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Prevalence of colonization with vancomycin-resistant enterococci in various population groups in Berlin, Germany.

In order to prevent the spread of vancomycin-resistant enterococci (VRE), the epidemiology of this micro-organism must be defined. The prevalence of colonization with VRE in various population groups in Berlin was investigated and the risk factors associated with VRE colonization assessed. In a cross-sectional study, rectal swabs were taken from seven population groups (healthy students, outpatients, home nursing patients, normal care and critical care patients of a community hospital and university hospital). Every one completed a questionnaire (age, gender, previous hospital stays, antibiotic therapy). Rectal swabs were examined for the presence of normal gut flora and VRE. All VRE isolates were typed by pulsed-field gel electrophoresis (PFGE). VRE colonization prevalence ranged from 0.9% (students) to 4.2% (nursing-home patients) in non-hospitalized subjects; in hospitalized patients prevalence ranged from 1.8% (regular care ward of a community hospital) to 16.3% (ICU patients of a university hospital). Location (university hospital, OR = 3.5) and age (> or = 60 years, OR = 2.2) were independent risk factors for VRE colonization. Within one population group, isolates with identical PFGE patterns were found in up to three people; one strain was found in four subjects belonging to different groups. Our findings suggest that VRE are imported from the community into hospitals with subsequent spread within the institution.

Adult↗

Detection of glycopeptide-resistant enterococci in routine diagnostic faeces specimens.

Faeces received in a diagnostic laboratory were screened for glycopeptide-resistant enterococci (GRE) on modified Lewisham medium, with and without enrichment in Enterococcosel broth. Colonization by GRE was detected in 102/838 patients (12.2%). In 74 (73%) of colonized patients GRE were detected by both methods and in 28 (27%) they were detected only after enrichment. The carriage rate in hospitalized patients was 32% (93/289) compared with 2.3% (11/425) in the community (GP patients and food-handlers). Carriage of GRE increased with age. Clostridium difficile isolation was associated with GRE colonization, odds ratio 6.76 (P<0.001). Fifty-nine percent (60/102) of the GRE had the VanA phenotype and 41% (42/102) had the VanB phenotype. In the community VanA predominated (91%), whereas 64% (57/89) of the isolates from hospitalised patients were of the VanB phenotype.

Adolescent↗

Nosocomial cross transmission as a primary cause of vancomycin-resistant enterococci in Austria.

Stool specimens from 226 patients from intensive care units (N=69), general wards (N=112), and outpatient-clinics (N=45) at the Innsbruck University Hospital and from 433 healthy volunteers were inoculated on to Enterococcosel Agar supplemented with 5 microg/mL vancomycin and 4 microg/mL cefodizime. Faecal specimens from 105 dairy cows, 171 pigs and 47 egg-laying hens were processed the same way. Thirteen of 226 patients (5.8%) harboured 14 vancomycin-resistant enterococci (VRE) of the vanA genotype; 12 E. faecium (from 11 patients) and two E. faecalis (ICU patients: 5.8%, general ward patients: 5.4%, outpatients: 6.7%). None of the faecal specimens from healthy volunteers or animals yielded VRE. Nine of the 13 patients harbouring VRE had received antibiotic therapy during the previous four weeks (broad-spectrum cephalosporins: six patients; i.v. vancomycin: five patients). Of the 14 VRE (vanA type) isolates six strains were indistinguishable by PFGE using Sma I as restriction endonuclease, six strains formed three pairs, and only two single isolates showed unique patterns. The results of our study supports the view that nosocomial cross transmission is currently the main cause of colonization and infection with VRE in Austria.

Animals↗

Experience of vancomycin-resistant enterococci in a children's hospital.

