Emergence of antibiotic-resistant bacteria is a consequence of increasing antibiotic selection pressure caused by the demand for new antibiotics for new and emerging infections, emergence of resistant organisms, inappropriate use of antibiotics in medical practice, and use of antibiotics in industry.
In 1988, after more than 30 years without the development of resistance, strains of vancomycin hydrochloride–resistant Enterococcus faecalis and Enterococcus faecium were isolated in England.1 Vancomycin-resistant Enterococcus (VRE) isolates were soon reported in France and the United States.1 High-level resistance to vancomycin and the other glycopeptide, teicoplanin, is due to the vanA gene located on transposon TN 1586. This complex produces an altered peptidoglycan precursor, D-alanine–D-lactate, that resists the interaction of the glycopeptides to inhibit cell wall synthesis in enterococci.1