An Enterococcus faecium isolate shows high-level resistance to vancomycin (MIC >256 µg/mL) and teicoplanin (MIC >128 µg/mL). Genotyping reveals vanA gene. What is the mechanism and what is the treatment option?

• A VanB: modification of D-Ala-D-Ala to D-Ala-D-Ser; treat with teicoplanin
• B VanC: intrinsic modification in motile enterococci; treat with high-dose penicillin
• C VanA: reprogramming of peptidoglycan precursor from D-Ala-D-Ala to D-Ala-D-Lac; treat with linezolid or daptomycin ✓
• D PBP5 overexpression causing reduced binding; treat with ampicillin

Explanation

VanA phenotype (high-level resistance to both vancomycin and teicoplanin) results from substitution of the terminal D-Ala-D-Ala in peptidoglycan precursors with D-Ala-D-Lac; this reduces vancomycin binding affinity 1000-fold. VanA is transferable on Tn1546 transposon. VanB phenotype shows high-level vancomycin resistance but susceptibility to teicoplanin (D-Ala-D-Lac substitution only induced by vancomycin, not teicoplanin). Treatment of VRE (vanA) infections: linezolid (bacteriostatic) or daptomycin (bactericidal); combination therapy may be needed for endocarditis. Tigecycline is an option for non-bacteraemic infections.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

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