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PubMed1999

Isolation and epidemiological study of vancomycin-resistant Enterococcus faecium from patients of a haematological unit in Poland.

Enterococcus faecium has recently emerged as a serious nosocomial pathogen. Vancomycin resistant enterococci (VRE) have been isolated in Europe and the USA since 1988. This is the first report on isolation of vancomycin resistant E. faecium (VREM) strains in Poland, from Haematological Unit patients in the Clinical Hospital in Gdańsk. In total, 6412 samples were examined between December 1996 and October 1997. Five hundred and five isolates of Enterococcus spp. were collected. One hundred and one were classified as Enterococcus faecium of which 49 were resistant to vancomycin (MIC > 256 mg/L) and teicoplanin (MIC > 256 mg/L), characteristic of the VanA phenotype. Twenty-nine patients were infected or colonized. A PCR-based specific diagnostic assay confirmed the phenotype. The multiplex PCR-restriction fragment length polymorphism patterns were consistent with VanA-type of vancomycin-resistant E. faecium for all isolates examined. These isolates were epidemiologically-related as shown by PCR-fingerprinting.

Adult↗

PubMed2003

Partial characterization of bacteriocins produced by environmental strain Enterococcus faecium EK13.

AIMS: The partial characterization of bacteriocins produced by an environmental strain Enterococcus faecium EK13, isolated from cattle dung water. METHODS AND RESULTS: A bacteriocin was partially purified by ammonium sulphate precipitation, followed by a SP-Sepharose column, reverse-phase chromatography and N-terminal region sequenced. The anti-microbial substance produced was found to be a heat-stable polypeptide with molecular mass 4.83 kDa, which was determined by N-terminal amino acid sequencing to be enterocin A. A second substance was specified by PCR as enterocin P. Bacteriocins were stable at 4 and -20 degrees C for long storage periods. The optimum of bacteriocin production was observed in the range of pH 5.0-6.5 at 30 and 37 degrees C. The most active substances are produced by strain EK13 in logarithmic growth phase and bacteriocins are produced after 1 h of fermentation. The highest activity detected in fermentation experiments was 51 200 AU ml(-1) and the most sensitive indicator strain was found to be Listeria innocua LMG 13568. Differences in bacteriocin activity against two indicators could be explained by more than one type of enterocin production by strain EK13, or with different mode of action or in different sensitivity of strains. CONCLUSION: Enterococcus faecium strain EK13 isolated from cattle dung water produces two bacteriocins, enterocin A and P, with an inhibitory effect against the strain of the genera Enterococcus, Leuconostoc, Lactobacillus, Streptococcus, Staphylococcus, Bacillus and Listeria (in different origin). SIGNIFICANCE AND IMPACT OF THE STUDY: Enterococcus faecium EK13 environmental strain is a new producer of enterocin A and P. The E. faecium EK13, isolated from cattle dung water, is presented with the further aim to utilize it for waste treatment by biotechnological processes.

Animals↗

PubMed2000

Virulence factors of Enterococcus faecalis and Enterococcus faecium blood culture isolates.

Known and potential virulence factors of enterococcal blood culture isolates were studied using 89 Enterococcus faecalis and 24 Enterococcus faecium isolates. The prevalence of the respective factors was (Enterococcus faecalis vs. Enterococcus faecium): hemolysin 16% vs. 0%, gelatinase 55% vs. 0%, aggregation substance 63% vs. 13%, lipase 35% vs. 4%, hemagglutinin 97% vs. 0%. Deoxyribonuclease was not detected in any isolate. The study showed that hemagglutinin and lipase may represent additional virulence factors of Enterococcus faecalis but not Enterococcus faecium. The significance of these factors in the pathogenesis of enterococcal infection needs to be elucidated in further studies.

Bacterial Proteins↗

PubMed1995

Hypocholesterolemic and immunostimulatory effects of orally applied Enterococcus faecium M-74 in man.

