Low prevalence of VRE gastrointestinal colonization of hospitalized patients in Manitoba tertiary care and community hospitals

al. Low prevalence of VRE gastrointestinal colonization of hospitalized patients in Manitoba tertiary care and community hospitals. Can J Infect Dis 2000;11(1):38-41. OBJECTIVE: To determine the prevalence of vancomycin-resistant enterococci (VRE) bowel colonization in hospitalized patients in Manitoba who had stool specimens collected for Clostridium difficile toxin and/or culture testing. DESIGN: Two tertiary care and five community hospitals in Winnipeg and three rural Manitoba community hospitals participated in this study. From January 1 to December 31, 1997 stool specimens, one per patient, submitted to hospital microbiology laboratories for C difficile toxin and/or culture testing were screened for VRE on colistin-nalidixic acid-vancomycin (6 (cid:1) g/mL) (CNAV) agar plates. The study was divided into six, eight-week intervals. Stool specimens received in the first two weeks of each eight week interval were screened for VRE. MAIN RESULTS: A total of 1408 stool specimens were submitted over the 48-week study period. Sixty-seven (4.8%) pa- tientswithVREcolonizationoftheirlowergastrointestinaltractwereidentified.Threeofthe67(4.5%)VREisolateswere Enterococcus faecium , with the remaining 64 (95.5%) were Enterococcus gallinarum . The three vancomycin-resistant E faecium (VREF) (from two different Winnipeg hospitals) demonstrated the van A genotype, and were resistant to vancomycin, teicoplanin and ampicillin. All three VREF isolates also demonstrated high level resistance to both gentamicin and streptomycin but were susceptible to quinuprisitin/dalfopristin and LY333328. CONCLUSION: VRE colonization in hospitalized patients in Manitoba is infrequent and most commonly due to E galli- narum . The prevalence of VREF colonization in the patients studied was 0.2% (three of 1408).

V ancomycin-resistant Enterococcus faecium (VREF) accounts for up to 65% of E faecium isolates in hospitalized patients across the United States and is endemic in many North American tertiary care institutions (1,2). The management of these infections presents a significant clinical challenge because species of the genus Enterococcus, and in particular E faecium, are frequently resistant to several antimicrobial agents (3). High level penicillin resistance, high level aminoglycoside resistance and most recently vancomycin resistance are emerging as significant concerns in the treatment of enterococcal infections. This has prompted the development and evaluation of new antimicrobial agents such as quinupristin/dalfopristin and LY333328, a glycopeptide, which may offer activity against enterococci resistant to conventional therapy (2).
VREF is not endemic in Manitoba hospitals, and infection with VREF is extremely rare (4). However, the prevalence of VREF lower gastrointestinal tract (GIT) carriage, which frequently precedes infection (5,6), is presently unknown for patients hospitalized in Manitoba. To determine whether the lack of VREF endemnicity correlated with an absence of lower GIT colonization, we assessed lower GIT carriage of VREF for patients hospitalized in 10 Manitoba hospitals from January 1 to December 31, 1997. Our study was consistent with Centers for Disease Control and Prevention guidelines (Atlanta, Georgia) that suggest surveillance programs for vancomycinresistant enterococci (VRE) be undertaken on an intermittent basis in areas where VRE is not known to be endemic (6). Isolates of VREF identified were phenotypically and genotypically characterized, and tested for their susceptibilities against a panel of antimicrobial agents. The study was divided into six, eight-week intervals, and extended from January 1 to December 31, 1997. Each hospital collected stool specimens submitted for Clostridium difficile toxin and/or culture testing in the first two weeks of each eight week interval from patients in their hospitals. One stool specimen per patient was considered. Stool specimens were frozen following collection and shipped to one of two central reference laboratories (Health Sciences Centre and the St Boniface General Hospital) where they were thawed and planted onto blood agar (BA), colistin-nalidixic acid agar (CNA), and colistinnalidixic acid agar supplemented with 6 m g/mL vancomycin (CNAV). All plates were incubated at 35°C for 48 h.

