers Facial protection for splash
waste; needlestick or spray
prevention devices Respirator use for
abortions, poultry
deaths, other aerosol risk
Footwear and head
cover when gross
contamination is
suspected
Pathogenic Prevent bats Control aerosolized Warn workers of risk Disposable footwear and
fungi and birds from dust, disinfect clothing, respirator
roosting in contaminated use, gloves
buildings material, dispose of
waste safety
Live vaccines Avoid use of live Substitute Needlestick Needlestick prevention Gloves, sleeves, leg
vaccines vaccine with prevention systems, training, avoid recapping coverings
less risk to sharps disposal needles, report exposures;
human beings containers use tick repellant, perform
frequent tick checks
Arthropods Control mites, Use of tick repellant, Protective clothing
ticks, fleas in frequent tick checks
animals
Physical
Bites, crush Avoid acquiring Substitute less- Rooms, corrals with Allow only trained Impermeable gloves for
injuries dangerous dangerous adequate exits individuals near certain tasks
animals animals dangerous or large
animals; bite prevention
Lifting animals, Design ergonomic Training in injury Footwear selection
carrying heavy solutions prevention; housekeeping
loads (mechanical lifts, training and maintenance
storage solutions
that reduce need
for lifting)
Slip, trip, and fall Eliminate fall risks Floor material Control access to areas
selection with slippery environment
and provide appropriate
signage
Continued
TABLE 12-1 n Occupational Hazards Encountered by Animal Workers and Relevant Hierarchy of
Control Strategies—cont’d
Administrative/ Work Personal Protective
Hazard Elimination Substitution Engineering Controls Practice Controls Equipment
Noise Eliminate noisy Substitute Noise shielding/ Motivate/train regarding Hearing protection
machines less-noisy barrier use of hearing protection;
machines or limit time in noisy areas
processes
Radiation Eliminate need for Substitute Appropriate Training in radiation safety, Use of sunscreen,
on-site x-rays, equipment radiologic housing sun exposure protection; protective clothing,
other radiation with less facility restrict access to and radiation shielding
radiation radiologic facilities (lead gowns, gloves,
hazard etc.)
Chemical
Anesthetic gases Substitute Adequate scavenging Follow MSDS with Gloves, respirators when
less-toxic systems chemical-specific indicated
compounds guidelines
Disinfectants, Substitute safer Adequate ventilation Safety policies to restrict Gloves, respirators when
cleaners, chemicals when cleaning; safe use to trained individuals indicated
pesticides application systems
Nitrogen Silage management, Safety policies regarding Air respirators, other
dioxide, H2S, manure entry into silos, manure respirators as indicated
ammonia management storage areas
(farms)
Psychosocial
Stress of Work with Safety equipment, Support groups, coping
euthanasia, different injury prevention as skills training, animal
compassion species above handling skills training
fatigue,
burnout; fear
of trauma,
isolation
MSDS, Material Safety Data Sheet.
diseases with occupational exposure potential are covered beings as an occupational disease among herdsmen engaged
in Chapter 9. Selected pathogens of relevance to particu- in activities such as assisting with cattle birthing and caring
lar worker groups are described in the sections that follow. for sick animals.22
For example, occupational cases of Campylobacter and Direct routes of exposure for zoonotic pathogens include a
Chlamydophila psittaci infection have been documented bite or scratch from an infected animal, exposure to infected
among poultry workers15,16 and reported human plague fluids through splashes to the eye or mucous membranes,
cases have been reported among veterinary staff attending touching of contaminated surfaces, needlestick or other sharp
to infected cats.17 With the increasing focus on emerging instrument injuries, or inhalation of infectious particles in
infectious diseases, it should be remembered that many such dusts. Vector-borne transmission can also occur in certain
diseases appear first or with greatest intensity in the occupa- workplaces (see arthropod exposures later in this chapter).
tional setting. The first recognized (index) human case for In addition to animal-human transmission, some zoonotic
the epidemic of severe acute respiratory syndrome (SARS) diseases can be “reverse zoonoses,” potentially transmitted
that began in China was a chef who had extensive exposure from human beings to animals in the occupational setting.
to wild game animals in his work.18 Nipah virus, another Examples include tuberculosis, which may be transmitted
deadly emerging viral pathogen, first broke out among by human beings to nonhuman primates,23 elephants,24 and
Malaysian pig farm workers.19 Human outbreaks of Ebola dogs.25
virus infection in Africa are believed to originate at least in
part from exposures to nonhuman primates and other wild- Live Vaccines
life during bushmeat hunting and butchering.20 A strain of
highly pathogenic avian influenza (HPAI) has caused fatal Accidental autoinoculation of live vaccines for diseases with
work-related infection in a veterinarian, and human cases zoonotic potential has been reported to result in worker
of H5N1 HPAI remain strongly associated with working in infections. An example is the vaccine for Brucella abortus
animal markets, poultry rearing, slaughtering, defeathering, strain RB51.26 A 1995 survey of veterinarians found that 23%
and preparing infected birds for consumption.21 Rift Valley of large animal veterinarian respondents reported accidental
fever, another emerging viral disease, often occurs in human self-inoculation with live Brucella vaccine.27
Endotoxin and Organic Dusts in immunocompromised individuals. However, C. neofor-

mans has not been extensively associated with occupational
Endotoxin is a biological hazard consisting of lipopolysaccha- or environmental exposures. In contrast, Cryptococcus gatii
ride compounds from the cell walls of gram-negative bacteria infection (a species formerly thought to be confined to the
that can grow in animal bedding or feed. When the bedding tropics) has been tied to environmental and occupational
or feed is disturbed, dusts are generated that can have endo- exposures to disturbed contaminated soil in both human
toxin concentrations of 3000 nanograms per meter cubed beings and domestic animals (including cats, a ferret, and a
(ng/m3), in excess of a proposed guideline2 of 9 ng/m3. Adverse llama) in North America. In these recent outbreaks, human
respiratory effects such as bronchitis and airway obstruction C. gatii infection has involved both chronic pulmonary man-
have been reported in workers who inhale such dusts, espe- ifestations as well as meningitis.32
cially when working in confined areas with less than adequate Another fungus associated with environmental expo-
ventilation.28 Organic dusts from moldy grain used for ani- sures is Blastomyces, which can cause chronic lung disease
mal feed can cause organic dust toxic syndrome (ODTS), a in human beings and other animals as well as extrapulmo-
self-limited disease with symptoms including fever, cough, nary manifestations. The typical human case of blastomy-
myalgias, headache, and shortness of breath.2 cosis related to occupational or environmental exposure is a
male who works or recreates outdoors where there is wildlife
Pathogenic Fungi activity. A history of a pet dog with the disease helps support
the diagnosis because dogs appear to act as sentinels for envi-
A hazard related to work around areas of bird or bat drop- ronmental exposure risk.33
pings is the exposure to potentially pathogenic fungi includ-
ing Histoplasma, Cryptococcus, and Blastomyces. Histoplasma
Arthropod Exposures
capsulatum is a fungus that exists in two forms: a mold form
in the soil environment and a yeast form that develops when Animal workers may be exposed to ticks, mites, and other
human beings or other animals inhale or ingest the spores. arthropods that may be attached to animals or in the vicinity.
Although many infected human beings are asymptomatic, Such exposures can lead to transmission of zoonotic patho-
some may develop complications ranging from mild flulike gens as well as bites and allergic reactions. Grain mites are a
illness to chronic lung and eye infections and pericardi- cause of allergy among agricultural workers.
tis.29 Skin infection can also occur. Immunocompromised
individuals are at increased risk of severe disease. The nutri-
Chemical Hazards
ents in bird or bat guano can encourage the growth of spores
in the environment. Therefore areas of pigeon and other bird Exposure to chemical hazards can occur in workers with
roosting where bird droppings accumulate may be more animal contact, especially among laboratory animal research
likely to have high levels of H. capsulatum spores that can lead staff and veterinary workers. Anesthetic gases are a signif-
to inhalation or ingestion by human beings. Poultry litter icant risk to veterinary personnel and are discussed below.
can also contain Histoplasma spores. Farmers, construction Other chemicals include immobilizing agents, disinfectants,
workers, forestry workers, and other workers exposed to dis- animal-related pesticides (see Chapter 8), rodenticides,
turbed soil or poultry guano can be at risk of infection, espe- and protocol-specific chemicals in animal research.34 These
cially if individuals are immunocompromised. Unlike birds, chemicals can cause a wide range of health effects from skin
bats appear to shed infectious Histoplasma in their drop- and mucous membrane irritation to neurological effects and
pings. Caves and other areas where bat guano accumulates adverse pregnancy outcomes (e.g., miscarriage from anes-
have been associated with human cases of histoplasmosis.30 thetic exposures).35 A Materials Safety Data Sheet (MSDS)
The National Institute for Occupational Safety and Health on the hazards, safe handling, and exposure management of
(NIOSH) has published guidelines for reduction of occupa- specific chemicals should be available to all animal workers
tional risk of Histoplasma infection that also can be applied to encountering chemicals in the workplace. Depending on the
the risk of other fungal pathogens such as Cryptococcus and particular exposure, specific types of decontamination and
Blastomyces. These guidelines include the use of respiratory acute medical care may be needed. In addition, inspection of
protection, disposable protective clothing and shoe coverings, the workplace should be considered in coordination with the
and gloves that avoid skin trauma to reduce the risk of skin industrial hygienist and other safety personnel.
infection. The types of respirators that should be worn during Farm workers, especially those working in animal con-
occupational activities with exposures to spore-contaminated finement facilities with large numbers of animals such as
dusts depend on intensity of exposure. In low-risk situations swine, may be exposed to pesticides as well as high levels
(e.g., site surveys of bird roosts), disposable, filtering face- of ammonia and hydrogen sulfide levels related to animal
piece respirators may be adequate, whereas extremely dusty waste. These irritating chemical fumes can cause toxic chem-
work such as removing accumulated bird or bat manure from ical pneumonitis and bronchitis.10 Hydrogen sulfide, pro-
an enclosed area such as a barn or attic may require full-face- duced by decaying organic waste, is a mitochondrial toxin
piece, powered air-purifying respirators.31 that can cause acute loss of consciousness, respiratory arrest,
Cryptococcus is another genus of potentially pathogenic and death.36
fungi found in soil. Like Histoplasma, high concentrations Cattle silage can be a source of nitrogen dioxide toxicity
of Cryptococcus spores can be found in soil enriched by bird causing “silo filler’s disease,” an acute syndrome character-
droppings. Cryptococcus neoformans is found worldwide ized by pulmonary edema, respiratory distress, and death in
and can cause significant infections, including meningitis, sufficiently high exposures.37
Physical Hazards most cost effective at preventing work-related health prob-

lems. For example, eliminating a zoonotic disease (such as
Common physical hazards faced by animal workers brucellosis) in an animal population through vaccination
include bites and crush injuries from animals; acute and and other preventive veterinary care may be more cost effec-
chronic musculoskeletal strain from handling animals tive over time than relying on personal protective equipment
and equipment; slip, trip, and fall injuries; and, in certain such as respirators and gloves for animal workers. Similarly,
settings, exposure to noise, extremes of temperature, and substituting a less-toxic cleaning agent (see Chapter 8) may
radiation.38 be more cost effective in reducing health complaints of eye
and throat irritation among exposed workers than the use of
Psychosocial Stressors gloves and respirators.
Although there are many psychosocial benefits of human-
animal interaction (see Chapter 5), animal workers may face OCCUPATIONAL MEDICINE SERVICES
particular psychosocial stressors. These can include fear of
attack and injury; fear of infectious disease; emotional reac- Because not all health hazards in the workplace can be elimi-
tions to performing euthanasia, necropsies, slaughtering, or nated or completely controlled by the methods listed above,
other procedures; compassion fatigue39; and professional animal workers may require occupational medicine services
burnout.40 to prevent and treat work-related illnesses and injuries. Such
services may involve both human health care providers and
other members of the occupational health team.
HAZARD CONTROLS
Once workplace hazards are identified, the goal is to reduce Preplacement Screening
exposures to these hazards. Taking an occupational health Preplacement examination (or post–job offer evaluation)
approach to such hazards involves using a hierarchy of con- is a medical evaluation conducted to determine if a newly
trols that range from most effective to least effective meth- hired worker is able to safely perform the essential functions
ods to reduce the health risks to workers. This hierarchy is of the job with or without accommodation. Such examina-
listed in Table 12-2. Many hazards can be eliminated at the tions can present an ideal opportunity for preventive risk
source, or a less-dangerous substance or process can be sub- assessment and counseling as well as prophylactic vaccina-
stituted. Engineering controls include physical methods to tion. However, for many animal workers such examinations
reduce exposures such as improved ventilation and use of are not required by law and may not be provided because an
nonporous surfaces on counters that can be easily disin- employer believes they are not necessary. Even when animal
fected. Administrative and work practice controls involve workers do have such clearance examinations, the service
job restrictions for susceptible persons, limiting individual may be provided by a personal physician or other health care
worker exposure times in high-exposure areas, and preven- provider who is not familiar with the health risks of animal
tive practices such as hand hygiene. Reliance on personal work. As a result, there may be many missed opportunities
protective equipment such as gloves, gowns, and respirators for prevention.
is considered to be the least effective and often most cumber- The content of the preplacement examination can vary
some approach to hazard control. depending on the particular job type and set of exposure
Table 12-1 shows examples of such controls for handling risks but often involves a screening medical history, physical
biological, chemical, physical, and psychosocial hazards in examination, and diagnostic testing, if indicated, to identify
animal work. Obviously the most effective controls vary important preexisting conditions that might place an indi-
by the specific type of hazard, and the occupational health vidual at increased risk of injury or illness, including immu-
team must consider the most feasible type of control for each nocompromising conditions41 or history of allergy. A history
particular hazard. Although they may require a greater up- of previous animal contacts and whether animals are kept
front investment, controls at the top of the hierarchy, such in the home may provide useful information. The use of
as elimination, substitution, or engineering controls, may be standardized history and physical forms may assist in this
process. Figure 12-2 shows an example of an animal worker
questionnaire that might be appropriate for a worker in an
TABLE 12-2 n Hierarchy of Controls for animal care facility or a veterinary practice.
Workplace Hazards If workers will be using respiratory protection involv-
ing N-95 respirators or other types of respirators, they
Control Strategy Effectiveness
should complete the Occupational Safety and Health
1. Eliminate the hazard Most effective Administration (OSHA) respirator questionnaire as part
of the respirator medical clearance required under the
2. Substitute for the hazard OSHA Respirator Standard 1910.134 (available at http://
3. Engineering controls www.osha.gov/pls/oshaweb/owadisp.show_document?p_
4. Administrative/work practice controls table=STANDARDS&p_id=9783). If latex is used in the
workplace, workers should be asked about any previous reac-
5. Use of personal protective equipment Least effective
(e.g., gloves, masks) tions to latex, including rash, hives, nasal or eye inflamma-
tion, breathing difficulties, or anaphylaxis.
Confidential Risk Assessment and Medical Questionnaire for Animal Workers
Name: Gender: Male Female Date of Birth:

Occupational exposure to animals and animal tissue:
Please state whether you work with live animals or animal tissue and which species you work with.
Amphibian Bird Cat Cattle Dog Ferret Fish Goat Horse Insect
Nonhuman primate Pig Rabbit Reptile Rodent Sheep Wildlife species (please list):
No animal or animal tissue contact
Other hazardous exposures:
Human blood/tissue Chemicals (please list):
Dust Noise Radiation Heavy lifting Other (please specify):
Personal protective equipment worn:
Mask/respirator (type): Gloves Other (please specify):
Pets, other nonoccupational animal exposures:
Please state whether outside of work you have contact with any of the following:
Bird Cat Dog Ferret Fish Horse Rabbit Reptile Rodent Other (please list):
Medical conditions:
Please list known allergies to medications, animals, or other environmental allergens:
Please list whether you have any of the following:

Asthma Rhinitis Eczema Other skin disease Diabetes Cancer Recurrent infections Other medical
conditions that could compromise immune system Heart murmur Hepatitis Back problems Other musculo-
skeletal problems Depression or anxiety
Please list current medications (prescription, over-the-counter, and supplements):
Symptoms:
Please check if you have any of the following symptoms:
Cough Shortness of breath Wheezing Runny/itchy eyes Runny/itchy/congested nose/sneezing Skin rash
Musculoskeletal pain Persistent diarrhea Weight loss Unexplained fevers Depression or anxiety Other
(please list):
Do you feel any of your symptoms are related to work? Yes No
Immunizations/tuberculosis testing:
Please state your most recent immunizations and tuberculosis (TB) test and date:
Immunization Date
Tetanus
Rabies
Influenza
Hepatitis B
TB testing
Figure 12-2 n Sample medical questionnaire for animal workers.
In addition to the history and physical, other baseline etry) is recommended for individuals with potential expo-
testing may be indicated. Audiometry at baseline is required sure to respiratory allergens, including veterinary workers
by OSHA if the worker will be exposed to noise at levels and workers in animal facilities. Allergy testing is not usu-
of 85 A-weighted decibels (dBA) or higher for an 8-hour ally performed routinely at baseline but may be warranted
time-weighted average. Testing of lung function (spirom- if the history suggests sensitization to particular allergens
found in the work setting. In certain settings baseline serol- attention for work-related problems, review unit inspection
ogy or serum banking may be indicated to detect immuno- standards, and evaluate future training needs.
logic response to zoonotic pathogens.
Based on the findings of the preplacement examination, Medical Surveillance
the medical provider can perform a risk assessment for the
individual and decide whether the individual can safely Depending on the degree of occupational risk, animal work-
do the job with or without accommodation. To do this, ers should receive periodic evaluations to detect evidence of
the medical provider may need to consult a veterinarian, work-related disease, reassess risk factors for occupational
biosafety professional, or other members of the occupational illness and injury, and ensure that vaccinations are current.
health team to learn more about specific risks of the job. For Table 12-1 suggests medical surveillance that may be appro-
example, a person with valvular heart disease may need to be priate for different types of animal workers.
restricted from working in a research facility with pregnant Questionnaires should ask about new health problems
sheep because of the risk of Q fever. A worker who devel- that have developed since the last examination, includ-
oped allergy to mice or rats in a previous job may need to ing symptoms of allergy or infection that could indicate
be restricted from future contact with such animals. In dis- increased risk of disease or the occurrence of work-related
cussing disease risks with other professionals, it is important disease or injury. A key aspect of such history is whether the
(although sometimes a challenge) to keep medical infor- symptoms show a temporal relation with work exposures.
mation about the worker confidential and prevent possible Box 12-2 shows characteristic symptom patterns suggesting
workplace discrimination because of a medical condition. If work-related occupational asthma. Similar temporal rela-
work restrictions are necessary, they can be indicated on a tions may occur with other occupational diseases.
work status form that can be given to the employer to out- Based on the results of screening questions, further test-
line such restrictions without revealing confidential health ing may be indicated, such as serial peak flow diaries, spirom-
information about the employee. In general, confidential etry, and methacholine testing of lung function in a worker
health information on employees should not be shared with reporting shortness of breath. Another example of periodic
the employer, supervisor, or other management personnel by medical surveillance testing is annual audiometry, which is
the human health clinician evaluating the worker.42 required by OSHA for workers exposed to noise and enrolled
in hearing conservation programs.
Vaccinations
Management of Acute Injuries, Exposures, and
A number of preventive vaccinations may be indicated for Illnesses
animal workers. Previous vaccination history should be assessed
at the preplacement evaluation and the need for additional vac- When an animal worker seeks medical attention for an acute
cination determined. As with other aspects of the preplacement illness or injury that may be work related, the health care
risk assessment, consultation with a veterinarian may be advis- provider should be familiar with the worker’s occupational
able or clear instructions conveyed to the health care provider hazards. As previously stated, many medical providers in
regarding necessary vaccinations. All animal workers should be emergency departments or clinics may not be aware of the
up to date with respect to tetanus vaccination. Table 12-3 lists zoonotic or other disease risks faced by animal workers. It
vaccines to consider for particular groups of workers. Rabies may therefore be advisable for workers with acute work-
vaccination is indicated for a number of workers.43 Table 12-4 related injuries or illnesses to carry a card listing relevant
shows recent recommendations for which individuals should zoonotic disease exposures and other work hazards and be
receive preexposure rabies vaccine. able to show the card to the health care provider. An exam-
ple of such a card is shown in Figure 12-3. This type of card
Training should be customized to the specific work setting.
If an animal worker has an acute exposure, illness, or injury
Training at the time of job entry is recommended by the work supervisor should document and report the incident.
the National Association of Public Health Veterinarians This documentation should include the date, time, location;
(NAPHV) for workers in veterinary facilities41 and is rele- persons injured or exposed; other persons present; description
vant for other animal workers as well. Aspects of such train- of the incident; the species, breed, and health status (vaccina-
ing include education about zoonotic disease risks, infection tion history, clinical signs, diagnostic testing) of any involved
control practices, use of personal protective equipment, safe animals; contact with public health and health care providers;
chemical handling techniques, and injury prevention, with and follow-up plans.41 If possible, pertinent documentation of
emphasis on proper animal handling, restraints, and recog- the incident should be made available to the treating medical
nition of behavioral cues in animals. Such training should provider. Because work-related injuries and illnesses must be
be provided by an individual familiar with the risks of a par- reported on the employer’s OSHA 300 Log, attending clini-
ticular workplace and the safety policies in place, such as a cians will need to provide a medical opinion and rationale on
safety officer. Training should be documented. Follow-up the work-relatedness of the injury, illness, or exposure.44
training in health and safety can take place on a regular A key part of the evaluation of any work-related illness or
basis with animal workers to identify and mitigate hazards, injury is determining whether it represents a sentinel health
address institutional occupational health policies (including event indicating a problem with existing hazard controls
record keeping), address personal hygiene, provide points of and potentially representing an index case in terms of other
contact for more information or for when to seek medical workers and possibly animals being at risk. This may require
TABLE 12-3 n Occupational Medicine Services for Animal Workers
Types of Animal Workers Requiring Occupational

Category of Medical Service Specific Medical Services Indicated Medicine Services
Preplacement screening Questionnaire regarding immune compromise, All

musculoskeletal problems, pets and other animal
contacts
Physical examination
Respirator clearance questionnaire, spirometry Workers exposed to respiratory hazards, workers
who will be using respirators
Audiometry Noise-exposed workers
HIV and TB screening Animal research and workers in contact with
nonhuman primates
Consider serum banking Zoological, wildlife, or research workers; others
with zoonotic exposures
Vaccination Rabies See Table 12-4
Tetanus (every 10 years) All
Annual influenza vaccine All (especially poultry and swine workers)
Anthrax Laboratory workers routinely working with
concentrations of anthrax or aerosol potential87
Q fever (consider)* Laboratory workers, researchers working with
pregnant sheep, slaughterhouse workers70
Hepatitis A and B, measles, polio Workers in contact with chimpanzees and other
nonhuman primates
Training Veterinary standard precautions, anesthetic safety, All
bite and injury prevention, OSHA training, safe
chemical handling
Medical surveillance Periodic questionnaire about allergy/respiratory NIOSH recommendations in all animal workers
symptoms with allergen exposures
Reassess zoonotic disease risk All animal workers with change in medical status
OSHA respirator questionnaire; spirometry; further Workers using respirators
evaluation in positive responses to questionnaire
TB testing (skin test or interferon assay) Animal workers with nonhuman primate and/or
elephant contact (see Figure 12-2)
Annual audiometry Workers with noise exposures ≥85 dBA (8-hour
average)
Acute injury and illness Treat acute problem, determine if work related, All
management identify sentinel health events indicating problem
with hazard control and risk to other workers and/
or patients
Consider whether human being with a zoonotic
disease is a sentinel for animal health problem as well
as indicator of occupational risk to other workers
Determine source of infectious exposure and
consider prophylactic treatment for exposure
(e.g., rat-bite fever, leptospirosis)
Herpes B exposure prophylactic treatment65 Workers with exposure to nonhuman primates
Confidential medical record Protect confidentiality of medical records All
management
*Not commercially available in the United States. Persons wishing to be vaccinated should first have a skin test to determine a history of previous exposure. Individuals who have
previously been exposed to C. burnetii should not receive the vaccine because severe reactions, localized to the area of the injected vaccine, may occur.
HIV, Human immunodeficiency virus; TB, tuberculosis; OSHA, Occupational Safety and Health Administration; dBA, decibels (acoustic).
communication between the health care provider and the case the medical provider should specify the necessary job
veterinarian and/or other members of the occupational restrictions that would allow the worker to safely return to
health team (see Figure 12-1). work and how long those restrictions are expected to be
After an episode of acute injury or illness, or because of required. Again, making appropriate recommendations
results of a periodic surveillance evaluation, the employee may require a team approach involving the veterinarian and
may not be able to resume full duties immediately. In this other professionals. As with preplacement evaluations, it is
TABLE 12-4 n Rabies Preexposure Prophylaxis Guide
Risk Category Nature of Risk Typical Population Preexposure Recommendations
Continuous Virus present continuously, often Rabies research laboratory Primary course*; serologic
in high concentrations; specific workers; rabies biologics testing every 6 months;
exposures likely to go unrecognized; production workers booster vaccination if
bite, nonbite, or aerosol exposure antibody titer is below
acceptable level
Frequent Exposure usually episodic and with Rabies diagnostic lab workers, Primary course; serologic
source recognized, but exposure spelunkers, veterinarians and testing every 2 years; booster
also may be unrecognized; bite, staff, animal control and wildlife vaccination if antibody titer is
nonbite, or aerosol exposure workers in rabies-endemic areas; below acceptable level
all persons who frequently
handle bats
Infrequent Exposure nearly always episodic with Veterinarians and terrestrial Primary course; no serologic
source recognized; bite or nonbite animal control workers in areas testing or booster vaccination
exposure where rabies is uncommon
to rare; veterinary students;
travelers visiting areas
where rabies is enzootic and
immediate access to appropriate
medical care, including
biologics, is limited
Rare (population Exposure always episodic with U.S. population at large, No vaccination necessary
at large) source recognized; bite or nonbite including persons in rabies-
exposure epizootic areas
From Manning SE et al, Centers for Disease Control and Prevention: Human rabies prevention–United States, 2008: recommendations of the Advisory Committee on
Immunization Practices, MMWR Recomm Rep 57(RR-3):1-28, 2008.
*Primary vaccination: three 1.0-mL injections of HDCV or PCEC vaccine should be administered intramuscularly (deltoid area)–one injection per day on days 0, 7, and 21 or 28.
i mportant that the worker’s privacy and the confidentiality

BOX 12-2 Pattern of Symptoms of Work-Related of medical information be respected during this process.
Asthma
• Symptoms of asthma develop after a worker starts a new job Management of Confidential Medical Records
or after new materials are introduced on a job (a substantial and Information
period of time may elapse between initial exposure and
development of symptoms). Medical evaluations of workers must uphold standards of
• Symptoms develop within minutes of specific activities or privacy and confidentiality in the provision of care and in
exposures at work. record keeping. In agreement with the Health Information
• Delayed symptoms occur several hours after exposure, during Portability and Accountability Act (HIPAA), the American
the evenings of workdays. College of Occupational and Environmental Medicine has
• Symptoms occur less frequently or not at all on days away from published a position paper in support of confidentiality of
work and on vacations. medical information in the workplace.45 Results of baseline
• Symptoms occur more frequently on returning to work. and periodic questionnaires and physical examinations
From National Institute for Occupational Safety and Health (NIOSH): NIOSH alert: (including, but not limited to, information about immuno-
preventing asthma in animal handlers, DHHS (NIOSH) Publication No. 97-116. http:// compromised conditions) represent medical information that
www.cdc.gov/Niosh/animalrt.html.
should be treated with the same confidentiality as information
in a hospital and not shared with the employer. Such informa-
tion should be kept in a secure chart in a medical office and
Name:
Job title: not placed in an employee’s personnel file in the workplace.
Name and telephone number of supervisor: Table 12-3 summarizes occupational medical services for
In case of an emergency, please be aware that the holder of this card, different groups of animal workers.
by virtue of work involving animals, is exposed to certain zoonotic
diseases. These include rabies, Q fever, leptospirosis, toxoplasmosis,
tularemia, psittacosis, cat-scratch fever, rat-bite fever, Pasteurella
multocida, Capnocytophaga canimorsus, viral encephalitis, Rocky OCCUPATIONAL HEALTH IN SPECIFIC SETTINGS
Mountain spotted fever, and herpes B. When possible, review the
specific animal exposure of this worker. Consult with local infectious
disease specialists, public health authorities, and other resources for Veterinary Personnel
appropriate management.
As a group, veterinarians and their staff are at increased risk
Figure 12-3 n Example of hazard card for animal workers seeking medical for work-related injuries and illnesses. A study of 10,000
care for acute illness or exposure (to be customized to particular work setting). veterinary practices in Europe found that the rate of work
a ccidents and occupational disease was almost three times as Zoonoses

great as that of general medical practitioners and their staff,
Many different zoonotic infections, including fatal cases,
and the rate of severe accidents resulting in lost work time
have been reported in veterinarians.41 In a European study
was nine times greater. The most common occupational dis-
of work-related claims by veterinary workers, the most
eases reported were skin disorders (39%), followed by allergic
frequent infections were ringworm, brucellosis, Lyme
respiratory diseases (31%) and infectious diseases (19%).46
disease, and psittacosis.46 A survey of American veterinari-
In the United States federal law requires veterinary practices
ans found that the occupational infections of current great-
to implement a workplace plan to comply with OSHA
est concern to small-animal veterinarians were ringworm,
Hazard Communication Standards (http://www.avma.org/
gastrointestinal bacteria, gastrointestinal parasites, lep-
issues/policy/workplace_hazards.asp). It also appears that
tospirosis, rabies, toxoplasmosis, and unknown or emerging
veterinarians may be held liable for harm if their employees
pathogens. Large-animal veterinarians were concerned about
develop a work-related illness such as a zoonotic infection.47
ringworm, gastrointestinal bacteria, leptospirosis, brucello-
It is not clear how many workers in veterinary practices
sis, gastrointestinal parasites, and rabies. Despite these con-
receive occupational medicine services from human health
cerns, most veterinarians responding to the survey reported
care providers or have access to members of the occupational
low rates of personal protective equipment use and other
health team, such as industrial hygienists or infection con-
protective behaviors currently recommended to protect
trol specialists. Many veterinary offices are located in rural or
against zoonotic disease transmission.51
other areas where shortages of occupational medicine pro-
Veterinarians and their staff have been identified as
viders exist.48 The practice director, who is often a veterinar-
a group at increased risk for many other zoonotic infec-
ian, or another staff member may have to perform a number
tions, including Q fever, salmonellosis, methicillin-resistant
of functions such as identifying hazards and designing con-
Staphylococcus aureus, avian influenza,51 cat-associated
trol strategies. The National Association of State Public
plague, animal bite infections including pasteurellosis, other
Health Veterinarians (NASPHV) has published a compen-
bacterial infections, and cat-associated sporotrichosis (see
dium of veterinary standard precautions that provides useful
Chapter 10).
practice guidelines as well as a model infection control plan
The NASPHV Veterinary Standard Precautions for
(Figure 12-4).41 The veterinarian may need to educate local
Zoonotic Disease Prevention in Veterinary Personnel includes
medical providers to ensure adequate and confidential pre-
a model infection control plan for veterinary offices.41 Figure
placement screening, medical surveillance, and acute injury/
12-4 shows this model plan.
illness follow-up of veterinary care workers. Having a des-
This NASPHV document recommends engineering
ignated medical provider as well as a designated emergency
controls such as single-purpose isolation rooms for sick
medical care facility that is aware of the special exposures of
animals; separate rooms for patient care and employee
the veterinary workers can help ensure improved preventive
breaks; designated sharps containers; the use of nonporous,
and acute care of exposure-related health problems.
easily cleaned surface materials in areas where animals are
housed, examined, or treated; and sealing up of rodent entry
Allergens
portals. Recommended work practice controls include train-
A survey of California veterinarians found that 40% reported ing new employees in practices such as hand hygiene before
animal-related allergic symptoms, especially to cats and and after each patient encounter and after contact with body
dogs.49 Allergens identified as hazards in veterinary practice fluids, secretions, or excretions as well as after eating, drink-
include animal hair and dander, feathers, latex, mites, organic ing, smoking, using lavatories, and cleaning animal areas.
dust, and amniotic fluid. Fortunately, a study of skin allergy Additional work practices include bite prevention and avoid-
in veterinarians found that most sensitized individuals were ance of needlesticks by not recapping needles. Bite preven-
allergic to only one species of animal.50 tion could include physical or chemical restraints, muzzles,
Hypersensitivity pneumonitis has been reported in vet- and bite-resistant gloves. Personal protective equipment
erinarians from exposure to antigens in animal feeds.46 recommendations include gloves or sleeves and facial pro-
Latex allergy is also a risk among veterinary personnel tection with a mask or goggles when splashes or sprays are
who use latex gloves and other latex equipment. expected. An N-95 respirator should be worn when evalu-
Measures to control these hazards in veterinary practices ating abortions in small ruminants, poultry deaths, sick
include frequent cleaning of facilities and adequate venti- psittacine birds, and other situations with the risk of aero-
lation. Personal protective devices such as gloves and res- solized pathogens.41 The NASPHV document also recom-
pirators can reduce allergen exposure. Box 12-3 shows the mends that immunocompromised individuals and pregnant
recommendations for animal handler allergen control pub- workers be counseled about their increased risk of zoonotic
lished by NIOSH that target veterinary and research animal disease, especially when working with high-risk animals such
workers. as young animals and animals that are parturient, unvacci-
However, even with these measures, sensitized individuals nated, stray or feral, housed in shelters or crowded condi-
may have difficulty working around animals to which they tions, fed raw meat diets, or with parasites; wildlife; reptiles
are allergic. Job modification may be necessary; there may and amphibians; and exotic or nonnative species.41 Such
be areas of the building with a lower allergy load that a sen- counseling should ideally be done by a health care profes-
sitized individual could tolerate. Allergy desensitization sional who is aware of the zoonotic disease risks faced by
should be considered as part of the management of some the worker. For this reason the NASPHV document recom-
allergic conditions. mends that all workers inform their health care providers
Figure 12-4 n NASPHV model infection control plan for veterinary practices, 2008. (Adapted from National
Association of State Public Health Veterinarians: NASPHV compendia. http://www.nasphv.org/documents
Compendia.html.
Figure 12-4—cont’d.
BOX 12-3 Preventing Asthma in Animal Handlers
WARNING! Exposure to animals or animal products in the workplace can cause asthma and allergies. Animal handlers should take steps to
protect themselves from exposure to animals and animal products.
• Perform animal manipulations within ventilated hoods or safety cabinets when possible.
• Avoid wearing street clothes while working with animals.
• Leave work clothes at the workplace to avoid potential exposure problems for family members.
• Keep cages and animal areas clean.
• Reduce skin contact with animal products such as dander, serum, and urine by using gloves, lab coats, and approved particulate respirators
with face shields.
• Employers of animal handlers should take steps to protect workers from exposure to animals and animal products.
• Modify ventilation and filtration systems:
• Increase the ventilation rate and humidity in the animal housing areas.
• Ventilate animal housing and handling areas separately from the rest of the facility.
• Direct airflow away from workers and toward the backs of the animal cages.
• Install ventilated animal cage racks or filter-top animal cages.
• Decrease animal density (number of animals per cubic meter of room volume).
• Keep cages and animal areas clean.
• Use absorbent pads for bedding. If these are not available, use corncob bedding instead of sawdust bedding.
• Use an animal species or sex that is known to be less allergenic than others.
• Provide protective equipment for animal handlers: gloves, lab coats, and approved particulate respirators with face shields.
• Provide training to educate workers about animal allergies and steps for risk reduction.
• Provide health monitoring and appropriate counseling and medical follow-up for workers who have become sensitized or have developed
allergy symptoms.
From National Institute for Occupational Safety and Health (NIOSH): NIOSH alert: preventing asthma in animal handlers, DHHS (NIOSH) Publication No. 97-116. http://www.
cdc.gov/Niosh/animalrt.html.
of their work activities, but additional direct communica- gases. These chemicals are capable of allergic, irritant, and
tion between a health care provider and a veterinarian about other toxic effects. Chemical irritant effects such as irritant
disease risks may be advisable. However, as previously men- contact dermatitis and eye irritation have been associated
tioned, such communication needs to respect patient privacy with the use of chemical disinfectants.52 Table 12-5 lists dis-
and confidentiality of medical information (see Chapter 2). infectant chemicals commonly used in veterinary practices.
As can be seen among the list of disadvantages, a number
of these chemicals are highly irritating to skin, eyes, and
Chemical Hazards
mucous membranes. If a particular disinfectant chemical
Chemical hazards in veterinary practices include disinfec- is causing adverse effects in workers, substitution should be
tant chemicals, pesticides (see Chapter 8), and anesthetic considered.
Approximately 50,000 veterinary workers in the United practice, but strategies used in other occupational groups
States risk potential exposure to anesthetic agents, including include job rotation and increased time off, coping skills
nitrous oxide and halogenated agents, mostly through training, support groups, and stress-reduction techniques.60
significant inhalation and accidental injections in veterinary
operating rooms.53,54 Many of these workers are women of Occupational Medicine Services for Veterinary Personnel
childbearing age. Adverse reproductive outcomes, such as
spontaneous abortion, have also been reported among work- As previously described, human health care providers who
ers exposed to these anesthetic agents.54 Control of anes- care for workers in a veterinary facility may not be famil-
thetic hazards involves ensuring 100% fresh air and 100% iar with the particular occupational health risks faced by
exhausted air for dilution of waste gases and odors in animal such workers. Such practitioners may need to be provided
rooms, filtering of supplied air prior to recirculation, and with information about the disease risks and the preventive
institution of a scavenging system for waste anesthetic gases services required. Table 12-3 outlines some suggested occu-
and vapors. This scavenging system should be checked peri- pational services for veterinary staff, including preplacement
odically to ensure it is working properly. Air levels of anes- evaluation, vaccination, and management of acute injuries
thetic gases can also be monitored periodically.55 and illnesses.
Preplacement Screening. Because all veterinary workers

