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Vancomycin-resistant enterococci: Epidemiology, prevention, and control

Vancomycin-resistant enterococci: Epidemiology, prevention, and control
Literature review current through: Jan 2024.
This topic last updated: Mar 06, 2023.

INTRODUCTION — Vancomycin-resistant enterococci (VRE) are a common and difficult-to-treat cause of hospital-acquired infection. The epidemiology of VRE and strategies for preventing its spread will be reviewed here. The infection control measures described are applicable to all resistant enterococci.

The mechanisms of vancomycin resistance, infections caused by VRE, and the treatment of VRE are discussed separately. (See "Mechanisms of antibiotic resistance in enterococci" and "Microbiology of enterococci" and "Treatment of enterococcal infections".)

DEFINITIONS — Vancomycin inhibits enterococci by binding to the D-alanyl-D-alanine (D-Ala-D-Ala) terminus of cell wall precursors, compromising the subsequent enzymatic steps in the synthesis of cell wall. High-level resistance to vancomycin is encoded by different clusters of genes referred to as the vancomycin-resistance gene clusters (eg, vanA, vanB, and vanD gene clusters).

The end result is the replacement of D-Ala-D-Ala-ending peptidoglycan precursors with D-alanyl-D-lactate termini, to which vancomycin binds with significantly lower affinity. The replacement of D-alanine by D-lactate, which disrupts one of the five hydrogen bonds required for the interaction of vancomycin with its target, increases the minimum inhibitory concentration (MIC) of vancomycin almost 1000-fold. (See "Mechanisms of antibiotic resistance in enterococci", section on 'Vancomycin resistance'.)

The Clinical and Laboratory Standards Institute has issued the following MIC definitions for vancomycin susceptibility and resistance in enterococci [1]:

Vancomycin susceptible – ≤4 mcg/mL

Vancomycin resistant – ≥32 mcg/mL

An MIC of 8 to 16 mcg/mL was considered vancomycin intermediate, but we do not recommend vancomycin therapy for such isolates.

EPIDEMIOLOGY — Colonization and clinical infection with VRE were first described in Europe in the 1980s [2,3] and soon thereafter in the United States [4]. The presence of VRE in Europe was related to the use of glycopeptides such as avoparcin as a food additive for growth promotion in animals for more than 20 years, a practice that was subsequently banned by the European Union.

Multiple epidemics of VRE infection have been described in diverse hospital settings (eg, medical and surgical intensive care units, and medical and pediatric wards) and, like methicillin-resistant Staphylococcus aureus, VRE is endemic in many large hospitals [5-12]. In 2008, the National Healthcare Safety Network (NHSN) published summary data on multidrug-resistant organisms suggesting that vancomycin resistance had increased to 33 percent among enterococci that caused health care-associated infections in 2006 and 2007 [13]. In fact, the rate of hospitalization with VRE essentially doubled during 2003 to 2006 from 4.60 to 9.48 hospitalizations per 100,000 population [14].

During the 2010s, epidemiologic trends varied with geography. In a review of trends from 890 United States hospitals and more than 41 million hospitalizations between 2012 and 2017, the incidence of VRE among hospitalized patients declined 39.2 percent, while the incidence of hospital-onset VRE declined 48.8 percent [15]. In contrast, a review of one million hospitalizations from 70 Canadian hospitals between 2014 and 2018 demonstrated a 148 percent increase in VRE infections [16].

Modern techniques have expanded our knowledge of the epidemiology of VRE. For example, pulsed-field gel electrophoresis (PFGE) has been utilized in analyses of both epidemic and endemic clusters of VRE infection and colonization [3,5,8,17,18]. These studies demonstrated that a single VRE clone can spread within an institution or a patient care unit. In fact, reports have demonstrated that these clonal outbreaks can persist for three to four years within an institution [19,20]. In addition, VRE strains can transfer resistance horizontally to unrelated strains. Both methods of spread can occur simultaneously in a single institution. One report using PFGE found 45 different profiles in a single medical center where VRE had become endemic [3].

