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PubMed2000

Vancomycin resistance emerging in a clonal outbreak caused by ampicillin-resistant Enterococcus faecium.

OBJECTIVES: To describe the first nosocomial outbreak of ampicillin-resistant Enterococcus faecium (ARE) in Norway, where a few vancomycin-resistant strains have also been identified. METHODS: All cases of ARE and vancomycin-resistant Enterococcus faecium (VRE) diagnosed by the medical microbiological laboratories in a region inhabited by approximately 1 million people were registered. Isolates obtained during the period 1 January 1995 to 31 December 1996 were characterized by pulsed field-gel electrophoresis and the clinical data were recorded. RESULTS: One hundred and forty-nine patients (64 males, 85 females, mean age 70.5 years) were infected with ARE. Isolates from 115 cases were genomically related to the outbreak strain. Infections included bacteremia (14), wound infections (31), urinary tract infections (97) and other infections (seven). Most had a severe underlying disease and 93% of the patients had received antibiotics for a mean time of 23 days. Twenty-four patients (16.1%) died during hospitalization. Four infections were caused by a vanB-type VRE that was genomically related to the ARE outbreak strain. The prescription rate for vancomycin was low, but an increase in vancomycin use paralleled the appearance of VRE. The highest monthly incidence rate was 2.5 per 1000 patient admissions in July 1996 declining to 0.5 in December 1996. CONCLUSIONS: The first nosocomial outbreak caused by ARE was observed in 1995 in Norway and is still ongoing. One year after the onset, VRE occurred in wards which had a relatively high consumption of vancomycin.

Aged↗

PubMed2002

Emergence of vancomycin-resistant Enterococcus faecium at a tertiary care hospital in Karachi, Pakistan.

Vancomycin-resistant enterococcus (VRE) has not been reported previously in Pakistan. This is the first report where in vancomycin-resistant Enterococcus faecium was isolated from the clinical specimens of six patients admitted to the intensive care unit (ICU) and neonatal intensive care unit (NICU) of the Aga Khan University Hospital, Karachi. To identify the extent of the outbreak, rectal swabs were obtained from all the patients admitted to the ICU and NICU at that time. A total of 10 strains of vancomycin-resistant Enterococcus faecium were isolated. All the strains showed high-level resistance to both glycopeptides (vancomycin and teicoplanin) with a vancomycin minimum inhibitory concentration greater than 256 mg/L. All isolates had the vanA gene detected by polymerase chain reaction. The contour-clamped homogeneous electric field (CHEF) pattern demonstrated that all but one of the isolates were of a single clone, suggesting that they were derived from common source. Use of vancomycin and prolonged hospitalization were common features in all cases investigated.

Adult↗

PubMed1993

Characterization of the chromosomal aac(6')-Ii gene specific for Enterococcus faecium.

Chromosomal gene aac(6')-Ii of Enterococcus faecium CIP 54-32, encoding a 6'-N-aminoglycoside acetyltransferase was characterized. The gene was identified as a coding sequence of 549 bp corresponding to a protein with a calculated mass of 20,666 Da. Analysis of the sequence of the deduced protein suggested that it was the second member of a subfamily of AAC(6')-I enzymes. Insertional inactivation of aac(6')-Ii led to aminoglycoside susceptibility of CIP 54-32, suggesting that this gene plays a role in resistance to AAC(6')-I substrates. The gene was detected by DNA hybridization in all 26 strains of E. faecium tested but not in 44 other enterococci of 13 species. These data suggest that the aac(6')-Ii gene is species specific and may be used to identify E. faecium.

Acetyltransferases↗

PubMed2003

Presence of a vanA-carrying pheromone response plasmid (pBRG1) in a clinical isolate of Enterococcus faecium.

