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PubMed1999

A polyclonal outbreak of predominantly VanB vancomycin-resistant enterococci in northeast Ohio. Northeast Ohio Vancomycin-Resistant Enterococcus Surveillance Program.

We studied the molecular epidemiology of vancomycin-resistant enterococci (VRE) isolated in northeast Ohio during 1996 and examined the association between isolation of VRE from samples other than stool and antimicrobial purchases for five Cleveland hospitals. Susceptibility testing and pulsed-field gel electrophoresis were used to analyze 363 isolates from individual patients from 13 hospitals. Susceptibility testing indicated that 287 strains (79%) expressed the VanB phenotype and 76 (21%) expressed the VanA phenotype. The outbreak was polyclonal, with 30 total genotypes. Both VanA and VanB VRE demonstrated multiple genotypes. One genotype was present in all hospitals, suggesting spread between hospitals. For five teaching hospitals, rates of isolation from non-stool sources and from blood correlated positively with purchases of ticarcillin/clavulanic acid (P = .005). In summary, this outbreak demonstrates transmission of VRE between several hospitals in a geographic region and suggests that use of certain beta-lactam antibiotics may be associated with an increased prevalence of VRE.

Disease Outbreaks↗

PubMed1998

Vancomycin-resistant and vancomycin-susceptible enterococcal bacteremia: comparison of clinical features and outcomes.

Vancomycin-resistant Enterococcus (VRE) is a major nosocomial pathogen. We collected clinical and laboratory data on 93 hospitalized adults with VRE bacteremia and 101 adults with vancomycin-susceptible enterococcal (VSE) bacteremia. Risk factors for VRE bacteremia included central venous catheterization, hyperalimentation, and prolonged hospitalization prior to the initial blood culture. VRE-infected patients were less likely to have undergone recent surgery or have polymicrobial bacteremia, suggesting a pathogenesis distinct from traditional VSE bacteremia. Prior exposure to metronidazole was the only significant pharmacologic risk factor for VRE bacteremia. Animal studies suggest metronidazole potentiates enterococcal overgrowth in the gastrointestinal tract and translocation into the bloodstream. An increasing APACHE II score was the major risk factor for death in a multivariate analysis, with VRE status being of only borderline significance.

Adult↗

PubMed2002

The effect of active surveillance for vancomycin-resistant enterococci in high-risk units on vancomycin-resistant enterococci incidence hospital-wide.

BACKGROUND: Vancomycin-resistant enterococci (VRE) have become a major cause of nosocomial infections and are now endemic in many geographic areas. The aim of this study was to describe the effect of active surveillance for patients with VRE in high-risk units on the VRE incidence rate hospital-wide. METHODS: We determined 4 time periods based on the intervention of active surveillance: preactive surveillance (period 1), active surveillance (period 2), no active surveillance (period 3), and reinstutition of active surveillance (period 4). VRE incidence rates based on first clinical culture for VRE per 10,000 patient days for each of these periods and incidence rate ratios were then calculated. RESULTS: Active surveillance in high-risk units was associated with a significant reduction in VRE incidence hospital-wide in 2 of the 3 comparisons made. The incidence rate ratio when comparing the first period of active surveillance (period 2) to the preactive surveillance period (period 1) was 0.63 (95% CI, 0.38-1.1); it was 0.36 (95% CI, 0.23-0.55) when comparing the first period of active surveillance (period 2) to the subsequent period (period 3) and 0.68 (95% CI, 0.54-0.85) when comparing the second period of active surveillance (period 4) to the prior period without active surveillance periods. CONCLUSIONS: Active surveillance culturing for VRE in the high risk-units prevented further VRE transmission, as evidenced by a significant increase in hospital-wide incidence rates when active surveillance was discontinued and a significant decrease in incidence rates when it was restarted.

Baltimore↗

PubMedDate not supplied

Inhibitory and bactericidal effects of telithromycin (HMR 3647, RU 56647) and five comparative antibiotics, used singly and in combination, against vancomycin-resistant and vancomycin-susceptible enterococci.

