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59 Cards in this Set

  • Front
  • Back
What is the role of Streptococcal Protein M in pathogenesis?
adhesion: binds to keratinocytes

immune evasion: binds fibrinogen, binds factor H (C3 convertase degradation), antiphagocytic

80 serotypes

mimics glomerular proteins --> glomerulonephritis
What is the role of Streptococcal LTA in pathogenesis of GAS?
binds epithelial fibronectin--aids adhesion and colonization of host.
What is the role of Streptococcal hyaluronic acid capsule in pathogenesis?

mimics our own connective tissue --> immune evasion
Why is Acute Rheumatic Fever often associated with streptococcal pharyngitis?
M protein mimics myosin --> autoimmunity

crossreactive AB's to sarcolemma membranes of heart valves and myocardium

lifelong susceptibility to bacterial endocarditis, cardiomyopathy
What is the significance of Streptococcal Pyrogenic Exotoxins?
SPE A, B, and C

SPE A and C are superantigens!
What secreted "weaponry" does Group A Strep have at its disposal?
Streptolysin O (all), S (85% of strains)
C5a peptidase (degrades C5a)
Protein M
What is the role of Streptokinase in pathogenesis of Streptococcus infections?
converts host plasminogen (zymogen)--> plasmin (enzyme). results in fibrin/blood clot degradation.
Describe pathogenesis of Scarlet Fever.
GAS, SPE intoxication.

pharyngitis with red, peeling rash. "strawberry tongue," hemorrhage on palate
Describe pathogenesis of Impetigo.

superficial skin infection of 2-5 y/o; traumatic inoculation resulting in crusty raised lesions
Describe pathogenesis of Erysipelas.
GAS, infection of lower dermis in fatty areas.

older or immunocompromised pts; lesions clearly demarcated with raised edges and orange-peel texture.
Describe the pathogenesis of cellulitis.
GAS infection of connective tissues in deeper dermal layers of skin.

risk grp: diabetics, immunocompromised, elderly

complications: sepsis, spread to necrotizing fasciitis
Describe the pathogenesis of acute glomerulonephritis.
antigen-antibody complexes, complement complexes in blood overwhelm and cause kidney inflammation.

M protein ≈ glomerulus proteins so AB's may attack kidneys too

1-3 weeks after pharyngitis
3-6 weeks after skin infection
Describe the pathogenesis of Streptococcal Toxic Shock Syndrome (STSS).
due to GAS production of SPE A, C --> superantigen-induced systemic inflammation, shock.

skin and soft tissue invasion; necrotizing fasciitis and myonecrosis

nausea, vomiting, diarrhea, kidney damage --> hypotension, organ failure, shock
How are GAS infections diagnosed?
Culture = gold standard. Anaerobic incubation on BA at 37C, beta-hemolytic, catalase neg GPC, bacitracin sensitive

Anti-Streptolysin O titer (ASO) used for Acute Rheumatic Fever

Lancefield Agglutination test for anti-Grp A antigen
What is the standard treatment for GAS infections?
What are the immune evasion techniques of Group B Strep?
capsular Sialic acid binds factor H --> complement C3b convertase degradation; prevents complement deposition; serves as anti-phagocytic
How many types of Group B strep exist and how are they characterized?
9 serotypes
characterized by capsular polysaccharides, all containing sialic acid
Type III most common
Prevalence of GBS colonization and infections in pregnant women and neonates?
10-40% of women colonized

50% of infants colonized at birth

2% develop infections
Normal habitat of GBS?
GI Tract, vagina; may colonize glans penis

may ascend into amniotic fluid
What types of infections are caused by GBS in neonates? Mortality rates?
Meningitis, pneumonia, sepsis

may cause premature birth or membrane rupture.

fatality 5-20%
What types of infections does GBS cause in adults and what are the mortality rates?
pregnant mothers: peripartum chorioamnionitis (infection of fetal membranes)

immunocompromised, elderly: bacteremia

~40% fatality
Tx of GBS infections?
Penicillin + aminoglycoside combo treatment.