The vast majority of VRE isolates are Enterococcus faecium. This was illustrated in a prospective analysis from the Surveillance and Control or Pathogens of Epidemiologic Importance (SCOPE) database of 24,179 nosocomial bloodstream infections occurring in 49 hospitals in the United States between 1995 and 2002 [21]. Vancomycin resistance was found in 60 percent of E. faecium isolates compared with 2 percent of E. faecalis isolates. Data from the NHSN suggest that resistance trends are worsening; 80 percent of the 987 isolates of E. faecium and 6.9 percent of the 1497 isolates of E. faecalis reported in 2006 and 2007 were vancomycin resistant [13].

VRE colonization frequently leads to subsequent infection. A systematic review and meta-regression of 14 studies concluded that 8 percent of patients with VRE colonization develop infection within 30 days [22]. VRE infections have been associated with adverse outcomes. The magnitude of this effect was illustrated in a meta-analysis of nine studies of 1614 enterococcal bloodstream infections, 42 percent of which were due to VRE [23]. The mortality rate was significantly higher in patients with VRE compared with vancomycin-susceptible enterococcal isolates (summary odds ratio 2.5, 95% CI 1.9-3.4).

Transmission — After vancomycin-resistant enterococci (VRE) have been introduced into a health care setting, transmission is determined by selective pressure due to antimicrobial use, the proportion of colonized patients, the availability of susceptible patients, and adherence to prevention efforts [24]. The risk increases significantly in an intensive care unit once the proportion of patients exceeds 50 percent.

VRE colonize the gastrointestinal tract and can be found on the skin due to fecal shedding. Colonization with VRE generally precedes infection, but not all patients with colonization become infected. Persons either colonized or infected with VRE can serve as sources for secondary transmission.

VRE colonization is identified through the use of rectal or perirectal swab cultures or stool cultures. The overall sensitivity of rectal swab cultures for detection of VRE was 58 percent in one report but varied directly with VRE density in stool from 100 percent at high densities (≥7.5 logs per gram) to 0 percent at low densities (≤4.5 logs per gram) [25]. Both prior antibiotic exposure and skin colonization with VRE were more common in patients with high stool densities. The authors speculated that the high false-negative rate of rectal swab cultures may contribute to the increasing prevalence of VRE.

Polymerase chain reaction techniques for identification of vanA and vanB genes from stool/rectal samples have been developed, but their impact on surveillance for VRE has yet to be determined.

Transmission can occur by both direct contact (eg, the hands of health care workers) and indirectly from environmental surfaces [26]. The following observations come from different studies that have evaluated VRE transmission:

In a study in which VRE were inoculated in different places, the strains survived for five to seven days on countertops, 24 hours without a reduction in counts on bedrails, 60 minutes on a telephone handpiece, and 30 minutes on the diaphragmatic surface of stethoscopes [26].

Rectal electronic thermometer probes were the means of transmission of VRE in an intensive care unit [27].

Environmental cultures for VRE were more likely to be positive when the stool density of the organism exceeded four logs per gram [28].

Health care workers can become colonized in their gastrointestinal tracts, but the rate of acquisition of stool colonization appears to be low and transmission to patients from this source has not been demonstrated [29].

Risk factors — There are a number of risk factors for vancomycin-resistant enterococci (VRE) colonization and infection. These include:

Previous antimicrobial therapy

Patient characteristics

Colonization pressure

Exposure to contaminated surfaces

Residence in long-term care facilities

Previous antimicrobial therapy — The most consistently observed risk factor for hospital acquisition of VRE is previous treatment with antimicrobials, particularly vancomycin and cephalosporins. As an example, a prospective study of 126 adult intensive care units (ICUs) in 60 hospitals found that vancomycin and cephalosporin use were significantly higher in patients with VRE, after controlling for the type of ICU and rates of VRE elsewhere in the institution [30]. In another report, colonization or infection was associated with a longer duration of therapy with ceftazidime (13.2 versus 4.6 days in noninfected controls [27]).

Use of multiple agents with a broad spectrum of activity may predispose patients to colonization with resistant enterococci, probably via alteration of the normal bowel flora [31]. Among patients with VRE in stool, the administration of antibiotics active against anaerobic organisms can increase the density of stool colonization with VRE, which decreases after discontinuation of these agents [28].

