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PubMed2005

Effect of hospitalization on the antibiotic resistance of fecal Enterococcus faecalis of surgical patients over time.

The prevalence of antibiotic resistant Enterococcus faecalis was determined in fecal samples of 263 patients admitted to the surgical wards of three university-affiliated hospitals on admission, at discharge, and at 1 and 6 months after discharge. A slight increase in the prevalence of antibiotic resistance of E. faecalis was found at discharge for the antibiotics tested compared to those on admission, vancomycin excepted. At 6 months after discharge, the prevalence of resistance for amoxicillin (0%), ciprofloxacin (3%), erythromycin (47%), and oxytetracycline (60%) decreased to the level on admission (respectively 0%, 8%, 45%, and 64%). Gentamicin resistance was the same at discharge (10%) as 1 month later (12%), but decreased 6 months after discharge (8%) to the level on admission (7%). In conclusion, hospitalization resulted in the study population in a slight increase in the prevalence of resistant fecal E. faecalis isolates at discharge, which decreased again (slowly) to the level on admission 6 months after discharge. Thus, the influence of hospitalization on the prevalence of antibiotic resistance in the extramural situation disappears between 1 and 6 months after discharge in this population.

Adult↗
PubMed2006

Multilocus sequence typing of hospital-associated Enterococcus faecium from Brazil reveals their unique evolutionary history.

We studied the genetic relationships between vancomycin-susceptible (n = 11) and -resistant Enterococcus faecium (VRE, n = 20) recovered from Brazil using a multilocus sequence typing (MLST) scheme. Grouping of allelic profiles revealed six clusters of related sequence types (STs) that differ in no more than two of the seven alleles. Of these, one cluster harbored 16 of the 20 isolates recovered during the first VRE outbreak in Brazil. The ampicillin and gentamicin resistance profiles were stable in the isolates that clustered within the groups I-III. Comparison with the allelic profiles of 139 E. faecium from different geographical regions and origins found in the international database http://www.mlst.net revealed that the Brazilian outbreak clone did not cluster in the previously named complex-17. This genetic complex contains hospital epidemic and clinical isolates recovered from different countries and continents. Twenty two of the 31 Brazilian isolates, including the VRE outbreak clone, clustered apart from the E. faecium isolates from the database, suggesting that these Brazilian isolates have a distinct evolutionary history.

Alleles↗
PubMed2006

Persistence of vanA-type Enterococcus faecium in Korean livestock after ban on avoparcin.

Prevalence of vancomycin-resistant enterococci (VRE) was investigated in Korean livestock 4 years after the ban of avoparcin in feed additives. VRE were isolated from approximately 16.7% of the chicken samples (57 strains from 342 meat samples) and 1.9% of the pig samples (4 from 214 fecal samples). No VRE, however, was isolated from 110 bovine fecal samples. All the 61 VRE isolates were vanA-type Enterococcus faecium expressing a high-level resistance to vancomycin, and showed resistance to teicoplanin as well except two poultry isolates. In addition, the VRE isolates had heterogeneous pulsed-field gel electrophoresis (PFGE) patterns of SmaI-digested DNA, although identical or closely related profiles were observed among strains isolated from the same farm. Although the chicken isolates were all poultry type with G at position 8,234 of the vanX gene, the pig isolates were all swine type with T at position 8,234 of the vanX gene.

Animal Feed↗
PubMed2006

A case of ventricular drainage infection with a rare pathogen in cerebrospinal fluid: vancomycin-resistant Enterococcus faecium.

The purpose of this study was to describe a patient, 7-month-old child with ventriculoperitoneal shunts for hydrocephalus with ventriculitis caused by vancomycin-resistant Enterococcus faecium. Two ventriculoperitoneal shunts were inserted just after birth and on the second month. On the sixth month, both shunts were removed because of dysfunction, and external drainage was inserted. The child developed fever, and lumbar puncture revealed a high leukocyte count and protein concentration after external drainage. Cerebrospinal fluid (CSF) cultures yielded E. faecium, which was resistant to ampicillin, erythromycin, gentamicin, penicillin G, vancomycin, and teicoplanin and was susceptible to chloramphenicol, ciprofloxacin, streptomycin, levofloxacin, and rifampin, as determined by the disk diffusion method. As a result of the antimicrobial susceptibility tests, multidrug antibiotic therapy was changed from vancomycin and ceftazidime to chloramphenicol, rifampin, and meropenem. In addition, a rifampin-clindamycin-impregnated shunt (The Codman Hakim Bactiseal, Raynham, MA) was inserted. The patient became afebrile, and CSF cultures were sterile after 15 days of yielding E. faecium. Implantation of the rifampin-clindamycin-impregnated shunt and timely use of appropriate antibiotics for 10 days according to antimicrobial susceptibility testing seem to be important in the resolution of vancomycin-resistant enterococci infections, especially in countries where linezolid and quinupristin-dalfopristin are not in use yet.