The inhibitory and bactericidal effects of telithromycin (HMR 3647, RU 66647) were compared with those of gentamicin, ampicillin, erythromycin, azithromycin and vancomycin against 74 strains of enterococci (34 Enterococcus faecalis and 40 Enterococcus faecium) by agar dilution, broth dilution, time kill assays and postantibiotic effect (PAE). The telithromycin MIC(90) for vancomycin-sensitive (VSE) E. faecalis strains tested using the agar dilution method was 8 microg/ml. For a different group of VSE E. faecalis strains tested using the broth dilution method it was 0.06 microg/ml The telithromycin MIC(90)s for vancomycin-resistant (VRE) and VSE E. faecium strains, determined using the agar dilution method, were 4 and 8 microg/ml, respectively, while for a different set of VRE and VSE E. faecium strains tested using the broth macrodilution method, they were 32 and 16 microg/ml, respectively. Telithromycin MBC(90)s for E. faecalis were 4-6 tubes higher and for E. faecium 3-5 tubes higher, respectively, than the MIC(90)s. In time kill assays, telithromycin had bactericidal activity against only 1 of 7 E. faecium strains; for all other E. faecium and E. faecalis strains, only inhibitory activity was demonstrated. Neither synergy nor drug interference was observed when telithromycin was used in combination with ampicillin, vancomycin or gentamicin. At 10 times the MIC, the PAE of telithromycin against E. faecalis was 2.8 h, while for E. faecium it was 1.6 h. Telithromycin should be evaluated for therapy of enterococcal infections, including those caused by VRE organisms. However, because of the strain-to-strain variability in susceptibility to telithromycin, MIC determinations are important, especially for erythromycin-resistant strains.

Anti-Bacterial Agents↗

PubMed2001

Prevalence of colonisation and resistance patterns of vancomycin-resistant enterococci in healthy, non-hospitalised persons in Switzerland.

In order to obtain data about the prevalence and the resistance profiles of vancomycin-resistant enterococci (VRE) in the community, we investigated fecal samples of employees (n = 1026) from food processing companies of different Swiss cantons. The susceptibility of the isolated VRE-strains against penicillin, ampicillin, tetracyclin, ciprofloxacin, chloramphenicol, streptomycin and gentamicin as well as the minimal inhibitory concentrations (MIC) for vancomycin and teicoplanin were determined by agar diffusion and microbroth dilution, respectively. The type of vancomycin-resistance (vanA, vanB, vanC1, -C2 or -C3) was confirmed by polymerase chain reaction (PCR). A ratio of 50 samples out of 1026 (4.9%) was found VRE-positive, all of the isolated strains carried the vanA-resistance gene. Compared to recent publications from other European countries, these results represent a rather high prevalence of VRE-carriers in the community.

Anti-Bacterial Agents↗

PubMed2002

Risk factors for development of vancomycin-resistant enterococcal bloodstream infection in patients with cancer who are colonized with vancomycin-resistant enterococci.

Vancomycin-resistant Enterococcus faecium (VRE) is a common nosocomial isolate, especially among patients with cancer. VRE infections have substantial attributable mortality among patients with cancer. The purpose of this study was to identify risk factors for developing bloodstream infection with VRE in patients with cancer who are colonized with VRE. VRE colonization was prospectively identified in 197 patients with cancer during 4-year period, of whom 179 (91%) had complete records for evaluation. Of these 179 patients, 24 (13.4%) developed hospital-acquired VRE bloodstream infections. Risk factors for VRE bloodstream infection included vancomycin use (relative risk [RR], 1.98; 95% confidence interval [CI], 1.25-3.14), diabetes mellitus (RR, 3.91; 95% CI, 1.20-12.77), gastrointestinal procedures (RR, 4.56; 95% CI, 1.05-19.7), and acute renal failure (RR, 3.10; 95% CI, 1.07-8.93). Strategies for preventing VRE bloodstream infection in VRE-colonized patients with cancer should include limiting vancomycin use and, perhaps, gastrointestinal procedures.

Bacteremia↗

PubMed2005

First report of vancomycin-resistant staphylococci isolated from healthy carriers in Brazil.

