Vancomycin kills bacteria by binding to the D-Ala–D-Ala terminus of peptidoglycan precursors. What consequence does this have at the molecular level?
- A Inhibits RNA polymerase, blocking transcription
- B Disrupts the cytoplasmic membrane by detergent action
- C Sterically blocks transglycosylase and transpeptidase, preventing peptidoglycan cross-linking ✓
- D Inhibits dihydrofolate reductase, depleting tetrahydrofolate
Correct answer: C. Sterically blocks transglycosylase and transpeptidase, preventing peptidoglycan cross-linking
Explanation
By tightly binding the D-Ala–D-Ala dipeptide end of lipid-II, vancomycin physically occludes the substrate from transglycosylase (polymerisation) and transpeptidase (cross-linking) enzymes, halting peptidoglycan synthesis and causing osmotic lysis of the bacterium. Resistance in VanA-type enterococci arises from substituting D-Ala–D-Ala with D-Ala–D-Lac, reducing vancomycin affinity 1000-fold. The other options describe mechanisms of rifampicin, polymyxins, and trimethoprim respectively.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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