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15 Cards in this Set

  • Front
  • Back
Superantigens
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
S. aureus
TSST-1 superantigen causes toxic shock syndrome
S. pyogenes
Scarlet fever-erythrogenic toxin causes toxic shock-like syndrome
ADP ribosylating A-B toxins
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
C. diphtheriae
Inactivates elongation factor (EF-2) casuses pharyngitis and pseudomembrane in throat. NEVER SCRAPE!
V. cholerae
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
E. coli
Heat labile toxin stim adenylate cyclase. head stable toxin stimulates guanylate cyclase. both cause watery diarrhea.
B. pertussis
Increases cAMP by inhibiting Gaphai, causes whooping cough, inhibits chemokine receptor, causing lymphocytosis
C. perfringes
alpha toxin, causes gas grene
C. tetani
blocks the release of GABA and glycine, causes "lockjaw"
C. botulism
blocks the release of Ach, causing anticholinergic symptoms, CNS paralysis, especially cranial nerves
B. anthracis
edema factor, part of toxin complex is an adenylate cyclase increasing cAMP
Shigella
Shiga toxin (also produced by E.coli O157:H7) cleaves host cell rRNA, enhances cytokine release, causing HUS
S. pyogenes
Streptolysin O is a hemolysin, antigen for ASO antibody which is the Dx for rheumatic fever
cAMP inducers
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