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PubMed1998

Activated cell-wall synthesis is associated with vancomycin resistance in methicillin-resistant Staphylococcus aureus clinical strains Mu3 and Mu50.

We have previously reported methicillin-resistant Staphylococcus aureus clinical strains, Mu50 and Mu3, representing two categories of vancomycin resistance: Mu50 representing vancomycin-resistant S. aureus (VRSA) with MICs > or = 8 mg/L, and Mu3 representing hetero-VRSA with MICs < or = 4 mg/L using standard MIC determination methods. The mechanisms of vancomycin resistance in these strains were investigated. These strains did not carry the enterococcal vancomycin-resistance genes, vanA, vanB, or vanC1-3, as tested by PCR using specific primers. However, both strains produced three to five times the amount of penicillin-binding proteins (PBPs) 2 and 2' when compared with vancomycin-susceptible S. aureus control strains with or without methicillin resistance; the amounts of PBP2 produced in Mu3 and Mu50 were comparable to those in the vancomycin-resistant S. aureus mutant strains selected in vitro. Incorporation of 14C-labelled Nacetyl-glucosamine into the cell was three to 20 times increased in Mu50 and Mu3, and release of the radioactive cell wall material was increased in Mu3 (and also in Mu50, though to a lesser extent), compared with control strains. The amounts of intracellular murein monomer precursor in these strains were three to eight times greater than those found in control strains. Transmission electron microscopy showed a doubling in the cell wall thickness in Mu50 compared with the control strains. Mu3 did not show obvious cell wall thickening. These data indicate that activated synthesis and an increased rate of cell wall turnover are common features of Mu3 and Mu50 and may be the prerequisite for the expression of vancomycin resistance in S. aureus.

Acetylglucosamine↗
PubMed1994

Development of a standardized screening method for detection of vancomycin-resistant enterococci.

The incidence of vancomycin resistance among enterococci is increasing in the United States and elsewhere in the world, but automated susceptibility testing methods have difficulty detecting resistance expressed by certain strains. The agar screening method described by Willey et al. (B. M. Willey, B. N. Kreiswirth, A. E. Simor, G. Williams, S. R. Scriver, A. Phillips, and D. E. Low, J. Clin. Microbiol. 30:1621-1624, 1992) has been proposed as a reliable method for confirming vancomycin resistance. In this study, we investigated various parameters associated with the agar screening method and, on the basis of the findings, established optimum testing conditions for the method. First, to evaluate media and vancomycin concentrations, one laboratory used Mueller-Hinton and brain heart infusion agars supplemented with 4, 6, and 8 micrograms of vancomycin per ml to test 100 genetically characterized enterococcal strains. On the basis of the results obtained, brain heart infusion agar supplemented with 6 micrograms of vancomycin per ml was selected for further study. Subsequently, eight laboratories used the medium to test both reference and clinical isolates. There was very good performance with the reference strains and, among 158 clinical isolates tested, the method demonstrated sensitivity and specificity of 100% and from 96 to 99%, respectively.

Culture Media↗
PubMed2005

Catheter-related vancomycin-resistant Enterococcus faecium bacteremia: clinical and molecular epidemiology.

OBJECTIVE: To study the clinical and molecular epidemiology of vancomycin-resistant Enterococcus faecium organisms causing catheter-related bacteremia in patients with cancer. DESIGN: Retrospective case-control study. SETTING: University of Texas M. D. Anderson Cancer Center, a tertiary-care hospital in Houston, Texas. PATIENTS: Case-patients were patients with cancer who had catheter-related vancomycin-resistant E. faecium bacteremia and control-patients were patients with cancer and vancomycin-resistant E. faecium gastrointestinal colonization without infection. RESULTS: Ten case-patients with catheter-related vancomycin-resistant E. faecium bacteremia were compared with 30 control-patients with gastrointestinal colonization by vancomycin-resistant E. faecium. Patients with catheter-related vancomycin-resistant E. faecium bacteremia were more likely to have required mechanical ventilation (P < .01), received total parenteral nutrition (P < .01), and had polyurethane catheters (P < .01) inserted in the femoral vein (P = .01). With the use of pulsed-field gel electrophoresis, 4 of the 10 catheter-related vancomycin-resistant E. faecium bacteremia isolates were genetically indistinguishable, whereas only 2 of the 30 control vancomycin-resistant E. faecium isolates displayed this same DNA pattern (P = .03). CONCLUSION: This study suggests that catheter-related vancomycin-resistant E. faecium bacteremia occurs more frequently in patients who receive total parenteral nutrition, mechanical ventilation, and femoral catheters.

