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This retrospective cohort study revealed that linezolid resistance in vancomycin-resistant Enterococcus faecium was dependent on prior linezolid exposure and duration of linezolid therapy. These strains of E. faecium were resistant to the entire class of oxazolidinones.
OBJECTIVE: To determine the efficacy of the use of gloves and gowns compared with that of the use of gloves alone for the prevention of nosocomial transmission of vancomycin-resistant enterococci. DESIGN: Epidemiologic study and controlled, nonrandomized clinical trial. SETTING: University-affiliated, 900-bed, urban teaching hospital in which vancomycin-resistant enterococci are endemic. PATIENTS: 181 consecutive patients admitted to the medical intensive care unit for 48 hours or more. INTERVENTION: It was determined that all hospital employees would always use gloves and gowns when attending 8 particular beds in the medical intensive care unit and would always use gloves alone when attending 8 others. Compliance with precautions was monitored weekly. Rectal surveillance cultures were taken from patients daily. Cultures of environmental surfaces, such as those of bed rails, bedside tables, and other frequently touched objects in patient rooms and common areas, were taken monthly. Pulsed-field gel electrophoresis was used for molecular epidemiologic typing of vancomycin-resistant enterococci. MEASUREMENTS: The number of patients becoming colonized by vancomycin-resistant enterococci; the number of days to acquisition of vancomycin-resistant enterococci; and other measurements, including nosocomial infections, length of hospital stay, and mortality rates. RESULTS: The 93 patients in glove-and-gown rooms and the 88 patients in glove-only rooms had similar demographic and clinical characteristics. Fifteen (16.1%) patients in the glove-and-gown group and 13 (14.8%) in the glove-only group had vancomycin-resistant enterococci on admission to the medical intensive care unit. Twenty-four (25.8%) patients in the glove-and-gown group and 21 (23.9%) in the glove-only group acquired vancomycin-resistant enterococci in the medical intensive care unit. The mean times to colonization among the patients who became colonized were 8.0 days in the glove-and-gown group and 7.1 days in the glove-only group. None of these comparisons were statistically significant. Risk factors for acquisition of vancomycin-resistant enterococci induced length of stay in the medical intensive care unit, use of enteral feeding, and use of sucralfate. Compliance with precautions was 79% in glove-and-gown rooms and 62% in glove-only rooms (P < 0.001). Only 25 of 397 (6.3%) environmental cultures were positive for vancomycin-resistant enterococci. Nineteen types of vancomycin-resistant enterococci were documented by pulsed-field gel electrophoresis during the study period. CONCLUSIONS: Universal use of gloves and gowns was no better than universal use of gloves only in preventing rectal colonization by vancomycin-resistant enterococci in a medical intensive care unit of a hospital in which vancomycin-resistant enterococci are endemic. Because the use of gowns and gloves together may be associated with better compliance and may help prevent transmission of other infectious agents, this finding may not be applicable to outbreaks caused by single strains or hospitals in which the prevalence of vancomycin-resistant enterococci is low.
Bacteraemia caused by vancomycin-resistant enterococci (VRE) is an important clinical problem because there are only a few potent antimicrobial agents against such bacteria. Therefore, understanding the pathogenic mechanisms of VRE bacteraemia is important for prophylaxis. This study shows that treatment of mice with cyclophosphamide and a combination of metronidazole, kanamycin and vancomycin reduced normal intestinal flora and induced systemic VRE bacteraemia. Translocation of VRE and the normal intestinal flora to the mesenteric lymph nodes, liver, spleen and blood, and mortality rate were dependent on treatment with cyclophosphamide and each of the three antimicrobial drugs. Among the different strains studied, C57BL/6 mice were the most susceptible to VRE. The virulence of vancomycin-resistant Enterococcus faecalis was greater than that of vancomycin-resistant Ent. faecium. On the day after inoculation of VRE, Escherichia coli was also detected in many VRE-positive specimens including blood, liver and the mesenteric lymph nodes. Moreover, both VRE and E. coli were detected simultaneously in almost all blood samples obtained from dead and dying mice, and VRE organisms outnumbered E. coli in those samples by 100:1 or more. These results indicate that changes in normal intestinal flora by administration of antimicrobial drugs and severity of neutropenia induced by cyclophosphamide are important factors that contribute to the development of systemic VRE bacteraemia. E. coli may be intimately associated with the establishment of VRE translocation.
