Emergence and epidemiology of vancomycin-resistant enterococci in Australia

Enterococci with acquired resistance to vancomycin and other glycopeptides (VRE) have emerged and spread rapidly through Europe and the United States since 1988. The first isolate of VRE in Australia occurred in 1994. Only one case was noted in 1995. Since March 1996 there has been a steady increase in the number of reports of VRE throughout the country. To August 1998 there have been 69 documented strains or clusters of strains detected in patients with documented infection, and about 3 times as many strains have been detected through screening procedures of contacts or in risk groups. 19% of strains whose source was known were blood isolates, while 34% came from urine and 47% came from other specimens. The strains have been found in 26 institutions in 10 widely separated cities or regions of the country (in 6/8 states or territories), without any obvious temporal associations in their appearance. All strains appear to have arisen locally except for one strain imported from the United Kingdom. Furthermore there was no direct evidence of interhospital transfer of strains. All clinical strains were examined by PCR to confirm species and to test for the presence of known vancomycin-resistance genes. Of the 69 strains, 42 were vanB E. faecium, 12 were vanA E. faecium, 9 were vanB E. faecalis, 3 were vanA E. faecalis. Three were negative for vanA, vanB, vanC1, vanC2/C3 and vanD. PGFE profiles on 38 strains have revealed at least 8 types of vanB E. faecium, 6 of vanA E. faecium, 4 of vanB E. faecalis and 2 of vanA E. faecalis. Isolates containing vanA always had different profiles from those containing vanB. Clinical clustering was confirmed by PFGE, and supported by extended antibiogram. 14 of 15 E. faecalis were ampicillin susceptible compared to only 2 of 54 E. faecium. One E. faecalis strain was beta-lactamase positive. The epidemiology of VRE in Australia appears to be different from that of Europe or the United States, since vanB E. faecium predominates and strains have appeared in diverse locations independently and are highly polyclonal.     

Emergence of vancomycin-resistant enterococci in Australia: phenotypic and genotypic characteristics of isolates

Enterococci with resistance to glycopeptides have recently emerged in Australia. We developed multiplex PCR assays for vanA, vanB, vanC1, and vanC2 or vanC3 in order to examine the genetic basis for vancomycin resistance in Australian isolates of vancomycin-resistant Enterococcus faecium and E. faecalis (VRE). The predominant genotype from human clinical E. faecium isolates was vanB. The PCR van genotype was consistent with the resistance phenotype in all but six cases. One vanA E. faecalis isolate had a VanB phenotype, one vanB E. faecium isolate had a VanA phenotype, and four E. faecalis isolates were consistently negative for vanA, vanB, vanC1, and vanC2 or vanC3, even though they exhibited a VanB phenotype. These four isolates were subsequently examined for the presence of vanD by published methods and were found to be negative. No vancomycin-susceptible strains produced a PCR product. On the basis of our findings the epidemiology of VRE in Australia appears to be different from that in either the United States or Europe. Our multiplex PCR assays gave a rapid and accurate method for determining the genotype and confirming the identification of glycopeptide-resistant enterococci. Rapid and accurate methods are essential, because laboratory-based surveillance is critical in programs for the detection, control, and prevention of the transmission of glycopeptide-resistant enterococci.     

Molecular analysis of glycopeptide-resistant Enterococcus faecium isolates collected from Michigan hospitals over a 6-year period

The purpose of this study was to evaluate the molecular relatedness of clinical isolates of glycopeptide-resistant Enterococcus faecium isolates collected from hospitals in Michigan. A total of 379 isolates used in this study were all vancomycin-resistant E. faecium isolates collected from 28 hospitals and three extended-care facilities over a 6-year period from 1991 to 1996. For the 379 isolates, there were 73 pulsed-field gel electrophoresis (PFGE) strain types. Within strain types, there were as many as six restriction fragment differences. Most isolates (70%) belonged to six strain types, which were designated M1 (36%), M2 (3%), M3 (18%), M4 (6%), M10 (4%), and M11 (3%). PFGE strain M1 was cultured from 135 patients in 13 hospitals during the period 1993 to 1996. Strain type M2 was cultured from 11 patients in two hospitals during the period 1991 to 1992 and was not observed after 1992. Strain type M3 was cultured from 70 patients in 10 hospitals during the period of 1994 to 1996. Both M4 and M10 were cultured from 23 patients in three hospitals and from 15 patients in two hospitals, respectively, during 1995 to 1996. M11 was cultured from 13 patients in four hospitals during 1996. A total of 23 of 28 hospitals had evidence of clonal dissemination of some isolates. Plasmid content and hybridization analysis done on 103 isolates from one hospital and two affiliated extended-care facilities indicated that the strains contained from one to eight plasmids. Mating experiments indicated transfer of vancomycin resistance from 94 of these isolates into plasmid-free E. faecium GE-1 at transfer frequencies of <10(-9) to 10(-4). Gentamicin resistance and erythromycin resistance were cotransferred at various frequencies. A probe for the vanA gene hybridized to the plasmids of 23 isolates and to the chromosomes of 72 isolates. A probe for the vanB gene hybridized to the chromosomes of 8 isolates. The results of this study suggest inter- and intrahospital dissemination of vancomycin-resistant E. faecium strains over a 6-year period in southeastern Michigan. The majority of isolates studied belonged to the same few PFGE strains, indicating that clonal dissemination was responsible for most of the spread of resistance that occurred.     

