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Difficulty: MediumInfectious Disease Mechanisms

Match each characteristic clinical presentation of a bacterial infection with the precise molecular mechanism of its primary exotoxin.

  • Profuse, watery diarrhea without fecal leukocytes in a recent travelerConstitutive activation of adenylate cyclase via ADP-ribosylation of Gs protein
  • Trismus, generalized muscle rigidity, and spasms triggered by sensory stimuliInhibition of GABA and glycine release via SNARE protein cleavage in the spinal cord
  • Sore throat, fever, and a grayish-white pharyngeal pseudomembraneInhibition of host cell protein synthesis via ADP-ribosylation of elongation factor-2
  • Prolonged paroxysmal coughing episodes with marked lymphocytosisDisinhibition of adenylate cyclase via ADP-ribosylation of Gi protein

Answer

The clinical presentations correctly map to the following toxin mechanisms: Cholera presentation matches with Gs ADP-ribosylation; Tetanus presentation matches with SNARE cleavage blocking GABA/glycine; Diphtheria presentation matches with EF-2 ADP-ribosylation; Pertussis presentation matches with Gi ADP-ribosylation.
Each bacterial pathogen presented produces a well-characterized exotoxin with a specific mechanism of action. Vibrio cholerae's toxin permanently activates Gs; Clostridium tetani's toxin cleaves SNARE proteins blocking inhibitory neurotransmitters; Corynebacterium diphtheriae's toxin inactivates EF-2 halting protein synthesis; and Bordetella pertussis's toxin disables Gi, removing its inhibitory effect on adenylate cyclase.

Step-by-Step Solution

1
Analyze the first clinical presentation (watery diarrhea in a traveler).
Identified as cholera, caused by Vibrio cholerae.
This is the classic presentation of cholera toxin action in the gastrointestinal tract.
2
Analyze the second presentation (trismus, rigidity, spasms).
Identified as tetanus, caused by Clostridium tetani.
Tetanospasmin is known to cause these symptoms by acting on the central nervous system.
3
Analyze the third presentation (pseudomembrane).
Identified as diphtheria, caused by Corynebacterium diphtheriae.
Diphtheria toxin is the classic cause of a pharyngeal pseudomembrane and potential myocarditis.
4
Analyze the fourth presentation (paroxysmal cough, lymphocytosis).
Identified as pertussis (whooping cough), caused by Bordetella pertussis.
Pertussis toxin causes systemic effects including characteristic lymphocytosis and respiratory tract damage.
5
Match the identified pathogens with their specific toxin mechanisms.
Cholera (Gs activation), Tetanus (SNARE cleavage), Diphtheria (EF-2 inactivation), Pertussis (Gi inhibition).
Accurate pairing of toxin mechanisms is required to understand the pathophysiology of these foundational infectious diseases.

Key Concept

Bacterial exotoxins exert their effects through highly specific molecular mechanisms, such as ADP-ribosylation of specific G-proteins (Gs, Gi) or translation factors (EF-2), or the proteolytic cleavage of neurotransmitter release machinery (SNARE proteins).
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Topics

Infectious Disease Mechanisms

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