Exposure to daptomycin, an antibiotic frequently used to treat VRE, can lead to VRE isolates with resistance to linezolid and daptomycin. In one study including more than 80 patients with daptomycin and linezolid non-susceptible VRE, risk factors included recent invasive surgical procedures and daptomycin exposure [32].

Patient characteristics — A number of patient characteristics other than antimicrobial therapy have been associated with a high risk of VRE colonization. These include hospitalization longer than 72 hours, significant underlying medical conditions (end-stage kidney disease requiring dialysis, cancer, transplant recipient), requirement for ICU, proton pump inhibitor use, and invasive devices [12,33].

Colonization pressure — Colonization pressure is an important risk factor for acquisition of VRE [24,34]. Colonization pressure in hospitals can lead to substantial increases in VRE colonization. A review of 1039 patients admitted to a general medicine ward demonstrated that colonization with VRE increased from 3.8 percent on admission to 32 percent during hospitalization; 60 percent of the VRE isolates were the same strain [35]. Indeed, hospitalization is strongly correlated with risk of VRE colonization [35,36]. Colonization pressure may outweigh other risk factors including antibiotic use once 50 percent or more of patients within the unit are colonized with VRE.

Exposure to contaminated surfaces — Exposure to contaminated surfaces in patient rooms, even after routine discharge cleaning, may be associated with VRE acquisition [37,38]. For example, several outbreaks caused by transmission of VRE from contaminated medical equipment have been reported. Implicated medical equipment included rectal thermometers, tympanic thermometers, and contaminated electrocardiogram leads [27,39,40].

Transmission of VRE from environmental surfaces to the hands or gloves of health care workers has been well documented. Forty-six percent of health care workers who touched bedrails and bedside tables in rooms of colonized patients in turn contaminated their gloves with VRE in one study [41]. Another study demonstrated that gloves or hands contaminated through contact with contaminated environmental surfaces can transfer VRE to approximately 10 percent of uncontaminated surfaces that are subsequently touched by other health care workers [42]. Patients with VRE colonization are associated with greater environmental contamination than patients with VRE infection [43].

Specific education of environmental services personnel leads to improved compliance with cleaning protocols and decreased environmental contamination with VRE [44]. A prospective quasi-experimental study showed that improved environmental cleaning significantly reduced the rate of VRE acquisition in a medical ICU [45]. This study was divided into four phases: a baseline period, a period including education to improve cleaning practices, a "washout" period, and a period including a multimodal hand hygiene initiative. Patients were screened for VRE on admission to ICU and daily thereafter. Enhanced cleaning with a detergent-disinfectant was found to reduce environmental and hand contamination as well as VRE acquisition. Novel technologies such as steam vapor [46], UV-C irradiation [47], and vaporized hydrogen peroxide [48] may further decrease environmental contamination and transmission of VRE.

Residence in long-term care facilities — Residents of long-term care facilities (LTCFs) appear to be a reservoir for VRE. In a prospective cohort study, 45 percent of patients admitted to an acute care hospital from an LTCF had rectal colonization with VRE; risk factors included prior use of antibiotics and the presence of a decubitus ulcer [49].

INFECTION CONTROL — Prevention of infection with VRE, as with any multidrug-resistant organism, requires a multifaceted approach including general infection prevention (eg, optimal management of vascular and urinary catheters), accurate and prompt diagnosis and treatment, prudent use of antimicrobial drugs, and prevention of transmission [50]. Methods for prevention will be summarized here.

Several different strategies for the prevention, control, and eradication of VRE have been studied. These include hand hygiene, contact precautions, cohorting of colonized patients, decolonization, surveillance cultures, and source control.

Judicious use of antimicrobial drugs (called antimicrobial stewardship) is another modality, but its relative importance for control of VRE is unclear. Agents that would be targeted include vancomycin, third-generation cephalosporins, and anti-anaerobic drugs.

The majority of published studies on the control of VRE have included multiple bundled approaches. As a result, it is often difficult to determine the attributable efficacy of individual interventions. Judicious use of antimicrobial drugs is another modality, but its relative importance for control of VRE is unclear [51].

