Enterococcus Species
Emily K. Shuman
Carol E. Chenoweth
Compared with other Gram-positive cocci such as Staphylococcus aureus and Streptococcus pyogenes, enterococci have been viewed as relatively avirulent, endogenous microorganisms with little potential for human infection. Despite their apparent lack of virulence, enterococci have emerged as important healthcare-associated pathogens (1,2,3). The enterococci possess several characteristics that allow them to survive and cause serious infections. They are intrinsically resistant to many commonly used antimicrobial agents, and they have considerable ability to acquire antimicrobial resistance through exchange of genetic elements with other Gram-positive cocci. They are hardy microorganisms and can survive in the environment and on the hands of healthcare personnel. These factors have allowed the enterococci to flourish and spread from patient to patient in healthcare settings (1,2,3).
ETIOLOGIES
Microbiologic Features and Taxonomy of Enterococci
Enterococci are catalase-negative, Gram-positive, facultative anaerobic cocci that classically belonged to the Lancefield group D streptococci. In the mid-1980s, they were officially classified, based on DNA-DNA and DNA-RNA homology, into their own genus (2,4,5). Their characteristic biochemical features include the ability to grow in the presence of 6.5% NaCl and at extremes of temperature (range of 10-45°C) and pH (up to 9.6). They share the ability to hydrolyze esculin in the presence of 40% bile salts with the remaining members of the group D streptococci. The ability of enterococci to hydrolyze L-pyrrolidonyl β-naphthylamide has been used as part of a rapid screening method for enterococci in the laboratory (2,5). Although other Grampositive microorganisms (e.g., Lactococcus, Aerococcus, Gemella, Leuconostoc, Lactobacillus) may show one or more of the previously listed characteristics, these microorganisms are rarely isolated from clinical infections. Therefore, these classic physiologic tests are still useful for initial identification of enterococci in clinical laboratories (2,5).
There are five recognized groups of enterococci, with a total of 33 species (4). Most species can be identified with conventional techniques using a combination of biochemical and morphologic characteristics, such as motility and pigmentation (2,5). The most clinically important species of enterococci are listed with their distinguishing biochemical features in Table 33-1. Enterococcus faecalis remains the major human pathogen, accounting for approximately 60% of clinical isolates of enterococci. Enterococcus faecium is the second most commonly isolated species, now accounting for about 30% of enterococcal clinical isolates (2,5). With the emergence of vancomycin resistance, the relative proportion of E. faecium in clinical isolates has been increasing. In 2006 to 2007, E. faecium represented 46% of enterococcal isolates from healthcareassociated infections (6). Enterococcus gallinarum, a motile strain of enterococcus that also exhibits intrinsic vancomycin resistance, has been associated with outbreaks of healthcare-associated infection (7,8).
Typing Methods
Early epidemiologic studies of healthcare-associated enterococcal infections were limited by a lack of typing methods. Biochemical tests and antibiograms were insufficient because enterococci rarely exhibit enough variation to allow for adequate strain differentiation. Total plasmid DNA analysis, with or without restriction enzyme digestion, was used in many studies to type enterococci (9, 10 and 11). However, these techniques have been uniformly replaced by newer methods for bacterial typing.
Pulsed-field gel electrophoresis (PFGE) or contourclamped homogeneous electric field electrophoresis of restriction enzyme-digested genomic DNA has been the dominant method used for typing enterococci (12, 13, 14 and 15). Enterococci have a relatively low guanine plus cytosine content of DNA, which, when digested with sma1 (a restriction enzyme seeking G-plus C-rich sequences), yields diverse, easily interpreted patterns. These techniques produce high-resolution, reproducible bands, which allow confident interpretation (12,14,15).
Newer methods of typing for enterococci have recently been applied. Ribotyping is a reproducible means of differentiating enterococcal strains, and automated systems have been developed for rapid typing. However, the reliability of the automated systems in comparison to other typing systems for enterococci has not been determined (15). Amplified fragment length polymorphism has been used
as a newer method of typing enterococci. This method is fast, reproducible, and appears to discriminate enterococcal strains well enough for the recognition of hospital outbreaks (16). Recently, a multilocus sequence typing scheme has been developed and compared with PFGE. This method appears promising for use in global epidemiologic analysis of E. faecalis and E. faecium, in addition to use in local outbreak investigations (14).
as a newer method of typing enterococci. This method is fast, reproducible, and appears to discriminate enterococcal strains well enough for the recognition of hospital outbreaks (16). Recently, a multilocus sequence typing scheme has been developed and compared with PFGE. This method appears promising for use in global epidemiologic analysis of E. faecalis and E. faecium, in addition to use in local outbreak investigations (14).