Characterization of glycopeptide-resistant enterococci from a Swiss hospital

Between August 1994 and September 1996, 28 glycopeptide-resistant enterococci (GRE) were isolated from 8 infected patients and 11 intestinal carriers hospitalized at the University Hospital of Geneva. Identification to the species was made by both phenotypic (API 20 STREP and Rapid ID 32 STREP systems, and Vitek Gram Positive Identification Card) and genotypic methods using a multiplex PCR assay developed also for the determination of the genotype of glycopeptide resistance (vanA, vanB, vanC1, and vanC2-C3 genes). Fifteen isolates were identified as Enterococcus faecium, 8 as E. gallinarum, 4 as E. faecalis, and 1 as E. hirae. All of the phenotypic identification methods failed to differentiate some isolates of E. gallinarum from E. faecium, or vice versa. Both vanA (n = 18) and vanB (n = 4) glycopeptide resistance genotypes were found. For the first time, the vanB determinant was found in two isolates of E. gallinarum. Two patients were colonized by two different species containing the vanA gene and one by two different species containing the vanB gene. All vanA isolates were highly resistant to both vancomycin and teicoplanin except for three isolates which were susceptible to teicoplanin. Molecular typing by pulsed-field gel electrophoresis showed identical or similar patterns among E. faecium isolates with the vanA gene in five patients for whom the epidemiological link could not be always elucidated. This study emphasizes the necessity of utilizing both phenotypic and genotypic methods to characterize GRE.     

Detection of vancomycin-resistant enterococci in fecal samples by PCR

Surveillance cultures for vancomycin-resistant enterococci (VRE) are time-consuming and expensive for the laboratory to perform. Therefore, we investigated the use of PCR as an alternative method of detecting and identifying VRE directly in fecal samples. PCR primers directed to vanA, vanB, vanC1, vanC2, and enterococcal ligase genes were used to detect and identify VRE in fecal material obtained by rectal or perirectal swabbing. Although PCR-inhibitory substances were present in DNA prepared directly from the swabs, the inhibitory substances could be reduced by processing the nucleic acid with two commercially available DNA preparation columns. Fecal material from 333 swabs was cultured on several selective agar media before and after broth enrichment. DNA was extracted from the fecal material and was analyzed by PCR. By using all four primer sets, only 59 (67.8%) of the samples were positive for vanA. However, after retesting the negative samples with only the vanA primer set, 77 (88.5%) of 87 specimens that were culture positive for Enterococcus faecium containing vanA were positive by PCR. One specimen was PCR positive for the vanA gene but culture negative for enterococci. The specificity of the vanA assay was 99.6%. PCR analysis of enrichment broth samples with all four primers sets after 15 to 18 h of incubation detected 74 (85.1%) of the 87 culture-positive specimens. The specificity of the vanA assay after the enrichment step was 100%. No vanB-containing enterococci were recovered by culture. Since 16 samples can be tested by PCR in 4 h (including electrophoresis), identification of VRE is possible within 8 h of specimen submission at a cost of approximately $10.12/assay. Thus, PCR may be a cost-effective alternative to culture for surveillance of VRE in some hospitals.     

