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Questions and Answers
What is the mechanism of action of the diphtheria toxin?
What is the mechanism of action of the diphtheria toxin?
- Inactivates the 60S ribosome
- Degrades cell membranes
- Increases fluid secretion by overactivating adenylate cyclase
- Inhibits protein synthesis through ADP-ribosylation of EF-2 (correct)
Which bacteria produce a toxin that increases intracellular cAMP levels leading to increased fluid secretion?
Which bacteria produce a toxin that increases intracellular cAMP levels leading to increased fluid secretion?
- Bacillus anthracis
- Enterohemorrhagic E coli (correct)
- Corynebacterium diphtheriae
- Vibrio cholerae (correct)
Which toxin is responsible for causing spastic paralysis by preventing the release of inhibitory neurotransmitters?
Which toxin is responsible for causing spastic paralysis by preventing the release of inhibitory neurotransmitters?
- Botulinum toxin
- Cholera toxin
- Erythrogenic exotoxin A
- Tetanospasmin (correct)
Which of the following manifestations is associated with the cholera toxin?
Which of the following manifestations is associated with the cholera toxin?
What type of toxin does Pseudomonas aeruginosa secrete?
What type of toxin does Pseudomonas aeruginosa secrete?
How does Shiga toxin affect cellular mechanisms?
How does Shiga toxin affect cellular mechanisms?
What is the role of the botulinum toxin?
What is the role of the botulinum toxin?
What distinguishes the action of Exotoxin A from Shiga toxin?
What distinguishes the action of Exotoxin A from Shiga toxin?
Which bacterium produces a toxin that degrades cell membranes and leads to spastic paralysis?
Which bacterium produces a toxin that degrades cell membranes and leads to spastic paralysis?
Which of the following toxins inhibits protein synthesis by inactivating the elongation factor EF-2?
Which of the following toxins inhibits protein synthesis by inactivating the elongation factor EF-2?
What mechanism does the cholera toxin use to affect the host?
What mechanism does the cholera toxin use to affect the host?
Which bacteria produce a toxin that results in a characteristic 'rice-water' diarrhea?
Which bacteria produce a toxin that results in a characteristic 'rice-water' diarrhea?
What kind of toxin does Enterotoxigenic E. coli produce?
What kind of toxin does Enterotoxigenic E. coli produce?
Which of the following best describes the action of Shiga toxin?
Which of the following best describes the action of Shiga toxin?
What is one of the effects of the anthrax toxin produced by Bacillus anthracis?
What is one of the effects of the anthrax toxin produced by Bacillus anthracis?
Which toxin is associated with the disease symptoms of whooping cough?
Which toxin is associated with the disease symptoms of whooping cough?
Which mechanism is associated with the anthrax toxin produced by Bacillus anthracis?
Which mechanism is associated with the anthrax toxin produced by Bacillus anthracis?
What is one of the primary effects of the shiga toxin produced by Shigella spp.?
What is one of the primary effects of the shiga toxin produced by Shigella spp.?
Which bacterium produces a toxin that leads to spastic paralysis by preventing inhibitory neurotransmitter release?
Which bacterium produces a toxin that leads to spastic paralysis by preventing inhibitory neurotransmitter release?
What symptom is characteristic of infection by Vibrio cholerae due to its cholera toxin?
What symptom is characteristic of infection by Vibrio cholerae due to its cholera toxin?
What effect does the diphtheria toxin from Corynebacterium diphtheriae have on host cells?
What effect does the diphtheria toxin from Corynebacterium diphtheriae have on host cells?
Which of the following toxins increases intracellular cAMP levels leading to diarrhea?
Which of the following toxins increases intracellular cAMP levels leading to diarrhea?
Which bacterium's toxin is associated with enhanced cytokine release and hemolytic-uremic syndrome?
Which bacterium's toxin is associated with enhanced cytokine release and hemolytic-uremic syndrome?
What type of effect is observed from the botulinum toxin in Clostridium botulinum?
What type of effect is observed from the botulinum toxin in Clostridium botulinum?
Which mechanism is associated with the diphtheria toxin?