TABLE 33-1 Phenotypic Characteristics of Clinically Significant Enterococcus Species | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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ANTIMICROBIAL RESISTANCE IN ENTEROCOCCI
Enterococcal infections are a therapeutic challenge because of the intrinsic resistance of enterococci to many antimicrobials. In addition to their intrinsic resistance, enterococci have a remarkable ability to acquire antimicrobial resistance genes (2,17). Enterococci with high-level resistance (HLR) to multiple antimicrobials have become endemic in many institutions (18, 19 and 20). As humans enter an era of decreased antimicrobial effectiveness, it becomes imperative to develop appropriate infection control procedures to decrease the transmission of these microorganisms in healthcare settings.
Intrinsic Resistance
Most enterococci are inherently resistant to many antimicrobials, as shown in Table 33-2. The gene coding for intrinsic resistance resides on the chromosome and confers resistance to cephalosporins and penicillinase-resistant penicillins, clindamycin, low levels of aminoglycosides, and trimethoprim-sulfamethoxazole (TMP-SMX) (1,2,3,21). Most clinical isolates of enterococci are inherently tolerant to all β-lactams and glycopeptides and are typically not killed by concentrations of antimicrobials many times higher than the minimum inhibitory concentration (MIC). The relative resistance to β-lactam antimicrobials is due to low affinity of the penicillin-binding proteins of enterococci for these antimicrobials. The MICs of E. faecalis to penicillin average 2 to 8 µg/mL, which is approximately
10 to 100 times greater than those for most streptococci (21). E. faecium strains are even more resistant, with MICs of 16 to 32 µg/mL and higher (21).
10 to 100 times greater than those for most streptococci (21). E. faecium strains are even more resistant, with MICs of 16 to 32 µg/mL and higher (21).
TABLE 33-2 Characteristics of Antimicrobial Resistance in Enterococci | ||||||||||||||||||||||||||||||||||||||||||||
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In addition, all enterococci exhibit resistance to low concentrations of aminoglycosides (MIC = 8-64 µg/mL for gentamicin). This resistance trait appears to be due to a decreased uptake of the drug. Even in the presence of low-level aminoglycoside resistance, aminoglycosides may be used in combination with a cell-wall active agent (i.e., a penicillin or vancomycin) to achieve synergistic killing (21,22). The combination of an aminoglycoside with a penicillin or vancomycin is required for reliable bactericidal therapy for the treatment of serious enterococcal infections (21,22).
Enterococci are intrinsically resistant to TMP-SMX because they are able to use exogenous folates to bypass the inhibitory effects of TMP-SMX. In vitro susceptibility testing is unreliable in enterococci because media used in these tests do not contain thymidine or folates (2). Animal studies confirm that TMP-SMX is ineffective in vivo despite apparent in vitro susceptibility (23,24).
Acquired Resistance
High-Level Aminoglycoside Resistance HLR to streptomycin and gentamicin was first identified in the 1970s (25). Over the next decade, the prevalence of these resistant strains increased dramatically in diverse geographic areas (25,26). HLR (MICs >2,000 µg/mL) confers resistance to the synergistic killing normally observed with combinations of cell-wall active agents and an aminoglycoside (25).
HLR to aminoglycosides in enterococci occurs primarily through acquisition of genes encoding aminoglycosidemodifying enzymes; these resistance genes are usually found on a transferable plasmid (21). Streptomycin is inactivated by an enzyme that adenylates its 6-hydroxyl position (25). A second mechanism of streptomycin resistance confers HLR (MICs up to 128,000 µg/mL) through ribosomal resistance (25).