Vancomycin resistant enterococci (VRE) are increasingly important nosocomial pathogens. This paper describes our experience of the epidemiology and clinical impact of VRE in the two years since the occurrence of our first case of VRE infection. Following introduction of surveillance, gastrointestinal colonization with VRE was detected in 38.3% of Haematology/Oncology and 11.1% of Hepatology/Gastroenterology patients, but in only 2.3% of children in the Paediatric Intensive Care and 1.5% of children in the Renal Unit. Only five patients with gastrointestinal colonization subsequently developed clinical infection with VRE, giving an annual incidence of 7.5%. A further six children were colonized at extra-intestinal sites. Twelve children had clinical infections with VRE, of whom three (25%) died. Contamination of bedspaces was found in association with 2/3 (66.7%) children with extraintestinal colonization and 5/7 (71.4%) children with clinical infections, compared with 6/28 (21.4%) cases of gastrointestinal colonization. In the latter group, bedspace contamination was usually associated with widespread contamination of the ward with VRE and may have been the cause rather than the result of patients acquiring VRE. Originally we employed control measures based closely on the North American HICPAC guidelines, but our control strategy has since evolved in response to epidemiological and clinical observations.

Adolescent↗

Effectiveness of a multifaceted infection control policy in reducing vancomycin usage and vancomycin-resistant enterococci at a tertiary care cancer centre.

We undertook a prospective cohort study to evaluate the role of a multifaceted infection control policy including the use of a "vancomycin order form," in decreasing the transmission of vancomycin-resistant enterococci (VRE). In January 1997, a multifaceted infection-control policy was implemented amongst patients admitted to the M. D. Anderson Cancer Center in whom neutropenic fever developed or who were found to be colonized or infected with VRE. As part of this programme, we initiated the use of a vancomycin order form to reduce the use of empirical vancomycin. The total incidence of VRE infections declined from 0.437/1000 patient days in 1996-97 to 0.229/1000 patient days in 1998-99 (P=0.008). The VRE bloodstream infections declined from 0.338/1000 patient days in 1996-97 to 0.181/1000 patient days in 1998-99 (P=0.027). Empiric vancomycin use decreased from 416 g/1000 patient days in 1996-97 to 208 g/1000 patient days in 1998-99 (P<0.001), resulting in a decreased vancomycin cost from $2561 US dollars/1000 patient days in 1996-97 to $1195 US dollars/1000 patient days in 1997-98 (P<0.001). We conclude that a multifaceted infection control policy incorporating the use of a vancomycin order form can effectively decrease the use of empirical vancomycin and can play a role in limiting the spread of VRE in an endemic setting.

Anti-Bacterial Agents↗

Vancomycin-resistant enterococci: 15 years and counting.

We review the history of vancomycin-resistant enterococci (VRE) and propose a causal model illustrating the roles of exposure to VRE reservoirs, patient characteristics, antimicrobial exposure, and prevalence of VRE in the progression from potential VRE reservoirs to active disease in hospitalized patients. Differences in VRE colonization and VRE infection are discussed with respect to hospital surveillance methodology and implications for interventions. We further document clonal transmission of VRE in a large, urban, teaching hospital and demonstrate VRE susceptibility to a wide array of antimicrobial agents. This model can guide the identification of mutable factors that are focal points for intervention.

Carrier State↗

Vancomycin-resistant enterococci: recent advances in genetics, epidemiology and therapeutic options.

Vancomycin-resistant enterococci (VRE) have gained much attention in the last decade. Currently, there are five known types of vancomycin resistance based on genes encoding ligase enzymes that the organisms use to produce their cell wall precursors, namely, VanA, VanB, VanC, VanD and VanE. An additional unclassified type was discovered in Australia. The basis of resistance among these phenotypes appears to be similar in that the resistant organisms produce peptidoglycan precursors that end in moieties other than D-alanyl-D-alanine, the usual target of vancomycin. The other dipeptide-like termini identified to date include D-alanyl-D-lactate and D-alanyl-D-serine, which have low affinity for glycopeptides. Recent evidence suggests that glycopeptide-producing organisms might be the remote origin of the vancomycin resistance genes. In European countries, avoparcin, a glycopeptide used in farm animals as a growth promoter, has been linked to the occurrence of VRE and occasional common strains have been identified in food products, farm animals, healthy subjects and hospitalized patients. There have been no such reports in the USA where heavy use of vancomycin and use of broad spectrum antibiotics such as cephalosporins have been identified as important risk factors for acquisition of VRE. Transmission within the same or between hospitals has been reported in many countries. Infection control measures and efforts to use antibiotics, particularly vancomycin, more appropriately have been implemented in a number of healthcare facilities with varying degrees of success. Many antibiotics, as a single agent or a combination of drugs, as well as various new antibiotics have been tested in vitro, in animal models, or used in anecdotal cases but clinical data from large comparative trials are not available to date. Because of the limited susceptibility of many VRE to other agents, efforts to control these organisms are particularly important. Copyright 1999 Harcourt Publishers LtdCopyright 1999 Harcourt Publishers Ltd.