Which mechanism is associated with the diphtheria toxin?
What effect does the anthrax toxin produced by Bacillus anthracis have?
What effect does the anthrax toxin produced by Bacillus anthracis have?
Which of the following toxins is known to lyse cell membranes?
Which of the following toxins is known to lyse cell membranes?
Which organism's toxin leads to the characteristic 'rice-water' diarrhea?
Which organism's toxin leads to the characteristic 'rice-water' diarrhea?
What is a primary mechanism by which shiga toxin affects intestinal function?
What is a primary mechanism by which shiga toxin affects intestinal function?
Which of the following best describes the action of botulinum toxin?
Which of the following best describes the action of botulinum toxin?
What effect is associated with the exfoliative toxin from Staphylococcus aureus?
What effect is associated with the exfoliative toxin from Staphylococcus aureus?
Which toxin from Enterotoxigenic E. coli mimics adenylate cyclase activity?
Which toxin from Enterotoxigenic E. coli mimics adenylate cyclase activity?
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Study Notes
Bacteria with Exotoxins
-
Corynebacterium diphtheriae
- Produces diphtheria toxin that inhibits protein synthesis by ADP-ribosylating elongation factor EF-2.
- Causes pharyngitis with pseudomembranes, severe lymphadenopathy ("bull neck"), and myocarditis leading to host cell death.
-
Pseudomonas aeruginosa
- Releases exotoxin A, which inhibits protein synthesis by inactivating the 60S ribosome via rRNA modification.
- Results in gastrointestinal mucosal damage, dysentery, and hemolytic-uremic syndrome (HUS), typically associated with EHEC serotype O157:H7. Unlike Shigella, does not invade host cells.
-
Shigella spp
- Produces Shiga toxin that overactivates adenylate cyclase, increasing cAMP and causing fluid secretion via increased Cl- and H2O efflux in the gut.
- Characterized by increased cAMP and associated gastrointestinal effects.
-
Enterohemorrhagic E. coli (EHEC)
- Also produces Shiga toxin; alters fluid secretion by overactivating guanylate cyclase, resulting in increased cGMP and decreased NaCl and H2O resorption in the gut.
- Bacteria linked to severe gastrointestinal disease.
-
Enterotoxigenic E. coli (ETEC)
- Produces heat-labile (LT) and heat-stable (ST) toxins that mimic adenylate cyclase, leading to elevated cAMP levels.
- Likely responsible for edema surrounding black eschar in cutaneous anthrax cases.
-
Bacillus anthracis
- Produces anthrax toxin that activates adenylate cyclase, raising cAMP levels by inhibiting the Gi subunit.
- Causes profuse "rice-water" diarrhea in affected individuals.
-
Vibrio cholerae
- Produces cholera toxin which disrupts neurotransmitter release by cleaving SNARE proteins, essential for vesicular fusion.
- Associated with severe diarrhea and "whooping cough" characterized by a cough that causes a "whoop" sound; can lead to significant symptoms in adults.
-
Bordetella pertussis
- Produces pertussis toxin, a phospholipase that degrades cell membranes, leading to spastic paralysis by preventing the release of inhibitory neurotransmitters such as GABA and glycine.
- Causes symptoms like risus sardonicus, trismus (lockjaw), and opisthotonos; linked to infant botulism from spore ingestion.
-
Clostridium tetani
- Produces tetanospasmin, a protein that degrades cell membranes contributing to spastic paralysis.
- Associated with symptoms of myonecrosis and characteristic "gas gangrene" observed on blood agar (double zone of hemolysis).
-
Clostridium botulinum
- Produces botulinum toxin, which acts as a superantigen causing shock by cross-linking the TCR beta region to MHC class II on APCs, leading to excessive release of IL-1, IL-2, and IFN-γ.
- Responsible for severe botulism when spores are ingested or toxin is consumed.
Bacteria with Exotoxins
-
Corynebacterium diphtheriae
- Produces diphtheria toxin that inhibits protein synthesis by ADP-ribosylating elongation factor EF-2.
- Causes pharyngitis with pseudomembranes, severe lymphadenopathy ("bull neck"), and myocarditis leading to host cell death.
