Exotoxins Flashcards
(16 cards)
What is the mechanism and manifestation of Diphtheria toxin?
Corynebacterium diphtheriae’s diphtheria toxin inactivates elongation factor (EF-2) which manifests as pharyngitis with psudomembranes in the throat and severe LAD (bull neck)
What is the mechanism and manifestation of Diphtheria toxin?
Corynebacterium diphtheriae’s diphtheria toxin inactivates elongation factor (EF-2) which manifests as pharyngitis with psudomembranes in the throat and severe LAD (bull neck)
What bacteria releases exotoxin A and what is the mechanism?
Psudomonas aeruginosa, the toxin inactivates EF-2 (elongation factor) and causes host cell death
Which bacteria release Shiga toxin and Shiga-like toxin and what is the mechanism of action?
Shigella spp -> shiga toxin causes GI mucosal damage -> dysentery; enhances cytokine release causing HUS EHEC (especially O157:H7) -> shiga-like toxin causes cytokine release -> HUS (does not invade host cells like shigella)
What bacteria releases Heat-labile toxin (LT) and Heat-stable toxin (ST)? What is the mechanism of each toxin?
Enterotoxigenic E. coli (ETEC) -> LT overactivates adenylate cyclase -> increase cAMP-> increase Cl- secretion in gut and water follows –> watery diarrhea ST-> overactivates guanylate cyclase-> increase cGMP-> decrease NaCl resorption (and water) in gut –> watery diarrhea “labile in the Air (adenylate cyclase), stable on the Ground (Guanylate cyclase)”
Edema toxin
Released by bacillus anthracis, mimics adenylate cyclase enzyme –> increases cAMP; likely responsible for characteristic edematous borders of black eschar
Cholera toxin
vibrio cholera, overactivates adenylate cyclase -> increase in cAMP by PERMANENTLY activating Gs -> increase Cl- secretion and water efflux –> voluminous “rice water” diarrhea
Pertussis toxin
Bordetella pertussis, toxin disables Gi -> overactivates adenylate cyclase -> increase cAMP, impairs phagocytosis
Tetanospasmin
clostridium tetani, protease cleaves SNARE and prevents release of inhibitory (GABA and glycine) NTs from Renshaw cells in spinal cord -> spasticity, risus sardonicus, “lock jaw”
Botulinum toxin
clostridium botulinum, protease cleaves SNARE and prevents release of stimulatory (ACh) NTs at NM junctions -> flaccid paralysis
Botulinum toxin
clostridium botulinum, protease cleaves SNARE and prevents release of stimulatory (ACh) NTs at NM junctions -> flaccid paralysis
alpha toxin
Clostridium perfingens, phospholipase (lecithinase) degrades tissue and cell membranes -> myonecrosis “gas gangrene” and hemolysis: “double zone” of hemolysis on blood agar
streptolysin O
Streptococcus pyogenes, toxin is a protein that degrades cell membrane -> lyses RBCs; contributes to beta-hemolysis; host Abs against toxin (ASO) used to diagnose RF
Toxic shock syndrome toxin (TSST-1)
Staph aureus, toxin binds to MHC II and TCR causing large release of IL-1, IL-2, IFN-gamma, TNF-alpha –> toxic shock syndrome: fever, rash, shock; other toxins can cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin)
Exotoxin A (causing toxic shock syndrome)
Strep pyogenes, exotoxin A binds to MHC II and TCR causing large release of IL-1, IL-2, IFN-gamma, TNF-alpha –> toxic shock syndrome: fever, rash, shock
What is the mechanism and resulting manifestations of endotoxin?
Endotoxin= LPS found in outer membrane of gram- bacteria
Activates macrophages-> IL-1 (fever), TNFalpha (fever and hypotension), NO (hypotension)
Activates compliment -> C3a (hypotension, edema), C5a (PMN chemotaxis)
Activates tissue factor -> coagulation cascade -> DIC