Cerebrospinal Fluid↗
PubMed1998

Antimicrobial susceptibility testing of a clinical isolate of vancomycin-dependent enterococcus using D-alanine-D-alanine as a growth supplement.

Bacteremia due to a vancomycin-dependent enterococcus (VDE) occurred during long-term vancomycin therapy in a renal transplant recipient with underlying pancreatitis and a vancomycin-resistant enterococcal (VRE) wound infection and bacteremia. The VDE was isolated from blood during vancomycin therapy and grew only in the presence of vancomycin and D-alanine-D-alanine (DADA), a substance required for cell-wall synthesis. Colonies beyond the periphery of growth of the VDE around a vancomycin disk contained vancomycin-independent revertant mutants after 48 hours of incubation. Pulsed-field gel electrophoresis of the VDE, revertant mutant, the initial blood culture isolate of VRE, and an autopsy isolate showed that the four strains were identical. Antimicrobial susceptibility testing was performed using standard macrobroth and microbroth dilution methods. DADA was used as a growth supplement for macrobroth dilution susceptibility testing of the VDE isolate. Minimum inhibitory concentrations (MICs) were similar for the VRE isolate and the VDE revertant, which were both resistant to ampicillin, high-level gentamicin, ciprofloxacin, imipenem, vancomycin, and daptomycin, and were susceptible to fusidic acid, high-level streptomycin, rifampin, and a quinupristin-dalfopristin combination. The MICs of teicoplanin were 2 microg/mL or less and 16 microg/mL for the clinical VRE isolate and the VDE revertant, respectively. The autopsy isolate was resistant to all antimicrobials tested and showed a fourfold increase in MICs for quinupristin-dalfopristin compared with that of the original blood isolate. The VDE was susceptible to all drugs tested except vancomycin.

Alanine↗
PubMed1993

Evaluation of modified MicroScan screening tests for high-level aminoglycoside resistance in Enterococcus faecalis.

Enterococcus faecalis strains that are refractory to aminoglycoside-penicillin synergistic killing can be predicted by their ability to grow in high concentrations of aminoglycoside (2,000 mg/L) or by disk diffusion tests using high content aminoglycoside disks. Forty-eight well-characterized clinical isolates of E. faecalis were used to evaluate recently reformulated gentamicin and streptomycin synergy screening tests on both overnight and rapid MicroScan (MS) Pos MIC panels (Baxter, West Sacramento, CA). The results obtained with the MS screening tests were compared with those from modified agar disk diffusion results. Discrepancies were resolved by an in-house broth microdilution method. The MS overnight tests detected 25 of 25 (100%) gentamicin high-level resistant strains and 23 of 24 (96%) streptomycin high-level resistant strains. No false high level resistance was found with the MS overnight tests. The MS rapid tests detected 100% of the gentamicin and 100% of the streptomycin high-level resistant strains, but one isolate was falsely high-level resistant to gentamicin (96% specific). The reformulated MS synergy screening tests were acceptable alternatives to disk diffusion for detection of high level aminoglycoside resistance in E. faecalis.

Anti-Bacterial Agents↗
PubMed2002

Enterococcus faecalis produces extracellular superoxide and hydrogen peroxide that damages colonic epithelial cell DNA.

