Vancomycin-resistant Enterococci Acquisition Research Articles

Role of environmental contamination as a risk factor for acquisition of vancomycin-resistant enterococci in patients treated in a medical intensive care unit.

Colonization pressure, proximity to another case, exposure to a nurse who cares for another case, enteral feeding, and the use of sucralfate, vancomycin hydrochloride, cephalosporins, or antibiotics are among the defined risk factors for acquisition of vancomycin-resistant enterococci (VRE) in the intensive care unit (ICU) setting. However, the role of rooms with contaminated environmental surfaces has not been well delineated. Retrospective case-control study conducted on patients admitted to the medical ICU (MICU) of a tertiary-care, university-affiliated medical center during a 9-month period. Patients who acquired VRE (cases) were matched with 2 randomly selected control subjects who did not acquire VRE and had been in the MICU for at least the same number of days. Thirty cases were matched with 60 appropriate controls. Cases were more likely to have been in the hospital for longer than 7 days before MICU admission (P =.009); to have occupied a specific room with persisting contaminated surfaces (P =.06); to have had a central venous catheter (P =.05); to have received vancomycin (P =.02), cephalosporins (P =.03), and quinolones (P =.006) before MICU admission; and to have received vancomycin (P =.02) and metronidazole sodium phosphate (P =.03) after MICU admission. Multivariate analysis showed that a hospital stay of longer than 1 week before MICU admission (P =.04), use of vancomycin before or after MICU admission (P =.03), use of quinolones before MICU admission (P =.03), and placement in a contaminated room (P =.02) were the best predictors of VRE acquisition. Among all other factors associated with VRE transmission, VRE acquisition may depend on room contamination, even after extensive cleaning. This study underscores the need for better cleaning and the role of the environment in transmission of VRE.

Effect of gastrointestinal bleeding and oral medications on acquisition of vancomycin-resistant Enterococcus faecium in hospitalized patients.

There has been minimal investigation of medications that affect gastrointestinal function as potential risk factors for the acquisition of vancomycin-resistant enterococci (VRE). We performed a retrospective case-control study, with control subjects matched to case patients by time and location of hospitalization. Strict exclusion criteria were applied to ensure that only case patients with a known time of acquisition of VRE were included. Control patients were patients with > or =1 culture negative for VRE. The risk factors identified were use of vancomycin (odds ratio [OR], 3.2; 95% confidence interval [CI], 1.7-6.0; P=.0003), presence of central venous lines (OR, 2.2; 95% CI, 1.04-4.6; P=.04), and use of antacids (OR, 2.9; 95% CI, 1.5-5.6; P=.002). Two protective factors included gastrointestinal bleeding (OR, 0.26; 95% CI, 0.08-0.79; P=.02) and use of Vicodin (Knoll Labs; hydrocodone and acetaminophen; OR, 0.93; 95% CI, 0.90-0.97; P=.0003). Changes in gastrointestinal function, whether due to bleeding or to the effects of oral medications, may affect whether patients become colonized with VRE.

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.

To gown or not to gown: the effect on acquisition of vancomycin-resistant enterococci.

Infection-control recommendations include the use of gowns and gloves to prevent horizontal transmission of vancomycin-resistant enterococci (VRE). This study sought to determine whether the use of a gown and gloves gives greater protection than glove use alone against VRE transmission in a medical intensive care unit (MICU). From 1 July 1997 through 30 June 1998 and from 1 July 1999 through 31 December 1999, health care personnel and visitors were required to don gloves and gowns upon entry into rooms where there were patients infected with nosocomial pathogens. From 1 July 1998 through 30 June 1999, only gloves were required under these same circumstances. During the gown period, 59 patients acquired VRE (9.1 cases per 1000 MICU-days), and 73 patients acquired VRE during the no-gown period (19.6 cases per 1000 MICU-days; P<.01). The adjusted risk estimate indicated that gowns were protective in reducing VRE acquisition in an MICU with high VRE colonization pressure.

The impact of persistent gastrointestinal colonization on the transmission dynamics of vancomycin-resistant enterococci.

