SEARCH · PubMed Health

Results for “Enterococcus faecium”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources

PubMed2003

Vancomycin-resistant Enterococcus faecium endocarditis in a premature infant successfully treated with linezolid.

A 4 1/2-month-old, 26-week premature infant with multiple complications of prematurity required a central venous catheter for venous access and antibiotic treatment of bacterial nosocomial infections. He developed tricuspid valve endocarditis with vegetation caused by Enterococcus faecium resistant to ampicillin, vancomycin and quinupristin-dalfopristin but susceptible to linezolid. He was successfully treated with linezolid intravenously (7 weeks) and then orally (2 weeks).

Acetamides↗

PubMed1994

An old antibiotic for a new multiple-resistant Enterococcus faecium?

Enterococci have become an important cause of nosocomial infections and may demonstrate high-level resistance to multiple antibiotics. We present the case of a 68-year-old man with a history of small cell lung cancer, who developed bacteremia due to a strain of Enterococcus faecium. The isolate was resistant to multiple antibiotics including vancomycin, ampicillin, aminoglycosides, quinolones, and macrolides. The patient was successfully treated with doxycycline and removal of an infected central venous catheter.

Aged↗

PubMed2003

Assessing risks for a pre-emergent pathogen: virginiamycin use and the emergence of streptogramin resistance in Enterococcus faecium.

Vancomycin-resistant enterococci (VRE) are an important cause of hospital-acquired infections and an emerging infectious disease. VRE infections were resistant to standard antibiotics until quinupristin/dalfopristin (QD), a streptogramin antibiotic, was approved in 1999 for the treatment of vancomycin-resistant Enterococcus faecium infections in people. After that decision, the practice of using virginiamycin in agriculture for animal growth promotion came under intense scrutiny. Virginiamycin, another streptogramin, threatens the efficacy of QD in medicine because streptogramin resistance in enterococci associated with food animals may be transferred to E faecium in hospitalised patients. Policy makers face an unavoidable conundrum when assessing risks for pre-emergent pathogens; good policies that prevent or delay adverse outcomes may leave little evidence that they had an effect. To provide a sound basis for policy, we have reviewed the epidemiology of E faecium and streptogramin resistance and present qualitative results from mathematical models. These models are based on simple assumptions consistent with evidence, and they establish reasonable expectations about the population-genetic and population-dynamic processes underlying the emergence of streptogramin-resistant E faecium (SREF). Using the model, we have identified critical aspects of SREF emergence. We conclude that the emergence of SREF is likely to be the result of an interaction between QD use in medicine and the long-term use of virginiamycin for animal growth promotion. Virginiamycin use has created a credible threat to the efficacy of QD by increasing the mobility and frequency of high-level resistance genes. The potential effects are greatest for intermediate rates of human-to-human transmission (R0 approximately equal 1).

Anti-Bacterial Agents↗

PubMed2004

Distribution of streptogramin resistance determinants among Enterococcus faecium from a poultry production environment of the USA.

OBJECTIVES: The impact of agricultural use of antimicrobials on the present and future efficacy of therapeutic drugs in human medicine is a growing public concern. Quinupristin/dalfopristin has been approved to treat human disease caused by vancomycin-resistant Enterococcus faecium and is related to virginiamycin, a streptogramin complex that has long been used in USA agriculture poultry production. METHODS: Streptogramin-resistant isolates of E. faecium from poultry production environments on the eastern seaboard were recovered without selection for streptogramin resistance and examined using ribotyping to evaluate clonal bias. Colony PCR screening for the previously described streptogramin resistance determinants erm(A), erm(B), msr(C), vgb(A), vat(D) and vat(E) was performed to determine the prevalence of streptogramin resistance mechanisms from these environments. RESULTS: The collection of E. faecium isolates was unevenly distributed among 28 ribogroups and did not cluster geographically. The most prevalent ribogroups was composed of isolates that possessed diverse antimicrobial resistance profiles. Of the 127 isolates examined, 63% were resistant to quinupristin/dalfopristin. The resistance determinants erm(A) and erm(B) were observed among 6% and 10%, respectively, of streptogramin-resistant isolates. msr(C) was detected in a single isolate that was resistant to macrolide and lincosamide antimicrobials. The streptogramin B hydrolase vgb(A) and the streptogramin A acetyltransferases genes vat(D) and vat(E) were not detected in any of the E. faecium isolates. CONCLUSIONS: These results indicate that there is widespread resistance to streptogramin antimicrobials among E. faecium throughout the poultry production region in this study and that the mechanisms of resistance to streptogramin antimicrobials within this population remain largely uncharacterized.