Enterococcus faecalis is a commensal microorganism of the human intestinal tract that produces substantial extracellular superoxide (O(-)(2)), and derivative reactive oxygen species such as H(2)O(2) and hydroxyl radical, through autoxidation of membrane-associated demethylmenaquinone. Because these oxidants may be important as a cause of chromosomal instability (CIN) associated with sporadic adenomatous polyps and colorectal cancer, the ability of E.faecalis to damage eukaryotic cell DNA was examined using the alkaline lysis single cell gel electrophoresis (comet) assay. Both Chinese hamster ovary and HT-29 intestinal epithelial cells showed increased DNA damage after co-incubation with wild-type E. faecalis strain OG1RF, but not a transposon-inactivated mutant with attenuated extracellular O(-)(2) production. E. faecalis-mediated DNA damage was prevented by catalase, but not manganese superoxide dismutase, indicating H(2)O(2) arising from O(-)(2) was the genotoxin. In a rat model of intestinal colonization, OG1RF resulted in significantly higher stool concentrations of H(2)O(2) and 5,5-dimethyl-1-pyrroline N-oxide adducts of hydroxyl and thiyl radicals, as identified by electron spin resonance-spin trapping, compared with rats colonized with a mutant strain having attenuated O(-)(2) production. Using the comet assay, luminal cells from the colon of rats colonized with O(-)(2)-producing E. faecalis showed significantly increased DNA damage compared with control rats colonized with the mutant. These findings suggest a potentially profound role for extracellular free radical production by E. faecalis in promoting CIN associated with sporadic adenomatous polyps and colorectal cancer.

Animals↗
PubMed1992

Bactericidal activity of antibiotics alone and in combination against Enterococcus faecalis in a pharmacodynamic model.

We evaluated the bactericidal kinetics of teicoplanin, mezlocillin, netilmicin, and ciprofloxacin alone and in dual combinations against strains of Enterococcus faecalis susceptible or resistant to ampicillin in a pharmacodynamic model reproducing in bacterial culture in active human plasma or Mueller-Hinton broth the serum kinetics of these antibiotics in humans. Killing was not different in cultures grown in plasma and those grown in broth. Antibiotics used alone had no or low bactericidal activity except for high-dose ciprofloxacin (600 mg intravenously [iv] twice daily or 750 mg orally twice daily), which achieved a 3- to 4-log reduction in colony-forming units (cfu). Netilmicin was equally active at 6 mg/kg once a day or 2 mg/kg three times daily in all combinations. No major increase in bactericidal activity was detected in any combination that included mezlocillin. Maximal synergistic killing was observed for the combination of teicoplanin plus netilmicin (both at three-times daily and once-daily dosing), which sterilized the bacterial cultures (initial inoculum, 10(6) cfu/mL). Combinations of ciprofloxacin at 600 mg iv twice daily and 750 mg orally twice daily plus either teicoplanin or netilmicin were less synergistic but equally effective in total killing as a result of the high bactericidal activity of ciprofloxacin alone.

Anti-Bacterial Agents↗
PubMed1993

Nosocomial outbreak due to Enterococcus faecium highly resistant to vancomycin, penicillin, and gentamicin.

In October 1990, Enterococcus faecium that was highly resistant to glycopeptides, penicillins, and aminoglycosides was isolated from the peritoneal dialysis fluid from a patient in an intensive care unit. Over the following 6 months, multiresistant E. faecium organisms were isolated from cultures of blood, urine, or surgical wound specimens from eight additional patients. Surveillance cultures of groin and/or rectal swabs were positive for eight of 37 patients and four of 62 employees at risk. Restriction endonuclease digestion of chromosomal DNA from outbreak isolates was consistent with dissemination of a single strain throughout the intensive care unit. Strict infection control interventions contained the outbreak after several weeks. Review of patient charts suggested that renal insufficiency, length of hospital stay, duration of antibiotic treatment, and prior treatment with vancomycin were risks for infection due to multiresistant E. faecium. The emergence of multiple-drug-resistant enterococci presents serious infection control and therapeutic dilemmas.

Aged↗
PubMedDate not supplied

High-level gentamicin resistance in Enterococcus: microbiology, genetic basis, and epidemiology.

Antibiotic resistance is an ever-increasing problem in enterococci. These bacteria are remarkable in their ability to acquire and disseminate antibiotic resistance genes by a variety of routes. Since first described in 1979, high-level resistance to gentamicin (MIC, greater than 2,000 micrograms/mL) has spread worldwide and has been responsible for serious infections. Resistance is plasmid-mediated and due to aminoglycoside-modifying enzymes. High-level gentamicin resistance indicates that there will be no synergistic bactericidal activity with penicillin-gentamicin combinations. The epidemiology of nosocomial enterococcal infections is remarkably similar to that of nosocomial infections caused by methicillin-resistant staphylococci and by multidrug-resistant gram-negative bacilli. The most likely way these resistant bacteria are spread among hospital patients is via transient carriage on the hands of hospital personnel. Patient-to-patient and interhospital transmission of strains has been reported recently. However, clonal dissemination is not the cause of the increased frequency of resistant strains, since gentamicin resistance appears in a variety of different conjugative and nonconjugative plasmids in Enterococcus.

