PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Enterococcus faecalis”

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 271 records · Page 15Linked to original sources
PubMed2002

A comparison of the antimicrobial efficacy of three calcium hydroxide formulations on human dentin infected with Enterococcus faecalis.

This study compared the antibacterial efficacy of three different formulations of calcium hydroxide by using human dentin specimens that were infected with Enterococcus faecalis. After exposure to three forms of calcium hydroxide (calcium hydroxide mixed with distilled water, calcium hydroxide mixed with 0.2% chlorhexidine, and calcium hydroxide mixed with camphorated paramonochlorophenol) for 7 days, dentin powder from the infected specimens was obtained and assessed for bacterial quantity by spectrophotometry. It was found that calcium hydroxide mixed with camphorated paramonochlorophenol killed all of the Enterococcus faecalis inside the dentinal tubules. This result was better than that obtained with calcium hydroxide mixed with distilled water or with 0.2% chlorhexidine (p < 0.05). Calcium hydroxide mixed with distilled water and calcium hydroxide mixed with 0.2% chlorhexidine were ineffective against these bacteria.

Anti-Infective Agents, Local↗
PubMed2005

Recovery of Enterococcus faecalis after single- or multiple-visit root canal treatments carried out in infected teeth ex vivo.

AIM: To assess the presence of Enterococcus faecalis after root canal treatment in single or multiple visits in an ex vivo model. METHODOLOGY: Forty-five premolar teeth were infected ex vivo with E. faecalis for 60 days. The canals were then prepared using a crowndown technique with System GT and Gates-Glidden burs and irrigated with 2% chlorhexidine gel. The specimens were divided into five groups (G1, G2, G3, G4 and G5) according to the time elapsed between chemical-mechanical preparation and root canal filling, the irrigant solution used and the use or nonuse of a calcium hydroxide intra-canal medicament. The teeth were then root-filled and incubated for 60 days at 37 degrees C. Dentine chips were removed from the canal walls with sequential sterile round burs at low speed. The samples obtained with each bur were immediately collected in separate test tubes containing Brain-Heart Infusion broth. These samples were placed onto agar plates and colony forming units were counted after 24 h at 37 degrees C. Data were ranked and analysed using the Kruskal-Wallis statistical test. RESULTS: Enterococcus faecalis was recovered from 20% (three of 15 specimens) of G1 (chlorhexidine irrigation and immediate root filling in a single visit), 25% (four of 15 specimens) of G2 (chlorhexidine irrigation and filling after 14 days use of a calcium hydroxide dressing in multiple visits), 40% (two of five specimens) of G3 (chlorhexidine irrigation and filling after 7 days), 60% (three of five specimens) of G4 (saline irrigation and filling after 7 days) and from 100% (five of five specimens) of G5 (saline irrigation and immediate filling without sealer). CONCLUSIONS: Neither single- nor multiple-visit root canal treatment ex vivo, eliminated E. faecalis completely from dentinal tubules. Up to 60 days after root filling, E. faecalis remained viable inside dentinal tubules. When no sealer was used, E. faecalis presented a higher growth rate.

Anti-Infective Agents, Local↗
PubMed2002

Inactivation of the antibacterial activity of iodine potassium iodide and chlorhexidine digluconate against Enterococcus faecalis by dentin, dentin matrix, type-I collagen, and heat-killed microbial whole cells.

The antibacterial activity of chlorhexidine digluconate and iodine potassium iodide on Enterococcus faecalis A197A was tested in the presence of dentin, dentin matrix, dentin pretreated by EDTA and citric acid, collagen, and heat-killed cells of Enterococcus faecalis and Candida albicans. Medications were preincubated for 1 h with each of the potential inhibitors and tested for their antibacterial activity against E. faecalis, strain A197A. Surviving bacteria were sampled after 1 and 24 h of incubation. Dentin matrix and heat-killed microbial cells were the most effective inhibitors of chlorhexidine, whereas dentin pretreated by citric acid or EDTA showed only slight inhibition. Dentin and skin collagen showed some inhibition at 1 h but not after 24 h. Iodine potassium iodide was effectively inhibited by dentin, dentin matrix, and heat-killed microbial cells. Skin collagen and dentin pretreated by EDTA or by citric acid showed little or no inhibitory effect on iodine potassium iodide. Different components of dentin are responsible for the divergent patterns of inhibition of the antibacterial activity of chlorhexidine digluconate and iodine potassium iodide. Chemical treatment of dentin before applying the medication into the root canal may alter the antibacterial effect of the medication.