Basic infection prevention principles

Hand hygiene — Hand hygiene is the most important and most practical means of preventing spread of VRE within the hospital, since VRE is primarily transmitted from patient to patient on the hands of health care workers [52]. Antimicrobial soaps (eg, chlorhexidine containing) may be more useful than plain soap for patients with VRE in contact precautions or during an epidemic. Alcohol-based hand rubs are as effective as soap and water and may improve compliance with hand hygiene among health care workers [53].

The duration of handwashing and the use of soap appear to affect efficacy. This was illustrated in a study in which VRE isolates were placed onto the hands of healthy volunteers [26]. A 30-second wash with water plus soap was necessary to completely eradicate the VRE hand carriage. In contrast, a five-second wash with water alone produced virtually no change in VRE recovery.

General principles regarding hand hygiene are discussed further separately. (See "Infection prevention: Precautions for preventing transmission of infection", section on 'Hand hygiene'.)

Contact precautions — Wearing gown and gloves when entering a patient room and removing them prior to exiting may decrease VRE transmission [54-57]. General principles regarding contact precautions are discussed further separately. (See "Infection prevention: Precautions for preventing transmission of infection", section on 'Contact precautions'.)

The optimal duration of contact precautions for VRE is uncertain and clinical practice is variable. In general, during the first year following VRE infection, we favor documentation of three negative weekly stool or rectal swabs to discontinue contact precautions; if more than one year has passed since VRE infection, we favor one negative stool or rectal swab.

Guidelines regarding the duration of contact precautions for acute care settings were published by the Society for Healthcare Epidemiology of America (SHEA) [58]. For patients previously infected or colonized with VRE, these guidelines recommend discontinuation of contact precautions after documentation of one to three negative weekly stool or rectal swab surveillance cultures and state that extension of contact precautions is reasonable for patients who are highly immunosuppressed, being treated with broad antibiotic therapy without VRE activity, or receiving care in protected environments (such as burn units) or in institutions with high VRE rates.

VRE colonization may be prolonged, with high relapse rates after multiple consecutive negative surveillance cultures [59,60]. The sensitivity of stool or rectal swab surveillance cultures for detecting VRE colonization is not well established.

Decolonization — No effective methods for decolonization of VRE have been identified, as attempts to eliminate intestinal VRE carriage with nonabsorbable oral antibiotics have been generally disappointing [61-63]. Thus, treatment specifically directed at decolonization of VRE is not recommended.

Surveillance cultures — Surveillance cultures for VRE are usually obtained from rectal swabs, perirectal swabs, or stool samples [51,61]. Samples for culture should also be obtained from areas of skin breakdown and draining wounds.

The standard approach to surveillance of hospitalized patients for VRE carriage consists of active surveillance of patients deemed to be at high risk. (See 'Active surveillance of patients at high risk' below.)

Surveillance cultures are not needed from patients known to have been colonized or infected with VRE within the past 6 to 12 months. Such patients typically remain culture positive regardless of therapy. Clinical cultures should not be used as a surrogate for VRE surveillance cultures due to a lack of correlation [64].

Rationale — The rationale for surveillance cultures to detect VRE carriage is threefold:

Patients colonized with VRE on admission or during hospitalization are at increased risk for VRE infection in-hospital or after discharge. The rate of infection varies with the health status of the patient, with an increased risk in severely ill or immunocompromised patients [65]. The magnitude of infection risk was assessed in a report from a university hospital over a five-year period [66]. Ninety VRE infections (60 urinary tract, 11 primary bloodstream, and 10 surgical site) occurred in 83 of 1050 patients who were colonized with VRE for an attack rate of 7.9 percent. A similar rate of infection (annual incidence 8.2 percent) was noted in 73 colonized children on a pediatric oncology ward [67].

VRE colonization may be spread to other patients, most often by health care workers whose hands or gloves have become transiently contaminated [26,52].

Intervention may reduce both the development of VRE infection and spread to other patients. (See 'Impact of infection control' below.)

Active surveillance of patients at high risk — Active surveillance reduces transmission of VRE when performed in outbreak settings [10,66,68,69] or in high-risk patient units such as ICUs and hematology-oncology wards [70-73]. The following observations illustrate the range of findings, some of which included combining surveillance cultures with other infection control measures:

In an outbreak in the Netherlands, surveillance cultures revealed that 27 patients in six wards were colonized, 93 percent with the outbreak strain [68]. The detection rate of non-outbreak VRE was only about 3 percent, which was comparable to a 2 percent prevalence in nonhospitalized persons. Surveillance cultures with isolation of carriers, preemptive isolation of patients at high risk for VRE colonization, and increased hand hygiene compliance controlled the outbreak. (See 'Impact of infection control' below.)

