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
Cevap
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.
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Anahtar Kavram
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).