Lyophilized Enterococcus faecium M-74 was administered to 12 adult subjects in a daily oral dose of 5 x 10(9) bacteria for six weeks. The bacterium temporarily colonized the host intestine and its excretion with stool persisted for five weeks after the last does. The mean levels of serum cholesterol and LDL showed a a biphasic effect--an elevation followed by a sharp decrease (on day 64 of investigation). The decrease corresponded in time with a significant increase in the ability to reduce iodonitrotetrazolium and superoxide production by peripheral neutrophils incubated with zymosan or phorbol myristate acetate, and also with an elevated production of IgG by peripheral blood mononuclear cells. Hence, intake of E. faecium may have a hypocholesterolemic and immunostimulatory effect. It was also demonstrated that E. faecium significantly reduced the average activity of beta-D-glucuronidase in stools.

Adjuvants, Immunologic↗

PubMed2004

Cytotoxicity of hydrogen peroxide produced by Enterococcus faecium.

Although the opportunistic bacterial pathogen Enterococcus faecium is a leading source of nosocomial infections, it appears to lack many of the overt virulence factors produced by other bacterial pathogens, and the underlying mechanism of pathogenesis is not clear. Using E. faecium-mediated killing of the nematode worm Caenorhabditis elegans as an indicator of toxicity, we determined that E. faecium produces hydrogen peroxide at levels that cause cellular damage. We identified E. faecium transposon insertion mutants with altered C. elegans killing activity, and these mutants were altered in hydrogen peroxide production. Mutation of an NADH oxidase-encoding gene eliminated nearly all NADH oxidase activity and reduced hydrogen peroxide production. Mutation of an NADH peroxidase-encoding gene resulted in the enhanced accumulation of hydrogen peroxide. E. faecium is able to produce hydrogen peroxide by using glycerol-3-phosphate oxidase, and addition of glycerol to the culture medium enhanced the killing of C. elegans. Conversely, addition of glucose, which leads to the down-regulation of glycerol metabolism, prevented both C. elegans killing and hydrogen peroxide production. Lastly, detoxification of hydrogen peroxide either by exogenously added catalase or by a C. elegans transgenic strain overproducing catalase prevented E. faecium-mediated killing. These results suggest that hydrogen peroxide produced by E. faecium has cytotoxic effects and highlight the utility of C. elegans pathogenicity models for identifying bacterial virulence factors.

Animals↗

PubMed1996

Heat tolerance of vancomycin resistant Enterococcus faecium.

The heat tolerance of 27 Enterococcus faecium isolates in water was studied. Stationary phase cultures including vancomycin resistant and sensitive clinical and food isolates were exposed to heat at 60 degrees, 65 degrees, 71 degrees, and 80 degrees C for one, three, 10, and 30 minutes and the log10 reductions in bacterial counts were determined. Exposure at 71 degrees and 80 degrees C resulted in > 6 log10 reduction in viable counts for all isolates. Seven (24%) isolates survived (< 5 log10 reduction) heat at 65 degrees C for 10 minutes. The E faecium isolates were more resistant to heat than the two E faecalis reference strains. No differences in heat tolerance were observed between vancomycin sensitive and resistant strains or between isolates of human or food origin.

Drug Resistance, Microbial↗

PubMed2002

Possible connection between a widely disseminated conjugative gentamicin resistance (pMG1-like) plasmid and the emergence of vancomycin resistance in Enterococcus faecium.

