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15 Cards in this Set
- Front
- Back
Superantigens
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bind directly to MHC II and T-cell receptor simultaneously, activating large numbers of T cells to stimulate release of IFN-gamma and I-2
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S. aureus
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TSST-1 superantigen causes toxic shock syndrome
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S. pyogenes
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Scarlet fever-erythrogenic toxin causes toxic shock-like syndrome
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ADP ribosylating A-B toxins
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interfere with host cells function. B component binds to a receptor on surface of host cell, enabling endocytosis. A component then attaches an ADP-ribosyl to a host cells protein, altering protein function
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C. diphtheriae
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Inactivates elongation factor (EF-2) casuses pharyngitis and pseudomembrane in throat. NEVER SCRAPE!
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V. cholerae
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ADP ribosylation of G protein stimulates adenylyl cyclase, increases the pumping of Cl into gut and decreases sodium absorption. H20 moves into gut lumen, causing voluminous rice-water diarrhea
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E. coli
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Heat labile toxin stim adenylate cyclase. head stable toxin stimulates guanylate cyclase. both cause watery diarrhea.
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B. pertussis
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Increases cAMP by inhibiting Gaphai, causes whooping cough, inhibits chemokine receptor, causing lymphocytosis
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C. perfringes
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alpha toxin, causes gas grene
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C. tetani
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blocks the release of GABA and glycine, causes "lockjaw"
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C. botulism
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blocks the release of Ach, causing anticholinergic symptoms, CNS paralysis, especially cranial nerves
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B. anthracis
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edema factor, part of toxin complex is an adenylate cyclase increasing cAMP
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Shigella
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Shiga toxin (also produced by E.coli O157:H7) cleaves host cell rRNA, enhances cytokine release, causing HUS
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S. pyogenes
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Streptolysin O is a hemolysin, antigen for ASO antibody which is the Dx for rheumatic fever
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cAMP inducers
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V. cholerae toxin
Pertusiss toxin E. coli heat labile toxin (ETEC) B. anthracis toxin cholera, ecoli, and pertussis active adenylate cyclase to increase cAMP, while pertussis is an adenylate cyclase to increase cAMP |