Foundations in Microbiology: The Cocci of Medical Importance Talaro
Foundations in Microbiology: The Cocci of Medical Importance Talaro
Foundations in Microbiology: The Cocci of Medical Importance Talaro
Foundations in
Microbiology
Sixth Edition
Talaro
Chapter 18
The Cocci of Medical
Importance
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
General Characteristics of the
Staphylococci
• Common inhabitant of the skin and mucous
membranes
• Spherical cells arranged in irregular clusters
• Gram-positive
• Lack spores and flagella
• May have capsules
• 31 species
2
3
Staphylococcus aureus
• Grows in large, round, opaque colonies
• Optimum temperature of 37oC
• Facultative anaerobe
• Withstands high salt, extremes in pH, and
high temperatures
• Carried in nasopharynx and skin
• Produces many virulence factors
4
5
Virulence factors of S. aureus
Enzymes:
• Coagulase – coagulates plasma and blood;
produced by 97% of human isolates; diagnostic
• Hyaluronidase – digests connective tissue
• Staphylokinase – digests blood clots
• DNase – digests DNA
• Lipases – digest oils; enhances colonization on
skin
• Penicillinase – inactivates penicillin
6
Virulence factors of S. aureus
Toxins:
• Hemolysins (α, β, γ, δ) – lyse red blood cells
• Leukocidin – lyses neutrophils and macrophages
• Enterotoxin – induce gastrointestinal distress
• Exfoliative toxin – separates the epidermis from the
dermis
• Toxic shock syndrome toxin (TSST) - induces
fever, vomiting, shock, systemic organ damage
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8
Epidemiology and Pathogenesis
• Present in most environments frequented by humans
• Readily isolated from fomites
• Carriage rate for healthy adults is 20-60%.
• Carriage is mostly in anterior nares, skin,
nasopharynx, intestine.
• Predisposition to infection include: poor hygiene and
nutrition, tissue injury, preexisting primary infection,
diabetes, immunodeficiency.
• Increase in community acquired methicillin resistance
- MRSA
9
Staphylococcal Disease
Range from localized to systemic
• Localized cutaneous infections – invade skin through
wounds, follicles, or glands
– folliculitis – superficial inflammation of hair follicle; usually
resolved with no complications but can progress
– furuncle – boil; inflammation of hair follicle or sebaceous
gland progresses into abscess or pustule
– carbuncle – larger and deeper lesion created by aggregation
and interconnection of a cluster of furuncles
– impetigo – bubble-like swellings that can break and peel
away; most common in newborns
10
11
Staphylococcal Disease
• Systemic infections
– osteomyelitis – infection is established in the
metaphysis; abscess forms
– bacteremia - primary origin is bacteria from
another infected site or medical devices;
endocarditis possible
12
13
Staphylococcal Disease
• Toxigenic disease
– food intoxication – ingestion of heat stable
enterotoxins; gastrointestinal distress
– staphylococcal scalded skin syndrome – toxin
induces bright red flush, blisters, then
desquamation of the epidermis
– toxic shock syndrome – toxemia leading to
shock and organ failure
14
15
Other Staphylococci
Coagulase-negative staphylococcus; frequently involved
in nosocomial and opportunistic infections
• S. epidermidis – lives on skin and mucous membranes;
endocarditis, bacteremia, UTI
• S. hominis – lives around apocrine sweat glands
• S. capitis – live on scalp, face, external ear
• All 3 may cause wound infections by penetrating
through broken skin.
• S. saprophyticus – infrequently lives on skin, intestine,
vagina; UTI
16
Identification of Staphylococcus in
Samples
• Frequently isolated from pus, tissue exudates,
sputum, urine, and blood
• Cultivation, catalase, biochemical testing,
coagulase
17
18
Clinical Concerns and Treatment
• 95% have penicillinase and are resistant to
penicillin and ampicillin.
• MRSA – methicillin-resistant S. aureus –
carry multiple resistance
• Abscesses have to be surgically perforated.
• Systemic infections require intensive
lengthy therapy.
19
Prevention of Staphylococcal Infections
20
General Characteristics of Streptococci
• Gram-positive spherical/ovoid cocci arranged in long
chains; commonly in pairs
• Non-spore-forming, nonmotile
• Can form capsules and slime layers
• Facultative anaerobes
• Do not form catalase, but have a peroxidase system
• Most parasitic forms are fastidious and require enriched
media.
• Small, nonpigmented colonies
• Sensitive to drying, heat and disinfectants
• 25 species
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22
Streptococci
• Lancefield classification system based on
cell wall Ag – 17 groups (A,B,C,….)
• Another classification system is based on
hemolysis reactions.