Sex pheromone plasmids, frequently found in Enterococcus faecalis, have rarely been detected in Enterococcus faecium. pBRG1 is an approximately 50-kb vanA-carrying conjugative plasmid of an E. faecium clinical isolate (LS10) that is transferable to E. faecalis laboratory strains. In cell infection experiments, E. faecium LS10 exhibited remarkably high invasion efficiency and produced cytopathogenic effects in Caco-2 cell monolayers. Growth in the presence of sex pheromones produced by E. faecalis JH2-2 was found to cause self-aggregation of both E. faecium LS10 and E. faecalis JH-RFV(pBRG1) (a transconjugant obtained by transfer of pBRG1 to E. faecalis JH2-2) and to increase the cell adhesion and invasion efficiencies of both E. faecium LS10 and E. faecalis JH-RFV(pBRG1). Sex pheromone cCF10 caused clumping of E. faecalis OG1RF(pBRG1) (a transconjugant obtained by transfer of pBRG1 to E. faecalis OG1RF) at a concentration approximately 100-fold higher than the one required for the control strain E. faecalis OG1RF(pCF10). PCR products of the expected sizes were obtained with primers internal to aggregation substance genes of E. faecalis pheromone response plasmids pAD1, pPD1, and pCF10 and primers internal to ash701 of E. faecium pheromone plasmid pHKK701. These findings suggest that pBRG1 of E. faecium LS10 is a sex pheromone response plasmid.

Bacterial Adhesion↗

PubMed1999

Alterations in GyrA and ParC associated with fluoroquinolone resistance in Enterococcus faecium.

High-level quinolone resistance in Enterococcus faecium was associated with mutations in both gyrA and parC genes in 10 of 11 resistant strains. On low-level resistant strain without such mutations may instead possess an efflux mechanism or alterations in the other subunits of the gyrase or topoisomerase IV genes. These findings are similar to those for other gram-positive bacteria, such as Enterococcus faecalis.

Amino Acid Sequence↗

PubMed2001

Aortic root replacement in a patient with vancomycin-resistant Enterococcus faecium endocarditis and leukemia.

Vancomycin-resistant Enterococcus faecium endocarditis is rare and usually occurs in immunocompromised patients. We describe a patient with hairy-cell leukemia and vancomycin-resistant E faecium endocarditis. The patient presented with severe aortic insufficiency. He underwent aortic root replacement with a cryopreserved aortic homograft and was treated with a combination of quinupristin/dalfopristin, ampicillin, and gentamicin.

Acute Disease↗

PubMed2006

[Comparative study of treatment with quinupristin-dalfopristin alone or in combination with gentamicin, teicoplanin, imipenem or levofloxacin in experimental endocarditis due to a multidrug-resistant Enterococcus faecium].

The incidence of multidrug-resistant Enterococcus faecium is increasing despite advances in antibacterial therapy. Thus, new antibiotics are required to treat hospital- or community-acquired infections caused by these multidrug-resistant organisms. The aim of this study was to compare the therapeutic efficacy of quinupristin-dalfopristin (QD) alone, or in combination with gentamicin (G), teicoplanin (T), imipenem (I) or levofloxacin (L) against a strain of multidrug-resistant E. faecium in an experimental model of aortic valve endocarditis in rabbits. The study group consisted of 28 control animals. Eighty-two animals were treated with one of the following antibiotic regimens: G1: 18 animals QD (30 mg/kg/8 h); G2: 18 animals QD+G (6 mg/kg/12 h); G3: 16 animals QD+T (20 mg/kg/12 h); G4: 14 animals QD+I (60 mg/kg/8 h); and G5: 16 animals QD+L (20 mg/kg/12 h). The response to therapy was determined by the comparison of the number of CFU/g of E. faecium in each vegetation. In vitro, time-kill studies looking for synergy for the combinations that showed better efficacy in vivo were done. The sensitivity of the strain was intermediate to QD, resistant to T and I, and sensitive to L. There was no high-level resistance to G. QD alone revealed a significant decrease (p <0.001) in the CFU/g in the control group (9.49 vs. 7.31). There were no differences in the average of CFU/g between the QD alone (G1), QD+G (G2) and QD+T (G3) groups. These three groups revealed a significant difference in decrease of CFU/g respect of the group control (p <0.001). There were no differences in the average of CFU/g between QD+I (G4) and QD+T (G5). These two groups revealed the greatest decrease in average CFU/g (G4: 4.38 and G5: 4.04) with differences respect of the group control (p <0.0001) and respect of the groups G1, G2 and G3 (p <0.001). We did not detect any alteration of MIC from QD in the course of the treatment for either of the final isolations. Only the time kill corresponding to concentrations of I 32 mg/l (0.25 x MIC) and QD 1 mg/l (0.25 x MIC presents a descending slope in the curve at 4 and 8 h, suggesting an early synergy phenomenon, which was lost after 8 h. In light of these results, the combination QD with I and L may be considered suitable alternatives for the treatment of multiresistant E. faecium.