Physical Hazards
encounter the risk of allergic reactions, preplacement exami-
Physical hazards in veterinary practices include bites and crush nation should focus on history of skin, respiratory, or other
injuries from animals; lifting hazards related to equipment allergies and any history of asthma or other underlying respi-
and patients; and slip, trip, and fall injuries. A survey of 2800 ratory conditions as well as medical conditions associated
Australian veterinarians found that more than half had sus- with immunocompromised status. The OSHA Respirator
tained a significant work injury.56 Animals have been reported Medical Evaluation questionnaire previously mentioned
to be the most common cause of occupational accidental inju- should be part of this baseline health history for any worker
ries, with cats and dogs causing the most accident-related who will be using respiratory protection.61
injuries in small-animal practices and horses and cows caus- Along with a thorough physical examination, baseline
ing the most injuries in large-animal practices. Large animal testing can include spirometry for anyone with allergen expo-
accidents were more likely to cause broken bones.46 Some of sures. Even nonclinical personnel such as office staff could be
the major causes of accidents involving animals are dangerous exposed to allergens in waiting rooms or other parts of the
animal behaviors, such as panic, male dominance aggression, facility.
fear aggression, and maternal aggression. Control of these Baseline vaccination should include a rabies preexposure
physical hazards includes bite prevention, proper animal han- series if not previously vaccinated against rabies (see Table
dling and restraint, training animals to voluntarily cooperate 12-4). All veterinary staff should have a current tetanus vac-
with veterinary procedures,57 and inadequate barriers or ani- cination and be encouraged to have an annual influenza vacci-
mal handling facilities to protect workers. nation. If the veterinary practice cares for pregnant sheep and
Repetitive trauma from carrying and handling animals and goats, baseline titers for the etiologic agent of Q fever (Coxiella
cages as well as acute trauma from lifting and carrying can burnetii) should be considered. Other components of the pre-
result in musculoskeletal injuries such as acute and chronic placement evaluation can be tailored depending on the specific
low back injury, carpal tunnel syndrome, and tendonitis. type of veterinary practice and the expected hazards.
Barking dogs, other noisy animals, and noisy machinery
can cause significant noise exposure to animal workers. Medical Surveillance. After a baseline medical evalu-
Veterinary staff can be exposed to significant noise, espe- ation, there are few guidelines for periodic examination
cially during the cleaning of cages with power washers. Noise of veterinary personnel by a medical provider. However,
levels above 85 dBA over an 8-hour period require inclusion NIOSH recommends that veterinary workers receive peri-
of workers in a hearing conservation program that complies odic monitoring for the development of allergy and asthma.
with the OSHA standard on occupational noise exposure.58 Such monitoring could be accomplished with a screening
If a person has to shout to converse with another person at questionnaire (see Figure 12-2) that could also assess any
arm’s length, the noise is likely to exceed 85 dBA. reported infectious disease symptoms or diagnoses that
Radiation is another physical hazard for staff in veterinary could be work related (such as febrile illnesses, diarrhea, and/
practices where radiographs are taken. Although evidence of or skin infections) as well as newly developed medical con-
adverse effects in veterinary staff from radiation exposure is ditions that could affect risk of zoonotic disease. If workers
limited, staff performing radiography should be monitored use respirators, repeat medical evaluations may be required
for radiation exposure. under the OSHA Respiratory Protection standard if a change
occurs in workplace conditions. NASPHV also recommends
that veterinary personnel who have a change in their health
Psychosocial Stressors
status, such as pregnancy, should discuss their work expo-
Psychosocial hazards of veterinary work include the stress of sures with their medical providers. They should also see their
euthanizing animals, compassion fatigue, and professional medical providers periodically for follow-up rabies vaccine
burnout.39 Increased rates of suicide have been reported for boosters. Workers enrolled in a hearing conservation pro-
veterinarians.59 There is little published evidence of successful gram because of excessive noise exposures require annual
interventions to reduce psychosocial stressors in veterinary audiometry.
360
TABLE 12-5 n Disinfectants Used in Veterinary Practices
Halogens: Halogens: Iodine
Alcohols Aldehydes Biguanides Hypochlorites Compounds Oxidizing Agents Phenols QACs
Sample trade Ethyl alcohol Formaldehyde Chlorhexidine Bleach Betadyne Hydrogen peroxide One-Stroke Roccal
names Isopropyl alcohol Glutaraldehyde Nolvasan Providone Peracetic acid Environ DiQuat
Virosan Virkon S Pheno-Tek II D-256
Oxy-Sept 333 Tek-Trol
Mechanism of Precipitates Denatures Alters membrane Denatures Denatures Denature proteins Denatures proteins; Denatures
action proteins; proteins; permeability proteins proteins and lipids alters cell wall proteins; binds
denatures lipids alkylates nucleic permeability phospholipids
acids of cell
membrane
Advantages Fast acting; leaves Broad spectrum Broad spectrum Broad spectrum; Stable in storage; Broad spectrum Good efficacy with Stable in storage;
no residue short contact relatively safe organic material; nonirritating to
time; noncorrosive; skin; effective
inexpensive stable in storage at high
temperatures
and high pH (9
to 10)
Disadvantages Rapid evaporation, Carcinogenic Only functions Inactivated Inactivated by Damaging to some Can cause skin and
flammable mucous in limited pH by sunlight; QACs; requires metals eye irritation
membrane and range (5 to 7); requires frequent frequent
tissue irritation; toxic to fish application; application;
only use in well- (environmental corrodes corrosive; stains
ventilated areas concern) metals; mucous clothes and
membrane and treated surfaces
tissue irritation
Precautions Flammable Carcinogenic Never mix with May be toxic
acids; toxic to animals,
chlorine gas will especially cats
be released and pigs
Vegetative Effective Effective Effective Effective Effective Effective Effective Yes, gram-
bacteria positive;
limited, gram-
negative
Mycobacteria Effective Effective Variable Effective Limited Effective Variable Variable
Enveloped viruses Effective Effective Limited Effective Effective Effective Effective Variable
Nonenveloped Variable Effective Limited Effective Limited Effective Variable Not effective
viruses
Spores Not effective Effective Not effective Variable Limited Variable Not effective Not effective
Fungi Effective Effective Limited Effective Effective Variable Variable Variable
Efficacy with Reduced Reduced ? Rapidly reduced Rapidly reduced Variable Effective Inactivated
organic matter
Efficacy with hard ? Reduced ? Effective ? ? Effective Inactivated
water
Efficacy ? Reduced Inactivated Inactivated Effective ? Effective Inactivated
with soap/
detergents
The use of trade names does not in any way signify endorsement of a particular product.
For additional product names, please consult the most recent Compendium of Veterinary Products.
Adapted from Linton AH, Hugo WB, Russel AD: Disinfection in veterinary and farm practice, Oxford, UK, 1987, Blackwell Scientific; Quinn PJ, Markey BK: Disinfection and disease prevention in veterinary medicine. In Block SS, ed:
Chapter 12
Disinfection, sterilization and preservation, ed 5, Philadelphia, Lippincott, 2001, Williams & Wilkins.
?, Information not available. QACs, quaternary ammonium compounds.
n
Occupational Health of Animal Workers
361
Acute Injury, Illness, or Exposure Evaluation and blow air to the back of cages from the aisles to reduce worker
Follow-up. As with other animal workers, it is ideal that exposures (see Box 12-3).63 Control by substitution may be
the health care provider treating veterinary workers for feasible in some situations because male rats are more aller-
acute work-related injuries and illnesses be familiar with the genic than female rats, and species such as rabbits are less
hazards in the workplace. Medical providers providing such allergenic than rats.1
care should take a careful history of occupational exposures.
Common acute injuries in veterinary personnel are animal Zoonoses
bites (see Chapter 10). In such situations use of a zoonotic
disease risk card (see Figure 12-3) may help guide the medi- Several zoonoses are of particular concern to animal facility
cal care provider to adequately consider zoonotic disease workers who work with nonhuman primates and rodents.64
risks. Care of animal bites in veterinary workers involves a Some can result in death. Therefore occupational exposures
review of rabies risk from the bite and rabies vaccination are considered medical emergencies. Unlike veterinary
status (see Chapter 9), as well as consideration of antibiotic hospitals where elimination of zoonotic hazards is not
treatment. possible, the control of many zoonotic diseases in animal
Any acute injury or illness in a veterinary worker can be facilities often involves control at the source through screen-
considered a sentinel event indicating a hazard in the working and eliminating disease in the animal colony. Separation
place that has not been adequately controlled. Therefore of species prevents interspecies transmission, and signage
communication between the medical care provider and the helps increase awareness of risks among employees. Use
veterinarian or other members of the occupational health of instruments and equipment with safety features such as
team can help turn an acute illness or injury event into an retractable needles can help prevent bloodborne pathogen
opportunity to identify and reduce workplace hazards. exposures.
In addition, the medical care provider will need to consider
whether and when the worker can safely return to work and Herpes B. Cercopithecine herpesvirus 1 infection, her-
whether job modification or restriction is necessary. Again, pes B, is endemic in monkeys of the genus Macaca. This
this may require communication between the medical pro- group of Asiatic monkeys includes rhesus macaques, pig-
vider and a work supervisor or veterinarian. Individuals with tailed macaques, and cynomolgus monkeys. Human beings
suspected allergy should be evaluated and may need to be who work with these monkeys can be infected by bites,
restricted from exposure to the animal to which they are scratches, needlesticks, and mucocutaneous exposure.65 In
sensitized (see Chapter 7). Individuals with musculoskeletal monkeys herpes B can be subclinical or cause lesions on the
injuries may need temporary job modification while they oral mucosa. In human beings herpes B can result in fatal
recover. The possibility of posttraumatic stress should be encephalomyelitis. Although rare, death has been reported in
considered in all employees returning to work after an acute up to 80% of cases. Workers dealing with these nonhuman
work-related injury or illness. primates must be informed of the risk of herpes B infec-
tion and receive training in proper use of appropriate per-
sonal protective equipment, including gowns, gloves, masks,
Workers in Animal Research Facilities
and face shields and the maintenance of a safe workplace.
Because many animal research facilities have affiliation They should seek medical care immediately if an exposure
with larger institutions, there is often a designated indus- occurs because early prophylaxis with antiviral agents has
trial hygienist and/or infection control specialist to help resulted in favorable outcomes.66 The Centers for Disease
design and implement preventive workplace hazard con- Control and Prevention (CDC) has developed guidelines for
trols. There is also often a designated medical care pro- assessment and medical management of monkey scratches
vider for the employees working in such facilities and a and bites, wound contaminations, cage scratches, and other
formal occupational health and safety program. In 1997 potential exposures.67
the Committee on Occupational Safety and Health in
Research Animal Facilities, Institute of Laboratory Animal Simian Retroviruses. A number of simian retroviruses,
Resources, published Occupational Health and Safety in the including simian immunodeficiency virus and simian foamy
Care and Use of Research Animals, which outlines guide- virus, are found in a variety of nonhuman primates. Cases
lines for occupational health programs for research animal of transmission of these viruses to laboratory workers with
workers.62 nonhuman primate exposure have been reported. Prevention
is similar to that for h
erpes B infection.68
Allergens
Measles. Measles (rubeola), a paramyxovirus infection, is
As with veterinary workers, allergy can be a significant primarily a disease of human beings. The primary concern
problem in workers in research animal facilities. Allergy for laboratory animal workers is therefore reverse zoonosis
to rodents is common, resulting in the spectrum of aller- (anthropozoonosis) when working with nonhuman primates
gic rhinitis, dermatitis, and asthma. Rodent allergy may be because measles can cause lethal infection in these animals.
species specific; individuals sensitized to mice may be able Outbreaks of measles in captive nonhuman primates usu-
to work safely with rats. ally originate from an infectious human animal handler.69
Control of allergens in animal facilities can involve engi- Therefore animal workers with contact with nonhuman
neering controls including adequate fresh air ventilation, primates must have documented measles vaccination and
filtering of any recycled air, and airflow of ventilation to receive booster vaccinations if necessary.
Viral Hepatitis. Hepatitis A, B, and C are primarily viral Q Fever. Laboratory animal personnel engaged in research
diseases of human beings. However, chimpanzees and other with pregnant sheep and goats are at risk for infection with Q
nonhuman primates have been experimentally infected.70 fever (see Chapter 9). High-risk individuals include immu-
Therefore there is risk of reverse zoonosis. Workers in nocompromised individuals and persons with valvular heart
animal facilities who have direct contact with nonhuman disease.
primates should be immunized against hepatitis A and B,64
have baseline serology for protective hepatitis B antibod- Human Immunodeficiency Virus. Another human
ies (HbSAb), and consider having baseline serology for isease with potential to be a reverse zoonosis in nonhuman
d
hepatitis C. primates is human immunodeficiency virus (HIV), and some
research facilities using nonhuman primates have adopted
Tuberculosis. Nonhuman primates are susceptible to policies requiring anonymous periodic HIV testing be part
infection with Mycobacterium tuberculosis (TB) and can of the job requirement. These HIV-related policies should
transmit the disease to human beings by the respiratory include outlining the steps undertaken to safeguard each
route. Likewise, human beings infected with TB can poten- individual worker’s privacy.
tially infect nonhuman primates. All animal workers with
nonhuman primate contact should have skin testing for Chemical Hazards
TB at baseline and annually. New employees who have not
had a TB skin test in the previous 5 years should be tested Chemical exposures in laboratory animal facilities include
with a two-step technique (retesting after 1 week if the first disinfectants and anesthetics, as previously mentioned.
test is negative) to detect boosted immunity from previous Protocol-specific chemicals such as medications and tox-
infection. Alternative testing methods include an assay for ins used in research can pose additional risks from a wide
interferon specific to TB (see Chapter 9).71 Workers with variety of chemicals. Eyewash stations and showers may
positive TB tests should be evaluated medically. Such evalu- be necessary for immediate decontamination by some
ation may include a chest radiograph to exclude active dis- agents.
ease and a determination of the need for treatment with Control of anesthetic gases and disinfectant chemical
antituberculous medication.72 risks is similar to that for veterinary personnel.
Rat-Bite Fever (Streptobacillosis). Rat-bite fever is Physical Hazards

caused by infection with the bacterium Actinobacillus
muris (formerly Streptobacillus moniliformis), usually as a Physical hazards for workers in animal care facilities are
result of a rat bite or contact with rat saliva or urine. The similar to those of veterinary workers and include ergonomic
incubation period is between 3 and 10 days. Symptoms risks for musculoskeletal injury, noise, and radiation.
include the acute onset of fever, headache, and muscle Sources of radiation exposure may include both diagnostic
pain, followed by the development of a maculopapu- and protocol-related radiation.73
lar rash on the extremities over the next several days. In
untreated cases complications can include endocarditis, Psychosocial Stressors
parotitis, and abscesses.
Doxycycline or penicillin can be used as a prophylactic Work-related stress, anxiety, uneasiness, and depression
treatment after a rat bite. Cases of infection are treated with have been reported in laboratory animal handlers. Particular
penicillin or tetracyclines (see Chapter 10).70 psychosocial stressors include developing strong attachments
to laboratory animals, having strong sentiments about “sac-
Lymphocytic Choriomeningitis Virus. Lymphocytic rificing” the animals, having friends and acquaintances who
choriomeningitis virus (LCMV) is an arenavirus infection are critical of animal experimentation, and having doubts
found especially in mice but also hamsters (see Chapter about the clinical value of animal research.74
9). Infected animals shed the virus in urine, saliva, and
feces. Nude mice, used in some animal research labo- Occupational Medicine Services for Animal Research Facility
ratories, appear to shed increased amounts of LCMV.70 Workers
Transmission to human beings can involve contact of
secretions with broken skin or oral or respiratory contact As previously mentioned, many animal research facilities
with dust or contaminated food. Handling contaminated have designated medical providers for both preventive and
surfaces and objects is considered a risk factor for infec- acute care services.
tion.70 Infection in human beings can range from mild
flulike symptoms to severe meningoencephalitis. Diagnosis Preplacement Screening. Preplacement evaluations are
involves viral cultures and serology. Cerebrospinal fluid similar to those for veterinary personnel. Particular work
can show lymphocytosis and decreased glucose level. The restrictions to consider based on the preplacement evalua-
disease is usually self-limiting in immunocompetent indi- tion include the risk of previously sensitized persons working
viduals. Immunocompromised individuals are at increased with animal allergens, the increased risk of immunocompro-
risk of severe disease, sometimes with hemorrhagic com- mised persons working with rodents possibly infected with
plications and fatal outcomes. There is no specific treat- LCMV as well as other zoonotic risks, and risks to women
ment. Control measures include screening of laboratory of childbearing age from working with pregnant sheep and
animals for infection (see Chapter 9). goats (Q fever). Baseline testing often includes spirometry,
serology to document immunity, and HIV and TB skin 60% reporting significant animal-related injury, more than
testing for primate workers. 30% reporting animal allergies, and more than 30% reporting
Vaccination services include ensuring that primate work- zoonotic infections. Formalin exposures and insect allergies
ers are current with measles, hepatitis B, hepatitis A, and have also been reported as significant concerns.77 A survey
polio immunizations. If wild stock animals that could carry of marine mammal workers found that 50% reported suf-
rabies (such as stray dogs) are used in the facility, rabies fering injuries from marine mammals (one third of which
vaccine should be considered for workers exposed to such were considered severe), and 23% reported skin rashes or
animals.75 reactions.78
Medical Surveillance. Many research animal workers are Allergens

enrolled in periodic medical surveillance on a yearly basis.
Periodic screening may include a questionnaire that inquires Zoo workers are exposed to allergens in both indoor and
about allergic and infectious symptoms. For primate work- outdoor environments. Aquariums may have additional
ers, HIV and TB testing is often repeated on a regular (every challenges with controlling mold. Control of allergens is
6 months or annual) basis. similar to that for veterinary personnel.
Acute Injury, Exposure, and Illness Evaluation and Zoonoses

Follow-up. Special issues in the acute care of animal care
workers include management of exposures to nonhuman Because of the diversity of species and the possibility of
primates and the need for possible herpes B prophylaxis. introduction of infectious agents from contact between
Workers with rodent exposures should ensure that acute captive and wild animals, zoo and aquarium workers are
febrile episodes are evaluated by medical providers for the exposed to perhaps the widest variety of zoonotic diseases
possibility of rat-bite fever and LCMV. As with veterinary compared with any other animal workers (see the species
workers, all acute injuries and illnesses should be consid- chart in Chapter 9). Guidelines for occupational health
ered possible sentinel health events with implications for programs for zoo workers have been published by the
the health of coworkers as well as the laboratory animals. American Association of Zoo Veterinarians.79 Zoonotic risks
Issues regarding job modifications and restrictions after to nonhuman primate handlers resemble those of workers
acute injuries and illnesses are similar to those of veterinary in primate research facilities. The care of wild ruminants
personnel. may expose workers to livestock pathogens such as brucel-
losis and Q fever. Reptile keepers are at risk of Salmonella
infection and envenomations, and bird workers are at risk of
Zoo and Aquarium Workers
Chlamydophila infection. Other enteric disease risks to zoo-
Although zoo and aquarium employees share many of the keepers include campylobacteriosis and shigellosis. Elephant
same occupational health issues as veterinary and animal handlers and staff working with nonhuman primates are at
research workers, there are particular challenges for occupa- risk of TB exposure (Figure 12-5). Zoonotic risk prevention
tional health programs targeting these workers. Depending on and control in zoo workers are similar to that in veterinary
the zoo, the diversity of species may far exceed that encoun- facilities.
tered by most other animal workers. Workers are employed Aquarium workers are at risk of Mycobacterium marinum
in only one area of the zoo or aquarium, and therefore their from tropical fish tanks. Other dermal exposure risks worthy
occupational health needs may differ widely. Although the of mention for aquarium workers include erysipeloid and
animals in a particular collection are likely captive bred, some Vibrio vulnificus.
have originated in the wild, where potential for zoonotic
infections could be greater. Many zoos and aquariums are also Erysipeloid. Erysipeloid is an infection from contact with
open to the outdoor environment, allowing contact between Erysipelothrix rhusiopathiae, a gram-positive rod bacterium
wild animals and the captive specimens, with the possibil- found in fish as well as birds and pigs. The bacteria usually
ity of disease introduction. For example, outbreaks of highly enter through broken skin. The most common manifesta-
pathogenic animal influenza (HPAI) have been reported in tion is local erythema and wound infection (Color Plate
captive birds in zoos after contact with wild birds. Cases of 12-1). Although rare, bacteremia and endocarditis can
avian influenza have also occurred in captive felids, presum- occur.80
ably as a result of feeding on infected poultry carcasses. Both
of these introductions posed infectious risks to zoo workers. Vibrio Vulnificus. Vibrio vulnificus is a marine bacteria
For these reasons, zoo workers (as well as zoo animals) may that can be encountered while handling tanks and marine
serve as sentinels of emerging infectious disease threats. For animals. It may infect wounds and cause local wound
example, primate workers in zoos have been found to have infections in immunocompetent individuals and fatal
evidence of possible infection with simian viruses consid- septicemia (Color Plate 12-2) in immunocompromised
ered to have potential for emergence.76 A special issue with persons.81 Careful hand hygiene after handling tanks and
zoo and aquarium workers is the significant number of vol- aquatic animals is essential.
unteers working in many facilities who may not receive med- Aquarium workers may also be at risk of exposure to
ical screening or prophylactic vaccinations. pathogens in marine mammals during regular care as well
Surveys of zoos have reported high rates of occupational as veterinary care and necropsies. Potential pathogens
injury and illness among zoo veterinarians, with more than include leptospirosis, brucellosis, and “seal finger” from
Figure 12-5 n Elephant being examined by a veterinarian. (From Fowler ME: Zoo and wild animal medicine
current therapy, ed 6, St Louis, 2007, Saunders Elsevier.)
bites or other direct contact with seals and other pinni- wheelbarrows and hoists. Special training is also needed for
peds. Seal finger is believed to be caused by infection with injury prevention for workers handling dangerous animals
Mycoplasma phocacerebrale 82 and is characterized by pain, and equipment.
cellulitis, and joint swelling (Color Plate 12-3). Treatment is
with tetracycline. Psychosocial Stressors
Zoo and aquarium workers may share psychosocial stressors
Chemical Hazards
with other animal workers, including grief after an animal
Disinfectant chemicals are used widely in zoos and aquar- death and fear of attack by dangerous animals. They also may
iums and may be capable of inducing irritation and develop stress related to encounters with the general public.
allergy. If a veterinary facility is present in the zoo, anes-
thetic exposures may resemble those in other veterinary Occupational Medicine Services for Zoo and Aquarium
facilities. Workers
Envenomations from reptiles, insects, fish, and other
marine organisms represent a significant hazard to reptile Because of the diversity and complexity of the occupational
handlers and aquarium workers. Emergency procedures exposures, it would seem advisable that zoos and aquariums
for treating envenomations should be in place, including designate a medical provider or group of providers for both
a stockpile or other resources to ensure the availability of routine and emergency medical services. This designated
antivenin for specific species housed at the facility (see provider should be familiar with both the infectious and
Chapter 8). noninfectious hazards that such workers face.
Preplacement Screening. Preplacement evaluations of

Physical Hazards
zoo and aquarium workers should consider the range of
Zoo and aquarium workers may have regular contact with species with which the worker is expected to have contact.
captive wild animals capable of inflicting serious and fatal Otherwise, baseline evaluations resemble those for veteri-
trauma, including large felids, bears, sharks, and elephants. nary and research animal workers.
Numerous other ergonomic risks exist, including transport Primate handlers should be screened for vaccination sta-
of feed and bedding. tus as listed for laboratory primate workers. Nonhuman pri-
Risks can be controlled by design of enclosures and train- mate handlers and elephant handlers should be screened for
ing of zoo workers in safe procedures for working near TB. Stool cultures and stool tests for ova and parasites have
dangerous animals as well as engineering solutions for trans- been recommended at baseline for zoo workers. Such cultures
port of heavy materials, such as ergonomically designed should include Salmonella, Shigella, and Campylobacter.79
Audiometry at baseline should be performed for work- v eterinary, animal research, and zoo settings, with the
ers entering noisy jobs. Because of the wide range of infec- difference being the lack of invasive procedures performed on
tious disease exposures, some with implications for disease animals. Chemical and physical hazards to pet store workers
emergence, it has been recommended that zoo workers bank are similar to those of other animal workers described.
serum at baseline and receive follow-up serology periodically
to detect zoonotic infections.83 Such serum banking should Occupational Medicine Services for Pet Store Workers
be done under strict protocols to preserve confidentiality of
workers and should be under the supervision of the consult- Preplacement Screening. As previously mentioned,
ing medical provider. many pet store workers do not receive occupational health
services, including preplacement examinations. It would
Medical Surveillance. Medical surveillance for zoo and seem reasonable, however, to offer such workers preplace-
aquarium workers is similar to that for veterinary and ani- ment examinations that resemble those for veterinary work-
mal research workers. ers. At the least, pet store workers should inform their health
care providers, if they have one, about their work activities.
Acute Injury, Illness, or Exposure Evaluation and The health care provider could then assess whether the indi-
Follow-up. Management of acute injuries and illnesses in vidual is at increased risk of zoonotic infection because of
zoo workers resembles that for veterinary and research ani- an immunocompromised condition or is at risk of develop-
mal workers. Designated emergency facilities should have ing allergic reactions from work exposures. As with other
protocols for antivenin treatment of reptile and other enven- animal worker occupational health issues, this requires that
omations (see Chapter 8). Nonhuman primate exposures the health care provider be aware of the health risks related
should be handled as emergencies, as with animal research to animal work or can consult a veterinarian to be updated
workers, because of the risk of herpes B infection. about such risks.
Vaccination. Vaccination for all workers should include

Pet Store Workers
tetanus if not up to date. Because ferrets can be susceptible
Pet store employees share many of the exposures of zoo and to human influenza, influenza vaccine should be encouraged
aquarium workers yet are rarely enrolled in formal occupa- for workers with ferret contact.
tional health programs and may not have access to medi-
cal providers with a knowledge of the particular risks of Medical Surveillance. Ongoing medical surveillance of pet
the workplace. Compared with zoos, veterinary practices, store workers is generally not performed. However, as with other
and animal research facilities, there is a lack of published animal handlers, NIOSH has recommended periodic monitor-
guidelines for occupational health services for this worker ing for allergic symptoms with a symptom questionnaire and
population. Despite this, the pet store industry is large and follow-up of positive responses as indicated. Such a screening
growing and employs thousands of workers nationwide. The questionnaire could cover infectious disease risk as well. Annual
recent multistate outbreak of monkeypox associated with audiometry should be performed on workers with significant
importation of African rodents underscored the potential noise exposures.
for disease emergence in pet stores and distribution facil-
ities related to trade in exotic pets (see Chapter 10). Pet Acute Injury, Illness, or Exposure Evaluation and
stores are generally required by local and federal regulations Follow-up. A wide range of acute infectious conditions
to have a designated veterinarian. Such an individual could can present in pet store workers and should be considered in
be in a position to advocate for preventive health services the differential diagnosis of ill employees. Animal bites and
for the employees. NASPHV has developed a compendium scratches should be treated according to the pathogens asso-
of measures to prevent disease associated with animals in ciated with particular species. In workers with bird contact
public settings, which gives general guidelines for infection who report respiratory symptoms, Chlamydophila infection
control in areas where the public has contact with animals, and hypersensitivity pneumonitis (see Chapter 7) should
including pet stores, but does not provide detailed guidance be considered. Job restrictions and modifications after
on the o ccupational health of pet store workers.84 acute illnesses and injuries are similar to those of zoo and
veterinary workers.
Hazards and Their Control in the Pet Store Setting
Farm Animal Workers
The hazards and principles of hazard control are similar
to those in zoos and veterinary offices, with the excep- Agricultural workers with animal contact may work in
tion that veterinary care procedures are not likely to take settings ranging from backyard farms with a small num-
place. Consequently, exposures to anesthetics and radia- ber of animals to intensive confinement facilities with hun-
tion are not expected. Ventilation systems and cleaning of dreds of thousands of animals. Therefore their work status
the facility may be geared to the retail setting, with less may vary from informal laborers without written job con-
attention to health concerns. There also is potential for tracts to registered employees in large and well-organized
inadequate ventilation and consequent increased risk of facilities. Job activities may range from feeding to manure
airborne allergy. management to slaughtering. The informal and varied set-
Zoonotic disease risks depend on the species of animals tings may make use of personal protective equipment dif-
sold in the facility but generally encompass risks seen in ficult, and there may be budgetary and other limitations
to implementing engineering controls. There are few com- Endotoxin and Organic Dusts
prehensive occupational health guidelines for farm animal
Farm workers in CAFOs have some of the highest exposure
workers as well as a lack of OSHA standards directly target-
to endotoxins and organic dusts, which can cause obstruc-
ing this setting. Farm managers may therefore be reluctant to
tive airway changes and the febrile syndrome known as
see any value in developing relationships with members of
organic toxic dust syndrome (ODTS).28 These organic dusts
an occupational health team or arranging for preplacement
may contain plant material from bedding and feed; animal
and periodic worker evaluations. Although veterinarians are
particulates, including feces, feathers, hair, skin cells, and
often involved in the care of farm animals, some of the first-
urine; bacteria; pathogenic fungi; endotoxins; antibiotics
aid and other medical treatment may be accomplished by
and other feed additives; and chemicals including pesticides,
the farmers themselves. Some of the occupational exposures
ammonia, hydrogen sulfide, and methane. Significant rates
may resemble those of workers in zoos, yet the high density
of OTDS have been reported among swine CAFO workers.2
of animals in some production facilities can present unique
Wetting dusts and regular cleaning of bedding as well as
exposure situations.
improved ventilation and manure management may reduce
Technological changes in swine and poultry production
worker exposure to organic dusts. When exposures are not
have increased the efficiency of husbandry operations over
able to be controlled, the use of respiratory protection may
the past several decades. A single concentrated animal feed-
be necessary.
ing operation (CAFO) facility may house hundreds of pigs
or more than 50,000 chickens or other poultry.2 Such facili-
ties produce high concentrations of airborne dusts and gases, Zoonoses
large quantities of manure, as well as the potential for rapid
spread of diseases among animals and workers. Many diseases of domestic livestock and poultry are poten-
tially communicable to workers. Table 12-6 shows some of
these pathogens.
Allergens Contact with rodents near animal operations can increase
A large variety of animal allergens on farms can pose a the risk of hantavirus and other rodent-borne infections.
significant health hazard to animal workers. Allergy from Control of zoonotic disease risks involves many of the pre-
pigs, horses, chickens, cattle, goats, and other domestic ani- ventive measures mentioned for veterinary and research
mals is well recognized (see Chapter 7). The development of animal workers, including control of disease in animals,
occupational allergy to such allergens may cause significant handwashing practices, disinfection of surfaces, and use of
difficulties in workers who are skilled in working with one personal protective equipment as necessary. Rodent manage-
particular type of animal, such as horses. Control strategies ment and tick control can further reduce zoonotic risks, as
include wetting dusts to avoid airborne exposures, frequent can reducing contact between farm animals and wildlife.
washing of animals, and use of respirators and gloves when
around animals. Workers may want to consider allergen Chemical Hazards
desensitization to allow them to continue working with
particular animal species. Chemical hazards encountered by farm animal workers
Other significant antigens around farms include those include animal pesticides such as tick dips, oxides of
produced by thermophilic bacteria growing on moldy hay nitrogen causing silo filler’s lung from decomposing silage,
or silage and in other moist environments that can cause and ammonia and hydrogen sulfide from manure waste in
hypersensitivity pneumonitis (farmer’s lung; see Chapter 7), swine CAFO facilities.28 Silo filler’s lung is a toxic pneu-
which can produce chills, fever, cough, and shortness of monitis that develops hours to days after a filling a silo and
breath. A survey of dairy farmers found antibodies to such inhaling the irritating oxides of nitrogen gas. This exposure
antigens in 75% of farmers tested and a history of symptoms can result in acute respiratory distress syndrome (ARDS)
consistent with farmer’s lung in 17%.2 and death in severe cases. Hydrogen sulfide can also cause
TABLE 12-6 n Specific Occupational Pathogens Associated With Animal Husbandry
Type of Production Pathogens High-Risk Activities
Poultry Salmonella, Campylobacter fetus, Chlamydophila, avian influenza Slaughtering, meat processing, close
virus, Newcastle disease virus, Erysipelothrix, Histoplasma contact with sick animals
Swine Salmonella, Campylobacter, Streptococcus suis, Brucella,
Erysipelothrix rhusiopathiae, vesicular stomatitis virus,
hepatitis E virus, Nipah virus, influenza
Cattle Brucella, B. anthracis Butchering meat, contact with birthing
products, skinning, inadequate
cooking of meat
Sheep Orf virus, Coxiella, B. anthracis Skinning, butchering, marketing
Bushmeat, wild game Francisella, Trichinella, other emerging pathogens, primate
viruses (non-U.S.)
ARDS and death in human beings and animals, often after of hypersensitivity pneumonitis. Cases of zoonotic disease
pumping liquid manure out of a pit. Ammonia fumes can in an animal worker should be considered a sentinel health
be highly irritating to the respiratory tract. These chemical event with relevance to both co-workers and herd health.
risks can be reduced by substitution of less-toxic pesticides, Communication back to the veterinarian responsible for the
proper silage and manure management, improvements in health of the farm animals should occur, perhaps mediated
ventilation, and personal protective equipment for short- by the public health department. The veterinarian may be
term, high-exposure tasks. simultaneously managing an outbreak in the domestic ani-
mals, and close communication between animal and human
health professionals is critical. Infectious disease exposures
Physical Hazards
requiring prophylaxis and follow-up may include anthrax
Work with large domestic animals carries a significant risk and Mycobacterium bovis. Similarly, acute exposures to chem-
of crush and other traumatic injuries from kicking, biting, icals could be a sign that other workers and animals are at
and other direct contact. Other physical hazards include risk. Acute injuries from animals and other physical factors
noise and traumatic injuries from farm machinery, ultra- should also be viewed as opportunities to review possible
violet radiation, and musculoskeletal strains from lifting breakdowns in safety measures and ways to further improve
objects and animals. Certain tasks such as animal slaughter safety. Decisions about job restriction and modification and
and processing may involve repetitive motions and result in confidentiality issues are similar to those for other animal
overuse injuries. Animal slaughter and butchering can also workers.
result in injuries from knives and other sharp tools.
Wildlife Rehabilitators, Hunters, and Other
Psychosocial Stressors Workers With Wildlife Contact
Psychosocial stressors in working with farm animals include Although often not included in discussions of occupational
fear of trauma or infection. There may also be feelings of risks to animal workers, several groups with significant
isolation for farmers working in rural locations.85 exposure to wild animals through informal or formal work
activities deserve mention. Wildlife rehabilitators are often
volunteers who care for injured and sick wild animals in a
Occupational Medicine Services for Farm Animal Workers
variety of settings, including wildlife sanctuaries and their
As previously mentioned, many farm animal workers are homes. Hunters may be amateur or professional and have
not currently enrolled in preventive occupational medicine intimate contact with blood and other body fluids of animals
screening and follow-up programs. Nonetheless, the fol- while butchering and skinning mammals and defeathering
lowing components of preventive occupational medicine birds, in addition to the consumption of wild game meat.
services for such workers should be considered based on the Other workers with potential wildlife contact include zoolo-
level of hazardous exposure. Sometimes screening is neces- gists, who may be trapping, dissecting, and otherwise com-
sary after an outbreak of disease among either workers or ing in contact with a wide variety of wild animals; forestry
animals; this process would be greatly simplified if baseline workers; and animal control officers and wildlife manage-
medical information were obtained on all workers. ment biologists, who may be involved in the immobilization
and transportation of wild animals and who are at risk of
Preplacement Screening. Because of the risk of allergy, zoonotic disease through direct contact as well as exposure
workers on farms should be screened for allergic symptoms to vectors, including ticks and mosquitoes.
at baseline and periodically thereafter. Baseline spirometry
is advisable. Workers with immunocompromised status are Hazards With Wildlife Contact
at increased risk of zoonotic transmission, and farm animal
workers, especially if zoonotic diseases are endemic, should Hazards faced by these groups include a wide range of
be screened and counseled for the risk of transmission in zoonotic disease exposures similar to those of zoo person-
immunocompromised individuals. Musculoskeletal prob- nel and vary according to the species encountered. Examples
lems at baseline should be identified and a preventive plan include Lyme disease, ehrlichioses, brucellosis, tularemia,
implemented to prevent injuries. If a respirator will be used, plague, rabies, giardiasis, and hantavirus.86 Vector-borne
the OSHA respirator medical evaluation and questionnaire diseases are a greater threat to these individuals compared
should be completed. with many other animal workers. Wildlife rehabilitators face
allergen and chemical exposures similar to those in veterinary
Vaccination. Vaccinations for all farm animal workers practice or zoos. Individuals working around areas of bird and
should include tetanus and seasonal influenza vaccine bat roosting, including caves, bridges, and abandoned build-
(especially for swine and poultry workers). Periodic exami- ings, are at risk for exposure to pathogenic fungi, including
nations should inquire about allergic and infectious disease Histoplasma, Cryptococcus, and Blastomyces. Chemical expo-
symptoms as well as problems related to contact with chemi- sures for wildlife management professionals may include
cals or physical hazards. inadvertent exposure to immobilizing (tranquilizer) agents
and envenomations from reptiles and arthropods. Physical
Acute Injury, Illness, or Exposure Evaluation and exposures for wildlife biologists include sun exposure, cold,
Follow-up. The acute care of farm animal workers should and heat stress. Individuals working with wild animals face
consider zoonotic and allergic risks as well as the possibility physical hazards of attacks and bites. Hunters risk similar
hazards as well as the risk of noise exposure from firearms appropriate management of acute illnesses and injuries,
and acute injuries and bloodborne disease transmission dur- which may involve unusual zoonotic diseases, enveno-
ing skinning and butchering game. mations, or other animal-related medical conditions
with which many human health clinicians will be less
familiar.
Occupational Health Services for Persons With
Wildlife Contact
Occupational medical services for wildlife workers are ONLINE RESOURCES
often less formalized than for other worker groups such as
research animal workers. Depending on the level of expo- • The National Institute for Occupational Safety and Health
sure, baseline medical screening that includes screening for (NIOSH): http://www.cdc.gov/NIOSH
allergy, immunocompromised status and other major medi- • Occupational Safety and Health Administration (OSHA):
cal conditions, and counseling about ways to reduce risk of http://www.osha.gov
exposure to zoonotic pathogens and avoid animal-related • Committee on Occupational Safety and Health in
injury would appear to be indicated. If individuals have con- Research Animal Facilities, Institute of Laboratory
tact with rodents in a hantavirus-endemic area, they should Animal Resources, Commission on Life Sciences, National
undergo respirator medical clearance and respirator fit test- Research Council: Occupational health and safety in the
ing as required under the OSHA respirator standard. Serum care and use of research animals, Washington DC: National
banking should be considered for individuals at high risk of Academy Press; 1997. Available at http://books.nap.edu/
zoonotic disease exposure. Immunizations should include openbook.php?isbn=0309052998
tetanus prophylaxis as well as vaccine rabies for individuals
working with bats, raccoons, skunks, or other potentially
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Public Health and
Human-Animal 13
Medicine
Peter M. Rabinowitz, Lisa A. Conti, and Hugh M. Mainzer
Both the human and veterinary medical oaths address the • Educate clinicians on ways to refocus clinical activities
need for the promotion of public health. This chapter deals toward prevention and to understand the links among
with human-animal health situations in which popula- environment, host, and agent.
tion health duties take primacy and where human and vet- • Consider surveillance of animals as well as human
erinary clinicians perform many functions that place them beings for early detection of disease risk.
together on the front line of public health practice (Color
Plate 13-1).
In ancient Greece, Asclepius, Apollo’s son, was charged Human Health Clinicians
by the gods with caring for the mortals of Greece (the classic • At a minimum, clinicians are required to report “noti-
symbol of medicine is Asclepius’ staff, around which is wound fiable diseases” to the state or local health department.
one snake).* His two daughters were Hygeia (Figure 13-1), the It is critical to contact the health department if an issue
guardian of health and champion of common sense practices of public health importance is even suspected.
as the basis of wellness (“cleanliness is next to godliness”), and • Practice preventive medicine.
Panacea, whose occupation was to cure individuals already
sick, one at a time. Mortals remained healthier when they fol-
lowed Hygeian principles, creating a healthy environment and
preventing disease. Individuals who lost their health sought Veterinary Clinicians
Panacea. • All veterinary clinicians must recognize that they are
Although in today’s culture, human and veterinary clini- essential parts of the public health system, with respon-
cians are more likely to practice solely as the hand of Panacea, sibility to protect and improve the health of human
the “one health” concept—drawing human, veterinary, and as well as animal populations. What the veterinarian
population health practices together—is focused on provid- observes, diagnoses, and treats in the clinical setting
ing a comprehensive approach to disease control and pre- can have a far-reaching population health impact.
vention and wellness promotion. • It is important to contact the health department (in
addition to requirements for reporting to agricul-
ture officials) if an issue of public health importance
Key Points for Clinicians and Public Health is suspected to discuss the situation. For example, if
Professionals leptospirosis is diagnosed in an animal, the public
health department can provide guidance for prevent-
ing human cases and be on the watch for human cases.
Public Health Professionals Contacting the health department regarding a commu-
nicable disease or other environmental health hazard
• Facilitate communication between human health care can also increase communication between veterinar-
providers and veterinary health care providers. ians and human health clinicians in the community.
• Recognize that veterinary and human health clinicians • Practice preventive medicine.
perform many functions that place them on the front
lines of public health practice.
THE 10 ESSENTIAL PUBLIC HEALTH SERVICES

