Match each clinical vignette with the molecular mechanism of the primary virulence factor responsible for the patient's symptoms.
- A 6-year-old unimmunized boy presents with a thick, grayish pseudomembrane over his tonsils and profound cervical lymphadenopathy.Toxin-mediated ADP-ribosylation of elongation factor-2 (EF-2), leading to inhibition of host cell protein synthesis and cell death.
- A 32-year-old man presents with painful muscle spasms in his jaw and face after sustaining a puncture wound to his foot.Metalloprotease-mediated cleavage of synaptobrevin, preventing the exocytosis of inhibitory neurotransmitters into the synaptic cleft.
- A 24-year-old aid worker develops sudden, severe, large-volume watery diarrhea without fever.Toxin-mediated ADP-ribosylation of the Gs alpha subunit, resulting in continuous adenylate cyclase activation and chloride efflux.
- A 3-month-old infant presents with paroxysms of severe, rapid coughing followed by a high-pitched inspiratory sound and post-tussive emesis.Toxin-mediated ADP-ribosylation of the Gi alpha subunit, preventing the inhibition of adenylate cyclase and impairing phagocyte function.
Cevap
1. Diphtheria matches with EF-2 ribosylation; 2. Tetanus matches with SNARE cleavage; 3. Cholera matches with Gs ribosylation; 4. Pertussis matches with Gi ribosylation.
Each clinical scenario corresponds to a classic toxin-mediated disease. The pseudomembrane of diphtheria is caused by EF-2 inhibition leading to cell death. The spastic paralysis of tetanus is caused by SNARE protein cleavage preventing inhibitory neurotransmitter release. The watery diarrhea of cholera is driven by Gs activation increasing cAMP. The whooping cough of pertussis involves Gi inhibition, which also increases cAMP and impairs host defenses.
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Anahtar Kavram
Molecular mechanisms of bacterial exotoxins
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