A patient with MRSA bacteremia is treated with vancomycin. The drug exerts its bactericidal effect by:
- A Inhibiting transpeptidase (PBP) to prevent cross-linking of peptidoglycan
- B Binding D-Ala–D-Ala terminus of lipid II precursor, blocking transglycosylation and transpeptidation ✓
- C Disrupting the bacterial cell membrane through detergent-like action
- D Inhibiting dihydropteroate synthase reducing folate synthesis
Explanation
Vancomycin binds with high affinity to the D-alanyl-D-alanine (D-Ala-D-Ala) terminus of the peptidoglycan precursor lipid II, physically blocking both transglycosylation and transpeptidation steps of cell wall synthesis. Beta-lactams inhibit transpeptidase (PBPs) but do not bind the substrate. MRSA acquires resistance through altered PBPs, not through altered D-Ala-D-Ala (that is the VRE mechanism with D-Ala-D-Lac substitution).
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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