Adult↗
PubMed2003

Molecular analysis of Tn1546-like elements mediating high-level vancomycin resistance in Enterococcus gallinarum.

OBJECTIVES: Four Enterococcus gallinarum isolates, all highly resistant to vancomycin, were studied in order to investigate their relationship and to gain insight into the molecular events responsible for their acquired resistance. METHODS: Extensive molecular analysis was performed to compare the four E. gallinarum isolates and their Tn1546-like elements. RESULTS: The four strains had very similar random amplified polymorphic DNA (RAPD) patterns and different but related PFGE profiles. Genotypic analysis demonstrated that all carried both vanC-1 and vanA genes. Using a vanA probe, no hybridization was detected to plasmid DNA, whereas hybridization to different SmaI fragments of the four strains was obtained with total DNA. Amplification and sequencing experiments showed that all four strains carried a Tn1546-like element that contained the orf2, vanR, vanS, vanH, vanA and vanX genes and was flanked at both ends by oppositely oriented IS1216V sequences. On the left side of the vanA cluster, all lacked IRL, and all had, upstream from orf2, 1029 bp of the 3' end of orf1. On the right side, one of the strains lacked vanY, vanZ and IRR, whereas in one of the other three there was an IS1542 element inserted within the vanZ gene. In one strain, an additional IS1216V element was inserted in the intergenic region vanX-vanY. CONCLUSIONS: This is the first study providing a molecular analysis of chromosomal Tn1546-like elements (possibly composite transposons) associated with high-level vancomycin resistance in human and animal strains of E. gallinarum. These molecular findings, together with those from PFGE and RAPD, suggest that the four E. gallinarum isolates are related and might have a common ancestor.

Animals↗
PubMed2000

Characterization of the first clinical isolate of vancomycin-resistant Enterococcus faecalis, AH803, in Taiwan.

We previously isolated a vancomycin-resistant strain of Enterococcus faecalis, designated AH803, from the sputum of a patient with pneumonia and bacteremia in Taiwan. AH803 was resistant to vancomycin (minimal inhibitory concentration, MIC = 512 micrograms/mL) but susceptible to teicoplanin (MIC = 8 micrograms/mL), and harbored the vanA gene but not the vanB gene. In this study, we further characterized E. faecalis AH803 and the plasmid it was found to contain. DNA from AH803 was analyzed for the presence of vanA and vanB resistance genes by polymerase chain reaction. The vancomycin resistant phenotype was transferable from AH803 to E. faecalis JH2-2, at a frequency of 4.8 x 10(-2). AH803 was also resistant to gentamicin and chloramphenicol, and these antibiotic resistance phenotypes cotransferred with vancomycin resistance. The genes responsible for resistance to all three antibiotics were located on a 42-kb conjugative plasmid (pBL101). This plasmid had the same restriction enzyme digestion patterns as Tn1546, found in pIP816 of E. faecalis BM4147. Epidemiologic studies of glycopeptide resistance should perhaps combine phenotypic and genotypic methods, rather than using phenotypic methods alone.

Bacterial Proteins↗
PubMed2005

Binding sites of VanRB and sigma70 RNA polymerase in the vanB vancomycin resistance operon of Enterococcus faecium BM4524.

The vanB operon of Enterococcus faecium BM4524 which confers inducible resistance to vancomycin is composed of the vanR(B)S(B) gene encoding a two-component regulatory system and the vanY(B)WH(B)BX(B) resistance genes that are transcribed from promoters P(RB) and P(YB) respectively. In this study, primer extension revealed transcription start sites at 13 and 48 bp upstream from the start codon of vanR(B) and vanY(B), respectively, that allowed identification of -10 and -35 promoter motifs. The VanR(B) protein was overproduced in Escherichia coli, purified and phosphorylated (VanR(B)-P) non-enzymically with acetylphosphate. VanR(B)-P and VanR(B) specifically bound to P(RB) and P(YB) promoters. VanR(B) bound at a single site at position -32.5 upstream from the P(RB) transcriptional start site and at two sites at positions -33.5 and -55.5 upstream from that of P(YB). The proximal VanR(B) binding site overlapped the -35 region of both promoters. VanR(B) was converted from a monomer to a dimer upon acetylphosphate treatment. VanR(B)-P had higher affinity than VanR(B) for its targets and appeared more efficient than VanR(B) in promoting open complex formation with P(RB) and P(YB). In the absence of regulator, E. coli RNA polymerase was able to interact with P(RB) but not with P(YB). Phosphorylation of VanR(B) significantly increased promoter interaction with RNA polymerase and led to an extended and modified footprint. In vitro transcription assays showed that VanR(B)-P activates P(YB) more strongly than P(RB). Analysis of the protected regions revealed one copy of a 21 bp sequence in the P(RB) promoter and two copies in the P(YB) promoter which may serve as recognition sites for VanR(B) and VanR(B)-P binding that are required for transcriptional activation and expression of vancomycin resistance.

