Vancomycin inhibits cell wall synthesis by a mechanism different from β-lactams. The specific step it inhibits is:
- A Transpeptidation (cross-linking of peptidoglycan strands)
- B Inhibition of MurA (UDP-N-acetylglucosamine enolpyruvyl transferase)
- C Binding to D-Ala-D-Ala terminus of peptidoglycan precursor, preventing transglycosylation and transpeptidation ✓
- D Inhibition of bactoprenol phosphatase, blocking lipid carrier recycling
Explanation
Vancomycin is a glycopeptide that forms hydrogen bonds with the D-Ala-D-Ala dipeptide terminus of the Park nucleotide (lipid II), physically blocking transglycosylase and transpeptidase access. Resistance in VRE involves substitution of D-Ala-D-Ala with D-Ala-D-Lac (reduced affinity ~1000-fold). β-Lactams, by contrast, inhibit transpeptidases (PBPs) by mimicking the D-Ala-D-Ala substrate. MurA is the target of fosfomycin; bactoprenol is affected by bacitracin.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.