A 68-year-old man has a relapsing MRSA bloodstream infection despite three weeks of therapeutic vancomycin dosing with troughs above 15 mg/L. Repeat E-test shows a vancomycin MIC of 3 mg/L, and population analysis reveals a subpopulation growing at 4 mg/L. PCR is negative for vanA and vanB. The best explanation is:
- A Plasmid-mediated transfer of the vanA operon from enterococci
- B Heterogeneous vancomycin-intermediate S. aureus due to a thickened cell wall trapping vancomycin ✓
- D Production of beta-lactamase degrading vancomycin
- C Loss of the mecA gene converting the isolate back to MSSA
Correct answer: B. Heterogeneous vancomycin-intermediate S. aureus due to a thickened cell wall trapping vancomycin
Explanation
hVISA/VISA arises without acquired van genes. The phenotype results from thickening of peptidoglycan layers and increased free D-Ala-D-Ala residues that trap vancomycin in the outer wall, slowing access to its division-septum target. This produces MIC creep into the intermediate range with a resistant subpopulation. VanA acquisition would give high-level resistance with D-Ala-D-Lac substitution, and vancomycin is not a beta-lactam substrate.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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