A vancomycin-resistant Staphylococcus aureus (VRSA) isolate is identified from a diabetic foot ulcer. The vancomycin MIC is 256 μg/mL. PCR confirms the presence of the vanA gene. The mechanism of vancomycin resistance in this isolate is:

• A Thickening of the peptidoglycan layer trapping vancomycin molecules
• B Acquisition of the vanA operon from vancomycin-resistant enterococci ✓
• C Overexpression of efflux pumps that expel vancomycin
• D Mutation in the vanSR two-component system without vanA acquisition

Explanation

VRSA strains have acquired the vanA operon from VRE via plasmid transfer, leading to synthesis of D-Ala-D-Lac instead of D-Ala-D-Ala, which reduces vancomycin binding affinity by 1000-fold. Option A describes VISA (vancomycin-intermediate S. aureus), not VRSA. Option C is not the mechanism for vancomycin resistance in S. aureus. Option D describes a VISA phenotype with thickened cell wall, not true VRSA with vanA.

Reference: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 9th ed.

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