A 55-year-old woman develops fever and a new murmur 3 months after prosthetic valve replacement. Blood cultures grow Gram-positive cocci in chains that are catalase-negative, grow in 6.5% NaCl, and hydrolyse esculin in the presence of 40% bile. Vancomycin resistance is detected (MIC >32 µg/mL). Which resistance mechanism is responsible?
- A Production of beta-lactamase hydrolysing vancomycin
- B Altered peptidoglycan precursor (D-Ala-D-Ala to D-Ala-D-Lac) reducing vancomycin binding affinity ✓
- C Efflux pumps actively exporting vancomycin from the cell
- D Modification of ribosomal 50S subunit preventing vancomycin binding
Correct answer: B. Altered peptidoglycan precursor (D-Ala-D-Ala to D-Ala-D-Lac) reducing vancomycin binding affinity
Explanation
Vancomycin-resistant Enterococcus (VRE) resistance is mediated by the van gene cluster (vanA, vanB) that reprogrammes peptidoglycan synthesis. The terminal D-Ala-D-Ala dipeptide is replaced with D-Ala-D-Lac, reducing vancomycin binding affinity 1000-fold. Beta-lactamases do not affect vancomycin. Ribosomal modification causes macrolide resistance. The isolate is Enterococcus based on growth in 6.5% NaCl, bile-esculin positivity, and catalase negativity.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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