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Vancomycin-resistant enterococci (VRE) are becoming a major concern in medical practice. Their increased prevalence and their ability to transfer vancomycin resistance to other bacteria (including methicillin-resistant Staphylococcus aureus) have made them a subject of close scrutiny and intense investigation. Colonization is usually acquired by susceptible hosts in an environment with a high rate of patient colonization with VRE (eg, intensive care units, oncology units). Vancomycin-resistant enterococci can survive in the environment for prolonged periods (>1 week), can contaminate almost any surface, and can be passed from one patient to another by health care workers. Whether VRE colonization leads to infection depends on the health status of the patient. Whereas immunocompetent patients colonized with VRE are at low risk for infection, weakened hosts (patients with hematologic disorders, transplant recipients, or severely ill patients) have an increased likelihood of developing infection following colonization. Quinupristin-dalfopristin and linezolid are among the anti-infective agents that have recently become available to treat infection caused by VRE. Other antimicrobials are currently under development. Molecular techniques such as polymerase chain reaction and standard culture studies are being used to detect VRE colonization, infection, and outbreaks.
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OBJECTIVES: To describe the population in whom bloodstream infections with vancomycin-resistant enterococci occur and the clinical and microbiologic features of infection. METHODS: From June 1, 1991, to January 31, 1994, 73 patients with bloodstream infections with vancomycin-resistant enterococci were identified by retrospective review of hospital charts and microbiology records. RESULTS: Fifty-two (73%) of 71 patients with evaluable data were hospitalized in an intensive care, unit, the adult oncology unit, or the acquired immunodeficiency syndrome unit. Before the development of the bloodstream infection with vancomycin-resistant enterococci, patients were hospitalized and received antibiotics for a median of 26 and 25.5 days, respectively. A hematologic malignancy, respiratory failure, or renal failure requiring dialysis was present in 59 patients (83%). Acute Physiology and Chronic Health Evaluation II scores of the patients ranged from 6 to 35 (median, 17). Forty-five (63%) of the patients died. Compared with 37 patients who had only a single positive blood culture, the 34 patients with 2 or more blood cultures positive for vancomycin-resistant enterococci more often were neutropenic or had acquired immunodeficiency syndrome (74% vs 35%; P = .002). CONCLUSIONS: Bloodstream infections with vancomycin-resistant enterococci predominantly affect severely ill patients who have received extensive antibiotic treatment during a prolonged hospitalization. Immunocompromised patients are more likely to have a persistent blood-stream infection with vancomycin-resistant enterococci.
BACKGROUND: The health and economic impact of vancomycin-resistant enterococci has not been quantified. METHODS: A retrospective matched cohort study was conducted comparing the outcomes of patients with vancomycin-resistant enterococci (cases) with those of control subjects matched for length of hospital stay until inclusion in the cohort, hospital location, and calendar date. The propensity to be a vancomycin-resistant enterococci case was modeled based on patient characteristics, and included in multivariable models to adjust for confounding. Analyses included the following: (1) conditional logistic regression for mortality, surgery, intensive care unit admission, and discharge to long-term care; (2) linear regression for the logarithm of cost; and (3) accelerated failure time model for length of stay. RESULTS: A total of 233 cases were compared with 647 controls. Groups were similar in age (mean, 62 years), sex (female, 47%), and length of stay before inclusion in the cohort (mean, 8.1 days), but differed in primary diagnosis and comorbidities, past infection or colonization with methicillin sodium-resistant Staphylococcus aureus or Clostridium difficile, and treatment with cephalosporins or metronidazole. These variables were included in the propensity score, which had good to excellent prediction. Outcomes for cases vs controls and adjusted risks (relative risks [RRs]) were as follows: (1) case fatality rate, 17% vs 6% (RR, 2.13; P =.04); (2) length of stay after inclusion in the cohort, 15.1 vs 8.5 days (RR, 1.73; P<.001); (3) hospital costs, $52 449 vs $31 915 (RR, 1.40; P<.001); (4) surgery after inclusion in the cohort, 18% vs 10% (RR, 2.74; P =.001); (5) intensive care unit admission after inclusion in the cohort, 25% vs 14% (RR, 3.47; P<.001); and (6) transfer to an institution, 51% vs 35% (RR, 2.01; P =.001). CONCLUSION: Compared with a matched hospital population, a population with vancomycin-resistant enterococci was associated with severe adverse outcomes: increased mortality, morbidity, and costs.