Aged↗

PubMed2001

Characterisation of VanA and VanB elements from glycopeptide-resistant Enterococcus faecium from Greece.

Ten glycopeptide-resistant Enterococcus faecium isolates from separate patients in Laikon General Hospital, Athens were studied. Eight isolates had the VanA phenotype and represented variants of three strains based on SmaI macrorestriction banding patterns. Their VanA elements were compared with the prototype element, Tn1546, by an overlapping PCR method. Three related isolates contained resistance elements indistinguishable from Tn1546 (designated Greek type I). The other five isolates all contained identical elements that differed from Tn1546 by the presence of IS1251 between vanS and vanH, by a point mutation (G --> T) at nucleotide position 8234 within vanX and by a partial loss of transposition gene orf1 (designated Greek type II). Two distinct strains of E. faecium with the VanB phenotype were obtained. HhaI digestion of an amplified fragment of the vanB gene indicated that both strains contained the vanB2 allele, and further PCR assays confirmed that the vanB2 gene cluster was located within a Tn5382-like element.

Alleles↗

PubMed1994

Outbreak of multidrug-resistant Enterococcus faecium with transferable vanB class vancomycin resistance.

Enterococcus faecium strains resistant to ampicillin, high levels of gentamicin, and vancomycin but susceptible to teicoplanin (vanB class vancomycin resistance) were recovered from 37 patients during an outbreak involving a 250-bed university-affiliated hospital. Three isolates with vancomycin MICs ranging from 8 to 256 micrograms/ml all hybridized with a vanB probe. Restriction endonuclease analysis of chromosomal and plasmid DNA suggested that all isolates tested were derived from a single clone. Vancomycin resistance was shown to be transferable. Risk factors for acquiring the epidemic strain included proximity to another case patient (P, 0.0005) and exposure to a nurse who cared for another case patient (P, 0.007). Contamination of the environment by the epidemic strain occurred significantly more often when case patients had diarrhea (P, 0.001). Placing patients in private rooms and requiring the use of gowns as well as gloves by personnel controlled the outbreak. These findings suggest that multidrug-resistant E. faecium strains with transferable vanB class vancomycin resistance will emerge as important nosocomial pathogens. Because extensive environmental contamination may occur when affected patients develop diarrhea, barrier precautions, including the use of both gowns and gloves, should be implemented as soon as these pathogens are encountered.

Adult↗

PubMed1996

Penicillin tolerance and modification of lipoteichoic acid associated with expression of vancomycin resistance in VanB-type Enterococcus faecium D366.

Induction of vancomycin resistance in Enterococcus faecium D366, which exhibits a VanB-type resistance, as well as its constitutive expression in MT9, a derivative of D366, was associated with penicillin tolerance as shown by decreased lysis and killing of the cells. This phenomenon was linked neither to decreased expression of the different autolysins nor to their decreased lytic activity on the different cell walls. The only change observed was that almost twice the normal amount of D-alanine was attached to the lipoteichoic acid.

Anti-Bacterial Agents↗

PubMed2004

Evidence for transmission between humans and the environment of a nosocomial strain of Enterococcus faecium.

An ampicillin- and ciprofloxacin-resistant Enterococcus faecium (ARE) strain, named FMSE1, with a characteristic biochemical phenotype, was in a recent study found to dominate among faecal ARE isolates from patients in several Swedish hospitals. In the present study, the prevalence of this strain among 9676 enterococcal isolates from healthy children, hospital sewage, urban sewage, surface water, slaughtered animals (broilers, pigs and cattle) and pig faeces and manure was investigated. Enterococcal isolates having the same biochemical phenotype as the FMSE1 were most common in samples of hospital sewage (50%), surface water (35%), treated sewage (28%) and untreated sewage (17%), but rare in samples from healthy children (0.8%) and animals (2%). PFGE typing of FMSE1-like isolates from hospital sewage indicated that they were closely related to the nosocomial FMSE1 strain. Thus, this study indicated a possible transmission route for nosocomial E. faecium from patients in hospitals to hospital sewage and urban sewage, and further via treatment plants to surface water and possibly back to humans. This proposed route of circulation of drug-resistant enterococci might be further amplified by antibiotic usage in human medicine. In contrast, such transmission from food animals seems to play a negligible role in Sweden.

