Vancomycin-resistant Enterococcus faecalis achieves resistance by which mechanism?

Vancomycin-resistant Enterococcus faecalis achieves resistance by which mechanism?

• A. Increased efflux pumps
• B. Substitution of D-Ala-D-Ala with D-Ala-D-Lac
• C. Inactivation by beta-lactamases
• D. Target mutation of ribosomal RNA

Answer: (B)

Vancomycin works by binding the D-Ala-D-Ala terminus of the nascent peptidoglycan, blocking cell-wall synthesis. In vancomycin-resistant Enterococcus faecalis, resistance is achieved when that terminus is altered to D-Ala-D-Lac. This substitution drastically reduces vancomycin’s binding affinity, so the drug can no longer inhibit the incorporation of new cell-wall material. As a result, cell-wall synthesis proceeds despite presence of the antibiotic. The resistance is often carried on mobile genetic elements (vanA/vanB clusters) and can spread between bacteria. Other proposed mechanisms, such as efflux pumps, beta-lactamase activity, or ribosomal RNA target mutations, do not explain vancomycin resistance because they affect different drugs or targets.

Vancomycin works by binding the D-Ala-D-Ala terminus of the nascent peptidoglycan, blocking cell-wall synthesis. In vancomycin-resistant Enterococcus faecalis, resistance is achieved when that terminus is altered to D-Ala-D-Lac. This substitution drastically reduces vancomycin’s binding affinity, so the drug can no longer inhibit the incorporation of new cell-wall material. As a result, cell-wall synthesis proceeds despite presence of the antibiotic. The resistance is often carried on mobile genetic elements (vanA/vanB clusters) and can spread between bacteria. Other proposed mechanisms, such as efflux pumps, beta-lactamase activity, or ribosomal RNA target mutations, do not explain vancomycin resistance because they affect different drugs or targets.