Journal Article↗

Antimicrobial activities of hydrophobic 2-arylbenzofurans and an isoflavone against vancomycin-resistant enterococci and methicillin-resistant Staphylococcus aureus.

Eight 2-arylbenzofurans and an isoflavone isolated from medicinal plants were tested for their antimicrobial activities against vancomycin-resistant enterococci (VRE) and methicillin-resistant Staphylococcus aureus (MRSA). Among these compounds, six hydrophobic 2-arylbenzofurans (log P = 4.4-8.7) exhibited considerable antibacterial activity against five VRE strains(VanA-, VanB-, and VanC-phenotypes) (MICs = 3.13-6.25 microg/mL). Five compounds also showed antibacterial activity against ten MRSA strains (MIC80 = 3.13 microg/mL).

Anti-Infective Agents↗

Vancomycin-resistant-enterococci--colonization of 24 patients on a pediatric oncology unit.

BACKGROUND: Colonization with multidrug-resistant vancomycin-resistant-enterococci (VRE) could become a serious problem, since there is no proven therapy in case of an infection or in case of transfer of glycopeptid-resistance to other organisms. PATIENTS: Description of 24 from 48 pediatric oncology patients with VRE-colonization. METHODS: Stool samples were taken from all patients of our pediatric oncology unit from March 1996 until June 1997. Barrier isolation was introduced in May 1996, a prudent use of glycopeptid antibiotica in July 1996. RESULTS: 193 stool sample examinations demonstrated that 24 (50%) of the 48 patients were colonized with VRE. 11 (46%) of these 24 patients were VRE-carriers at the time of their first examination; 9 (37%) patients acquired VRE during their therapy and 4 (17%) patients had come from other hospitals and already were VRE-positive when they entered our unit. In March 1997, one year after the outbreak only four patients still were VRE-positive, in June 1997 all of them were VRE-negative. The average time of colonization was 12.5 weeks. 17 (70%) of the 24 colonized patients had received glycopeptide antibiotics, 16 of them within two months before the appearance of VRE in their stool. Five colonized patients died, four of them because of their oncological illness, one because of a sepsis without proof of VRE in his blood. In the end none of our patients suffered from a VRE-infection, and besides that, the transfer of glycopeptid-resistance to other organisms was not observed. CONCLUSION: With barrier isolation and a very restrictive use of glycopeptid-antibiotica, colonization can be decreased and even stopped. Inspite of the high number of colonized patients no VRE-infectious disease occurred.

Adolescent↗

Persistent contamination of fabric-covered furniture by vancomycin-resistant enterococci: implications for upholstery selection in hospitals.

Vancomycin-resistant enterococci (VRE) have emerged as important nosocomial pathogens in hospitals throughout the United States. An increasing concern with respect to VRE dissemination is survival on, and potential transmission from, environmental surfaces within health care institutions. Therefore, we assessed survival of VRE on fabric chairs in an attempt to determine the optimal upholstery for the health care setting. VRE was identified on 3 of 10 seat cushions sampled, including 2 chairs in a room of a patient with known VRE. After performing simulated contamination experiments, all samples were positive at 72 hours and 1 week after inoculation. Contamination of the upholstery could be prevented by placing a sheet folded 4 times or a bath blanket folded in half on the seat cushion. In conclusion, VRE are capable of prolonged survival on fabric seat cushions and can be transferred to hands. Environmental surfaces such as chairs may serve as a potential reservoir for nosocomial transmission of VRE, and an easily cleanable, nonporous material is the preferred upholstery in hospitals.

Chicago↗

Vancomycin-resistant enterococci in intensive-care hospital settings: transmission dynamics, persistence, and the impact of infection control programs.

