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PubMedDate not supplied

In vitro and in vivo antibacterial activities of TOC-50, a new parenteral cephalosporin, against Enterococcus faecalis.

In vitro and in vivo antibacterial activities of TOC-50, a new parenteral cephalosporin, were assessed against Enterococcus faecalis. In vitro, TOC-50 had excellent activity, stronger than that of penicillin G, sulbactam/ampicillin, tazobactam/piperacillin, the cephalosporins tested, imipenem, vancomycin, gentamicin, tobramycin, arbekacin, amikacin, minocycline and ofloxacin against clinically isolated strains. In addition, TOC-50 was more active than penicillin G, sulbactam/ampicillin and imipenem against vancomycin-resistant E. faecalis NCTC 12201. In terms of bactericidal effect against the same strain, TOC-50 was superior to sulbactam/ampicillin and imipenem. In murine systemic infection models, TOC-50 had a potent protective activity against E. faecalis 42. Its protective activity was stronger than that of imipenem or vancomycin.

Animals↗

PubMed1992

Conjugative transfer of Enterococcus faecalis plasmid pAD1: nucleotide sequence and transcriptional fusion analysis of a region involved in positive regulation.

The Enterococcus faecalis plasmid pAD1 undergoes conjugative transfer in response to cAD1, a peptide sex pheromone emitted by potential bacterial recipients. Regulation of pAD1 transfer involves a number of plasmid-encoded determinants:iad, which determines a peptide-competitive inhibitor iAD1; signal sensing and transducing elements; and negative and positive regulators. The key positive regulator(s) of the pheromone response is believed to be encoded within a segment designated the E region of the plasmid. In this study, we analyzed the nucleotide sequence and transcription within the E region. An open reading frame designated traE1 was identified; its inferred protein consists of 118 amino acids. Insertional mutagenesis of traE1 resulted in a complete loss in plasmid transfer capability. Analysis of Tn917-lac insertions giving rise to transcriptional lacZ fusions showed that traE1 is transcribed only under cAD1 inducing conditions. Analysis of additional lacZ fusions within the region provided some insight into the roles of potential regulatory signals within and around the nucleotide sequences reported here. A regulatory role appearing to involve read-through of certain key transcription termination sequences seemed evident.

Amino Acid Sequence↗

PubMed2000

A pAD1-encoded small RNA molecule, mD, negatively regulates Enterococcus faecalis pheromone response by enhancing transcription termination.

pAD1 is a 60-kb hemolysin-bacteriocin plasmid in Enterococcus faecalis that encodes a conjugative mating response to a peptide sex pheromone, cAD1, secreted by plasmid-free bacteria. The pheromone response is regulated by two proteins: TraE1, which positively regulates all or most conjugative structural genes, and TraA, which negatively regulates traE1. TraA binds to pAD1 DNA at the iad (encoding the inhibitor peptide iAD1) promoter but is released upon binding to imported pheromone. This leads to enhanced transcription through two closely spaced downstream terminators (t1 and t2) into traE1. TraE1 is believed to then upregulate itself from a site located within t2; thus, a small amount of transcription through t1-t2 could lead to overall induction. It is important therefore that the t1-t2 terminators be tightly controlled to keep the response shut down in the absence of pheromone. A small (200-nucleotide) RNA molecule designated mD is encoded just upstream of t1 by a determinant (traD) oriented in the direction opposite to that of transcripts utilizing t1. mD is expressed at high levels in the uninduced state, but it decreases significantly upon induction. Here we present results of genetic studies relating to the activity of t1-t2 and show that mD strongly enhances transcriptional termination at t1. The mD activity is shown to influence transcription well downstream and can affect the determinant for aggregation substance asa1. The phenomenon is specific in that there is no effect of mD on the unrelated pheromone-responding plasmids pPD1 and pCF10.

Bacterial Proteins↗

PubMed1992

Hyperhemolytic phenomena associated with insertions of Tn916 into the hemolysin determinant of Enterococcus faecalis plasmid pAD1.

Members of the Tn916 family of conjugative transposons are able to insert themselves into Enterococcus faecalis hemolysin/bacteriocin plasmid pAD1 (and related elements) in such a way as to generate hyperexpression of the hemolysin/bacteriocin. To examine this phenomenon in more detail, E. faecalis (pAD1::Tn916) derivatives defective or altered in hemolysin expression were isolated and characterized with respect to production of the L (lytic) or A (activator) component (also known as CylA) and the specific location of the transposon. The mutants fell into five classes. Class 1 strains were nonhemolytic, and the related insertions mapped in a location known to affect expression of the L component. The other four classes varied from an inability to express hemolysin (class 2) to different degrees of hyperhemolytic expression (classes 3 to 5); the insertions in these classes mapped in a similar place within cylA, near the 3' end of the determinant. A previous study provided evidence that CylA is also necessary for bacteriocin immunity; however, these insertions did not destroy this function. (A Tn917 insertion in the 5' half of the determinant eliminates immunity.) In mutant classes 3 to 5, the presence of tetracycline enhanced hemolysin expression. In late-exponential-phase broth cultures, hemolysin could not be detected in supernatants of classes 2 to 5, in contrast to a wild-type control strain; however, different amounts of the L component could be detected, with the lowest in class 2 and greater-than-normal amounts in classes 3 to 5. Although nucleotide sequencing showed that the Tn916 insertions in classes 2 to 5 were at identical sites, the transposon junction sequences differed in some cases. The data indicated that cylA translation into the transposon would result in different truncation sites, and these differences were probably related to phenotype differences.