Bacterial Proteins↗
PubMed1999

Interspecies recombination between enterococci: genetic and phenotypic diversity of vancomycin-resistant transconjugants.

Handwerger and colleagues demonstrated that a particular clinical isolate of Enterococcus faecium, designated GUC, and here redesignated as GUCR, can conjugatively transfer vancomycin resistance. The vancomycin resistance is encoded by a chromosomally born linked set of genes in the donor, designated the vanA cluster, to the chromosome of an E. faecalis recipient, JH2-2. Here it is reported that an earlier isolate of E. faecium from the same patient who later harbored the vancomycin-resistant E. faecium GUCR lacks the vanA gene cluster but is otherwise similar (by SmaI chromosomal fingerprint and metabolic fingerprinting) to the vancomycin-resistant GUCR. Therefore, "GUCS" is a strong suspect as the base strain for the clinical acquisition of the vanA cluster present in GUCR. Thirteen laboratory-generated vanA transconjugants derived from conjugation between GUCR and JH2-2 were subjected to further analysis, allowing a comparison between transfer in the laboratory and transfer that occurred in the clinical setting. Surprisingly, each JH2-2 transconjugant had a unique constellation of abilities to oxidize various members of a panel of potential carbon sources. This pattern was stable for each transconjugant, and it was not changed by growing the strains with or without vancomycin. Transconjugants had pulsed-field gel electrophoretic (PFGE) patterns largely consistent with that of JH2-2, the recipient in conjugation experiments. However, PFGE analysis showed that a large but variable amount of DNA, between 145 kb and 277 kb, was transferred into different transconjugants. The mechanism appears to be conjugative transposition in which new DNA is added to the pre-existing genome rather than substituting for a segment in the recipient. Mapping and hybridization studies of several transconjugants showed that each received similar, but not exactly the same, DNA fragment of at least 30 kb from the donor. Sequencing of 16S ribosomal genes was used to confirm that the recipient and donor strains used in transconjugation experiments were different species. Sequence analysis was also used to consider the possibility that rRNA operons might be mobilized in conjugation, but no evidence for the transfer of rDNA operons was found. An apparent insertion sequence in E. faecium almost identical to IS 1485 and 57% sequence identity to IS 199 of Streptococcus mutans was found in the region of DNA transferred. The results imply new consequences of conjugative transfer and interspecies recombination.

Anti-Bacterial Agents↗
PubMed1995

Overexpression, purification, and characterization of VanX, a D-, D-dipeptidase which is essential for vancomycin resistance in Enterococcus faecium BM4147.

Vancomycin resistance in Enterococcus faecium requires five genes: vanR, vanS, vanH, vanA, and vanX. The functions and mechanism of four gene products have been known, with VanR/S for signal transduction and transcriptional regulation and VanH/A to synthesize D-Ala-D-lactate. But the function of the fifth gene product, VanX, has been unknown until very recently, when Reynolds and colleagues discovered D-, D-dipeptidase activity in crude extracts of a VanX overproducer [Reynolds, P. E., et al. (1994) Mol. Microbiol. 13, 1065-1070]. We report here the expression of VanX in Escherichia coli and its purification to homogeneity. VanX has been characterized as a metal-activated D-, D-dipeptidase with an optimal pH range of 7-9. The kcat and Km of D-Ala-D-Ala in the absence of divalent metal are determined to be 4.7 s-1 and 1 mM, respectively. However, in the presence of metal cations, kcat can be as high as 788 s-1. VanX is unable to hydrolyze D-Ala-D-lactate, the substituted moiety in the peptidoglycan that leads to vancomycin resistance, not only because of low binding affinity (Ki estimated at 242 mM) but also due to a kcat less than 0.005 s-1. The more than 10(5)-fold differential in catalytic efficiency of VanX for hydrolysis of D-Ala-D-Ala vs D-Ala-D-lactate leaves D-Ala-D-lactate intact for subsequent incorporation into peptidoglycan.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed2004

Aggressive control measures for resistant Acinetobacter baumannii and the impact on acquisition of methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus in a medical intensive care unit.