The transmission dynamics of vancomycin-resistant enterococci (VRE) and factors contributing to their dissemination are complex. Mathematical modeling was used to simulate patterns of dissemination among patients and health care workers (HCWs) and to quantify the contribution of specific factors and infection control interventions on the endemic prevalence (EP) of VRE in a long-term hemodialysis unit. The model predicted that (1) an EP of 12% would be reached over time, regardless of the number of patients initially colonized, (2) endemicity would be sustained by the constant influx of newly colonized patients discharged from the hospital, (3) duration of VRE gastrointestinal colonization would have the most impact on the number of secondary cases, increasing the EP to a maximum of 70%, and (4) decreasing the patient:HCW ratio or improving hand hygiene would decrease the EP to 3%. Decreasing the duration of colonization, limiting hospital acquisition of VRE, and improving compliance with hand hygiene in the hemodialysis unit may decrease the rapidly rising rates of VRE in the patient population.

Epidemiology and clinical consequences of vancomycin-resistant enterococci in liver transplant patients.

Vancomycin-resistant enterococci (VRE) are increasingly important as pathogens in liver transplant patients. To guide control efforts, we conducted an epidemiological study of the frequency, source, and modes of transmission of VRE at our center. During September 1998 through August 1999, we obtained weekly surveillance cultures from consenting liver transplant patients and surfaces in their rooms. Pooled handwash specimens from personnel also were obtained. Specimens were processed on selective media to detect VRE, and isolates were typed by pulsed field gel electrophoresis. Information was collected from patient records concerning in-hospital treatment and clinical course. Serial cultures were obtained during 33 admissions of 29 patients. VRE were detected in initial specimens from 6 admissions, and nosocomial acquisition of VRE occurred in 12 (44%) of the remaining 27 admissions. Seven different strain types of VRE were detected. The initial site of acquisition was stool in all cases; bile became culture-positive in only two patients. Overall, 16 (55%) of the 29 patients became colonized, usually after transplantation. VRE were detected in environmental cultures during 10 admissions and in 2 of 21 pooled handwashes. No statistically significant differences in clinical status or treatment were found when colonized patients were compared to noncolonized controls. The only VRE infection resulted from a choledochojejunostomy anastomotic leak. Alimentary tract colonization by VRE occurred commonly in liver transplant patients, probably by cross-transmission. The clinical consequences were modest in the patients studied, but colonized transplant patients provide a substantial reservoir for continued VRE transmission in hospitals.

Acquisition of vancomycin-resistant enterococci during scheduled antimicrobial rotation in an intensive care unit.

Scheduled rotation of treatment of gram-negative antimicrobial agents has been associated with reduction of serious gram-negative infections. The impact of this practice on other nosocomial infections has not been assessed. The purpose of this study was to determine if scheduled antimicrobial rotation reduced rates of acquisition of enteric vancomycin-resistant enterococci (VRE) among 740 patients admitted to an intensive care unit (ICU). The preferred gram-negative agent was ceftazidime during rotation 1 and ciprofloxacin during rotation 2. Unadjusted VRE acquisition rates were 8.5 cases per 1000 ICU days and 11.7 cases per 1000 ICU days during rotations 1 and 2, respectively (P<.01). However, scheduled antimicrobial rotation of ceftazidime with ciprofloxacin had no effect on the risk of acquiring VRE in the ICU after adjustment for known risk factors. Independent predictors of acquisition of VRE were enteral feedings, higher colonization pressure, and increased duration of anaerobic therapy. Our findings can confirm no additional beneficial or adverse effect on VRE acquisition among ICU patients as a result of this practice.

Vancomycin-resistant enterococci among chronic hemodialysis patients: a prospective study of acquisition.