Ampicillin Resistance↗

PubMed1995

vanA-mediated high-level glycopeptide resistance in Enterococcus faecium from animal husbandry.

Glycopeptide-resistant Enterococcus faecium strains were isolated from a pig farm and a poultry farm both using avoparcin as a food additive. Such organisms were not isolated in a hen's eggs-producing farm not using avoparcin. Glycopeptide-resistant enterococci were also detected in broiler chicken carcasses that were delivered to a hospital's kitchen. The resistance was determined by the vanA gene as indicated by the detection of the inducible 39-kDa cytoplasmic membrane protein and of a vanA-specific DNA sequence amplified by polymerase chain reaction. Genomic DNA fragment patterns of strains from animal sources were different from each other and also from those of strains isolated in hospitals and from sewage treatment plants. This findings suggest the dissemination of the vanA determinant among different enterococcal strains of distinct ecological origin.

Animal Husbandry↗

PubMed2006

Molecular epidemiology of urinary tract isolates of vancomycin-resistant Enterococcus faecium from North America.

Vancomycin-resistant Enterococcus faecium (VRE) are a common cause of nosocomial infections and are important agents of gastrointestinal colonisation. As the prevalence of VRE in hospitalised patients continues to increase, implementation of appropriate infection control measures requires routine surveillance of VRE transmission patterns. The purpose of the present study was to investigate the molecular epidemiology of VRE isolates within the USA and Canada. Two hundred and eighty-three urinary tract isolates of VRE were collected in the year 2000 from ten Canadian hospitals and 28 US tertiary care medical centres representing seven of the nine geographic regions of the United States Bureau of the Census. The in vitro activity of vancomycin, teicoplanin and nine comparators was determined by broth microdilution. The genetic relatedness among isolates was evaluated by pulsed-field gel electrophoresis (PFGE). Resistance rates (intermediate and resistant) were 100% for vancomycin and 78.7% for teicoplanin. Resistance was lowest with linezolid, chloramphenicol and nitrofurantoin at 0.3%, 0.3% and 0.5%, respectively. PFGE revealed that genetic heterogeneity amongst isolates from each of the medical centres varied considerably. Despite some intracentre and intercentre VRE dissemination, the present study found no evidence for the emergence of a dominant clonal strain. This suggests that the spread of VRE within North America is a complex process involving both the horizontal transfer of glycopeptide resistance determinants and polyclonal dissemination.

Canada↗

PubMed2006

Genotyping and preemptive isolation to control an outbreak of vancomycin-resistant Enterococcus faecium.

BACKGROUND: Control of vancomycin-resistant Enterococcus faecium (VRE) in European hospitals is hampered because of widespread asymptomatic carriage of VRE by healthy Europeans. In 2000, our hospital (The University Medical Center Utrecht, Utrecht, The Netherlands) was confronted with a large outbreak of VRE. INTERVENTION: On the basis of genotyping (by pulsed-field gel electrophoresis), epidemic and nonepidemic VRE strains were distinguished, and infection-control measures were exclusively targeted toward epidemic VRE. The outbreak was retrospectively divided into 3 periods of different infection-control measures. Compliance with use of alcohol-based hand rubs was enforced during all periods. Period I involved active surveillance, isolation of carriers, and cohorting (duration, 4 months); preemptive isolation of high-risk patients for VRE colonization was added in period II (7 months); and cohorting and preemptive isolation were abandoned in period III (18 months). METHODS: When the outbreak was identified, 27 patients in 6 wards were colonized; 93% were colonized with an epidemic VRE strain. Detection rates of nonepidemic VRE were 3.5%, 3.0%, and 2.9% among 683, 810, and 977 screened patients in periods I, II, and III, respectively, comparable to a prevalence of 2% (95% confidence interval [CI], 1%-3.5%) among 600 nonhospitalized persons. The relative risks of detecting epidemic VRE in periods II and III, compared with period I, were 0.67 (95% CI, 0.41-1.10) for period II and 0.02 (95% CI, 0.002-0.6) for period III. Infection-control measures were withheld for patients colonized with nonepidemic VRE (76 [54%] of 140 patients with a test result positive for VRE). Use of alcohol-based hand rubs increased by 31%-275% in outbreak wards. CONCLUSION: Genotyping-targeted infection control, isolation of VRE carriers, enhancement of hand-hygiene compliance, and preemptive isolation successfully controlled nosocomial spread of epidemic VRE infection.