HLR to gentamicin in most clinical isolates is mediated by a bifunctional aminoglycoside-modifying enzyme with 6′-acetyltransferase and 2″-phosphotransferase activity. The presence of this enzyme confers HLR to gentamicin, tobramycin, kanamycin, amikacin, sisomicin, and netilmicin (25). The gene encoding for HLR to gentamicin has a DNA sequence homologous to the gene-conferring gentamicin resistance in S. aureus (26,27), and has been localized to transposons found on conjugative plasmids and chromosomes, which has allowed spread to multiple unrelated strains of enterococci (11,28,29). Additional gentamicin resistance genes encoding other 2″-phosphorylating enzymes have been identified in clinical isolates (26,30). Arbekacin may have synergistic activity against enterococci with HLR to aminoglycosides (31).
HLR to gentamicin does not always correlate with HLR to streptomycin; therefore, screening for HLR to both streptomycin and gentamicin is important (26). There are several screening methods currently available, but the disk method and the single-concentration agar plate method are most reliable for detecting high-level aminoglycoside resistance in enterococci and are recommended by the Clinical Laboratory Standards Institute (CLSI) (formerly the National Committee for Clinical Laboratory Standards) (32). Disks containing 120 µg of gentamicin generate a zone of 15 mm or less in strains with HLR to gentamicin. For streptomycin, disks containing 300 µg give rise to zones of 12 mm or less in HLR strains (7). Automated susceptibility testing is now also being used to screen for high-level aminoglycoside resistance in enterococci (33).
β-Lactam Resistance Penicillin resistance in enterococci occurs through two distinct mechanisms (21,34, 35 and 36). The most common mechanism of penicillin resistance occurs primarily in E. faecium and correlates with increased amounts of a low affinity penicillin-binding protein (21,34,35). A large, multicenter study of enterococcal bloodstream isolates reported that only 12.5% of E. faecium isolates were susceptible to penicillin (37). In the United States, ampicillin resistance is highly associated with vancomycin resistance in E. faecium (37, 38 and 39), but in Sweden an outbreak of ampicillin- and quinolone-resistant E. faecium was identified (40). In vitro penicillin or ampicillin susceptibility generally predicts susceptibility to imipenem (41). However, imipenem-resistant, ampicillin-sensitive E. faecium have been identified (42).
Since 1981, numerous centers have reported β-lactamase-producing strains of enterococci (10,36,43). The β-lactamase gene has been localized to transferable plasmids or to the chromosome in some isolates (36). The β-lactamase gene in enterococci is homologous with the S. aureus β-lactamase gene and has features suggesting that it resides on a transposon similar to S. aureus transposon Tn4201 (44). Routine susceptibility tests may not reliably detect β-lactamase-producing strains (43). Several β-lactamase tests, including nitrocefin disks, have been used to successfully identify β-lactamase production (36).
Vancomycin Resistance Vancomycin-resistant enterococci (VRE), first detected in Europe in 1988, have increased in prevalence dramatically in the United States (1,45,46,47) and worldwide (48,49). There are several phenotypes and genotypes for vancomycin resistance in enterococci, and some of these phenotypes have been studied in detail (Table 33-3). vanA and vanB are the most predominant phenotypes in clinical isolates of VRE (1,45,47). All phenotypes code for alternate biosynthetic pathways that alter the D-ala-D-ala cell wall precursors that normally bind vancomycin. vanA, vanB, and vanD genes code for D-ala-D-lac ligases (50,51), whereas vanC and vanE genes code for D-ala-D-ser ligases (52).
vanA strains exhibit high-level, inducible resistance (MICs >64 µg/mL) to both vancomycin and teicoplanin (53). The vanA trait is carried by a gene cluster located in a transposon, Tn1546 (54). The transposon is usually found on a plasmid, which is transferable to other Grampositive cocci. This accounts for the presence of vanA genes in widely heterogeneous strains of enterococci (37,55). Although vanA is usually found in E. faecium and E. faecalis, it has been identified in E. gallinarum and other enterococcal species (45). In addition, there have now been nine reported cases of infection with vanA-mediated vancomycin-resistant S. aureus in the United States (56,57).