To determine the prevalence and rate of acquisition of vancomycin-resistant enterococci (VRE) among patients undergoing chronic (i.e., long-term) hemodialysis who were admitted to a tertiary care center, serial rectal cultures for VRE were performed at hospital admission and every 5 days until hospital discharge. A total of 7 (6%) of the 119 patients were colonized with VRE at admission. Six (19%) of the 32 patients who remained in the hospital > or =4 days acquired VRE. A nonambulatory status was significantly associated with colonization at admission (OR, 9.7; 95% CI, 1.8-53; P=.01), and vancomycin exposure was significantly associated with VRE acquisition (relative risk, 1.8; 95% CI, 1.1-2.9; P=.02). All patients acquired VRE from epidemiologically linked dialysis patients colonized with similar VRE genotypes. Hospital acquisition of VRE contributes substantially to the increasing prevalence of VRE in the chronic hemodialysis patient population.

Outbreak of vancomycin-resistant enterococci in a burn unit.

To investigate and control an outbreak of colonization and infection caused by vancomycin-resistant enterococci (VRE) in a burn intensive care unit (BICU). Epidemiological investigation, including multiple point-prevalence culture surveys of patients and environment, cultures from hands of healthcare workers (HCWs), pulsed-field gel electrophoresis (PFGE) typing of patient and environmental isolates, case-control study, and institution and monitoring of control measures. BICU in an 800-bed university medical center in Galveston, Texas. Between June 6, 1996, and July 14, 1997, 21 patients were colonized by VRE, and 4 of these patients developed bacteremia. Of 2,844 environmental cultures, 338 (11.9%) were positive, but all hand cultures from HCWs were negative. PFGE typing indicated that the outbreak was clonal, with VRE isolates from patients differing by < or =4 bands from the index case. Thirteen of 14 environmental isolates varied by < or =4 bands from the pattern of the index case. A case-control study analyzed by exact logistic regression identified diarrhea (odds ratio [OR], 43.9; 95% confidence interval [CI95], 5.5-infinity; P=.0001) and administration of an antacid (OR, 24.2; CI95, 2.9-infinity; P=.002) as independent risk factors for acquisition of VRE. During a 5-week period in October and November 1996, all patient and 317 environmental cultures were negative for VRE. The outbreak recurred from a contaminated electrocardiogram lead that had not been identified during the prior 5 weeks. VRE were finally eradicated from the BICU in July 1997, using barrier isolation and a very aggressive environmental decontamination program. A VRE outbreak in a BICU over 13 months was caused by a single clone. After apparent eradication of VRE from a BICU, recrudescence of the outbreak occurred, evidently from a small inapparent source of environmental contamination. Changes in gastrointestinal (GI) tract function (motility) and administration of medications, other than antibiotics, that have an effect on the GI tract may increase the risk of GI tract colonization by VRE in burn patients. Application of barrier isolation and an aggressive environmental decontamination program can eradicate VRE from a burn population.

Prevalence and determinants of fecal colonization with vancomycin-resistant Enterococcus in hospitalized patients in The Netherlands.

To determine the prevalence and determinants of fecal carriage of vancomycin-resistant enterococci (VRE) in intensive care unit (ICU), hematology-oncology, and hemodialysis patients in The Netherlands. Descriptive, multicenter study, with yearly 1-week point-prevalence assessments between 1995 and 1998. All patients hospitalized on the testing days in ICUs and hematology-oncology wards in nine hospitals in The Netherlands were included. Rectal swabs obtained from 1,112 patients were screened for enterococci in a selective broth and subcultured on selective media with and without 6 mg/L vancomycin. Resistance genotypes were determined by polymerase chain reaction. Further characterization of VRE strains was done by pulsed-field gel electrophoresis (PFGE). We studied possible determinants of VRE colonization with a logistic regression analysis model. Determinants analyzed included gender, age, and log-transformed length of prior hospital stay. The results showed that 614 (55%) of 1,112 patients were colonized with vancomycin-sensitive enterococci, and 15 (1.4%) of 1,112 carried VRE. No increase in VRE colonization was observed from 1995 to 1998. Eleven strains were identified as Enterococcus faecium and four as Enterococcus faecalis. All E faecium and one E faecalis carried the vanA gene; the other E faecalis strains harbored the vanB gene. PFGE revealed that three vanB VRE isolated from patients hospitalized in one single ICU were related, suggesting nosocomial transmission. Though higher age seemed associated with VRE colonization, exclusion of patients with the nosocomial strain from the regression analysis decreased this relation to nonsignificant. Duration of hospital stay was not associated with VRE colonization. VRE colonization in Dutch hospitals is an infrequent phenomenon. Although nosocomial spread occurs, most observed cases were unrelated, which suggests the possibility of VRE acquisition from outside the hospital. Prolonged hospital stay, age, and gender proved unrelated to VRE colonization.