-hemolysis – A,B,C,G and some D strains
–hemolysis – S. pneumoniae and others
collectively called viridans
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24
Human Streptococcal Pathogens
• S. pyogenes
• S. agalactiae
• Viridans streptococci
• S. pneumoniae
• Enterococcus faecalis
25
-hemolytic S. pyogenes
• Most serious streptococcal pathogen
• Strict parasite
• Inhabits throat, nasopharynx, occasionally
skin
26
Virulence Factors of -hemolytic
S. pyogenes
Produces surface antigens:
– C-carbohydrates – protect against lysozyme
– Fimbriae - adherence
– M-protein – contributes to resistance to
phagocytosis
– Hyaluronic acid capsule – provokes no
immune response
27
28
Virulence Factors of -hemolytic
S. pyogenes
Extracellular toxins:
streptolysins – hemolysins; streptolysin O (SLO)
and streptolysin S (SLS) – both cause cell and
tissue injury
pyogenic toxin (erythrogenic) – induces fever
and typical red rash
superantigens – strong monocyte and
lymphocyte stimulants; cause the release of
tissue necrotic factor
29
Virulence Factors of -hemolytic
S. pyogenes
Extracellular enzymes
streptokinase – digests fibrin clots
hyaluronidase – breaks down connective tissue
DNase – hydrolyzes DNA
30
Epidemiology and Pathogenesis
• Humans only reservoir
• Inapparent carriers
• Transmission – contact, droplets, food, fomites
• Portal of entry generally skin or pharynx
• Children predominant group affected for
cutaneous and throat infections
• Systemic infections and progressive sequelae
possible if untreated
31
Scope of Clinical Disease
Skin infections
• Impetigo (pyoderma) – superficial lesions that break
and form highly contagious crust; often occurs in
epidemics in school children; also associated with
insect bites, poor hygiene, and crowded living
conditions
• Erysipelas – pathogen enters through a break in the
skin and eventually spreads to the dermis and
subcutaneous tissues; can remain superficial or become
systemic
Throat infections
• Streptococcal pharyngitis – strep throat
32
33
34
Scope of Clinical Disease
Systemic infections
• Scarlet fever – strain of S. pyogenes
carrying a prophage that codes for
pyrogenic toxin; can lead to sequelae
• Septicemia
• Pneumonia
• Streptococcal toxic shock syndrome
35
Long-Term Complications of Group
A Infections
• Rheumatic fever – follows overt or subclinical
pharyngitis in children; carditis with extensive
valve damage possible, arthritis, chorea, fever
• Acute glomerulonephritis – nephritis,
increased blood pressure, occasionally heart
failure; can become chronic leading to kidney
failure
36
Group B: Streptococcus agalactiae
• Regularly resides in human vagina, pharynx
and large intestine
• Can be transferred to infant during delivery
and cause severe infection
– most prevalent cause of neonatal pneumonia,
sepsis, and meningitis
– 15,000 infections and 5,000 deaths in US
– Pregnant women should be screened and treated.
• Wound and skin infections and endocarditis in
debilitated people
37
Group D Enterococci and Groups C and
G Streptococci
• Group D:
– Enterococcus faecalis, E. faecium, E. durans
– normal colonists of human large intestine
– cause opportunistic urinary, wound, and skin
infections, particularly in debilitated persons
• Groups C and G:
– common animal flora, frequently isolated from
upper respiratory; pharyngitis, glomerulonephritis,
bacteremia
38
Identification
• Cultivation and diagnosis ensure proper
treatment to prevent possible complications.
• Rapid diagnostic tests based on monoclonal
antibodies that react with C-carbohydrates
• Culture using bacitracin disc test, CAMP test
39
40
41
Treatment and Prevention
• Groups A and B are treated with penicillin.
• Sensitivity testing needed for enterococci
• No vaccines available
42
-Hemolytic Streptococci:
Viridans Group
• Large complex group
– Streptococcus mutans, S. oralis, S. salivarus,
S. sanguis, S. milleri, S. mitis
• Most numerous and widespread residents of the
gums and teeth, oral cavity and also found in
nasopharynx, genital tract, skin
• Not very invasive; dental or surgical procedures
facilitate entrance
43
Viridans Group
• Bacteremia, meningitis, abdominal infection, tooth
abscesses
• Most serious infection – subacute endocarditis –
blood-borne bacteria settle and grow on heart
lining or valves
• Persons with preexisting heart disease are at high
risk.
• Colonization of heart by forming biofilms
44
Viridans Group
• S. mutans produce slime layers that adhere
to teeth, basis for plaque.
• Involved in dental caries
• Persons with preexisting heart conditions
should receive prophylactic antibiotics
before surgery or dental procedures.
45
Streptococcus pneumoniae: The
Pneumococcus
• Causes 60-70% of all bacterial pneumonias
• Small, lancet-shaped cells arranged in pairs
and short chains
• Culture requires blood or chocolate agar.