Animal Husbandry↗

PubMed1997

Pharmacodynamic evaluation of a new glycopeptide, LY333328, and in vitro activity against Staphylococcus aureus and Enterococcus faecium.

The objectives of the present study were to compare the in vitro activity of LY333328 (LY) to that of vancomycin (V) alone and in combination with gentamicin (G) and rifampin (R) against methicillin-resistant Staphylococcus aureus (MRSA) and V-resistant Enterococcus faecium (VREF), by using the killing curve methods. In addition, the effect of the inoculum size and protein on LY's activity was evaluated by using MICs and killing curves. MICs, MBCs, and killing curves were determined with supplemented Mueller-Hinton broth (B), B with albumin (4 g/dl) (A), and B with 50% pooled human serum (S). For MRSA, time to 99.9% killing after exposure to LY at four times the MIC (4x MIC) was achieved at 0.5 +/- 0 h (mean +/- standard deviation) and was significantly faster than that by V (8.54 +/- 0.10 h; P = 0.001). Against VREF, LY decreased the inoculum by 2.2 log10 CFU/ml at 24 h (P = 0.002). With a large inoculum of MRSA, the activity of LY and V at 4x MIC was decreased compared to that with the standard inoculum (P = 0.0003) and regrowth occurred at 24 h. The reduction in the number of CFU per milliliter at 24 h to 2 log10 CFU/ml was restored by increasing the LY concentration to at least 16x MIC. At 24 h, the combinations of LY and G, LY and R, LY and V, and V and G were better than either LY or V alone against a large inoculum of MRSA (P = 0.0002). LY and G achieved 99.9% killing at 1.01 +/- 0.03 h and was more rapid (P < 0.007) than all the other regimens studied except for V and G, which achieved 99.9% killing at 3.59 +/- 0.01 h. Killing curves determined with different media against a standard inoculum of MRSA did not demonstrate a significant difference between LY and V at 24 h. Time to 99.9% killing was more rapid with LY than with V in B, A, and S (P = 0.0002). Times to 99.9% killing by LY in B, A, and S were not significantly different from each other. Against VREF, LY killed better than V in B, A, or S at 24 h (P = 0.0002). LY in B was more active than LY in A or S (P = 0.0002). LY is a new potent glycopeptide with a unique activity profile. It has a greater activity than that of V against MRSA and has activity against VREF. LY demonstrated synergism in combination with gentamicin against MRSA. LY was affected by large inoculum sizes and proteins in time-kill studies. However, the effect was compensated for by increasing the drug concentration to 16x MIC.

Anti-Bacterial Agents↗

PubMed1997

Influence of inducible cross-resistance to macrolides, lincosamides, and streptogramin B-type antibiotics in Enterococcus faecium on activity of quinupristin-dalfopristin in vitro and in rabbits with experimental endocarditis.

The influence of inducible cross-resistance to macrolides, lincosamides, and streptogramin B (MLS(B)) type antibiotics (inducible MLS(B) phenotype) on the activity of quinupristin-dalfopristin was investigated against Enterococcus faecium in vitro and in rabbits with experimental endocarditis. In vitro, quinupristin-dalfopristin displayed bacteriostatic and bactericidal activities against a MLS(B)-susceptible strain similar to those against two strains with the inducible MLS(B) phenotype. In addition, induction of the two MLS(B)-resistant strains with quinupristin (0.016 to 1 microg/ml) or quinupristin-dalfopristin (0.08 to 0.25 microg/ml) increased the MICs of quinupristin from 8 microg/ml to 32 to > 128 microg/ml, but did not modify the MIC of dalfopristin (2 microg/ml) or quinupristin-dalfopristin (0.5 microg/ml). In a rabbit endocarditis model, quinupristin-dalfopristin was as active as amoxicillin against the MLS(B)-susceptible E. faecium strain. In contrast, the activity of quinupristin-dalfopristin was significantly decreased in animals infected with either of the two inducible MLS(B)-resistant strains (P < 0.05), although no mutants resistant to quinupristin-dalfopristin were detected. Against the clinical strain with the inducible MLS(B) phenotype, quinupristin-dalfopristin was not effective and was less active than amoxicillin (P < 0.001); however, the activity of the combination of amoxicillin and dalfopristin-quinupristin was superior to that of amoxicillin (P < 0.01). The different impact of the inducible MLS(B) phenotype in E. faecium on the activity of quinupristin-dalfopristin in vitro and in experimental endocarditis may be related to the reduced diffusion of dalfopristin compared with that of quinupristin into cardiac vegetations that we previously reported. This result emphasizes the importance of the constant presence of dalfopristin at the site of infection to ensure synergism with quinupristin.

