Microbiology MCAT Practice Question
A 68-year-old man with type 2 diabetes presents with severe watery diarrhea, fever (38.9°C), and abdominal cramping after 2 weeks of ciprofloxacin use for a urinary tract infection. Stool testing is positive for Clostridium difficile toxins. Colonoscopy reveals pseudomembranous colitis with focal ulcerations and loss of epithelial integrity. A research colleague explains that C. difficile toxins A and B exert their pathologic effects by glucosylating threonine residues within the switch regions of Rho family GTPases (Rac, Rho, and Cdc42). This glucosylation modification is critical to the disease pathogenesis observed in this patient. Which of the following best explains how glucosylation of these GTPases leads to the cytoskeletal disruption and epithelial barrier dysfunction seen in this infection?
Answer choices
- AGlucosylation blocks the nucleotide binding pocket, preventing GTPase cycling between inactive GDP-bound and active GTP-bound statesCorrect answer
- BGlucosylation directly polymerizes actin filaments by cross-linking actin monomers into rigid, non-functional bundles
- CGlucosylation hyperactivates GTPases by mimicking the structural conformation of GTP-bound active state
- DGlucosylation activates downstream serine/threonine kinases that phosphorylate and degrade tight junction proteins
- EGlucosylation competitively inhibits guanine nucleotide exchange factors (GEFs), preventing the normal GTPase activation cycle
- FGlucosylation enhances GTPase GTPase hydrolysis activity, causing rapid depletion of cellular GTP pools
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