[Table of Contents]

Canada Communicable Disease Report - Supplement
Volume: 23S8
December 1997

INFECTION CONTROL GUIDELINES

Preventing the Spread of Vancomycin-Resistant Enterococci (VRE) in Canada

Antibiotic Resistance in Enterococci

Enterococcal species are intrinsically resistant to many antibiotics and have demonstrated a remarkable capacity to acquire resistance^(20-22). Enterococci have constitutive resistance to cephalosporins, penicillinase-resistant penicillins, clindamycin, low-level aminoglycosides, and probably trimethoprim-sulfamethoxazole^(23-25). For serious enterococcal infections, the combination of a cell-wall active agent (a ß-lactam or glycopeptide) and an aminoglycoside is necessary to achieve bactericidal activity^(26-29).

Over the past 2 decades there have been an increasing number of reports of Enterococcus species with induced resistance to multiple antibiotics, and therapeutic options have become increasingly limited. The first evidence of high-level resistance of Enterococcus species to streptomycin and gentamicin (minimum inhibitory concentration [MIC] > 2,000 µg/L) was documented in the 1970s^(30,31), and during the 1980s the prevalence of these resistant strains increased dramatically in several locales in North America and Europe^(2,32). High-level aminoglycoside resistance eliminates the option of using aminoglycosides in combination with cell-wall active agents (e.g., penicillin or ampicillin) for synergistic activity⁽³³⁾. Resistance to ampicillin^(34-36) is being seen with increasing frequency and may be due to a decreased ability to bind to penicillins or to the production of ß-lactamase by the microorganism.

The development of resistance to vancomycin, which is potentially much more problematic, was first reported in Europe in 1986⁽³⁷⁾. Since then, outbreaks of VRE infections have been described in several institutions and other health settings^(38-43) in the United States. The mechanisms of resistance to vancomycin have been described⁽⁴⁴⁾, but the concern from a clinical perspective is the loss of vancomycin and other glycopeptide antibiotics for the treatment of serious enterococcal infections. With an increasing incidence of Enterococcus species resistant to both penicillins and aminoglycosides, the addition of vancomycin resistance would severely limit therapeutic options. The vancomycin-resistance trait in Enterococcus species is transferable, and perhaps the greatest threat of VRE is the potential emergence of vancomycin resistance in methicillin-resistant Staphylococcus aureus (S. aureus) or S. epidermidis, which would create a major concern^(45,46).

There is some variability in the phenotypic and genotypic characteristics of VRE (see Table 2). The strains can be classified phenotypically according to the level of their resistance (low or high) to vancomycin and teicoplanin⁽⁴⁷⁾. Four phenotypes of glycopeptide resistance have been recognized. The phenotype usually corresponds to the genotype of the same name, as determined by detection of the gene responsible for the resistance pattern. Van A phenotype constitutes a high-level resistance to vancomycin and teicoplanin⁽³⁷⁾. Van B phenotype represents a low- to high-level resistance to vancomycin only⁽⁴⁸⁾. Van C phenotype is associated with low-level resistance to vancomycin⁽⁴⁹⁾. For the purpose of this document, only Van A and Van B phenotypes are considered. Vancomycin resistance, in the case of E. faecium and E. faecalis, is either of Van A or Van B phenotype and is acquired, inducible and capable of transfer to other gram-positive cocci. Vancomycin resistance in E. gallinarum and E. casseliflavus is intrinsic, and transferability of the vancomycin-resistance genes has never been observed.

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