*Commercial, military, and American medical organizations use the cadu-
ceus of Hermes (rod entwined by two snakes and topped by a pair of wings)
as their symbol. Most medical associations around the world, including the In 1994, the U.S. Public Health Service assembled and
World Health Organization and the veterinary profession, use the staff of tasked the Public Health Functions Steering Committee to
Asclepius, which has a single serpent encircling a staff. develop a working definition of public health and a guiding
372
Chapter 13 n Public Health and Human-Animal Medicine 373
DISEASE SURVEILLANCE AND INFORMATION

FLOW BETWEEN HUMAN AND ANIMAL HEALTH
PROFESSIONALS
Much of this book discusses the need for enhanced commu-

nication between animal health and human health profes-
sionals. Not always evident is the key role that public health
professionals and the public health system play in such
communication.
The first three core functions of public health systems
are to monitor the status of the health of the community; to
diagnose and investigate health problems and health hazards
affecting communities; and inform, educate, and empower
communities to improve health. To accomplish these func-
tions, accurate information is required on the prevalence
and incidence of disease events and risk factors as well as the
extent of environmental health hazards. A major method of
obtaining this information is from surveillance data gath-
ered through mandated reporting systems. These data,
reported by clinicians, laboratories, and others, are used to
identify emerging diseases, plan for disasters, track trends,
and evaluate progress of intervention strategies. Reportable
disease events in animals could be sentinel events for human
health hazards, and vice versa.
In the United States each state can set its own priorities
for disease reporting. The Council of State and Territorial
Epidemiologists (CSTE; http://www.cste.org) and National
Association of State Public Health Veterinarians (NASPHV;
Figure 13-1 n The bust of the Greek muse of health, Hygeia, on the http://www.nasphv.org) provide guidance for such report-
CDC’s Roybal campus in Atlanta, Ga. (From Centers for Disease Control and able condition criteria and for both communicable and
Prevention Public Health Image Library. Photo courtesy John P. Anderton.)
noncommunicable conditions. State and local health depart-
ments then provide selected data to the Centers for Disease
f ramework for the responsibilities of local public health sys- Control and Prevention (CDC).2 Most states have required
tems.1 The resulting 10 Essential Public Health Services are animal disease reporting of agricultural importance to agri-
the following: cultural agencies as well (see state requirements at http://
1. Monitor health status to identify and solve community www.biosecuritycenter.org/reportDisease.php). Box 13-1
health problems. lists the human infectious diseases that are nationally notifi-
2. Diagnose and investigate health problems and health able to the public health system. One animal disease, rabies, is
hazards in the community. also required to be reported. For a complete listing of nation-
3. Inform, educate, and empower people about health ally notifiable diseases and other conditions of public health
issues. importance (including injury and lead), see http://www.cdc.
4. Mobilize community partnerships and action to identify gov/ncphi/disss/nndss/phs/files/NNDSS_event_code_list_
and solve health problems. January_2008.doc.
5. Develop policies and plans that support individual and In individual states, additional diseases may also be
community health efforts. reportable to state health and/or agriculture departments.
6. Enforce laws and regulations that protect health and In the United States veterinarians may be required to
ensure safety. report selected clinical conditions to either public health
7. Link people to needed personal health services and authorities, who may perform further disease investigations
ensure the provision of health care when otherwise to protect human health, or to their state veterinarian at the
unavailable. state department of agriculture for the protection of animal
8. Ensure a competent public and personal health care and human health. Ideally, the public health and agriculture
workforce. authorities then communicate. State veterinarians provide
9. Evaluate effectiveness, accessibility, and quality of selected data to the U.S. Department of Agriculture (USDA).
personal and population-based health services. Every 6 months the USDA reports to the World Organization
10. Research for new insights and innovative solutions to for Animal Health (OIE) regarding the presence or absence
health problems. of reportable animal diseases in the United States.3 Box 13-2
lists reportable diseases tracked by the OIE.
The actions of public health professionals as well as human When veterinarians report clinical illness in animals to
and veterinary clinicians that are mentioned in many sec- public health authorities, public health professionals can
tions of this book encompass these 10 core responsibilities. assist with providing prevention guidance to minimize
Box 13-1 Nationally Notifiable Infectious Diseases, United States, 2009
AIDS Mumps
Anthrax Novel influenza A virus infections
Arboviral neuroinvasive and nonneuroinvasive diseases Pertussis
• California serogroup virus disease Plague
• Eastern equine encephalitis virus disease Poliomyelitis, paralytic
• Powassan virus disease Poliovirus infection, nonparalytic
• St. Louis encephalitis virus disease Psittacosis
• West Nile virus disease Q Fever
• Western equine encephalitis virus disease • Acute
Botulism • Chronic
• Foodborne Rabies
• Infant • Animal
• Other (wound and unspecified) • Human
Brucellosis Rocky Mountain spotted fever
Chancroid Rubella
Chlamydia trachomatis, genital infections Rubella, congenital syndrome
Cholera Salmonellosis
Coccidioidomycosis Severe acute respiratory syndrome–associated coronavirus
Cryptosporidiosis (SARS-CoV) disease
Cyclosporiasis Shiga toxin–producing Escherichia coli
Diphtheria Shigellosis
Ehrlichiosis/anaplasmosis Smallpox
• Ehrlichia chaffeensis Streptococcal disease, invasive, group A
• Ehrlichia ewingii Streptococcal toxic-shock syndrome
• Anaplasma phagocytophilum Streptococcus pneumoniae, drug resistant, invasive disease
• Undetermined Streptococcus pneumoniae, invasive disease, non–drug resistant, in
Giardiasis children <5 years
Gonorrhea Syphilis
Haemophilus influenzae, invasive disease • Primary
Hansen disease (leprosy) • Secondary
Hantavirus pulmonary syndrome • Latent
Hemolytic uremic syndrome, postdiarrheal • Early latent
Hepatitis, viral, acute • Late latent
• Hepatitis A, acute • Latent, unknown duration
• Hepatitis B, acute • Neurosyphilis
• Hepatitis B virus, perinatal infection • Late, nonneurologic
• Hepatitis, C, acute • Syphilitic stillbirth
Hepatitis, viral, chronic Syphilis, congenital
• Chronic hepatitis B Tetanus
• Hepatitis C virus infection (past or present) Toxic-shock syndrome (other than streptococcal)
HIV infection Trichinellosis (trichinosis)
• Adult/adolescent (age ≥13 years) Tuberculosis
• Child (age ≥18 months and <13 years) Tularemia
• Pediatric (age <18 months) Typhoid fever
Influenza-associated pediatric death Vancomycin-intermediate Staphylococcus
Legionellosis aureus
Listeriosis Vancomycin-resistant Staphylococcus aureus
Lyme disease Varicella (morbidity)
Malaria Varicella (deaths only)
Measles Vibriosis
Meningococcal disease Yellow fever
From Centers for Disease Control and Prevention: National notifiable infectious diseases. Available at http://www.cdc.gov/ncphi/disss/nndss/phs/infdis.htm. Accessed April 8, 2009.
AIDS, Acquired immunodeficiency syndrome; HIV, human immunodeficiency virus.
human risk of disease. In addition, an inquiry into possible Surveillance for disease can be both passive and active.
associated human cases may ensue. Passive surveillance involves tracking the number of diag-
Both human medical reporting requirements and nosed cases of disease in a community that are reported to
agricultural requirements vary from state to state, but the public health authorities. Active surveillance involves per-
nationally notifiable diseases and the OIE list represent forming surveys or other systematic investigations to detect
a minimum dataset for which ongoing surveillance is cases not reported through passive systems. Active surveil-
conducted. lance can take place for both human and animal diseases.
Box 13-2 Animal Diseases Reportable to the World Organization for Animal Health
Multiple Species Diseases Equine influenza

Anthrax Equine piroplasmosis
Aujeszky’s disease Equine rhinopneumonitis
Bluetongue Equine viral arteritis
Brucellosis Glanders
• Brucella abortus Surra (Trypanosoma evansi)
• Brucella melitensis Venezuelan equine encephalomyelitis
• Brucella suis Swine Diseases
Crimean Congo hemorrhagic fever African swine fever
Echinococcosis/hydatidosis Classical swine fever
Foot and mouth disease Nipah virus encephalitis
Heartwater Porcine cysticercosis
Japanese encephalitis Porcine reproductive and respiratory syndrome
Leptospirosis Swine vesicular disease
New world screwworm (Cochliomyia hominivorax) Transmissible gastroenteritis
Old world screwworm (Chrysomyia bezziana)
Paratuberculosis Avian Diseases
Q fever Avian chlamydiosis
Rabies Avian infectious bronchitis
Rift Valley fever Avian infectious laryngotracheitis
Rinderpest Avian mycoplasmosis (Mycoplasma gallisepticum)
Trichinellosis Avian mycoplasmosis (Mycoplasma synoviae)
Tularemia Duck virus hepatitis
Vesicular stomatitis Fowl cholera
West Nile fever Fowl typhoid
Highly pathogenic avian influenza and low-pathogenic avian
Cattle Diseases
influenza in poultry*
Bovine anaplasmosis Infectious bursal disease (Gumboro disease)
Bovine babesiosis Marek’s disease
Bovine genital campylobacteriosis Newcastle disease
Bovine spongiform encephalopathy Pullorum disease
Bovine tuberculosis Turkey rhinotracheitis
Bovine viral diarrhea
Contagious bovine pleuropneumonia Lagomorph Diseases
Enzootic bovine leukosis Acarapisosis of honey bees
Hemorrhagic septicemia American foulbrood of honey bees
Infectious bovine rhinotracheitis/infectious pustular vulvovaginitis Bee diseases
Lumpy skin disease European foulbrood of honey bees
Malignant catarrhal fever (wildebeest only) Myxomatosis
Theileriosis Rabbit hemorrhagic disease
Trichomonosis Small hive beetle infestation (Aethina tumida)
Trypanosomosis (tsetse-transmitted) Tropilaelaps infestation of honey bees
Varroosis of honey bees
Sheep and Goat Diseases
Caprine arthritis/encephalitis Fish Diseases
Contagious agalactia Epizootic hematopoietic necrosis
Contagious caprine pleuropneumonia Epizootic ulcerative syndrome
Enzootic abortion of ewes (ovine chlamydiosis) Gyrodactylosis (Gyrodactylus salaris)
Maedi-visna Infectious hematopoietic necrosis
Nairobi sheep disease Infectious salmon anemia
Ovine epididymitis (Brucella ovis) Koi herpesvirus disease
Peste des petits ruminants Red sea bream iridoviral disease
Salmonellosis (Salmonella abortus ovis) Spring viremia of carp
Scrapie Viral hemorrhagic septicemia
Sheep pox and goat pox Mollusk Diseases
Equine Diseases Abalone viral death
African horse sickness Infection with Bonamia exitiosa
Contagious equine metritis Infection with Marteilia refringens
Dourine Infection with Perkinsus marinus
Equine encephalomyelitis (Eastern) Infection with Perkinsus olseni
Equine encephalomyelitis (Western) Infection with Xenohaliotis californiensis
Equine infectious anemia Infection with Bonamia ostreae
Continued
Box 13-2 Animal Diseases Reportable to the World Organization for Animal Health—Cont’d
Crustacean Diseases Crayfish plague (Aphanomyces astaci)

Infectious hypodermal and hematopoietic necrosis Infectious myonecrosis
Spherical baculovirosis (Penaeus monodon–type baculovirus) White tail disease
Taura syndrome Other Diseases
Tetrahedral baculovirosis (Baculovirus penaei) Camelpox
White spot disease Leishmaniosis
Yellowhead disease
As of January 21, 2008.

From World Organisation for Animal Health: OIE listed diseases. http://www.oie.int/eng/maladies/en_classification2008.htm?e1d7. Accessed March 3, 2008.
*Per Chapter 2.7.12 of the Terrestrial Animal Health Code.
For specific diseases, public health authorities may cre-

ate and maintain surveillance systems using animal sentinels. OUTBREAKS
Examples are the use of sentinel chickens for West Nile virus
and other encephalitis viruses (Figure 13-2) and routine tick When outbreaks of disease occur in human or other animal
and mosquito surveillance for Lyme disease and West Nile populations, they are ideally detected by the surveillance sys-
virus, respectively. tems described above. Such detection can lead to a response
Ongoing monitoring for the appearance of disease out- on both the public health and clinical levels (Figure 13-4). If
breaks in both human beings and other animals takes place an outbreak involves both human and animal health, com-
on local, state, national, and international levels. Figure 13-3 munication and coordination between human and animal
depicts some of the mandated and potential information health professionals becomes critical. Specific roles for clini-
flow between animal and human health. As with any sys- cians and public health professionals are mentioned in many
tem of such complexity, there is potential for information chapters of this book.
to be lost or for miscommunication to occur. Public health The occurrence of a disease outbreak in human beings or
professionals can play an important role in facilitating com- other animals can be a sign of an emerging health hazard in
munication between human health and animal health care the environment. Examples include an unintentional release
providers. However, for nonreportable conditions, and even of a toxic chemical such as chlorine gas from a tanker truck,
in the case of conditions that have reporting requirements, which could sicken both human beings and animals, or the
veterinarians and human health clinicians should consider introduction of a novel pathogen into an ecosystem.
contacting each other in addition to the relevant authorities, Public health systems need to be alert to the possibil-
while respecting patient confidentiality (see Chapter 14). ity of intentional releases of pathogens or chemicals as in a
Fostering such communication in a community is an biological or chemical terrorism attack. In such scenarios,
example of the fourth public health function—to “mobilize there is potential for animals to serve as sentinels for human
community partnerships and action to identify and solve beings if they develop signs of illness before it is recognized
health problems.” Such information is fundamental to the in human populations. As Table 13-1 shows, in the event of
ability for the public health service to “develop policies and a bioterrorism attack in the United States, different animal
plans that support individual and community health efforts,” species may either provide early warning to human beings,
the fifth essential service. serve as indicators of ongoing risk in the environment or, in
Figure 13-2 n A caged sentinel chicken flock used to detect the presence of a specific arbovirus. (From Centers
for Disease Control and Prevention Public Health Image Library, Atlanta, Ga.)
National and international animal National and international health authorities,

health authorities, including USDA OIE including DHHS, CDC, FDA, and WHO
Department of agriculture; State or local department of public health;

state veterinarian state public health veterinarian
(www.usaha.org/members.shtml) (www.nasphv.org)
Human diseases reportable

Animal diseases reportable to agriculture
to public health department
Select animal diseases
Disease prevention coordination

Veterinary Human
health care health care
providers providers
Figure 13-3 n Flow of disease information between animal health and human health. Solid line, Mandated
reporting; hatched line, recommended communication.
Figure 13-4 n This victim of Venezuelan equine encephalitis was reported and permitted public health
authorities to alert the community to take precautions against mosquito bites. (From Centers for Disease Control
and Prevention Public Health Image Library, Atlanta, Ga. Courtesy James Stewart.)
some situations, help spread or maintain an outbreak though from an industrial facility in Georgia. In the days after
propagation of infection in an a nimal population. the release, electronic records from pet hospitals in the
Similarly, animals could provide early warning of an area showed that respiratory signs in cats, gastrointesti-
intentional release of chemical warfare agents.4,5 For animals nal signs in dogs, and eye inflammation signs in dogs and
to serve as effective sentinels for either biological or chemical cats increased significantly in areas of greater chemical
classes of agents, there must be adequate surveillance systems exposure. These signs were consistent with chemical irri-
in place (particularly for animal populations) and working tation, and such data provided information about high-
channels of communication between human and animal risk exposure areas for both animals and human beings
health, with the public health system playing a vital role in in the vicinity.6
such channels. The prospect for another global pandemic of human
An example of the use of electronic animal surveil- influenza derived from a highly pathogenic animal strain has
lance for public health benefit occurred after the unin- strengthened existing partnerships and created new ones in
tentional release of propyl mercaptan (a chemical with a the human, veterinary, and public health realms. Surveillance
strong onionlike odor and potential for irritant effects) of wild birds for subclinical viral carriage, as well as morbidity
Table 13-1 n Public Health Implications of Animals Exposed to Bioterrorism Agents*

Animals That Can Provide
Early Warning of Acute Animals That Could Be Markers Animals That Can Propagate
Agent/Disease Bioterrorism Attack for Ongoing Exposure Risk or Maintain Epidemic
Category A
Anthrax Sheep, cattle‡ Sheep, cattle‡
Dogs and pigs*
Plague Cats* Dogs, cats*; multiple species† Cats, camels, goats‡
Tularemia None‡ Rodents† Ticks, rodents, prairie dogs†
Horses, cows†
Botulism None‡ None‡ None‡
Filovirus infection Unknown Unknown Wildlife‡
Category B
Q fever Sheep* Wild hogs, goats† Cats, sheep, goats, cattle‡
Brucellosis None‡ Cattle† Wildlife, cattle, dogs‡
Foodborne illness: Cattle‡ Unknown Unknown
Salmonella spp., Shigella
spp., Cryptosporidium
spp., etc.
Glanders Unknown Horses† Horses†
Alphaviruses (VEE/EEE) Horses‡ Birds* Wild birds†
Rift Valley fever Cattle, sheep‡ Sheep* Mosquitoes, rodents*
Ricin toxin Unknown Unknown Unknown
Epsilon toxin Unknown Unknown Unknown
Category C (Emerging Diseases)
Nipah virus Unknown Multiple species‡ Pigs*
Hantavirus None† Multiple species† Rodents†
Flavivirus (WN, JE) Wild birds‡ Mosquitoes, birds† Birds*
From Rabinowitz P, Gordon Z, Chudnov D, et al: Animals as sentinels of bioterrorism agents, Emerg Infect Dis 12:647, 2006.
*Level 1 evidence available; experimental or cohort study or randomized clinical trial.
†Level 2 evidence available: case-control or cross-sectional study.
‡Level 3 evidence available: Case reports or case series, expert opinion.
Unknown, Insufficient evidence found; VEE/EEE, Venezuelan equine encephalitis/Eastern equine encephalitis; WN, West Nile; JE, Japanese encephalitis.
and mortality, is taking place on an unprecedented scale

through efforts such as the Global Avian Influenza Network INSPECTIONS AND REGULATIONS OF
for Surveillance (GAINS)7 and the Highly Pathogenic Avian FACILITIES
Influenza Early Detection Data System (HEDDS).8 Reports
of disease events in animals are being collected on a real-time A number of clinical conditions discussed in this book are
basis by the Emergency Prevention System for Transboundary related to facilities such as petting zoos, pet stores, and vet-
Animals and Plant Pests and Diseases (EMPRES), coordinated erinary clinics, where members of the public come in con-
by the United Nations Food and Agriculture Organization tact with animals. It can often be confusing to the clinician
(FAO).9 Such efforts may provide the first clue to possible regarding which agency has responsibility for the inspec-
impending human outbreaks of highly pathogenic avian tion and regulation of particular facilities, an example of
influenza. the sixth essential public health service. Table 13-2 lists a
The public health response to outbreaks can involve a number of different types of facilities, and whether ani-
number of measures to control the spread of disease. These mal health or human health officials tend to be involved in
include environmental health measures to ensure clean air, inspections and regulations. In some of these settings, such
water, food supplies, and housing as well as elimination of as food processing, both animal health and human health
specific hazards, vector control, and public health messaging agencies may be involved. In certain situations, local ani-
regarding risk reduction measures for affected populations. mal control divisions are also often involved; this division is
Specific control measures are mentioned in many of the dis- usually separate from both public health departments and
ease-specific sections of this book. departments of agriculture.
Table 13-2 n Inspection and Regulation of Various Settings Involving Human Animal Contact
Public Health Inspections/ Local Animal Control Department of Agriculture
Type of Facility or Scenario Regulations Officer Inspections/Regulations
Pet store, petting zoo, Recommendations for Ensures animal health

country fair with animal handwashing facilities and
exhibits, pet swap meets other infection control
measures, zoonoses
investigation
Beaches (pet policies) Beach water monitoring for Enforces pet policies
pathogens
Veterinary clinics Occupational health of Management of reportable
veterinary staff and diseases
biomedical waste
Quarantine of dog or cat after Oversees quarantine Ensures dog or cat is
bite to human being quarantined
Farms Occupational health of Health of animals, biosecurity,
workers management of reportable
diseases
Food processing facilities/ Occupational health of workers, Food safety
abattoirs/live bird markets food safety (including FDA)
Building with lead Oversees screening of persons,
contamination remediation
Local regulations and scope of jurisdiction may vary.

FDA, Food and Drug Administration.
include the medical reserve corps of Health and Human

DISASTERS AND HUMAN-ANIMAL MEDICINE Services Office of the Surgeon General as well as the Disaster
Medical Assistance Team (DMAT; http://www.hhs.gov/aspr/
In a disaster situation, there is a need to coordinate ser- opeo/ndms/teams/dmat.html)* and the National Veterinary
vices for animals as well as human beings. The seventh and Response Team (http://www.dhhs.gov/aspr/opeo/ndms/
eighth public health services, linking people to health care teams/vmat.html).†
and ensuring a competent workforce are never more criti- The USDA has its own emergency response unit, the
cal than during a disaster. People often keep themselves in National Animal Health Emergency Response Corps, which
harm’s way if their pets’ safety and health needs are not can address herd health or flock health issues such as out-
addressed. Recent experience with hurricanes has dem- breaks of foot and mouth disease, Newcastle’s disease of
onstrated that some directly in the path of these storms poultry, or avian influenza (see http://www.aphis.usda.gov/
would not leave their homes when there was no place to emergency_response). Such efforts may involve mass vacci-
take their pets. The extended public health community is nation, culling, or quarantine.
now addressing this. The Pets Act authorizes the Federal
Emergency Management Agency (FEMA) to provide shel-
ter for the animals belonging to those persons beings shel- *The National Response Framework (NRF) uses the National Disaster Medical
tered, at least close enough in proximity so that they can System (NDMS), a part of the U.S. Department of Health & Human Services. Under
the NRF, NDMS serves as a component of Emergency Support Function #8 (ESF-8),
have access to the animals.10 States have animal emergency Health and Medical Services. The National Veterinary Response Team (NVRT) is a
response teams that can be and have been mobilized to cadre of individuals within the NDMS system who have professional expertise in
areas of veterinary medicine, public health, and research. In addition to supporting
address animal emergency management issues, includ- the NRF mission requirements of NDMS under ESF-8, operational support may also
ing assisting with the movement of animals to emergency be rendered by the NVRT to other federal partners such as the U.S. Department of
shelters and caring for the animals in the shelters. They Agriculture (USDA) under ESF-11, Agriculture, and Federal Emergency Management
Act (FEMA) under ESF-6, Mass Care, in the support of the Pets Evacuation and
often collaborate extensively with local communities Transportation Standards Act (PETS Act). The NVRT provides assistance in identi-
as well as a number of nongovernmental organizations fying the need for veterinary services after major disasters, emergencies, and public
working to provide shelter and care of human and animal health or other events requiring federal support and in assessing the extent of dis-
ruption to animal and public health infrastructures. The NVRT is a fully supported
populations. federal program.
Box 13-3 shows that many of the health risks that occur †Under the National Response Framework, USDA is a primary agency for Emergency
after a natural disaster are shared by both human beings and Support Function #11, Agriculture and Natural Resources. The Animal and Plant
Health Inspection Service (APHIS) is expected to play a significant role in a wide
other animals. variety of emergency incidents. APHIS’ Veterinary Services program safeguards U.S.
Both human health clinicians and veterinarians can vol- poultry and livestock from the introduction, establishment, and spread of foreign
animal diseases. Veterinary Services National Center for Animal Health Emergency
unteer for clinical roles in disaster response, including car- Management develops strategies and policies for effective incident management, and
ing for individuals and animals in shelters. Opportunities coordinates incident responses.
Figure 13-5 n Abandoned pools are a source for emerging mosquito populations.
for animal health professionals managing animals in emer-

Box 13-3 Human and Other Animal Health gency shelters and other facilities after a natural disas-
Hazards After Disasters ter (Figure 13-6).11 These guidelines are provided in Box
13-4.
• Bites from injured or stray animals
The care of displaced domestic animals in emergency
• Rodent infestation and rodent-borne disease
• Mosquito-borne disease after flooding (Figure 13-5)
shelters can present occupational health hazards for indi-
• Leptospirosis after floods viduals handling such animals. The National Institute for
• Potential for occupational exposures of persons working in Occupational Safety and Health (NIOSH) has published
emergency human and animal shelters guidelines for the prevention of occupational injury and
• Posttraumatic stress in animal owners who have lost pets illness among emergency first responders and animal res-
• Heat or cold stress, depending on the disaster cue workers handling animals during a disaster.12 Identified
• Food or waterborne illness health and safety hazards include animal bites and scratches,
• Carbon monoxide poisoning from generators rabies and other zoonoses, sharps-related injuries, heavy
• Envenomations from displaced animals lifting, skin rashes and other dermatologic conditions, ani-
mal allergy, latex allergy, noise, and pesticide exposure.
Guidelines for Management of Animals After Recommended steps to reduce these risks are shown in
a Disaster Box 13-5.
The last two essential public health services—evaluate
The CDC, in cooperation with the American Veterinary effectiveness, accessibility, and quality of personal and pop-
Medical Association, has prepared a set of detailed guidelines ulation-based health services and research for innovative
Figure 13-6 n A bird in a pet carrier. (From Mitchell M, Tully TN Jr:

Manual of exotic pet practice, St Louis, 2008, Saunders Elsevier.)
Box 13-4 CDC Guidelines for Animal Health and Control of Disease Transmission in Pet Shelters
solutions to health problems—require thoughtful reflec- tion on the current system as well as collective insight for
These interim guidelines have been developed by consultation for other forms of identification such as a tag or tattoo. Tattoos
between the American Veterinary Medical Association and the on dogs may correspond to an AKC registration number and
CDC and are advisory in nature. They are intended to provide this information should be used to trace the animal, if possible.
guidance for the care of animals entering shelters and for persons Animal Health Management and Prevention and
working with or handling the animals in response to natural Treatment of Zoonotic and Nosocomial Diseases
disasters.
Animals arriving at shelters as a result of a natural disaster need Intestinal Parasitism
special care. Because they may have been exposed to contaminated • Dogs should be treated prophylactically for internal parasites,
water and may not have had access to safe food and fresh water, including Giardia, roundworms, hookworms, and whipworms.
many are stressed and dehydrated and some may be injured and/or • Exposure to mosquitoes in flood-ravaged areas presents an
ill. Stressed animals may or may not show signs of illness and may increased risk of heartworm disease. If possible, dogs should
also exhibit behavioral disorders. Following some simple animal be tested for heartworms and appropriate preventatives or
management and disease control guidelines can help improve ani- treatment should be administered.
mal health and reduce the risk of disease transmission and injury
between animals and people. External Parasitism
What follows are some recommendations for pets arriving at • Dogs and cats should be examined for flea or tick infestation
animal shelters. and treated appropriately.
• Preventive flea and tick treatments should be considered for all
Animal Health History, Examinations, and Identification dogs and cats housed in shelters.
• Each animal should be examined at a triage site. Particular
attention should be paid to hydration status, cuts and Vaccinations
abrasions, paw/hoof/foot health (e.g., pads and claws, area • While the American Veterinary Medical Association normally
between toes), ear health (e.g., redness, discharge), oral injuries recommends that vaccination programs be customized to
(may have occurred if animal was foraging for food), vomiting individual animals, in disaster situations vaccination status may
and/or diarrhea, respiratory disease, and evidence of parasite be difficult, if not impossible, to determine. For this reason,
infestation. administration of “core” vaccines to animals upon admission
• Animals should be bathed upon entry, particularly if they to shelters when vaccination status is unavailable or not
may have been in contact with contaminated flood water. current is considered appropriate. Vaccines take some time to
Commercial dish soap can remove petroleum and some other become effective and will not address preexisting exposures, so
toxic chemicals, but care should be taken with use on sensitive personnel are cautioned to be alert for clinical signs of disease.
species (e.g., horses). Those bathing the animals should wear • A rabies vaccination should be administered to dogs, cats, and
protective clothing (e.g., rain suits, ponchos), gloves, and a ferrets. This is especially important for dogs and cats housed in
face shield or goggles with a surgical mask to avoid mucous group settings. Personnel should be aware that rabies vaccines
membrane contact with droplets and splashes that may contain may take as long as 28 days to become effective.
toxic materials. • Additional core vaccinations for dogs include distemper,
• Intake personnel should ask whether the pet has been in the hepatitis, and parvovirus.
custody of the owner since the beginning of the evacuation • Additional core vaccinations for cats include feline viral
and should inquire about the animal’s health and vaccination rhinotracheitis, panleukopenia, and calicivirus. Vaccination
history, paying particular attention to any current medical against feline leukemia should be considered for young kittens
needs or chronic health problems (e.g., diabetes, which would that will be housed in contact with other cats.
signal a need for insulin injections). In addition, owners should • Vaccination (intranasal) against Bordetella bronchiseptica and
be questioned about the animal’s usual temperament (e.g., parainfluenza should be considered for all dogs to reduce the
whether the animal can safely be housed with others of the incidence of kennel cough.
same species, whether it might be aggressive toward caretakers). • Because leptospirosis risk is higher in flood-ravaged areas
• A health record for each animal should be created and updated and because the disease is zoonotic, vaccination should be
as needed. Identification information for the animal should considered. Personnel are cautioned that leptospirosis vaccines
correspond to that for the owner so that animals and their are serovar specific and that the potential for adverse reactions
owners can be reunited. Owned animals should be clearly may be higher than for some other vaccines.
marked as “owned” and not “abandoned” to reduce the risk Diarrheal Disease
of mix-ups. Photographs should be taken, if possible. Collars • Animals presenting with (or developing) diarrhea should be
(leather or nylon, not choke chains) containing readily legible separated from healthy animals.
identification information should be placed on all animals. • Nosocomial agents of concern that may be transmitted by feces
Ideally, all animals should be microchipped. include parvovirus, panleukopenia, Giardia, and intestinal parasites.
• Cages should be clearly labeled so that newly arriving personnel • Zoonotic agents of concern for small animals include
are easily apprised of the health status and temperament of Campylobacter and Salmonella, which are highly infectious
sheltered animals. and have been associated with outbreaks in shelters and
• Animals arriving without owners should be scanned for veterinary clinics.
microchip identification. Microchips are most often placed
between the shoulder blades, but earlier models were prone to Ill Birds
migration, so animals should be scanned from the shoulder • Ill birds are usually lethargic, depressed, and inappetent. Care
blade down to the ventral chest. All scanners are not capable should be taken when handling ill birds because they may be
of reading all microchips, so if multiple types of scanners are infected with the zoonotic bacteria Chlamydophila psittaci, which
available, scan with each type before declaring an animal to be causes psittacosis. Face masks should be worn when handling
microchip-free. Animals without microchips should be checked birds of unknown origin that are exhibiting signs of illness.
Continued
Box 13-4 CDC Guidelines for Animal Health and Control of Disease Transmission in Pet
Shelters—cont’d
Behavioral Concerns • Behavioral exercises and behavioral medications may be