The medical ICU implemented aggressive control measures following an outbreak of multidrug-resistant, clonal Acinetobacter baumannii. Multivariable regression analyses comparing acquisition (6 months preceding to 6 months during or following the outbreak) revealed decreased VRE and MRSA acquisition. Aggressive control measures can reduce VRE, and perhaps MRSA, transmission.

Acinetobacter↗
PubMed1992

Detection of vancomycin resistance in Enterococcus species.

Enterococcus faecalis and Enterococcus faecium isolates that are resistant to vancomycin have recently been identified in North America and Europe. Of 155 clinical isolates of enterococci (113 E. faecium and 42 E. faecalis), we found that 98 were resistant, 52 were moderately susceptible, and 5 had intermediate susceptibilities to vancomycin by using broth microdilution susceptibility testing according to the National Committee for Clinical Laboratory Standards (NCCLS) (Approved Standard M7-A2). Using NCCLS disk diffusion methodology (Approved Standard M2-A4), we evaluated the NCCLS supplemental M100-S3 revisions for zone diameter interpretive standards and incubation conditions and found 5.8% minor errors. A total of 234 isolates, which included an additional 79 E. faecium isolates that were moderately susceptible to vancomycin, were used to evaluate the Vitek GPS-TA card (bioMerieux, Inc., Hazelwood, Mo.) and the Pos MIC type 6 panel (MicroScan; Baxter Health Care Corp., West Sacramento, Calif.) for the detection of vancomycin resistance. The Vitek card was 100% specific and 72% sensitive, whereas the MicroScan panel with the Walk/Away system was 98% specific, with a sensitivity of 93% which increased to 99% when readings were performed manually. An agar screen plate method was evaluated with vancomycin concentrations of 6, 8, 10, or 12 micrograms/ml; plates were inoculated so as to obtain a final concentration of 10(5) CFU per spot. This method was found to be 100% sensitive and specific at all concentrations.

Drug Resistance, Microbial↗
PubMed1998

[Increase of non-amidated muropeptides in the cell wall of vancomycin-resistant Staphylococcus aureus (VRSA) strain Mu50].

The mechanism of resistance was studied with vancomycin-resistant Staphylococcus aureus (VRSA) strain Mu50. It was demonstrated that the incorporation of 14C-N-acetylglucosamine into the cell wall of Mu50 was not suppressed in the presence of 8 microliters/ml of vacomycin, whereas it was completely suppressed in vancomycin-susceptible strains FDA209P and H-1. Increased binding of vancomycin to the wall of Mu50 was observed compared to the control strains: 1.7 x 10(16) (Mu50), 6.1 x 10(15) (209P), and 6.7 x 10(15) (H-1) vancomycin molecules/mg cell wall, respectively. Remarkable proportion of the cell-wall component muropeptides were non-amidated in the cell wall of Mu50. In concordance with this phenomena, peptidoglycan cross-linkage decreased strikingly in the Mu50 strain. Free D-Ala-D-Ala residues at the end of muropeptides in the pre-existing cell wall generated by decreased cross-linkage seems to account for increased vancomycin binding. The increase of vancomycin-resistance level is presumably caused by sequestration of vancomycin molecules from primary target point on cell membrane. It was considered that at least two phenotypic changes are required for the vancomycin resistance in the Mu50 strain. First, as we have described previously, is the activated cell wall synthesis, and second, the reduction of cross-linkage of peptidoglycan by production of non-amidated muropeptide precursors.

Acetylglucosamine↗
PubMed1997

Vancomycin-resistant enterococci: improving treatments.

Recent issues of Morbidity and Mortality Weekly Report (MMWR), a publication of the Centers for Disease Control and Prevention (CDC), described clinical isolates of Staphylococcus aureus with intermediate resistance to vancomycin in patients in Michigan and New Jersey. As described last month in the first installment of this article, vancomycin has been the only approved antibiotic to which S. aureus had been uniformly sensitive. Media coverage of this latest example of increasing antibiotic resistance included the September 4, 1997, issue of The Wall Street Journal, which carried a report of a large study of the appropriateness of vancomycin use being coordinated by the Health Care Financing Administration (HCFA). The article reported study findings that "63 percent of orders for the drug vancomycin violated guidelines from the Centers for Disease Control and Prevention." In this report, we provide additional details about that study, as well as results specific to the Pennsylvania hospitals that participated in this project. The journal article failed to point out that each of the hospitals volunteered to participate in this 15-state study, beginning in late 1995, as part of their strategy to prevent and control the spread of vancomycin-resistant enterococci (VRE). These facilities agreed with experts that optimizing vancomycin use was an important part of this strategy, in addition to traditional infection control measures such as appropriate handwashing practices, prompt and accurate identification of resistant organisms, and isolation of infected and colonized patients when indicated.

