To determine the molecular epidemiology of vancomycin-resistant enterococci (VRE) at our medical center in order to identify the extent of strain clonality and possible transmission patterns of this pathogen.

An important facet of our infection control program includes molecular typing of all clinical and surveillance isolates of VRE to determine transmission patterns in the hospital. Molecular strain typing is performed by restriction endonuclease analysis (REA) of genomic DNA. REA patterns are visually compared to categorize VRE strains into type and subtype designations.

A 588-bed, university-affiliated, tertiary-care hospital and a neighboring 155-bed rehabilitation facility.

From January 1995 through December 1996, 379 VRE isolates were collected from 197 patients. Thirty-three genotypes were determined by REA typing; 15 genotypes were implicated in 29 instances of potential nosocomial transmission. Three major clusters of VRE involving patients on multiple nursing units and two adjacent hospitals were identified. The remaining instances of nosocomial transmission occurred in small patient clusters.

In conclusion, the VRE epidemic at this medical center is polyclonal. VRE transmission patterns are complex, and, while large clusters do occur, the usual pattern of nosocomial acquisition of this pathogen occurs in the setting of “mini-clusters”.

To determine the role of mucositis severity in the development of vancomycin-resistant enterococcal (VRE) bloodstream infection (BSI).

A tertiary-care university medical center.

Hematology-oncology-unit inpatients.

Patients with VRE BSI (case-patients) were compared with VRE-colonized (control) patients from September 1994 through August 1997. Oral mucositis severity was recorded on the day of VRE BSI for case-patients and on hospital day 22 (median day of hospitalization of case-patient VRE BSI) for controls. There were 19 case-patients and 31 controls.

In univariate analysis, case-patients were significantly more likely than controls to have a higher mucositis severity score, diarrhea, or a higher severity of illness score. In multivariate analysis, only mucositis remained as an independent risk factor, and increasing mucositis score was significantly associated with VRE BSI.

Mucositis severity was independently associated with an increasing risk for VRE BSI. Interventions to alter mucositis severity may help to prevent VRE BSI in hospitalized cancer patients.

To identify independent risk factors for enteric carriage of vancomycin-resistant Enterococcus faecium (VREF) in hospitalized patients tested for Clostridium difficile toxin.

Retrospective case-cohort study.

Tertiary-care teaching hospital.

Convenience sample of 215 adult inpatients who had stool tested for C difficile between January 29 and February 25,1996.

41 (19%) of 215 patients had enteric carriage of VREF. Five independent risk factors for enteric VREF were identified: history of prior C difficile (odds ratio [OR], 15.21; 95% confidence interval [CI95], 3.30-70.10; P<.001), parenteral treatment with vancomycin for ≥5 days (OR, 4.06; CI95, 1.54-10.73; P=.005), treatment with antimicrobials effective against gram-negative organisms (OR, 3.44; CI95, 1.20-9.87; P=.021), admission from another institution (OR, 2.95; CI95, 1.21-7.18; P=.017), and age >60 years (OR 2.57; CI95, 1.13-5.82; P=.024). These risk factors for enteric VREF were independent of the patient's current C difficile status.

Antimicrobial exposures are the most important modifiable independent risk factors for enteric carriage of VREF in hospitalized patients tested for C difficile.

To assess state-based surveillance for isolation from a sterile site of vancomycin-resistant enterococci (VRE) in Connecticut.

Clinical laboratory reporting (passive surveillance) of VRE isolates to the Connecticut Department of Public Health (CDPH) was followed by state-initiated validation, laboratory proficiency testing, and review of hospital demographic characteristics.

All 45 clinical laboratories and all 37 (36 for 1995 and 1996) acute-care hospitals in Connecticut were included in the study.

The outcome measures included determination of the statewide incidence of VRE and the accuracy of passive reporting, determination of clinical laboratory proficiency in detecting VRE, and analysis of hospital characteristics that might be associated with an increased incidence of VRE.

During 1994 through 1996, 29 (78%) of 37 hospital-affiliated clinical laboratories and 1 (11%) of 9 commercial or other laboratories in Connecticut reported to the CDPH the isolation of VRE from sterile sites; 158 isolates were reported for these 3 years. Based on verification, we discovered that these laboratories actually detected 58 VRE isolates in 1994, 104 in 1995, and 104 in 1996 (total, 266). The age-standardized incidence rate of VRE was 14.1 cases per million population in 1994 and 26.8 cases per million population for both 1995 and 1996. Laboratory proficiency testing revealed that high-level vancomycin resistance was identified accurately and that low- and moderate-level resistance was not detected. The incidence of VRE isolates was three times greater in hospitals with over 300 beds compared with categories of hospitals with fewer beds. Increases in the number of VRE isolates were at least twice as likely in hospitals located in areas with a higher population density, or with a residency program or trauma center in the hospital.

Passive reporting of VRE isolates from sterile sites markedly underestimated the actual number of isolates, as determined in a statewide reporting system. Statewide passive surveillance systems for routine or emerging pathogens must be validated and laboratory proficiency ensured if results are to be accurate and substantial underreporting is to be corrected.

To evaluate the in vitro activity of antiseptics and detergents against Candida.

One strain each of Candida albicans, Candida tropicalis, Candida lusitaniae, Candida parapsilosis, Candida kefyr, Candida glabrata, and an American Type Culture Collection strain of Escherichia coli (control) were studied. Clinical isolates were obtained from patients in a bone marrow unit of a large tertiary hospital. Antiseptic and disinfectant agents studied were used in the hospital where isolates were identified for cleaning of inanimate surfaces or hand washing. In vitro susceptibility was determined using a broth macrodilution method with exposure times to antiseptic or disinfectant agent of 15 seconds to 4 minutes and concentrations of agents that ranged from undiluted to 1:10,000 dilution.

A 900-bed teaching hospital.

Of disinfectants tested, Vestal and Sparquat inhibited growth of all species at dilutions of ≤1:100 at all contact times for all species. Clorox showed inhibition of growth at 1:100 dilution after 30 seconds of contact time for all isolates. Of antiseptics studied, Hibiclens inhibited growth of all species except C tropicalis at dilutions of ≤1:100 at all contact times and for C tropicalis after 60 seconds. Clinidine inhibited growth of all species at dilutions of ≤1:100 at all contact times for all species with the exception of C glabrata and C tropicalis, which grew at the undiluted concentration. Ultradex failed to demonstrate killing of any species for any dilutions tested.

The results of this study show varying degrees of in vitro inhibition of growth by a variety of antiseptics and disinfectants against clinical isolates of Candida species from hospitalized patients.