Reduced susceptibility or resistance to vancomycin has been reported among clinical isolates of staphylococci in previous studies. In the present study we report on the isolation of four vancomycin-resistant staphylococcal strains from healthy carriers inside and outside the hospital environment. These carriers did not receive treatment with any antibiotic. All coagulase-negative staphylococcal strains showed variable levels of resistance to several antimicrobial agents, including oxacillin, and unstable resistance to vancomycin, with decreased vancomycin MICs (<4 mg/liter) after 10 days of passage in a nonselective medium. However, exposure of these revertants to vancomycin selected staphylococcal strains resistant to vancomycin at very high frequencies (10(-2) and 10(-3)). The vancomycin resistance in these staphylococcal strains was not mediated by the van gene. The cell wall of the staphylococcal strains studied became thickest after culture in medium containing vancomycin, and the differences in cell wall thickness were statistically significant (P < 0.001). Thus, the thickening of the cell wall in these staphylococcal strains may be an important contributor to vancomycin resistance.

Anti-Bacterial Agents↗

PubMed1989

Activity of glycopeptides against vancomycin-resistant gram-positive bacteria.

Gram-positive bacteria resistant to vancomycin are rare; but they include members of the genera Leuconostoc, Lactobacillus, and Pediococcus, as well as recently emerging vancomycin-resistant strains of Enterococcus faecium and Enterococcus faecalis. Vancomycin, teicoplanin, and several vancomycin derivatives were tested for their activities against vancomycin-resistant gram-positive bacteria. Vancomycin-resistant E. faecium and E. faecalis were generally cross-resistant to other glycopeptides, but some N-substituted vancomycin derivatives were active against the resistant strains, with MICs of 2 to 32 micrograms/ml. These vancomycin derivatives also had significant levels of activity against intrinsically vancomycin-resistant organisms such as Leuconostoc sp. While vancomycin resistance in E. faecium and E. faecalis was inducible, resistance in members of the genera Leuconostoc, Lactobacillus, and Pediococcus appeared to be expressed constitutively. Antibody to a vancomycin-induced membrane protein found in membranes of resistant enterococci did not detect a cross-reacting protein in other vancomycin-resistant species.

Drug Resistance, Microbial↗

PubMed2005

Nosocomial infections due to methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci at a university hospital in Taiwan from 1991 to 2003: resistance trends, antibiotic usage and in vitro activities of newer antimicrobial agents.

A rapid increase of nosocomial methicillin-resistant Staphylococcus aureus (MRSA) infection (from 39% in 1991 to 75% in 2003) and vancomycin-resistant enterococci (VRE) (from 1.2% in 1996 to 6.1% in 2003) at a university hospital in Taiwan was found. The noticeable rise of MRSA and VRE was significantly correlated with the increased consumption of glycopeptides, beta-lactam-beta-lactamase inhibitor combinations, extended-spectrum cephalosporins, carbapenems and fluoroquinolones (Pearson's correlation coefficient, P < 0.05). Minimum inhibitory concentrations (MICs) of 100 non-duplicate blood isolates of MRSA (in 2003) and of 25 non-duplicate isolates of vancomycin-resistant Enterococcus faecalis and 172 vancomycin-resistant Enterococcus faecium (in 1996-2003) causing nosocomial infection recovered from various clinical specimens of patients treated at the hospital to nine antimicrobial agents were determined by the agar dilution method. All of these isolates were susceptible to linezolid and were inhibited by 0.5mg/L of tigecycline, and all MRSA isolates were inhibited by daptomycin 1mg/L, including two isolates of MRSA with heteroresistance to vancomycin. Daptomycin had two-fold better activity against vancomycin-resistant E. faecalis (MIC90, 2 mg/L) than against vancomycin-resistant E. faecium (MIC90, 4 mg/L). Decreased susceptibilities of vancomycin-resistant E. faecium and MRSA to quinupristin/dalfopristin (non-susceptibility 25% and 8%, respectively) were found. Telithromycin had poor activity against the isolates tested (MIC90, 8 mg/L). Linezolid, daptomycin and tigecycline may represent therapeutic options for infections caused by these resistant Gram-positive organisms.