Third-Generation Cephalosporins and Vancomycin as Risk Factors for Postoperative Vancomycin-Resistant Enterococcus Infection

S INCE THE late 1980s, group D enterococcus (GDEN), including Enterococcus faecalis and Enterococcus faecium, has emerged as an important nosocomial pathogen. Once thought to be a nonpathogen or a copathogen, GDEN has been shown to have the virulence factors necessary to cause infections in varied patient populations. Strains of GDEN resistant to multiple antibiotics have been studied as clinically problematic pathogens in surgical patients. Increased incidence of vancomycin-resistant enterococcus (VRE) has been identified as a serious complication in recipients of solid organ transplants. Throughout the emergence of GDEN as a recognized pathogen, antibiotic use has been cited consistently as a significant risk factor for infection. As antibiotic resistance among enterococci developed and VRE became endemic in many institutions, vancomycin hydrochloride and third-generation cephalosporins (3CGs) have been associated repeatedly with acquisition of VRE. The most commonly held theory on the mechanism by which broad-spectrum antibiotics such as 3GCs select for VRE is a disruption of the patient’s endogenous intestinal microbial flora. This disruption allows for accelerated growth of opportunistic pathogens, such as enterococci. Fairview-University Medical Center, in Minneapolis, Minn, is a large (.300bed) tertiary care teaching hospital. A marked increase in the number of surgical patients with VRE beginning on September 3, 1993, prompted the design of a 1:1 matched case-control study to investigate 3GC use as a risk factor for infection with VRE. By matching patients with VRE infections and those with vancomycinsensitive enterococcus (VSE) infections, we sought to identify the risk factors specific for infection with VRE as opposed to infection with enterococci in general. PAPER

Vancomycin-resistant enterococci: recent advances in genetics, epidemiology and therapeutic options.

Vancomycin-resistant enterococci (VRE) have gained much attention in the last decade. Currently, there are five known types of vancomycin resistance based on genes encoding ligase enzymes that the organisms use to produce their cell wall precursors, namely, VanA, VanB, VanC, VanD and VanE. An additional unclassified type was discovered in Australia. The basis of resistance among these phenotypes appears to be similar in that the resistant organisms produce peptidoglycan precursors that end in moieties other than D-alanyl-D-alanine, the usual target of vancomycin. The other dipeptide-like termini identified to date include D-alanyl-D-lactate and D-alanyl-D-serine, which have low affinity for glycopeptides. Recent evidence suggests that glycopeptide-producing organisms might be the remote origin of the vancomycin resistance genes. In European countries, avoparcin, a glycopeptide used in farm animals as a growth promoter, has been linked to the occurrence of VRE and occasional common strains have been identified in food products, farm animals, healthy subjects and hospitalized patients. There have been no such reports in the USA where heavy use of vancomycin and use of broad spectrum antibiotics such as cephalosporins have been identified as important risk factors for acquisition of VRE. Transmission within the same or between hospitals has been reported in many countries. Infection control measures and efforts to use antibiotics, particularly vancomycin, more appropriately have been implemented in a number of healthcare facilities with varying degrees of success. Many antibiotics, as a single agent or a combination of drugs, as well as various new antibiotics have been tested in vitro, in animal models, or used in anecdotal cases but clinical data from large comparative trials are not available to date. Because of the limited susceptibility of many VRE to other agents, efforts to control these organisms are particularly important. Copyright 1999 Harcourt Publishers LtdCopyright 1999 Harcourt Publishers Ltd.

The role of "colonization pressure" in the spread of vancomycin-resistant enterococci: an important infection control variable.