Vancomycin-resistant enterococci (VRE) recently have emerged as a nosocomial pathogen especially in intensive-care units (ICUs) worldwide. Transmission via the hands of health-care workers is an important determinant of spread and persistence in a VRE-endemic ICU. We describe the transmission of nosocomial pathogens by using a micro-epidemiological framework based on the transmission dynamics of vector-borne diseases. By using the concept of a basic reproductive number, R0, defined as the average number of secondary cases generated by one primary case, we show quantitatively how infection control measures such as hand washing, cohorting, and antibiotic restriction affect nosocomial cross-transmission. By using detailed molecular epidemiological surveillance and compliance monitoring, we found that the estimated basic reproductive number for VRE during a study at the Cook County Hospital, Chicago, was approximately 3-4 without infection control and 0.7 when infection control measures were included. The impact of infection control was to reduce the prevalence from a predicted 79% to an observed 36%. Hand washing and staff cohorting are the most powerful control measures although their efficacy depends on the magnitude of R0. Under the circumstances tested, endemicity of VRE was stabilized despite infection control measures, by the constant introduction of colonized patients. Multiple stochastic simulations of the model revealed excellent agreement with observed pattern. In conjunction with detailed microbiological surveillance, a mathematical framework provides a precise template to describe the colonization dynamics of VRE in ICUs and impact of infection control measures. Our analyses suggest that compliance for hand washing significantly in excess of reported levels, or the cohorting of nursing staff, are needed to prevent nosocomial transmission of VRE in endemic settings.

Anti-Bacterial Agents↗

Lectin-like binding and antibiotic sensitivity of enterococci from wild herbivores.

Fifty eight enterococcal isolates from wild herbivores were tested for their antibiotic sensitivity pattern and lectin-like binding of extracellular matrix (ECM) and serum proteins. Kanamycin resistance was very frequent; many multiresistant strains were also isolated. All isolates were sensitive to rifampicin. Resistance to gentamicin, novobiocin, and tetracycline was widely distributed in the microflora of wild herbivores breeded in zoological garden in Kosice. No autoaggregating strains were detected among these 58 enterococcal isolates. Various degrees of binding of mucins, fetuin, heparin, fibrinogen, and fibronectin were observed in individual strains. However, bovine lactoferrin binding by enterococci from deers and chamoises was either negative (0) or strongly positive (3). With regard to influence of growth media, TH agar was found to be better for the expression of lectin-like binding than blood agar, TH broth and Nutrient broth. A significant effect (P < 0.001 or P < 0.05) of proteolytic treatment was observed in six selected strains. However, there is a difference between the effect of trypsin and pronase P. Pronase treatment more effectively decreased binding of some strains (1H, 6A, EF 1111, EC 1292), while trypsin treatment decreased more binding of other enterococcal strains (EF 953 and 1E). Significant (P < 0.001) influence of metaperiodate, which cleaves the C-C bond between vicinal groups of sugars, on collagen I binding by three selected strains (1E, 1H, 6A) and bovine lactoferrin binding (by EF 1111, EC 1292, EF 953) was also observed. However, its influence was very different. In two strains (1H and EC 1292), ECM binding was decreased, while in four other strains (1E, 6A, EF 1111, EF 953) it was increased.

Animals↗

Antibiotic resistance and genomic analysis of enterococci in an intensive care unit and general wards.

Fifty-nine enterococci isolated from 18 patients in an intensive care unit (ICU) and 21 patients in general wards (GW) at Royal Perth Hospital (RPH) during a period of 14 months were examined for antibiotic resistance by susceptibility testing and DNA polymorphism by pulsed-field gel electrophoresis. The study showed that penicillin-resistant Enterococcus faecium is a common nosocomial isolate in ICU. The DNA patterns of various strains of E. faecium and E. faecalis were closely related in most consecutive isolates from the same patients but were generally different for isolates from different patients. Thirty two different DNA patterns were identified for 59 isolates from 39 patients. Identical or similar DNA patterns were also identified for some isolates from different patients, suggesting that cross-infection had occurred between patients in ICU and GW. These data suggest that cross-infection occurred more commonly in ICU than in GW and are consistent with the known higher risk of ICU patients for nosocomial infection.