Anti-Bacterial Agents↗

PubMed2002

Osteomyelitis attributable to vancomycin-resistant enterococci.

Vancomycin-resistant enterococcus first was described in 1988, and has become a major problem in nosocomial infections. This is a retrospective review of 10 patients, seen at the authors' hospital during a 2-year period, with confirmed vancomycin-resistant enterococcal osteomyelitis: four patients had total joint arthroplasty infections, one patient had an infected tibial nail, three patients had infections associated with external fixators, and two patients had osteomyelitis of the femur. Four of the 10 patients had underlying medical illnesses (diabetes mellitus, systemic lupus erythematosus, human immunodeficiency virus infection); four of the 10 patients were intravenous drug users. Two patients had vancomycin-resistant enterococci on admission, and the other eight patients were admitted to the hospital for a mean of 21.3 days (range, 3-73 days) before vancomycin-resistant enterococci were identified in the bone. Eight of the 10 patients had monomicrobial infections with vancomycin-resistant enterococci. Patients were treated by surgical debridement, removal of hardware, and antibiotics (chloramphenicol in eight patients, quinupristin and dalfopristin (Synercid) in two patients). All patients initially improved with therapy, but one patient had a recurrence of vancomycin-resistant enterococcal osteomyelitis and died of bacteremia. Bone infections with vancomycin-resistant enterococcus still may be uncommon, but with time and selective antibiotic pressures, vancomycin-resistant enterococci may become a more prominent entity in orthopaedic infections.

Adult↗

PubMed2005

[Case report: a nosocomial infection caused by vancomycin resistant enterococcus].

Vancomycin resistant enterococcus (VRE) was recovered from the urine culture of a 61 years old female patient, who was being treated for sepsis, on the 15th day of hospitalization in Ondokuz Mayis University Hospital Infectious Disease Unit. The underlying diseases of this patient were chronic renal failure and diabetes mellitus. The patient died due to septic shock on the day of VRE isolation. Since this case was the first VRE infection in our hospital, a point prevalence study was planned. For this purpose, rectal swab samples collected from 10 patients from the same unit and 27 personnel who worked in the same unit, were screened for the presence of VRE. Nasal swabs and finger tip samples were also taken from the staff to determine if the transmission has occured in this way. As a result, a second VRE strain was isolated from another patient with chronic renal failure who was under treatment due to multiple pulmonary abscesses. Immediate isolation of this patient prevented a possible epidemic in this specific unit. In this report, the importance of VRE screening and isolation of the patients after the recovery of VRE has been emphasized.

Bacteriuria↗

PubMed2004

Relative susceptibilities to vancomycin and quinupristin-dalfopristin of adhered and planktonic vancomycin-resistant and vancomycin-susceptible coagulase-negative staphylococci.

Quinupristin-dalfopristin, a novel streptogramin antibiotic, has proven efficacious against multi-drug-resistant, Gram-positive bacteria, particularly glycopeptide-resistant coagulase-negative staphylococci (CoNS), and CoNS within biofilms. We examined its activity, along with the glycopeptide antibiotic vancomycin, against laboratory-derived, vancomycin-resistant (van R) CoNS and their vancomycin-susceptible (van S) parent strains, both in the planktonic state and after their adhesion to silicone urinary catheters. The laboratory-derived van R CoNS displayed lower adhesion and biofilm formation capabilities than did their van S parent strains. Compared with silicone, the adhesion to hydrogel-silver urinary catheters was approximately one log lower for both van R and van S CoNS. Adhesion of van R and van S CoNS to silicone catheters increased their tolerance to vancomycin. However, adhered van R CoNS succumbed to concentrations of quinupristin-dalfopristin markedly (16- to 32-fold) lower than adhered van S CoNS. This anomaly may be due to the presence of vancomycin sequestered in the cell wall of van R CoNS. Quinupristin-dalfopristin in combination with vancomycin may provide enhanced inhibitory effects against van R CoNS in the adhered state.

