Prevalence and acquisition of vancomycin-resistant enterococci in a medical intensive care unit.

Patients admitted to a medical intensive care unit during 21 days had rectal and urine samples cultured for vancomycin-resistant enterococci (VRE). The prevalence rate was 55.3%. Only enteral feedings were associated with acquisition of VRE. One-quarter of VRE transmission resulted from acquisition in the study unit, 35% arrived from other units, and 15% from other hospitals.     

Outbreak of vancomycin-resistant Enterococcus faecium in a neonatal intensive care unit.

An outbreak of vancomycin-resistant Enterococcus faecium involving 28 infants in a neonatal intensive care unit was observed. Successful control of the outbreak was achieved following use of patient and staff cohorting, contact isolation precautions, patient and environmental surveillance cultures, environmental decontamination, molecular typing, introduction of an alcohol-based hand disinfectant, and decreased use of vancomycin.     

Control of vancomycin-resistant enterococci in the neonatal intensive care unit.

BACKGROUND AND OBJECTIVE: Multidrug-resistant organisms (MDROs), such as vancomycin-resistant enterococci (VRE), cause serious infections, especially among high-risk patients in NICUs. When VRE was introduced and transmitted in our NICU despite recommended infection control practices, we instituted active surveillance cultures to determine their efficacy in detecting and controlling spread of VRE among high-risk infants. METHODS: Active surveillance cultures, other infection control measures, and a mandatory in-service education module on preventing MDRO transmission were implemented. Cultures were performed on NICU admission and then weekly during their stay. Molecular DNA fingerprinting of VRE isolates facilitated targeting efforts to eliminate clonal spread of VRE. Repetitive sequence PCR (rep-PCR)-based DNA fingerprinting was used to compare isolates recovered from patients with VRE infection or colonization. Environmental VRE cultures were performed around VRE-colonized or -infected patients. DNA fingerprints were prepared from the products of rep-PCR amplification and analyzed using software to determine strain genetic relatedness. RESULTS: Active surveillance cultures identified 65 patients with VRE colonization or infection among 1,820 admitted to the NICU. Rep-PCR performed on 60 VRE isolates identified 3 clusters. Cluster 1 included isolates from 21 patients and 4 isolates from the environment of the index patient. Clusters 2 and 3 included isolates from 23 and 3 patients, respectively. Similarity coefficients among the members of each cluster were 95% or greater. CONCLUSIONS: Control of transmission of multi-clonal VRE strains was achieved. Active surveillance cultures, together with implementation of other infection control measures, combined with rep-PCR DNA fingerprinting were instrumental in controlling VRE transmission in our NICU.     

Management of an outbreak of vancomycin-resistant enterococci in the medical intensive care unit of a cancer center.

Between November 1996 and February 1997, 17 episodes of vancomycin-resistant enterococci (VRE) infection or colonization (9 infections, 8 colonizations), all with the same or a similar genomic DNA pattern, were identified in the medical intensive care unit (MICU) of a tertiary-care cancer hospital. The cases were genotypically traced to a patient who was admitted to the hospital in September 1996 and who, by December 1996, had four different admissions to the MICU. Multifaceted infection control measures, including decontamination of the environment and of nondisposable equipment, halted the nosocomial transmission of VRE in the MICU.     

Emergence of vancomycin-resistant enterococci

Vancomycin and ampicillin resistance in clinical Enterococcus faecium strains has developed in the past decade. Failure to adhere to strict infection control to prevent the spread of these pathogens has been well established. New data implicate the use of specific classes of antimicrobial agents in the spread of vancomycin-resistant enterococci (VRE). Extended-spectrum cephalosporins and drugs with potent activity against anaerobic bacteria may promote infection and colonization with VRE and may exert different effects on the initial establishment and persistence of high-density colonization. Control of VRE will require better understanding of the mechanisms by which different classes of drugs promote gastrointestinal colonization.     

The changing epidemiology of vancomycin-resistant enterococci.