-
Pseudomonas aeruginosa
- Releases exotoxin A, which inhibits protein synthesis by inactivating the 60S ribosome via rRNA modification.
- Results in gastrointestinal mucosal damage, dysentery, and hemolytic-uremic syndrome (HUS), typically associated with EHEC serotype O157:H7. Unlike Shigella, does not invade host cells.
-
Shigella spp
- Produces Shiga toxin that overactivates adenylate cyclase, increasing cAMP and causing fluid secretion via increased Cl- and H2O efflux in the gut.
- Characterized by increased cAMP and associated gastrointestinal effects.
-
Enterohemorrhagic E. coli (EHEC)
- Also produces Shiga toxin; alters fluid secretion by overactivating guanylate cyclase, resulting in increased cGMP and decreased NaCl and H2O resorption in the gut.
- Bacteria linked to severe gastrointestinal disease.
-
Enterotoxigenic E. coli (ETEC)
- Produces heat-labile (LT) and heat-stable (ST) toxins that mimic adenylate cyclase, leading to elevated cAMP levels.
- Likely responsible for edema surrounding black eschar in cutaneous anthrax cases.
-
Bacillus anthracis
- Produces anthrax toxin that activates adenylate cyclase, raising cAMP levels by inhibiting the Gi subunit.
- Causes profuse "rice-water" diarrhea in affected individuals.
-
Vibrio cholerae
- Produces cholera toxin which disrupts neurotransmitter release by cleaving SNARE proteins, essential for vesicular fusion.
- Associated with severe diarrhea and "whooping cough" characterized by a cough that causes a "whoop" sound; can lead to significant symptoms in adults.
-
Bordetella pertussis
- Produces pertussis toxin, a phospholipase that degrades cell membranes, leading to spastic paralysis by preventing the release of inhibitory neurotransmitters such as GABA and glycine.
- Causes symptoms like risus sardonicus, trismus (lockjaw), and opisthotonos; linked to infant botulism from spore ingestion.
-
Clostridium tetani
- Produces tetanospasmin, a protein that degrades cell membranes contributing to spastic paralysis.
- Associated with symptoms of myonecrosis and characteristic "gas gangrene" observed on blood agar (double zone of hemolysis).
-
Clostridium botulinum
- Produces botulinum toxin, which acts as a superantigen causing shock by cross-linking the TCR beta region to MHC class II on APCs, leading to excessive release of IL-1, IL-2, and IFN-γ.
- Responsible for severe botulism when spores are ingested or toxin is consumed.
Bacteria with Exotoxins
-
Corynebacterium diphtheriae
- Produces diphtheria toxin that inhibits protein synthesis by ADP-ribosylating elongation factor EF-2.
- Causes pharyngitis with pseudomembranes, severe lymphadenopathy ("bull neck"), and myocarditis leading to host cell death.
-
Pseudomonas aeruginosa
- Releases exotoxin A, which inhibits protein synthesis by inactivating the 60S ribosome via rRNA modification.
- Results in gastrointestinal mucosal damage, dysentery, and hemolytic-uremic syndrome (HUS), typically associated with EHEC serotype O157:H7. Unlike Shigella, does not invade host cells.
-
Shigella spp
- Produces Shiga toxin that overactivates adenylate cyclase, increasing cAMP and causing fluid secretion via increased Cl- and H2O efflux in the gut.
- Characterized by increased cAMP and associated gastrointestinal effects.
-
Enterohemorrhagic E. coli (EHEC)
- Also produces Shiga toxin; alters fluid secretion by overactivating guanylate cyclase, resulting in increased cGMP and decreased NaCl and H2O resorption in the gut.
- Bacteria linked to severe gastrointestinal disease.
-
Enterotoxigenic E. coli (ETEC)
- Produces heat-labile (LT) and heat-stable (ST) toxins that mimic adenylate cyclase, leading to elevated cAMP levels.
- Likely responsible for edema surrounding black eschar in cutaneous anthrax cases.
-
Bacillus anthracis
- Produces anthrax toxin that activates adenylate cyclase, raising cAMP levels by inhibiting the Gi subunit.