vanB strains have variable resistance to vancomycin (MICs 16 to (1,000 µg/mL) but in general remain susceptible to teicoplanin. The genes that code for vanB trait are
very similar to vanA genes, are usually found within large mobile elements located on the chromosome, and can be transferred to other enterococci. The vanC phenotype is typically found intrinsically on the chromosome of motile species of enterococci, E. gallinarum (vanC-1) and E. casseliflavus (vanC-2 and vanC-3) (58, 59 and 60). These strains are moderately resistant to vancomycin (MICs, 8-16 µg/mL) but remain susceptible to teicoplanin. The resistance in these isolates is not inducible or transferable (58,59).
very similar to vanA genes, are usually found within large mobile elements located on the chromosome, and can be transferred to other enterococci. The vanC phenotype is typically found intrinsically on the chromosome of motile species of enterococci, E. gallinarum (vanC-1) and E. casseliflavus (vanC-2 and vanC-3) (58, 59 and 60). These strains are moderately resistant to vancomycin (MICs, 8-16 µg/mL) but remain susceptible to teicoplanin. The resistance in these isolates is not inducible or transferable (58,59).
TABLE 33-3 Characteristics of Phenotypes of Glycopeptide-Resistant Enterococci | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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The vanD phenotype has constitutive intermediate resistance to vancomycin and low-level resistance to teicoplanin (51,61). vanE resistance is nontransferable and confers a low-level resistance phenotype (62,63). The vanG phenotype has moderate-level resistance to vancomycin (MIC = 16 µg/mL), has no resistance to teicoplanin, and is negative by polymerase chain reaction (PCR) for vanA, vanB, vanC, or vanE (64). Vancomycin-resistant strains of enterococci that are dependent on vancomycin for growth have been identified from clinical isolates (65, 66 and 67).
Many laboratories have difficulty detecting vancomycin resistance when the MICs are less than 64 µg/mL (68); however, HLR can be detected more readily (69). The agar screen test using 6 µg/mL of vancomycin in brain-heart infusion agar is a simple, sensitive, confirmatory test and is recommended by CLSI (7,68). Automated susceptibility testing of isolates is also commonly performed (70). Heteroresistance to vancomycin, confirmed by presence of the vanA gene by PCR, has been identified recently in a clinical isolate (71). PCR assays have been developed for identification of VRE isolates and are now commonly used (72).
Resistance to Newer Antimicrobials E. faecalis is inherently resistant to the combination antimicrobial quinupristin/dalfopristin, with MICs of 4 to 32 µg/mL (73,74). This is thought to be a species characteristic and may be related to an efflux mechanism (74). E. faecium does not have inherent resistance, and most strains of E. faecium remain susceptible to quinupristin/dalfopristin (75). Mechanisms of resistance to quinupristin/dalfopristin in E. faecium include inactivation by enzymes, structural or conformational alterations in ribosomal target binding sites, and efflux of the antimicrobial out of cells (75,76).
Linezolid, an oxazolidinone, has activity against most enterococci, including VRE (77). However, linezolid resistance was reported in isolates from 9 of 501 patients treated with linezolid during the manufacturer’s compassionate use program and was related to ribosomal mutations (78). Although large prevalence studies reveal near universal susceptibility of enterococci to linezolid (79), healthcareassociated outbreaks of linezolid-resistant strains of VRE have occurred (18,20).
Daptomycin, a new cyclic lipopeptide antimicrobial, also has activity against most enterococci, including VRE (80). Enterococcal isolates have been almost universally susceptible to daptomycin in large surveillance studies (81,82). However, sporadic cases of resistance have been reported in patients with and without prior exposure to daptomycin (83, 84, 85 and 86). Resistance mechanisms have not been fully elucidated. Proposed mechanisms include decreased ability to adequately disrupt cell membrane potential, physical changes in the bacterial cell wall, protein binding leading to low serum concentrations, and chromosomal mutations (83,85,86).
Tigecycline is a new broad-spectrum glycylcycline antimicrobial that is active against most enterococci, including VRE (87). Tigecycline is closely related to the tetracycline class of antimicrobials but overcomes common resistance mechanisms associated with this class, including efflux pumps and ribosomal protection (87). Thus far, surveillance studies have demonstrated nearly universal susceptibility of enterococci to tigecycline (88). There is one reported case of resistance, in which tigecycline-resistant E. faecalis was isolated from the urine of a patient after prolonged therapy with tigecycline (89). The mechanism of resistance was not fully elucidated in this case but was not related to tetracycline-resistance mechanisms.
