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Micro toxins

QuestionAnswer
inactivate EF2 Corynebacterium, diphtheriae
exotoxin A psuedomonas
inactivate 60s ribosome by cleaving rRNA Shigella, EHEC
overactivates adenylate cyclase (increased cAMP) -> increased Cl secretion in gut and H2O efflux ETEC (heat labile toxin) vibrio cholearae
heat labile toxin increased adenylate cyclase ETEC
heat stabile toxin increased guanylate cyclase ETEC
mimics the adenylate cyclase enzyme (increased cAMP) bacillus anthracis
edema factor bacillus anthracis
pertussis toxin bordetella pertussis
overactivates adenylate cyclase by disabling Gi, impairing phagocytosis to permit survival of microbe Bordetella pertussis
cleave SNARE protein required for NT release Clostridium tetai Clostridium botulinum
toxin precvents release of inhibitory (GABA and glycine) NT in spinal cord bordetella - tetanospasmin toxin
toxin prevents release of stimulatory Ach signals at musculoskeleat junction, -> flaccid paralysis botulinum toxin
alpha toxin clostridium perfringens
phospholipase that degrades tissue, cell membranes clostridium perfringens
degradation of phospholipids -> myonecrosis ("gas gangrene") and hemolysis ("double zone" of hemolysis on blood agar) clostridium perfringens
protein that degrades cell membrane streptococcus pyogenes
streptolysin O streptococcus pyogenes
lyses RbCs; contributes to beta hemolysis; host antibodies against toxin ASO; used to diagnose rheumatic fever (do not confuse with immune complexes of poststreptococcal glomerulonephritis( streptococcus pyogenes
lyses cell membranes clostridium perfringens streptococcus pyogenes
brinch MHC II and TcR in proximity to cause overwhelming release of IFN gamma and IL2 -> shock strep pyogenes staph aureus
exotoxin A streptococcus pyogenes
TSST-1 staph aureus
toxic shock syndrome: fever, rash, shock strep pyogenes
toxic shock syndrome: fever rash, shock; other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin) staph aureus
Created by: ilovemusic007
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