The spread of nosocomial multiresistant microorganisms is affected by compliance with infection control measures and antibiotic use. We hypothesized that "colonization pressure" (ie, the proportion of other patients colonized) also is an important variable. We studied the effect of colonization pressure, compliance with infection control measures, antibiotic use, and other previously identified risk factors on acquisition of colonization with vancomycin-resistant enterococci (VRE). Rectal colonization was studied daily for 19 weeks in 181 consecutive patients who were admitted to a single medical intensive care unit. A statistical model was created using a Cox proportional hazards regression model including length of stay in the medical intensive care unit until acquisition of VRE, colonization pressure, personnel compliance with infection control measures (hand washing and glove use), APACHE (Acute Physiology and Chronic Health Evaluation) 11 scores, and the proportion of days that a patient received vancomycin or third-generation cephalosporins, sucralfate, and enteral feeding. With survival until colonization with VRE as the end point, colonization pressure was the most important variable affecting acquisition of VRE (hazard ratio [HR], 1.032; 95% confidence interval [C1], 1.012-1.052; P=.002). In addition, enteral feeding was associated with acquisition of VRE (HR, 1.009; 95% CI, 1.000-1.017; P=.05), and there was a trend toward association of third-generation cephalosporin use with acquisition (HR, 1.007; 95% CI, 0.999-1.015; P=.11). The effects of enteral feeding and third-generation cephalosporin use were more important when colonization pressure was less than 50%. Once colonization pressure was 50% or higher, these other variables hardly affected acquisition of VRE. Acquisition of VRE was affected by colonization pressure, the use of antibiotics, and the use of enteral feeding. However, once colonization pressure was high, it became the major variable affecting acquisition of VRE.

Vancomycin-Resistant Enterococci (VRE) as Intestinal Flora from Poultry in Riyadh

2-5 The number of cases infected with VRE, as reported by the US Centers for Disease Control and Prevention, had jumped from 99 in 1992 to 278 in 1994, with a rapid increase in colonization, and a fecal carriage rate of 86%. 6 Since colonized patients as well as domestic animals and environment can serve as significant reservoirs for human acquisition of VRE, we determined the presence of these organisms in sewage and fecal samples of poultry, camels, goats and sheep in Riyadh and its vicinity. Our findings are reported in this paper.

Epidemiology of colonisation of patients and environment with vancomycin-resistant enterococci

Vancomycin-resistant enterococci (VRE) have emerged as nosocomial pathogens during the past 5 years, but little is known about the epidemiology of VRE. We investigated colonisation of patients and environmental contamination with VRE in an endemic setting to assess the importance of different sources of colonisation. Between April 12, and May 29, 1995, cultures from body sites (rectum, groin, arm, oropharynx, trachea, and stomach) and from environmental surfaces (bedrails, drawsheet, blood-pressure cuff, urine containers, and enteral feed) were obtained daily from all newly admitted ventilated patients in our medical intensive-care unit (MICU). Rectal cultures were obtained from all non-ventilated patients in the MICU. Strain types of VRE were determined by pulsed-field gel electrophoresis. There were 97 admissions of 92 patients, of whom 38 required mechanical ventilation. Colonisation with VRE on admission was more common in ventilated than in non-ventilated patients (nine [24%] vs three [6%], p < 0.05). Of the nine ventilated patients colonised with VRE on admission, one acquired a new strain of VRE in the MICU. Of the 29 ventilated patients who were not colonised with VRE on admission, 12 (41%) acquired VRE in the MICU. The median time to acquisition of VRE was 5 days (interquartile range 3-8). Of the 13 ventilated patients who acquired VRE, 11 (85%) were colonised with VRE by cross-colonisation. VRE were isolated from 157 (12%) of 1294 environmental cultures. The rooms of 13 patients were contaminated with VRE, but only three (23%) of these patients subsequently acquired colonisation with VRE. Pulsed-field gel electrophoresis of 262 isolates showed 20 unique strain types of VRE. Frequent colonisation with VRE on MICU admission and subsequent cross-colonisation are important factors in the endemic spread of VRE. Persistent VRE colonisation in the gastrointestinal tract and on the skin, the presence of multiple-strain types of VRE, and environmental contamination may all contribute to the spread of VRE.