Animals↗

PubMed2005

First nosocomial outbreak of vancomycin-resistant Enterococcus faecium expressing a VanD-like phenotype associated with a vanA genotype.

Although enterococci expressing acquired vancomycin resistance phenotype have been reported increasingly worldwide, they have been rarely reported in France. From August to December 2004 we faced an outbreak of vancomycin-resistant Enterococcus faecium (VRE) isolates in the nephrology department at Bicêtre Hospital (K.-Bicêtre, France). The expression of the glycopeptide resistance varied among the 26 VRE isolates, with vancomycin MICs ranging from 12 to >256 microg/ml, whereas teicoplanin MICs ranged from 4 to 48 microg/ml. However, several strains appeared to be susceptible to glycopeptides according to disk diffusion testing and expressed resistance only after subculture with glycopeptides. In addition, a heterogeneous expression of glycopeptide resistance was also observed. This so-called VanD-like phenotype of resistance (low-level resistance to vancomycin and mostly susceptibility to teicoplanin) was surprisingly associated with a vanA gene. Plasmid extraction and mating-out experiments indicated that the vanA gene was located on a 200-kb self-transferable plasmid. Pulsed-field gel electrophoresis identified mostly dissemination of a single clone, whereas diffusion of the VanA-positive plasmid in different genomic backgrounds had also occurred. The vanA gene was part of a vanA-type operon for expression of resistance located on a Tn1546-like transposon. Sequencing of this transposon identified insertion of insertion sequence IS16 in the vanY gene that encodes a d,d-carboxypeptidase that might explain in part the peculiar VanD-type phenotype of resistance. This report is the first description of a VRE outbreak in France and underlines the difficulty in detecting this organism due to variability on the expression of the glycopeptide resistance trait, if any.

Adult↗

PubMed1998

Treatment of vancomycin-resistant Enterococcus faecium with RP 59500 (quinupristin-dalfopristin) administered by intermittent or continuous infusion, alone or in combination with doxycycline, in an in vitro pharmacodynamic infection model with simulated endocardial vegetations.

Quinupristin-dalfopristin is a streptogramin antibiotic combination with activity against vancomycin-resistant Enterococcus faecium (VREF), but emergence of resistance has been recently reported. We studied the activity of quinupristin-dalfopristin against two clinical strains of VREF (12311 and 12366) in an in vitro pharmacodynamic model with simulated endocardial vegetations (SEVs) to determine the potential for resistance selection and possible strategies for prevention. Baseline MICs/minimal bactericidal concentrations (microg/ml) for quinupristin-dalfopristin, quinupristin, dalfopristin, and doxycycline were 0.25/2, 64/>512, 4/512, and 0.125/8 for VREF 12311 and 0.25/32, 128/>512, 2/128, and 0.25/16 for VREF 12366, respectively. Quinupristin-dalfopristin regimens had significantly less activity against VREF 12366 than VREF 12311. An 8-microg/ml simulated continuous infusion was the only bactericidal regimen with time to 99.9% killing = 90 hours. The combination of quinupristin-dalfopristin every 8 h with doxycycline resulted in more killing compared to either drug alone. Quinupristin-dalfopristin-resistant mutants (MICs, 4 microg/ml; resistance proportion, approximately 4 x 10(-4)) emerged during the quinupristin-dalfopristin monotherapies for both VREF strains. Resistance was unstable in VREF 12311 and stable in VREF 12366. The 8-microg/ml continuous infusion or addition of doxycycline to quinupristin-dalfopristin prevented the emergence of resistance for both strains over the 96-h test period. These findings replicated the development of resistance reported in humans and emphasized bacterial factors (drug susceptibility, high inoculum, organism growth phase) and infectious conditions (penetration barriers) which could increase chances for clinical resistance. The combination of quinupristin-dalfopristin with doxycycline and the administration of quinupristin-dalfopristin as a high-dose continuous infusion warrant further study to determine their potential clinical utility.