Emergence and dissemination of a highly vancomycin-resistant vanA strain of Enterococcus faecium at a large teaching hospital

We prospectively identified patients at the Massachusetts General Hospital from whom vancomycin-resistant enterococci (VRE) were isolated from a clinical specimen from 1 January 1991 through 31 December 1995. VRE strains were available from 139 (82%) of the 169 patients with clinical cases. Of these, 39 (28%) were identical or closely related by pulsed-field gel electrophoresis (i.e., VRE type A strain), including 38 (43%) of 89 VRE strains in 1995. By multivariate analysis, acquisition of the VRE type A strain was associated with receipt of clindamycin (odds ratio [OR] = 10.5), 15 or more days of hospitalization before the first isolation of VRE (OR = 2.9), and residence on one of the general medical floors (OR = 7.8). The VRE type A strain was a vanA strain of Enterococcus faecium and was highly resistant to all antimicrobial agents tested except chloramphenicol. These findings document the rapid dissemination of a highly resistant strain of E. faecium among patients and among other extant VRE strains at the Massachusetts General Hospital in 1995.     

Structure-based design of a dimeric zinc finger protein

In 1996, the dominant (43%) strain of vancomycin-resistant enterococci (VRE; type A) at Massachusetts General Hospital was identified at Brigham and Women's Hospital (BWH). To characterize the epidemiology of infection with type A isolates of VRE at BWH, we collected demographic and clinical data for all patients from whom VRE were isolated from a clinical specimen through September 1996. The first clinical isolates from all BWH patients from whom VRE were isolated were typed by pulsed-field gel electrophoresis of SmaI digests of chromosomal DNA. Among patients hospitalized after the first patient at BWH infected with a type A isolate of VRE was identified, exposures were compared between patients who acquired type A isolates of VRE and those who acquired other types of VRE. Isolates from 99 patients identified to have acquired VRE were most commonly from blood (n = 27), urine (n = 19), or wounds (n = 19). Three months after the index patient arrived at BWH and at a time when > or =12 types of strains of VRE were present, type A isolates of VRE became dominant; 39 of 75 (52%) of the study cohort had acquired type A isolates of VRE. We found no association between the acquisition of type A isolates of VRE and transfer from another institution or temporal overlap by service, ward, or floor with patients known to have acquired type A isolates of VRE. By multivariate analysis, only residence in the medical intensive care unit (adjusted odds ratio [OR], 3.2; 95% confidence interval [CI], 1.4 to 107) and the receipt of two or more antibiotics per patient-day (adjusted OR, 12.2; 95% CI, 1.2 to 9.0) were associated with the acquisition of strain A. This strain of VRE, dominant at two Boston hospitals, was associated with intensity of antibiotic exposures (i.e., two or more antibiotics per patient-day). We hypothesize that this strain may have unidentified properties providing a mechanism favoring its spread and dominance over other extant isolates, and further studies are needed to define these properties.     

Low-level vancomycin resistance in Clostridium innocuum

Low-level vancomycin resistance was observed for 28 clinical Clostridium innocuum isolates and C. innocuum NCIB 10674, whereas teicoplanin was active. DNA from three clinical isolates and the type strain could not be amplified by PCR with primers specific for the genes vanA, vanB, and vanC, suggesting that C. innocuum is intrinsically resistant to vancomycin.     

A fundamental study of 99mTc-HMPAO double injection method and clinical application to stress scintigraphy in orthostatic hypotension

Enterococcus faecium, which was highly resistant to vancomycin (MIC 256 mg/liter), but susceptible to teicoplanin (MIC 2 mg/liter), caused two distinct episodes of infection on a renal unit in the United Kingdom. Pulsed field gel electrophoresis (PFGE) indicated that a single strain caused the first episode, while the second episode, which occurred 1 year later, involved multiple strains, all of which were distinct from the original strain. Vancomycin resistance in all but one of these strains was mediated by transferable plasmids that carried the vanB glycopeptide resistance gene. Transfer either of resistance plasmids or the vanB resistance determinant itself to different strains occurred during the second episode. Plasmid-mediated vanB resistance has not been widely documented. A retrospective study of a reference collection revealed two other vanB-encoding plasmids from an E. faecalis and an E. faecium referred from two further UK centers. Although restriction analysis indicated no similarity between the plasmids from the three different centers, all contained a 2.1-kb EcoRV fragment that hybridized with a probe for the vanB gene. This suggests that there has been dissemination of a conserved glycopeptide resistance determinant, of which vanB is a part.     