Anti-Bacterial Agents↗

PubMed2006

Recovery and characterization of a 30.7-kDa protein from Bacillus licheniformis associated with inhibitory activity against methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and Listeria monocytogenes.

Of 131 bacterial isolates from seaweed, a culture of Bacillus licheniformis produced a novel protein with antibacterial activity against methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and Listeria monocytogenes. The antibacterial activity was maximal in cultures prepared in Columbia broth containing pieces of synthetic polyurethane sponge and shaken at 210 to 230 rpm. Antibacterial activity was not found in cultures grown statically or with different speeds of rotary shaking. Reduced activity was apparent in supernatants prepared from marine 2216E broth and tryptone soya broth with or without 1% (wt/vol) sodium chloride. The antibacterial compound was sensitive to proteinase K, pronase, and trypsin, but was not affected by Tween-20, -40, -60, or -80, or alpha- or beta-amylase. Activity was not adversely affected by heating up to 40 degrees C or treatment at pH 5 to 14. The bioactive compound was determined to be associated with a protein of 30.7 kDa, which had homology to the YbdN protein of B. licheniformis ATCC 14580.

Amino Acid Sequence↗

PubMed2005

The role of the novel Fem protein VanK in vancomycin resistance in Streptomyces coelicolor.

The non-pathogenic, non-glycopeptide-producing actinomycete Streptomyces coelicolor carries a cluster of seven genes (vanSRJKHAX) that confers inducible, high level resistance to vancomycin. The vanK gene has no counterpart in previously characterized vancomycin resistance clusters, yet vanK is required for vancomycin resistance in S. coelicolor. VanK belongs to the Fem family of enzymes, which add the branch amino acid(s) to the stem pentapeptide of peptidoglycan precursors. Upon exposure to vancomycin, the VanRS two-component system switches on expression of all seven van genes, and the VanHAX enzymes reprogram the cell wall such that precursors terminate D-Ala-D-lactate (Lac) rather than D-Ala-D-Ala, thus conferring resistance to vancomycin, which only binds D-Ala-D-Ala-containing precursors. Here we provide biochemical and genetic evidence that VanK is required for vancomycin resistance because the constitutively expressed FemX enzyme, encoded elsewhere on the chromosome, cannot recognize D-Lac-containing precursors as a substrate, whereas VanK can. Consistent with this view, D-Lac-containing precursors carrying the Gly branch are present in the wild type transiently exposed to vancomycin but are undetectable in a vanK mutant treated in the same way. Further, femX null mutants are viable in the presence of vancomycin but die in its absence. Because only VanK can recognize D-Lac-containing precursors, vancomycin-induced expression of VanHAX in a vanK mutant is lethal, and so vanK is required for vancomycin resistance.

Amino Acids↗

PubMed2006

7-O-malonyl macrolactin A, a new macrolactin antibiotic from Bacillus subtilis active against methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and a small-colony variant of Burkholderia cepacia.

We report here the discovery, isolation, and chemical and preliminary biological characterization of a new antibiotic compound, 7-O-malonyl macrolactin A (MMA), produced by a Bacillus subtilis soil isolate. MMA is a bacteriostatic antibiotic that inhibits a number of multidrug-resistant gram-positive bacterial pathogens, including methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and a small-colony variant of Burkholderia cepacia. MMA-treated staphylococci and enterococci were pseudomulticellular and exhibited multiple asymmetric initiation points of septum formation, indicating that MMA may inhibit a cell division function.

Animals↗

PubMed2004

Glycopeptide-resistance transferability from vancomycin-resistant enterococci of human and animal source to Listeria spp.