EPIDEMIOLOGY OF HEALTHCARE-ASSOCIATED INFECTIONS
Descriptive Epidemiology
The prevalence of enterococci in healthcare-associated infections has increased over the past three decades. In current reports from the National Healthcare Safety Network (NHSN) at the Centers for Disease Control and Prevention (CDC), enterococci rank as the third most common cause of all healthcare-associated infections hospital wide (6). In data from January 2006 through October 2007, enterococci accounted for 16% and 15% of healthcare-associated bloodstream infections (BSIs) and UTIs, respectively, and for 12% of all healthcare-associated infections (6).
At the same time their prevalence has increased, the enterococci have also developed increased antimicrobial resistance. One institution reported its first clinical isolate of high-level gentamicin-resistant enterococci in 1981, but, by 1989, 20% of clinical isolates were high-level gentamicinresistant and, by 1992, 23% of nonurinary isolates were highly resistant to gentamicin (90). Other institutions noted a similar increase in prevalence of high-level gentamicinresistant isolates; some centers reported that 50% to 55% of clinical isolates exhibited HLR (9,91). In a recent survey of more than 8,000 enterococcal isolates, 14% to 32% of enterococcal strains were gentamicin resistant, and 30% to 46% were streptomycin resistant, with variations reflected by geographic area (92).
Even more dramatic has been the continued increase in the prevalence of VRE in the United States (6,45,46). Between January 2006 and October 2007, the NHSN reported that 36% of enterococcal isolates from healthcare-associated infections were vancomycin resistant (6). E. faecium were more frequently vancomycin resistant (79%) compared with E. faecalis (7.5%) (6). Rates of VRE vary between geographic areas and institutions (92). Other areas of the world report lower prevalence of VRE than the United States (45,46,92). Latin America reports 0% to 4% VRE, whereas Europe reports 1% to 3% VRE (45,46,92). The prevalence of VRE in Canada may have increased in recent years, with VRE accounting for 6.7% of enterococcal isolates in a recent study (93).
Reservoirs
Enterococci are normal inhabitants of the human gastrointestinal tract. E. faecalis is found in concentrations of 105 to 107 colony-forming units (CFUs)/g of feces in 80% of hospitalized patients. E. faecium is recovered in smaller amounts in 30% of adult patients (2,3,90). Other parts of the gastrointestinal tract such as the oropharynx and hepatobiliary tract may also harbor enterococci (90,94). The gastrointestinal tract of hospitalized patients is the major reservoir for resistant enterococci (10,95, 96, 97, 98, 99 and 100). Rectal colonization was found in 100% of patients with VRE BSI and may persist for years after identification (100, 101, 102 and 103). Prolonged colonization has been associated with prolonged hospitalization, ICU care, and antimicrobial use (96,102). In addition, higher density colonization by VRE has been associated with use of antianaerobic antimicrobial regimens (95).
Enterococci may also colonize the gastrointestinal tract of healthcare personnel, as illustrated by an outbreak of a β-lactamase-producing enterococcus on an infant/toddler ward, where the resistant strain was isolated from 8 of 33 personnel (10). Healthcare personnel colonization with VRE is uncommon, but a recent study showed that 12 of 228 healthcare personnel carried VRE (104). In addition, identical strains of VRE were identified in household members of two colonized healthcare personnel (104). Antimicrobial therapy may place healthcare personnel at risk for colonization with VRE (105). The significance of colonization of healthcare personnel with VRE in the transmission of VRE has not been defined.
Other major sites of colonization that are reservoirs for enterococci in hospitalized patients include skin, wounds, and chronic pressure ulcers (101,106). In patients with VRE BSI, 86% were found to have VRE colonizing their skin in the inguinal or the antecubital fossa areas (97). Enterococci, when present in wounds, are usually found in mixed culture (2,90). Asymptomatic women may also carry enterococci in high numbers in their vagina, and more than 60% of men in the hospital may carry enterococci in their perineal or meatal areas (2,90,107).