The impact of screening hospitalized high-risk patients on admission and then weekly for rectal colonization with VRE was evaluated in 14 units at four academic medical centers in the United States [73]. Ten units were ICUs; the other four cared for immunocompromised and transplant patients. The study population consisted of 8266 admissions and approximately 61,000 patient-days over 165 unit-months. The following findings were noted:

The admission prevalence of VRE colonization varied from 2 to 27 percent, with admission surveillance cultures increasing the detection rate 3.3-fold (range 2- to 17-fold).

The monthly incidence of VRE acquisition was 1 to 10 percent, with weekly surveillance cultures increasing the detection rate 6.1-fold (range 3- to 15-fold).

Active surveillance prevented the misclassification of 43 percent of "incident" carriers on the basis of clinical cultures alone and increased precaution days 2.4-fold.

By advancing the initiation of contact precautions, active surveillance consistently reduced VRE transmission over a 12-month period (0.22 percent per month).

Environmental disinfection — VRE can be transmitted to hospitalized patients via contaminated hospital environment. Efforts to improve environmental disinfection decrease this risk. Studies have demonstrated a reduction in VRE acquisition after improving room disinfection through education and performance feedback for environmental services personnel [74]. Enhanced disinfection strategies such as vaporized hydrogen peroxide and ultraviolet (UV) light also reduce the risk of VRE transmission in hospitalized patients. (See "Infection prevention: General principles", section on 'Health care environment: Cleaning and disinfection'.)

Patient bathing — Patient bathing with chlorhexidine has been shown to be useful for reducing enterococcal colonization and infection; this issue is discussed further separately. (See "Infection prevention: Precautions for preventing transmission of infection", section on 'Patient bathing'.)

Impact of infection control — A number of studies have demonstrated the beneficial clinical effects of infection control [12,66,68,72,73,75,76]. The following observations illustrate the potential benefits of infection control measures:

The impact of screening for VRE on the rate of VRE bacteremia was evaluated in a study of two similar neighboring hospitals, one of which actively screened high-risk patients and one of which did not [77]. Over a six-year period, the hospital that did not screen had a 2.1-fold higher rate of VRE bacteremia (17.1 versus 8.2 per 100,000 hospital days) with a higher incidence of clonally related isolates, suggesting more horizontal transmission.

In a VRE outbreak in the Netherlands cited above, the outbreak was retrospectively divided into three periods of different infection control measures [68]. The use of alcohol-based hand rubs was enforced during all periods. Period I (duration four months) involved active surveillance cultures, isolation of carriers and cohorting; preemptive isolation of high-risk patients for VRE colonization was added in period II (duration seven months); and cohorting and preemptive isolation were discontinued in period III (duration 18 months). Compared with period I, the relative risk (RR) of detecting epidemic VRE was 0.67 (95% CI, 0.41-1.10) in period II and 0.02 (95% CI, 0.002-0.6) in period III, demonstrating control of the outbreak.

In a study in an oncology unit in which VRE was endemic, 184 patients received standard infection control measures and 259 received an enhanced infection control strategy [75]. Both regimens included surveillance rectal swab cultures on admission and weekly, handwashing before and after patient contact, and contact precautions for VRE colonized and infected patients. The enhanced regimen included gown and glove use on room entry rather than for patient contact, cohorting with VRE-unknown patients being placed on a separate unit until culture results were available, and more infectious diseases input with emphasis of reducing all antimicrobial drugs. Enhanced infection control was associated with reductions in the incidence of both VRE colonization (10.3 versus 20.7 patients per 1000 patient-days) and VRE bacteremia (0.45 versus 2.1 patients per 1000 patient-days). A side benefit of the program was a significant decrease in the use of all antimicrobial drugs except for clindamycin and amikacin.