• Fear, panic, separation anxiety, noise and storm phobias, and administered short or long term, as required, to help animals
other behavioral disorders are common problems in displaced recover. Shelters are encouraged to seek assistance from
animals. Animals that have never had these problems may qualified animal and veterinary behaviorists who can assist
develop them, and preexisting problems are likely to worsen. them in meeting these needs.
• Providing housed animals with fresh food and water on a Euthanasia
regular basis and establishing other familiar routines will help • Animals that are irreversibly ill or exhibiting intractable signs
animals adjust to their new environment. Food and water of aggression should be euthanized. Records should be kept of
should be provided at multiple smaller and dispersed stations, animals euthanized.
rather than a few large clumped stations, to minimize fear • Animals that have been previously associated with transmission
competition and fighting among unfamiliar animals. of monkeypox (i.e., prairie dogs, African rodents) are under
• Animals without a prior history of aggression may snap, bite, legal restrictions for movement except to a veterinarian for
or hiss as a result of fear or uncertainty. Shelter personnel care. If one of these high-risk species is presented for veterinary
should approach rescued animals calmly, but cautiously. Only care at a shelter, it must be kept isolated from other animals
experienced personnel should handle animals that exhibit and housed in a separate cage. If this cannot be accomplished,
significant behavioral disorders. these animals must be humanely euthanized.
From Centers for Disease Control and Prevention: Disaster recovery information: Interim guidelines for animal health and control of disease transmission in pet shelters. http://www.
bt.cdc.gov/disasters/animalhealthguidelines.asp. Accessed April 8, 2009.
Box 13-5 Guidance to Prevent Injuries and Illnesses from working with displaced domestic animals
Recommendations for Workers • Wear sturdy clothing and protective footwear with nonslip
Workers can reduce their risk of occupational hazards associated soles; tennis shoes or sneakers do not provide protection
with displaced domestic animals by taking the following steps: from bite, puncture, or crush injuries.
• Wear hearing protection if you must raise your voice to talk to
Sanitation and Hygiene someone an arm’s length away (e.g., when working in enclosed
• Wash your hands frequently with soap and water: spaces with barking dogs).
• Before and after handling animals.
• After coming in contact with animal saliva, urine, feces, or
Animal Bites and Scratches
blood. • Complete the rabies preexposure vaccination series before
• After cleaning cages or equipment. directly handling dogs, cats, ferrets, or other mammals that may
• Before eating, drinking, smoking, taking breaks, or leaving be infected with rabies.
work. • Thoroughly clean all bite wounds and scratches with soap and water.
• After removing gloves. • Report any bite injury to your supervisor.
• Use alcohol-based hand sanitizers for cleaning hands when • Immediately receive medical evaluation of any bite wound and
soap and water are not available. the need for possible rabies postexposure treatment.
• Change into clean clothing before leaving the workplace. Other Hazards
• Wear disposable outerwear or clothing that can be removed • Take precautions when using scalpels, forceps, and other sharp
before leaving the workplace if clean clothing or laundry instruments.
facilities are not available. • Dispose of sharp devices in labeled, puncture-resistant, leak-
• Keep your nails trimmed to 1/4 inch and do not use artificial proof sharps disposal containers immediately after use.
nails. • Do not recap, bend, or remove contaminated needles and sharps.
• Use personal protective clothing and equipment. • Do not shear or break contaminated needles.
• Wear medical examination gloves that provide your skin • Take precautions when lifting heavy or awkward loads.
with a protective barrier when handling animals, animal • Use proper lifting techniques.
waste, cages, equipment, and pesticides. • Reduce the weight of loads when possible.
• Wear two pairs of gloves if one pair alone might tear. • Work together to lift loads that are unsafe for one person to
• Make sure that latex gloves are reduced-protein, powder-free handle.
gloves to reduce exposure to allergy-causing proteins. • Pregnant or immunocompromised workers should avoid
• Use nonlatex gloves if you need or want to avoid latex. contact with cat feces and pet rodents to reduce their risk of
• Wear cotton or leather work gloves as the outer pair when zoonotic disease.
heavy work gloves are needed. • Immediately report to the supervisor:
• Remember that cotton, leather, and other absorbent gloves • Any needlestick or other sharps-related injury.
are not protective when worn alone. • Any symptoms of infectious disease or zoonosis.
• Wear protective eyewear (safety glasses with side shields) • Any other workplace injury or illness.
or face shields if there is a risk of spitting or splashing of • Consult a health care provider about any occupational injury
contaminated material. or illness.
Box 13-5 Guidance to Prevent Injuries and Illnesses from working with displaced domestic
animals—cont’d
Recommendations for Employers • Provide medical examination gloves that provide workers’
Employers should protect their workers from the hazards skin with barrier protection.
associated with working with displaced domestic animals by • Provide nonlatex gloves for those workers who need or want
taking the following steps. to avoid latex.
• Provide training in: • Provide heavy work gloves or restraints for use with
• Workplace-specific hazards, including bites and scratches, aggressive animals.
zoonoses, sharps-related injuries, heavy lifting, dermatologic • Provide hearing protection for workers when
conditions, allergies, excessive noise, and pesticide exposure. needed.
• Good housekeeping, sanitation, hygiene, and infection • Provide preexposure rabies vaccination for workers with
control procedures. direct animal contact; only workers who have completed
• Animal handling procedures and use of equipment. the preexposure rabies vaccination series should work
• The use and maintenance of personal protective clothing with dogs, cats, ferrets, or other mammals that may be
and equipment. infected.
• Provide handwashing and sanitation facilities. • Provide a medical surveillance system that monitors and
• Provide alcohol-based hand sanitizers for cleaning hands records all occupational injuries and illnesses.
when soap and water are not available. • Stress to workers the importance of reporting all work-related
• Provide appropriate personal protective clothing and injuries and illnesses as soon as possible.
equipment. • Ensure that any worker with a bite injury is immediately
• Provide disposable outerwear or clothing if laundry facilities evaluated by a health care provider for rabies risk and possible
are not available. postexposure treatment and vaccination.
Modified from National Institute for Occupational Safety and Health: NIOSH interim guidance on health and safety hazards when working with displaced domestic animals. http://
www.cdc.gov/niosh/topics/flood/pdfs/displacedanimals.pdf. Accessed September 22, 2008.
continuous system improvement. This cannot happen with- 6. Maciejewski R, Glickman N, Moore G, et al. Companion animals as sen-
out the partnerships, the communication, and the feedback tinels for community exposure to industrial chemicals: the Fairburn, GA,
propyl mercaptan case study. Public Health Rep. 2008;123(3):333–342.
from the human, veterinary, and public health communi- 7. Global Avian Influenza Network for Surveillance. http://www.gains.org.
ties’ coordinated approach to animal and human health. Accessed September 23, 2008.
8. Highly Pathogenic Avian Influenza Early Detection Data System.
What does the HEDDS system do? http://wildlifedisease.nbii.gov/ai/
References abouthedds.jsp. Accessed September 23, 2008.
9. Food and Agriculture Organization of the United Nations. Emergency
1. Centers for Disease Control and Prevention. National Public Health Prevention System. http://www.fao.org/ag/AGAinfo/programmes/en/
Performance Standards Program: ten essential public health services. empres/home.asp. Accessed September 23, 2008.
http://www.cdc.gov/od/ocphp/nphpsp/EssentialPHServices.htm. 10. Public Law 109-308. Pets evacuation and transportation standards act
Accessed March 3, 2008. of 2006. http://www.animallaw.info/statutes/stusfd2006pl109_308.htm.
2. Centers for Disease Control and Prevention. National notifiable infec- Accessed September 7, 2008.
tious diseases. http://www.cdc.gov/ncphi/disss/nndss/phs/infdis.htm. 11. Centers for Disease Control and Prevention. Interim guidelines for ani-
Accessed March 3, 2008. mal health and control of disease in pet shelters. http://www.bt.cdc.gov/
3. World Organisation for Animal Health. OIE listed diseases. http://www.oie. disasters/pdf/petshelterguidelines.pdf. Accessed March 3, 2008.
int/eng/maladies/en_classification2008.htm?e1d7. Accessed March 3, 2008. 12. National Institute for Occupational Safety and Health. NIOSH
4. Rabinowitz P, Gordon Z, Chudnov D, et al. Animals as sentinels of bio- interim guidance on health and safety hazards when working with dis-
terrorism agents. Emerg Infect Dis. 2006;12(4):647–652. placed domestic animals. http://www.cdc.gov/niosh/topics/emrs/pdfs/
5. Rabinowitz P, Wiley J, Odofin L, et al. Animals as sentinels of chemical displacedanimals.pdf. Accessed October 21, 2009.
terrorism agents. Clin Toxicol (Phila). 2008;46(2):93–100.
Shared Strategies to
Maximize Human and 14
Animal Health
This textbook has outlined numerous scenarios in which

the health of human beings and other animals is closely
Professionals
aligned. The majority of the health conditions discussed
are considered preventable. Key prevention roles for human
health care providers, veterinarians, and public health pro-
fessionals are outlined in each section.
These professionals traditionally have worked in parallel, • Include veterinarians in public health outreach efforts
seeing different parts of the human-animal medicine picture in the community.
and responding to the issues that fell within one particular • Adopt a “one health” model and maximize the role of
domain (see Chapter 1). However, the growing convergence the public health department in enhancing commu-
of human and animal health and interest in a “one health” nication between human health care providers and
approach to human-animal disease issues suggest that more animal health care providers.
direct communication and cooperation among veterinar-
ians, physicians and other human health care providers, and
public health officials will become increasingly important to
better prevent disease threats. This chapter presents steps to • Identify opportunities for direct referrals to veterinar-
facilitate such cooperation. Some of the case scenarios are ians while respecting patient privacy.
based on actual cases. They illustrate the concept of veter- • Encourage other direct communication with veteri-
inarians and human health care providers making formal narians, including shared efforts to improve environ-
patient referrals to each other, just as specialty consultation mental health risks.
referrals are routinely made between members of the same • Use the health department as a means for communi-
profession. Although local public health authorities may be cating with animal health professionals regarding envi-
a conduit for information flow between human health care ronmental health problems and other shared health
providers and animal health care providers in a community, risks.
there is a role for direct communication as well. In doing so, • For patients with pets and farm animals, perform pre-
care must be taken to both convey necessary information and ventive disease risk assessments.
also respect patient privacy considerations, including HIPAA
(see Chapters 2 and 3). The use of standardized forms may
facilitate such communication. Forms shown in the case sce-
narios that follow are suggested examples of communication • Identify opportunities for direct referrals to physi-
templates for transmitting information. cians and other health care providers while respecting
The focus of many of the chapters of this book has been patient privacy.
the clinical recognition of shared environmental health risks • Use the health department as a means for commu-
facing both human beings and other animals. Enhanced clin- nicating with human health care providers regard-
ical awareness, communication, and improved history taking environmental health problems and other shared
ing can gather important information about environmental health risks.
health risks. A preventive risk assessment checklist can add • Educate human health care providers about the impor-
to such information. Home or other site visits provide an tance of the human-animal bond and alternatives to
opportunity to gain detailed information about clinically giving up a pet for health reasons.
relevant environmental risks. This chapter outlines mecha- • For owners with pets and farm animals, perform pre-
nisms for preventive risk assessments geared toward max- ventive disease risk assessments.
imizing the health of human beings and animals living in • Use home visits as an opportunity for a preventive risk
proximity. assessment.
384
Chapter 14 n Shared Strategies to Maximize Human and Animal Health 385
asks Mr. Doe’s permission to contact the family veterinarian to

REFERRALS FROM HUMAN HEALTH CARE request a consultation, and Mr. Doe agrees. The physician writes
PROVIDERS TO VETERINARIANS a note of referral to the veterinarian that does not mention the
patient’s medical condition (Box 14-2).
At times a busy physician or other human health care pro- The veterinarian evaluates the patient’s exposure to the
vider may suspect that a patient’s clinical condition may patient’s pets, other animals that may be in the household, and
be affected by contact with animals in the home or vicin- other potential animal exposures. It is not necessary for the
ity. However, clinicians are limited by time and experience veterinarian to know details about the patient’s medical con-
at addressing such issues in depth. At such times the health dition. Preventive services are provided to the pets during the
care provider can advise the patient to consult his or her vet- visit. The veterinarian writes a consultation letter back to the
erinarian. A direct referral from the health care provider to physician (Box 14-3).
the veterinarian may facilitate this process. One example is This communication illustrates the possibility of coopera-
an immunocompromised patient who reports having com- tion between human health care providers and veterinarians
panion animals. Such a patient is in need of a detailed discus- regarding the care of immunocompromised patients without
sion of zoonotic disease risks (see Chapter 10). Studies have needing to share confidential medical data (see Chapter 2).
shown that human health care providers do not feel com- Another situation in which the human health care pro-
fortable providing in-depth counseling about zoonotic dis- vider may want to directly refer a patient to a veterinarian
ease risk reduction and believe veterinarians are best suited is the occurrence of dermatophytes (see Chapter 9). Some
to do so.1 Mechanisms by which human health care provid- animals remain subclinically infected and may contribute to
ers could make direct referrals of patients to a veterinarian clinical disease in human beings. The following case scenario
for zoonotic disease risk reduction assessment and counsel- illustrates this.
ing are therefore appropriate. Box 14-1 shows the possible
components of such a referral visit.
Many medical insurance plans pay for preventive med- Case Scenario: Dermatophyte Associated
icine counseling sessions, but whether a veterinarian’s With Animal in the Home
services would be compensable at this point by such human A physician diagnoses a 9-year-old with ringworm and cul-
health insurance plans is not clear. However, if such consul- tures Microsporum canis as the causative agent (Figure 14-1).
tations become increasingly frequent, this situation could During the history taking, the mother reports that for the past
change. In addition, some pet insurance policies may cover 2 years there has been a cat living in the house and the family is
such referrals from a human health care provider as preven- attached to the cat. The mother has not noticed skin problems
tive visits under either a wellness rider (e.g., routine care, in the cat. In addition to prescribing symptomatic medication,
including vaccinations and parasite testing) or the illness the physician suggests that the mother contact the veterinarian
portion for medical coverage if the pet was suspected of to determine if the cat’s condition is associated with the child’s
having or exhibiting clinical signs of a zoonosis.2 infection. The mother requests a letter that she can take to the
veterinarian. The physician writes the veterinarian the referral
Case Scenario: Referral for Zoonotic Disease letter shown in Box 14-4.
Counseling and Risk Reduction Again, this form demonstrates the possibility of direct com-
munication between human health and animal health pro-
A nephrologist is providing ongoing care for a patient (Mr. Doe) fessionals without sharing confidential medical information
who has been on dialysis in the past but who just recently received about individuals. In this case the veterinarian can respond to
a kidney transplant. The patient is now taking a number of the human health care provider, with the owner’s permission,
immunosuppressive medications to prevent transplant rejection.
At a follow-up visit, the patient asks whether there is any risk of
infection from the animals in the house. The physician suspects
that the risk of zoonotic disease could be increased but is interested Box 14-2 Referral of Patient to Veterinarian for
in having the family veterinarian review this issue and provide Zoonotic Risk Reduction Counseling
recommendations. The physician is particularly concerned about Human-Animal Medicine Consultation
Referral Form
the patient’s cat, since she knows that toxoplasmosis can be a
severe disease in immunocompromised persons. The physician Anytown Nephrology Associates
48 Medical Drive, Anytown, State, 10001
Phone 000-000-0000, Fax 111-222-3333
Box 14-1 Components of a medical referral
visit for preventive risk reduction Patient Name: Mr. John Doe
counseling by a veterinarian Date of referral: November 7, 2009
To: Preventive Family Veterinary Associates
• Inventory animal contacts in home and around home. Referring Provider: Alan O. Pathic, MD
• Review animal husbandry practices.
• Review biosafety measures taken. Reason for referral: Zoonotic disease risk reduction with
• Identify specific infectious disease risks. Mr. Doe’s permission
• Provide counseling on disease risk reduction. Services requested: Please provide counseling on zoonotic risk
• Provide a summary of recommendations to human health care reduction, including the types of pets in the house and risks
provider (see Box 14-3). associated with each type.
Box 14-3 Sample Consultation Letter Sent From Veterinarian to Physician Regarding Zoonotic Disease
Risk Reduction
Human-Animal Medicine Consultation Report (Zoonotic Disease Prevention)
Preventive Family Veterinary Associates

100 Urban Street, Anytown, State, 10001
Phone 000-00-000, Fax 111-222-3333
To: Alen O. Pathic, MD
Anytown Nephrology Associates
48 Medical Drive, Anytown, State, 10001
Dear Dr. Pathic,
Thank you for referring Mr. Doe to me for zoonotic disease risk assessment and preventive counseling in regard to reducing his risk of
zoonotic disease. He was seen in our office on December 12, 2009. His evaluation consisted of an inventory of animal contacts in the home
and peridomestic environment, a review of animal husbandry and biosafety practices in the home, and a discussion of specific risk reduc-
tion measures. I also examined his puppy and cat and performed their preventive care. I am writing this summary evaluation with Mr. Doe’s
permission.
Mr. Doe and his wife live in a one-story single-family dwelling on a city lot. There is a lawn outside and a park nearby. They recently
acquired a puppy in addition to their cat and iguana.
The puppy is currently 9 weeks old and is a Labrador–German Shepherd cross. According to the records Mr. Doe provided, the puppy
received its core vaccinations at 6 weeks of age, along with deworming, and did not reportedly have any health problems when they acquired
it from the city animal shelter. It is eating a puppy diet of dried food, but Mr. Doe also reported that he likes to feed it “special puppy treats.”
It has a bed in the kitchen, and Mr. Doe reports that he likes to sit in a chair and read a book with the puppy in his lap. He also reports that
he likes to let the puppy lick his face. Handwashing after handling the puppy is inconsistent. The puppy is still being housebroken. Mr. Doe
and his wife take turns cleaning up after the puppy and dispose of the waste in the trash. During the past week, Mr. Doe reports that the
puppy’s feces have “been a little loose” but without blood or mucus. Mr. Doe takes the puppy for a short walk twice a day in the backyard.
If the puppy defecates on the lawn, he picks up the feces with a plastic bag. The puppy’s physical examination was unremarkable. I did not
see evidence of abnormal behavior or other signs of illness. A fecal flotation test was negative for ova and parasites, and I submitted a fecal
sample for culture. I administered core vaccination boosters and deworming and scheduled a rabies vaccination to be provided when the
puppy is 12 weeks.
The cat is a domestic short-hair that is 2 years old and has been previously seen by a veterinarian. Mr. Doe reported that it is allowed
in the kitchen on counters and is an indoor-outdoor cat, spending several hours visiting the neighborhood park before returning for an
evening meal of a commercial wet diet. There is a litterbox in the corner of the kitchen that Mr. Doe and his wife take turns cleaning every
3 days. The cat also appeared healthy and was negative for feline leukemia virus and feline immunodeficiency virus but positive for
roundworms. It was dewormed and provided its core vaccinations. Because I recommended that the cat not go outdoors (see below), we
trimmed the nails.
The pet iguana lives in a conservatory room off the living room, and it sometimes likes to sit on a person’s shoulder. Mr. Doe’s wife is
responsible for cleaning and feeding the iguana.
Mr. Doe denies other pets or animal contacts, including petting zoos, other farm exposures, caged birds, or fish.
Mr. Doe is obviously attached to his puppy and cat, and they provide him with a great deal of emotional comfort and satisfaction.
In general, the risk of zoonotic disease from these animals is low. However, there are several important risks that should be addressed:
1. Puppies are at increased risk of infection with a number of zoonotic disease agents, including Salmonella, Giardia, and Cryptosporidium.
Therefore it would be better for anyone at increased risk of infection to avoid any contact with puppy feces and to use careful
handwashing precautions around the animal. I communicated this to Mr. Doe. Allowing the puppy to lick one’s face is not advisable,
and Mr. Doe was counseled about this. I recommended that they discontinue feeding the special puppy treats because the ingredients
included raw meat, which can be a source of Salmonella or E. coli.
2. Overall, many authorities consider that the positive health benefits of a pet such as the family cat, in terms of the human-animal bond,
greatly outweigh any risk of infection. To reduce disease transmission risk, I have recommended that they move the litterbox from the
kitchen. We discussed methods to train the cat to stay off kitchen counters and to keep the cat indoors only. I also recommended that an
immunocompetent person take responsibility for changing the cat litter, removing solids daily, and washing the box on a weekly basis.
These steps will greatly reduce any potential risk of toxoplasmosis. Another risk to consider is Bartonella infection, although this disease
in human beings is generally associated with kittens. Nevertheless, I trimmed the cat’s nails and provided a flea prevention treatment
that will reduce this risk further.
3. Reptiles, such as the pet iguana, can be carriers for Salmonella infection and are not advised for families with children younger than
5 years or with immunocompromised persons. If Mr. Doe is at increased risk of zoonotic infection, he and his wife should seriously
consider finding another home for this pet.
Mr. Doe was provided printed information about zoonotic disease risk reduction. He has a return appointment for his puppy in 3 weeks
when it is the appropriate age for rabies vaccination, and I will revisit these issues at this time.
Thank you again for the referral of this pleasant gentleman. If you have any questions regarding this report, please do not hesitate to contact
me. I will let you know the results of the puppy fecal culture when it is available next week.
Sincerely,
Jane Q. Veterinarian
Box 14-4 Communication from Medical Provider

to Veterinarian
Communication to Veterinary Provider Regarding
Human-Animal Medicine Issue
Alice O. Pathic, MD
242 Medical Drive, Anytown, USA
Phone 111-112-1111, Fax 111-112-1112
John Q. Veterinarian:
With permission of the owner, I am contacting you regarding a
potential zoonotic disease or other shared health issue. In particu-
lar, I am requesting an:
 Evaluation of pet(s) for internal parasites, especially_______
 Evaluation report of health problems in pet(s)
 Evaluate risks from specific pet for: ____________
dermatophyte________________________(name health
concern)
 Other_______________________________________
Reason for communication: There is concern that the family
cat may be the source of dermatophyte infection for people in the
house. Please evaluate the cat and advise the family whether there
is anything they can do to reduce zoonotic transmission if the cat
is infected.
Please call if you need more information and/or want to discuss.
Health department contacted? Yes No
Person contacted:
Date of contact:
Sincerely,
Alice O. Pathic, MD
02/20/09
Figure 14-1 Scalp ringworm in which an ectothrix infection of the hair

is caused by Microsporum canis. (From Mandell GL, Bennett JE, Dolin R:
Principles and practice of infectious diseases, ed 6, New York, 2005, Churchill
Livingstone Elsevier.)
that the cat was cultured (Figure 14-2) and treated appropri-
ately and that recommendations were made regarding clean-
ing the environment. The veterinarian can also educate the
physician about the therapeutic importance of the human-
animal bond between the family and the pet.
REFERRALS FROM VETERINARIANS TO HUMAN

HEALTH CARE PROVIDERs
Figure 14-2 Dermatophytosis. Paronychia in a cat caused by Microsporum
As discussed in Chapter 2, veterinarians are restricted by canis. The nailbed is erythematous and alopecic. (From Medleau L,
scope of practice guidelines from providing human medi- Hnilica KA: Small animal dermatology: a color atlas and therapeutic guide,
ed 2, St Louis, 2006, Saunders Elsevier.)
cal advice to owners and other clients. At the same time,
there may be liability if they do not adequately communi-
cate information about zoonotic and other health risks to the veterinarian finds that there are two smokers living in the
their clients. In the following case scenario, the veterinarian house. In discussion, the veterinarian mentions that second-
suspects an environmental health risk and brings it to the hand cigarette smoke has been linked to malignant lymphoma
attention of the health care provider. in cats.3 In this case, the cat may be a sentinel for the health risk
of second-hand smoke to human beings in the household. The
two smokers in the family decide they want to start a smoking
Case Scenario: Shared Environmental Toxic Risk
cessation program but are not sure how to start. The veterinar-
The family cat is diagnosed with malignant lymphoma by the ian suggests that they contact their family physician. The fam-
veterinarian. Despite treatment, the cat dies. The family is upset ily requests that the veterinarian write a letter about the cat’s
about the loss of the pet and asks if the veterinarian has any cancer that they can share with the physician. The veterinarian
ideas about what caused the cancer. In talking with the family, writes the letter shown in Box 14-5.
Box 14-5 Letter From Veterinarian to Physician Box 14-6 Letter From Veterinarian to Human
Regarding Animal Sentinel Event for Health Care Provider Regarding Dog
Environmental Toxic Risk Obesity
Human-Animal Medicine Communication to Human-Animal Medicine Communication to
Medical Provider Medical Provider
John Q. Veterinarian, DVM Preventive Family Veterinary Associates

200 Parkside Road, Anytown, State 100 Urban Street, Anytown, State, 10001
Phone 111-111-1111, Fax 111-111-1112 Phone 000-00-000, Fax 111-222-3333
Alice O. Pathic, MD: Alan O. Pathic, MD:
An evaluation was recently performed on animals that may An evaluation was recently performed on animals that may
have been in contact with one of your patients. have been in contact with one of your patients.
Findings: Family cat has developed malignant lymphoma. Findings: Family dog is obese
Reason for communication: According to mother in Reason for communication: Owner reports not taking his
household, the husband and nephew living in the house are heavy dog on walks. I have recommended that the dog get more exercise.
smokers. Exposure to secondhand smoke could have played a role Owner is interested in starting exercise program with the dog but
in the development of the cat’s neoplasia. The family has asked that mentions he has medical questions. Please evaluate. I have sug-
I provide you with this documentation because they are interested gested a nearby dog park as an exercise area because there are no
in participating in smoking cessation. Please contact me if you sidewalks in the neighborhood near his house. Please contact me if
have any questions. you would like to discuss this further.
Health department contacted? Yes No Health department contacted? Yes No
Person contacted: Person contacted:
Date of contact: Date of contact:
Thank you for your collaboration. Thank you for your collaboration.
John Q. Veterinarian, DVM Jane Q. Veterinarian
02/20/09 03/21/09
The physician, receiving this letter, is able to use it in of both human beings and companion animals in the commu-
motivating the husband and nephew to start a smoking ces- nity. It takes some time, but eventually, due in part to the efforts
sation program. of the health professionals, the walking paths are constructed.
Such direct communication between veterinarians and
human health care providers can lead to further cooperative
efforts, as shown in the following case scenario. HEALTH DEPARTMENT COORDINATION OF
CARE BETWEEN HUMAN AND ANIMAL HEALTH
Case Scenario: Shared Behavioral Risks
As outlined in Chapter 13, public health professionals can
A veterinarian is seeing a 3-year-old dog for a routine checkup. play a key role in coordinating preventive actions between
She notices that the dog has gained 10 pounds over the past 18 human and animal health care providers. Public health
months and is now significantly overweight. The owner is also departments are dedicated to improving the environmental
overweight. In asking about exercise routines for the dog, the vet- health of communities, and these efforts can obviously bene-
erinarian learns that the dog spends most of the time in a small fit the health of both human beings and nonhuman animals,
yard and is rarely walked. The veterinarian asks whether the as shown in the following scenario.
owner has considered getting more exercise himself. The owner
says yes, that he used to jog regularly, but in the suburban devel- Case Scenario: Shared Environmental
opment where they live there are currently no sidewalks. The Exposure to Lead
veterinarian agrees that this makes taking walks more difficult,
but tells the owner about a nearby dog park within a 10-minute A self-employed painter is seen in an emergency department for
drive that has a walking path around the perimeter. The veteri- abdominal pain and nausea. His blood test shows anemia. The
narian recommends a modified diet for the dog and also advises physician assistant seeing the patient suspects lead poisoning
the owner to get evaluated by his health care provider before and orders a test of venous lead. The level comes back several
starting an exercise program. With the owner’s permission, she days later markedly elevated (112 mcg/dL). The painter is seen
writes a communication to the health care provider (Box 14-6). in follow-up and reports that he has been sanding paint on the
The next week the veterinarian receives a phone call from exterior an old house that is being renovated and that a cou-
the patient’s nurse practitioner, who has seen the patient and ple is living in the house. The health department is contacted
is grateful that the veterinarian helped motivate him to start and investigates the house. The environmental health officer for
an exercise program. The nurse practitioner and the veterinar- the health department contacts the couple living in the house
ian agree to set goals for exercise and weight loss for both the and asks whether they have any children who could have been
patient and the dog and to separately provide reinforcement for exposed to paint dust from the renovation. The couple reports
the healthy change in behavior. They also agree to co-write a let- that they do not have any children, but that their two cats have
ter to the town mayor pointing out the need for construction of a been acting strangely, refusing to eat, and appearing drowsy.
walking path in the patient’s neighborhood to benefit the health The health department recommends that they take the cats to
the veterinarian for evaluation for possible lead poisoning. The pose.5 This database captures the occurrence of ticks detected
environmental health officer contacts the veterinarian person- during physical examination of pets and reports this as an
ally to inform him of the toxic risk. It is determined that the incidence rate based on the number of animals examined.6
cats are suffering from severe lead toxicosis (see Chapter 8) and Increases in the incidence of ticks found on the animals are
require chelation treatment. Meanwhile, the environmental thereby able to provide early warning of risk of Lyme disease
health department supervises the cleanup of the lead-contam- and other tickborne illness to both animals and human beings.
inated environment around the house. Based on this case, the The health department uses this information to send out alerts
health department starts an educational initiative with both to both veterinary and human health clinicians about the tick-
medical providers and veterinarians in the community to raise borne disease risk in the community.
awareness of lead poisoning risks.
Box 14-7 shows text from a sample brochure produced
as part of this educational initiative. This type of document PREVENTIVE ENVIRONMENTAL RISK
could be distributed to both human health care and veteri- ASSESSMENTS FOR HUMAN BEINGS AND
nary offices in the community. OTHER ANIMALS
A cornerstone of prevention is ensuring that health threats

Case Scenario: Shared Environmental Exposure
in the environment are recognized and minimized, and that
to Tickborne Disease
living environments are designed and maintained to foster
A state health department is engaged in tracking tickborne dis- optimal health status. Direct assessment of environments are
ease risk and alerting clinicians and the general public to areas often not performed as part of clinical care but can have a
and seasons of increased risk. To do this, the health department positive effect on outcomes.
decides to use data from a large companion animal database of An example of a commercially available form for assess-
electronic records of pets seen in animal hospitals around the ing disease risk in dogs is shown in Figure 14-3.
state. Such databases have already been developed for this pur- This disease risk assessment process can be expanded into
a comprehensive assessment of the home environment.
Box 14-7 Example of Public Health

Communication to Human and Animal
Healthy Home Environments
Health Care Providers, Patients, and As discussed throughout this book, homes shared by human
Clients beings and other animals can be healthy and nurturing envi-
ronments, but the risks of zoonotic disease transmission and
Lead—It’s Everywhere: Facts for Families, Human Health shared environmental health risks must be addressed and
Care Providers, and Veterinarians minimized. National programs such as the Healthy Homes
Sources of Lead in the Environment initiative (http://www.uwex.edu/healthyhome/tool) provide
• Peeling paint (houses built before 1978) information about toxic hazards in homes, but it is also impor-
• Dust and dirt contaminated with lead tant to assess other human-animal medical issues related to
• Lead pipes home environments.
• Toys, cans, other household objects containing lead Figure 14-4 gives an example of a home environment risk
Lead Is Harmful to People assessment checklist. Such a form can be given to patients
• 310,000 children aged 1 to 5 years in the United States have by their medical care providers or their veterinarians. The
elevated blood lead levels.4 information provided can supplement the basic medical
• Children are particularly vulnerable to lead poisoning and are history forms included in Chapter 3.
exposed by ingesting paint chips, lead objects, and dirt and dust While clinicians can ask questions about environmen-
contaminated with lead. tal health hazards during a medical history (see Chapter 8),
• Some children show no obvious symptoms; others may develop home visits can provide even greater information. Although
anemia, developmental delay, abdominal pain and, in high physicians are less likely to make home visits, a number of
doses, seizures. other health care providers routinely visit homes, including
• Talk to your medical provider about getting screened for lead
visiting nurse and physical therapy services. Some veterinar-
exposure.
ians and public health workers routinely make home visits.
Lead Is Harmful to Pets Most of these professionals should be able to make a cursory
• Pets get lead poisoning, too. Dogs and cats may have physical assessment and decide if further evaluation and/or counsel-
contact with dust and dirt contaminated with lead. They ing is needed. It is useful to identify a network of health pro-
then lick their fur and ingest even more lead. Sometimes they fessionals who are comfortable performing in-depth home
develop signs before human beings do.
environmental health assessments that include pets and
• Signs to look for include fatigue, vomiting, and weight loss.
• Talk to your veterinarian about getting pets screened for lead other animals if the situation seems more complex.
exposure. Figure 14-4 reviews steps that should be in place in a
household to ensure that the risk of disease transmission is
Questions about lead? Call the Environmental Health Division
reduced. This checklist can be given to patients and clients
at 111-222-3333.
to fill out or be used by visiting nurses, other home health or
Anytown Department of Health, Division of Environmental
public health personnel, and veterinarians performing home
Health
visits.
Canine Disease Risk Assessment Form
Being a dog is risky business. Disease risks vary by region and individual animal. Answering these questions will help your
veterinary team develop a disease protection plan that's right for your dog.
Date:
Your name:
Your dog's age:
Your dog's name:
Part 1: Risk assessment (to be completed by veterinary technician and pet owner)
Y N
Does your dog go outdoors unsupervised?
Do you have multiple pets?
Does your dog come in contact with other people's pets?
Other than visiting the clinic, does your dog ever leave your premises?
Is there wildlife in your area, including deer, mice, squirrels, birds, opossums, raccoons, rats, or skunks?
Have you seen ticks on your dog recently?
Do you frequently see mosquitoes near where your dog goes outdoors?
Has your dog been spayed or neutered?
Does your dog have an opportunity to drink from water outdoors (ponds, puddles, water bowls, etc.)?
Do you ever take your dog to a groomer or boarding facility?
Do you ever take your dog to dog shows?
Do you hunt with your dog?
If your dog is on monthly heartworm preventative, have you ever missed a dose by more than 2 weeks?
Does your dog have any known diseases?
Is your dog on any medications?
Has your dog ever become sick after a vacation?
Figure 14-3 Example of disease risk assessment for dogs. Courtesy Fort Dodge Animal Health, Madison, NJ.
It is also important to assess if the animals are being taken clinicians or for completion by a veterinarian during a farm
care of properly in terms of mental and social well being visit. In the United States many issues related to the health of
(e.g., appropriate exercise, attention, appropriate discipline). farm animals are managed by state and federal departments
Mental or physical neglect can be signs of social or psychiat- of agriculture. Therefore efforts to improve environmen-
ric dysfunction in the home (see Chapters 3 and 5). tal health around farms require close cooperation between
animal and human health care providers.
Healthy Backyards and Neighborhoods
If there is a yard connected to the house, or if the house is OTHER PARTNERSHIPS
located in a suburban area that may be encroaching on wild-
life habitat, further steps can also be taken to reduce risk of Following are other recent examples of successful clinical
disease transmission between local wildlife and domestic veterinary-human medical partnerships that are expanding
pets and people. The checklist shown in Figure 14-5 can be the horizons of medical care.
given to patients and families to make their own assessments
of the animal-associated health risks in their backyard and Case Scenario: Development of Novel Surgical
what can be done to reduce them. Procedure for the Care of a Pet Dog
A pet dog is found to have a congenital heart defect that is not
Healthy Farms
treatable with traditional veterinary cardiac surgical tech-
Individuals living in proximity to farm animals have addi- niques. The veterinary cardiologist contacts a human pediat-
tional environmental health and occupational health issues ric cardiac surgeon to discuss the case. The cardiac surgeon has
to consider in a preventive risk assessment (see Chapter 12).7 experience in the performance of a particular surgical tech-
Figure 14-6 is a checklist of farm-related health issues for nique designed to cure similar cardiac defects in human beings
patients and animal owners to complete and return to their but has not attempted an operation on the type of lesion that
Healthy Home with Animals Checklist (Check All the Following That Apply):
Pets in household (list numbers):

Adult dogs Puppies Adult cats Kittens Birds Reptiles Rodents Fish
Farm animals Other (please identify)
Local wildlife being fed or living in close proximity
Name of veterinarian(s):
Name of human health care provider(s):
Type of home: Apartment Single-family house Trailer Other (please describe)
Urban Suburban Rural
Separation between pets and any food preparation
Separation between storage of animal food and toys and human food
Separation between storage of animal medications and human medications
Family does not smoke inside the house
Absence of peeling paint that could represent a risk of lead poisoning
Family has a smoke alarm
Family has a carbon monoxide alarm
Household cleaners and other toxic chemicals are out of reach of children, dogs, and other pets
Household pets are kept inside and, when taken outside, are supervised and prevented from having direct contact with
wildlife or unfamiliar domestic animals
Family has a policy of handwashing after handling all animals and their food and bedding
Pets are up to date with appropriate vaccinations, are regularly screened for ectoparasites and endoparasites, and are
placed on a proper preventative medicine plan
Flea and tick medications are low toxicity (list chemicals)
Family physician or other primary care provider is aware of pets in house
Any persons with immunodeficiency are taking extra precautions with pet contact
Pets are restricted from bedroom(s) of individual(s) with allergies
Family regularly cleans cages, litter boxes, shed hair, etc.
Animal waste is immediately disposed of in a sanitary manner and animals are discouraged from relieving themselves in
inappropriate places (e.g., uncovered sandboxes)
Figure 14-4 Healthy home with animals checklist.
the dog has because such a specific procedure has not yet been c ollaboratively, the cardiologist and the veterinarian detected
developed for human beings. With the appropriate consents evidence of cardiomyopathy and heart failure in a number
and approvals, arrangements are made for the pediatric cardiac of animals in the captive colony. The cardiologist helped the
surgeon to perform a novel procedure on the dog in partner- veterinarian develop clinical treatment protocols for the ani-
ship with the veterinary cardiologist. The procedure proves to mals. When another tamarin dies, the heart is examined by
be lifesaving for the dog. In the process, the veterinary cardiolo- both a veterinary pathologist and a human pathologist, who
gist learns skills that could allow him to help other animals in agree on the diagnosis of sclerosing cardiomyopathy. The car-
the future, and the pediatric surgeon gains experience to better diologist learns from zoo veterinarians that animals can suffer
perform the novel procedure on children with congenital heart from “capture myopathy” as a result of stress. This condition
disease.8 has been recognized in animals for several decades. The cardi-
ologist notes the similarity to a recently described condition in
human beings (Tako-Tsubo, or stress cardiomyopathy),9 which
Case Scenario: Echocardiography for Zoo
could be underdiagnosed. This overlap of clinical conditions
Primates
between animals and human beings impels the physician to
After several nonhuman primates (tamarins) in a zoo die of search the medical literature to find other disease syndromes in
apparent heart failure, the zoo veterinarian contacts a car- human beings and nonhuman animals that could benefit from
diologist at a nearby medical school. The cardiologist agrees increased communication between human health care provid-
to perform echocardiograms on the tamarins. Working ers and animal health care providers.10
Healthy Backyard and Neighborhood Checklist (Check all the Following That Apply):
Date: Person completing form:

Address of the house/apartment:
1. Outside the house:
Wildlife (deer, raccoons, skunks, coyotes, etc.) are restricted from coming near the house, and garbage and pet food
containers are secured to not attract wildlife.
Any feces is cleaned up and disposed in the trash can quickly.
Sandbox is covered when not in use.
Any bird feeder is regularly cleaned and away from the house to not attract rats and mice.
If in area where ticks are a problem, vegetation is kept cut short around the house.
There is no standing water (e.g., old tires, clogged gutters, pots, toys, buckets or barrels filled with water) that could be a
breeding area for mosquitoes.
Firewood is kept at least 100 feet from house (it can attract rodent nests).
2. In the neighborhood:
There are adequate walking paths and other exercise areas for people and pets.
There are policies on cleaning up after pets in playgrounds and other public areas.
There are no recognized toxic hazards in the neighborhood that could be a risk to animals or people.
Comments:
Figure 14-5 Healthy backyard and neighborhood checklist.
Healthy Farms Checklist (Check all the Following That Apply)
Individuals working with horses, cows, and other large animals are aware of injury prevention.
Species are separated as appropriate.
Diseased animals are isolated.
Food bins are secured against vermin and other scavenging animals and are away from toxic chemicals.
Adequate handwashing facilities are available.
Food product handlers are aware of safety and hygiene procedures for all animal products (eggs, milk, etc.).
Dairy products are pasteurized.
If home slaughter for meat production, meat is cooked or cured adequately to destroy parasites.
Wells are properly constructed to prevent contamination from livestock, human, and wildlife wastes.
Farm has a manure management and animal disposal plan. Animal waste and carcasses are disposed of in ways that
do not leak into water supply or attract scavengers.
Workers are using adequate and appropriate personal protective equipment.
Wildlife are kept from contact with farm animals.
Animals have proper access to preventive and acute veterinary care (vaccines, parasite control, reproductive care,
injuries, infections, etc.).
Workers have access to preventive occupational health care for injuries, allergies, infectious diseases, and other
occupational health risks.
Workers have access to adequate personal protective equipment.
Figure 14-6 Farm animal safety and health checklist.
References
2. Dr. J. Stephens. Personal communication. November 19, 2008.
1. Grant S, Olsen CW. Preventing zoonotic diseases in immunocompro- 3. Bertone ER, Snyder LA, Moore AS. Environmental tobacco smoke
mised persons: the role of physicians and veterinarians. Emerg Infect Dis. and risk of malignant lymphoma in pet cats. Am J Epidemiol.
1999;5(1):159–163. 2002;156(3):268–273.
4. Centers for Disease Control and Prevention. Lead: topic home. 8. Carey S. Human, animal doctors report success in dog’s open heart
http://www.cdc.gov/lead/. Accessed November 15, 2008. surgery. University of Florida Health Science Center News. http://
5. Glickman LT, Moore GE, Glickman NW, et al. Purdue University- news.health.ufl.edu/news/story.aspx?ID=3487. Accessed May 5, 2009.
Banfield National Companion Animal Surveillance Program for emerg- 9. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-
ing and zoonotic diseases. Vector Borne Zoonotic Dis. 2006;6(1):14–23. Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarc-
6. Raghavan M, Glickman N, Moore G, et al. Prevalence of and risk factors tion. Am Heart J. 2008;155(3):408–417.
for canine tick infestation in the United States, 2002–2004. Vector Borne 10. Cima G. One-health wonders. J Am Vet Med Assoc. 2008;233(7):1026.
Zoonotic Dis. 2007;7(1):65–75.
7. Will LA. Shared human-animal diseases. Safe Farm Fact Sheet. Ames, IA:
Iowa State University Extension; 1994. http://www.cdc.gov/nasd/docs/
d001001-d001100/d001073/d001073.pdf.
Index
Note: Page numbers followed by f indicate figures; t, tables; and b, boxes.
A Alopecia Anatoxin-a, HAB-related illness and, 97t

