Vancomycin-resistant Enterococcus (VRE) most commonly carries which resistance gene, and what structural alteration does it produce?
- A vanB gene — changes D-Ala-D-Ala to D-Ala-D-Ser, reducing affinity 7-fold
- B mecA gene — alters PBP2a reducing vancomycin binding
- C vanA gene — changes D-Ala-D-Ala terminus to D-Ala-D-Lac, reducing vancomycin affinity 1000-fold ✓
- D blaVIM gene — produces metallo-beta-lactamase that inactivates vancomycin
Explanation
The vanA gene cluster (most common and clinically significant) in VRE encodes enzymes that reprogramme cell wall biosynthesis, replacing the terminal D-Ala-D-Ala of peptidoglycan precursors with D-Ala-D-Lac (D-lactate). This single oxygen-to-sulphur change reduces vancomycin binding affinity approximately 1000-fold (because vancomycin hydrogen bonds to D-Ala-D-Ala). vanB changes to D-Ala-D-Ser with only ~7-fold reduced affinity and usually retains teicoplanin susceptibility. mecA is the MRSA resistance gene; blaVIM is a Gram-negative resistance gene.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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