Candida albicans↗
PubMed2005

The expression of alpha4 integrins by human polymorphonuclear neutrophils in response to sonicated extracts of Enterococcus faecalis.

This study was undertaken to investigate immunopathologic mechanism of Enterococcus faecalis in relation to persistent apical periodontitis. We monitored the expression levels of alpha4 integrin in human polymorphonuclear neutophils (PMNs) after stimulated with sonicated extracts of E. faecalis (SEF) and compared with lipopolycaccarides (LPS) of Escherichia coli for various incubation time. Venous blood was collected from healthy volunteers and then PMNs were isolated and cultured with various concentrations of SEF for different periods of time. The levels of alpha4 integrin were measured by flow cytometry analysis. E. coli LPS group was used as a positive control and untreated PMNs as a negative control. Results showed that the expressions levels of alpha4 integrin were increased in human PMNs stimulated with E. coli LPS in comparison with unstimulated control cells (p < 0.05). In case of SEF stimulated group, the expression levels were decreased in time-dependent manner in comparison to E. coli LPS group (p < 0.05). Notably, after 12 h for incubation with SEF, the expression of alpha4 integrin was decreased in dose-dependent manner (p < 0.05). These findings suggest that E. faecalis seem to suppress PMNs recruiting activity by down-regulating alpha4 integrin expression, providing the possible mechanism that E. faecalis may play a crucial role in persistent apical periodontitis.

Analysis of Variance↗
PubMed1996

Molecular analysis of the rpoD gene of Enterococcus faecalis.

The complete nucleotide sequence of the rpoD gene of Enterococcus faecalis ATCC19433 has been determined. This gene encodes a putative 368 amino acids (aa) polypeptide of a predicted Mr of 41842 named sigma 42. Upstream of the rpoD gene and beginning from the end of the cloned chromosomal fragment is an open reading frame encoding a putative 264-aa polypeptide. It is reminiscent of the C-terminal domain of known DNA primase from Gram-positive bacteria indicating that the E. faecalis rpoD gene is included in a macromolecular synthesis (MMS) operon, as it was described for Escherichia coli, Bacillus subtilis and Lactococcus lactis rpoD gene.

Amino Acid Sequence↗
PubMed1991

Antimicrobial susceptibility and molecular epidemiology of beta-lactamase-producing, aminoglycoside-resistant isolates of Enterococcus faecalis.

beta-Lactamase-producing (BL+), aminoglycoside-resistant (AR) Enterococcus faecalis is endemic in our hospital, having caused widespread colonization and infection. Suitable therapy for infections caused by these organisms has been problematic. We compared the antimicrobial and bactericidal activities, by broth macrodilution and time-kill methods, of several antibiotics, alone and in combination, against BL+, AR isolates of E. faecalis and determined the transmissibility of antibiotic resistance markers. Ampicillin-sulbactam, imipenem, daptomycin, and ciprofloxacin were the most active antibiotics with MICs for 90% of isolates tested of 2, 1, 2, and 1 microgram/ml, respectively, against inocula of 10(3) and 10(5) CFU/ml. Little inoculum effect was noted with imipenem, vancomycin, daptomycin, or ciprofloxacin, while the addition of sulbactam to ampicillin partially inhibited the effect of the increased inoculum. Penicillin-sulbactam and ampicillin-sulbactam combinations in a 2:1 ratio were most frequently bactericidal (greater than or equal to 3-log10-unit decrease in bacterial titers at 24 h for 13 of 20 isolates), followed by daptomycin (8 of 20 isolates) and ciprofloxacin (2 of 20 isolates). Bactericidal activity was not demonstrated for imipenem or teicoplanin. beta-Lactamase production and aminoglycoside resistance were associated with a 60- to 65-MDa plasmid which was easily transferred to a plasmid-free E. faecalis recipient. The 840-bp beta-lactamase gene probe hybridized to purified plasmid DNA from BL+ donor isolates of E. faecalis and transconjugants but not from BL- isolates. Ampicillin-sulbactam and daptomycin (an investigational antibiotic) seem to be reasonable choices for the empiric therapy of presumed enterococcal infections in hospitals in which BL+, AR E. faecalis strains are isolated. Their use should ideally be supported by tests for bactericidal activity.

