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59 Cards in this Set
- Front
- Back
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What is the role of Streptococcal Protein M in pathogenesis?
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adhesion: binds to keratinocytes
immune evasion: binds fibrinogen, binds factor H (C3 convertase degradation), antiphagocytic 80 serotypes mimics glomerular proteins --> glomerulonephritis |
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What is the role of Streptococcal LTA in pathogenesis of GAS?
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binds epithelial fibronectin--aids adhesion and colonization of host.
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What is the role of Streptococcal hyaluronic acid capsule in pathogenesis?
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anti-phagocytic
mimics our own connective tissue --> immune evasion |
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Why is Acute Rheumatic Fever often associated with streptococcal pharyngitis?
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M protein mimics myosin --> autoimmunity
crossreactive AB's to sarcolemma membranes of heart valves and myocardium lifelong susceptibility to bacterial endocarditis, cardiomyopathy |
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What is the significance of Streptococcal Pyrogenic Exotoxins?
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SPE A, B, and C
SPE A and C are superantigens! |
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What secreted "weaponry" does Group A Strep have at its disposal?
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SPE A, B, C
Streptolysin O (all), S (85% of strains) C5a peptidase (degrades C5a) Protein M LTA Streptokinase |
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What is the role of Streptokinase in pathogenesis of Streptococcus infections?
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converts host plasminogen (zymogen)--> plasmin (enzyme). results in fibrin/blood clot degradation.
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Describe pathogenesis of Scarlet Fever.
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GAS, SPE intoxication.
pharyngitis with red, peeling rash. "strawberry tongue," hemorrhage on palate |
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Describe pathogenesis of Impetigo.
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GAS
superficial skin infection of 2-5 y/o; traumatic inoculation resulting in crusty raised lesions |
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Describe pathogenesis of Erysipelas.
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GAS, infection of lower dermis in fatty areas.
older or immunocompromised pts; lesions clearly demarcated with raised edges and orange-peel texture. |
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Describe the pathogenesis of cellulitis.
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GAS infection of connective tissues in deeper dermal layers of skin.
risk grp: diabetics, immunocompromised, elderly complications: sepsis, spread to necrotizing fasciitis |
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Describe the pathogenesis of acute glomerulonephritis.
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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 |
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Describe the pathogenesis of Streptococcal Toxic Shock Syndrome (STSS).
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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 |
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How are GAS infections diagnosed?
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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 |
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What is the standard treatment for GAS infections?
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penicillin.
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What are the immune evasion techniques of Group B Strep?
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capsular Sialic acid binds factor H --> complement C3b convertase degradation; prevents complement deposition; serves as anti-phagocytic
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How many types of Group B strep exist and how are they characterized?
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9 serotypes
characterized by capsular polysaccharides, all containing sialic acid Type III most common |
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Prevalence of GBS colonization and infections in pregnant women and neonates?
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10-40% of women colonized
50% of infants colonized at birth 2% develop infections |
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Normal habitat of GBS?
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GI Tract, vagina; may colonize glans penis
may ascend into amniotic fluid |
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What types of infections are caused by GBS in neonates? Mortality rates?
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Meningitis, pneumonia, sepsis
may cause premature birth or membrane rupture. fatality 5-20% |
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What types of infections does GBS cause in adults and what are the mortality rates?
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pregnant mothers: peripartum chorioamnionitis (infection of fetal membranes)
immunocompromised, elderly: bacteremia ~40% fatality |
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Tx of GBS infections?
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Penicillin + aminoglycoside combo treatment.
prophylactic screening of pregnant mothers prior to delivery |
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Which spp. of viridans strep contribute to dental caries and bacterial endocarditis (in untreated sepsis)?
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S. mutans, S. sanguis
normal inhabitants of mouth; produce glucans to adhere to teeth |
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Which spp. of viridans strep contributes to colon carcinomas?
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S. bovis, Group D strep but differentiated from Enterococci
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Which spp. of viridans strep causes deep tissue infections, bacteremia, and oral infections?
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S. milleri group
more prone to spreading than most other Streptococcal infections. |
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What are the benefits offered by commensal bacteria?