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A point-prevalence study of vancomycin-resistant enterococci colonization of the gastrointestinal tract in an Israeli hospital revealed that 14.7% of the 320 inpatients were colonized. Vancomycin-resistant enterococci colonization was detected in most departments except the neonatal intensive care unit. Hence, a prospective longitudinal study of the prevalence of vancomycin-resistant enterococci colonization in the neonatal intensive care unit was conducted. A rectal swab was obtained from every newborn on admission to the neonatal intensive care unit and once weekly thereafter until the patient was discharged. Enterococci were isolated and tested for susceptibility to vancomycin. A total of 84 neonates were enrolled and monitored on average for 3 weeks (SD +/- 3.9, range 1-20 weeks). Mean gestational age was 35.7 weeks (SD +/- 3.9, range 25-42 weeks), and mean birth weight was 2.4 kg (SD +/- 0.9, range 0.45-4.1 kg). Most patients had one or more of the known risk factors associated with colonization with vancomycin-resistant enterococci. Eighty percent of the patients received antibiotics during the study, and 14.3% received vancomycin. The median duration of vancomycin treatment was 12.5 days (SD +/- 16.8, range 5-55 days). Fifty-one of 84 (61%) patients acquired enterococci sensitive to vancomycin during the study period, but no newborn had vancomycin-resistant enterococci. Possible explanations for this finding may be physical isolation of the neonatal intensive care unit from the rest of the hospital, intrinsic differences in the bowel milieu of this age group and the lack of exposure to food and other environmental sources of vancomycin-resistant enterococci from the community.
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BACKGROUND: Enterococcus species are major nosocomial pathogens and are exhibiting vancomycin resistance with increasing frequency. Previous studies have not resolved whether vancomycin resistance is an independent risk factor for death in patients with invasive disease due to Enterococcus species or whether antibiotic therapy alters the outcome of enterococcal bacteremia. OBJECTIVE: To determine whether vancomycin resistance is an independent predictor of death in patients with enterococcal bacteremia and whether appropriate antimicrobial therapy influences outcome. DESIGN: Prospective observational study. SETTING: Four academic medical centers and a community hospital. PATIENTS: All patients with enterococcal bacteremia. MEASUREMENTS: Demographic characteristics; underlying disease; Acute Physiology and Chronic Health Evaluation (APACHE) II scores; antibiotic therapy, immunosuppression, and procedures before onset; and antibiotic therapy during the ensuing 6 weeks. The major end point was 14-day survival. RESULTS: Of 398 episodes, 60% were caused by E. faecalis and 37% were caused by E. faecium. Thirty-seven percent of isolates exhibited resistance or intermediate susceptibility to vancomycin. Twenty-two percent of E. faecium isolates showed reduced susceptibility to quinupristin-dalfopristin. Previous vancomycin use (odds ratio [OR], 5.82 [95% CI, 3.20 to 10.58]; P < 0.001), previous corticosteroid use (OR, 2.43 [CI, 1.22 to 4.86]; P = 0.01), and total APACHE II score (OR, 1.06 per unit change [CI, 1.02 to 1.10 per unit change]; P = 0.003) were associated with vancomycin-resistant enterococcal bacteremia. The mortality rate was 19% at 14 days. Hematologic malignancy (OR, 3.83 [CI, 1.56 to 9.39]; P = 0.003), vancomycin resistance (OR, 2.10 [CI, 1.14 to 3.88]; P = 0.02), and APACHE II score (OR, 1.10 per unit change [CI, 1.05 to 1.14 per unit change]; P < 0.001) were associated with 14-day mortality. Among patients with monomicrobial enterococcal bacteremia, receipt of effective antimicrobial therapy within 48 hours independently predicted survival (OR for death, 0.21 [CI, 0.06 to 0.80]; P = 0.02). CONCLUSIONS: Vancomycin resistance is an independent predictor of death from enterococcal bacteremia. Early, effective antimicrobial therapy is associated with a significant improvement in survival.
Twenty-seven isolates of vancomycin-resistant enterococci were obtained at monthly intervals from a bed-ridden man with hypoxic encephalopathy. During the 28-month period of the patient's hospitalization, 3 episodes of bacteremia and one episode of catheter-related infection caused by vancomycin-resistant enterococci occurred. Rectal swabs showed colonization of vancomycin-resistant enterococci for more than 2 years. Three months after termination of antimicrobial therapy, the rectal colonization for vancomycin-resistant enterococci was eradicated. Four species (Enterococcus faecium, Enterococcus gallinarum, Enterococcus faecalis, and Enterococcus casseliflavus) were identified among the 27 vancomycin-resistant enterococcus isolates. Three non-clonal related patterns were found among 17 strains of E. faecium by pulsed-field gel electrophoresis. All of the 3 E. faecalis isolates were of the VanB phenotype, but of the vanA genotype. Linezolid had the most potent in vitro activity against these vancomycin-resistant enterococcus isolates, with minimum inhibitory concentrations >2 microg/mL. Eighty-five percent of these vancomycin-resistant enterococcus isolates were susceptible to tetracycline and 66% were susceptible to quinupristin-dalfopristin. Although a high genetic correlation of E. faecium was identified in the patient with prolonged hospitalization, the isolation of 3 genetically unrelated colonized isolates suggested a lack of correlation between infection and colonization. Precautions against resistant organisms, adapted antibiotic policies, and elimination of patient carriage are useful for controlling the spread of vancomycin-resistant enterococci.