Enterococci are also hardy microorganisms, which allow them to survive well on environmental surfaces (13,104). Resistant enterococci have been cultured from environmental surroundings of infected or colonized patients in many studies (9,10,100,108, 109, 110, 111, 112 and 113). Heavy contamination of the surrounding environment is more likely to occur when the patient has diarrhea or is incontinent (100,112,114,115). Medical equipment may also become contaminated with resistant enterococci and serve as a reservoir for these microorganisms. In one notable outbreak of infection resulting from VRE, the epidemic strain was cultured from electronic thermometers within the ICU (116). VRE has since been found to contaminate electronic ear thermometers, blood pressure cuffs, patient gowns and linens, fabric seat cushions, beds, bed rails, bedside tables, and commodes (13,100,109,112,117,118). Recent studies showed that ICU patients are more likely to acquire VRE if prior room occupants were VRE-positive, demonstrating the role of environmental contamination in VRE transmission (113,119).
Residents of long-term care facilities may serve as a reservoir for introduction of resistant enterococci into the hospital (13,106,120). Rectal VRE colonization of patients in a single long-term care facility increased from 9% in December 1994 to 22% in January 1996 (13). In another hospital where VRE has become endemic, it was found that 45% of patients admitted to the hospital from long-term care facilities were colonized with VRE (106). VRE colonization at admission was associated with the presence of a pressure ulcer and prior use of antimicrobials (106).
In Europe, VRE colonization of nonhospitalized people was identified in the early 1990s. Evidence suggested that foodborne VRE may lead to human colonization in the community setting (121,122). Avoparcin, a glycopeptide used as a food supplement in animals, was identified as an important factor in the emergence of VRE in the community setting (121,122). Use of avoparcin has now been banned in many countries, but VRE colonization of animals has persisted at lower rates, likely due to horizontal transfer of resistance determinants, environmental contamination, and use of other antimicrobials in animal feed (123). One study demonstrated that persons who ingested meat products contaminated with antimicrobial-resistant
enterococci developed transient intestinal colonization with VRE (124). In the United States, avoparcin has not been approved for use as a food additive; however, resistant enterococci have been found in the community (125,126). In 200 patients admitted to a community hospital, 10 patients were colonized with enterococci with HLR to aminoglycosides, and two patients were colonized with ampicillin-resistant enterococci (125). VRE colonization of outpatients without hospital exposures is rare in the United States (125, 126 and 127), but person-to-person transmission of VRE has been reported in the household setting (128,129). Virginiamycin, a streptogramin similar to quinupristin/dalfopristin, has been used in animal feed since 1974 in the United States. A large proportion of chicken sold in the United States was contaminated with quinupristin/dalfopristin-resistant enterococci (130). At this point, persons living in the community are not a major reservoir for VRE or other resistant enterococci, but the potential for increased dissemination in the community is concerning.
enterococci developed transient intestinal colonization with VRE (124). In the United States, avoparcin has not been approved for use as a food additive; however, resistant enterococci have been found in the community (125,126). In 200 patients admitted to a community hospital, 10 patients were colonized with enterococci with HLR to aminoglycosides, and two patients were colonized with ampicillin-resistant enterococci (125). VRE colonization of outpatients without hospital exposures is rare in the United States (125, 126 and 127), but person-to-person transmission of VRE has been reported in the household setting (128,129). Virginiamycin, a streptogramin similar to quinupristin/dalfopristin, has been used in animal feed since 1974 in the United States. A large proportion of chicken sold in the United States was contaminated with quinupristin/dalfopristin-resistant enterococci (130). At this point, persons living in the community are not a major reservoir for VRE or other resistant enterococci, but the potential for increased dissemination in the community is concerning.
Modes of Transmission
Early studies suggested that enterococci isolated from sites of infection were from the host’s own gastrointestinal tract (107). Since the emergence of antimicrobial resistance and more sophisticated molecular typing tools, numerous studies have shown that person-to-person spread of enterococci is a significant mode of transmission in healthcare settings (9,10,39,43,91,112,131). Zervos et al. (91) used total plasmid content and a high-level gentamicin-resistance marker, which was uncommon at that time, to show exogenous acquisition of enterococci. Since the emergence of VRE, the understanding of the spread of enterococci within healthcare settings has become more complete. The most important method of spread of VRE and other resistant enterococci is through transient carriage on the hands of healthcare personnel (10,13,107,112,132). Regional dissemination of VRE has resulted from interfacility transfer of colonized patients (133,134).
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