RESULTS
The number of stool specimens evaluated in the first two weeks of each eight week period between January 1 and December 31, 1997 ranged from 187 to 265. A total of 1408 stool specimens were tested. Sixty-seven of the 1408 (4.8%) hospitalized patients evaluated had VRE colonization of their lower GIT. Three of the 67 (4.5%) VRE identified were E faecium, while the remaining 64 isolates (95.5%) were Enterococcus gallinarum. Three of 1408 (0.2%) patients hospitalized in Manitoba, who had a stool specimen submitted for C difficile testing during the study period, were colonized with VREF. One isolate of VREF was identified at the Misericordia General Hospital, a Winnipeg community hospital, between April 23 and May 7, 1997. The two remaining isolates of VREF were identified between June 18 and July 2, 1997 at the Health Sciences Centre, a Winnipeg tertiary care hospital.
All three VREF identified possessed the vanA genotype (Table 1). The two isolates of VREF, from the Health Sciences Centre, possessed the same PFGE pattern while the third isolate, collected from a patient at the Misericordia General Hospital, had a different PFGE pattern (Table 1). Both PFGE patterns have been previously identified in VREF isolated in Manitoba (unpublished data), suggesting they may have been acquired locally or nosocomially. Using NCCLS serum breakpoints (14), the three isolates of VREF demonstrated uniform resistance to teicoplanin, ampicillin, streptomycin, gentamicin, and ciprofloxacin, but were sensitive to quinuprisitin/dalfopristin and LY333328 (Table 1).

DISCUSSION
Enterococci are normal constituents of the human GIT, and may also colonize the oral cavity, vagina, biliary tract and upper respiratory tract of healthy people. Most clinical isolates of enterococci represent colonization, not infection (15). Enterococci may however cause infection, most commonly urinary tract infections (15). Cholecystitis, cholangitis, peritonitis, septicemia, endocardititis, meningitis and wound infections have also been documented (15). The GIT is the major reservoir for enterococci, and serves as the source of dissemination. However, the ability of enterococci to survive on environmental surfaces for extended periods (up to a week) can also facilitate their spread (15).
Traditionally, enterococcal infections have been treated with the penicillins, usually in combination with an aminoglycoside for serious infections. However, with penicillin and aminoglycoside resistance rates increasing vanconiycin is now often used to treat enterococcal infections. VRE were extremely rare before 1988 with just two isolates (MIC greatern than 100 m g/mL) documented in the previous two decades (16,17). In 1988, VRE began to emerge as a clinical concern, with the description of 55 clinical isolates of VRE (seven Enterococcus faecalis and 48 E faecium) (MICs greater than 64 m g/mL) from 22 British patients with renal impairment (18). In 1993, the American National Nosocomial Infections Surveillance (NNIS) system reported an increase in the incidence of nosocomial VRE from 0.3% in 1989 to 7.9% in 1993 (19). Many scientific publications from the United States and Europe have followed with reports of as many as 65% of E faecium isolates being vancomycin resistant in some American hospitals (1). The epidemiology of VRE in Canada before 1997 has been succinctly summarized (20), with the first isolate of VRE reported in Edmonton in 1993 and the first VRE outbreak, involving 38 patients, occurring in a Toronto hospital in 1995. A 1996 Canadian VRE surveillance study demonstrated a VRE (E faecalis or E faecium) point prevalence of 0.7% overall (26 of 3773), 0.1% in nonendemic hospitals, 3.7% in endemic hospitals and 5.3% in endemic patient groups within endemic hosptials (21). Twenty-three of the 26 patients identified in this study were from a single tertiary care institution with all isolates (three E faecalis and 23 E faecium) being colonizers (21). VRE were not identified in a previous study over a fourmonth period in 1995 at the Health Sciences Centre in Winnipeg, one of the 10 Manitoba hospitals included in this survey