Abattoir fever, 222 chemotherapy and, 314f Ancylostoma
Abnormal behavior, cause and appropriate action generalized, 48f effects of, 174
for, 20t Alphavirus (VEE/EEE), animal exposure to, hookworm dermatitis and, 176
Abuse implications of, 378t in visitation dogs, 31–32
domestic violence and, 33 Alveolar cyst, 156f Ancylostoma braziliense, 174–175
health care professional reporting, 33 Alveolar echinococcosis, Echinococcus multilocularis cutaneous larva migrans and, 175
potential for, 13 and, 153 geographic occurrence of, 175
warning signs of, 34b Alveolar hydatid disease, 153 hosts, reservoir species, vectors for, 175
Acariasis, 254 Amanita rubescens, 56f life cycle of, 175
Acetaminophen, toxicity of, 54, 55t Amanita toxin, 56 Ancylostoma caninum, 174–175
Acid-fast bacilli (AFB), mycobacteria and, 282 Amantadine, 184 characteristics of, 175
Active disease surveillance, 374–376 Amblyomma, heartwater and, 310 geographic occurrence of, 175
Active living, built environment and, 37–38 Amblyomma cajennense, 238 hosts, reservoir species, vectors for, 175
Active tuberculosis, 282–283 American Association of Poison Control Centers life cycle of, 175
Activities of daily living, pet ownership and, 28 poisonous plants reported to, 56t Ancylostoma ceylanicum, 175
Acute care visit substances reported to Ancylostomiasis, 174
animal contact history and, 12–13 human exposures, 53t Andes virus, 172
screening/follow-up questions for, 13t nonhuman exposures, 54t Anesthetic agent, 359
Acute Chlamydophila species conjunctivitis, in toxic agent percentages reported to, 54t Anesthetic gas, animal workers and, control
heifer, 137f American dog tick (Dermacentor variabilis), strategies for, 346t
Acute febrile illness, Francisella tularensis and, 289 159–160 Angioedema, from insect sting, 80f
Acute toxic exposure, 52–57 Rocky Mountain spotted fever and, 237–238 Animal
household/environmental sources of, 55–57 sizes of, 199f allergic conditions in, 47–49
identification of, 57 American Medical Association (AMA) anthrax in
of medication, 54–55 One Health Initiative and, 5 clinical presentation of, 116–117, 116t
Aerosolized anthrax, release of, 114 One Health Task Force and, 5 diagnosis of, 118
African elephant bluff-charge, 302f American Society for the Prevention of Cruelty to treatment of, 118t
African hedgehog Animals (ASPCA), 53–54 Bartonella henselae in, 121–122
Salmonella and, 310 American Society of Heating, Ventilating, bioterrorism exposure, 378t
view of, 310f Refrigerating, and Air Conditioning Engineers brucellosis in, 126–127
Africanized bee, 80 (ASHRAE), 41 Campylobacter disease in, 131
African tick fever, travel and, 303 American Veterinary Medical Association (AVMA) carbon monoxide poisoning in, 64
Agar gel immunodiffusion (AGID), 184 animals after disaster, management of, 380 cat-scratch disease in, 121–122
Agricultural animal, animal cruelty laws and, 11 One Health Initiative and, 5 Chlamydophila psittaci in, 136
Agricultural tourism, 302 One Health Task Force and, 5 Coxiella burnetii and, 224
Agriculture, U.S. Department of, Animal and Plant Amikacin, 285 cryptosporidiosis in, 142–143
Health Inspection Service (APHIS), 4 Ammonia after disaster, management of, 380–383
Airborne dust particle, 41 acute toxic exposure to, 55–56 disease/pathogen reported in, 110t
Airborne mold, 41 animal workers and, control strategies for, 346t
Airway obstruction, recurrent, in companion ehrlichiosis/anaplasmosis in, 161
toxic exposure of, 58t Escherichia coli infection in, 166
animal, 47t Amoxicillin
Albendazole, for echinococcosis, 156–157 as food, 1
bite infection, treatment for, 329t foodborne illness, evaluation of, 340–341
Alcohol for tularemia, 293t
toxicity in animals, 53t giardiasis in, 170
Amphibian, Salmonella prevention in, 248b
use of, in veterinary practice, 360t hantavirus infection in, 174
Amphibian intoxication, 84–88
Aldehyde, use of, in veterinary practice, 360t healthy home with, checklist, 391f
symptoms and treatment of, 85t
Aleppa ulcer, 186 hookworm infections in, 176
Ampicillin, bite infection, treatment for, 329t
Algae bloom. See Harmful algae bloom illegal importing of, 308–309
Amyotrophic lateral sclerosis-parkinsonism
Allergen dementia complex (ALS/PDC), 99–100 immunodeficient, care for, 318
animal research facility worker and, 362 Anaphylaxis, 45 LCM infection in, 208
animal workers and, 345 from insect sting, treatment for, 80 lead toxicity in, 68–70
as biological hazard, types of, 345 Anaplasma, 198 leishmaniasis in, 189–190
control strategies for, 346t Anaplasmataceae, 158–159 leptospirosis in, 194
farm animal worker and, 367 Anaplasmataceae phagocytophilum, 159 Lyme disease in, 201–202
sentinel events from, 41t geographic occurrence of, 159 medication toxicity in, 54–55
veterinary personnel and, 354 hosts, reservoir species, vectors for, 159–160 MRSA in, 212
zoo/aquarium worker and, 364 Anaplasmataceae platys, 159 orf virus in, 216
See also specific types of hosts, reservoir species, vectors for, 159–160 pesticides used on, 73–76, 75t
Allergen load reduction, 47 Anaplasmosis pesticide toxicity in, 77
Allergic conditions, 43–49 in animals, 161 Pets Act, The, 379
Allergy cause of, 157–159 plague in, 220
to cats/dogs, 43–44 clinical presentation of, 162t preventive environmental risk assessment for,
See also Animal allergy environmental risk factors for, 160–161 389–390
Allergy desensitization, 354 in goat, 161f Q fever in, 225
Allergy skin test, 48f hosts, reservoir species, vectors for, 159–160 rabies in, 231
Alligator, West Nile virus in, 298 in human beings, 161 Rift Valley fever in, 246
Alligator bite, 325 risk groups for, 159 Rocky Mountain spotted fever in, 240
395
396 Index
Animal (Continued) human health and, 18–19 Anthozoa (Sea anemone) sting, 88, 89t
Salmonella in, 251–252 consequences of, 18–19 Anthrax
scabies and, 257–258 Animal disease symptoms acquiring, routes of, 2f
as sentinel, 51–52 human health and animal carcass and, 118
toxic exposures in, 58t cause and appropriate action for, 20t animal exposure to, implications of, 378t
toxoplasmosis in, 268–269 relevance to, 19, 19f animal husbandry and, 367t
transmissible spongiform encephalopathy in, Animal feed in animals
273–274 foodborne illness risk and, 332–333, 332t clinical presentation of, 116–117, 116t
tuberculosis in, 281–282 occupational exposure to, 333b diagnosis of, 118
tularemia in, 292 Animal health treatment of, 118t
West Nile virus in, 296–298 environmental, human and, 2f bushmeat and, 303–304
Animal abuse. See Abuse ethical principles in, 11 camel slaughter and, 302
Animal allergen, 345 human health and, 1 causative agents of, 113
Animal allergy convergence of, 7–8 environmental risk of, 114
allergen load reduction, 47 zoonotic disease and, 1–3 example of, 23f
anaphylaxis and, 45 Animal health risk assessment form, 16f geographic occurrence of, 113–114
animal/person, removal of, 46–47 Animal hide, as souvenir, 304–305 hosts, reservoir species, vectors for, 114
asthma and, 44–45 Animal-human disease transmission, in human beings
diagnosis of, 46 immunodeficiency and, 315 clinical presentation in, 116t
in human beings, 43–44 Animal husbandry diagnosis of, 116–117
management of, 46–47 immunocompromised individual and, 317–318 treatment of, 118, 118t
rhinitis/upper airway symptoms and, 44 occupational pathogens and, 367t types of, 115–116
risk factors for, 44 Animal Poison Control Center, 53–54 life cycle of, 115f
sources of, 44t Animal research facility worker outbreaks of, 106–107
Animal and Plant Health Inspection Service allergens and, 362 risk groups for, 114
(APHIS), 4 chemical hazards and, 363 transmission of, 114
Animal-assisted activity (AAA), 24 herpes B infection and, 362 See also Cutaneous anthrax
benefits of, 27 HIV and, 363 Anthrax vaccine, 118–119
contraindications for, 34 injury, exposure, illness management for, 364 Anthropophilic dermatophyte
credentialing for, 30–31 lymphocytic choriomeningitis and, 363 classification of, 145t
exclusion criteria for, 32t measles and, 362–363 transmission of, 144
infectious disease/risks, minimizing, 31–32 medical surveillance for, 364 Antibiotic-resistant Escherichia coli, in visitation
psychological/psychosocial effects of, 26 occupational medicine services for, 362–364 dogs, 31–32
recommendation, guidelines for, 29t physical hazards and, 363 Antifreeze
referral for, 29 preplacement screening of, 363–364 acute toxic exposure to, 55
social work and, 29 psychosocial hazards and, 363 toxic exposure of, 58t
use of, 25 Q fever and, 363 Antimicrobial prophylaxis, 118–119
Animal-assisted therapy (AAT), 24 rat-bite fever (streptobacillosis), 363 Antivenin
benefits of, 27 tuberculosis and, 363 for snakebite, 82–83
contraindications for, 34 vaccinations and, 364 for spider bite, 81
credentialing for, 30–31 viral hepatitis and, 363 Antiviral medication, types of, 184
exclusion criteria for, 32t zoonotic disease and, 362–363 Anxiety, animal interaction reducing, 26
infectious disease/risks, minimizing, 31–32 Animal sentinel Aquarium, in long-term care setting, 26, 27f
psychological/psychosocial effects of, 26 for arbovirus detection, 376f Aquarium worker. See Zoo/aquarium worker
recommendation, guidelines for, 29t as disease surveillance system, 376 Arboviral disease, 294
referral for, 29 for pathogen/chemical warfare, 376–377 animal sentinel for, 376f
social work and, 29 Animal shelter Arenaviridae, 205–206
use of, 25 health/disease control at, 381b Arthritis, cause and appropriate action, 21t
Animal bite, 300 injury/illness prevention at, 382b Arthropod, animal workers and
antibiotic prophylaxis and therapy, 325 Animal slaughter, anthrax and, 302 control strategies for, 346t
epidemiologic characteristics of, 323t Animal travel, 299 exposure to, 348
in human beings Animal welfare, freedoms of, 11b Arthropod-borne disease (arboviral), 294
history of, 322–324 Animal workers Ascariasis, 261
physical examination of, 324 allergens and, 345 Asia, travel advisory for, 302
prevention of, 322 asthma in Aspirin, toxicity of, 54, 55t
prevention of, 358b Association of Reptilian and Amphibian
immunocompromised individual and, 325
symptoms of, 353b Veterinarians, Salmonella brochure by, 250f
infection, risk factors for, 324t
biological hazards and Asthma, 44–45
prevalence of, 321
allergens as, 345 in companion animal, 47t
radiograph of, 324–325, 325f
biological, 345–348 work-related
wound, site for, 323t
zoonotic pathogens as, 345–347 prevention of, 358b
See also Wound
chemical hazards and, 348–349 symptoms of, 353b
Animal bite, animal workers and, control strategies
hazard card for, 353f Ataxia, cause and appropriate action for, 20t
for, 346t
hazards and Atopic dermatitis, 46
Animal certification, for national/international
control strategies for, 346t in companion animal, 47t
movement, 341
Animal contact, 12–13 types of, 345 diagnosis/treatment of, 48–49
medical questionnaire for, 350f Atopy
abuse/neglect, potential for, 13
occupational health of, 343–371 in dog, 48f
checklist for, 14f
preplacement screening of, 349–351 in feline, 48f
farm visits and, 302
psychosocial hazards and, 349 Atypical cutaneous leishmaniasis, 188
at festivals, 302
risk assessment for, 351 Atypical mycobacterial infection, 276
risk reduction, counseling for, 300
Atypical pneumonia, bird exposure and, 136
travel and, 299 training for, 351
Audiometry at baseline, for animal workers, 350–351
injuries and, 300–302 types of, 344
Australian pressure-immobilization technique, 87f
Animal cruelty law, agricultural animals and, 11 vaccinations and, 351
Australian Q fever, 222
Animal dander, as indoor air contaminant, 38–39 zoonotic pathogens and, 345–347 Autism spectrum disorder, animal interaction
Animal disease/illness Antemortem toxicology testing, samples needed
and, 27
for, 59t
Index 397
Autopsy, necropsy rate versus, 3 animal health and, 11 Bovine tuberculosis, travel and, 303
Avian flu, 177 definition of, 10–11 Box jellyfish
Avian influenza Biguanide, 360t envenomation from, 88
animal husbandry and, 367t Biliary tract, cryptosporidiosis in, 140 picture of, 90f
animal workers and, 345–347 Bioaerosol, as indoor air contaminant, 39t sting, treatment of, 90f
chicken manure and, 333 Biological hazard Brain, toxicology testing and, 59t
classification of, 181, 182 allergens as, 345 Breast cancer, 58–59
effects of, 183–184 control strategies for, 346t Breathing, labored, cause and appropriate action
farm visits and, 302 zoonotic pathogens as, 345–347 for human health care provider, 20t
hosts, reservoir species, vectors for, 181 Biological warfare, Yersinia pestis as, 219 for veterinarian, 21t
live bird market and, 302–303 Bioterrorism agent Brevetoxin
risk factors for, 182 animal exposure to, implications of, 378t effects of, 95t, 101
Avian salpingitis, 252f Category A, Bacillus anthracis as, 113 Karenia brevis producing, 94
Avian tuberculosis, 276 Category B toxicity of, humans versus animals, 99t
cause of, 287 Burkholderia mallei as, 113 Broken bone, cause and appropriate action, 21t
clinical presentation of, 287–288 Pseudomonas pseudomallei bacteria as, 108t Bromethalin
Avian vacuolar myelinopathy (AVM), 99–100 Bird hindlimb ataxia from, 57f
Avocado, toxicity in animals, 53t breast/leg meant, removal of, 2f toxic effects of, 57
Azithromycin, bite infection, treatment for, 329t carboxyhemoglobin and, 64 toxic exposure of, 58t
Chlamydiae infection in, 137t Bronchus epithelium, bronchus, 40f
HIV-infected person and, 319t Brown bat (Eptesicus fuscus), rabies and, 232f
B
lead toxicity in, 68–69, 69t Brown dog tick, 159, 238f
Babesia, 198
sick, animal shelter guidelines for, 381b Brown recluse spider
Babesia bigemina, 5
Babesiosis, acquiring, routes of, 2f toxic exposures in, 58t envenomation from, 81
Bacillary angiomatosis, 122t West Nile virus and, 296–297, 297t picture of, 81f
Bacillus anthracis, 113 See also Chlamydophila psittaci Brucella
animal husbandry and, 367t Bird fancier’s lung, 45 animal husbandry and, 367t
characteristics of, 113 Bird flu, 177 hosts for, 124t
drum head contamination by, 114f Bison goring, 302f species of, 124
photomicrograph of, 114f Bite Brucella abortus, 124
Backyard, healthy, 390 animal workers and, control strategies for, 346t clinical presentation of, 124, 125t
checklist for, 392f dog quarantine after, 379t in cow/cattle, 126
Bacteremia, anthrax and, 115–116 from monkey, 362 Brucella melitensis, 124
Bacterial enteritis Black Creek Canal Hantavirus, 172 clinical presentation of, 124, 125t
Campylobacter species and, 128 Black Death, 218 Brucella ovis, 126
travel and, 303 Blacklegged tick. See Ixodes scapularis Brucellosis
Bacterial pneumonia Black widow spider animal exposure to, implications of, 378t
influenza and, 177 neurotoxic envenomation from, 81 in animals, 126–127
radiographs showing, 181f picture of, 81f cause of, 124
Baghdad boil, 186 Blastomyces, animal workers and, 348 clinical presentation of, 125t
Bait, toxicology testing and, 59t Blastomycosis, 348 diagnosis of, 127
Balkan influenza, 222 Bleach discitis/spondylitis from, 126f
Bang’s disease, 123 acute toxic exposure to, 55–56 environmental risk factors for, 125f, 126
Bartonella elizabethae, 122t toxic exposure of, 58t farm visits and, 302
Bartonella henselae Blood, toxicology testing and, 59t geographic occurrence of, 124
in animals, 121–122 Blood lead level, treatment and, 70t hosts, reservoir species, vectors for, 124–125
characteristics of, 120 Body fluid, toxicology testing and, 59t in human beings, 126
clinical presentation of, 122t Bone, toxicology testing and, 59t overview of, 123
transmission/life cycle of, 121, 121f Bone disease, nontuberculosis mycobacteria postexposure prophylaxis for, 127
treatment of, 122t and, 287 risk groups for, 124
Bartonella infection Bordetella, 108t transmission/life cycle of, 125–126
Bordetella bronchiseptica, 316 treatment of, 127, 127t
cat bite/scratches and, 328
Borrelia burgdorferi, 195–196 Bruising, cause and appropriate action, 21t
causative agent for, 119
cystic form of, 197f Bubonic plague
clinical presentation of, 122t
micrograph of, 197f clinical presentation of, 221t
diagnosis of, 122
transmission/life cycle of, 198 in human beings, 220
environmental risk factors for, 121
Borrelia burgdorferi sensu stricto, 196 treatment of, 222t
exposure to, reducing, 316
Borrelial arthritis, in dog, 202f Bufo marinus (cane/marine toad), 88f
HIV-infected person and, 319t Borrelia species, 196
travel and, 300 Building, with lead contamination, inspection and
Botulism regulation of, 379t
treatment of, 122–123 animal exposure to, implications of, 378t
Bartonella spp. Built environment
in cow/cattle, 338f active living and, 37–38
disease, reservoir species, vectors for, 120t in dog, 335
hosts, reservoir species, vectors for, 120–121 animals, effect on, 38
overview of, 335 clinical conditions related to, 38, 39t
Bartonella vinsonii subsp. arupensis, 122t Bovine amyloidal spongiform encephalopathy
Bartonella vinsonii subsp. Berkhoffii, 122t definition of, 37
(BASE), 273 health hazards and, 39t
Bat, as disease reservoir, 303 Bovine hypersensitivity pneumonitis (HP), 49
Baylisascaris procyonis, 261–262 healthy communities as, 38
Bovine spongiform encephalopathy (BSE), 271 Bunyaviridae family, 243, 243f
Beach
in cattle, 273f Bunyavirus, 172
animal contact and, 304
clinical presentation of, 275t Burkholderia mallei, 113
inspection and regulation of, 379t
diagnosis of, 275 Buruli ulcer, Mycobacteria ulcerans and, 287
Behavior
hosts, reservoir species, vectors for, 272 Bushmeat
abnormal, cause and appropriate action for, 20t
outbreak of, 271 amount sold and types of, 304t
concerns for, animal shelter guidelines for, 381b
signs and symptoms of, 273 consumption of, 303–304
human, pets as indicators of, 33–34
transmission/life cycle of, 272 as delicacy, 303–304
problems with, educating about, 9–10
transmission of, 272 South African market selling, 303f
Behavioral evaluation, for therapy dog, 32f
variant Creutzfeldt-Jakob disease and, 273 viruses associated with, 367t
Beneficence
398 Index
C toxicity of, humans versus animals, 64t, 67f Cervidae, tuberculosis in, 281
Cadmium-induced renal disease, environmental Carboxyhemoglobin (COHb) Chagas disease, 108t
exposures and, 60t air levels of, 64 Chamois, with clinical scabies, 258f
Caffeine, toxicity in animals, 53t dogs and, 64 Chelation therapy, 68
Cavalryman’s scabies, 254 effects of, 63, 63f guidelines for, 71t
Campylobacter formation and characteristics of, 62–63 indications for, 70
animal husbandry and, 367t in smokers, 63 Chemical
animal workers and, 345–347 Cat as indoor air contaminant, 38–39, 39t
chicken sashimi and, 303 allergy to, 43–44 intentional release of, 376–377
Campylobacter coli, bacterial enteritis and, 128 bite infection, treatment for, 329t Chemical hazard
Campylobacter disease black widow envenomation and, 82 animal workers and
farm visits and, 302 Chlamydiae infection in, 137t control strategies for, 346t
in human beings, 130–131 cryptosporidiosis in, 142–143 types of, 348–349
Campylobacter fetus, 128 dog bite in, 328f farm animal worker and, 367–368
characteristics of, 130 Escherichia coli infection in, 166, 166t veterinary personnel and, 358–359
Campylobacteriosis HIV-infected person and, 319t zoo/aquarium worker and, 365
in animals, 131 as mercury poisoning sentinel, 60 Chemotherapy, alopecia and, 314f
clinical presentation of, 132t plague in, 220 Cheyletiella species, 255
diagnosis of, 131–132 toxicant exposure and, 58t zoonotic potential of, 255t
treatment of, 132t indoors, 52 Chicken
in animals, 132–133 outdoors, 52 carboxyhemoglobin and, 64
in human beings, 132 toxoplasmosis and, 265 Salmonella and, 316
Campylobacter jejuni tularemia in, 292, 293t Chicken sashimi, Campylobacter and, 303
bacterial enteritis and, 128 West Nile virus in, 297t, 297–298 Chiclero ulcer, 186
case study for, 129b See also Toxocara infection Chikungunya, 108t
presentation/management of, 336t Cat bite travel and, 303
Campylobacter species abscess on wrist, 324f Child proofing, 51
canine fecal smear of, 130f Bartonella infection from, 328 Children
characteristics of, 129–130 epidemiologic characteristics of, 323t Dipylidiasis in, 150–152, 151f
dark-field microscopy of, 129f infection risk from, 325 lead exposure and, 66–67
effects of, 128 Category A bioterrorism agent, anthrax as, 113 risk of, 68
electron micrograph of, 129f Caterpillar, 80–81 toxicity of, 68
environmental risk factors for, 130, 131f Cat mascot, for older adult, 25–26 therapeutic horsemanship for, 26
geographic occurrence of, 130 Cat-scratch disease (CSD), 328 Visceral larva migrans in, 263
hosts, reservoir species, vectors for, 130 in animals, 121–122 Chirodopoid box jellyfish, 88
risk groups for, 130 causative agent for, 119 Chives, toxicity in animals, 53t
transmission/life cycle of, 130 diagnosis of, 122 Chlamydia, Chlamydophila versus, 135t
Canary enlarged lymph nodes from, 121f Chlamydiae infection, 137t
carbon monoxide and, 52, 61–62 in human beings, 121 Chlamydial conjunctivitis, conjunctival scraping
mines and, 50 risk groups for, 120 of, 138f
photo of, 52f Chlamydia trachomatis, 138
treatment of, 122–123, 122t
Cancer Chlamydophila
Cattle
chronic toxic exposures and, 57–60 animal husbandry and, 367t
botulism in, 338f
environmental exposures and, 59–60, 60t farm visits and, 302
bovine spongiform encephalopathy in, 273f
Canine distemper, 107t Chlamydophila abortus, pregnancy and, 136
brucellosis in, 126
Canine eosinophilic bronchopneumopathy Chlamydophila psittaci
dermatophytosis in, 146
in companion animal, 47t in animals, 136
Escherichia coli infection in, 166, 166f, 166t
diagnosis/treatment of, 48 animal workers and, 345–347
granulomatous enteritis/Johne’s disease in, 287f
Canine flu, 177 atypical pneumonia and, 136
HAB-related illness in, 99t
Canine hemorrhagic fever, 157 cause of, 133
hypersensitivity pneumonitis in, 47t, 49
Canine influenza, 183 chest radiograph of girl with, 136f
lead toxicity in, 68, 69f, 69t
Canine leishmaniasis, 189f Chlamydia versus, 135t
listeriosis in, 338f
Canine monocytic ehrlichiosis, 157 diagnosis of, 136–138
with rabies, 233f
Canine parvovirus infection, 107t environmental risk factors for, 135
tuberculin skin test in, 284
Canine rickettsiosis, 157 hosts, reservoir species, vectors for, 135
tuberculosis in, 281, 285
Canine scabies, 258f in human beings, 135–136
viruses associated with, 367t
Canine typhus, 157 necropsy, diagnosis by, 137–138
Cattle fever, 5
Capnocytophaga canimorsus, 328 pregnancy and, 136
Cattle silage, hazards of, 348–349
Capnocytophaga infection, 328 prevention of, 134b
Cefotaxime, bite infection, treatment for, 329t
Carbamate risk groups for, 135
Cellular prion protein (PrPc), transmissible
animal toxicity from, 76 strains of, 134–135
spongiform encephalopathy and, 272
poisoning from, 77 transmission/life cycle of, 135, 136f
use of, in animals, 75t treatment of, 138, 138t
animals after disaster, management of, 380
Carbon dioxide, measurements of, 41 Chloramphenicol
Asia, travel advisory for, 302
Carbon monoxide bite infection, treatment for, 329t
Bacillus anthracis, 113
canaries and, 52 for tularemia, 293t
calf, outbreak investigation of, 4f
characteristics of, 62 Chocolate
EIS training at, 4
exposure to animal exposure frequency, 54t
foodborne illness, cases of, 331
metabolism and routes of, 62 toxicity in animals, 53t
inhalation anthrax screening guidelines for, 117f
prevention of, 62b Chorioretinitis, 207f
monkey scratch/bite guidelines, 362–363
poisoning from, 61–62 Chronic toxic exposure
psittacosis, surveillance criteria for, 137
acute/chronic effects of, 63 cancer and, 57–60
Special Pathogens Unit at, 4
in animals, 64 health effects of, 57
travel regulations by, 306
infarction from, 64f Chronic wasting disease (CWD) of deer and elk, 271
veterinarian role at, 4
management of, 65f clinical presentation of, 275t
Central nervous system, lead exposure and, 67–68
risk groups for, 63 diagnosis of, 275
Cerebrospinal fluid, toxicology testing and, 59t
treatment of, 64–65 environmental risk factors for, 272–273
Index 399
geographic occurrence of, 272 environmental risk factors for, 224–225 in human beings, 188
host for, 272 geographic occurrence of, 223 transmission/life cycle of, 187
signs and symptoms of, 273 reservoir for, 224 treatment of, 190t
in wapiti, 274f as Select Agent, 225 Cyanide poisoning, 52
Ciguatera fish poisoning, 101 Coxiella burnetii-infected caprine placenta, 223f Cyanobacterial toxin
Ciguatoxin, 95t Coxiellosis, 222 in domestic animals, 101
Ciprofloxacin, for tularemia, 293t Creeping eruption, 174 effects of, 101
Cleaning product from beaches, 304 toxicity of, humans versus animals, 99t
acute toxic exposure to, 55–56 Creutzfeldt-Jakob disease (CJD), 271 Cylindrospermopsin, HAB-related illness and, 97t
toxic exposure of, 58t diagnosis of, 274 Cystic echinococcosis, 153
Clindamycin, bite infection, treatment for, 329t transmission of, 272–273 cause of, 153
Clinical health history treatment of, 275–276 Cysticercosis
approach to, 12–17 variants of, 273 life cycle of, 340f
See also Medical history Crocodile, Chlamydophila psittaci and, 137f overview of, 338
Clinical scabies, chamois with, 258f Crotalid envenomation, 83f Cystic hydatid disease, 153
Clinician. See Human health clinician; physician symptoms and treatment of, 85t
Clonorchis sinensis, 303 Crusted scabies, 254 D
Clostridial food poisoning, 335 clinical presentation of, 257t Dairy farming, animal workers in, 344
Clostridium botulinum occurrence of, 257 Dancing cats disease, 51
overview of, 335 treatment of, 259t Dander, as indoor air contaminant, 38–39
presentation/management of, 336t Crusting Death
Clostridium difficile, in visitation dogs, 31–32 cause and appropriate action for, 20t animal abuse causing, 33
Clostridium perfringens dermatophytosis and, 22f cause and appropriate action for, 20t
overview of, 335 Cryptococcus Chlamydophila psittaci and, 136
presentation/management of, 336t animal workers and, 348 environmental exposures and, 60t
Cochliomyia hominivorax, 217 cockatoo shedding, 316–317 Deer-fly fever, 289
Coelenterate envenomation, 88 Cryptococcus neoformans, 348 Deerfly fever, 289
Coffee, toxicity in animals, 53t Cryptosporidia baileyi, 141 Deer mouse, as Hantavirus carrier, 38f
Colibacillosis, 164 Cryptosporidia hominis, 140t DEET, 73
Collaboration reservoir for, 141 application of, 74f
human-animal medicine and, 5 Cryptosporidial diarrhea, 18–19 guidelines for use, 75b
public/human/animal health professionals and, 7 Cryptosporidia muris, 141 poisoning from
Communication Cryptosporidia parvum, 140t in animals, 77
human-animal medicine and, 4–5 geographic occurrence of, 140 in human beings, 77
medical provider to veterinarian, human-animal oocysts of, 142f use of, 74t
medicine issue, 387b reservoir for, 141 Delhi boil, 186
public/human/animal health professionals Cryptosporidiosis Depression, pet attachment and, 28
and, 7 in animals, 142–143 Dermacentor andersoni. See Rocky Mountain wood tick
See also Disease surveillance; Letter clinical presentation of, 143t Dermacentor variabilis. See American dog tick
Community, building healthy, 38 diagnosis of, 143 Dermanyssus gallinae, 255
Community-dwelling older adult, “loaner” dog and, effects of, 139 zoonotic potential of, 255t
26–27 environmental risk factors for, 142 Dermatitis
Companion animal geographic occurrence of, 140 characteristics of, 46
allergic conditions/diseases in, 47t hosts, reservoir species, vectors for, 141 Salmonella and, 252f
feline asthma as, 47–48 in human beings, 142 Dermatomycosis, 144
types of, 47t risk groups for, 140–141 Dermatophyte
bite infection, treatment for, 329t site for, 140 acquiring, routes of, 2f
contaminated fish and, 102 in small intestine, 140f classification of, 144
cyanobacteria toxins and, 100 transmission/life cycle of, 141–142, 141f transmission/features of, 145t
home health assessment of, 13 treatment of, 143, 143t Dermatophytosis
lead toxicity in, 68, 69t Cryptosporidium in animals, 146–147
pet trade and, 309 animal exposure to, implications of, 378t cause of, 144
service animal versus, 26 oocysts of, 141 clinical presentation of, 147t
tuberculosis in, 282, 285–286 presentation/management of, 336t crusting and, 22f
See also Pet species of, 140 diagnosis of, 147
Comparative oncology, 58–59 types of, 140t environmental risk factors for, 145–146, 145f
Congenital toxoplasmosis Cryptosporidium cyst, 142 focal alopecia from, 146f
clinical presentation of, 270t Ctenocephalides canis, 149 fungus causing, 144
with hydrocephalus, 269f Ctenocephalides felis, 149 geographic occurrence of, 144
Conjunctivitis, Chlamydophila psittaci and Culex mosquito, 296, 296f hosts, reservoir species, vectors for, 144–145
in cats, 136 Cultural festival, animal contact and, 302 in human beings, 146
in crocodile, 137f Cutaneous acariasis, 254 Microsporum canis as cause of, 387f
Consumer Cutaneous anthrax risk groups for, 144
foodborne illness risk and, 332t in child, 115f signs of, 146f
Consumer, foodborne illness risk and, 334–335 clinical presentation of, 116t
Contagious abortion, 123 transmission/life cycle of, 145, 145f
example of, 23f treatment of, 147–148, 148t
Contaminant, in indoor air, 41t life cycle of, 115–116
identification/evaluation of, 40–41 Desensitization therapy, 46, 47
transmission of, 114 Dew itch, 174
types of, 39t treatment of, 118t Diarrhea
Copperhead snake, tissue necrosis from, 83f Cutaneous larva migrans, 174
Coronavirus, SARS-like, 303 animal shelter guidelines for, 381b
from beaches, 304 cause and appropriate action
Cortisol level, animal interaction and, 26 Cutaneous leishmaniasis
Coughing, cause and appropriate action for human health care provider, 20t
cause of, 187 for veterinarian, 21t
for human health care provider, 20t diagnosis of, 190–191
for veterinarian, 21t cause and appropriate action for, 20t
environmental risk factors for, 187–188 See also Giardiasis
Coxiella, animal husbandry and, 367t geographic occurrence of, 187
Coxiella burnetii, 222 Diffuse cutaneous leishmaniasis, 188
hosts, reservoir species, vectors for, 187 Difloxacin, bite infection, treatment for, 329t
400 Index
Digoxin toxicity, 56 Domestic animal. See Companion animal geographic occurrence of, 159
Dipylidiasis, 148t Domestic violence transmission/life cycle of, 159–160, 160f
in animals, 152, 152t pets as indicators of, 33–34 Ehrlichia ewingii, 157–158
in children, 150–152, 151f warning signs of, 34b effects of, 159
diagnosis of, 152 Domoic acid hosts, reservoir species, vectors for, 159–160
environmental risk factors for, 152 effects of, 95t Ehrlichiosis
geographic occurrence of, 149 toxicity of, humans versus animals, 99t in animals, 161
hosts, reservoir species for, 150 Dobrava-Belgrade virus, 172 cause of, 157–159
in human beings, 152, 152t Doxycycline clinical presentation of, 162t
risk groups for, 149–150 bite infection, treatment for, 329t diagnosis of
transmission/life cycle of, 150–152, 150f for Chlamydophila psittaci infection, 138, 138t in animals, 162
treatment of, 152, 152t for leptospirosis, 194 in human beings, 161–162
Dipylidium caninum Q fever and, 225 environmental risk factors for, 160–161
characteristics of, 149 for Rocky Mountain spotted fever, 241, 241t geographic occurrence of, 159
example of, 149f for tularemia, 293t hosts, reservoir species, vectors for, 159–160
structure and egg packet of, 151f Dryness, winter discomfort and, 41 in human beings, 161
Dirofilariasis, 108t Duck risk groups for, 159
Disaster avian vacuolar myelinopathy in, 99–100 transmission/life cycle of, 160, 160f
animals after, management of, 380–383 HAB-related illness in, 99t treatment of, 162–163, 163t
health hazards after, 380b Salmonella and, 316 in animals, 163
human-animal medicine and, 379–383 Dumb rabies, 231 in human beings, 162–163
Discomfort, freedom from, 11b dog with, 234f Ehrlichiosis ewingii, 157
Disease Dust Elapidae, 84
animals reported in, 110t as indoor air contaminant, 39t Australian pressure-immobilization technique
animal symptoms/human relevance, 19 organic for, 87f
freedom from, 11b animal workers and, 348 envenomation from, 89t
human symptoms/animal relevance, 19–23 farm animal workers and, 367 symptoms and treatment of, 85t
OIE, reporting to, 373, 375b Elephant, examination of, 365f
outbreak of, 341, 376–378 E Emergency Prevention System for Transboundary
with zoonotic potential, 108t Eagle Animals and Plant Pests and Diseases (EMPRES),
See also Zoonotic disease avian vacuolar myelinopathy in, 99–100 377–378
Disease ecology, 6 HAB-related illness in, 99t Encephalitis
Disease prevention, handwashing for, 316f Eastern diamondback rattlesnake, horse bitten rabies causing, 227
Disease surveillance, 6 by, 84f toxoplasmosis and, 268
as active/passive, 374–376 Eastern Equine encephalitis (EEE), 294 Encephalopathy, lead exposure and, 68
information flow, human/animal disease, Ebola virus infection, first case of, 345–347 Endocrine disruption, 60
373–376, 377f Echinococciasis, 153 Endotoxin
Disinfectant/cleaners Echinococcosis animal workers and, 348
animal workers and, control strategies for, 346t cause of, 153 farm animal worker and, 367
use of, in veterinary practice, 360t clinical presentation of, 155t Enrofloxacin, 285
Distal radius, lead in, 67f diagnosis of, 156 bite infection, treatment for, 329t
Distemper, canine, 107t Echinococcus multilocularis as cause of, 154–156 for tularemia, 293t
Distress, freedom from, 11b in human beings, 154–156 Enteritis, treatment for, 253
Dog risk groups for, 153–154 Enterobacteriaceae family, 249
allergy to, 43–44 transmission/life cycle of, 154 Enterohemorrhagic E. coli (EHEC), 164
bite infection, treatment for, 329t treatment of, 156–157, 157t diagnosis of, 166
botulism in, 335 Echinococcus granulosus, 153 geographic occurrence of, 164–165
brucellosis in, 126 echinococcosis from, 154 hosts, reservoir species, vectors for, 165
carboxyhemoglobin and, 64 example of, 154f in human beings, 165–166
cryptosporidiosis in, 142–143 geographic occurrence of, 153 serotype of, 164
Escherichia coli infection in, 166, 166t hosts, reservoir species, vectors for, 154 treatment of, 166
with rabies, 233f, 234f hosts for, 153, 156 Enteroinvasive E. coli (EIEC), 164
risk assessment for, 390f Enteropathogenic E. coli, 164
transmission/life cycle of, 155f
with scabies, 258f Enterotoxigenic E. coli (ETEC), 164
Echinococcus multilocularis
toad poisoning and, 88 micrograph of, 165f
alveolar cyst from, 156f
toxicant exposure and presentation/management of, 336t
alveolar echinococcosis and, 153
indoors, 52 Envenomation
echinococcosis from, 154–156
outdoors, 52 from hymenoptera, 80
hosts for, 154
toxic exposures in, 58t marine, 88–91
risk factors for, 154
tularemia in, 292, 293t from reptile, 82–84
transmission/life cycle of, 154
West Nile virus in, 297t, 297–298 risk factors for, 79–80
Echinococcus oligarthus
See also Toxocara infection from scorpion, 82
geographic occurrence of, 153
Dog bite from spider bite, 81
polycystic hydatid disease and, 156
dog quarantine after, 379t Echinococcus vogelii travel and, animal contact during, 302
epidemiologic characteristics of, 323t geographic occurrence of, 153 types, symptoms, treatment for, 85t
infection risk from, 325 Environment
polycystic hydatid disease and, 156
Dog cestodiasis, 149 Echinodermata (Sea urchin), 88–90, 89t health community and, 38
Dog tapeworm. See Dipylidiasis Ecthyma contagiosum, 215 healthy backyard/neighborhood, 390
Dog tick, 159–160 Ectothrix infection, Microsporum canis as cause healthy home, 389–390
Rocky Mountain spotted fever and, 237–238 of, 387f indoor, 38–42
sizes of, 199f Eczema/dermatitis See also Built environment
Dog-walking program, 26–27 characteristics of, 46 Environmental disaster, effects of, 1–3
for exercise/stress reduction, 39f on hand, 46f Environmental hazard, animal disease/illness and,
Doherty, Peter C., 5 Ehrlichia canis, 159–160 18–19, 37
Dolphin Ehrlichia chaffeensis, 157–158 Environmental health
HAB-related death of, 101 effects of, 159 animal, human and, 2f
HAB-related illness in, 99t benefits of, 11
Index 401
importance of, 1–3 F Florida red tide, 94b