A total of 640 vancomycin-resistant Enterococcus faecium (VRE) isolates, which were obtained between 1994 and 1999 from the Medical School Hospital of the University of Michigan, Ann Arbor, were used in this study. Of the 640 strains, 611 and 29 were VanA and VanB VRE, respectively, based on PCR analysis. Four hundred ninety-two (77%) of the strains exhibited resistance to concentrations of gentamicin from 64 micro g/ml (MIC) to more than 1,024 micro g/ml (MIC). The gentamicin resistance of each of 261 (53%) of the 492 gentamicin-resistant strains was transferred to E. faecium at a frequency of about 10(-5) to 10(-6) per donor cell in broth mating. More than 90% of vancomycin resistances of the 261 strains cotransferred with the gentamicin resistances to E. faecium strains by filter mating. The conjugative gentamicin resistance plasmids were identified and were classified into five types (A through E) with respect to their EcoRI restriction profiles. The transfer frequencies of each type of plasmid between E. faecium strains or Enterococcus faecalis strains were around 10(-3) to 10(-5) per donor cell or around 10(-6) to 10(-7) per donor cell, respectively, in broth mating. Type A and type B were the most frequently isolated, at an isolation frequency of about 40% per VRE isolate harboring the gentamicin resistance conjugative plasmid. The plasmids did not show any homology in Southern hybridization with the pheromone-responsive plasmids and broad-host-range plasmids pAMbeta1 and pIP501. The EcoRI or NdeI restriction fragments of each type of plasmids hybridized to the conjugative gentamicin resistance plasmid pMG1 (65.1 kb), which was originally isolated from an E. faecium clinical isolate, and transfer efficiently in broth mating.

Anti-Bacterial Agents↗

PubMed2006

Case report vancomycin -resistant Enterococcus faecium VanA phenotype: first documented isolation in India.

In recent years, vancomycin-resistant enterococci, especially Enterococcus faecium has emerged as an important nososcomial pathogen and represents a serious threat to patients with impaired host defences. We report infection with vancomycin-resistant Enterococcus faecium in a 3-year-old child with patent ductus arteriosus. The organism, isolated from a central venous catheter tip, exhibited a high-level resistance to vancomycin (minimum inhibitory concentration > or = 256 microg/ ml) and was also resistant to teicoplanin. The child probably died due to sepsis from this highly resistant organism. To the best of our knowledge, this is the first reported isolation of VanA phenotype Enterococcus faecium in India.

Bacterial Proteins↗

PubMed1998

RP59500 (Quinupristin/dalfopristin): three case reports of its use in infection due to Enterococcus faecium.

We describe three cases of Enterococcus faecium sepsis arising in immunocompromised patients, severely ill with other conditions, who were treated with the new injectable streptogramin RP59500. There are still few reports of clinical experience with this drug. All had bacteriological resolution, with one patient recovering fully. Although two of the three patients died, this was due to underlying disease in one case and a gram-negative superinfection in another. Quinupristin/dalfopristin therapy was not associated with significant adverse effects in any of the patients.

Adolescent↗

PubMed2003

Linkage of erm(B) and aadE-sat4-aphA-3 in multiple-resistant Enterococcus faecium isolates of different ecological origins.

Enterococcus faecium shares its antibiotic resistance gene pool with various Gram-positive bacteria. A gene cluster aadE-sat4-aphA-3, which was first described in staphylococci, has been recently identified also in E. faecium. In staphylococci, this gene cluster was mostly integrated into the transposable element, Tn5405. We identified five different cluster types of Tn5405-like elements that were linked to erm(B) in 47 of 67 aadE-sat4-aphA-3 and erm(B) positive isolates (70.1%). Clusters differed by insertion of additional DNA between the IS1182 transposase gene and the left inverted repeat of IS1182, an integration of IS1216 between erm(B) and ORF X deleting IS1182 and the 5' end of ORF X, or a loss of the left end of Tn5405 including IS1182, ORF X, and the 5' end of ORF Y. Twenty isolates (29.8%) possessed neither a link between erm(B) and aadE-sat4-aphA-3 nor an arrangement of aadE-sat4-aphA-3 in a Tn5405-like element. A 17-kb composite cluster was identified in a single hospital isolate linking determinants for glycopeptide (vanA), macrolide-lincosamide-streptogramin B [erm(B)], and aminoglycoside-streptothricin (aadE-sat4-aphA-3) resistances.