Cross Infection↗
PubMed1992

Nosocomial bacteremia due to Enterococcus faecalis without endocarditis.

During a 2-year observation period at a 2,200-bed university hospital, bacteremia due to Enterococcus faecalis was observed in 111 patients. Fifty-five patients with nosocomial bacteremia due to E. faecalis could be evaluated. The most common entry sites were the urinary tract (25%), the intraabdominal cavity (13%), and burn and decubital wounds (11%). Bacteremia was preceded by administration of cephalosporins, imipenem, and aztreonam (n = 39); ciprofloxacin (n = 11); and other antibiotics (n = 4). Age, sex, underlying disease, portal of entry, previous antibiotic therapy, and bacteremia due to other organisms had no influence on mortality. Treatment of bacteremia with penicillins (n = 45) and glycopeptides (n = 4) resulted in a mortality rate of 37%. The addition of a high-dose aminoglycoside to a penicillin did not result in a better survival rate.

Adult↗
PubMed1993

Bacteremia due to Enterococcus avium.

Enterococcus avium, formerly "group Q streptococcus," has rarely been reported as a pathogen in humans. To determine the clinical significance of this organism, we reviewed the records of all patients whose blood cultures were positive for E. avium who were seen at our institution from 1986 through 1991 and identified nine cases of bacteremia due to E. avium. All isolates were believed to be clinically significant. Five of nine cases developed in patients with significant gastrointestinal illnesses. The remaining clinical scenarios included intravenous catheter sepsis and factitious disorders. E. avium bacteremias were polymicrobial in seven cases; in six cases, the coisolates were gastrointestinal organisms. These observations suggest that E. avium bacteremia most often originated from a gastrointestinal tract source. We conclude that, though rare, E. avium can be pathogenic in humans and that E. avium bacteremia is associated with gastrointestinal abnormalities.

Adult↗
PubMed1994

Successful treatment of meningitis due to multiply resistant Enterococcus faecium with a combination of intrathecal teicoplanin and intravenous antimicrobial agents.

Following neurosurgery necessitated by intractable seizures, Enterococcus faecium meningitis that was resistant to ampicillin, a high-level aminoglycoside (MIC, > 2,000 micrograms/mL), and vancomycin developed in a 6-year-old boy. Treatment with intrathecal teicoplanin in combination with intravenous clindamycin, rifampin, and ampicillin was successful. The role of intravenous and intrathecal antibiotics in treatment of this infection is discussed. This case is illustrative of the safety and potential usefulness of intrathecally administered teicoplanin.

Child↗
PubMed1995

Clinical and molecular epidemiology of Enterococcus faecalis bacteremia, with special reference to strains with high-level resistance to gentamicin.

The objective of this study was to characterize the clinical and molecular epidemiology of Enterococcus faecalis bacteremia, specifically that involving strains with high-level resistance to gentamicin (HLGR). Episodes of E. faecalis bacteremia at the Buffalo Veterans Affairs Medical Center from January 1986 to September 1989 were retrospectively identified. Of 94 episodes, 45 (48%) were due to strains with HLGR. Hemolytic activity was detected with greater frequency (85%) among the latter strains than among those without HLGR (P < .001). Of the 54 episodes for which medical charts were available for review, 94% were hospital acquired, and 46% were due to strains with HLGR. An examination of the plasmid DNA content of isolates revealed restriction-fragment-length polymorphism. One plasmid pattern was identified in 15 isolates with HLGR (P < .001), and chromosomal DNA digest patterns suggested a common clonality; there was no direct evidence for patient-to-patient spread of these strains. The use of antibiotics, the presence of invasive devices, surgery, and admission to an intensive-care unit were not significantly associated with HLGR bacteremia. Mortality during hospitalization was 65%, with no difference between figures for HLGR and non-HLGR infections. This high mortality regardless of gentamicin susceptibility status suggests that E. faecalis bacteremia is a marker for severe illness. In contrast to previous studies, this investigation identified no clinical factors associated with HLGR E. faecalis bacteremia.

Bacteremia↗
PubMed1995

Bacteremia due to vancomycin-dependent Enterococcus faecium.