AIMS: The glycopeptide-resistance transferability from vancomycin-resistant enterococci (VRE) of clinical and animal origin to different species of Listeria was investigated. METHODS AND RESULTS: Of 36 matings, performed on membrane filter, the glycopeptide resistance was successfully transferred in six attempts, five with donors of animal origin and only one with donors from clinical source. The acquired glycopeptide resistance in Listeria transconjugants was confirmed by the presence of the conjugative plasmid band and by the amplification of the 732-bp fragment of vanA gene in transferred plasmids. CONCLUSIONS: Despite the lower number of bacteria used in this study, the source of enterococci influenced the outcome of mating. Moreover transferred VanA plasmid induced a different expression in Listeria transconjugants, suggesting that gene expression might be influenced by species affiliation of recipients. SIGNIFICANCE AND IMPACT OF THE STUDY: Our data strengthen the opinion that enterococci are an important source of resistance genes for Listeria via the transfer of movable genetic elements. As these strains are commonly found in the same habitats, a horizontal spread of glycopeptide resistance in Listeria spp. could be possible.

Animals↗

PubMed2002

Characterization of Tn1546 in vancomycin-resistant Enterococcus faecium isolated from canine urinary tract infections: evidence of gene exchange between human and animal enterococci.

Thirty-five enterococcal isolates were recovered from dogs diagnosed with urinary tract infections at the Michigan State University Veterinary Teaching Hospital over a 2-year period (1996 to 1998). Isolated species included Enterococcus faecium (n = 13), Enterococcus faecalis (n = 7), Enterococcus gallinarum (n = 11), and Enterococcus casseliflavus (n = 4). Antimicrobial susceptibility testing revealed several different resistance phenotypes, with the majority of the enterococcal isolates exhibiting resistance to three or more antibiotics. One E. faecium isolate, CVM1869, displayed high-level resistance to vancomycin (MIC > 32 micro g/ml) and gentamicin (MIC > 2,048 micro g/ml). Molecular analysis of this isolate revealed the presence of Tn1546 (vanA), responsible for high-level vancomycin resistance, and Tn5281 carrying aac6'-aph2", conferring high-level aminoglycoside resistance. Pulsed-field gel electrophoresis analysis revealed that CVM1869 was a canine E. faecium clone that had acquired Tn1546, perhaps from a human vancomycin-resistant E. faecium. Transposons Tn5281 and Tn1546 were located on two different conjugative plasmids. Sequence analysis revealed that in Tn1546, ORF1 had an 889-bp deletion and an IS1216V insertion at the 5' end and an IS1251 insertion between vanS and vanH. To date, this particular form of Tn1546 has only been described in human clinical vancomycin-resistant enterococcus isolates unique to the United States. Additionally, this is the first report of a vancomycin-resistant E. faecium isolated from a companion animal in the United States.

Animals↗

PubMed1996

Differences in outcomes for patients with bacteremia due to vancomycin-resistant Enterococcus faecium or vancomycin-susceptible E. faecium.

To determine the differences in outcome in cases of enterococcal bacteremia due to vancomycin-resistant organisms, we compared consecutive patients on a liver transplant service who had clinically significant bacteremia due to vancomycin-resistant Enterococcus faecium (VREF) (n = 54) with a contemporaneous cohort of patients who had vancomycin-susceptible E. faecium (VSEF) bacteremia (n = 48). VREF bacteremia occurred significantly later in the hospitalization than did VSEF bacteremia (43 days vs. 24 days, respectively; P < .01); in addition, VREF was more frequently the sole blood pathogen isolated (91% of patients) than was VSEF (56% of patients) (P = .0002). Invasive interventions for intraabdominal and intrathoracic infection were required more often in the VREF cohort than in the VSEF cohort (34 of 45 patients vs. 20 of 41 patients, respectively; P = .01). Vancomycin resistance more frequently resulted in recurrent bacteremia (22 of 54 patients infected with VREF vs. 7 of 48 patients infected with VSEF; P = .006), persistent isolation of Enterococcus species at the primary site (27 of 33 patients infected with VREF vs. 7 of 18 patients infected with VSEF; P = .005), and endovascular infection (4 patients infected with VREF vs. none infected with VSEF). The decrement in patient survival, as measured from the last bacteremic episode, was greater in the VREF cohort (P = .02). Vancomycin resistance, shock, and liver failure were independent risk factors for Enterococcus-associated mortality. Higher rates of refractory infection, serious morbidity, and attributable death occurred in the VREF cohort and were partially mediated by the lack of effective antimicrobial therapy.

Adult↗