OBJECTIVE: To determine the distribution of vancomycin-resistant enterococci (VRE) cases in our hospital and those from outside of our hospital from 1993 through 1998. METHODS: Weekly rectal surveillance was instituted whenever there were two or more cases present in the units. Cases were divided into acquired in our hospital, acquired outside of our hospital (VRE positive after and within 72 hours of admission, respectively), and indeterminate. Hospital cases were attributed to the originating ward or intensive care unit (ICU) if patients were noted to be positive within 72 hours of transfer. RESULTS: From 1993 to 1998, the rate of VRE per 1,000 admissions increased threefold, from 3.2 to 9.8, for the hospital. VRE cases acquired outside of the hospital increased by approximately 5% per year (r = 0.87; P = .03). The rate of VRE per 1,000 admissions increased 1.7-fold in the ICUs and 3.6-fold in the wards. The ICUs had an average of 75.3 cases per year, with the number of new cases per year increasing by approximately 9 (r = 0.80; P = .028). In the wards, there were an average of 22.0 new cases per year, with a slight upward trend of 3 additional new cases per year (r = 0.69; P = .64). There was a highly significant increasing linear trend (P = .0007) for VRE colonization and infection. CONCLUSION: Although VRE still predominate in the ICUs, cases originating from outside of our hospital and the wards are becoming more common. VRE colonization remained more frequent than infection.     

Outcomes associated with vancomycin-resistant enterococci: a meta-analysis.

BACKGROUND: Because patients with vancomycin-resistant Enterococcus bacteremia (VREB) usually have a higher severity of illness, it has been unclear whether VREB is worse than vancomycin-susceptible Enterococcus bacteremia (VSEB). METHODS: Data on morbidity and case fatality rates and costs were pooled from studies comparing VREB and VSEB, identified by Medline January 1986 to April 2002) and meeting abstracts. Heterogeneity across studies was assessed with contingency table chi-square. Multivariate analyses (MVAs) controlling for other predictors were evaluated. RESULTS: Thirteen studies compared case-fatality rates of VREB and VSEB. VREB case fatality was significantly higher (48.9% vs 19%; RR, 2.57; CI95, 2.27 to 2.91; attributable mortality = 30%). Five studies compared VREB with VSEB when bacteremia was the direct cause of death; VREB case fatality was significantly higher (39.1% vs 21.8%; RR, 1.79; CI95, 1.28 to 2.5; attributable mortality = 17%). Four MVAs found significant increases in case-fatality rates (OR, 2.10 to 4.0), 3 showed trends toward increase (OR, 1.74 to 3.34 with wide confidence intervals), and 3 with low statistical power found no difference. VREB recurred in 16.9% versus 3.7% with VSEB (P < .0001). Three studies reported significant increases in LOS, costs, or both with VREB. CONCLUSION: Most studies have had inadequate sample size, inadequate adjustment for other predictors of adverse outcomes, or both, but available data suggest that VREB is associated with higher recurrence, mortality, and excess costs than VSEB including multiple studies adjusting for severity of illness.     

Experience of vancomycin-resistant enterococci in a children's hospital

Vancomycin resistant enterococci (VRE) are increasingly important nosocomial pathogens. This paper describes our experience of the epidemiology and clinical impact of VRE in the two years since the occurrence of our first case of VRE infection. Following introduction of surveillance, gastrointestinal colonization with VRE was detected in 38.3% of Haematology/Oncology and 11.1% of Hepatology/Gastroenterology patients, but in only 2.3% of children in the Paediatric Intensive Care and 1.5% of children in the Renal Unit. Only five patients with gastrointestinal colonization subsequently developed clinical infection with VRE, giving an annual incidence of 7.5%. A further six children were colonized at extra-intestinal sites. Twelve children had clinical infections with VRE, of whom three (25%) died. Contamination of bedspaces was found in association with 2/3 (66.7%) children with extraintestinal colonization and 5/7 (71.4%) children with clinical infections, compared with 6/28 (21.4%) cases of gastrointestinal colonization. In the latter group, bedspace contamination was usually associated with widespread contamination of the ward with VRE and may have been the cause rather than the result of patients acquiring VRE. Originally we employed control measures based closely on the North American HICPAC guidelines, but our control strategy has since evolved in response to epidemiological and clinical observations.     

Occurrence of co-colonization or co-infection with vancomycin-resistant enterococci and methicillin-resistant Staphylococcus aureus in a medical intensive care unit.

