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Microbiology · Antimicrobial resistance: vancomycin-resistant enterococci
Sample itemEnterococcus faecium from a dialysis patient's blood shows a vancomycin MIC above 256 mg/L and is also resistant to teicoplanin. Which gene and mechanism explain this phenotype?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. vanA, with replacement of D-Ala-D-Ala by D-Ala-D-Lac in the peptidoglycan precursor
In vanA-type resistance, a ligase produces D-Ala-D-Lac instead of D-Ala-D-Ala, which lowers vancomycin binding about 1000-fold. It confers high-level resistance to both vancomycin and teicoplanin and is carried on a transposon, usually in Enterococcus faecium. Linezolid or daptomycin is used for treatment.
Option by option
A. mecA, with an altered penicillin-binding protein
mecA gives methicillin resistance in staphylococci and does not affect vancomycin.
B. vanC, with D-Ala-D-Ser causing high-level resistance to both drugs
vanC gives low-level intrinsic vancomycin resistance in species such as Enterococcus gallinarum, with teicoplanin remaining susceptible.
C. vanA, with replacement of D-Ala-D-Ala by D-Ala-D-Lac in the peptidoglycan precursor (correct)
The vanA cluster alters the precursor terminus and causes resistance to both glycopeptides.
D. vanB, with D-Ala-D-Lac and preserved teicoplanin susceptibility
vanB also uses D-Ala-D-Lac, but teicoplanin remains active, which does not match this isolate.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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