Aminoglycosides↗
PubMed2001

Antibodies to a surface-exposed, N-terminal domain of aggregation substance are not protective in the rabbit model of Enterococcus faecalis infective endocarditis.

The aggregation substance (AS) surface protein from Enterococcus faecalis has been implicated as an important virulence factor for the development of infective endocarditis. To evaluate the role of antibodies specific for Asc10 (the AS protein from the conjugative plasmid pCF10) in protective immunity to infective endocarditis, an N-terminal region of Asc10 lacking the signal peptide and predicted to be surface exposed (amino acids 44 to 331; AS(44-331)) was cloned with a C-terminal histidine tag translational fusion and expressed from Escherichia coli. N-terminal amino acid sequencing of the purified protein revealed the correct sequence, and rabbit polyclonal antisera raised against AS(44-331) reacted specifically to Asc10 expressed from E. faecalis OG1SSp, but not to other proteins as judged by Western blot analysis. Using these antisera, flow cytometry analysis demonstrated that antibodies to AS(44-331) bound to a surface-exposed region of Asc10. Furthermore, antibodies specific for AS(44-331) were opsonic for E. faecalis expressing Asc10 in vitro but not for cells that did not express Asc10. New Zealand White rabbits immunized with AS(44-331) were challenged intravenously with E. faecalis cells constitutively expressing Asc10 in the rabbit model of experimental endocarditis. Highly immune animals did not show significant differences in clearance of organisms from the blood or spleen or in formation of vegetations on the aortic valve, in comparison with nonimmune animals. Although in vivo expression of Asc10 was demonstrated by immunohistochemistry, these experiments provide evidence that immunity to Asc10 does not play a role in protection from experimental infective endocarditis due to E. faecalis and may have important implications for the development of immunological approaches to combat enterococcal endocarditis.

Amino Acid Sequence↗
PubMed2005

Development of a method for markerless genetic exchange in Enterococcus faecalis and its use in construction of a srtA mutant.

Enterococcus faecalis is a gram-positive commensal bacterium of the gastrointestinal tract and an important opportunistic pathogen. Despite the increasing clinical significance of the enterococci, genetic analysis of these organisms has thus far been limited in scope due to the lack of advanced genetic tools. To broaden the repertoire of genetic tools available for manipulation of E.faecalis, we investigated the use of phosphoribosyl transferases as elements of a counterselection strategy. We report here the development of a counterselectable markerless genetic exchange system based on the upp-encoded uracil phosphoribosyl transferase of E. faecalis. Whereas wild-type E. faecalis is sensitive to growth inhibition by the toxic base analog 5-fluorouracil (5-FU), a mutant bearing an in-frame deletion of upp is resistant to 5-FU. When a cloned version of upp was ectopically introduced into the deletion mutant, sensitivity to 5-FU growth inhibition was restored, thereby providing the basis for a two-step integration and excision strategy for the transfer of mutant alleles to the enterococcal chromosome by recombination. This method was validated by the construction of a DeltasrtA mutant of E. faecalis and by the exchange of the surface protein Asc10, encoded on the pheromone-responsive conjugative plasmid pCF10, with a previously isolated mutant allele. Analysis of the DeltasrtA mutant indicated that SrtA anchors Asc10 to the enterococcal cell wall, facilitating the pheromone-induced aggregation of E. faecalis cells required for high-frequency conjugative plasmid transfer in liquid matings. The system of markerless exchange reported here will facilitate detailed genetic analysis of these important pathogens.