OBJECTIVE: To determine the occurrence of co-colonization or co-infection with VRE and MRSA among medical patients requiring intensive care. DESIGN: Prospective, single-center, observational study. SETTING: A 19-bed medical ICU in an urban teaching hospital. PATIENTS: Adult patients requiring at least 48 hours of intensive care and having at least one culture performed for microbiologic evaluation. RESULTS: Eight hundred seventy-eight consecutive patients were evaluated. Of these patients, 402 (45.8%) did not have microbiologic evidence of colonization or infection with either VRE or MRSA, 355 (40.4%) were colonized or infected with VRE, 38 (4.3%) were colonized or infected with MRSA, and 83 (9.5%) had co-colonization or co-infection with VRE and MRSA. Multiple logistic regression analysis demonstrated that increasing age, hospitalization during the preceding 6 months, and admission to a long-term-care facility were independently associated with colonization or infection due to VRE and co-colonization or co-infection with VRE and MRSA. The distributions of positive culture sites for VRE (stool, 86.7%; blood, 6.5%; urine, 4.8%; soft tissue or wound, 2.0%) and for MRSA (respiratory secretions, 34.1%; blood, 32.6%; urine, 17.1%; soft tissue or wound, 16.2%) were statistically different (P < .001). CONCLUSIONS: Co-colonization or co-infection with VRE and MRSA is common among medical patients requiring intensive care. The recent emergence of vancomycin-resistant Staphylococcus aureus and the presence of a patient population co-colonized or co-infected with VRE and MRSA support the need for aggressive infection control measures in the ICU.     

Molecular epidemiology of vancomycin-resistant enterococci: a 2-year perspective.

OBJECTIVE: 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. DESIGN: 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. SETTING: A 588-bed, university-affiliated, tertiary-care hospital and a neighboring 155-bed rehabilitation facility. RESULTS: 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. CONCLUSIONS: 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".     

Risk factors for colonization with vancomycin-resistant enterococci in a Melbourne hospital.

OBJECTIVE: To determine risk factors for colonization with vancomycin-resistant enterococci (VRE) in a hospital outbreak. DESIGN: Outbreak investigation and case-control study. SETTING: A referral teaching hospital in Melbourne, Australia. PARTICIPANTS: Cases were inpatients colonized (with or without clinical disease) with VRE between July 26 and November 28, 1998; controls were hospitalized patients without VRE. METHODS: Five cases of VRE were identified between July 26 and November 8, 1998, by growth of VRE from various sites. Active case finding by cultures of rectal swabs from patients surveyed in wards was commenced on July 26, after the first isolate of VRE. RESULTS: There were 19 cases and 66 controls. All the VRE identified were vanB, and all were Enterococcus faecium. One molecular type predominated (18/19 cases). In a logistic-regression model, being on the same ward as a VRE case was the highest risk factor (odds ratio [OR], 82; 95% confidence interval [CI95], 5.7-1,176; P=.001). Having more than five antibiotics (OR, 11.9; CI95 1.1-129.6; P<.05), use of metronidazole (OR, 10.9; CI95, 1.7-69.8; P=.01), and being a medical patient (OR, 8.1; CI95, 1.4-47.6; P<.05) also were significant. Intensive care unit admission was associated with decreased risk (OR, 0.1; CI95, 0.01-0.8; P<.05). CONCLUSION: Our findings are consistent with an acute hospital outbreak. Monitoring and control of antibiotic use, particularly metronidazole, may reduce VRE in our hospital. Ongoing surveillance and staff education also are necessary.     

Efficacy of hand disinfectants against vancomycin-resistant enterococci in vitro.