Aged↗
PubMed1999

Clinical and molecular biological analysis of a nosocomial outbreak of vancomycin-resistant enterococci in a neonatal intensive care unit.

Vancomycin-resistant enterococci (VRE) have emerged as important nosocomial pathogens since 1988. We report here an outbreak of VRE between April 1997 and May 1997 in our neonatal intensive care unit (NICU). All isolates from four patients were identified as Enterococcus faecium positive and were resistant to vancomycin and teicoplanin. All of the patients with VRE were isolated for at least 5 d after admission to the unit and the positive cultures lasted between 13 and 31 d. There were no cases of sepsis or mortality in the patients with VRE. Two cases had previously received vancomycin therapy. All isolates were shown to have the vanA gene and had the same band pattern on repetitive PCR. After the four episodes, all equipment used to care for the patients were decontaminated and the staff engaged in therapy used disposable gloves and gowns. There were no more episodes. However, the NICU is no longer a safety area with regards to vancomycin-resistant enterococcal infection.

Anti-Bacterial Agents↗
PubMed2006

Short course of linezolid treatment for vancomycin-resistant Enterococcus faecium meningitis.

Enterococci might be one of the meningitis pathogens, but meningitis is rarely caused by vancomycin-resistant enterococci. In this report, we present a 69-year-old man who had the underlying chronic obstructive pulmonary disease with long-term steroid treatment suffered from a meningitis episode after hospitalisation for the urinary tract infection. The cerebrospinal fluid culture of the patient grew Enterococcus faecium which was resistant to vancomycin. A vancomycin-resistant E. faecium was also isolated from the rectal swab of the patient. These two E. faecium isolates were found to harbour the vanA gene and to be identical by pulsed field gel electrophoresis typing. The patient was treated successfully with intravenous linezolid, 600 mg every 12 h for 2 weeks. This was the first case of meningitis caused by vancomycin-resistant E. faecium in Taiwan.

Acetamides↗
PubMed2000

Efficacy of percutaneous abscess drainage in patients with vancomycin-resistant enterococci.

OBJECTIVE: We reviewed a 4-year experience draining fluid collections infected with vancomycin-resistant enterococci to determine the outcome of percutaneous intervention in patients with this highly resistant and increasingly common organism. MATERIALS AND METHODS: Charts of patients from whom vancomycin-resistant enterococci had been isolated during percutaneous drainage were reviewed to determine patient response to drainage, catheter management, and outcome of treatment. RESULTS: Twenty-one patients underwent percutaneous drainage of 28 fluid collections from which vancomycin-resistant enterococci were isolated, including 16 intraabdominal abscesses, seven biliary or urinary obstructions, and five empyemas. The drainage of 27 (96%) of 28 collections were technically successful. In seven patients, drainage provided the first isolation of vancomycin-resistant enterococci from the patient. Five patients also had blood cultures with positive findings for vancomycin-resistant enterococci, and 14 collections were coinfected with other bacteria or with fungi. Twenty collections (71%) or obstructions were successfully treated with percutaneous drainage. Drainage was unsuccessful in treating eight collections in seven patients. CONCLUSION: Despite high-level antibiotic resistance, fluid collections infected with vancomycin-resistant enterococci can be successfully drained percutaneously, resulting in a favorable likelihood of recovery for patients.

Abscess↗
PubMed2002

Monitoring antimicrobial use and resistance: comparison with a national benchmark on reducing vancomycin use and vancomycin-resistant enterococci.

To determine if local monitoring data on vancomycin use directed quality improvement and decreased vancomycin use or vancomycin-resistant enterococci (VRE), we analyzed data from 50 intensive-care units (ICUs) at 20 U.S. hospitals reporting data on antimicrobial-resistant organisms and antimicrobial agent use. We compared local data with national benchmark data (aggregated from all study hospitals). After data were adjusted for changes in prevalence of methicillin-resistant Staphylococcus aureus, changes in specific prescriber practice at ICUs were associated with significant decreases in vancomycin use (mean decrease -48 defined daily doses per 1,000 patient days, p<0.001). These ICUs also reported significant decreases in VRE prevalence compared with those not using unit-specific changes in practice (mean decrease of 7.5% compared with mean increase of 5.7%, p<0.001). In this study, practice changes focused towards specific ICUs were associated with decreases in ICU vancomycin use and VRE prevalence.

Anti-Bacterial Agents↗