Aminoglycosides↗

PubMed1994

Identification of the DNA-binding site for the phosphorylated VanR protein required for vancomycin resistance in Enterococcus faecium.

The vancomycin resistance operon of Enterococcus faecium encodes a two-component regulatory system comprising VanS and VanR. In vitro experiments showed that about 5% of a labile phosphorylated VanR (P-VanR) was accumulated from ATP and a maltose-binding protein-VanS fusion protein (MBP-VanS). Alternatively, about an 8% abundance of P-VanR was produced with acetyl phosphate. In such incubations, gel shift experiments revealed that P-VanR selectively bound to a 254-bp DNA fragment that contains the vanH promoter for the vanH, vanA, and vanX structural genes. When VanS was added with a mole ratio for VanS:VanR of higher than 1:1, VanS competed with DNA for P-VanR and abolished the gel shift. P-VanR bound 500-fold more tightly to the vanH promoter region, with an estimated EC50 of 40 nM, than the unphosphorylated VanR. A second DNA fragment of 197 bp containing the proposed vanR promoter for the vanR and vanS regulatory genes also exhibited gel shift, but with much lower affinities. A mutant VanR(D53A) was shown to be incompetent for phosphorylation by phosphorylated MBP-VanS or by acetyl phosphate; however, it still bound DNA specifically, albeit with low affinity. DNase I footprinting by P-VanR revealed that a ca. 80-bp region was protected on the vanH promoter and a ca. 40-bp region was protected on the vanR promoter. The unphosphorylated VanR footprinted the same 80 bp on the vanH promoter, but only 20 bp on the vanR promoter.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗

PubMed2025

Novel, rapid, and reliable typing of vancomycin-resistant Enterococcus faecium CC17/ST80 strains using MALDI-TOF MS.

Vancomycin-resistant Enterococcus faecium (VREfm) is an important nosocomial pathogen. The recent emergence of the highly virulent clonal complex 17 (CC17) is posing a challenge for both therapeutic interventions and hospital infection control measures. Hence, prompt discrimination of CC17 VREfm from unrelated and less-virulent VREfm strains is essential for preventing its spread in hospitals and beyond. Between January 2022 and November 2024, 340 VREfm primary isolates have been identified in our lab and underwent genotyping by pulsed-field gel electrophoresis (PFGE) to survey a potential outbreak in the Tyrol region. In addition, whole-genome sequencing (WGS) was performed on a selected subset (n = 40). To curtail the lengthy time-to-result (TTR) of these methods, a novel typing protocol using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) was established, validated, and optimized for rapid sample processing. PFGE and WGS showed that 61.2% of isolates (n = 208) belonged to a specific VREfm cluster identified as CC17 sequence type (ST) 80 vanA VREfm. A comprehensive MALDI-TOF MS analysis identified a distinct peak pattern specific to this lineage. This phenotypic characterization was used as a novel typing method with excellent performance (sensitivity: 1.00 [0.98-1.00], specificity: 0.89 [0.70-0.97]) and demonstrated a short TTR of 1 day after the cultural growth of VREfm. A rapid and novel MALDI-TOF MS-based typing approach for a specific CC17/ST80 vanA VREfm cluster was developed and enabled real-life application in routine diagnostics to assure accurate infection prevention and control measures. Future outbreak investigations may benefit from adopting this cost- and labor-efficient approach.IMPORTANCEThis study addresses the urgent need for faster ways to detect problematic hospital bacteria. A highly transmissible strain of Enterococcus faecium (CC17) has been spreading in healthcare settings, making infections harder to treat and control. Traditional methods to identify and track outbreaks are accurate but slow and resource-intensive, delaying critical infection control actions. By developing and validating a new method using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, the researchers demonstrated that this strain can be identified quickly, reliably, and at lower cost. Importantly, the new approach delivers results within a day, compared to the lengthy turnaround times of existing methods. This rapid detection tool provides hospitals with a practical solution to respond to outbreaks more effectively, prevent further spread, and protect vulnerable patients. The findings highlight a valuable step forward in strengthening hospital infection control and improving patient safety.