Aminoacyltransferases↗
PubMedDate not supplied

Does aggregation substance of Enterococcus faecalis contribute to development of endocarditis?

Aggregation substance (AS) of Enterococcus faecalis which is encoded by so-called sex pheromone plasmids enables the bacteria to bind to in vitro-cultured pig kidney tubular cells. It is reported that the presence of AS is not of pivotal importance for the ability of E. faecalis to cause infective endocarditis (EN). The lines of evidence for this are twofold: 1) sex pheromone plasmids and, therefore, the gene for AS were not present more often in epidemiologically unrelated strains of E. faecalis isolated from human cases of EN than in isolates from well-water (26 vs. 18%); 2) the presence of the adhesin did not correlate with the establishment of EN in an animal (rat) model. The data are discussed with respect to the specificity of interaction of AS with eukaryotic cells and the results of other studies.

Adhesins, Bacterial↗
PubMed2002

Invasion of HeLa cells by Enterococcus faecalis clinical isolates.

We examined the in vitro ability of Enterococcus faecalis clinical isolates to adhere to and to invade HeLa cells, suggested to be a valuable model system to study bacteria-directed endocytosis. Using a variety of compounds that act on eukaryotic cell structures, both microtubules and microfilaments were found to be involved in enterococcal entry into cells. Two distinct modes of interaction were observed: in one, a close proximity of bacteria with the cell membrane was observed, possibly leading to direct engulfment of the bacterial cell. In the other mode, cellular pseudopodal formation seemed to be stimulated by vicinity of bacterial cells; in some cases, such associations involved formation of clathrin-coated-like vesicles before internalizing enterococci. The above-mentioned experimental data together with the use of monodansylcadaverine, amiloride and NH4Cl, all involved in cytosol acidification and inhibition of receptor-mediated endocytosis (RME), led us to conclude that E. faecalis is internalized within HeLa cells by more than one invasion pathway. One, sensitive to amiloride, is most likely a macropinocytic, actin-dependent uptake mechanism, which determines the production of large smooth-membrane vacuoles engulfing enterococci. The other is RME, in which entry is dependent on both microfilament and microtubule structural integrity.

Acids↗
PubMed1987

Location of antibiotic resistance markers in clinical isolates of Enterococcus faecalis with similar antibiotypes.

Eight wild-type strains of Enterococcus faecalis, resistant to chloramphenicol (Cmr), erythromycin (Emr), tetracycline (Tcr), and minocycline (Mnr), were examined for the genetic basis of their antibiotic resistance, Five of the strains transferred all of their antibiotic resistance markers by conjugation, while the other three strains transferred only Tcr and Mnr. Cmr and Emr determinants were localized by DNA-DNA hybridization experiments, in which the Cmr gene of plasmid pIP501, of group B Streptococcus origin, and the Emr gene of transposon Tn917, of E. faecalis origin, served as probes. A chromosomal location was found for the nonconjugative Cmr and Emr markers of one wild-type strain. In two strains these markers were carried by nonconjugative plasmids, and in the other strains they were carried by plasmids that transferred by conjugation. Plasmids isolated from three transconjugants resistant to tetracycline but susceptible to minocycline bore nucleotide sequences homologous to the tetL gene. Nucleotide sequences homologous to conjugative transposon Tn916, of E. faecalis origin, were detected by hybridization in the tetracycline-minocycline-resistant transconjugants. Three of these transconjugants were plasmid free, while four harbored conjugative cryptic plasmids. Sequences homologous to Tn916 were also found on two conjugative plasmids, one of which appeared to be a conjugative cryptic plasmid that had acquired chromosomal Tcr Mnr markers during transfer.

Chloramphenicol Resistance↗
PubMed2006

Antimicrobial susceptibility and molecular analysis of Enterococcus faecalis originating from endodontic infections in Finland and Lithuania.