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-compete w/pathogens for host receptors
-compete w/pathogens for nutrients -exclusion of pathogens -nutritional efficiency (vitamin K) -priming of immune system |
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Conc of bacteria per mL of saliva?
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10e8/mL
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Conc of bacteria per gm of feces?
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10e10 to 10e11 per mL volume in colon; feces 25% bacteria by weight
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Oxygen requirements of microbiota in colon?
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90% anaerobes
10% aerobes --> use up all O2 quickly. |
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What population is most prone to Streptococcal meningitis?
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infants.
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What factors increase risk of colonization with Strep pneumoniae?
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crowding
child contact 2/3 of children colonized 5-70% of adults depending on conditions. |
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Protocol for dx of Strep pneumoniae infection?
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culture: optochin sensitive, alpha hemolysis on blood agar
PCR, antibody detection (quellung reaction, slide agglutination test) |
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Abx for tx of Strep pneumoniae infections?
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Penicillin
Erythromycin Levofloxacin Vancomycin "PELVi's" |
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What is the problem with clinical rapid Ag detection for dx of Strep pyogenes pharyngitis?
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only 90-95% accurate.
must follow up with culture. |
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Define Infectivity.
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(# diseased) / (# susceptible exposed) x 100%
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Define "carrier state/latency."
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not evident but potentially discernible (ex. by PCR)
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What are the two types of pharyngitis and which is more common?
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Viral <--more common
Bacterial (Strep throat) |
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What is the primary limiting nutrient for bacteria in our bodies?
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IRON.
thus we have lactoferrin (mucus) and transferrin (serum); bacteria have siderophores |
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When is Streptococcal pneumonia most frequent?
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winter (some also say early spring)
reasons unknown |
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For A/B subunit toxins, what are the roles of each subunit?
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A = catalytic subunit
B = membrane binding subunit, translocates A into cytoplasm once endocytotic vesicle is acidified. |
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What is Fibrinogen?
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Serum protein cleaved by THROMBIN to form FIBRIN blood clots
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What is Fibronectin?
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Protein component of connective tissue.
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What is Plasminogen?
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Zymogen. Activated to form PLASMIN which degrades blood clots.
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What is Thrombin/Prothrombin?
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Enzyme that cleaves fibrinogen --> fibrin for blood clots.
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What are some forms of mobile virulence determinants?
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-bacteriophage infection/lysogeny
-plasmids (conjugation) -transposons |
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Principle of ELISA assay?
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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) |
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Principle of Western Blot?
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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. |
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Principle of competitive EIA (Enzyme Immunoassay)?
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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. |
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Principle of Agglutination test?
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mix pt serum + Ab-coated latex beads.
formation of immune complexes = clumping = + result. |
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When is PCR most useful in the clinical lab?
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ID organisms that are difficult or impossible to cultivate in vitro.
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Possible shortcomings of PCR?
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-contamination yields false results
-can't observe properties of organism/run phenotypic tests--all you have is genetic markers. |
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What are the main inflammatory cytokines?
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IL-1
IL-6 IL-8 TNF-alpha |
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What is myeloperoxidase?
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enzyme produced by NEUTROPHILS.
makes BLEACH. cool! |
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Examples and functions of cationic peptides involved in innate immune response?
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alpha/beta defensins. bind to (-) charged bacterial membrane.
from epi/endothelial cells, phagocytes broad-spectrum antimicrobial, helps ramp up innate immune response |
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Examples of phagocytes' O2-dependent mechanisms of pathogen destruction?
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Myeloperoxidase: H2O2 + Cl- --> HOCl, bleach
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Examples of phagocytes' O2-INdependent mechanisms of pathogen destruction?
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defensins
lysozyme proteases other enzymes, etc. |
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How can one distinguish a primary from a secondary immune responses?
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Primary IgM > IgG (no CSR yet)
Secondary IgG > IgM Onset of secondary response much faster and [Ig] much higher |
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Function of pneumolysin?
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lung damage, may impair phagocytes
release of inflammatory cell guts |
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Function of autolysin?
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contributes to the release of inflammatory mediators (cell guts)
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