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Difficulty: MediumInfectious Disease Mechanisms

Match each patient's clinical presentation with the primary mechanism of action of the responsible bacterial toxin.

  • A 6-year-old unimmunized boy presenting with a thick, grayish pharyngeal exudate and severe cervical lymphadenopathy.Inhibition of protein synthesis via ADP-ribosylation of elongation factor 2 (EF-2)
  • A 35-year-old woman presenting with profound, watery diarrhea and severe dehydration after consuming undercooked seafood.Overactivation of adenylate cyclase via ADP-ribosylation of the Gs alpha subunit
  • A 22-year-old man presenting with severe jaw stiffness and painful muscle spasms after sustaining a deep puncture wound.Blockade of inhibitory neurotransmitter release via cleavage of synaptobrevin
  • A 4-year-old girl presenting with bloody diarrhea and new-onset oliguria following consumption of an undercooked hamburger.Inhibition of protein synthesis via inactivation of the 60S ribosomal subunit

Answer

The unimmunized boy (diphtheria) matches with ADP-ribosylation of EF-2. The woman with watery diarrhea (cholera) matches with ADP-ribosylation of Gs alpha. The man with muscle spasms (tetanus) matches with cleavage of synaptobrevin. The girl with bloody diarrhea (EHEC) matches with inactivation of the 60S ribosomal subunit.
Each pathogen relies on a specific exotoxin to produce its characteristic clinical disease. Corynebacterium diphtheriae uses an A-B toxin to ADP-ribosylate EF-2. Vibrio cholerae uses an A-B toxin to ADP-ribosylate Gs alpha. Clostridium tetani produces a protease (tetanospasmin) that cleaves SNARE proteins. Enterohemorrhagic E. coli produces a Shiga-like toxin that inactivates the 60S ribosomal subunit.

Step-by-Step Solution

1
Analyze the first clinical vignette.
Identified Corynebacterium diphtheriae as the causative agent.
The unimmunized status, grayish pharyngeal pseudomembrane, and severe cervical lymphadenopathy (bull neck) are classic for diphtheria.
2
Determine the mechanism of diphtheria toxin.
Matched with ADP-ribosylation of EF-2.
Diphtheria toxin is an A-B exotoxin that halts cellular protein synthesis by inactivating elongation factor 2.
3
Analyze the second clinical vignette.
Identified Vibrio cholerae as the causative agent.
Profuse watery diarrhea after seafood consumption is the hallmark of cholera.
4
Determine the mechanism of cholera toxin.
Matched with ADP-ribosylation of the Gs alpha subunit.
Cholera toxin increases cAMP by permanently activating the stimulatory G-protein (Gs), leading to chloride and water efflux.
5
Analyze the third clinical vignette.
Identified Clostridium tetani as the causative agent.
Jaw stiffness (trismus) and muscle spasms following a puncture wound are characteristic of tetanus.
6
Determine the mechanism of tetanospasmin.
Matched with cleavage of synaptobrevin.
Tetanus toxin acts as a protease that cleaves SNARE proteins, blocking the release of inhibitory neurotransmitters and causing spastic paralysis.
7
Analyze the fourth clinical vignette.
Identified Enterohemorrhagic E. coli (EHEC) complicated by hemolytic uremic syndrome (HUS).
Bloody diarrhea followed by acute kidney injury in a child after eating undercooked beef is typical for EHEC.
8
Determine the mechanism of Shiga-like toxin.
Matched with inactivation of the 60S ribosomal subunit.
Shiga and Shiga-like toxins cleave host cell 28S rRNA (part of the 60S subunit), halting protein synthesis and causing cell death.

Key Concept

Bacterial exotoxins cause specific clinical syndromes through distinct intracellular mechanisms, such as inhibition of protein synthesis, overactivation of intracellular signaling pathways, or disruption of neurotransmitter release.
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Topics

Infectious Disease Mechanisms

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