e Accurate detection of vancomycin-resistant enterococci (VRE) is essential in preventing transmission in health care settings. Chromogenic media are widely used for screening VRE because of fast turnaround times (TAT) and high sensitivity. We report an outbreak of Enterococcus faecium bearing vanA yet susceptible to vancomycin (vancomycin-variable Enterococcus [VVE]). Between October 2009 to March 2011, clinical and screening specimens (n โซุโฌ 14,747) were screened for VRE using VRE-selective medium and/or PCR. VVE isolates were genotyped to determine relatedness. Plasmids from these isolates were characterized by sequencing. Overall, 52 VVE isolates were identified, comprising 15% of all VRE isolates identified. Isolates demonstrated growth on Brilliance VRE agar (Oxoid) at 24 h of incubation but did not grow on brain heart infusion agar with 6 g/ml vancomycin (Oxoid) or bile esculin azide agar with 6 g/ml vancomycin (Oxoid) and were susceptible to vancomycin. Genotyping of 20 randomly selected VVE isolates revealed that 15/20 were identical, while 5 were highly related. PCR of the VVE transposon confirmed the presence of vanHAXY gene cluster; however, vanS (sensor) and vanR (regulator) genes were absent. The outbreak was controlled through routine infection control measures. We report an emergence of a fit strain of E. faecium containing vanA yet susceptible to vancomycin. Whether this new strain represents VRE has yet to be determined; however, unique testing procedures are required for reliable identification of VVE.
Vancomycin-resistant enterococcus (VRE) colonization and infection are increasingly common in both hospital and outpatient settings. Since the initial discovery of VRE during the 1980s in the United Kingdom and France, it has spread to many countries throughout the world (1, 2). In Canada, there has been a small but steady increase in rates of detection of VRE from 0.37 case per 1,000 patient admissions in 1999 to 1.32 in 2005 (3). VRE infection rates increased from 0.02 to 0.05 case per 1,000 admitted patients. Six different types of glycopeptide resistance (vanA, vanB, vanC, vanD, vanE, and vanG) have been described, of which the vanA-and vanB-mediated types are clinically significant in enterococci. Typically, vanA-mediated vancomycin resistance is found in Enterococcus faecium. VRE resistance in vanA-bearing isolates is mediated by the group of genes vanR, vanS, vanH, vanA, and vanX, which are usually carried on the Tn1546 transposon. The expression of these genes leads to replacement of the C-terminal D-Ala residue with D-Lac during cell wall synthesis, thus modifying the vancomycin-binding target. The transposon is often contained on plasmids, making it easy to transfer among enterococcal strains. Historically, there has been little sequence variation in this gene cluster (4).Various studies have shown that infections caused by VRE lead to longer hospital stays, higher mortality, and significantly higher cost than infections caused by vancomycin-susceptible enterococci (5). Therefore, ac...