prophylactic screening of pregnant mothers prior to delivery
Which spp. of viridans strep contribute to dental caries and bacterial endocarditis (in untreated sepsis)?
S. mutans, S. sanguis

normal inhabitants of mouth; produce glucans to adhere to teeth
Which spp. of viridans strep contributes to colon carcinomas?
S. bovis, Group D strep but differentiated from Enterococci
Which spp. of viridans strep causes deep tissue infections, bacteremia, and oral infections?
S. milleri group

more prone to spreading than most other Streptococcal infections.
What are the benefits offered by commensal bacteria?
-compete w/pathogens for host receptors
-compete w/pathogens for nutrients
-exclusion of pathogens
-nutritional efficiency (vitamin K)
-priming of immune system
Conc of bacteria per mL of saliva?
Conc of bacteria per gm of feces?
10e10 to 10e11 per mL volume in colon; feces 25% bacteria by weight
Oxygen requirements of microbiota in colon?
90% anaerobes
10% aerobes --> use up all O2 quickly.
What population is most prone to Streptococcal meningitis?
What factors increase risk of colonization with Strep pneumoniae?
child contact

2/3 of children colonized
5-70% of adults depending on conditions.
Protocol for dx of Strep pneumoniae infection?
culture: optochin sensitive, alpha hemolysis on blood agar

PCR, antibody detection (quellung reaction, slide agglutination test)
Abx for tx of Strep pneumoniae infections?

What is the problem with clinical rapid Ag detection for dx of Strep pyogenes pharyngitis?
only 90-95% accurate.

must follow up with culture.
Define Infectivity.
(# diseased) / (# susceptible exposed) x 100%
Define "carrier state/latency."
not evident but potentially discernible (ex. by PCR)
What are the two types of pharyngitis and which is more common?
Viral <--more common
Bacterial (Strep throat)
What is the primary limiting nutrient for bacteria in our bodies?

thus we have lactoferrin (mucus) and transferrin (serum); bacteria have siderophores
When is Streptococcal pneumonia most frequent?
winter (some also say early spring)

reasons unknown
For A/B subunit toxins, what are the roles of each subunit?
A = catalytic subunit
B = membrane binding subunit, translocates A into cytoplasm once endocytotic vesicle is acidified.
What is Fibrinogen?
Serum protein cleaved by THROMBIN to form FIBRIN blood clots
What is Fibronectin?
Protein component of connective tissue.
What is Plasminogen?
Zymogen. Activated to form PLASMIN which degrades blood clots.
What is Thrombin/Prothrombin?
Enzyme that cleaves fibrinogen --> fibrin for blood clots.
What are some forms of mobile virulence determinants?
-bacteriophage infection/lysogeny
-plasmids (conjugation)
Principle of ELISA assay?
1. pt serum bound to solid substrate
2. pthg-specific AB bound
3. Fc-specific, enzyme tagged AB binds to mark where initial AB bound.
4. level of enzyme activity assayed (usu. by color change)
Principle of Western Blot?
1. pthg proteins run on gel.
2. bands transferred (blotted) onto solid filter.
3. filter incubated w/pt serum to see which Ag's pt has mounted a response to.
Principle of competitive EIA (Enzyme Immunoassay)?
1. Ag specific AB bound to substrate.
2. pure radiolabeled Ag + pt serum added.
3. Ag in serum competes w/radiolabeled Ag for Ab binding.
4. Reduced radioactivity indicates Ag present in pt serum.
Principle of Agglutination test?
mix pt serum + Ab-coated latex beads.

formation of immune complexes = clumping = + result.
When is PCR most useful in the clinical lab?
ID organisms that are difficult or impossible to cultivate in vitro.
Possible shortcomings of PCR?
-contamination yields false results
-can't observe properties of organism/run phenotypic tests--all you have is genetic markers.
What are the main inflammatory cytokines?
What is myeloperoxidase?
enzyme produced by NEUTROPHILS.

makes BLEACH. cool!
Examples and functions of cationic peptides involved in innate immune response?
alpha/beta defensins. bind to (-) charged bacterial membrane.

from epi/endothelial cells, phagocytes

broad-spectrum antimicrobial, helps ramp up innate immune response
Examples of phagocytes' O2-dependent mechanisms of pathogen destruction?
Myeloperoxidase: H2O2 + Cl- --> HOCl, bleach
Examples of phagocytes' O2-INdependent mechanisms of pathogen destruction?
other enzymes, etc.
How can one distinguish a primary from a secondary immune responses?
Primary IgM > IgG (no CSR yet)
Secondary IgG > IgM

Onset of secondary response much faster and [Ig] much higher
Function of pneumolysin?
lung damage, may impair phagocytes

release of inflammatory cell guts
Function of autolysin?
contributes to the release of inflammatory mediators (cell guts)