Match each patient's clinical presentation with the precise molecular mechanism of the primary virulence factor responsible for their condition.
- A 2-month-old infant with severe paroxysmal coughing episodes followed by an inspiratory whoop, accompanied by marked lymphocytosis.Inactivates the inhibitory G-protein subunit (Gi) via ADP-ribosylation, leading to unrestrained adenylate cyclase activity.
- A 6-year-old unvaccinated child presenting with a tightly adherent, grayish oropharyngeal pseudomembrane and new-onset complete heart block.Catalyzes the ADP-ribosylation of elongation factor-2 (EF-2), thereby inhibiting eukaryotic host cell translation.
- A 35-year-old construction worker with a recent puncture wound who develops severe trismus and sustained facial muscle spasms.Functions as a zinc-dependent endopeptidase that cleaves synaptobrevin, blocking inhibitory neurotransmitter exocytosis.
- A 5-year-old girl with bloody diarrhea who subsequently develops oliguria, thrombocytopenia, and schistocytes on a peripheral blood smear.Cleaves a specific adenine residue from the 28S rRNA of the 60S ribosomal subunit, halting protein synthesis.
- A 45-year-old woman with profound, painless, watery diarrhea and severe dehydration shortly after consuming raw oysters.Permanently activates the stimulatory G-protein subunit (Gs) via ADP-ribosylation, resulting in massive chloride and water efflux.
Cevap
The clinical vignettes must be matched to their respective exotoxin mechanisms: Pertussis involves Gi inactivation; Diphtheria involves EF-2 ADP-ribosylation; Tetanus involves synaptobrevin cleavage; EHEC/Shigella involves 60S ribosome inactivation; and Cholera involves Gs activation.
This question assesses the ability to link classic clinical syndromes to the exact molecular pathogenesis of bacterial exotoxins. Bordetella pertussis produces pertussis toxin, which ADP-ribosylates and disables Gi. Corynebacterium diphtheriae produces diphtheria toxin, which ADP-ribosylates elongation factor-2. Clostridium tetani produces tetanospasmin, a protease that cleaves the SNARE protein synaptobrevin. Enterohemorrhagic E. coli and Shigella produce Shiga/Shiga-like toxins that inactivate the 60S ribosomal subunit. Vibrio cholerae produces cholera toxin, which ADP-ribosylates and permanently activates Gs.
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Anahtar Kavram
Bacterial exotoxins cause specific clinical syndromes through precise intracellular disruption, such as altering G-protein signaling pathways (cAMP), halting protein synthesis, or cleaving vesicular transport proteins.
Tahmini Süre:2m 30s