Bacterial Typing Techniques↗

Vancomycin-resistant enterococci in neonates.

Fecal-oral transmission of vancomycin-resistant strains of Enterococci (VRE), which colonize the human gastrointestinal tract, has led to nosocomial epidemics in recent years. The aim of this study was to establish the incidence and associated factors of fecal colonization with VRE in neonates. In our hospital 110 rectal swab specimens collected in the neonatal intensive care unit (NICU) were examined for VRE. For comparison, rectal swabs collected from 42 healthy neonates on the obstetrics ward were also analyzed. Of the NICU patients, 8 had VRE MICs of 8-64 microg/ml for vancomycin and 2-32 microg/ml for teicoplanin, whereas none of the healthy newborns, had VRE (p < 0.05). All patients positive for VRE had factors known to be associated with VRE carriage, such as low birth weight or long-term antibiotic therapy.

Cross Infection↗

Low faecal carrier rate of vancomycin resistant enterococci in Norwegian hospital patients.

The faecal carrier rate of vancomycin resistant enterococci (VRE) was surveyed among 616 patients in selected departments of 7 Norwegian hospitals. One Enterococcus gallinarum isolate harbouring a vanB2 element was recovered from a child with malignant disease treated with vancomycin and ceftazidime. No vancomycin resistant Enterococcus faecalis or Enterococcus faecium were detected and no VRE isolates of the VanA type were identified. The low level of VRE carriage corresponds to the limited use of glycopeptide antibiotics for human therapeutic purposes in Norway. It indicates a low risk of acquiring VRE infections in Norwegian hospitals.

Anti-Bacterial Agents↗

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↗

Comparative in-vitro activity of fourteen antibiotics against clinical isolates of enterococci.

The in-vitro antibacterial activities of fourteen antimicrobial agents, including ampicillin, amikacin, Augmentin, ceftazidime, cefotaxime, ceftriaxone, ciprofloxacin, erythromycin, gentamicin, penicillin G, piperacillin, rifampicin, streptomycin and vancomycin, were compared against 195 enterococcal strains isolated from clinical specimens received at the King Abdulaziz University Hospital in Saudi Arabia. The antibacterial susceptibility was determined by the minimal inhibitory concentration (MIC) using an agar dilution method. Ampicillin, Augmentin and vancomycin exhibited the greatest activity, inhibiting 90% of the tested strains (MIC90) at 2 micrograms/ml, followed by penicillin G and piperacillin with MIC90 of 4 micrograms/ml. Erythromycin, third generation cephalosporins, aminoglycosides and rifampicin, on the other hand, had poor activity against enterococci with MIC90s well above the obtainable serum concentrations. The clinical implications of resistance to aminoglycosides and the alternative antimicrobial therapy in serious enterococcal infections are discussed in the text.

Anti-Bacterial Agents↗

Antimicrobial activity of isepamicin (SCH21420, 1-N-HAPA gentamicin B) combinations with cefotaxime, ceftazidime, ceftriaxone, ciprofloxacin, imipenem, mezlocillin and piperacillin tested against gentamicin-resistant and susceptible gram-negative bacilli and enterococci.

Isepamicin, formerly SCH21420 or 1-N-HAPA gentamicin B, is an aminoglycoside that was tested alone or in combination with one of seven broad spectrum drugs against 80 clinical isolates. Half of the strains were gentamicin-resistant but only one isolate (1.3%) was resistant to isepamicin. The broadest spectrum comparison drugs tested alone (ciprofloxacin at 3.8% resistance and imipenem at 5.0% resistance) were associated with the lowest synergy rates when combined with isepamicin. The rank order of synergy (complete or partial) was; cefotaxime = ceftazidime = ceftriaxone = mezlocillin = piperacillin (75% to 80%) greater than imipenem (66%) greater than ciprofloxacin (38%). Isepamicin/ampicillin combinations produced synergistic killing of those enterococci not having high-grade resistance to gentamicin or kanamycin. Enterococcus faecium strains were also refractory to isepamicin/ampicillin synergy. Isepamicin appears to be widely useable against gentamicin-resistant gram-negative bacilli either alone or combined with most commonly used broad spectrum beta-lactams.

Cefotaxime↗