Random amplified polymorphic DNA typing versus pulsed-field gel electrophoresis for epidemiological typing of vancomycin-resistant enterococci

Sixty vancomycin-resistant vanA mutant Enterococcus faecium (VRE) isolates, collected during a 40-month period from 48 patients hospitalized in a French Cancer Referral Center, were typed by using random amplified polymorphic DNA (RAPD), and the results were compared with those previously obtained by typing with SmaI pulsed-field gel electrophoresis (PFGE), which is currently recognized as the "gold standard." The discriminating power of RAPD typing, with seven primers and 11 combinations of primers, was tested on 18 strains, and only the most discriminating combination was further tested on the whole collection. We compared the epidemiological usefulness of RAPD typing of 60 clinical VRE isolates with that of SmaI PFGE typing. With primers AP4 and ERIC1R, RAPD generated 30 patterns versus the 36 patterns generated by SmaI PFGE. However, this did not hamper the epidemiologically correct clustering of 15 related strains and the detection of multiple colonization in nine patients. We conclude that this simple RAPD technique is well suited to the epidemiological typing of VRE and the monitoring of its nosocomial spread.     

Comparison of agar dilution, broth microdilution, E-test, disk diffusion, and automated Vitek methods for testing susceptibilities of Enterococcus spp. to vancomycin

An evaluation was undertaken to determine the optimal method for testing the susceptibilities of 100 clinical isolates and two reference strains of Enterococcus spp. to vancomycin in vitro. Six testing methods were studied by using the following media and incubation times: agar screen with the Synergy Quad Plate (Remel, Lenexa, Kans.), an in-house-prepared brain heart infusion (BHI) agar plate, and an in-house-prepared Mueller-Hinton (MH) agar plate, all incubated for 24 or 48 h; broth microdilution (Sensititre Just One Strip; AccuMed International, Inc., West Lake, Ohio) with BHI or cation-adjusted MH broth incubated for 24 or 48 h; agar dilution with BHI or MH agar incubated for 24 or 48 h; epsilometer test (E test; AB BioDisk, Solna, Sweden) with BHI or MH agar incubated for 24 or 48 h; disk diffusion with BHI or MH agar incubated for 24 or 48 h; and the automated Vitek method with the gram-positive susceptibility Staphylococcus aureus card and R02.03 software (bioMerieux, Inc., Hazelwood, Mo.). Growth failures occurred with MH media (n = 6) but not with BHI media. One growth failure occurred with the Vitek method. Results for each testing method for each Enterococcus strain were interpreted as susceptible, intermediate, or resistant according to current National Committee for Clinical Laboratory Standards (NCCLS) criteria and compared to the vancomycin resistance genotype (i.e., vanA, vanB, vanC-1, or vanC-2/3). For all methods, extension of the incubation time from 24 h to 48 h either produced no difference in the results or gave poorer results. The following methods produced no very major or major interpretive errors: broth microdilution with BHI media incubated for 24 h, agar dilution with BHI media incubated for 24 or 48 h, and E test with BHI media incubated for 24 or 48 h. Unacceptable frequencies of very major errors (> 1%) occurred with all methods for which MH media were used. Minor interpretive errors were frequent with all methods. These minor interpretive errors also occurred most frequently with Enterococcus strains with vanC genes, which encoded low-level vancomycin resistance (MIC < or = 8 microg/ml), as opposed to Enterococcus strains which possessed vanA or vanB genes, which encoded higher-level vancomycin resistance (MIC > or = 64 microg/ml). Modification of NCCLS breakpoints, especially for motile Enterococcus spp. (E. casseliflavus, E. flavescens, and E. gallinarum), may resolve this problem; however, in the current study, one E. faecalis strain and one E. faecium strain carried only the vanC gene. The agar screen method may also require reformulation. The current agar screen plate contains 6 microg of vancomycin per ml, which may not detect all low-level resistance associated with vanC genotypes. Nevertheless, the clinical significance of this low-level vancomycin resistance remains unknown.     

Genetically programmed development of salivary gland abnormalities in the NOD (nonobese diabetic)-scid mouse in the absence of detectable lymphocytic infiltration: a potential trigger for sialoadenitis of NOD mice

