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Microbiology > Endotoxins of Bacteria > Flashcards

Endotoxins of Bacteria Flashcards

1
Q

What are the six general ways bacterial exotoxins assist in the pathogenesis of infectious disease?

A
  • 1) inhibit host cell protein synthesis (causes cell death)
  • 2) increase fluid secretion
  • 3) inhibit phagocytic ability (promotes survival)
  • 4) inhibit release of NTs
  • 5) lyse cell membranes (causes cell death)
  • 6) shock (these exotoxins are superantigens)
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2
Q

How do endotoxins cause damage?

A
  • (toxic portion of LPS is largely lipid A)
  • endotoxins activate:
  • IL-1, TNF, and nitric oxide (causes fever and hypotension)
  • complement (causes edema and neutrophil chemotaxis)
  • tissue factor III AKA thromboplastin (causes DIC)
  • note that endotoxins are extremely heat stable, but also require very large doses to cause damage/disease
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3
Q

What are the two mechanisms exotoxins use to inhibit host cell protein synthesis? Which toxins (and organisms) use each?

A
  • 1) inactivate elongation factor (EF-2): diphtheria toxin (Corynebacterium diphtheriae) and exotoxin A (Pseudomonas aeruginosa)
  • 2) inactivate the 60S ribosomal subunit: shiga toxin (Shigella spp.) and shiga-like toxin (EHEC)
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4
Q

Which toxins (and organisms) increase fluid secretion?

A
  • heat-labile toxin (LT) and heat-stable toxin (ST) of ETEC
  • edema factor of Bacillus anthracis
  • cholera toxin of Vibrio cholerae
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5
Q

Which toxins (and organisms) inhibit phagocytic ability?

A
  • pertussis toxin of Bordetella pertussis
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6
Q

Which toxins (and organisms) inhibit NT release? How do these toxins work in general?

A
  • tetanospasmin of Clostridium tetani
  • botulinum toxin of Clostridium botulinum
  • both are proteases that cleave SNARE proteins (SNARE proteins are required for NT release)
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7
Q

Which toxins (and organisms) lyse cell membranes?

A
  • alpha toxin of Clostridium perfringens

- streptolysin O: Strep. pyogenes

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8
Q

Which toxins are superantigens? How do superantigens work?

A
  • toxic shock syndrome toxin (TSST-1) of Staph. aureus
  • exotoxin A of Strep. pyogenes (group A beta-hemolytic Strep)
  • superantigens are able to activate any T-cell, resulting in a massive release of cytokines (especially IL-1 and TNF-alpha), resulting in shock
  • manifests as toxic shock syndrome: fever, rash, shock
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9
Q

What exotoxin is released by Corynebacterium diphtheriae? How does it work? How does the disease manifest as a result?

A
  • diphtheria toxin
  • inhibits protein synthesis by inactivating elongation factor (EF-2) [same mechanism as Pseudomonas’ exotoxin A]
  • manifests as pharyngitis and severe lymphadenopathy with grey pseudomembranes in the throat
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10
Q

What exotoxin is released by Pseudomonas aeruginosa? How does it work? How does the disease manifest as a result?

A
  • exotoxin A
  • inhibits protein synthesis by inactivating elongation factor (EF-2) [same mechanism as diphtheria toxin]
  • manifests just as cell death
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11
Q

What exotoxin is released by Shigella spp.? How does it work? How does the disease manifest as a result?

A
  • shiga toxin (ST)
  • inhibits protein synthesis by inactivating the 60S ribosomal subunit [same mechanism as EHEC’s shiga-like toxin]
  • manifests as dysentery and hemolytic-uremic syndrome
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12
Q

What exotoxin is released by EHEC? How does it work? How does the disease manifest as a result?

A
  • shiga-like toxin (SLT)
  • inhibits protein synthesis by inactivating the 60S ribosomal subunit [same mechanism as Shigella’s shiga toxin]
  • manifests as dysentery and hemolytic-uremic syndrome
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13
Q

What exotoxin is released by ETEC? How does it work? How does the disease manifest as a result?

A
  • heat-labile and heat-stable toxins (LT and ST); both increase fluid secretion
  • LT over activates adenylate cyclase (raises cAMP) to increase Cl- gut secretion
  • ST over activates guanylate cyclase (raises cGMP) to decrease gut NaCl absorption
  • both result in excess water in the gut, manifesting as watery diarrhea
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14
Q

What exotoxin is released by Bacillus anthracis? How does it work? How does the disease manifest as a result?

A
  • edema factor
  • increases fluid secretion by mimicking adenylate cyclase (raises cAMP) to increase Cl- secretion
  • manifests as the edematous borders of the black lesions seen in cutaneous anthrax
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15
Q

What exotoxin is released by Vibrio cholera? How does it work? How does the disease manifest as a result?

A
  • cholera toxin
  • increases fluid secretion by permanently ACTIVATING Gs in the gut to increase adenylate cyclase (raises cAMP) to increase Cl- gut secretion
  • manifests as severe “rice-water” diarrhea
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16
Q

What exotoxin is released by Bordetella pertussis? How does it work? How does the disease manifest as a result?

A
  • pertussis toxin
  • inhibits phagocytic ability by INHIBITING Gi to increase adenylate cyclase (raises cAMP), impairing phagocytosis
  • manifests as whooping cough, as the organism is unable to be destroyed by phagocytosis
17
Q

What exotoxin is released by Clostridium tetani? How does it work? How does the disease manifest as a result? What about Clostridium botulinum?

A
  • C. tetani: tetanospasmin; prevents the release of inhibitory NTs (GABA and glycine), resulting in tetany (spasticity, rises sardonic, and lockjaw)
  • C. botulinum: botulinum toxin; prevents the release of ACh at the NMJ, resulting in flaccid paralysis/floppy baby
18
Q

What exotoxin is released by Clostridium perfringens? How does it work? How does the disease manifest as a result?

A
  • alpha toxin (lecithinase, which is a phospholipase)
  • lyses cell membranes by degrading phospholipids
  • manifests as myonecrosis and gas gangrene
19
Q

What exotoxin is released by Strep. pyogenes? How does it work? How does the disease manifest as a result?

A
  • streptolysin O
  • lyses cell membranes of RBCs
  • ASO (antibodies against streptolysin O) are used to diagnose rheumatic fever
20
Q

Which exotoxins are A-B toxins? How do these toxins generally function?

A
  • diphtheria toxin, exotoxin A (Pseudomonas), shiga toxin, shiga-like toxin (EHEC); (these all act to inhibit protein synthesis)
  • heat-labile toxin only (ETEC), cholera toxin; (these act to increase fluid secretion)
  • pertussis toxin (acts to inhibit phagocytic ability)
  • A-B toxins have 2 subunits; a B or “binding” subunit and an A or “active” subunit that attaches ADP-ribosyl to disrupt host cell proteins (this is why these toxins are AKA ADP-ribosylating toxins)

Microbiology (16 decks)

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