- Causes profuse "rice-water" diarrhea in affected individuals.
-
Vibrio cholerae
- Produces cholera toxin which disrupts neurotransmitter release by cleaving SNARE proteins, essential for vesicular fusion.
- Associated with severe diarrhea and "whooping cough" characterized by a cough that causes a "whoop" sound; can lead to significant symptoms in adults.
-
Bordetella pertussis
- Produces pertussis toxin, a phospholipase that degrades cell membranes, leading to spastic paralysis by preventing the release of inhibitory neurotransmitters such as GABA and glycine.
- Causes symptoms like risus sardonicus, trismus (lockjaw), and opisthotonos; linked to infant botulism from spore ingestion.
-
Clostridium tetani
- Produces tetanospasmin, a protein that degrades cell membranes contributing to spastic paralysis.
- Associated with symptoms of myonecrosis and characteristic "gas gangrene" observed on blood agar (double zone of hemolysis).
-
Clostridium botulinum
- Produces botulinum toxin, which acts as a superantigen causing shock by cross-linking the TCR beta region to MHC class II on APCs, leading to excessive release of IL-1, IL-2, and IFN-γ.
- Responsible for severe botulism when spores are ingested or toxin is consumed.
Bacteria with Exotoxins
-
Corynebacterium diphtheriae
- Produces diphtheria toxin that inhibits protein synthesis by ADP-ribosylating elongation factor EF-2.
- Causes pharyngitis with pseudomembranes, severe lymphadenopathy ("bull neck"), and myocarditis leading to host cell death.
-
Pseudomonas aeruginosa
- Releases exotoxin A, which inhibits protein synthesis by inactivating the 60S ribosome via rRNA modification.
- Results in gastrointestinal mucosal damage, dysentery, and hemolytic-uremic syndrome (HUS), typically associated with EHEC serotype O157:H7. Unlike Shigella, does not invade host cells.
-
Shigella spp
- Produces Shiga toxin that overactivates adenylate cyclase, increasing cAMP and causing fluid secretion via increased Cl- and H2O efflux in the gut.
- Characterized by increased cAMP and associated gastrointestinal effects.
-
Enterohemorrhagic E. coli (EHEC)
- Also produces Shiga toxin; alters fluid secretion by overactivating guanylate cyclase, resulting in increased cGMP and decreased NaCl and H2O resorption in the gut.
- Bacteria linked to severe gastrointestinal disease.
-
Enterotoxigenic E. coli (ETEC)
- Produces heat-labile (LT) and heat-stable (ST) toxins that mimic adenylate cyclase, leading to elevated cAMP levels.
- Likely responsible for edema surrounding black eschar in cutaneous anthrax cases.
-
Bacillus anthracis
- Produces anthrax toxin that activates adenylate cyclase, raising cAMP levels by inhibiting the Gi subunit.
- Causes profuse "rice-water" diarrhea in affected individuals.
-
Vibrio cholerae
- Produces cholera toxin which disrupts neurotransmitter release by cleaving SNARE proteins, essential for vesicular fusion.
- Associated with severe diarrhea and "whooping cough" characterized by a cough that causes a "whoop" sound; can lead to significant symptoms in adults.
-
Bordetella pertussis
- Produces pertussis toxin, a phospholipase that degrades cell membranes, leading to spastic paralysis by preventing the release of inhibitory neurotransmitters such as GABA and glycine.
- Causes symptoms like risus sardonicus, trismus (lockjaw), and opisthotonos; linked to infant botulism from spore ingestion.
-
Clostridium tetani
- Produces tetanospasmin, a protein that degrades cell membranes contributing to spastic paralysis.
- Associated with symptoms of myonecrosis and characteristic "gas gangrene" observed on blood agar (double zone of hemolysis).
-
Clostridium botulinum
- Produces botulinum toxin, which acts as a superantigen causing shock by cross-linking the TCR beta region to MHC class II on APCs, leading to excessive release of IL-1, IL-2, and IFN-γ.
- Responsible for severe botulism when spores are ingested or toxin is consumed.
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