Vancomycin exerts its cell wall inhibitory effect by binding to:
- A The D-Ala-D-Ala terminus of peptidoglycan precursor (lipid II), sterically blocking transglycosylation and transpeptidation ✓
- B Penicillin-binding proteins (PBPs), preventing transpeptidation of peptidoglycan strands
- C Undecaprenyl pyrophosphate (bactoprenol), preventing recycling of the lipid carrier and halting cell wall synthesis
- D The 50S ribosomal subunit, inhibiting peptidyl transferase activity in rapidly dividing bacteria
Correct answer: A. The D-Ala-D-Ala terminus of peptidoglycan precursor (lipid II), sterically blocking transglycosylation and transpeptidation
Explanation
Vancomycin is a glycopeptide that binds with high affinity to the D-Ala-D-Ala C-terminal dipeptide of the pentapeptide portion of lipid II (the peptidoglycan precursor). This non-covalent binding sterically blocks both transglycosylation (cross-linking of glycan strands) and transpeptidation (cross-linking of peptide stems), inhibiting cell wall synthesis. VRE resistance arises from ligases (VanA, VanB) that replace D-Ala-D-Ala with D-Ala-D-Lac, reducing vancomycin binding affinity 1000-fold. Beta-lactams target PBPs; bacitracin targets bactoprenol.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.