SPIROCHETES • Isolation and identification

o Culture – Fletcher’s, Stuart’s, or Ellinghausen-McCullough-

• Helical-shaped, motile, unicellular bacteria
Johnson-Harris (EMJH) medium (use 1-2 drops of patient
o 0.1-3.0 um wide by 5-20 um long
sample)
o Exhibit various types of motion in liquid media
o Serology – microscopic agglutination test (MAT) for serotyping
o Free-living or survive in association with animal or human hosts
o Immunoglobulin M (IgM) enzyme-linked immunosorbent assay
• Treponema pallidum subsp. pallidum (syphilis)
(ELISA) test
• T. pallidum other subspecies
• Borrelia – relapsing fever; Lyme disease
• Leptospira – leptospirosis ANTIMICROBIAL SUSCEPTIBILITY
• Spirillum minor – rat-bite fever • Susceptible to
o Streptomycin
o Tetracycline
o Doxycycline
LEPTOSPIRES o Penicillin
• Leptospira o Some limited effectiveness if used early (before fourth day of
o Obligate aerobic helical rods 0.1 um by 5-15 um long that are illness)
tightly coiled, thin, and flexible
o Leptospirosis - L. interrogans
• 20 serovars
o Most common – Icterohaemorrhagiae, Australis, and Canicola BORRELIAE
• Virulence factors (unknown but may include): • Borrelia spp.
o Reduced phagocytosis o Helical bacteria 0.2-0.5 um by 3-20 um in length
o Soluble hemolysin o Spirals vary between 3-10 per organism
o Endotoxins o Less tightly coiled than leptospires
• Relapsing fever
o B. recurrentis and B. duttonii
- Pediculus humanus louse-borne infection (epidemic
INFECTIONS CAUSED BY LEPTOSPIRES
relapsing fever)
• Organisms in mud or water enter through breaks in the skin or intact - Transmission by crushing or scratching lice into skin
mucosa o B. hermsii
• Symptoms - Tick-borne infection – Ornithodoros ticks
o Initial phase - Endemic relapsing fever – transmitted by saliva during
- Fever, headache, malaise, and severe myalgia bite
- Conjunctival suffusion seen in less than half
- Can involve hepatic, renal, and central nervous systems
VIRULENCE FACTORS
(renal lesions are interstitial nephritis with glomerular
swelling and hyperplasia) Relapsing fever
o Illness lasts from less than 1 week to 3 weeks • Evade complement by acquiring and displaying suppressive
• Late manifestations caused by host immunologic response to complement regulators
infections o C3b-BP
• Weil’s disease – severe systemic disease o Factor H
o Jaundice, acute renal failure, hepatic failure, intravascular • Relapses are caused by antigenic variation
disease (can be fatal) o Specific antibodies are rendered ineffective
• Symptoms
o Incubation period is 2-15 days
EPIDEMIOLOGY o High fever (104°C) with shaking chills (3-7 days)
ZOONOTIC DISEASE o Delirium
• Animal workers or in rat-infested surroundings o Severe muscle aches and pain in bones and joints – followed by
o Dogs, rats, and other rodents are principal hosts (excreted in remission and subsequent repeat of symptoms – sometimes
urine) hepatosplenomegaly and jaundice
• Freshwater recreational exposure o Neurologic symptoms – lymphocytic meningitis and facial palsy
o Water contaminated by urine (can survive for months in water) o Rarely fatal
• Laboratory diagnosis
o Direct examination of spirochetes in blood (thick and thin films
INFECTION
of Giemsa or Wright-stained smears)
• Enters by contact with infected urine o Culture – Kelly medium, Animal inoculation (rarely), serology is
difficult and impractical
• Antimicrobial susceptibility
o Tetracyclines are the drugs of choice
LABORATORY DIAGNOSIS o Death of spirochetes can cause sudden endotoxin release
• Specimen collection (Jarisch-Herxheimer reaction) – fevers, chills, headache, myalgia
o Collect blood or cerebrospinal fluid (CSF) during first week of
illness
o Collect urine – yield higher after first week (direct microscopic
detection is not recommended)
B. BURGDORFERI SYPHILITIC INFECTION
VIRULENCE FACTORS • Transmission
• Bacterial spread o Infection caused by sexual contact (mucous membranes)
o Binds plasminogen and urokinase-type plasminogen activator to o Can enter via cuts, abrasions, or directly through intact mucous
its surface (could act as a protease to promote tissue invasion) membranes
• Complement evasion o Can enter other sites such as the lip or transplacentally
o Binds factor H • Incubation period
o Disseminate throughout the body
o 10-90 days (usually about 3 weeks)
CLINICAL MANIFESTATION
• Primary syphilis
• Stage 1 o Chancre at infection site (usually one but sometimes several in
o Erythematous papule that rapidly expands human immunodeficiency virus [HIV]-positive patients)
o Erythema chronicum migrans – classic “bulls-eye rash” in 60% - Clean, smooth base, edge slightly raised, and firm
of patients (peripheral edema with central clearing) - Painless but may be tender
• Stage 2 (Acute) - Heals in 3-6 weeks
o Disseminated infection o Base contains spirochetes that can be identified by dark field
o Secondary skin lesions microscopy or immunofluorescence or serology
o Joint and bone pain • Secondary syphilis
o Neurologic and cardiac pathology o Begins 2-12 weeks after chancre appearance
o Splenomegaly o Widespread macular rash (syphilitic roseola), particularly palms
o Malaise and fatigue and soles of feet
• Stage 3 (Chronic) o Secondary lesions (Condylomata lata) – moist, gray-white
o Chronic cardiac symptoms plaques teeming with spirochetes
o Chronic neurologic symptoms o Systemic symptoms – lymphadenopathy, headache, lesions of
o Chronic arthritis (most common symptom) the mucous membranes and the skin, and rash
• Tertiary (late) syphilis
EPIDEMIOLOGY o Complications – central nervous system (CNS) disease,
• Lyme disease (B. burgdorferi) cardiovascular abnormalities, aortitis and valve insufficiency,
o First described in Lyme, Connecticut and granulomatous lesions (gummas) in any organ
o North America and Europe o Asymptomatic CNS disease – CSF abnormalities without
• B. garinii and B. afzelii symptoms (pleocytosis, elevated proteins levels, depressed
o Asia and Europe glucose)
o Congenital syphilis
• Transmission
- Intrauterine infection
o Tick bites
- Non-immune hydrops – disease of placenta that causes
o Protective clothing and repellent prevent infection
fetal death
- Hepatosplenomegaly, meningitis, thrombocytopenia,
TREATMENT
anemia, and bones lesions
• Antibiotics – early stages doxycycline - Visible deformities (deformed tibias or teeth)
• Late stages show no usefulness of antibiotics