• Growth improved by 5-10% CO2
• Lack catalase and peroxidases – cultures die in
O2
46
47
S. pneumoniae
• All pathogenic strains form large capsules –
major virulence factor.
• Specific soluble substance (SSS) varies among
types.
• 84 capsular types have been identified
• Causes pneumonia and otitis media
48
Epidemiology and Pathology
• 5-50% of all people carry it as normal flora in the
nasopharynx; infections are usually endogenous.
• Very delicate, does not survive long outside of its
habitat
• Young children, elderly, immune compromised, those
with other lung diseases or viral infections, persons
living in close quarters are predisposed to pneumonia
• Pneumonia occurs when cells are aspirated into the
lungs of susceptible individuals.
• Pneumococci multiply and induce an overwhelming
inflammatory response.
• Gains access to middle ear by way of eustachian tube
49
50
Cultivation and Diagnosis
• Gram stain of specimen – presumptive
identification
• α hemolytic; optochin sensitivity
• Quellung test or capsular swelling reaction
51
Treatment and Prevention
• Traditionally treated with penicillin G or V
• Increased drug resistance
• Two vaccines available for high risk
individuals:
– capsular antigen vaccine for older adults and
other high risk individuals-effective 5 years
– conjugate vaccine for children 2 to 23 months
52
Family Neisseriaceae
• Gram-negative cocci
• Residents of mucous membranes of warm-
blooded animals
• Genera include Neisseria, Moraxella,
Acinetobacter.
• 2 primary human pathogens:
– Neisseria gonorrhoeae
– Neisseria meningitidis
53
Genus Neisseria
• Gram-negative, bean-shaped, diplococci
• None develop flagella or spores.
• Capsules on pathogens
• Pili
• Strict parasites, do not survive long outside of the host
• Aerobic or microaerophilic
• Oxidative metabolism
• Produce catalase and cytochrome oxidase
• Pathogenic species require enriched complex media
and CO2.
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55
Neisseria gonorrhoeae:
The Gonococcus
• Causes gonorrhea, an STD
• Virulence factors:
– pili, other surface molecules for attachment;
slows phagocytosis
– IgA protease – cleaves secretory IgG
56
Epidemiology and Pathology
• Strictly a human infection
• In top 5 STDs
• Infectious dose 100-1,000
• Does not survive more than 1-2 hours on
fomites
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58
Gonorrhea
Infection is asymptomatic in 10% of males and 50%
of females.
• Males – urethritis, yellowish discharge, scarring
and infertility
• Females – vaginitis, urethritis, salpingitis (PID)
mixed anaerobic abdominal infection, common
cause of sterility and ectopic tubal pregnancies
• Extragenital infections – anal, pharygeal,
conjunctivitis, septicemia, arthritis
59
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Gonorrhea in Newborns
• Infected as they pass through birth canal
• Eye inflammation, blindness
• Prevented by prophylaxis immediately after
birth
62
Diagnosis and Control
• Gram stain – Gram-negative intracellular (neutrophils)
diplococci from urethral, vaginal, cervical, or eye
exudate – presumptive identification
• 20-30% of new cases are penicillinase-producing
PPNG or tetracycline resistant TRNG
• Combined therapies indicated
• Recurrent infections can occur.
• Reportable infectious disease
63
64
Neisseria meningitidis: The
Meningococcus
Virulence factors:
– capsule
– pili
– IgA protease
– endotoxin
• 12 strains; serotypes A, B, C cause most
cases
65
Epidemiology and Pathogenesis
• Prevalent cause of meningitis; sporadic or epidemic
• Human reservoir – nasopharynx; 3-30% of adult
population; higher in institutional settings
• High risk individuals are those living in close
quarters, children 6months-3 years, children and
young adults 10-20 years.
• Disease begins when bacteria enter bloodstream, pass
into cranial circulation, and multiply in meninges
• Very rapid onset; neurological symptoms; endotoxin
causes hemorrhage and shock; can be fatal
66
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68
Clinical Diagnosis
• Gram stain CSF, blood, or nasopharyngeal
sample
• Culture for differentiation
• Rapid tests for capsular antigen
69
Treatment and Prevention
• Treated with IV penicillin G, chloramphenicol
• Prophylactic treatment of family members,
medical personnel, or children in close contact
with patient
• Vaccines exist for group A and C.
70
Other Gram-negative Cocci and
Coccobacilli
• Genus Branhamella
– Branhamella catarrhalis – found in nasopharynx:
significant opportunist in cancer, diabetes, alcoholism
• Genus Moraxella
– bacilli; found on mucous membranes
• Genus Acinetobacter
– Gram-negative bacilli; nonliving reservoir; source of
nosocomial infections
71