BACKGROUND/AIMS: Enterococcus faecalis strains with multiple antibiotic resistances can cause infections that are difficult to treat. The microbial flora in treatment-resistant apical periodontitis is dominated by E. faecalis, and is a potential source of infections at other sites. MATERIAL AND METHODS: Sensitivities to a range of antibiotics were determined for 59 endodontic E. faecalis isolates from Finland and Lithuania. The DNA sequence of the gene responsible for the species' intrinsic quinupristin-dalfopristin resistance, lsa, was determined from two isolates with diminished resistance. Four pairs of isolates from the same root canal were typed by pulsed-field gel electrophoresis. RESULTS: A high prevalence of resistance to rifampicin was found, whereas all isolates were susceptible or showed intermediate susceptibility to penicillin and ampicillin and four isolates were unusually susceptible to cefotaxime. No vancomycin or high-level gentamicin resistance was detected. Nine of 59 isolates were susceptible to quinupristin-dalfopristin. A fully quinupristin-dalfopristin-susceptible isolate also susceptible to clindamycin produced a truncated Lsa polypeptide, and an isolate with borderline quinupristin-dalfopristin-susceptibility had mutations proximal to the predicted ribosomal binding site. Pulsed-field gel electrophoresis showed that the same root canal could harbor two different strains of E. faecalis during the course of the same infection. CONCLUSION: Despite the differing antibiotic usage in Finland and Lithuania, E. faecalis from endodontic infections in these countries showed similar susceptibility patterns with levels of resistance considered typical for the species, and decreased resistance to clindamycin and quinupristin-dalfopristin as well as lesions in the lsa gene which were similar to those described in other clinical isolates.

ATP-Binding Cassette Transporters↗
PubMed1992

Antimicrobial susceptibility changes in Enterococcus faecalis following various penicillin exposure regimens.

Penicillin-"virgin" strains of Enterococcus faecalis collected from a population of individuals with no previous antibiotic exposure were subjected in vitro to penicillin delivered as repeated pulses, stepwise increasing concentrations, or sustained levels of a single concentration. Changes in resistance to penicillin were assessed by determination of MICs, and time-kill studies were performed to evaluate changes in tolerance to the bactericidal effects of penicillin. Isogenic clones, derived from various exposure regimens, which exhibited changes in either resistance or tolerance were further examined for changes in penicillin-binding proteins. Exposure to repeated pulses of penicillin resulted in the development of tolerance to penicillin without changes in the level of resistance. Clones derived from a regimen of stepwise increases in the penicillin concentration acquired both increased penicillin resistance and tolerance. Clones selected after prolonged continuous exposure to a fixed concentration of penicillin displayed minimally increased resistance to penicillin, but they retained the lytic, nontolerant response to the bactericidal effect of penicillin. Clones which acquired tolerance to the bactericidal effect of penicillin without changes in penicillin resistance exhibited a penicillin-binding protein pattern identical to that of the parental strain. Increased labeling of several penicillin-binding proteins accompanied the development of increased penicillin resistance in both penicillin-tolerant and nontolerant strains. Exposure of E. faecalis to penicillin in repeated pulses of brief duration, for prolonged periods at a constant concentration, or in stepwise graded concentrations can result in the selection of clones with increased resistance to the inhibitory or bactericidal effects of penicillin, or both. These observations may be relevant to the selection of dosing regimes for penicillin in the treatment of enterococcal infections, when bactericidal synergism cannot be achieved with penicillin-aminoglycoside combinations.

Bacterial Proteins↗
PubMed2001

Aggregation substance-mediated adherence of Enterococcus faecalis to immobilized extracellular matrix proteins.