Enterococcus faecium↗

PubMed2005

Binding sites of VanRB and sigma70 RNA polymerase in the vanB vancomycin resistance operon of Enterococcus faecium BM4524.

The vanB operon of Enterococcus faecium BM4524 which confers inducible resistance to vancomycin is composed of the vanR(B)S(B) gene encoding a two-component regulatory system and the vanY(B)WH(B)BX(B) resistance genes that are transcribed from promoters P(RB) and P(YB) respectively. In this study, primer extension revealed transcription start sites at 13 and 48 bp upstream from the start codon of vanR(B) and vanY(B), respectively, that allowed identification of -10 and -35 promoter motifs. The VanR(B) protein was overproduced in Escherichia coli, purified and phosphorylated (VanR(B)-P) non-enzymically with acetylphosphate. VanR(B)-P and VanR(B) specifically bound to P(RB) and P(YB) promoters. VanR(B) bound at a single site at position -32.5 upstream from the P(RB) transcriptional start site and at two sites at positions -33.5 and -55.5 upstream from that of P(YB). The proximal VanR(B) binding site overlapped the -35 region of both promoters. VanR(B) was converted from a monomer to a dimer upon acetylphosphate treatment. VanR(B)-P had higher affinity than VanR(B) for its targets and appeared more efficient than VanR(B) in promoting open complex formation with P(RB) and P(YB). In the absence of regulator, E. coli RNA polymerase was able to interact with P(RB) but not with P(YB). Phosphorylation of VanR(B) significantly increased promoter interaction with RNA polymerase and led to an extended and modified footprint. In vitro transcription assays showed that VanR(B)-P activates P(YB) more strongly than P(RB). Analysis of the protected regions revealed one copy of a 21 bp sequence in the P(RB) promoter and two copies in the P(YB) promoter which may serve as recognition sites for VanR(B) and VanR(B)-P binding that are required for transcriptional activation and expression of vancomycin resistance.

Bacterial Proteins↗

PubMed2006

Molecular epidemiology of vancomycin-resistant Enterococcus faecium in Argentina.

OBJECTIVE: To characterize the mechanism of glycopeptide resistance and to determine the genetic relatedness among strains by pulsed-field gel electrophoresis (PFGE) in vancomycin-resistant Enterococcus faecium from Argentina. MATERIALS AND METHODS: A total of 189 vancomycin-resistant single-patient isolates of Enterococcus faecium recovered between January 1997 and December 2000 from 30 hospitals in Argentina were studied. Minimum inhibitory concentrations were determined by the agar dilution method and van genes were detected by PCR. PFGE was used for molecular typing. RESULTS: All isolates except three (vanB) were of genotype vanA. For 189 vancomycin-resistant Enterococcus faecium, SmaI-PFGE indicated 35 clonal types. Most of the isolates (56%) belonged to the same clonal type 1, which was present in 19 hospitals and dominant in 17. CONCLUSIONS: The emergence of vancomycin-resistant Enterococcus faecium in Argentina seems to be related to the intra- and inter-hospital dissemination of an epidemic clone carrying the vanA element.

Argentina↗

PubMed2005

Varying linezolid susceptibility of vancomycin-resistant Enterococcus faecium isolates during therapy: a case report.