In a study designed to gain data on the in vitro transferability of vancomycin resistance from enterococci of the VanA phenotype to listeriae of different species, three clinical Enterococcus isolates-Enterococcus faecium LS10, Enterococcus faecalis LS4, and Enterococcus faecalis A3208, all harboring a plasmid that strongly hybridized with a vanA probe-were used as donors in transfer experiments. Strains of five Listeria species were used as recipients. From Enterococcus faecium LS10, glycopeptide resistance was transferred to Listeria monocytogenes, Listeria ivanovii, and Listeria welshimeri recipients, whereas no transfer occurred to Listeria seeligeri or Listeria innocua strains. From the two Enterococcus faecalis isolates, no transfer occurred to any Listeria recipient. MICs of both vancomycin and teicoplanin were > or = 256 mg/l for all transconjugants tested. Furthermore, all transconjugants harbored a plasmid that strongly hybridized with the vanA probe, with vanA consistently located in an EcoRI fragment of about 4 kb. Exposure of Listeria transconjugants to vancomycin resulted in synthesis of a membrane protein similar in size (39 kDa) to a vancomycin-induced membrane protein of Enterococcus faecium LS10. In retransfer experiments with Listeria transconjugants used as donors, glycopeptide resistance was transferred to all Listeria recipients tested, including strains of Listeria innocua and Listeria seeligeri, which were unable to receive the resistance from Enterococcus faecium LS10. The frequency of vanA transfer to listerial recipients was greater in retransfer experiments than in the primary matings. These findings suggest that the vanA resistance determinant might spread to the established pathogen Listeria monocytogenes, both directly from a resistant enterococcus and through strains of nonpathogenic Listeria species acting as intermediate resistance vehicles.     

Phage types and ribotypes of Salmonella enteritidis in southern Italy

Differently from other European countries, Southern Italy was affected by a considerable increase in human infections due to Salmonella enterica subsp. enterica serovar Enteritidis (S. Enteritidis) only after 1990. On the present investigation, two groups of S. Enteritidis strains isolated during the low-incidence period 1980-1984 and the epidemic period 1990-1993, respectively, have been submitted to phage-typing and ribotyping in order to ascertain whether the epidemic increase was determined by the spread of a foreign bacterial clone or not. Among the 150 isolates relative to the aforesaid two periods, 12 different phage types (PTs) were observed. PT4 was the most common phage type among the strains isolated in 1980-1984 (61%) as well as in those of the epidemic period 1990-1993 (72%). PT8 was the second most frequent (33%) phage type in 1980-1984. It was substituted by PT1 (19%) in the 1990-1993 period. Analysis of rDNA patterns obtained after Hinc II digestions and Escherichia coli rRNA hybridizations showed 8 different patterns, A to H. The great majority of the strains studied (140 isolates, 93%) belonged to the ribotype A, showing a similar frequency both in 1980-1984 (36 of 39, 92%) and in 19901993 (104 of 111, 94%). The predominance of PT4 and ribotype A among both preepidemic and epidemic strains is in agreement with the hypothesis that host genetic diversity decline and modern farming practices in the poultry industry have facilitated a widespread dissemination of preexisting endemic strains. This hypothesis urges to plan new strategies in preventing S. Enteritidis infections.     

Investigation of an outbreak of vancomycin-resistant Enterococcus faecium in a low prevalence university hospital

BACKGROUND: Until 1995, there were no cases of vancomycin resistant enterococcus (VRE) identified at our university hospital. From May 1995 to August 1996, we investigated a cluster of 10 cases of phenotypic class Van B Enterococcus faecium. METHODS: Patients were matched with controls who were on the same unit for at least 7 days prior to the case developing VRE. Control patients were age and sex matched if possible, and had duration of hospitalization at least as long as the number of days it took the patient to become VRE positive. We analyzed 16 independent risk factors using Epi-info version 6. Environmental cultures were obtained in the MICU where 5 of the patients were located. All 10 patient isolates and environmental isolates were analyzed by pulsed field gel electrophoresis (PFGE). RESULTS: PFGE confirmed the genetic relatedness of all 10 patient isolates and environmental isolates. The VRE-positive group was more likely to be immunosuppressed and to have exposure to 3 physicians. In the MICU, significant, P < 0.05) risk factors for VRE were higher Apache scores, location adjacent to a VRE case, duration of vancomycin and amino-glycoside use, duration of invasive catheter use, and diarrhea. Among the VRE-positive environmental cultures was a blood pressure cuff wash that was used on several patients. CONCLUSION: We hypothesize that a VRE strain was introduced into our hospital environment and was spread by personnel or contaminated equipment. As a consequence of this study, a hospital-wide VRE policy was implemented.     

Infection with T-lymphotropic virus in Dutch blood donors, 1993-1996]

Infection with human T-lymphotrophic virus (HTLV) type 1 causes a neurological disorder or leukaemia in a minority of infected persons. Since January 1993 the Dutch blood banks screen each donation for presence of HTLV-1 infection. Approximately 4,000,000 donations from 700,000 donors have been tested. The numbers of confirmed HTLV-1 positive donors were: 1993: 15; 1994: 6; 1995: 8; 1996: 3. In 1995 one case of HTLV-2 infection was detected as well. In 26/32 (81%) of the HTLV-1 positive cases either the donor or his/her partner originated from HTLV-1 endemic areas. The introduction of HTLV screening prevents the silent spread of HTLV via blood transfusion.     

