Vancomycin-resistant enterococci (VRE) carrying the vanA gene cluster differ from vanB-carrying VRE primarily by:

• A vanA confers resistance to vancomycin only; vanB confers resistance to both vancomycin and teicoplanin
• B vanA confers high-level resistance to both vancomycin (MIC > 256 µg/mL) and teicoplanin (MIC > 16 µg/mL); vanB confers resistance to vancomycin but remains susceptible to teicoplanin ✓
• C vanA is intrinsic resistance in E. gallinarum; vanB is acquired
• D vanA replaces D-Ala-D-Ala with D-Ala-D-Ser; vanB replaces with D-Ala-D-Lac

Explanation

Both vanA and vanB substitute D-Ala-D-Lac for D-Ala-D-Ala in peptidoglycan precursors, reducing glycopeptide binding by 1000-fold. However, vanA is inducible by both vancomycin and teicoplanin and confers high-level resistance to both glycopeptides (MIC ≥ 256 and ≥ 16 µg/mL respectively). vanB is inducible only by vancomycin and confers variable vancomycin resistance while retaining teicoplanin susceptibility — a clinically important distinction for treatment planning. D-Ala-D-Ser (with lower-level resistance) is the mechanism of the intrinsic vanC gene cluster in E. gallinarum/E. casseliflavus.

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

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