In a system-wide study, a comprehensive infection control intervention was evaluated for the control of endemic colonization and infection in 30 acute care and long-term facilities in Iowa, Nebraska, and South Dakota [12]. The prevalence of VRE colonization fell from 2.2 percent at baseline to 1.4 percent at one year and 0.5 percent at two years after intervention.

Guideline recommendations — The Society for Healthcare Epidemiology of America and the Hospital Infection Control Practices Advisory Committee of the Centers for Disease Control and Prevention published recommendations to prevent transmission of multidrug-resistant organisms, including VRE [51,52].

Although the two guidelines agree in large part, they offer different recommendations regarding the use of surveillance cultures. The SHEA guideline strongly recommends that facilities implement a program of active surveillance cultures in patients at high risk and contact precautions to reduce the transmission of VRE [52]. In contrast, the HICPAC guideline contains a two-tiered set of recommendations [51]:

Tier 1–level recommendations, which represent general measures for all health care facilities, do not include the use of active surveillance cultures.

Tier 2–level recommendations include intensified interventions that should be implemented when the incidence or prevalence of multidrug-resistant organisms such as VRE is not decreasing despite implementation of and adherence to routine control measures. Active surveillance cultures of high-risk patients are recommended as part of Tier 2–level interventions.

As described above, the main components of a program aimed at reducing the transmission of VRE in health care facilities include hand hygiene, contact precautions (gloves, gowns, and isolation or cohorting) for infected and colonized patients, active surveillance cultures of patients at high risk, and decontamination of the environment and equipment [51]. In contrast, attempts to eliminate intestinal VRE carriage with nonabsorbable oral antibiotics have been generally disappointing [61-63], and the 2006 HICPAC guidelines concluded that no recommendation for such therapy can be made [51].

The specific components of these infection control measures and the definition of patients at high risk are similar to those used for the prevention of transmission of MRSA and are discussed elsewhere. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Prevention and control".)

The only major difference is the site of culture, which, as noted above, consists of rectal, perirectal, or stool cultures as opposed to nares cultures for MRSA surveillance [51]. A mathematical model suggested that, in intensive care units, active surveillance cultures alone could reduce VRE transmission by 39 percent and by 65 percent when combined with preemptive isolation [72]. The 2006 HICPAC guidelines also concluded that the judicious use of vancomycin, third-generation cephalosporins, and anti-anaerobic antibiotics may reduce that rate of VRE colonization [51].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Infection control".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Basics topic (see "Patient education: Vancomycin-resistant enterococci (The Basics)")

SUMMARY AND RECOMMENDATIONS

Definitions - Vancomycin-resistant enterococci (VRE) are differentiated from other strains of Enterococcus by an increased minimum inhibitory concentration for vancomycin and the presence of vancomycin-resistance gene clusters such as vanA. (See 'Definitions' above.)

Epidemiology

Transmission – Health care-associated VRE is transmitted on the hands of health care workers; as a result, good hand hygiene is considered an essential measure for reducing the spread of this pathogen. (See 'Transmission' above and 'Hand hygiene' above.)

Colonization – Colonization with VRE typically precedes infection. Colonization most commonly occurs in patients with previous antimicrobial therapy and residents in long-term care facilities. Patients who are colonized with VRE have approximately an 8 percent rate of developing a VRE infection in-hospital or after discharge, with a higher rate in patients who are severely ill or immunocompromised. In addition, VRE colonization may be spread to other patients, most often by health care workers whose hands or gloves have become transiently contaminated. (See 'Risk factors' above.)

Infection control

Contact precautions – We recommend that contact precautions be followed for patients with VRE infection or colonization (Grade 1A). (See 'Contact precautions' above and "Infection prevention: Precautions for preventing transmission of infection", section on 'Contact precautions'.)

Surveillance cultures – Routine active surveillance cultures are not warranted to identify patients colonized with VRE in non-epidemic situations. Active surveillance cultures in high-risk patients can be used if the incidence or prevalence of VRE in the facility is not decreasing despite implementation of and rigorous adherence to routine control measures (eg, hand hygiene, contact precautions). (See 'Guideline recommendations' above.)

Decolonization – We recommend NOT attempting to decolonize VRE carriers (Grade 1B). (See 'Decolonization' above.)

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Topic 4045 Version 37.0

References

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