A recipient of small-bowel and liver transplants developed recurrent fever and polymicrobial bacteremia due to multiply resistant Enterobacter cloacae and an inducible VanB strain of Enterococcus faecium while receiving therapy with amikacin, imipenem, and vancomycin. These organisms could not be subcultured onto blood agar but did grow around the vancomyin disk on a direct-susceptibility test plate. Additional testing confirmed the strain as E. faecium, which would not grow in the absence of vancomycin. Growth around a disk containing D-alanyl-D-alanine was demonstrated. Spontaneous vancomycin-independent revertants were obtained at a frequency of approximately 1 x 10(-6). Two classes of vancomycin-independent revertants were obtained: one that was constitutively vancomycin resistant and one that was nonconstitutively vancomycin resistant. We hypothesize that the normal D-ala ligase is not expressed in the vancomycin-dependent strain; thus survival of these strains is dependent on expression of the VanB ligase, which produces a depsipeptide precursor that is resistant to vancomycin binding. This is the second reported case involving a clinically important vancomycin-dependent enterococcal strain. Awareness of the existence of these strains is important, especially when clinical and microbiological data are consistent with infection due to a fastidious or nutritionally-deficient organism.

Bacteremia↗
PubMed1995

Vancomycin-resistant Enterococcus faecium bacteremia: risk factors for infection.

We describe an outbreak of vancomycin-resistant Enterococcus faecium (vanA phenotype) bacteremia on the oncology ward of a tertiary care community hospital. In 10 of the 11 cases the patients had leukemia and were neutropenic (median duration of neutropenia, 21 days) at the time of bacteremia. On average, patients received six antibiotic agents for a total of 61 agent-days prior to development of vancomycin-resistant E. faecium bacteremia. The mortality rate was 73%. Molecular typing of 22 isolates revealed that the majority (83%) represented a common strain, indicating nosocomial spread. When the 11 cases were compared to 22 matched control patients, gastrointestinal colonization with vancomycin-resistant E. faecium (odds ratio [denominator, 0] infinity, P = .005) and the use of antimicrobial agents with significant activity against anaerobes (metronidazole, clindamycin, and imipenem; odds ratio infinity, P = .02) were found to be risk factors for the development of vancomycin-resistant E. faecium bacteremia. Since no proven therapy for such infection exists, there is an urgent need to identify effective measures to prevent and control the development of vancomycin-resistant E. faecium bacteremia.

Adult↗
PubMed1995

Clinical and molecular epidemiology of vancomycin-resistant Enterococcus faecium during its emergence in a city in southern Texas.

During a 19-month period from April 1993 to October 1994, 41 isolates of vancomycin-resistant Enterococcus faecium (VREF) were detected in seven different hospitals in a city in southern Texas. A case-control study to determine the risk factors for acquisition was done in the hospital in which the majority of isolates were detected. Pulsed-field gel electrophoresis (PFGE) of whole-cell DNA was used to determine strain identity. Thirty-five (85%) of the 41 VREF isolates were of the vanB phenotype. Of these, 32 (91%) of 35 were the same strain by PFGE typing. The same vanB strain was documented in five different hospitals in the city. In contrast, 4 (67%) of 6 of the vanA phenotype VREF isolates were distinct strains by PFGE typing. Significant risk factors for colonization or infection with VREF were prior exposure to antibiotics (P = .04), the previous use of third-generation cephalosporins (P = .03), and the previous use of parenteral vancomycin (P = .002). Infection-control and antibiotic-utilization measures were implemented to control cross-transmission and selection of VREF isolates. During the emergence of VREF in our city, clonal dissemination of a single strain of vanB VREF among six hospitals was documented. Limited cross-transmission of vanA phenotype VREF isolates occurred, but most vanA VREF isolates were distinct strains selected in individual hospital environments.

Anti-Bacterial Agents↗
PubMed1996

A citywide survey of vancomycin-resistant Enterococcus--New York City, 1993.

Vancomycin-resistant Enterococcus (VRE) has become an increasingly important nosocomial pathogen. Questionnaires were sent to all New York City (NYC)-licensed laboratories to ask about testing procedures used, number of isolates identified, species identified, and vancomycin susceptibility for enterococcal isolates in 1993. Of 127 laboratories, 118 (93%) responded. Fifty-three (45%) of the 118 laboratories reported both the number of enterococcal isolates tested and the number of VRE isolates identified during 1993; 15 (28%) of the 53 laboratories did not isolate VRE, and the remaining 38 laboratories identified 3,822 (8.1%) VRE isolates. VRE was first identified by a NYC-licensed (commercial) laboratory in 1988. Among NYC hospital laboratories, 65 (97%) of 67 identified at least one VRE isolate during 1989-1993. This survey demonstrates that there has been a marked increase in the number of VRE isolates identified in NYC laboratories.

Data Collection↗