Environmental mycobacteria (EM), 277 Falling effects of, 101
Environmental sentinel event, potential, 19–23 animal workers and Flu, 177
Environmental toxic exposure control strategies for, 346t Fluorosis, 60t
cancer and, 59–60, 60t Farm Food
lead as, 66–67 foodborne illness risk and, 333–334 animal as, 1
noncancer disorders from, 60, 60t healthy, 390 toxicity in animals, 53t
Enzootic hepatitis, 242 checklist for, 392f Food and Agriculture Organizations (FAO), 5
Epidemic Intelligence Service (EIS) training, 4 inspection and regulation of, 379t Food and Drug Administration (FDA), equine-
Epidermophyton, 144 Farm animal worker derived antivenin from, 81–82
Epigenetics, Human Genome Project and, 6 allergens and, 367 Foodborne Diseases Active Surveillance Network,
Epinephrine level, animal interaction and, 26 chemical hazards and, 367–368 role of, 331
EpiPen, 80, 80f endotoxins/organic dust and, 367 Foodborne Diseases Outbreak Response and
Epizootic abortion, 123 occupational health/safety of, 366–367 Surveillance Team, role of, 341
Epsilon toxin, animal exposure to, implications occupational medicine services for, 368 Foodborne illness
of, 378t injury, exposure, illness management for, 368 animal exposure to, implications of, 378t
Equine anaplasmosis, 157 preplacement screening of, 368 in animals
Equine chronic obstructive pulmonary disease, 49 vaccinations and, 368 laboratory test, 341
Equine-derived antivenin, for spider bite, 81–82 physical examination, 341
physical hazards and, 368
Equine encephalitis, victim of, 377f cases of, 331
psychosocial stressors and, 368
Equine influenza, 182–183 in human beings
zoonotic disease and, 367
Equine monocytic ehrlichiosis, 157 laboratory test, 339–340
Farm environment
Erysipeloid, 108t patient history, 339
foodborne illness risk and, 332t
zoo/aquarium worker and, 364 physical examination, 339
Farmer’s lung, 45
Erysipelothrix rhusiopathiae, 364 presentation/management of, 336t
Farm visits, animal contact and, 302
animal husbandry and, 367t reporting of, 341
Fat, toxicology testing and, 59t
Erythematous wheal, in cat, 48f treatment for, 341
Fatal familial insomnia (FFI), 271
Eschar, cause and appropriate action, 21t types of, 335–339
Fatal human encephalitis, 227
Escherichia coli Food chain, risks along, 332–335, 332t
Fatigue, cause and appropriate action
micrograph of, 165f Food poisoning
for human health care provider, 20t
presentation/management of, 336t clostridial, 335
for veterinarian, 21t
reporting of, 341 staphylococcal, 335–338
Fatty food, toxicity in animals, 53t
ruminants and, 316 Fear, freedom from, 11b Food processing facility, inspection and regulation
serogroup classification for, 164 Federal Emergency Management Agency (FEMA), of, 379t
strains of, 164 Pets Act, The, 379 Food safety, in home, 333b
Escherichia coli infection, 163t Feed, toxicology testing and, 59t Formaldehyde, as indoor air contaminant, 39t
in animals, 166 Feline asthma, 47–48 Four corners’ disease, 171
clinical presentation of, 166t Feline atopy, 48f Fowl pest, 177
complications from, 166 Feline cowpox, 108t Fowl plague, 177
diagnosis of, 166 Feline immunodeficiency virus infection (feline Francis disease, 289
environmental risk factors for, 165, 165f AIDS), 107t Francisella, animal husbandry and, 367t
geographic occurrence of, 164–165 Feline leukemia virus infection, 107t Francisella tularensis
hosts, reservoir species, vectors for, 165 Feline spongiform encephalopathy (FSE), 271 effects of, 289
in human beings, 165–166 clinical presentation of, 275t subspecies of, 290
risk groups for, 165 geographic occurrence of, 272 Francisella tularensis holarctica (Jellison type B),
transmission/life cycle of, 165, 165f host for, 272 290
treatment of, 166 signs and symptoms of, 273 Francisella tularensis mediasiatica, 290
Espundia, 186 transmission/life cycle of, 272 Francisella tularensis tularensis (Jellison type A), 290
Ethambutol (EMB), 284–285, 284t Festival, animal contact and, 302 Freedom, five, of animal welfare, 11b
Ethanol, toxicity in animals, 53t Fetal loss, cause and appropriate action for, 20t Fungi. See Pathogenic fungi
Ethical issues, professionalism and, 10 Fever, cause and appropriate action, 21t Fungus
Ethical principles Fiber, as indoor air contaminant, 39t classification of, 144
in animal health, 11 Fiddleback spider. See Brown recluse spider dermatophytosis and, 144
in human health, 10–11 Fiduciary duty, 10 Funnel-web spider, neurotoxic envenomation
Ethylene glycol (EG) Filovirus infection, animal exposure to, implications from, 82
acute toxic exposure to, 55 of, 378t Furious rabies, 231
toxic exposure of, 58t Fipronil
Eucalyptus, oil of lemon, 73, 74t toxicity of, 73–76 G
Euthanasia, animal shelter guidelines for, 381b use of, 75t Gambian-pouched rat
Excoriation “First Strike” campaign, 33–34 monkeypox and, 310
cause and appropriate action Fish view of, 310f
for veterinarian, 21t brevetoxins killing, 94 Garlic, toxicity in animals, 53t
Exhaust marine HABs and, 101 Gastric ulcer, from NSAID use, 55f
as indoor air contaminant, 39t seabird deaths from, 101 Gastroenteritis, 251
Exotic animal Fish envenomation, 90, 90f Gastrointestinal anthrax
infections linked to, 310–311 Fish tank, types of, 318f clinical presentation of, 116t
risks associated with, 309–310 Fistulous withers, 126 life cycle of, 116
Exotic pet, 1 Flame-retardant polybrominated diphenyl ether treatment of, 118t
malpractice liability and, 9 (PBDE), 60, 60t Gastrointestinal system
Exotic ungulate encephalopathy, 271 Flavivirus contents of, toxicology testing and, 59t
clinical presentation of, 275t animal exposure to, implications of, 378t lead exposure and, 68
Extensively drug-resistant tuberculosis (XDR-TB), West Nile virus and, 295–296 Generalized alopecia, 48f
284–285 Flea, 74f Genome, 6
External parasitism, animal shelter guidelines for, 381b dog tapeworm and, 149 Gentamicin, for tularemia, 293t
Extracorporeal membrane oxygenation, 174 as plague vector, 219 Geophilic dermatophyte
Extraintestinal pathogenic E. coli (ExPEC), 164 types of, 149 classification of, 145t
Extrinsic allergic alveolitis, 45 Flea bite, 23f transmission of, 144
402 Index
GeoSentinel Surveillance Network Hand eczema, 46 Health risk assessment form, animal, 16f
Bartonella infection and, 300 Handwashing, for disease prevention, 316f Healthy backyard/neighborhood, 390
dog bites and, 300 Hantavirus checklist for, 392f
Gerstmann-Sträussler-Scheinker disease (GSS), 271 deer mouse as carrier of, 38f Healthy farm, 390
Giardia rodents and, 172 checklist for, 392f
example of, 168f Hantavirus infection Healthy home
presentation/management of, 336t animal exposure to, implications of, 378t with animals, checklist, 391f
site and forms of, 168 in animals, 174 concept of, 50
Giardia, in visitation dogs, 31–32 diagnosis of, 174 Heartwater, Amblyomma and, 310
Giardia cyst environmental risk factors for, 173 Heartworm, 108t
diagnosis of, 170 geographic occurrence of, 172 Heaves, in horses, 47t, 49
example of, 168f hosts, reservoir species, vectors for, 172–173 Helicobacter infection, 108t
Giardia duodenalis, 167 in human beings, 173 Heloderma horridum (Mexican beaded lizard), 84
Giardia intestinalis, 167 risk groups for, 172 Heloderma suspectum (Gila monster), 84
geographic occurrence of, 168 syndromes of, 171 Hematochezia, cause and appropriate action, 21t
in human beings, 168 transmission/life cycle of, 173, 173f Hemolytic uremic syndrome (HUS)
See also Giardiasis travel and, 303 as E. coli complication, 166
Giardia lamblia, 167 treatment of, 174 EHEC infection and, 165
in reptile, 170f Hantavirus pulmonary syndrome (HPS), 171 Hemoptysis, cause and appropriate action, 21t
Giardiasis geographic occurrence of, 172 Hemorrhage, cause and appropriate action for, 20t
in animals, 170 in human beings, 173 Hemorrhagic fever
clinical presentation of, 170t prevention of, 172b bushmeat and, 303–304
diagnosis of, 170 Haplorchis pumilio, 303 Rift Valley fever and, 246
environmental risk factors for, 170 Harmful algal bloom travel and, 303
geographic occurrence of, 168 effects of, 91 Hemorrhagic fever with nephropathy, 171
hosts, reservoir species, vectors for, 168 exposure to cause of, 172
in human beings, 170 metabolism and routes of, 99–100 stages of, 173–174
infectious diarrhea and, 167 risk groups for, 100 Hepatitis A infection, reporting of, 341
transmission/life cycle of, 168–170, 169f sites of, 92, 100f Hepatitis E virus, animal husbandry and, 367t
treatment of, 170–171, 171t Herpes B infection
toxicity of, 95t
See also Giardia intestinalis animal research facility worker and, 362
in animals, 101–102
Gila monster (Heloderma suspectum), 84, 87f fatal viral meningitis and, 328
in human beings, 100–101
Glanders, 108t Old World monkeys and, 300
humans versus animals, 99t
animal exposure to, implications of, 378t in rhesus monkey, 328f
types by site of, 100f
Glandular tularemia, 292 Highly Pathogenic Avian Influenza Early Detection
See also HAB-related illness
Global Avian Influenza Network for Surveillance Data System (HEDDS), 377–378
Harmful Algal Bloom Incidence Surveillance System
(GAINS), 377–378 High pathogenicity avian influenza, 182
(HABISS), 94
Glycol, animal exposure frequency, 54t Hilar lymphadenopathy, 282–283
Harvest/processing
Gnathostomiasis, 303 Histoplasma, animal husbandry and, 367t
foodborne illness risk and, 332t
Goat Histoplasma capsulatum, animal workers and, 348
Harvest/processing, foodborne illness risk and, 334
anaplasmosis in, 161f Histoplasmosis, 2f
Haverhill fever (Rat bite fever), 108t
Chlamydiae infection in, 137t Hives, animal allergy and, 46
Hay, moldy, 45
Chlamydophila abortus and, 136 HIV. See Human immunodeficiency virus (HIV)
cattle and, 49
See also Orf virus Home, as healthy environment, 389–390
Hazard
Granulomatous conjunctivitis, 121 Honeybee, 80
animal research facility worker and, 362–364 Hookworm dermatitis, 176
Granulomatous enteritis, in cow/cattle, 287f animal workers and, 345
Grapes, toxicity in animals, 53t Hookworm infection
biological in animals, 176
Gravid proglottid, 150–152 allergens as, 345, 354
Green Building Council, U.S., LEED rating system, 40 from beaches, 304
zoonotic pathogens as, 345–347 clinical presentation of, 176t
“Green” chemistry, 51 chemical, 348–349
Green iguana, 309f diagnosis of, 176–177
control strategies for, 346t, 349t effects of, 174–175
Ground itch, 174 elimination of, 349
Guillain-Barré syndrome, 298 environmental risk factors for, 176f
OSHA Hazards Communication Standards, geographic occurrence of, 175
Guinea pig, sarcoptic mange in, 258f
353–354 hosts, reservoir species, vectors for, 175
in pet store setting, 366 in human beings, 175
H physical, 349 life cycle of, 176f
H (flagellar) antigen, 164 psychosocial, 349 risk groups for, 175
H5N1. See Avian influenza See also Animal research facility worker; Farm species of, 175
Habitat destruction, species diversity and, 37–38 animal worker; Pet store worker; Veterinary
HAB-related illness transmission/life cycle of, 175
personnel; Wildlife rehabilitator; Zoo/aquarium treatment of, 177t
causative agents of, 94–99 worker
cyanobacteria associated with, 97t in animals, 177
Hazard card, for animal workers, 353f in human beings, 177
detection, surveillance, education for, 93–94 Health community, building, 38
diagnosis of, 102 See also Toxocara infection
Health department, human-animal health,
Hookworm ova, 176f
eutrophication, prevention of, 94 coordination of care, 388–389
Horse
management of, 102–103 Health hazard, built environment and, 39t
brucellosis in, 126
prevention of, 93 Health history
dermatophytosis in, 146–147, 146f
reporting of, 94 approach to, 12–17
equine encephalitis, 377f
treatment of baseline checklist for, 14f
fistulous withers in, 126f
in animals, 103 See also Medical history
heaves in, 47t, 49
in human beings, 102–103 Health home environment, 389–390
Health Insurance Portability and Accountability Act lead toxicity in, 68, 69t
See also Harmful algal bloom
(HIPAA) leishmaniasis in, 190f
Hair, toxicology testing and, 59t
Halogen, 360t animal worker medical records, 353 sarcoptic mange in, 258
Hamster covered entities under, 10 tularemia in, 292, 293t
lymphochoriomeningitis virus and, 317 purpose of, 10 West Nile virus in, 297t
view of, 317f veterinarians and, 10 Household cleaner, 58t
Index 403
House mouse (M. musculus). See Lymphocytic rabies in, 230–231 Hyperthyroidism, environmental exposures and, 60t
choriomeningitis (LCM) Rift Valley fever in, 246 Hypochlorite, 360t
Human-animal bonding, 13 Rocky Mountain spotted fever in, 239–240
immunocompromised individual and, 313 Salmonella in, 251 I
Human-animal bond phenomenon, 1 scabies and, 257 Iatrogenic Creutzfeldt-Jakob disease (CJD),
Human-animal contact, in veterinary history, 13–17 toxic exposures in, 58t transmission of, 272–273
Human-animal disease risk form, 17f Toxocara infection in, 263 IFA visualization, cryptosporidiosis and, 143
Human-animal interaction (HAI) toxoplasmosis in, 268 IFN-γ-releasing assay (IGRA), 284
child with dog, 25f transmissible spongiform encephalopathy in, 273 Iguana
facilitation of, 29–32 tuberculosis in, 276, 279–281 green, 309f
Giardia infection and, 167 tularemia in, 291–292, 293t lead poisoning in, 69f
health benefits of, 25–29 West Nile virus in, 296, 297t Imidacloprid
in older adults, 25–26 Human bite, 325 toxicity of, 76
long term versus casual encounter, 26 Human dander, as indoor air contaminant, 38–39 use of, 75t
in occupational setting, 343 Human disease symptoms Immunocompromise, etiology of, 314t
pain level and, 26 animal health and, 22f Immunocompromised individual
physiological benefits of, 26 cause and appropriate action for, 20t animal bite and, 325
psychological benefits of, 26t relevance to, 19–23 animal husbandry and, 317–318
psychosocial/therapeutic aspects of, 24–36, 27t types of, 19–23 care for pet of, 318
research needs for, 34 Humane Genome Project, 6 human-animal bonding and, 313
types of, 24–25 Humane Society of the United States, “First Strike” occupational/recreational risk and, 316
Human-animal medicine campaign, 33–34 pet ownership and, 315
case scenario, shared behavior risk, 388 Human granulocytic anaplasmosis (HGA), 157 pet selection for, 316–317
collaboration for, 5 peripheral blood smear showing, 163f reptiles and, 317f
communication for, 4–5 Human health veterinarian role in care of, 318–320
medical provider to veterinarian, 387b animal disease/illness and, 18–19 zoonotic disease prevention for, 315–318
coordination of care, 388–389 consequences of, 18–19 Immunocompromised pet
disasters and, 379–383 animal health and, 1 animal bites in, 328, 329t
legal/ethical issues in, 7–11 convergence of, 7–8 veterinarian role in care of, 318–320
malpractice liability and, 8–9 baseline history for veterinarian, 13–15 Immunodeficiency, animal-human disease
One Health approach to, 384 companion animals and, 13 transmission and, 315
professionals involved in, 4 echinococcosis in, 154–156 Immunodeficient animal
public health and, 381 environmental, animal and, 2f care for, 318
tickborne disease, shared environment ethical principles in, 10–11 guidance for owner, 318–320
exposure, 389 training/practice statistics for, 3–4, 3t Immunoglobulin E, anaphylaxis and, 45
See also Veterinary-human medical partnerships veterinarian role in, 3–4 Immunosuppression, etiology of, 314–315
Human being Human health clinician Importing, of animal, 308–309
animal bite in, 322–327 disease reporting/notification by, 10 Inadequate ventilation, 39–40
anthrax in human-animal medicine, key points for, 7 sentinel events from, 41t
clinical presentation of, 116t veterinarian, referral to, 385–387 Indoor air quality
diagnosis of, 116–117 Human health risk clinical conditions related to, 40
treatment of, 118 human-animal disease risk survey for, 17f definition of, 37
types of, 115–116 screening/follow-up questions for, 17t illness associated with, checklist for, 40b
brucellosis in, 126 travel and, animal contact during improvement of, 42b
Campylobacter disease in, 130–131 injuries and, 300–305 LEED rating system and, 40
carbon monoxide poisoning in, 63–64 prevention of, 301t problems in
cat-scratch disease in, 121 Human immunodeficiency virus (HIV) conditions associated with, 41t
Chlamydiae infection in, 137t animal research facility worker and, 363 evaluation of, 40–42
Chlamydophila psittaci in, 135–136 infection, prevention of, 319t Indoor environment, 38–42
cryptosporidiosis in, 142 nontuberculosis mycobacteria and, 287 contaminants in, 39t
disease outbreak in, 376 tuberculosis and, 279–280 Industrial hygienist, 345
ehrlichiosis/anaplasmosis in, 161 zoonotic disease and, 318 Infection control/biosafety specialist, 345
Escherichia coli infection in, 165–166 Human monocytic ehrlichiosis (HME), 157 Infection control plan for veterinary practice, model
foodborne illness, evaluation of, 339–340 Human toxic exposure, sentinels for, 51–52 for, 355f
Giardia intestinalis in, 168 Humidity, effects of, 41 Infectious canine cyclic thrombocytopenia, 157
giardiasis in, 170 Hunger, freedom from, 11b Infectious diarrhea. See Giardiasis
HAB-related illness in, 99t Hurricane Katrina, effects of, 1–3 Infectious disease
Hantavirus infection in, 173 Hydatid cyst, 153 animal research facility worker exposure to, 364
hookworm infections in, 175 CT image of, 156f animal worker exposure to, 351–353
influenza in, 182 in horse liver, 156f environmental driver versus outcome, 106f
insect repellent for, 73 Hydatid disease, 153 exotic/ wildlife pets and, 310–311
LCM infection in, 207–208 Hydatidosis, 153 farm animal worker exposure to, 368
Hydatid sand, 153f nationally notifiable, 374b
lead toxicity in, 68
Hydrocephalus, congenital toxoplasmosis and, 269f nontraditional pets and
leishmaniasis in, 188
Hydrozoa, 88, 89t prevention guidelines for, 312b
leptospirosis in, 193–194
Hygeia, bust of, 373f risk groups for, 310t
Lyme disease in, 201
Hymenopteran envenomation, 80 as non-zoonotic, 106–107, 107t
marine envenomation in, 89t
symptoms and treatment of, 85t outbreak of, 376–378
medication toxicity in, 54–55
Hyperkeratosis, Sarcoptes scabiei and, 256f pet store worker exposure to, 366
MRSA in, 212 Hyperkeratotic scabies, occurrence of, 257
orf virus in, 216 scenarios for, 299–330
Hypersensitivity pneumonitis (HP), 45–46 shared risk of, us versus them, 105–106
pesticide toxicity in, 76–77 in cattle, 47t, 49
plague in, 220 traveling pet and, 305
chest radiograph of, 45f travel medicine and, 299–300
preventive environmental risk assessment for, diagnosis of, 45
389–390 veterinary personnel exposure to, 362
symptoms of, 45 zoo/aquarium worker exposure to, 366
prion disease in, 273 treatment of, 45–46
Q fever in, 225 as zoonotic, 1, 105
in veterinary personnel, 354
404 Index
Influenza larvae from, 88 hosts, reservoir species, vectors for, 187

animal husbandry and, 367t venom of, 88 in human beings, 188
bacterial pneumonia and, 177, 181f Jellyfish envenomation, 88 risk groups for, 187
clinical presentation of, 183t Jiggers (Tunga penetrans), 304 transmission/life cycle of, 187, 188f
diagnosis of Johne’s disease traveling pet and, 305
in animals, 184 cause of, 287 treatment of, 190t, 191
in human beings, 184 in cow/cattle, 287f ulcer from, 190f
effects of, 177 Justice Leishmaniasis recidivans, 188
environmental risk factors for, 182 application of, 11b Lemon eucalyptus, oil of, 73, 74t
evolvement of, 180 definition of, 10–11 Leopard/spurred tortoise, heartwater and, 310
hosts, reservoir species, vectors for, 181 Lepidopterism, 80–81
in human beings, 182 K Leprosy, 276
micrograph of, 180f Kala-azar, 186 Mycobacterium leprae and, 288
risk groups for, 181 Karenia brevis, 94 Leptospira, 192
species affected by, 178 Kennel, animal workers at, 344 Leptospira interrogans, 192f
transmission/life cycle of, 181–182, 182f Kennel cough, 108t Leptospirosis
treatment of Keratinophilic mycosis, 144 acquiring, routes of, 2f
in animals, 184–185 Kidney in animals, 194
in human beings, 184, 185t lead exposure and, 68 cause of, 192
types of, 180 toxicology testing and, 59t clinical presentation of, 193t
vaccination for, 179 Kilborne, F. L., 5 diagnosis of, 194
Influenza A virus Kuru, 271 doxycycline and, 194
diagnosis of, 184 Kyphosis, 281f environmental risk factors for, 193
schematic model of, 178f geographic occurrence of, 192
subtypes of, 180 hosts, reservoir species, vectors for, 192–193
L in human beings, 193–194
Influenza A virus H3N8/H7N7, 182–183 Laboratory testing, for foodborne illness
Influenza B, 180 phases of, 194f
in animals, 341
Influenza C, 180 prevalence of, 191
Influenza pandemic, 177–178 risk groups for, 192
Labored breathing, cause and appropriate action
types and duration of, 180f transmission/life cycle of, 193, 193f
for human health care provider, 20t
Inhalational anthrax treatment of, 194–195, 195t
for veterinarian, 21t
chest x-ray of, 117f Letter
La Crosse encephalitis (LAC), 294
clinical presentation of, 116t animal sentinel event, environmental toxic
Lamblia intestinalis, 167
life cycle of, 116 Larvae (sea bather’s eruption), 88 risk, 388b
screening guidelines for, 117f Lassa fever, travel and, 303 dog obesity, 388b
treatment of, 118t Latent tuberculosis zoonotic disease counseling/risk reduction, 386b
Inhalational tularemia, 293t diagnosis of, 283–284 Liability
Injury treatment of, 285 malpractice, 8–9
animal abuse causing, 33 Latex allergy, animal worker and, 349–350 personal injury and, 9–10
animal research facility worker and, 364 α-Latroxin, 81 workers’ compensation, 9
animal workers and Lead Listeria, presentation/management of, 336t
control strategies for, 346t characteristics of, 65f Listeria monocytogenes, 335
management of, 351–353 in distal radius, 67f Listeriosis
farm animal worker and, 368 exposure to in cow/cattle, 338f
freedom from, 11b metabolism and routes of, 67–68 overview of, 335
pet store worker and, 366 sources of, 66–67 Litterbox, cleaning, 316, 316f
veterinary personnel and, 362 Live animal market, 302–303
in intestines, 67f
zoo/aquarium worker and, 366 Severe acute respiratory syndrome and,
public health communication about, 389b
Insect repellent 302–303
risk groups for, 68
for human beings, 73 Live bird market, H5N1 avian influenza and,
shared environment exposure to, 388–389
types of, 74t 302–303
toxicity of
See also Pesticide Liver, toxicology testing and, 59t
in animals, 68–70, 69t Livestock
Insect sting chelation therapy guidelines, 71t
anaphylaxis from, 80 Rift Valley fever in, 246
in human beings, 68, 69t toxicant exposure and, 52
angioedema from, 80f treatment and level of, 70t
International animal trade, 310–311 tuberculosis in, 276
See also Lead poisoning Livestock confinement, animal workers in, 344, 348
International travel. See Travel Leading, service dogs and, 25
Intestinal parasitism, animal shelter guidelines for, 381b Live vaccine, animal workers and, 345–347
Lead lines, 66–67, 67f control strategies for, 346t
Intestine, lead in, 67f Lead poisoning
In vitro carcinogen, 101 Lizard, poisonous, 84
blood lead level, 70t symptoms and treatment of, 85t
Iodine compound, 360t diagnosis of, 70
Isoniazid (INH), 284–285, 284t “Loaner” dog, 26–27
presentation/management of, 336t Lone star tick, size of, 199f
Itching, animal allergy and, 46
treatment of Long-term care, animal interaction and, 26
Ixodes pacificus, 159
for animals, 71 Loss, of pet, impact of, 32–33
Lyme disease and, 198
for human beings, 70–71 Lower respiratory tract symptoms, cause and
Ixodes scapularis, 159
See also Lead appropriate action, 21t
host for, 198
LEED rating system, 40 Low pathogenicity avian influenza, 182
Lyme disease and, 198
Leek, toxicity in animals, 53t Lufenuron
size of, 199f
Leishmania, 186 toxicity of, 76
view of, 198f Leishmaniasis
Ixodid ticks, Rocky Mountain spotted fever use of, 75t
in animals, 189–190 Lunar New Year festival, travel during, 302
and, 237–238
in canine, 189f Lung, toxicology testing and, 59t
diagnosis of, 190–191 Lung disease
J environmental risk factors for, 187–188 environmental exposures and, 60t
Jellyfish forms of, 186 See also Tuberculosis
groupings of, 88 geographic occurrence of, 187 Lung function test, for animal workers, 350–351
Index 405
Lyme arthropathy, 201–202 dermatophyte, cat in home, 385–387 Minamata disease, 51

Lyme disease shared environment toxic risk, 387–388 Mine, canaries and, 50
acquiring, routes of, 2f zoonotic disease counseling/risk reduction, 385 Mite
in animals, 201–202 form for, 385b Sarcoptes scabiei as, 255
antibiotics for, 203, 203t human health care provider to veterinarian, zoonotic potential of, 255t
cause of, 195–196 385–387 Mobility, animal assistance for, 25
clinical presentation of, 202t for preventive risk reduction, 385b Model Veterinary Practice Act (MVPA), 8
diagnosis of veterinarian to human health care provider, Mold
in animals, 202 387–388 as indoor air contaminant, 38–39
in human beings, 202 zoonotic disease counseling/risk reduction, 386b water damage and, 41
environmental risk factors for, 199–201 Medical surveillance Moldy food, toxicity in animals, 53t
example of, 22f for animal research facility worker, 364 Moldy hay, 45
geographic occurrence of, 196–198, 198f for animal workers, 351 cattle and, 49
hosts, reservoir species, vectors for, 198 for pet store workers, 366 Monkey, scratch/bite from, 362
in human beings, 201 for veterinary personnel, 359–362 Monkeypox, 108t
MRI and, 201f for zoo/aquarium worker, 366 example of, 311f
risk groups for, 198 Medication exotic rodents and, 310–311
transmission/life cycle of, 198–199, 200f judicious prescription of, 51 Gambian pouched rat and, 310–311
treatment of, 203, 203t toxicity of, 54–55, 55t wildlife importation and, 311f
Lyme nephropathy, 201–202 Mediterranean fever, 123 Monkey temple, 300
Lymphatic disease, nontuberculosis mycobacteria Melamine Moon blindness, 191
and, 287 effects of, 51 Morbidity, swine influenza and, 182
Lymph node, cat-scratch disease and, 121f presentation/management of, 336t Mosquito, 74f
Lymphochoriomeningitis virus (LCMV), outbreak Melioidosis (pseudoglanders), 108t abandoned pools and, 380f
of, hamster and, 317 Meningeal plague Culex, 296f
Lymphocytic choriomeningitis (LCM) clinical presentation of, 221t Rift Valley fever and, 243, 244
animal research facility worker and, 363 in human beings, 220 See also West Nile virus (WNV)
in animals, 208 Meningoencephalitis, Rift Valley fever and, 246 Mosquito-borne virus, West Nile virus as, 296
Arenaviridae family and, 205–206 Mental suffering, freedom from, 11b Mosquito repellent, 74f
clinical presentation of, 208t Mercury poisoning Mucocutaneous leishmaniasis, 188
CT of infant with, 207f environmental exposures and, 60t Mud fever, 191
diagnosis of, 208 sentinels of, 60 Multidrug-resistant tuberculosis (MDR-TB),
effects of, 204 Mesothelioma, 52 284–285
environmental risk factors for, 207 Metabolism, toxicant exposure and, 52 Mushroom
geographic occurrence of, 206 Metaflumizone acute toxic exposure to, 56
hosts, reservoir species, vectors for, 206 toxicity of, 76 toxic exposure of, 58t
use of, 75t Mushroom worker’s lung, 45
Metaldehyde Mycobacteria
pregnancy and, 328
acute toxic exposure to, 56 acid-fast bacilli and, 282
risk groups for, 206
toxic exposure of, 58t classification of, 277
transmission/life cycle of, 206–207, 206f
p-methane 3,8-diol (PMD), 73 geographic occurrence of, 278
treatment of, 208–209
Methicillin-resistant coagulase-negative identification of, 282
Lyssavirus, 228
Staphylococcus (MRCoNS), 211 Mycobacteria growth indicator tube, 282
Lyssavirus, bat as reservoir for, 303
Methicillin-resistant Staphylococcus aureus infection Mycobacterial interspersed repetitive unit
in animals, 212 (MIRU), 282
M clinical presentation of, 212t Mycobacteria other than tuberculosis
Macadamia nut, toxicity in animals, 53t (MOTT), 277
diagnosis of, 212
Mad cow disease, 271 Mycobacteria ulcerans, Buruli ulcer and, 287
effects of, 209–210
Malaria, travel and, 303 Mycobacteriosis, 276
environmental risk factors for, 211–212
Malnutrition, freedom from, 11b Mycobacterium avium, 288f
geographic occurrence of, 210–211
Malpractice liability Mycobacterium bovis, 276, 278
hosts, reservoir species, vectors for, 211
management techniques for, 9 acquiring, routes of, 2f
in human beings, 212
for physician/veterinarian, 8–9 radiograph of, 282f
Malta fever, 123 life cycle of, 211f
Mycobacterium genavense, 287
Manatee, HAB-related death of, 101 micrograph of, 206f
Mycobacterium leprae, 288
Mannitol, for HAB-related illness, 102–103 prevalence of, 210 Mycobacterium marinum, 276, 287, 288
Marbofloxacin, 285 risk groups for, 211 aquarium workers and, 364
bite infection, treatment for, 329t transmission of, 211 Mycobacterium paratuberculosis, 287
Marburg virus, bats and, 303 treatment of, 212–213, 212t Mycobacterium prototuberculosis, 278
Marine animal, HAB-related death of, 101 β-methylamino-L-alanine (BMAA), 99–100 Mycobacterium tuberculosis, 276
Marine envenomation, 88–91, 89t Metronidazole, bite infection, treatment for, 329t Mycobacterium tuberculosis complex
Marine HAB, fish and, 101 Mexican beaded lizard (Heloderma horridum), 84 (MTBC), 276
Market men’s disease, 289 Microagglutination test (MAT), 194 geographic occurrence of, 278
Material Data Safety Sheet (MSDS), 57 Microcystin hosts for, 278t
chemical hazards and, 348 HAB-related illness and, 97t species and cause of, 277–278
Measles, animal research facility worker and, 362–363 as in vitro carcinogen, 101 Mycobacterium tuberculosis direct test, 282
Mediastinal lymphadenopathy, 282–283 Microphytosis, 144 Mycoplasma phocicerebrale, 364–365
Medical chart, baseline information for, 13 Microsporum, 144 Myiasis, 217
Medical evaluation, for animal workers, 349, 353 Microsporum audonii, geographic occurrence of, 144
Medical history Microsporum canis
animal health information on, 12–13 in culture, 148f N
ectothrix infection from, 387f Nasal cancer, polyaromatic hydrocarbon and, 52
approach to, 12–17
geographic occurrence of, 144 Nasal/sinus congestion
lead exposure risk and, 70b
paronychia in cat from, 387f cause and appropriate action
Medical questionnaire, for animal workers, 350f
Medical record, confidentiality for animal workers, Tinea capitis and, 146, 146f for human health care provider, 20t
353 Microsporum nanum, 144–145 for veterinarian, 21t
Medical referral Milk pasteurization National Animal Health Policy and Programs, 341
case scenario Q fever and, 224 National Animal Health Reporting System, 341
406 Index
National Association of Public Health Veterinarians O One Health Initiative

animal workers training and, 351 Occupational allergen, types of, 43 disease ecology and, 6
infection control plan for veterinary practice, Occupational disease, types of, 353–354 disease surveillance and, 6
model for, 355f Occupational exposure, HIV-infected person and, logo for, 5f
veterinary standard precautions and, 353–354 319t objectives for, 5
Veterinary Standard Precautions for Zoonotic Occupational health approach, 344, 344b overview of, 5–6
Disease Prevention in Veterinary Personnel, 354 Occupational health/safety research approaches for, 6
National Asthma Education and Prevention for animal research facility worker, 362 One Health Task Force, 5
Program Expert Panel Report 3, 46–47 for farm animal worker, 366–367 Onion, toxicity in animals, 53t
National Center for Zoonotic, Vector-Borne, and for veterinary personnel, 353–362 Oocyst
Enteric Disease (NCZVED), 4 for wildlife rehabilitator, 369 of Cryptosporidia, 141
National Health and Nutrition Examination Survey for zoo/aquarium worker, 364 of Cryptosporidia parvum, 142f
(NHANES), toxoplasmosis and See also Animal worker O polysaccharide antigen, 164
geographic occurrence of, 266 Occupational health team Orbifloxacin, bite infection, treatment for, 329t
risk groups for, 266 industrial hygienist role in, 345 Orf virus
National Highly Pathogenic Avian Influenza (HPAI), infection control/biosafety specialist role affects and transmission of, 214
179 in, 345 animal husbandry and, 367t
Necropsy, autopsy rate versus, 3 members of, 344, 345f in animals, 216
Neglect of pet store worker, 366 clinical presentation of, 217t
cause and appropriate action for, 20t veterinarian role in, 344–345 diagnosis of
potential for, 13 Occupational medicine, 349 in animals, 217
Neighborhood, healthy, 390 Occupational medicine services in human beings, 216–217
checklist for, 392f for animal research facility worker, 363–364 environmental risk factors for, 216
Nematocyst, structure of, 90f for animal workers, 352t geographic occurrence of, 215
Neoplasia, 20t injury, exposure, illness management for, hosts, reservoir species, vectors for, 215–216
Neorickettsia sennetsu, 159 351–353 in human beings, 216
Neosaxitoxin, HAB-related illness and, 97t medical records, confidentiality of, 353 life cycle of, 216f
Nephropathia epidemica, 172 medical surveillance for, 351 Parapoxvirus ovis and, 215
Neuropathology, cause and appropriate action for, 20t preplacement screening of, 349–351 risk groups for, 215
Newcastle disease virus, animal husbandry and, 367t training for, 351 transmission/life cycle of, 216
New World spotted fever, 236 vaccinations and, 351 treatment of, 217
Nine-mile fever, 222 for farm animal worker, 368 Organic compound, as indoor air contaminant, 39t
Nipah virus, 105–106
injury, exposure, illness management for, 368 Organic dust
animal exposure to, implications of, 378t
preplacement screening of, 368 animal workers and, 348
animal husbandry and, 367t
vaccinations and, 368 farm animal worker and, 367
bats and, 303 Organic toxic dust syndrome (ODTS), 367
for pet store workers
first case of, 345–347 Organophosphate compound
injury, exposure, illness management for, 366
Nitenpyram animal toxicity from, 76
medical surveillance for, 366
toxicity of, 76 human being, effect on, 72
preplacement screening of, 366
use of, 75t poisoning from, 77–78
vaccinations and, 366
Nitrogen dioxide
for veterinary personnel, 359–362 use of, 75t
animal workers and, control strategies for, 346t Oriental sore, 186
injury, exposure, illness management for, 362
source of, 348–349 Oropharyngeal tularemia, 292
medical surveillance for, 359–362
N-methyl carbamate Orthomyxoviridae, 180
preplacement screening of, 359
toxicity of, 76 Oseltamivir (Tamiflu), 184, 185t
for zoo/aquarium worker, 365–366
See also Carbamate OSHA Hazards Communication Standards, 353–354
Nodularin, HAB-related illness and, 97t injury, exposure, illness management for, 366
medical surveillance for, 366 OSHA Respiratory Standard, 349–350, 359–362
Noise, control strategies for, 346t wildlife rehabilitator and, 369
Nonaccidental injury, 33 preplacement screening of, 365–366
Occupational Safety and Health Administration Osler, Sir William, 5
Nonallergic asthma, 45 Osteosarcoma, 58–59
Nonhealing wound, cause and appropriate action, 20t (OSHA)
carbon monoxide exposure, 62–63 Otitis externa
Nonhuman primate, exposure to, 300 in dog, 315f
Nonsteroidal antiinflammatory drug (NSAID) disease/injury reporting to, 10
Respiratory Standard, 349–350 immunocompromised patient and, 315
gastric ulcer from, 55f Otodectes cynotis, 255
toxicity of, 54–55, 55t workplace plan for hazards, 353–354
Occupational setting zoonotic potential of, 255t
Nontuberculosis mycobacteria (NTM), 277 Outer surface protein A (OSP A), vaccine for, 203
clinical/epidemiological presentation of, 286 human-animal interaction in, 343
reverse zoonosis in, 347 Oxidizing agent, 360t
HIV and, 287
lymphatic disease and, 287 veterinarian role in, 344–345
pulmonary, diagnosis of, 287 Ocular larva migrans, 261 P
site and symptoms of, 286–287 clinical presentation of, 263t Pain
skin, soft tissue, bone disease and, 287 development of, 263 freedom from, 11b
transmission of, 286 in human beings, 263 human-animal interaction and, 26
types and presentation of, 287t treatment of, 264t Pancreas, toxicology testing and, 59t
Non-tuberculosis mycobacterial disease, 276 Ocular toxoplasmosis, 268 Panton-Valentine leukocidin (PVL), 210
Non-typhoid Salmonella gastroenteritis, 251 Oculoglandular tularemia, 292 Papules, cause and appropriate action, 21t
Non-zoonosis, infectious disease as, 106–107, 107t Ohara’s disease, 289 Paragonimiasis, 303
North American tick typhus, 236 Oil of lemon eucalyptus, 73, 74t Paragonimus, 303
Norwegian scabies, 254 Okadaic acid, 95t Parapox virus infection, 215
occurrence of, 257 as in vitro carcinogen, 101 Parapoxvirus ovis, 215
Nosocomial zoonosis, immunocompromised patient Older adult micrograph of, 215f
and, 315 animal interaction with, 26 Parasitism, animal shelter guidelines for, 381b
Notification, of disease/conditions, 10 cat mascot for, 25–26 Paretic patient, example of, 32f
Notoedres cati, 255 “loaner” dog and, 26–27 Parinaud’s oculoglandular syndrome, 121
zoonotic potential of, 255t Old World monkeys, herpes B infection, 300 Paronychia, Microsporum canis as cause of, 387f
Nucleic acid amplification (NAA) test, 282 Old World virus, 172 Particulate, 41
Nursing home resident, dog visits and, 26 Oleander, acute toxic exposure to, 56 Parvovirus, canine, 107t
One Health approach, 384 Pasteurella
Index 407
travel and, 300 Pet trade human exposures, 53t