Anti-Bacterial Agents↗

PubMed1995

Long-term effects of Enterococcus faecium SF68 versus lactulose in the treatment of patients with cirrhosis and grade 1-2 hepatic encephalopathy.

In 40 patients with cirrhosis on a dietary protein regimen of 1 g/kg b.w., we determined the effect on chronic hepatic encephalopathy of long-term administration of Enterococcus faecium (SF68) versus lactulose. The patients received one of the two treatments for three periods of 4 weeks, each separated by drug-free 2-week intervals. The efficacy of treatment was assessed by arterial blood ammonia concentration, mental status, number connection (Reitan's part A) test and flash-evoked visual potentials. At the end of the third period the reduction in both blood ammonia concentrations and Reitan's test times was more enhanced in patients on SF68 than in patients on lactulose. Furthermore, while patients on lactulose tended to return to basal values during drug-free intervals, responders in the SF68 group maintained improvement throughout the study. In conclusion, SF68 is at least as useful as lactulose for the chronic treatment of chronic hepatic encephalopathy; it has no adverse effects, and treatment can be interrupted for 2 weeks without losing the beneficial effects.

Adult↗

PubMed2000

Typing of Enterococcus faecium by polymerase chain reaction and pulsed field gel electrophoresis.

Polymerase chain reaction (PCR) with JB1 or REP consensus oligonucleotides and pulsed field gel electrophoresis (PFGE) were used to study genomic DNA extracted from 31 strains of enterococci. Eleven ATCC strains, representative of 11 species of Enterococcus, were initially tested by JB1-PCR, revealing that Enterococcus malodoratus and Enterococcus hirae presented identical banding patterns. Eight Enterococcus faecium isolates from Stanford University and 12 from São Paulo Hospital were studied by JB1-PCR, REP-PCR (1/2)R and PFGE. Among the isolates from Stanford University, 5 genotypes were defined by JB1-PCR, 7 by REP-PCR (1/2)R and 4 by PFGE. Among the isolates from São Paulo Hospital, 9 genotypes were identified by JB1-PCR, 6 by REP-PCR and 5 by PFGE. The three methods identified identical genotypes, but there was not complete agreement among them.

Bacterial Typing Techniques↗

PubMed1999

Synergy testing of vancomycin-resistant Enterococcus faecium against quinupristin-dalfopristin in combination with other antimicrobial agents.

Using checkerboard and time-kill assays, we evaluated the in vitro activity of quinupristin-dalfopristin (RP 59500) alone and in combination with five other antimicrobial agents against 12 clinical strains of vancomycin-resistant Enterococcus faecium (VREF). In time-kill studies, six VREF strains exhibited synergism with the combination of quinupristin-dalfopristin and doxycycline and three exhibited synergism with quinupristin-dalfopristin plus ampicillin-sulbactam. Combinations of quinupristin-dalfopristin with these and other agents warrant further clinical evaluation for the treatment of serious VREF infections.

Anti-Bacterial Agents↗

PubMed2002

The 2.4-A crystal structure of the penicillin-resistant penicillin-binding protein PBP5fm from Enterococcus faecium in complex with benzylpenicillin.