Vancomycin-resistant enterococci (VRE) may be spread within a hospital via the contaminated hands of the healthcare worker. Effective hand disinfectants are necessary to break chains of transmission. We determined the bactericidal activity of 1-propanol, chlorhexidine digluconate (0.5 and 4%). Sterillium (45% 2-propanol, 30% 1-propanol and 0.2% mecetronium etilsulphate), Skinsept F (70% 2-propanol, 0.5% chlorhexidine digluconate and 0.45% hydrogen peroxide) and Hibisol (70% 2-propanol and 0.5% chlorhexidine gluconate) against 11 clonally distinct enterococcal isolates in a quantitative suspension test. Four isolates were vancomycin susceptible, four were vanA and the remainder vanB positive. Eight isolates were identified as Enterococcus faecium, two as Enterococcus faecalis and one as Enterococcus gallinarum. The investigator was blinded to the species and the genotype. Four parallel experiments were carried out for each isolate, each preparation, each dilution and each reaction time. 1-Propanol (60%), Sterillium, Skinsept F and Hibisol were all highly bactericidal after 15 and 30 s against VRE and vancomycin-susceptible enterococci (VSE) with reduction factors (RF) > 6.4, even in dilution of 50% (v/v). No significant difference was observed between vanA isolates, vanB isolates and VSE. Chlorhexidine digluconate (0.5% and 4%) was found to be less bactericidal after 30, 60 and 300 sec (RF < or = 2.5). The vanB genotype isolates were found to be significantly more susceptible to chlorhexidine (0.5%) than the vanA isolates (60 sec; one-way ANOVA model; P = 0.05). After 300 sec the vanB genotype isolates were found to be significantly more susceptible to chlorhexidine (0.5%) than the other two genotype isolates (P = 0.016). The vanA isolates were found to be significantly more susceptible to chlorhexidine (4%) than the vanB isolates (300 s; P = 0.024). E. faecium was found to be less susceptible to chlorhexidine than E. faecalis at all concentrations and reaction times, but significant differences between RF were only observed at 60 sec for both chlorhexidine concentrations (P < 0.05; t-test for independent samples). Propanol is much more effective against enterococci than chlorhexidine and combination of the two may be useful in providing an immediate and long lasting effect.     

Characteristics of a large cluster of vancomycin-resistant enterococci in an Australian hospital.

Investigation of a cluster of hospital inpatients colonized with vancomycin-resistant enterococci (VRE) revealed a point-prevalence of 19.1%. The outbreak was controlled using established guidelines and additional strategies, including minimizing patient transfers and enforcing appropriate antibiotic prescribing. The incidence of VRE has remained low during the ensuing 30 months.     

An outbreak of vancomycin-resistant enterococci in a hematology-oncology unit: control by patient cohorting and terminal cleaning of the environment.

We describe the impact of enhanced infection control interventions on controlling the spread of vancomycin-resistant enterococci (VRE) in our hematology-oncology unit. Between April and September 1998, 13 patients on this unit were identified as having VRE. In addition to contact precautions, other measures that were needed to control the outbreak included closure of the unit to new admissions, creation of a cohort of VRE-positive patients and staff, and thorough cleaning of patients' rooms with 0.5% sodium hypochlorite.     

Characterizing vancomycin-resistant enterococci in neonatal intensive care

Repetitive sequence-based polymerase chain reaction fingerprinting was used to characterize 23 vancomycin-nonsusceptible enterococcal isolates from 2003 to 2004. Five genetically related clusters spanned geographically distinct referring centers. DNA fingerprinting showed infant-to-infant transmission from referring institutions. Thus, community healthcare facilities are a source of vancomycin-nonsusceptible enterococci and should be targeted for increased infection control efforts.     

Fecal colonization with vancomycin-resistant enterococci in Australia

To assess the rate of fecal vancomycin-resistant enterococci (VRE) colon ization in Austalia, we examined specimens from 1,085 healthy volunteers. VRE was cultured from 2(0.2%) of 1,085 specimens; both were vanB Enter ococcus faecium, identical by pulsed-field gel electrophoresis, but with a pattern rare in Melbourne hospitals.     

Lack of transmission of vancomycin-resistant enterococci in three long-term-care facilities.

Three patients colonized with vancomycin-resistant Enterococcus were admitted to one or more of three long-term-care facilities. Six point-prevalence surveys revealed no transmission of vancomycin-resistant Enterococcus after a total of 234 days of exposure during which moderately strict infection control measures were implemented. Four of 116 environmental cultures were positive.     

High-level vancomycin-resistant enterococci causing hospital infections

Nosocomial infection or colonization due to enterococci with high-level resistance to vancomycin (minimal inhibitory concentrations [MICs] between 64 and greater than 2000 mg/L) has occurred in 41 patients with renal disease. These vancomycin-resistant enterococci were cultured from many sources including blood. All but one strain contained one or more plasmids ranging in molecular weight from 1.0 to 40 Megadaltons (MDa). Vancomycin resistance was transferable by conjugation to a susceptible recipient strain of Enterococcus faecalis but this was not always associated with plasmid DNA. The emergence of transferable high-level vancomycin resistance in enterococci causing significant clinical infections is of particular importance since vancomycin is widely regarded as a reserve drug for the management of infections with multi-resistant Gram-positive organisms.