in visitation dogs, 31–32 companion animals and, 309 nonhuman exposures, 54t
Pasteurella infection, 327 control efforts for, 311–313 toxic agent percentages reported, 54t
Pasteurella multocida, 327, 327f infections linked to, 310–311 See also Carbon monoxide; Lead; Pesticide
Pasteurellosis, 108t reptiles and, 309 Poisonous lizard, 84
Pasteurization, Q fever and, 224 wildlife and, 309 Poisonous plant
Pasture fever, 157 Pet travel. See Travel acute toxic exposure to, 56
Pathogen PFOA fumes exposures reported, 56t
animal research facility worker exposure to, 364 acute toxic exposure to, 57 Poll evil, 126
animals reported in, 110t toxic exposure of, 58t Polyaromatic hydrocarbon (PAH), nasal cancer
animal worker exposure to, 351–353 Pharmaceutical, animal exposure and, 52
farm animal worker exposure to, 368 frequency, 54t Polycystic hydatid disease, 156
intentional release of, 376–377 Pharyngeal plague Polymer fume fever, 57
pet store worker exposure to, 366 clinical presentation of, 221t Pool, abandoned, mosquitos and, 380f
zoo/aquarium worker exposure to, 366 in human beings, 220 Portuguese man-o-war, 88
Pathogenic fungi Phenol, 360t Postmortem toxicology testing, samples needed for,
animal workers and, 348 Phlebovirus, 243, 243f 59t
control strategies for, 346t Physical examination, for foodborne illness Posttravel assessment, 305, 305b
Pedestrian path, 38f in animals, 341 for pet, 307b
Pelican, HAB-related illness in, 99t in human beings, 339 Potomac horse fever, 157
Peliosis hepatitis, 121f, 122t Physical hazard Poultry, virus associated with, 367t
Peripheral nervous system, lead exposure and, 68 animal workers and Powdered air purifying respirator (PAPR), 369f
Permethrin/pyrethroid control strategies for, 346t Prairie dog, plague and, 219, 220
characteristics of, 72 types of, 349 Pregnancy
use of, in animals, 75t farm animal worker and, 368 Chlamydophila abortus and, 136
Persin, toxicity in animals, 53t veterinary personnel and, 359 Chlamydophila psittaci and, 136
Personal protective equipment, anthrax and, 119 zoo/aquarium worker and, 365 complications and appropriate action, for
Pesticide Physician veterinarian, 21t
animal exposure frequency, 54t disease reporting/notification by, 10 lymphocytic choriomeningitis and, 328
for animals, 73–76, 75t home/worksite visits by, 3 raw food handling during, 316f
animal toxicity from malpractice liability for, 8–9 toxoplasmosis and, 268
high levels of, 76 practice, scope of, 8 Preplacement screening
low levels of, 73–76 Physician-veterinary contact, advantages of, 9 for animal research facility worker, 363–364
moderate levels of, 76 Picaridin, 73, 74t for animal workers, 349
toxicity of, 72 Pigeon breeder’s lung, 45 for farm animal worker, 368
in animals, 77 Pig-handler’s itch, 254 for pet store workers, 366
in human beings, 76–77 Pit viper for veterinary personnel, 359
risk groups for, 76 domestic animal bites from, 84 for zoo/aquarium worker, 365–366
See also Rodenticide head of, 83f Pretragal lymphadenopathy, 121
Pesticide poisoning treatment for bite, 83–84 Pretravel risk assessment, 300, 305
diagnosis of, 77–78 types of, 83 for pet, 307b
management of, 78 venom of, 83 Primary bronchus epithelium, 40f
treatment of, 78t Plague Primary pneumonic tularemia, 292
Pet acquiring, routes of, 2f Prion disease, 271
acute care visit and, 12–13 animal exposure to, implications of, 378t development of, 273f
benefits/percentage of, 1 in animals, 220 in human beings, 273
bite infection, treatment for, 329t cause and effects of, 218 outbreak of, 271
cyanobacteria toxins and, 100 clinical presentation of, 221t treatment of, 275–276
human behavior/domestic violence, as indicators diagnosis of, 220–221 Privacy Rule. See Health Insurance Portability and
of, 33–34 environmental risk factors for, 220 Accountability Act (HIPAA)
immunocompromised patient and, 315 epidemiological features of, 219f Professionalism, ethical principles and, 10–11
lead exposure and geographic occurrence of, 219 Proglottid
risk of, 68 hosts, reservoir species, vectors for, 219 elements of, 149
as sentinel of, 68 in human beings, 220 example of, 149f
separation/loss of, impact of, 32–33 risk groups for, 219 micrograph of, 150f
toxicant exposure and, 52 transmission/life cycle of, 219–220 Proportionalism, 10–11
See also Companion animal Propyl disulfide, toxicity in animals, 53t
treatment of, 222t
Pet allergy, risk factors for, 44 Propyl mercaptan, 377
in animals, 221
Pet ownership Prostate cancer, 58–59
Protein allergen, 43–44
medical recommendations for, 29–30 Plant
Proteinase-sensitive prionopathy (PSPr), 273
physical/cognitive ability and, 29 animal exposure frequency, 54t
Pruritus, from eczema/dermatitis, 46
physiological/psychosocial effects of, 27–29 toxic exposure of, 58t Pseudomembranous colitis, 108t
recommendation, guidelines for, 29t toxicology testing and, 59t Pseudomonas pseudomallei bacteria as, 108t
Pet proofing, 51 See also Poisonous plant Pseudoscabies, 254, 256
Pets Act, The, 379 Plant crop, safe fertilizer for, 332–333 clinical presentation of, 257t
Pet shelter Plasmodium knowlesi, travel and, 303 treatment of, 259t
health/disease control at, 381b Pneumonia, Q fever and, 226f Psittacine bird (parrot family), 133
injury/illness prevention at, 382b Pneumonic plague See also Chlamydophila psittaci
Pet store, inspection and regulation of, 379t clinical presentation of, 221t Psittacosis
Pet store worker in human beings, 220 CDC surveillance criteria for, 137
hazards and, 366 radiograph of, 220f diagnosis of, 136
occupational health/safety of, 366 treatment of, 222t Psychosocial stressor
occupational medicine services for Pneumonic tularemia, 291 animal workers and
injury, exposure, illness management for, 366 Poisoning control strategies for, 346t
medical surveillance for, 366 acute toxic exposure and, 52 types of, 349
preplacement screening of, 366 from cyanide, 52 farm animal worker and, 368
vaccinations and, 366 substances reported
408 Index
Psychosocial stressor (Continued) dog with, 233f Reverse zoonosis, 19

veterinary personnel and, 359 effects of, 227 in occupational setting, 347
zoo/aquarium worker and, 365 environmental risk factors for, 230 Rhabdovirus, 228
PTFE fumes geographic occurrence of, 228–229 Rhesus monkey, herpes B infection in, 328f
acute toxic exposure to, 57 Holstein with, 233f Rhinitis, 44
toxic exposure of, 58t hosts, reservoir species, vectors for, 229–230 Ribavirin, 174
Public disclosure, 10–11 in human beings, 230–231 Rice field fever, 191
Public health first aid for, 231 Ricin toxin, animal exposure to, implications of,
human-animal medicine and, 381 management of, 231 378t
training/practice statistics for, 3–4, 3t risk assessment of, 231 Rickettsiae, disease caused by, 236–237
veterinarian role in, 4, 318–320 monitoring for, 232 Rickettsial infection, travel and, 303
Public health information (PHI), veterinarian role no indigenous cases of, 306t Rickettsia rickettsii
in, 10 pathogenesis of, 231f effects in dog, 240f
Public health professional, human-animal medicine, postexposure prophylaxis handling of, 236
key points for, 7 decision tree for, 234f Rifampin (RIF), 284–285, 284t
Public Health Service, HIV and zoonotic disease, 318 immunization and, 232–234 Rift Valley fever (RVF)
Public health system indications for, 232–234 animal exposure to, implications of, 378t
essential services of, 372–373 risk groups for, 229 in animals, 246
functions of, 373 transmission of, 230, 232f animal workers and, 345–347
lead, communication about, 389b traveling pet and, 305 clinical presentation of, 247t
pathogen/chemical warfare and, 376–377 travel risks and, 300 diagnosis of, 246
Public health veterinarian, role of, 4 treatment of effects of, 242
Pulmonary nontuberculosis mycobacteria, 287 in animals, 235 environmental risk factors for, 245–246
Pulmonary tuberculosis, 282f in human beings, 235 fatalities from, 246
Pumaala virus, 172 geographic occurrence of, 243
vectors for, 229f
Puncture-aspiration-injection-reaspiration (PAIR), hemorrhagic fever and, 246
Rabies vaccination
for echinococcosis, 156–157 hosts, reservoir species, vectors for, 244
availability of, 235t
Purple jellyfish, 88 in human beings, 246
indications for, 227
Pyrazinamide (PZA), 284–285, 284t meningoencephalitis and, 246
Pyrethroid/permethrin postexposure prophylaxis, 325
rabid animals and, 328 micrograph of, 243f
characteristics of, 73 Phlebovirus and, 243
use of travel and, 306
Radiation, animal workers and, control strategies retinitis and, 246
in animals, 75t risk groups for, 243–244
for, 346t
in human beings, 74t risk map for, 245f
Radioallergosorbent testing (RAST), 44
Pyrethrum, poisoning from, 77 transmission/life cycle of, 244–245, 244f
Radon, sentinel events from, 41t
Raisins, toxicity in animals, 53t treatment of, 246–247
Q Rash, cause and appropriate action Rimantadine, 184
QAC, 360t for human health care provider, 20t Ringworm. See Dermatophytosis
Q fever for veterinarian, 21t Risk assessment
animal exposure to, implications of, 378t Rat bite fever (Haverhill fever), 108t, 327–328 for animal workers, 351
animal research facility worker and, 363 animal research facility worker and, 363 for dog, 390f
in animals, 225 Raw food, pregnancy and, 316f River otter attack, 325, 327f
antibiotics for, 227t Raw milk Rocky Mountain spotted fever
cause and transmission of, 222 bovine tuberculosis and, 303 acquiring, routes of, 2f
clinical presentation of, 225t Coxiella burnetii and, 224 in animals, 240
Coxiella burnetii and, 223 Real-time reverse transcriptase polymerase chain antibiotics for, 241t
diagnosis of, 225 reaction (RRT-PCR), 184 clinical presentation of, 263t
environmental risk factors for, 224–225 Red poultry mite, 255 diagnosis of, 240–241
farm visits and, 302 Red tide, 92 effects of, 236
geographic occurrence of, 223 Florida, 94b environmental risk factors for, 239
hosts, reservoir species, vectors for, 224 Redwater of calves, 191 example of, 22f
in human beings, 225 Reed, Walter, 5 exanthem of, 239f
life cycle of, 224f Referral. See Medical referral geographic occurrence of, 237
phases of, 223 Rehabilitation, animal-assisted therapy and, 25 hosts, reservoir species, vectors for,
pneumonia and, 226f Relenza (zanamivir), 184 237–238
risk groups for, 223–224 Religious festival, animal contact and, 302 in human beings, 239–240
sheep and, 224f Renal disease, environmental exposures and, 60t risk groups for, 237
transmission/life cycle of, 224 Reporting, of disease/conditions, 10 transmission of, 239f
Reptile, 87f treatment of, 241
travel and, animal contact during, 302f
Giardia lamblia in, 170f Rocky Mountain wood tick (Dermacentor
treatment of, 225–226
Quadrilateral fever, 222 immunocompromised individual and, 317f andersoni)
Query fever, 222 lead toxicity in, 69–70, 69t Rocky Mountain spotted fever and,
pet trade and, 309 237–238
Salmonella prevention in, 248b view of, 237–238
R Reptile envenomation Rodent
Rabbit, tularemia in, 292, 293t cases reported, 82t plague and, 219
Rabbit fever, 289 incidence and risk groups of, 82 tularemia in, 292
Rabies types, symptoms, treatment for, 85t Rodenticide
acquiring, routes of, 2f Research. See Animal research facility worker acute toxic exposure to, 56–57
in animals, 231 Respiratory medical clearance, 349–350 animal exposure frequency, 54t
management of, 234–235 Retail sector toxic exposure of, 58t
bats and, 303 foodborne illness risk and, 332t See also Pesticide
brown bat and, 232f Retail sector, foodborne illness risk and, 334 Rodent infestation, prevention of, 172b, 218
cases reported, 230t Retinitis, Rift Valley fever and, 246 Roundworm infection, 261
cause of, 228 Retrieval, animal assistance with, 25 traveling pet and, 305
clinical presentation of, 233t Reverse transcriptase polymerase chain reaction See also Toxocara infection
diagnosis of, 235 (RT-PCR), 184 Ruminant, Escherichia coli and, 316
Index 409
S Schwabe, Dr. Calvin W., 5 Simian immunodeficiency virus

Safari, zoonotic disease and, 303 Scorpion, 82f animal research facility worker and, 362
Salmonella, 249 Scorpion sting, 82 bushmeat and, 303–304
African hedgehog and, 310 symptoms and treatment of, 85t Simple cutaneous leishmaniasis, 188
animal exposure to, implications of, 378t Scrapie, 271, 274f Skin, Sarcoptes scabiei and, 254–255
animal husbandry and, 367t clinical presentation of, 275t Skin disease, nontuberculosis mycobacteria and, 287
in animals, 251–252 diagnosis of, 275 Skin prick testing, 44, 48f
avian salpingitis and, 252f geographic occurrence of, 272 Skin rash, cause and appropriate action, 20t
box turtles and, 250f host for, 272 Skin scraping, scabies and, 258
brochure for, 249f signs and symptoms of, 273 Slow virus infection, transmissible spongiform
in chicks/ducks, 316 transmission/life cycle of, 272 encephalopathy and, 272
dermatitis and, 252f Screening/follow-up questions Slug bait, 58t
effects of, 248 for acute care visit, 13t Small intestine, cryptosporidiosis in, 140, 140f
environmental risk factors for, 251–252 for human health risk, 17t Smith, Dr. Theobald, 5
exposure to, reducing, 316 Scyphozoa, 88, 89t Smoking
family Enterobacteriaceae and, 249 Sea anemone sting, 88 carboxyhemoglobin levels from, 63
farm visits and, 302 Sea bather’s eruption (larvae), 88 cessation of, 51f
geographic occurrence of, 249 Seabird sentinel events from, 41t
in human beings, 251 contaminated fish and, 101 Snake
international animal trade and, 310 HAB-related illness in, 99t cryptosporidiosis in, 142–143
presentation/management of, 336t Seal finger, 364–365 elapid family of, 84
reporting of, 341 Sea lion venomous, families of, 82–83
reptile pet trade and, 309 HAB-related death of, 101 See also Pit viper
HAB-related illness in, 99t Snakebite
risk groups for, 249–250
Seal pox, 215 Australian pressure-immobilization technique
transmission/life cycle of, 250–251
Sea snake for, 87f
transmission prevention, 248b
toxicity of, 90–91 cases reported, 82t
in visitation dogs, 31–32
Salmonella choleraesuis, 251 types, manifestation, treatment for, 89t renal tissue after, 87f
Salmonella dublin, 251 Seasonal flu, 177 swelling from, 83f, 84f
Salmonella enteritidis, 249 Sea urchin (Echinodermata), 88–90 Sneezing, cause and appropriate action for, 20t
Salmonella gastroenteritis Selamectin Social interaction, animal-assisted activity and, 25
effects of, 251 toxicity of, 76 Social work, animal-assisted activity/therapy and, 29
use of, 75t Soft tissue disease, nontuberculosis mycobacteria
pathogenesis of, 251f
Salmonella paratyphi, 250 Select Agent and, 287
Salmonella typhi, 250 Coxiella burnetii as, 225 Solid agar media, 282
Salmonella typhimurium, 249 Rickettsia rickettsii as, 236 Somnolence, 20t
Salmonellosis Sentinel, animals as, 51–52 Sore throat, 21t
Sentinel disease, 18–23 Sound discrimination, service dogs and, 25
acquiring, routes of, 2f
Sentinel event, 1–3 Souvenir, animal hide as, 304–305
antibiotics for, 253t
from indoor air quality problems, 41t Special Pathogens Unit, 4
clinical presentation of, 252t
potential environmental, 19–23 Species diversity, habitat destruction and, 37–38
diagnosis of, 252–253 Spider
effects of, 248 Separation, from pet, impact of, 32–33
Septicemic plague population of, 81
hosts, reservoir species, vectors for, 250 types of, 81
risk groups for, 249–250 clinical presentation of, 221t
in human beings, 220 Spider bite, 81–82
treatment of symptoms and treatment of, 85t
Serpiginous rash, cause and appropriate action, 21t
in animals, 253 Spinosad
Serum, toxicology testing and, 59t
in human beings, 253 toxicity of, 76
Service animal
Sandbox, animal contact and, 304 use of, 75t
companion animals versus, 26
Sandworm, 174 Spirometry, for animal workers, 350–351
São Paolo fever, 236 health clearance examination for, 31b
Service dog Spoligotyping, 282
Sarcoptes scabiei, 254 Spongiform encephalopathy, scrapie, 274f
characteristics of, 254–255 behavioral evaluation for, 32f
use of, 25 Sporadic Creutzfeldt-Jakob disease (sCJD)
hyperkeratosis and, 256f characteristics of, 273
view of, 255f visually impaired, helping, 25f
Severe acute respiratory syndrome (SARS), 302–303 clinical presentation of, 275t
zoonotic potential of, 255t Sporotrichosis, 328
Sarcoptic itch/mange, 254 first case of, 345–347
Shared risk approach, 106 Spurred/leopard tortoise, heartwater and, 310
in guinea pig, 258f Staphylococcal cassette chromosome mec
Sheep
in horses, 258 (SCCmec), types of, 210
brucellosis in, 126
SARS-like coronavirus, 303 Staphylococcal food poisoning, 335–338
Saxitoxin, 95t Chlamydiae infection in, 137t
Chlamydophila abortus and, 136 Staphylococcus aureus
HAB-related illness and, 97t antibiotic resistance of, 210
Scabies Escherichia coli infection in, 166
Q fever and, 224f effects of, 209–210
in animals, 257–258 food poisoning and, 335–338
clinical presentation of, 257t tularemia in, 292, 293t
viruses associated with, 367t geographic occurrence of, 210–211
diagnosis of, 258–259 presentation/management of, 336t
in dog, 258f See also Orf virus
Shiga toxin, 164 scabies and, 256, 257
environmental risk factors for, 256–257 See also Methicillin-resistant Staphylococcus
Shigella dysenteriae, 164
geographic occurrence of, 255 aureus infection
animal exposure to, implications of, 378t
in human beings, 257 Staphylococcus pseudintermedius, 211
reporting of, 341
risk groups for, 255–256 State public health veterinarian, role of, 4
Sick animal visit
Sarcoptes scabiei and, 254 Stinging nettle, 88
animal health risk assessment form, 16f
transmission/life cycle of, 256, 256f Stingray envenomation, 89t
health assessment during, 15–17
treatment of, 259t St. Louis encephalitis (SLE), 294
human-animal disease risk survey for, 17f
in animals, 260 Streptobacillus moniliformis, 327
Silo filler’s disease, 333, 348–349
in human beings, 259–260 Streptococcosis, 108t
Simian foamy virus infection, 300
wet mount prep of, 259f Streptococcus, scabies and, 256, 257
animal research facility worker and, 362
Scalp ringworm, 387f Streptococcus suis, animal husbandry and, 367t
410 Index
Streptococcus zooepidemicus, 2f Toxic exposure, 50–104 outbreak of, 271

Streptomycin, 285 acute, 52–57 treatment of, 275–276
for tularemia, 293t identification of, 57 Transparency, 10–11
Stress. See Psychosocial stressor metabolism and, 52 Trauma, cause and appropriate action
Stuttgart disease, 191 prevention of, 51 for human health care provider, 20t
Subacute spongiform encephalopathy, 271 See also Acute toxic exposure; Chronic toxic for veterinarian, 21t
Sudden death. See Death exposure Travel
Swamp fever, 191 Toxicology testing, samples need for, 59t animal contact during, 299
Swine, 181 Toxocara beaches and sandboxes, 304
Bordetella bronchiseptica and, 316 sandboxes and, 304 bushmeat consumption and, 303–304
tularemia in, 293t in visitation dogs, 31–32 farm visits and, 302
viruses associated with, 367t Toxocara canis festivals and, 302
Swine flu, 177 characteristics of, 261–262 injuries and, 300–302
Swineherd fever, 191 clinical presentation of, 263t live animal market and, 302–303
Swine influenza A H1N1 virus, 178 life cycle of, 262f safaris and wilderness, 303
effects of, 181 ocular larva migrans and, 263 souvenirs and, 304–305
morbidity from, 182 ova from, 264f assessment for
signs of, 182 signs of, 263 posttravel, 305, 305b, 307b
Symptomatic cyst disease, 156 size of, 261f pretravel, 300, 307b
Toxocara cati CDC regulations for, 306
T characteristics of, 261–262 foodborne illness reporting and, 341
Taenia saginata, 338 clinical presentation of, 263t illness after, 307
Taeniasis life cycle of, 262f with pet
life cycle of, 339f Toxocara infection, 261 documentation/regulations for, 305–307
overview of, 338 diagnosis of, 263–264 infectious disease and, 305
presentation/management of, 336t geographic occurrence of, 262 logistics for, 305
Taenia solium, 338 in human beings, 263 reasons for, 305
Tamiflu (oseltamivir), 184 risk groups for, 262 risks associated with, 305
Tapeworm. See Dipylidiasis traveling pet and, 305 zoonotic disease, reduction of, 302–303
See also Echinococcosis treatment of Travel medicine
Tarantula, 81 in animals, 264 elements of, 300t
Teflon fumes in human beings, 264 infectious disease and, 299–300
acute toxic exposure to, 57 Toxocara infestation, 261 Tremorgenic mycotoxins, toxicity in animals, 53t
toxic exposure of, 58t Toxocariasis Trichinella, 338
Tenosynovitis, of hand, 287 clinical presentation of, 263t animal husbandry and, 367t
Tetanus vaccination, 300–302, 325–327 treatment of, 264t presentation/management of, 336t
indications for, 327t Toxoplasma, 336t Trichinella spiralis, 341f
Tetracycline Toxoplasma abscess, MRI image of, 268f Trichinellosis, 338–339
for Chlamydophila psittaci infection, 138, 138t Toxoplasma gondii Trichophyton, 144
seal finger and, 364–365 infection, source of, 315 Trichophyton, Tinea capitis and, 146
for tularemia, 293t photomicrograph of, 269f Trichophyton mentagrophytes
Theobromine, toxicity in animals, 53t stages of, 266 in culture, 147f
Therapeutic horsemanship, 26 Toxoplasma gondii–induced abortion, 269f geographic occurrence of, 144
Therapy dog, behavioral evaluation for, 32f Toxoplasmosis host for, 144–145
Thermophilic bacteria, 45 in animals, 268–269 Trichophyton tonsurans, 144
Thimble jellyfish, 88 clinical presentation of, 270t Trichophyton verrucosum, 144
Thirst, freedom from, 11b congenital, with hydrocephalus, 269f Trichophytosis, 144
Ticarcillin, bite infection, treatment for, 329t diagnosis of Trophozoites, 168f, 169f
Tick in animals, 269 Tropical canine pancytopenia, 157
Borrelia burgdorferi and, 198 in human beings, 269 Trypanosomiasis, 303
Coxiella burnetii and, 224 effects of, 265 Tuberculin skin test
Lyme disease and, 195–196 environmental risk factors for, 267–268 in cattle, 284
pest management for, 158b geographic occurrence of, 266 in human beings, 283–284
Rickettsia rickettsii and, 238 histopathology of, 266f indications for, 283
Rocky Mountain spotted fever and, 237–238 HIV-infected person and, 319t positivity, criteria for, 283t
sizes of, 199f hosts, reservoir species, vectors for, 266 technique for, 283f
See also Anaplasmosis; Ehrlichiosis; Tularemia in human beings, 268 Tuberculoma, MRI image of, 281f
Tickborne fever/disease, 157, 236 lipemia retinalis and, 269f Tuberculosis
shared environment exposure to, 389 risk groups for, 266 aerosol transmission of, 279b
Tinea capitis, Microsporum canis causing, 146f sandboxes and, 304 animal research facility worker and, 363
Tinea corporis, 146 Toxoplasma gondii and, 266 in animals, 281–282
Tinea infection. See Dermatophytosis transmission/life cycle of, 266–267, 267f in companion animal, 285–286
Tinea pedis, 146 treatment of, 269–271, 270t diagnosis of
Toad Tracker dog disease, 157 active disease, 282–283
Bufo marinus (cane/marine toad), 88f Training, for animal workers, 351 latent infection, 283–284
dog poisoning by, 88 Transmissible mink encephalopathy, 271 environmental risk factors for, 279
Toad intoxication, 84–88 clinical presentation of, 275t HIV and, 279–280
symptoms and treatment of, 85t geographic occurrence of, 272 hosts, reservoir species, vectors for, 278
Toadstool signs and symptoms of, 273–274 in human beings, 279–281
acute toxic exposure to, 56 transmission/life cycle of, 272 phases of infection, 280f
toxic exposure of, 58t Transmissible spongiform encephalopathy, 271 prevalence of, 276
Tobacco smoke in animals, 273–274 pulmonary, radiograph of, 282f
elimination of, 51f cellular prion protein (PrPc) and, 272 radiograph of, 282–283, 282f
sentinel events from, 41t clinical presentation of, 275t risk factors for, 280b
Tobramycin, for tularemia, 293t risk groups for, 278, 279b
environmental risk factors for, 272–273
Total airborne hydrocarbon, 41 of spine, 281f
Toxascaris leonina, 261–262 transmission of, 278
Index 411
treatment of cat-scratch disease and, 120 Walking dandruff mite, 255

in animals, 285–286 CDC, role at, 4 Wapiti, chronic wasting disease in, 274f
drug regimen for, 284t disease reporting/notification by, 10 Warfarin
in human beings, 284–285 elephant examination by, 365f acute toxic exposure to, 56–57
Tuberculosis culture, methods of, 282 home/worksite visits by, 3 toxic exposure of, 58t
Tufts Animal Care and Condition Scale, 33 human-animal medicine, key points for, 7 Water
Tularemia, 289 human health, role in, 3–4 cyanobacteria toxins in, 101
acquiring, routes of, 2f malpractice liability for, 8–9 toxicology testing and, 59t
animal exposure to, implications of, 378t occupational health/safety role of, 343 Water damage, mold and, 41
in animals, 292 occupational health team role, 344–345 Weakness, cause and appropriate action
clinical presentation of, 293t practice, scope of, 8 for human health care provider, 20t
cutaneous lesion and, 292f public health role of, 318–320 for veterinarian, 21t
diagnosis of state public health, role of, 4 Weight loss, cause and appropriate action
in animals, 292 at zoo, occupational illness/injury, 364 for human health care provider, 20t
in human beings, 292 Veterinarian oath, 8b for veterinarian, 21t
environmental risk factors for, 291, 291f Veterinary-human medical partnerships Weil’s disease, 191
geographic occurrence of, 290 cardiac surgical procedure for dog, 390–391 Western equine encephalitis (WEE), 294
hosts, reservoir species, vectors for, 290–291 echocardiography for primate, 391–392 West Nile virus (WNV)
in human beings, 291–292, 293t examples of, 390 in animals, 296–298
postexposure prophylaxis, 293t See also Human-animal medicine clinical presentation of, 297t
risk groups for, 290 Veterinary medicine diagnosis of, 298
transmission/life cycle of, 291 practice of, definition of, 8b discovery of, 294
treatment of, 292, 293t training/practice statistics for, 3–4, 3t environmental risk factors for, 296
wildlife pets and, 311 Veterinary personnel Flavivirus and, 295–296
Tunga penetrans (Jiggers), 304 allergens and, 354 geographic occurrence of, 296
Tungiasis, 304 anesthetic agent and, 359 hosts, reservoir species, vectors for, 296
Typhoidal tularemia, 292 chemical hazards and, 358–359 in human beings, 296, 297t
treatment of, 293t medical surveillance for, 359–362 microscopy of, 295f
occupational health/safety of, 353–362 outbreaks of, 294
occupational medicine services for, 359–362 risk groups for, 296
U
physical hazards and, 359 transmission/life cycle of, 296, 296f
Ulceroglandular tularemia, 292
Undulant fever, 123 preplacement screening of, 359 treatment of, 298
Unilocular hydatid disease, 153 psychosocial stressors and, 359 Whale, HAB-related death of, 101
United Nations Children’s Emergency Fund zoonotic disease and, 354–358 Wheezing, 20t
(UNICEF), 5 Veterinary practice White-footed mouse (Peromyscus leucopus), 198, 199f
United Nations System Influenza Coordination, 5 behavioral services offered by, 30t White-tailed deer (Odocoileus virginanus), 198
Upper airway disorder, 44 chemical hazards in, 358–359 Whole blood, toxicology testing and, 59t
Upper respiratory disease, Chlamydophila psittaci disinfectant/cleaners used in, 360t Widow spider bite
and, 136 infection control plan for veterinary practice, effects of, See also Black widow spider, 81–82
Upper respiratory signs, cause and appropriate action model for, 355f Wilderness, zoonotic disease and, 303
for human health care provider, 20t inspection and regulation of, 379t Wildlife
for veterinarian, 21t Veterinary Practice Act, 8 cyanobacteria toxins and, 101–102
Urine, toxicology testing and, 59t Veterinary Standard Precautions for Zoonotic Disease infections linked to, 310–311
USDA, animal disease/health and, 341 Prevention in Veterinary Personnel, 354 pet trade and, 309
“Us versus them” approach, 105–106 Vibrio vulnificus toxicant exposure and, 52
Uta, 186 wound infection and, 364 tuberculosis in, 276
Uveitis, toxoplasmosis and, 268 zoo/aquarium worker and, 364 Wildlife pet, 1
Viral hepatitis malpractice liability and, 9
animal research facility worker and, 363 Wildlife rehabilitator
V hazards with, 368–369
Vaccination travel and, 303
Virchow, Dr. Rudolf, 5 occupational health/safety of, 369
animal research facility worker and, 364 Wood dust, 45
animal shelter guidelines for, 381b Visceral larva migrans
clinical presentation of, 263t Wood tick
animal workers and, 351 Rocky Mountain spotted fever and, 237–238
for farm animal worker, 368 in human beings, 261, 263
treatment of, 264t view of, 237–238
live vaccine, as hazard, 346t Workers’ compensation liability, 9
pet store worker and, 366 Visceral leishmaniasis, 186
cause of, 187 Work-related asthma
tetanus, 300–302, 325–327 prevention of, 358b
See also Rabies vaccination diagnosis of, 190–191
environmental risk factors for, 187–188 symptoms of, 353b
Variant Creutzfeldt-Jakob disease (vCJD), 271 Work-related injury/illness, liability and, 9
bovine spongiform encephalopathy and, 273 geographic occurrence of, 187
hosts, reservoir species, vectors for, 187 World Bank, 5
clinical presentation of, 275t World Health Organization (WHO), 5
diagnosis of, 274 in human beings, 188–189
World Organization for Animal Health, 5
geographic occurrence of, 272 transmission/life cycle of, 187
disease outbreak reporting and, 341
photomicrograph of, 275f treatment of, 190t
disease reporting to, 373, 375b
risk groups for, 272 Vomiting, cause and appropriate action for
Wound
transmission/life cycle of, 272 for human health care provider, 20t
animal bite, infection risk, 324t
Vascular peliosis, 121f for veterinarian, 21t
care for, 324
Vector-borne disease, traveling pet and, 305 Vomitoxin
closure of, 325
Ventilation, inadequate, 39–40 effects of, 339
culture of, 324
sentinel events from, 41t presentation/management of, 336t
nonhealing, cause and appropriate action, 20t
Verocytotoxin, 164 tetanus prophylaxis, indication for, 327t
Vertebral tuberculosis, 281f W Vibrio vulnificus and, 364
Vesicular stomach virus, animal husbandry and, 367t Walking
Veterinarian dog-walking program, 26–27
baseline human health history for, 13–15 pedestrian paths for, 38f Y
Brucella inoculation of, 124 Yeast dough, toxicity in animals, 53t
pet ownership and, 28
Yellow fever
412 Index
Yellow fever (Continued) erysipeloid and, 364 infectious disease and, 1

transmission of, 5 occupational health/safety of, 364 malpractice liability and, 8–9
travel and, 303 occupational medicine services for, 365–366 in pet store setting, 366
Yellow jacket, 80f injury, exposure, illness management for, 366 reverse, 19
Yersinia enterocolitica medical surveillance for, 366 routes of, 2f
overview of, 338 preplacement screening of, 365–366 as sentinel event, 1–3
presentation/management of, 336t physical hazards and, 365 training/practice statistics for, 3
Yersinia pestis, 218 psychosocial stressors and, 365 veterinary personnel and, 354–358
as biological warfare, 219 veterinarian, occupational illness/injury of, 364 zoo/aquarium worker and, 364
Yersiniosis, 108t, 338 zoonotic disease and, 364–365 See also specific types of
Zoonotic disease, 105–298 See also Travel
Z animal health and, 1–3 Zoonotic pathogen
Zanamivir (Relenza), 184, 185t animal research facility worker and, 362–363 animal workers and, 345–347
Zinc sulfur concentration test (ZCST), 170 control of, 11 control strategies for, 346t
Zinkernagel, Rolf, 5 farm animal worker and, 367 exposure to, routes of, 347
Zoo/aquarium worker HIV and, 318 Zoophilic dermatophyte
allergens and, 364 in human, 19 classification of, 145t
chemical hazards and, 365 immunocompromised patient and, 315–318 transmission of, 144
CP 6-1 n Mold on drywall under leaky sink. (From Environmental
Protection Agency, Washington, DC. Courtesy John Martyny.) CP 8-2 n Oleander (Nerium oleander). (From Plumlee K: Clinical vet-
erinary toxicology, St Louis, 2004, Mosby Elsevier. Courtesy K.H. Plumlee.)
CP 8-1 n Malignant mesothelioma. Note the thick, firm, white, pleu-

ral tumor that ensheaths this bisected lung. (From Kumar V, Abbas AK,
Fausto N et al: Robbins basic pathology, ed 8, Philadelphia, 2007, Saunders
Elsevier.)
CP 8-3 n Hemorrhage, anticoagulant (warfarin-containing) rodenti-
cide toxicosis, skin and subcutis, medial aspect of the right hindleg, dog.
There is a large area of extensive hemorrhage in the subcutis. This lesion
was attributed to decreased production of coagulation factors II, VII, IX,
and X and proteins C and S resulting from a deficiency of vitamin K induced
by warfarin. (From McGavin MD, Zachary JF: Pathologic basis of veterinary
disease, ed 4, St Louis, 2007, Mosby Elsevier. Courtesy D.A. Mosier, College
of Veterinary Medicine, Kansas State University.)
CP 8-4 n Carbon monoxide poisoning, brain, human. The blood in the
brain is cherry red from the carboxyhemoglobin formed by the inhalation
of carbon monoxide in exhaust gases. (From McGavin MD, Zachary JF:
Pathologic basis of veterinary disease, ed 4, St Louis, 2007, Mosby Elsevier.
Courtesy J.C. Parker, School of Medicine, University of Louisville, Ky.)
CP 8-6 n Worker using a power sander with a high-efficiency particu-

late air (HEPA) filter exhaust system that collects paint particulates, demon-
strating an exterior renovation method used on residences where lead-based
paint was present. This was a low-exposure method. (From Centers for
Disease Control and Prevention Public Health Image Library, Atlanta, Ga.)
CP 8-7 n Basophilic stippling. Presence of irregular basophilic granules

CP 8-5 n Worker removing a wood baseboard covered with lead-based either fine or coarse; commonly seen in increased red blood cell production.
paint, demonstrating renovation methods typically used on residences Coarse stippling is usually seen in lead poisoning (×1000). (From McPherson
where lead-based paint was present. (From Centers for Disease Control and RA, Pincus MR: Henry’s clinical diagnosis and management by laboratory
Prevention Public Health Image Library, Atlanta, Ga.) methods, ed 21, Edinburgh, 2006, Saunders Elsevier.)
CP 8-11 n Scorpions fluoresce in ultraviolet light. (From Auerbach PS:
Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.)
CP 8-8 n Fire ant lesions. (From Auerbach PS: Wilderness medicine,

ed 5, Philadelphia, 2007, Mosby Elsevier.)
CP 8-12 n A case of severe envenomation by a western diamondback

rattlesnake (Crotalus atrox) 4 days after the bite. Note the soft tissue swell-
ing and hemorrhagic and serum-filled vesicles. (From Townsend CM,
Beauchamp RD, Evers BM: Sabiston textbook of surgery, ed 18, Philadelphia,
2008, Saunders Elsevier. Courtesy David Hardy.)
CP 8-9 n Lepidopterism. Toxic irritative caterpillar dermatitis. (From

Spiegel W, Maier H, Maier M: A non-infectious airborne disease, Lancet
363:1438, 2004.)
CP 8-13 n Melting corneal ulcer secondary to a bite from a copperhead

CP 8-10 n Caterpillar of the io moth, Automeris io. Widespread in the snake to the upper eyelid, which penetrated, but did not perforate, the cor-
eastern United States, this species can inflict a painful sting. (From Auerbach nea. (From Dziezyc J, Millichamp NJ: Color atlas of canine and feline oph-
PS: Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.) thalmology, St Louis, 2005, Saunders Elsevier.)
CP 8-16 n Skin destruction 3 weeks after an untreated box jellyfish
CP 8-14 n A Texas coral snake, Micrurus tener tener, in Galveston
(Chironex fleckeri) envenomation. (From Auerbach PS: Wilderness medi-
County, Texas. The eastern coral snake, Micrurus fulvius fulvius, is similar
cine, ed 5, Philadelphia, 2007, Mosby Elsevier. Courtesy John Williamson.)
in appearance and differs primarily in the distribution of black mottling
within the red segments. In contrast to the vipers, the fangs of coral snakes
and other elapids are short, hollow structures that are permanently fixed
in position on the anterior maxillary bones (i.e., proteroglyphous denti-
tion). Because of their small size and short fangs, the North American coral
snakes pose little risk to individuals wearing appropriate clothing and foot-
wear. Most human envenomations occur on the hands after a coral snake
is erroneously identified as a harmless king snake and intentionally hand-
led. (From Centers for Disease Control and Prevention Public Health Image
CP 8-15 n Many marine invertebrates contain venoms and poisons.