Penicillin-binding proteins (PBPs) are membrane proteins involved in the final stages of peptidoglycan synthesis and represent the targets of beta-lactam antibiotics. Enterococci are naturally resistant to these antibiotics because they produce a PBP, named PBP5fm in Enterococcus faecium, with low-level affinity for beta-lactams. We report here the crystal structure of the acyl-enzyme complex of PBP5fm with benzylpenicillin at a resolution of 2.4 A. A characteristic of the active site, which distinguishes PBP5fm from other PBPs of known structure, is the topology of the loop 451-465 defining the left edge of the cavity. The residue Arg464, involved in a salt bridge with the residue Asp481, confers a greater rigidity to the PBP5fm active site. In addition, the presence of the Val465 residue, which points into the active site, reducing its accessibility, could account for the low affinity of PBP5fm for beta-lactam. This loop is common to PBPs of low affinity, such as PBP2a from Staphylococcus aureus and PBP3 from Bacillus subtilis. Moreover, the insertion of a serine after residue 466 in the most resistant strains underlines even more the determining role of this loop in the recognition of the substrates.

Amino Acid Sequence↗

PubMed2003

Antimicrobial susceptibility of vancomycin-resistant Enterococcus faecium: potential utility of fosfomycin.

The increasing prevalence of vancomycin-resistant enterococcal (VRE) infections has necessitated a search for drugs that are effective in treating these infections, and a need to determine whether currently available antimicrobials are effective. 75 consecutive clinical isolates of vancomycin-resistant Enterococcus faecium (VRE faecium) (40 blood and 35 urine isolates) isolated over 1 y at the Cleveland Clinic Foundation were tested for susceptibility to linezolid, quinupristin-dalfopristin, fosfomycin and nitrofurantoin using the Etest. The minimum inhibitory concentrations were read independently by 3 observers and compared, and a final reading was obtained by predetermined criteria. The proportion of isolates susceptible to linezolid, quinupristin-dalfopristin, fosfomycin and nitrofurantoin was 100%, 98.7%, 98.7% and 78.7%, respectively. No single isolate was resistant to more than 1 of the 4 drugs tested. Etest presented significant unexpected difficulties in testing for VRE faecium susceptibility to nitrofurantoin. Fosfomycin may be a useful alternative to linezolid and quinupristin-dalfopristin in the treatment of VRE infections in certain clinical situations, e.g. uncomplicated urinary tract infections. In addition, the use of fosfomycin could limit the use of newer agents, thus reducing the chance of development of further resistance in the enterococci.

Anti-Bacterial Agents↗

PubMed1998

Genetic linkage and cotransfer of a novel, vanB-containing transposon (Tn5382) and a low-affinity penicillin-binding protein 5 gene in a clinical vancomycin-resistant Enterococcus faecium isolate.

Mechanisms for the intercellular transfer of VanB-type vancomycin resistance determinants and for the almost universal association of these determinants with those for high-level ampicillin resistance remain poorly defined. We report the discovery of Tn5382, a ca. 27-kb putative transposon encoding VanB-type glycopeptide resistance in Enterococcus faecium. Open reading frames internal to the right end of Tn5382 and downstream of the vanXB dipeptidase gene exhibit significant homology to genes encoding the excisase and integrase of conjugative transposon Tn916. The ends of Tn5382 are also homologous to the ends of Tn916, especially in regions bound by the integrase enzyme. PCR amplification experiments indicate that Tn5382 excises to form a circular intermediate in E. faecium. Integration of Tn5382 in the chromosome of E. faecium C68 has occurred 113 bp downstream of the stop codon for the pbp5 gene, which encodes high-level ampicillin resistance in this clinical isolate. Transfer of vancomycin, ampicillin, and tetracycline resistance from C68 to an E. faecium recipient strain occurs at low frequency in vitro and is associated with acquisition of a 130- to 160-kb segment of DNA that contains Tn5382, the pbp5 gene, and its putative repressor gene, psr. The interenterococcal transfer of this large chromosomal element appears to be the primary mechanism for vanB operon spread in northeast Ohio. These results expand the known family of Tn916-related transposons, suggest a mechanism for vanB operon entry into and dissemination among enterococci, and provide an explanation for the nearly universal association of vancomycin and high-level ampicillin resistance in clinical E. faecium strains.

Anti-Bacterial Agents↗

PubMed2000

A strain of Enterococcus faecium (18C23) inhibits adhesion of enterotoxigenic Escherichia coli K88 to porcine small intestine mucus.