Aggregation substance (AS) of Enterococcus faecalis (E. faecalis), a sex pheromone plasmid encoded cell surface protein, mediates the formation of bacterial aggregates, thereby promoting plasmid transfer. The influence of pAD1-encoded AS, Asa1, on binding to immobilized extracellular matrix proteins was studied. The presence of AS increased enterococcal adherence to fibronectin more than eight-fold, to thrombospondin more than four-fold, to vitronectin more than three-fold, and to collagen type I more than two-fold (P<0.001). In contrast, binding to laminin and collagen type IV occurred independently of AS. Adherence of the constitutively AS expressing E. faecalis OG1X(pAM721) to immobilized fibronectin was found to be approximately five times higher than that of Staphylococcus aureus Cowan and approximately 30 times higher than that of Streptococcus bovis. Investigation of strains with various deletions within the structural gene of asa1 suggests that attachment to immobilized fibronectin is mainly mediated by amino acids within the variable region or by neighbouring residues. Thus, AS may promote adherence to injured epithelium and endothelium, where extracellular matrix proteins are exposed, thereby facilitating colonization and infection.

Bacterial Proteins↗
PubMed2006

Topoisomerase mutations and efflux are associated with fluoroquinolone resistance in Enterococcus faecalis.

To understand better the mechanisms of fluoroquinolone resistance in Enterococcus faecalis, fluoroquinolone-resistant mutants isolated from Ent. faecalis ATCC 29212 by stepwise selection with sparfloxacin (SPX) and norfloxacin (NOR) were analysed. The results showed the following. (i) In general, fluoroquinolone-resistance mechanisms in Ent. faecalis are similar to those in other Gram-positive bacteria, such as Staphylococcus aureus and Streptococcus pneumoniae, namely, mutants with amino acid changes in both GyrA and ParC exhibited high fluoroquinolone resistance, and single GyrA mutants and a single ParC mutant were more resistant to SPX and NOR, respectively, than the parent strain, indicating that the primary targets of SPX and NOR in Ent. faecalis are DNA gyrase and topoisomerase IV, respectively. (ii) Alterations in GyrB (DeltaKGA, residues 395-397) and ParE (Glu-459 to Lys) were associated with fluoroquinolone resistance in some mutants. Moreover, the facts that the NOR MIC, but not the SPX MIC, decreased in the presence of multidrug efflux pump inhibitors, that NOR accumulation decreased in the cells, and that the EmeA mRNA expression level did not change, strongly suggested that a NorA-like efflux pump, rather than EmeA, was involved in resistance to NOR.

Anti-Infective Agents↗
PubMed1994

Conjugal transfer of transposon Tn916 from Enterococcus faecalis to Bacillus licheniformis.

Transposon Tn916 was conjugally transferred from Enterococcus faecalis to Bacillus licheniformis bacterial strains ATCC 10716 and ATCC 9945A by filter and broth matings. The Tn916 transfer frequencies to B. licheniformis ranged from 10(-7) to 10(-5) selecting for tetracycline-resistant (Tcr) transconjugants depending on broth or filter mating. Movement of Tn916 was demonstrated when Tcr B. licheniformis transconjugants were mated with Bacillus subtilis strain W23. Tn916 insertion caused several auxotrophic and bacitracin deficient mutants. Southern blot analyses of HindIII chromosomal digests extracted from Tcr transconjugants showed that the transposon inserted at different sites in the B. licheniformis chromosome and the copy number of Tn916 varied. This approach should be useful for genetic studies of B. licheniformis.

Bacillus↗
PubMed1996

Enterococcus faecalis cytolysin and lactocin S of Lactobacillus sake.

Strains of Enterococcus faecalis and Lactobacillus sake have been found to express lantibiotics with unusual properties. The enterococcal lantibiotic is unusual in that it consists of two dissimilar subunits, both putatively containing modifications consistent with those found in other lantibiotics. The enterococcal lantibiotic is also unusual in the number of proteolytic steps involved in secretion signal removal and activation. Moreover, it has been observed to contribute to enterococcal disease in humans and in animal models. Structural studies of lactocin S, expressed by a strain of L. sake highlight unique properties including the presence of D-alanine within its structure, and a protease putatively responsible for lactocin S secretion signal peptide removal which, itself, lacks a signal or propeptide sequence. Despite the unusual properties of each of these lantibiotics, the operons encoding each, and accompanying auxiliary functions, are collinear suggesting a common ancestry. The accretion of interdigitating DNA sequences between genes encoded within the lactocin S determinant are unique to that determinant, however, and are of unknown function.

Amino Acid Sequence↗