Polyarthritis with perinuclear antineutrophil cytoplasmic antibody inaugurating microscopic polyangiitis. Report of a case

The prevalence of, and clinical risk factors associated with, vancomycin-resistant enterococcal colonization were investigated in patients suspected of having Clostridium difficile infection. Stools submitted for C difficile cytotoxin testing were screened for vancomycin-resistant enterococci (VRE). Isolates were speciated and characterized further by antibiotic susceptibility testing, DNA fingerprinting, and DNA:DNA hybridization for detection of specific vancomycin resistance genes. Of the 79 evaluable patients identified during a 3-month period, 16.5% were VRE-positive. The VRE isolates were genetically heterogeneous, although all carried the vanA gene. DNA fingerprinting data suggest that patient-to-patient transmission occurred, implicating colonized patients as potential reservoirs for VRE transmission. A positive C difficile cytotoxin assay and diabetes mellitus were the only identifiable risk factors associated with VRE colonization. Patients at risk for C difficile infection therefore may serve as reservoirs for VRE.     

Survival of vancomycin-resistant and vancomycin-susceptible enterococci on dry surfaces

We compared the abilities of Enterococcus faecium strains (three vancomycin-resistant enterococci [VRE] and five vancomycin-susceptible enterococci [VSE]) and Enterococcus faecalis strains (one VRE and 10 VSE) to survive under dry conditions. Bacterial suspensions of the strains were inoculated onto polyvinyl chloride and stored under defined conditions for up to 16 weeks. All strains survived for at least 1 week, and two strains survived for 4 months. A statistical model was used to distribute the 19 resulting survival curves between two types of survival curves. The type of survival curve was not associated with the species (E. faecalis versus E. faecium), the source of isolation (patient versus environment), or the susceptibility to vancomycin (VRE versus VSE). Resistance to dry conditions may promote the transmissibility of a strain, but VRE have no advantages over VSE with respect to their ability to survive under dry conditions.     

Taking care of the elderly: the unmentioned abuses

A total of 10,427 diarrhoeal stool specimens were cultured for Vibrio cholerae between 1992 and 1997. The isolation rates were 2%, 2.6%, 6.7%, 7.08%, 0.9% and 2.6% in the years from 1992 to 1997 respectively. Till 1992, Vibrio cholerae 01 ogawa was the predominant strain. In 1993, 81.3% of the isolates were of 0139 Bengal strain and the rest were V. cholerae 01. From 1994 to 1997, V. cholerae 01 ogawa was the predominant strain and there were no isolation of 0139 strain. The predominant phage type in 1992 and 1993 were T2 and T27 thereafter. Most Vibrio cholerae strains were sensitive to tetracycline, gentamycin, netromycin, norfloxacin and furazolidine. Strains were resistant to cotrimaxozole till 1996, but were 100% sensitive in 1997. Strains were sensitive to chloramphenicol till 1993 but acquired resistance thereafter.     

Transferable, plasmid-mediated vanB-type glycopeptide resistance in Enterococcus faecium

An approximately 60-kb transferable, vanB-carrying plasmid has been identified in a clinical Enterococcus faecium strain. A similar plasmid has been observed in an unrelated E. faecium strain, suggesting that plasmid transfer of vanB operons occurs in nature and plays a role in the dissemination of VanB-type resistance among strains of E. faecium.     

Vancomycin-resistant enterococci

Vancomycin-resistant enterococci (VRE) are a major problem in numerous institutions in the United States. Most VRE are resistant to all available antimicrobial agents, resulting in serious therapeutic dilemmas. The resistance genes are transmitted on transposons, so the potential for dissemination to other species is significant. Risk factors associated with VRE infection and colonization are vancomycin and cephalosporin use, but numerous patient-related factors also contribute. Although resistant strains appear to arise from the patient's endogenous flora, VRE may be spread through direct contact with contaminated environmental surfaces and hands of caregivers. Published guidelines for preventing such spread suggest implementing infection-control practices and vancomycin restrictions. The ideal drug regimen for the treatment of VRE is unknown. Various drug combinations have been studied in the laboratory, but patient treatment data are scarce. There is an urgent need for new antimicrobial agents.