Venoms in corals, anemones, and jellyfish are contained within special cel-
lular stinging organelles called nematocysts. Nematocysts contain a stinging
thread that penetrates the skin and injects venom. Many of these inver-
tebrates are visually attractive, and children are particularly liable to be
stung. (From Page C, Hoffman B, Curtis M et al: Integrated pharmacology,
ed 3, Edinburgh, 2006, Mosby Elsevier. Courtesy Ron Kertesz, permission of
the Vancouver Aquarium.)
CP 8-17 n Seabather’s eruption on the neck of a diver in Cozumel,

Mexico. (From Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007,
Mosby Elsevier. Courtesy Paul Auerbach.)
CP 8-19 n Vesiculation of the hand 48 hours after the sting of a lion-
CP 8-18 n Lionfish from the Red Sea. (From Auerbach PS: Wilderness
fish. (From Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007,
medicine, ed 5, Philadelphia, 2007, Mosby Elsevier. Courtesy Paul
Mosby Elsevier. Courtesy Howard McKinney.)
Auerbach.)
CP 8-20 n Sampling cyanobacteria. (Courtesy Andy Reich, Aquatic

Toxins Coordinator, Florida Department of Health.)
CP 8-21 n Approximate areas of the U.S. coast affected by various HAB poisoning syndromes and other
effects. Note that cyanoHAB dots portray geographically general representations of outbreaks and may represent
events occurring in more than one water body within a state. Note also that not all HABs are depicted in this gen-
eralized view of the United States. (From U.S. National Office for Harmful Algal Blooms: Distribution of HABs in
the U.S. http://www.whoi.edu/redtide/page.do?pid=14898.)
CP 8-22 n Blue-green algae. Facial and lip swelling after accidental inges-
tion of contaminated water. (From Auerbach PS: Wilderness medicine, ed 5,
Philadelphia, 2007, Mosby Elsevier. Courtesy Edgar Maeyens, Jr.)
CP 9-1 n Gray flying fox (Pteropus griseus), East Timor. Host of Nipah
virus. (Courtesy Andrew C. Breed. From Fowler ME, Miller RE: Zoo and wild
animal medicine: current therapy, ed 6, St Louis, 2008, Saunders Elsevier.)
A B
C D
E
CP 9-2 n Typical clinical findings of Bartonella henselae infection (cat-scratch disease). Simple papule at the
scratch site on the leg (A) of a young boy and the face of a young girl (B). Papular lesion on the arm and axil-
lary lymphadenopathy in an adolescent (C). Papular lesion and fluctuant, enlarged lymph nodes in the supra-
clavicular and neck areas of an adolescent girl who frequently cuddled her kitten over her chest and shoulder
(D). Granulomatous conjunctivitis and preauricular lymphadenopathy in a 12-year-old boy (E). (From Long SS,
Pickering LK, Porber CG: Principles and practice of pediatric infectious disease, ed 3, Philadelphia, 2009, Saunders
Elsevier.)
CP 9-5 n Epididymitis (Brucella ovis), tunic adhesions, epididymis, ram.
Note the dramatic enlargement of the epididymis and the adhesion of the
parietal tunica vaginalis to the visceral tunica vaginalis around the affected
epididymis. (From McGavin MD: Pathologic basis of veterinary disease,
ed 4, St Louis, 2007, Mosby Elsevier. Courtesy K. McEntee, Reproductive
Pathology Collection, University of Illinois; and J. King, College of Veterinary
Medicine, Cornell University.)
CP 9-3 n Cutaneous bacillary angiomatosis lesions on the elbow of a

patient with AIDS. (From Mandell GE, Bennett JE, Dolin R: Principles and
practice of infectious diseases, ed 6, Philadelphia, 2005, Churchill Livingstone
Elsevier.)
CP 9-6 n Anterior uveitis in a 3-year-old female German Shepherd

CP 9-4 n Liver from a dog with peliosis hepatis associated with B. hense- diagnosed with Brucella canis. Conjunctival and ciliary injection, corneal
lae infection. (From Greene CE: Infectious diseases of the dog and cat, ed 3, edema, and iridal congestion and petechiae are present. (From Maggs DJ,
St Louis, 2006, Saunders Elsevier. Courtesy Tim Fan, University of Illinois, Miller PE, Ofri R (eds): Slatter’s fundamentals of veterinary ophthalmology,
Urbana.) ed 4, St Louis, 2008, Saunders Elsevier.)
CP 9-7 n Milk ring test. Stained Brucella remains suspended in the milk
in a negative test but rises with the cream in a positive reaction (second
tube). (From Tizard IR: Veterinary immunology: an introduction, ed 8, St
Louis, 2009, Saunders Elsevier. Courtesy John Huff.) CP 9-9 n Ovine abortion resulting from Campylobacter fetus spp.
fetus. (From Songer JG, Post KW: Veterinary microbiology: bacterial and
fungal agents of animal disease, St Louis, 2005, Saunders Elsevier. Courtesy
J. Glenn Songer.)
CP 9-8 n Foodborne transmission probably accounts for the majority of diarrheal illness in travelers and
expatriates. The high rates of shigellosis and campylobacteriosis compared with cholera among travelers in
cholera-endemic areas suggest that they may be better able to avoid exposure to contaminated water than to
contaminated food. (From Cohen J, Powderly G: Infectious diseases, ed 2, Philadelphia, 2004, Mosby Elsevier.)
CP 9-12 n This micrograph of a direct fecal smear is stained to detect
Cryptosporidium spp., an intracellular protozoan parasite. Using a modified
CP 9-10 n To many, the Amazon parrot is considered the typi- cold Kinyoun acid-fast staining technique, and under an oil immersion lens,
cal companion psittacine. (From Bewig M: Manual of exotic pet practice, the Cryptosporidium oocysts—which are acid-fast—stain red, and the yeast
St Louis, 2009, Saunders Elsevier.) cells, which are not acid-fast, stain green. (From CDC/Journal of Infectious
Diseases, Vol. 137, no. 5, pp 824-828, May 1983, and Pearl Ma, Director of
Microbiology, St. Vincent’s Hospital, New York.)
CP 9-11 n This snake had severe gastritis develop from a cryptospo-

ridial infection. Infected animals typically vomit their meals 2 to 3 days after
ingestion. An animal may commonly keep a meal down, then vomit again
on the next feeding, confusing the keeper into thinking that the problem
has self-corrected. (From Mader DR: Reptile medicine and surgery, ed 2, St CP 9-13 n Tinea corporis due to T. mentagrophytes. (From Cohen J,
Louis, 2006, Saunders Elsevier.) Powderly G: Infectious diseases, ed 2, Philadelphia, 2004, Mosby Elsevier.)
CP 9-15 n Dermatophytosis. Crusting alopecic dermatitis typical of
dermatophytosis on the face of a cat. (From Medleau L, Hnilica KA: Small
animal dermatology: a color atlas and therapeutic guide, ed 2, St Louis, 2006,
Saunders Elsevier.)
CP 9-14 n Dermatophytosis. The severe crusting on the entire head of

this Jack Russell Terrier was caused by a Trichophyton infection. The furun-
culosis resulted in severe cellulitis with subsequent scarring. (From Medleau
L, Hnilica KA: Small animal dermatology: a color atlas and therapeutic guide,
ed 2, St Louis, 2006, Saunders Elsevier. Courtesy J. MacDonald.)
A B
CP 9-16 n Dermatophytosis in a cow, luminal folliculitis, skin, haired. A, Dermatophytosis, presumed to
be Trichophyton verrucosum. Note irregularly ovoid, hairless areas with mild surface crusting. B, Dermatophyte
infection presumed to be Microsporum canis involving hair follicle, dog. Note spores (arrow) along periphery
and hyphae (arrowhead) within hair shaft. The hair loss is due to breakage of hair shafts and mural and lumi-
nal folliculitis, which interfere with production of new hairs and cause increased loss of old hairs. Gomori’s
methenamine silver nitrate H&E counterstain. (From McGavin MD, Zachary JF: Pathologic basis of veterinary
disease, ed 4, St Louis, 2007, Mosby Elsevier. A, Courtesy H. Denny Liggitt, University of Washington. B, Courtesy
Ann M. Hargis, Dermato Diagnostics.)
CP 9-17 n Dermatophytosis. A, Tufted papules and annular areas of crust and alopecia on brisket. B, Annular
areas of alopecia, scaling, and erythema on the face. C, Annular areas of alopecia, scale, and crust near base of ear.
D, Alopecia and scaling in the girth area. E, Alopecia, scaling, and crusting on leg. F, Crusting and alopecia on
caudal pastern. (From Scott DW, Miller WH: Equine dermatology, Philadelphia, 2003, Saunders Elsevier. Courtesy
W. McMullen.)
CP 9-19 n Dermatophytosis. Close-up of a dermatophyte test medium
fungal culture demonstrating the typical white colony growth and red color
CP 9-18 n A guinea pig with a crusted area on the dorsal pinna con- change. This is suggestive of dermatophytosis, but microscopic identifica-
sistent with dermatophytosis. A Trichophyton organism was cultured tion should be performed to identify Microsporum canis. (From Medleau L,
from the site. (From Mitchell M, Tully TN: Manual of exotic pet practice, Hnilica KA: Small animal dermatology: a color atlas and therapeutic guide, ed
St Louis, 2008, Saunders Elsevier.) 2, St Louis, 2006, Saunders Elsevier.)
CP 9-20 n Slaughtering sheep near dogs. (From Craig PS, McManus DP, Lightowlers MW, et al: Prevention
and control of cystic echinococcosis, Lancet Infect Dis 7(6):385-94, 2007.)
APPROXIMATE DISTRIBUTION IN THE UNITED STATES OF VECTOR TICK
SPECIES FOR HUMAN MONOCYTOTROPIC EHRLICHIOSIS,
HUMAN GRANULOCYTOTROPIC ANAPLASMOSIS AND LYME BORRELIOSIS
Ixodes scapularis distribution

Ixodes pacificus distribution
Amblyomma americanum distribution
Overlapping distribution (I. scapularis and A. americanum)
CP 9-21 n Hydatidosis (echinococcosis), lung, sheep. A large hydatid
cyst is present in the pulmonary parenchyma. Inset, Hydatid cyst, cut-open
section. The cyst contains fluid and larvae and is often enclosed by a fibrous CP 9-22 n Approximate distribution in the United States of vector tick
capsule. (From McGavin MD, Zachary JF: Pathologic basis of veterinary species for human monocytotropic ehrlichiosis, human granulocytotropic
disease, ed 4, St Louis, 2007, Mosby Elsevier. Courtesy Manuel Quezada, anaplasmosis, and Lyme borreliosis. (From Chapman AS et al: MMWR
Universidad de Concepción, Chile.) Recomm Rep 55:1-27, 2006.)
CP 9-23 n Tick vectors of agents of human rickettsial diseases. An unengaged nymph (A), engorged nymph
(B), and adult female (C) of Ixodes scapularis (deer tick), the vector of Anaplasma phagocytophilum, the cause
of human granulocytic anaplasmosis. An adult female (D) of Amblyomma americanum (lone star tick), the vector
of Ehrlichia chaffeensis and Ehrlichia ewingii, the causes of human monocytic ehrlichiosis and ewingii ehrlichiosis,
respectively. An adult female (E) of Dermacentor variabilis (American dog tick), the vector of Rickettsia rickettsii,
the cause of Rocky Mountain spotted fever. (From Siberry GK, Dumler JS: Spotted fever group Rickettsioses.
In Kliegman RM, Behrman RE, Jenson HB et al (eds): Nelson textbook of pediatrics, ed 18, Philadelphia, 2007,
Saunders Elsevier.)
CP 9-26 n Canine ehrlichiosis. Petechiae and ecchymotic hemorrhages
caused by thrombocytopenia resulting from the infection. (From Medleau
CP 9-24 n Flat retinal detachment in a dog with E. canis infection. L, Hnilica KA: Small animal dermatology: a color atlas and therapeutic guide,
Note the shadowing of retinal vessels. Also note the absence of retinal ed 2, St Louis, 2006, Saunders Elsevier.)
hemorrhage, which often accompanies the thrombocytopenia that occurs
with this disease. (From Dziezyc J, Millichamp NJ: Color atlas of canine and
feline ophthalmology, St Louis, 2005, Saunders Elsevier.)
CP 9-27 n Epistaxis in canine ehrlichiosis. (From Songer JG, Post KW:

Veterinary microbiology: bacterial and fungal agents of animal disease, St
CP 9-25 n Canine ehrlichiosis. A focal erythematous, alopecic lesion Louis, 2005, Saunders Elsevier. Courtesy Raymond E. Reed.)
with superficial erosions in a dog with ehrlichiosis. (From Medleau L,
Hnilica KA: Small animal dermatology: a color atlas and therapeutic guide, ed
2, St Louis, 2006, Saunders Elsevier.)
CP 9-29 n Colonoscopic appearance of the sigmoid colon in a patient
with enterohemorrhagic Escherichia coli infection. The mucosa is edematous
and violaceous, with diffuse subepithelial hemorrhage. (From Feldman M,
et al (eds): Sleisenger and Fordtran’s gastrointestinal and liver disease, vol 1, ed
CP 9-28 n Peripheral blood smear (buffy coat preparation) show- 8, Philadelphia, 2006, Saunders Elsevier.)
ing intracellular inclusions (arrows) in mononuclear cells of a patient with
ehrlichiosis. (Wright stain, original magnification, ×400.) (From Mandell
GL, Bennett JE, Dolin R: Principles and practice of infectious diseases, ed 6,
Philadelphia, 2005, Churchill Livingstone Elsevier.)
CP 9-30 n Field biologists using protective equipment for hantavirus infection while examining wild
mice. (From Centers for Disease Control and Prevention, Atlanta, Ga.)
CP 9-31 n Deer mouse (Peromyscus maniculatus), the principal reser-
voir species for hantavirus in the United States. (From Centers for Disease
Control and Prevention, Atlanta, Ga.)
CP 9-34 n Leishmaniasis. Microscopic image of the protozoal amastig-
otes as viewed with a ×100 (oil) objective. (From Medleau L, Hnilica KA:
Small animal dermatology: a color atlas and therapeutic guide, ed 2, St Louis,
2006, Saunders Elsevier.)
CP 9-32 n Third-stage larva of Ancylostoma caninum. (From Long SS,

Pickering LK, Prober CG (eds): Principles and practice of pediatric infectious
diseases, ed 2, Philadelphia, 2003, Elsevier. Courtesy E. Gravé.)
CP 9-35 n Skin ulcer due to leishmaniasis on the hand of a Central

American adult. (From Centers for Disease Control and Prevention Public
Health Image Library, Atlanta, Ga. Courtesy D.S. Martin.)
CP 9-33 n Cutaneous larva migrans. (From Goldman L, Ausiello

DA (eds): Cecil textbook of medicine, ed 23, Philadelphia, 2008, Saunders
Elsevier.)
CP 9-38 n Cutaneous ulcer in cat with leishmaniasis. (From Greene
CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders
Elsevier. Courtesy Maria Grazia Pennisi, University of Messina, Italy.)
CP 9-36 n Mucocutaneous leishmaniasis. (From Cohen J, Powderly

WG: Infectious diseases, ed 2, Edinburgh, 2003, Elsevier.)
CP 9-39 n Subconjunctival hemorrhages and jaundice in leptospiro-

sis. Asymptomatic or atypical infection probably occurs in 90% of cases. In
some tropical areas, leptospirosis may account for up to 15% of all patients
with undiagnosed pyrexia. Although this form can be mild, the infection
may develop into a generalized septic form with confusion within 1 to 2
weeks. This is characterized by fever, myalgia, and often subconjuncti-
val hemorrhages. The patient illustrated was in the second week after the
onset of symptoms. The most dangerous form (Weil’s disease) may be quite
severe and can involve several organs, with jaundice, renal failure, hemor-
rhagia, vascular collapse, and obtundation. (From Cohen J, Powderly WG:
Infectious diseases, ed 2, Edinburgh, 2004, Mosby Elsevier.)
CP 9-37 n Epistaxis in a Saint Bernard with leishmaniasis and no der-

mal lesions. (From Greene CE: Infectious diseases of the dog and cat, ed 3, St
Louis, 2006, Saunders Elsevier.)
CP 9-42 n Preretinal petechiae on the fundus of a 7-year-old blood-
hound diagnosed with canine Lyme disease. (From Maggs D, Miller P, Ofri
R: Slatter’s fundamentals of veterinary ophthalmology, ed 4, St Louis, 2008,
Saunders Elsevier.)
CP 9-40 n Pathognomonic erythematous rash of Lyme disease in the
pattern of a bull’s-eye, which manifested at the site of a tick bite on this
Maryland woman’s posterior right upper arm. (From Centers for Disease
Control and Prevention Public Health Image Library, Atlanta, Ga. Courtesy
James Gathany.)
CP 9-43 n Posterior synechiae, iris bombé, and cataract associated with

a high enzyme-linked immunosorbent assay titer to Borrelia burgdorferi
CP 9-41 n Rash on patient’s back—presumptive southern tick-asso- in a mixed-breed dog. (The linear opacity on the cornea is a hair.) (From
ciated rash illness, a differential for Lyme disease. (From Auerbach PS: Dziezyc J, Millichamp NJ: Color atlas of canine and feline ophthalmology, St
Wilderness medicine, ed 5, Philadelphia, 2007, Mosby Elsevier.) Louis, 2005, Saunders Elsevier.)
CP 9-44 n Necrotizing fascitis. (From Roberts JR, Hedges JR: Clinical
procedures in emergency medicine, ed 5, Philadelphia, 2010, Saunders
Elsevier.) CP 9-47 n Orf in finger. (From Centers for Disease Control and
Prevention, Atlanta, Ga. Courtesy Sue Meidel, National Center for Zoonotic,
Vector-Borne, and Enteric Disease.)
CP 9-45 n Methicillin-resistant Staphylococcus aureus soft tissue

infection. (From Centers for Disease Control and Prevention Public Health
Image Library, Atlanta, Ga.) CP 9-48 n World distribution of Plague, 1998. (From Centers for
Disease Control and Prevention, Division of Vector Borne Infectious
Diseases, Atlanta, Ga.)
CP 9-46 n Severe crusting erosive dermatitis on the face of an adult

Boxer. This dog also had a secondary methicillin-resistant Staphylococcus
aureus infection, possibly obtained from the owner, who worked in the
human health care industry. (From Medleau L, Hnilica KA: Small ani- CP 9-49 n Prairie dog that died of a Yersinia pestis infection. (From
mal dermatology: a color atlas and therapeutic guide, ed 2, St Louis, 2006, Centers for Disease Control and Prevention Public Health Image Library,
Saunders Elsevier.) Atlanta, Ga.)
Actual size
CP 9-50 n Xenopsylla cheopis (oriental rat flea) engorged with

blood. (From Centers for Disease Control and Prevention, Division of
Vector Borne Infectious Diseases, Atlanta, Ga.)
CP 9-52 n Septicemic plague with ecchymoses and petechiae from dis-

seminated intravascular coagulation. (From Mandell GL, Bennett JE, Dolin
R: Principles and practice of infectious diseases, ed 6, Philadelphia, 2005,
Churchill Livingstone Elsevier.)
CP 9-51 n Axillary bubo in bubonic plague. (From Marx J, Hockberger

R, Walls R (eds): Rosen’s emergency medicine: concepts and clinical practice, ed
6, Philadelphia, 2006, Mosby Elsevier. Courtesy of Frederick M. Burkle, Jr.)
CP 9-53 n Cat recovering from bubonic plague. Centers for Disease

Control and Prevention: Emergency preparedness and response: plague: veter-
inary issues: dogs and ungulates. http://www.bt.cdc.gov/agent/plague/train-
ingmodule/7/07.asp.)
CP 9-56 n Intercotyledonary placentitis (Coxiella burnetii), goat. Note
CP 9-54 n Dog with submandibular lymphadenopathy. (Courtesy Ted the opacity of the intercotyledonary placenta caused by thickening from
Brown, New Mexico Environment Department.) inflammation and fibrosis. The cotyledons have variable areas of gray dis-
coloration, indicating necrosis and inflammatory exudates. The gross
appearance of the lesions of placentitis tends to be similar, regardless of the
etiologic agent identified by microbiological examination. (From McGavin
MD, Zachary JF: Pathologic basis of veterinary disease, ed 4, St Louis, 2007,
Mosby Elsevier. Courtesy R.A. Foster, Ontario Veterinary College, University
of Guelph.)
CP 9-55 n Q fever endocarditis on bioprosthetic valve leaflet. The CP 9-57 n Immunofluorescent micrograph revealing a positive result
ridge in the center of the photograph is the area infiltrated with C. bur- for the presence of rabies virus antigens in a specimen. (From Centers for
netii. (From Raoult D, Raza A, Marrie TJ: Q fever endocarditis and other Disease Control and Prevention Public Health Image Library, Atlanta, Ga.
forms of chronic Q fever. In Marrie TJ (ed): Q fever: the disease, Boca Raton, Courtesy Dr. Tierkel.)
FL, 1990, CRC Press.)
N
N
3
4 1
2
4 4 2 1 15
5 2
30 3 7
2
16 14
11
1 14 6 6
2 4 7 75
14 45
3
535
106 DC
4 190 188 64
2
23 NYC
28 54 78
20 5 AS
22 CNMI
GU
PR
0 ≥1 VI
CP 9-58 n The number of reported cases of Rocky Mountain spotted fever (RMSF) in the United States and
its territories, 2004. Changes in the number of reported cases of RMSF might reflect alterations to surveillance
algorithms for this and other tickborne diseases. Biological factors (e.g., changes in tick populations resulting
from fluctuating environmental conditions) might also be involved. (From Long SS, Pickering LK, Prober CG:
Principles and practice of pediatric infectious diseases, ed 3, London, 2009, Churchill Livingstone Elsevier. Data
from Centers for Disease Control and Prevention: Summary of Notifiable Disease— United States, 2004, MMWR
Morbid Mortal Wkly Rep 53:61, 2006.)
CP 9-59 n Child’s right hand and wrist displaying the characteristic

rash of Rocky Mountain spotted fever. (From Centers for Disease Control
and Prevention Public Health Image Library, Atlanta, Ga.)
CP 9-60 n Anterior uveitis in the left eye of a 9-year-old mixed-breed

dog seropositive to Rickettsia rickettsii. Iridal congestion, blood, and fibrin
in the anterior chamber, and secondary glaucoma (iris bombé) can be
seen. (From Maggs D, Miller P, Ofri R: Slatter’s fundamentals of veterinary
ophthalmology, ed 4, St Louis, 2008, Saunders Elsevier.)
CP 9-63 n Fresh blood clots mixed with feces of a cow that had a type C
Salmonella spp. enterocolitis. (From Divers TJ, Peek SF: Rebhun’s diseases of
dairy cattle, ed 2, St Louis, 2008, Saunders Elsevier.)
CP 9-61 n Stricture, colon, pig. This lesion in pigs has been attributed to
thrombosis of the cranial hemorrhoidal artery from vasculitis and throm-
bosis caused by salmonella. (From McGavin MD, Zachary JF: Pathologic
basis of veterinary disease, ed 4, St Louis, 2007, Mosby Elsevier. Courtesy C.S.
Patton, College of Veterinary Medicine, University of Tennessee.)
CP 9-64 n Systemic lesions of Salmonella infection in a cockatiel. (From

Songer JG, Post KW: Veterinary microbiology: bacterial and fungal agents of
animal disease, St Louis, 2005, Saunders Elsevier. Courtesy Raymond E.
Reed.)
CP 9-62 n Fibrinous cholecystitis, gallbladder, cow. Fibrinous cholecys-

titis caused by Salmonella enteritidis serotype dublin has produced a fibrin-
ous cast, which has sloughed into the lumen of the gallbladder. (From
McGavin MD, Zachary JF: Pathologic basis of veterinary disease, ed 4, St
Louis, 2007, Mosby Elsevier. Courtesy D.A. Mosier, College of Veterinary
Medicine, Kansas State University.)
CP 9-65 n Feline scabies. Generalized alopecia and crusting papu-

lar dermatitis on the head of an adult cat. (From Medleau L, Hnilica
KA: Small animal dermatology: a color atlas and therapeutic guide, ed 2,
St Louis, 2006, Saunders Elsevier.)
CP 9-68 n Larva of Toxocara in retina manifesting as granuloma. (From
Long SS, Pickering LK, Porber CG: Principles and practice of pediatric infec-
tious disease, ed 3, Philadelphia, 2009, Saunders Elsevier.)
CP 9-66 n Scabies. Pustules on the palms of an infant. Note the papular

lesions on the wrist. (From Habif TP: Clinical dermatology: a color guide to
diagnosis and therapy, ed 4, St Louis, 2004, Mosby Elsevier.)
CP 9-69 n Chorioretinitis due to toxoplasmosis. (From Cohen J,

Powderly WG: Infectious diseases, ed 2, Edinburgh, 2004, Mosby Elsevier.)
CP 9-67 n Marked hyperkeratosis on arms of a patient with crusted

(“Norwegian”) scabies. (From Mandell GL, Bennett JE, Dolin R: Principles
and practice of infectious diseases, ed 6, Philadelphia, 2005, Churchill
Livingstone Elsevier. Courtesy Kenneth E. Greer, Charlottesville, Va.)
CP 9-70 n Pneumonia and necrosis in heart of a kitten congenitally

infected with toxoplasmosis. (From Greene CE: Infectious diseases of the dog
and cat, ed 3, St Louis, 2006, Saunders Elsevier.)
A
CP 9-71 n Punctate chorioretinitis caused by Toxoplasma gondii in an

experimentally inoculated cat. (From Lappin MR: Polysystemic protozoal
infections. In Nelson RW, Couto CG (eds): Small animal internal medicine,
ed 4, St Louis, 2009, Mosby Elsevier.)
B
CP 9-72 n A, Tracheal wash and bronchioalveolar lavage from a dog
with toxoplasmosis. A ciliated columnar cell, red blood cells, scattered neu-
trophils, and an extracellular Toxoplasma gondii organism (arrow) are shown.
(Wright’s stain, original magnification ×250.) B, Ciliated columnar cells are
present both individually and in a cluster. The morphology of the cells in
the cluster cannot be discerned. Cilia are evident on the cells that are well
spread out. Many of the cells are traumatized, as evidenced by their irregu-
lar nuclear outlines. (Wright’s stain, original magnification ×160.) (From
Cowell RL, Tyler RD, Meinkoth JH, et al: Diagnostic cytology and hematology
of the dog and cat, ed 3, St Louis, 2008, Mosby Elsevier.)
A B
CP 9-73 n Feline spongiform encephalopathy. A, Area in the thalamus with many small and large vacuoles
in the neuropil (H&E stain, ×100). B, Area with spongiform change. Punctate and plaquelike deposits (red) of
the protease resistant PrP (immunocytochemical staining with polyclonal anti-PrP; avidin biotinylated enzyme
complex [ABC] technique, ×250). (From Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis, 2006,
Saunders Elsevier.)
CP 9-74 n Scheme of the proposed evolutionary pathway of the tubercle bacilli illustrating successive loss of
DNA in certain lineages (gray boxes). (From Brosch R, Gordon SV, Marmiesse M et al: A new evolutionary sce-
nario for the Mycobacterium tuberculosis complex, Proc Natl Acad Sci U S A 99(6):3684, 2002. Copyright © 2002
The National Academy of Sciences.)
CP 9-75 n Typical granuloma resulting from infection with

Mycobacterium tuberculosis showing central caseous necrosis, activated
epithelioid macrophages, many giant cells, and a peripheral accumulation
of lymphocytes. (From Kumar V, Abbas AK, Fausto N et al: Robbins basic
pathology, ed 8, Philadelphia, 2007, Saunders Elsevier.)
CP 9-76 n Axillary lymphadenitis caused by Mycobacterium tuber-

culosis in a patient with AIDS. (From Mandell GL, Bennett JE, Dolin R:
Principles and practice of infectious diseases, ed 6, New York, 2005, Churchill
Livingstone Elsevier.)
CP 9-80 n Thumb with skin ulcer of tularemia. (From Centers for
CP 9-77 n Multiple caseous granulomas, tuberculosis, Mycobacterium Disease Control and Prevention Public Health Image Library, Atlanta, Ga.)
bovis, liver, cow. Hepatic tuberculosis is characterized by random, multifo-
cal, pale white to yellow caseous granulomas on the capsular and cut sur-
faces. (From McGavin MD, Zachary JF: Pathologic basis of veterinary disease,
ed 4, St Louis, 2007, Mosby Elsevier. Courtesy M. Domingo, Autonomous
University of Barcelona, and Noah’s Arkive, College of Veterinary Medicine,
The University of Georgia.)
CP 9-81 n Ulceroglandular tularemia. (From Reintjes R, Dedushaj I,

Gjini A, et al: Tularemia outbreak investigation in Kosovo: case control and
environmental studies, Emerg Infect Dis 8(1):69, 2002.)
CP 9-78 n Mycobacterium marinum in a pet store worker. (From

Nguyen C: Images in clinical medicine. Mycobacterium marinum, N Engl J
Med 350(9):e8, 2004.)
CP 9-82 n Multifocal necrosis with fibrinosuppurative and granu-

CP 9-79 n Conjunctival mycobacteriosis (Mycobacterium avium) in an lomatous inflammation in the spleen of a cat infected with F. tularen-
ostrich. (From Songer JG, Post KW: Veterinary microbiology: bacterial and sis. (From Greene CE: Infectious diseases of the dog and cat, ed 3, St Louis,
fungal agents of animal disease, St Louis, 2005, Saunders Elsevier. Courtesy 2006, Saunders Elsevier. Courtesy Brad M. DeBey, Department of Veterinary
J. Glenn Songer.) Pathology, Kansas State University, Manhattan.)
CP 9-83 n Photomicrograph depicting Francisella tularensis bacteria as CP 9-85 n Blood being extracted from the wing vein of a pigeon to be
seen with a fluorescent antibody stain. (From Centers for Disease Control tested for the presence of arboviruses. (From Centers for Disease Control
and Prevention Public Health Image Library, Atlanta, Ga.) and Prevention Public Health Image Library, Atlanta, Ga.)
CP 9-84 n Flock of sentinel chickens. (From Scott County Health Department: Mosquito surveillance pro-
gram. http://www.scottcountyiowa.com/health/images/mosquito_surveillance02.jpg.)
CP 10-2 n Toddler victim of moose attack. Hoof mark on chest wall
overlies rib fractures and pulmonary contusion. (From Auerbach PS:
CP 9-86 n Fibrinous colitis in an alligator with West Nile virus. This Luanne Freer.)
animal was unable to submerge itself. (From Nevarez J: Crocodilians. In
Mitchell M, Tully Jr TN (eds): Manual of exotic pet practice, St Louis, 2009,
Saunders Elsevier.)
CP 10-3 n Lion attack victim. This African victim was rescued by

CP 9-87 n Young alligator (Alligator mississippiensis) with the head tilt bystanders while his head was in the lion’s mouth. His only injury was a
typical of those affected with West Nile virus. Notice that it still maintains an degloving scalp laceration. (From Auerbach PS: Wilderness medicine, ed 5,
aggressive stand with the mouth open. (From Mader DR: Reptile medicine Philadelphia, 2007, Mosby Elsevier. Courtesy Harold P. Adolph.)
and surgery, ed 2, St Louis, 2006, Saunders Elsevier.)
CP 10-1 n Many amphibians bite. Some, such as the Argentine horned

frog (Ceratophrys ornata), can inflict severe wounds on the human han-
dler. (From Mader DR: Reptile medicine and surgery, ed 2, St Louis, 2006,
Saunders Elsevier. Courtesy D. Mader.) CP 10-4 n Live animal market. (From U.S. Agency for International
Development: Congress approves $25 million to fight avian flu in Asia,
FrontLines, July/August 2005.)
CP 10-8 n Maculopapular rash with small, dark-red eruptions on hand
of person with rat-bite fever. (From Van Nood E, Peters SH: Rat-bite fever,
Neth J Med 63:319, 2005.)
CP 10-5 n A nematode in the accessory lung lobe (at tip of forceps) in a
chameleon. Small numbers of lung parasites do not usually cause a problem.
However, in immunocompromised patients, parasites can lead to inflamma-
tion and pneumonia. (From Mader DR: Reptile medicine and surgery, ed 2,
St Louis, 2006, Saunders Elsevier. Courtesy D. Mader.)
CP 10-9 n Localized lesion in sporotrichosis. The most common clini-

cal presentation is a localized cutaneous or subcutaneous lesion, which
develops at the site of implantation of the etiologic agent, Sporothrix
schenckii. (From Cohen J, Powderly WG: Infectious diseases, ed 2, London,
2004, Mosby Elsevier.)
CP 10-6 n Subcutaneous abscess. Feline abscess caused by a cat bite.
The syringe contains purulent material aspirated from the abscess. (From
Medleau L, Hnilica KA: Small animal dermatology: a color atlas and thera-
peutic guide, ed 2, St Louis, 2006, Saunders Elsevier.)
CP 12-1 n Erysipeloid. Approximately 3 days after animal or fish con-

CP 10-7 n Infected cat bite. Note the streak of erythema extending proximally tact, a dull red erythema appears at the inoculation site and extends centrif-
along the anterior forearm. (From Zaoutis LB, Chiang VW: Comprehensive ugally. (From Habif TP: Clinical dermatology: a color guide to diagnosis and
pediatric hospital medicine, Philadelphia, 2007, Mosby Elsevier.) therapy, ed 4, St Louis, 2004, Mosby Elsevier.)
CP 12-2 n Torso of a victim with Vibrio vulnificus sepsis. (From
Auerbach PS: Wilderness medicine, ed 5, Philadelphia, 2007, Mosby
Elsevier.)
CP 12-3 n Seal finger secondary to Mycoplasma. (From Auerbach PS:
Edgar Maeyens, Jr.)
CP 13-1 n Protecting animal and human health. (From Centers for Disease Control and Prevention, Atlanta, Ga.)

2010 - Human-Animal Medicine

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Human-Animal

Lisa A. Conti, DVM, MPH, DACVPM, CEHP

with more than 400 illustrations

HUMAN-ANIMAL MEDICINE: CLINICAL APPROACHES TO ZOONOSES, ISBN 978-1-4160-6837-2

Copyright © 2010 by Saunders, an imprint of Elsevier Inc.

Library of Congress Cataloging-in-Publication Data

Cover image (woman with cat) © Inti St. Clair/Corbis.

Vice President and Publisher: Linda Duncan

Printed in the United States of America

Matthew S. Alkaitis Russell W. Currier, DVM, MPH, DACVPM

Thomas P. Monath, MD Judy Sparer, CIH, MSCE

Lynda U. Odofin, DVM, MSPH Oyebode A. Taiwo, MD, MPH

Alina Alonso, MD Emily Beeler, DVM

Philip W. Askenase, MD Tegan K. Boehmer, PhD, MPH

Michele Barry, MD, FACP Victoria E. Bridges, DVM, MS

Stanley D. Bruntz, DVM, MPH Paul Ettestad, DVM, MS

Zimra J. Gordon, DVM, MPH Anne E. Justice-Allen, DVM

Robert Hood, PhD, CIP Leonard C. Marcus, VMD, MD

Jennifer McQuiston, DVM, MS, DACVPM Mark A. Pokras, DVM

Kathleen A. Smith, DVM, MPH †

We believe that human and animal health clinicians have an

intellectual and practical contributions of this book and will

James H. Steele, DVM, MPH

Lonnie King, DVM, MS, MPA

How human and animal health Food Animals

Environmental health (biologic,

“Shared risk” and

Human health Animal health

Figure 1-1 n Relationships among environmental, human, and animal

EXAMPLES OF ROUTES BY WHICH ZOONOSES ARE ACQUIRED

­ onoxide. Just as canaries once warned coal miners of the

in important ways. Table 1-1 outlines some of the key points

*As of October 31, 2007.

Similarly, veterinarians are licensed to evaluate and treat

Baseline Animal Health History Checklist (to be completed by the patient)

Date: Name and telephone number of veterinarian:

Does your work involve contact with animals? Y N

If yes, please describe.

Farms where animals are kept Y N

Residential contact with wildlife:

Dwelling (check one): House Apartment Other

Size of property: acres

Property is: Urban Suburban Rural

Lawn Woods Pond or other wetlands

Have you noticed ticks around your yard? Y N

Have you noticed mice or rats near your home? Y N

Figure 3-1 n Self-administered checklist for a patient’s animal contact history.

Deer Coyotes Foxes Canada geese

Other (please specify):

Other (please specify):

Hunting and other wild game exposures:

Please check which of the following apply.

I or another household member regularly hunt for:

Deer Waterfowl Other gamebirds Rabbits Feral hogs

Other (please specify):

Such hunting involves:

Skinning carcasses without gloves or other protection Eating wild meat

Other (please specify):

Figure 3-1 n Cont’d

onoxide. Just as canaries once warned coal miners of the

1. Are any persons in the If yes, go to #2.

long-term care.2 Subsequently, despite a growing number and

Figure 6-1 n Tree-lined, designated pedestrian paths increase the likeli