DETECTION SYPHILIS EPIDEMIOLOGY AND SPECIMEN COLLECTION

• Generally only screen those with symptoms and high-risk factors • Transmission – sexual contact, direct injection, direct contact with
• Generally test by serology lesions, transplacental transmission
• Specimen collection – primary or secondary lesion is cleaned with
SEROLOGIC TEST saline and gently abraded with dry, sterile gauze
• ELISAs to demonstrate reactive antibody o Transfer serous fluid to slide with saline
• Western blot to verify specificity • Usually use serology or direct exam (do not use oral lesions because
o Detection of 2-3 IgM bands of non-pathogenic oral flora)
- 24 (OspC), 39 and 41 (flagellin) kDa
o Detection of 5-10 IgG bands DETECTION
- 18, 21, 28, 30, 39, 41, 45, 58, 66, 93 kDa • Non-treponemal tests (primary or secondary stage only, later stage
less than 1%)
• Venereal disease research laboratory (VDRL)
o Cardiolipin antigen is mixed with patient serum or CSF (if
TREPONEMES positive, flocculation occurs and can be read macroscopically)
• Treponema pallidum subsp. pallidum – Syphilis • Rapid plasma reagin (RPR)
• Treponema pallidum subsp. pertenue – Yaws o Black carbon particles are bound to cardiolipin and mixed with
• Treponema pallidum subsp. endemicum – Endemic syphilis patient sera (particles agglutinate, thus indicating a positive test)
• Treponema pallidum subsp. carateum – Pinta • Treponemal tests (all stages, although more effective for secondary
and late stages)
o Confirm non-treponemal tests
VIRULENCE FACTORS
o Titers remain high despite treatment
• Penetrate intact mucous membranes • Fluorescent treponemal antibody absorption test (FTA-ABS)
• Crosses placenta o Patient sera is absorbed against non-pallidum spirochetes
• Dissemination throughout the body and organ systems o Absorbed serum is then placed with T. pallidum organisms and
• Antigenic variation – may help evade immune system secondary anti-human antibody conjugate to a fluorescein is
added
• T. pallidum-particulate agglutination test (TP-PA)
o Antigens to T. pallidum are absorbed to gelatin particles
o Patient sera is added, and gelatin agglutinates
• Enzyme immunoassay (EIA) test kits are not comparable

TREATMENT
• Penicillin – long acting is preferred (Benzathine penicillin)
• Doxycycline and tetracycline – if penicillin allergies
• Can develop Jarisch-Herxheimer reactions

OTHER TREPONEMAL DISEASES

• T. pallidum subsp. pertenue
o Yaws (chronic non-venereal disease)
- Central Africa, South America, India, Indonesia, and
Pacific Islands
- Primary, secondary, and tertiary stages (lesions are
elevated, granulomatous nodules)
• T. pallidum subsp. endmicum
o Endemic syphilis (bejel) – spread by direct contact or eating
utensils
o Resembles yaws
- Middle East and desert regions
- Papules that usually go unnoticed (gummas of skin,
bones, and nasopharynx)
• T. pallidum subsp. carateum
o Pinta – ulcerative or papulosquamous skin lesions that
depigment
o South and Central America