B Lynn Johnston MD FRCPC, John M Conly MD FRCPC In the July/August 1997 issue of the The Canadian Journal of Infectious Diseases, the Adult Infectious Disease Notes was entitled “The emerging epidemiology of vancomycin-resistant enterococci (VRE) in Canada”(1). At that time, it was acknowledged that VRE’s Canadian epidemiology was not fully elucidated. The first isolate of VRE had been reported in Edmonton in 1993, and the first outbreak of VRE in Canada occurred in Toronto in 1995 (1). This outbreak was presented as “A casecontrol analysis of the ‘call bell’ outbreak” (2). This was in reference to the contaminated call bells, a previously unrecognized reservoir and potential vector. But was it also alluding to a wake-up call for Canada to the emergence of VRE in its hospitals? In response to the need for more data describing the epidemiology of VRE in Canada, the Canadian Nosocomial Infection Surveillance Program (CNISP), a collaborative effort of the Canadian Hospital Epidemiology Committee (CHEC), a subcommittee of the Canadian Infectious Disease Society, and the Laboratory Centre for Disease Control (LCDC), Health Canada undertook several initiatives including two-point prevalence surveys, establishment of the Passive Reporting Network (PRN) for VRE occurrences in Canada and the VRE Incidence Surveillance Project for determining the incidence rate of VRE in CHEC facilities. What have we learned about VRE since 1997? Four major phenotypes of VRE are now recognized: van A, van B, van C and van D (3). The van A phenotype is characterized by high level resistance to both vancomycin and teicoplanin. It has been found in a number of enterococcal species. The van B phenotype has low to moderate level resistance to vancomycin with preserved teicoplanin susceptibility. It is seen primarily in Enterococcus faecalis and Enterococcus faecium. Van C resistance, found in non-E faecalis and non-E faecium, is nontransferrable (constitutive) and exhibits low level resistance to vancomycin. Finally, the van D phenotype is characterized by low to moderate level resistance to both vancomycin and teicoplanin. In the United States, data from the National Nosocomial Infection Surveillance System (NNIS) of the Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, have revealed a dramatic national outbreak of VRE. Between 1989 and 1997, the percentage of enterococci isolated from nosocomial infections in intensive care unit (ICU) patients that were resistant to vancomycin rose from 0.4% to 23.2% and the percentage from non-ICU patients rose from 0.3% to 15.4% (5). From January to December 1999, VRE accounted for 25.2% of enterococci associated with nosocomial infections in ICU patients participating in NNIS, a 43% increase in resistance over the previous five years (5). Rates of vancomycin resistance in enterococci remained lower in non-ICU inpatient areas (11.7%) and in outpatient areas (3.6%) (4). Initially found mainly in large hospitals, VRE is now found in American hospitals of all sizes (4). At the 4th Decennial International Conference on Nosocomial and Healthcare-associated Infections, held March 5 to 9, 2000, a number of American centres described their experience with VRE. Dialysis patients remain a group with increased rates of VRE colonization. Tokars et al (6) found a prevalence of 9.2% at seven outpatient dialysis centres in Virginia and Maryland where patients were screened over several months in early 1998. During 1997 and 1998, VRE was isolated from 15.6% of dialysis patients screened within two days of admission to hospital in Atlanta, Georgia (7). For the nine outpatient clinics from where more than 20 patients were cultured in this study, VRE carriage ranged from 10% to 23% (7). While adult ICUs have previously been recognized as high prevalence settings for VRE, De Santis et al (8) reported an