Few studies, if any, have addressed the adhesion of enterococci to the intestinal mucosa and their interference with the adhesion of pathogens, although more than 60% of probiotic preparations in the market contain strains of enterococci. The objective of this study was to investigate if Enterococcus faecium 18C23 has the ability to inhibit the adhesion of Escherichia coli K88ac and K88MB to the small intestine mucus of piglets. Approximately 9% of E. faecium 18C23 organisms adhered to the small intestine mucus, and the adhesion was found to be specific. Living E. faecium 18C23 culture efficiently inhibited the adhesion of E. coli K88ac and K88MB to the piglet intestine mucus. Inhibition of the adhesion of E. coli K88ac to the small intestine mucus was found to be dose dependent. Inhibition of >90% was observed when 10(9) CFU or more of living E. faecium 18C23 culture per ml was added simultaneously with E. coli to immobilized mucus. The substances from both the 18C23 cells and the spent culture supernatant contributed to the inhibition of adhesion of E. coli K88 to the small intestine mucus receptors. The inhibiting effect was not solely a pH effect since considerable inhibitory action was demonstrated after neutralizing the mixture or spent culture supernatant to pH 7.0. Part of the inhibition of adhesion of E. coli K88ac by E. faecium 18C23 or its supernatant might occur through steric hindrance.

Animals↗

PubMed2004

Emerging linezolid-resistant, vancomycin resistant Enterococcus faecium from a patient of a haematological unit in Poland.

The oxazolidinone antimicrobial, linezolid, has been approved for the treatment of infections caused by various gram-positive bacteria, including vancomycin-resistant enterococci (VRE). This is the first report on isolation of a linezolid resistant, vancomycin-resistant Enterococcus faecium (LRVREF) strain in Poland, from a Haematological Unit patient in the Clinical Hospital in Gdańsk. PCR-RFLP analysis of rDNA and allele-specific PCR of the domain V region of the 23S ribosomal RNA gene demonstrated the presence of the G2576U mutation previously reported to be associated with linezolid resistance. Both assays detected heterozygous in this position.

Acetamides↗

PubMed1996

Peptidoglycan structure of Enterococcus faecium expressing vancomycin resistance of the VanB type.

Resistance to glycopeptide antibiotics in enterococci is due to the synthesis of UDP-MurNAc-tetrapeptide-D-lactate (where Mur is muramic acid) replacing the normal UDP-MurNAc-pentapeptide precursor. The peptidoglycan structures of an inducible VanB-type glycopeptide-resistant Enterococcus faecium, D366, and its constitutively resistant derivative, MT9, were determined. Using HPLC, 17 muropeptides were identified and were present regardless of whether resistance was expressed or not. The structures of 15 muropeptides were determined using MS and amino acid analysis. The cross-bridge between D-alanine and L-lysine consisted of one asparagine. No monomer pentapeptide or tetrapeptide-D-lactate could be identified. These results obtained with D366 (non-induced) and MT9 indicate that, in the absence of vancomycin, the cell wall synthetic machinery of E. faecium can process the lactate-containing precursor as efficiently as the normal pentapeptide. In contrast, the presence of subinhibitory inducing concentrations of vancomycin interfered with the synthesis of oligomers.

Amino Acid Sequence↗

PubMed2001

Effect of different complex carbon sources on growth and bacteriocin synthesis of Enterococcus faecium.

Different criteria are followed in order to select bacteria to be used in probiotic and symbiotic supplements. A new parameter to choose strains could be fermentation by intestinal bacteria of some complex carbohydrates because they are prebiotics and promote the development of beneficial microorganisms in the intestinal environment. An Enterococcus faecium strain, isolated from the crop of a free-range chicken, was assayed in order to determine the utilization of commercial sugars and/or crude carbohydrate samples from a sugar mill. The production of antimicrobial substances, under these conditions, was also considered. Ent. faecium CRL1385 grew well in the presence of complex carbohydrates and its ability to produce bacteriocin, active against poultry pathogens such as Ent. hirae, Salmonella pullorum and Listeria monocytogenes, was not significantly modified. These results are promising because the trend today is to employ eubiotic or symbiotic products and their use in the poultry industry could be a natural way to protect the flocks against potential pathogens.

Animals↗