OBJECTIVES: Linezolid is an oxazolidinone antibiotic used in the treatment of infections caused by vancomycin-resistant enterococci. Resistance to linezolid has been associated with a G2576U mutation in domain V of the 23S rRNA. PATIENT AND METHODS: We present clinical details and susceptibility data from multiple Enterococcus faecium strains isolated from a liver transplant patient over 13 months. MICs of linezolid, vancomycin and quinupristin/dalfopristin were determined using Etest. Molecular typing was performed by pulsed-field gel electrophoresis. Domain V of the 23S rRNA gene in the vancomycin-resistant Enterococcus faecium was amplified. Linezolid concentrations were analysed by HPLC. RESULTS: We report the emergence of resistance to linezolid in a vancomycin-resistant Enterococcus faecium during linezolid treatment. After discontinuation of the linezolid therapy, the isolate reverted to susceptibility. However, after re-administration of linezolid the vancomycin-resistant Enterococcus faecium became resistant to linezolid again. The isolates that were resistant to linezolid had a G2576T mutation in their 23S rDNA. CONCLUSION: We describe a clinical case that shows the shift of a vancomycin-resistant Enterococcus faecium from linezolid resistance to susceptibility and then back to resistance again related to linezolid therapy.

Acetamides↗

PubMed1989

Effect of cell cycle stages on the central density of Enterococcus faecium ATCC 9790.

Cultures of Enterococcus faecium growing at various rates were examined for timing of cell division cycle events by using the method of residual divisions and a morphological analysis. Both methods gave essentially the same timing for the onset of D1 (completion of chromosome replication) and of D2 (completion of septation). Frequencies of cells exhibiting a phase-reversed center in bovine serum albumin at various growth rates were determined. The data fit a model in which rapidly growing cells increase in refractive index (which is assumed to represent central density) at completion of the chromosome replication cycle involved in the ongoing division, whereas slowly growing cultures increase in central density at the time of completion of septation. There was no correlation between the timing of increase in central density and the timing of initiation of new sites of surface growth.

Cell Cycle↗

PubMed2006

Bacteriocin T8, a novel class IIa sec-dependent bacteriocin produced by Enterococcus faecium T8, isolated from vaginal secretions of children infected with human immunodeficiency virus.

Enterococcus faecium T8, isolated from vaginal secretions of children with human immunodeficiency virus, produces a class IIa sec-dependent bacteriocin that is structurally different from three other class IIa sec-dependent bacteriocins, i.e., enterocin P and an enterocin P-like bacteriocin, produced by Enterococcus faecium, and bacteriocin 31, produced by Enterococcus faecalis, and from a class III bacteriocin produced by E. faecalis. The genes encoding the bacteriocin, immunity protein, mobilization protein, and relaxase nuclease are located on a 7-kb plasmid. Bacteriocin T8 has a molecular mass of 5.1 kDa based on its DNA sequence, similar to the 5.0 kDa recorded for bacteriocin 31 but larger than the 4.6 kDa reported for enterocin P. At the amino acid level, bacteriocin T8 is 69% homologous to bacteriocin 31 and 47% homologous to enterocin P. Bacteriocin T8 is active against E. faecalis isolated from patients diagnosed with vaginosis, against Lactobacillus sakei, and against a Propionibacterium sp. The peptide is heat stable (60 min at 100 degrees C) and remains active in phosphate buffer from pH 4.0 to 10.0. The mode of activity is bactericidal, as determined with E. faecalis.

Amino Acid Sequence↗

PubMed2000

In vitro adherence of Enterococcus faecalis and Enterococcus faecium to urinary catheters.

The in vitro adherence of ten strains of Enterococcus faecalis and ten strains of Enterococcus faecium to siliconized latex urinary catheters and to silicone elastomer was evaluated. Bacterial suspensions (2.5x10(5) cfu/ml) in tryptic soy broth containing 0.5 cm segments from each type of catheter were incubated at 37 degrees C. At specified intervals, the segments were washed to remove nonadherent bacteria and sonicated for 1 min, and colony-forming units were quantified. Bacterial adherence occurred rapidly, reaching maximal peaks after 24 h of incubation. Enterococcus faecium adherence to both biomaterials was significantly lower than that of Enterococcus faecalis. No differences were observed between the two elastomers. Bacterial adherence was not related to bacterial surface hydrophobicity, hemolysin or gelatinase production.

Bacterial Adhesion↗