Vancomycin-resistant enterococci (VRE) have emerged as an important nosocomial pathogen. Since 1989, a rapid increase in the incidence of enterococcal bacteremia and endocarditis by VRE has been reported. The use of avoparcin in animal husbandry is reportedly associated with the appearance of VRE. In this study, a multiplex polymerase chain reaction (PCR) method was established to detect and differentiate resistant types of enterococci, which specifically amplify the four van genes that encode vancomycin resistance elements. Using this method, we investigated the incidence rates and types of VRE from two types of farms: those that had used avoparcin and those that had not used avoparcin. A total of 1091 animal fecal samples were collected from 70 pig farms and 32 poultry farms. A total of 425 enterococci were isolated from the fecal samples. Among the 425 isolates, six showed a pattern of high-level vancomycin resistance (Minimal Inhibitory Concentration, MIC: 64-256 microg/ml). Out of six high-level VRE, three were isolated from poultry farms that had used avoparcin and three were not. The six high-level VRE harbored the vanA gene. Sixty-seven of 425 isolates that showed a pattern of low-level vancomycin resistance (MIC: 4-8 microg/ml) were associated with the presence of vanC-1 or vanC-2/3 gene. We also performed a repetitive extragenic palindromic PCR (rep-PCR) method to compare the genetic relatedness between the high-level VRE of six animal isolates and 31 human isolates. None of the animal isolates had a similar rep-PCR pattern as the human isolates but similarities between human VRE isolates were observed.
BACKGROUND: Between 1990 to 1992 and 1993 to 1995 there was a >5-fold increase (16.7% to 89.8%) in vancomycin-resistant Enterococcus faecium isolates as a percentage of all isolates of vancomycin-resistant enterococci on the pediatric units of The New York Hospital-Cornell Medical Center (NYH-CMC). A molecular epidemiologic investigation was undertaken to determine the extent to which this increase was associated with the spread of a vanA-containing clone of vancomycin-resistant E. faecium that had been previously defined in adults hospitalized at NYH-CMC or with the spread of another vanA clone that had been defined in children hospitalized on the pediatric service at Memorial Sloan-Kettering Cancer Center, which shares a common pediatric intensive care unit and pediatric house staff with NYH-CMC. METHODS: Molecular genotyping of vancomycin-resistant E. faecium isolates obtained from pediatric patients from 1993 to 1995 was performed by pulsed field gel electrophoresis of chromosomal SmaI digests. Southern hybridization was performed using vanA- and vanB-specific probes. Medical records of patients were reviewed for pertinent clinical and demographic information. RESULTS: A single vanB clone of vancomycin-resistant E. faecium was responsible for 17 (77.3%) of 22 isolates in the neonatal intensive care unit (NICU) of NYH-CMC. Two other vanB strains of vancomycin-resistant E. faecium and 2 vanA strains were identified among the 5 remaining NICU isolates. Vancomycin-resistant E. faecium isolates from the other pediatric units represented a heterogeneous population of primarily vanA strains, but vanA clonal strains previously identified from patients on adult services at NYH-CMC and from children hospitalized at Memorial Sloan-Kettering Cancer Center were not detected. CONCLUSION: A newly identified vanB clone was responsible for the increase in vancomycin-resistant E. faecium isolates in the NICU of NYH-CMC. The increase of vancomycin-resistant E. faecium among children hospitalized at NYH-CMC was unrelated to the spread of vancomycin-resistant E. faecium among adults in the same hospital or among children at an affiliated facility cared for by the same house staff and sharing a common pediatric intensive care unit.
Screening for Vancomycin Resistant Enterococci (VRE) is recommended for preventing nosocomial infections with VRE. The aim of this study was to assess the performance of VCA3 agar (bioMérieux) in VRE isolation from fecal specimens. 220 specimens were cultured on VCA3 agar, which contains vancomycin and in parallel, on CAP agar (Oxoid), which is vancomycin-free. 36 vancomycin resistant enterococci were isolated: 24 isolates of Enterococcus faecium expressed a high-level resistance to vancomycin and 12 isolates of E. gallinarum/casseliflavus exhibited resistance at low-level. The sensitivity of VCA3 appeared greater than that of CAP for VRE isolation: 92% (22/24) vs 79% (19/24) for E. faecium (NS, P>0.05) ; 83% (10/12) vs 50% (6/12) for E. gallinarum/casselliflavus (NS, P>0.05). As expected, initial cultures of multiple gram positive organisms were far more frequent on CAP agar than on VCA3 agar. The isolation rate of vancomycin susceptible gram positive strains was impressively lower on VCA3 medium than on CAP medium. VCA3 agar avoided therefore additional subcultures, useless identification and susceptibility tests. In conclusion, VCA3 medium could be useful for the direct, rapid and selective isolation of VRE from fecal specimens.