Disease Outbreaks↗

PubMedDate not supplied

[Regulation of enzymes of the first and last stage of lysine biosynthesis in Streptococcus bovis and Enterococcus faecium].

Regulation of aspartate kinase and diaminopimelate decarboxylase activities in Streptococcus bovis and Enterococcus faecium cell-free extracts was studied. The levels of synthesis of aspartate kinase and diaminopimelate decarboxylase in both microorganisms are growth-dependent. The synthesis of these enzymes is depressed by lysine, but the activity of aspartate kinase is induced by addition of this amino acid and threonine to the reaction system. Meso-diaminopimelate dehydrogenase activity was not found in the extracts of Streptococcus bovis and Enterococcus faecium. The data excludes the possibility of lysine formation via six enzyme reactions.

Aspartate Kinase↗

PubMed2004

Identification of a new peptide deformylase gene from enterococcus faecium and establishment of a new screening model targeted on PDF for novel antibiotics.

OBJECTIVE: To identify a new peptide deformylase (PDF) gene (Genebank Accession AY238515) from Enterococcus faecium and to establish a new screening model targeted on PDF. METHODS: A new PDF gene was identified by BLAST analysis and PCR and was subsequently over-expressed in the prokaryotic expression host E. coli B121(DE3). Over-expressed protein was purified for enzymatic assay by metal affinity chromatography and a new screening model was established for novel antibiotics. RESULT: A new PDF gene of Enterococcus faecium was identified successfully. Ten positive samples were picked up from 8000 compound library and the microbial fermentation broth samples. CONCLUSION: A new PDF of gene Enterococcus faecium was first identified and the model had a high efficacy. Positive samples screened may be antibacterial agents of broad spectrum.

Amidohydrolases↗

PubMed1995

Quinupristin/dalfopristin (RP 59500) therapy for vancomycin-resistant Enterococcus faecium aortic graft infection: case report.

A 46-year-old woman was admitted to the hospital with severe peripheral vascular disease, requiring multiple vascular surgical procedures. During the sixth hospital week, after prior therapy with multiple antibiotics, Enterococcus faecium was isolated as the only organism from an operating room culture of an infected aortic graft. Histological examination of the graft showed infiltration with polymorphonuclear leukocytes. Subsequently, cultures of an infected inguinal wound yielded Enterococcus faecium with mixed bacterial growth. Both isolates of Enterococcus faecium were resistant to all available antimicrobials, including ampicillin, vancomycin, tetracycline, chloramphenicol, and ciprofloxacin. Compassionate use therapy with quinupristin/dalfopristin (RP59500) was administered for 25 days, the patient's clinical condition improved, and wound healing occurred. Transient elevation of serum alkaline phosphatase was noted. This case demonstrates successful eradication of deep VREF infection by quinupristin/dalfopristin with good tolerance of prolonged therapy.

Anti-Bacterial Agents↗

PubMed1996

Modification of penicillin-binding protein 5 associated with high-level ampicillin resistance in Enterococcus faecium.

High-level ampicillin resistance in Enterococcus faecium has been shown to be associated with the synthesis of a modified penicillin-binding protein 5 (PBP 5) which had apparently lost its penicillin-binding capability (R. Fontana, M. Aldegheri, M. Ligozzi, H. Lopez, A. Sucari, and G. Satta. Antimicrob. Agents Chemother. 38:1980-1983, 1994). The pbp5 gene of the highly resistant strain E. faecium 9439 was cloned and sequenced. The deduced amino acid sequence showed 77 and 54% homologies with the PBPs 5 of Enterococcus hirae and Enterococcus faecalis, respectively. A gene fragment coding for the C-terminal part of PBP 5 containing the penicillin-binding domain was also cloned from several E. faecium strains with different levels of ampicillin resistance. Sequence comparison revealed a few point mutations, some of which resulted in amino acid substitutions between SDN and KTG motifs in PBPs 5 of highly resistant strains. One of these converted a polar residue (the T residue at position 562 or 574) of PBP 5 produced by susceptible and moderately resistant strains into a nonpolar one (A or I). This alteration could be responsible for the altered phenotype of PBP 5 in highly resistant strains.

Amino Acid Sequence↗