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15 Cards in this Set
- Front
- Back
Corynebacterium diphtheriae
toxin is an ADP ribosylating A-B toxin -B = binding component -- binds to host cell surface receptor, enabling endocytosis -A = active component -- attaches ADP-ribosyl to disrupt host cell proteins |
-inhibits protein synthesis
-diphtheria toxin (an A-B toxin) -inactivates elongation factor (EF-2) -manifests as phrayngitis with pseudomembranes in throat and severe lymphadenopathy (bull neck) |
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Psudomonas aeruginosa
-A-B toxin |
-inhibits protein synthesis
-exotoxin A (an A-B toxin) -inactivates elongation factor (EF-2) -causes host cell death |
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Shigella species
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-inhibits protein synthesis
-Shiga toxin (ST), an A-B toxin -inactivates 60S ribosome by removing adenine from rRNA -GI mucosal damage --> dysentery -ST also enhances cytokine release, causing hemolytic-uremic syndrome (HUS) |
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EHEC: entero-hemorrhagic E. coli
-includes O157:H7 strain |
-inhibits protein synthesis
-shiga-like toxin (SLT), an A-B toxin -inactivates 60S ribosome by removing adenine from rRNA -SLT enhances cytokine releases, causing HUG -but unlike Shigella, EHEC does not invade host cells |
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ETEC: enterotoxigenic E. coli
-two toxins -cause watery diarrhea |
-Increases fluid secretion
-Heat-labile toxin (LT), an A-B toxin -overactivates adenylate cyclase (inc. cAMP), causing inc. Cl- secretion in gut and H2O efflux -Heat-stable toxin (ST) -overactivates guanylate cyclase (inc. cGMP), causing decreased resorption of NaCl and H2O in gut -"stable on the Ground" (cGMP) |
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Bacillus anthracis
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-increases fluid secretion
-toxin is Edema factor -mimics the adenylate cyclase enzyme (inc. cAMP) -likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax* |
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Vibrio cholerae
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-increases fluid secretion
-cholera toxin, an A-B toxin -overactivates adenylate cyclase (inc. cAMP) by permanently activating Gs --> inc. Cl- secretion in gut and H2O efflux -"CHolera causes CHloride secretion" -->voluminous rice-water diarrhea |
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Bordatella pertussis
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-pertussis toxin, an A-B toxin
-inhibits phagocytic ability -overactivates adenylate cyclase (inc cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe -Whooping cough: --child coughs on expiration and "whoops" on inspiration --toxin may not actually cause cough --can cause "100-day cough" in adults |
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Clostridium tetani
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-inhibits release of neurotransmitter
-toxin = tetanospasmin -protease that cleaves SNARE proteins required for neurotransmitter release -spasticity, risus sardonicus, "lockjaw" -toxin prevents release of INHIBITOR neurotransmitters (GABA, glycine) from Renshaw cells and spinal cord [Renshaw cells = inhibitory interneurons found in gray matter of spinal cord] |
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Clostridium botulinum
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-inhibits release of neurotransmitter
-botulinum toxin -like tetanospasmin, botulinum toxin is a protease that cleaves SNARE proteins required for neurotransmitter release -flaccid paralysis, floppy baby syndrome (infant exhibits no muscular tone whatsoever) -toxin prevents release of STIMULATORY signals (ACh) at neuromuscular junction --> flaccid paralysis |
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Clostridium perfringens
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-lyses cell membranes
-alpha toxin -a phospholipse (lecithinase) that degrades tissue and cell membranes -degradation of phospholipids --> myonecrosis ("gas gangrene"), and hemolysis ("double zone" hemolysis on blood agar) |
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Streptococcus pyogenes
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-lyses cell membranes
-toxin = streptolysin O -protein that degrades cell membrane -lyses RBCs – contributes to beta-hemolysis -host antibodies against toxin (ASO) used to diagnose rheumatic fever* --do not confuse with immune complexes of post-streptococcal glomerulonephritis |
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Staphylococcus aureus
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-superantigen causes shock
-toxic shock syndrome toxin (TSST-1) -brings MHCII and TCR in proximity to outside of antigen binding cite --> overwhelming release of IFN-gamma and IL-2 --> shock -toxic shock shyndrome: fever, rash shock -other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin |
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Streptococcus pyogenes
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-superantigen causes shock
-Exotoxin A -brings MHC II and TCR in proximity to outside of antigen binding site --> overwhelming release of IFN-gamma and IL-2 --> shock -toxic shock syndrome: fever, rash, shock |
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Endotoxin
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-an LPS found in outer membrane of gram-negative bacteria (cocci and rods)
-three major effects of endotoxin (especially lipid A) -Activates macrophages --IL-1 --> fever --TNF --> fever and hypotension --nitric oxide --> hypotension -Activates complement --C3a --> hypotension, edema --C5a --> neutrophil chemotaxis -activates tissue factor --coagulation cascade --> DIC |