Amino Acid Sequence↗

PubMed2000

Branched-chain alpha-keto acid catabolism via the gene products of the bkd operon in Enterococcus faecalis: a new, secreted metabolite serving as a temporary redox sink.

Recently the bkd gene cluster from Enterococcus faecalis was sequenced, and it was shown that the gene products constitute a pathway for the catabolism of branched-chain alpha-keto acids. We have now investigated the regulation and physiological role of this pathway. Primer extension analysis identified the presence of a single promoter upstream of the bkd gene cluster. Furthermore, a putative catabolite-responsive element was identified in the promoter region, indicative of catabolite repression. Consistent with this was the observation that expression of the bkd gene cluster is repressed in the presence of glucose, fructose, and lactose. It is proposed that the conversion of the branched-chain alpha-keto acids to the corresponding free acids results in the formation of ATP via substrate level phosphorylation. The utilization of the alpha-keto acids resulted in a marked increase of biomass, equivalent to a net production of 0.5 mol of ATP per mol of alpha-keto acid metabolized. The pathway was active under aerobic as well as anaerobic conditions. However, under anaerobic conditions the presence of a suitable electron acceptor to regenerate NAD(+) from the NADH produced by the branched-chain alpha-keto acid dehydrogenase complex was required for complete conversion of alpha-ketoisocaproate. Interestingly, during the conversion of the branched-chain alpha-keto acids an intermediate was always detected extracellularly. With alpha-ketoisocaproic acid as the substrate this intermediate was tentatively identified as 1, 1-dihydroxy-4-methyl-2-pentanone. This reduced form of alpha-ketoisocaproic acid was found to serve as a temporary redox sink.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed1997

Cloning and genetic analysis of the UV resistance determinant (uvr) encoded on the Enterococcus faecalis pheromone-responsive conjugative plasmid pAD1.

The conjugative pheromone-responsive plasmid pAD1 (59.6 kb) of Enterococcus faecalis encodes a UV resistance determinant (uvr) in addition to the hemolysin-bacteriocin determinant. pAD1 enhances the UV resistance of wild-type E. faecalis FA2-2 and E. faecalis UV202, which is a UV-sensitive derivative of E. faecalis JH2-2. A 2.972-kb fragment cloned from between 27.7 and 30.6 kb of the pAD1 map conferred UV resistance function on UV202. Sequence analysis showed that the cloned fragment contained three open reading frames designated uvrA, uvrB, and uvrC. The uvrA gene is located on the pAD1 map between 28.1 and 29.4 kb. uvrB is located between 30.1 and 30.3 kb, and uvrC is located between 30.4 and 30.6 kb on the pAD1 map. The uvrA, uvrB, and uvrC genes encode sequences of 442, 60, and 74 amino acids, respectively. The deduced amino acid sequence of the uvrA-encoded protein showed 20% homology of the identical residues with the E. coli UmuC protein. Tn917 insertion mutagenesis and deletion mutant analysis of the cloned fragment showed that uvrA conferred UV resistance. A palindromic sequence, 5'-GAACNGTTC-3', which is identical to the consensus sequence found within the putative promoter region of the Bacillus subtilis DNA damage-inducible genes, was located within the promoter region of uvrA. Two uvrA transcripts of different lengths (i.e., 1.54 and 2.14 kb) which terminate at different points downstream of uvrA were detected in UV202 carrying the deletion mutant containing uvrA. The longer transcript, 2.14 kb, was not detected in UV202 carrying the deletion mutant containing both uvrA and uvrB, which suggests that uvrB encodes a terminator for the uvrA transcript. The uvrA transcript was not detected in any significant quantity in UV202 carrying the cloned fragment containing uvrA, uvrB, and uvrC; on the other hand, the 1.54-kb uvrA transcript was detected in the strain exposed to mitomycin C, which suggests that the UvrC protein functions as a regulator of uvrA.

Adenosine Triphosphatases↗

PubMed1998

Generation and testing of mutants of Enterococcus faecalis in a mouse peritonitis model.

A previously described mouse peritonitis model was used to study derivatives of Enterococcus faecalis strain OG1RF. The addition of sterile rat fecal extracts (SRFE) lowered the LD50 of OG1RF >10-fold. Hemolysin production caused a 35-fold lower LD50 and a much shorter survival, similar to previous results using a peritonitis model without SRFE. A purine (but not a pyrimidine) auxotroph was considerably less lethal than wild type; gelatinase mutants were also attenuated. A suicide vector was generated with an enterococcal selectable marker in order to disrupt a gene encoding an E. faecalis antigen; the resulting mutant was not attenuated despite a slower growth rate. In conclusion, this model allows attenuated mutants to be detected, corroborates prior reports that hemolysin is a virulence factor, and suggests a role for gelatinase in virulence of E. faecalis in mice; the attenuated purine auxotroph may provide a system for developing vectors for in vivo expression systems.

Animals↗

PubMed2006

Acquired gentamicin resistance by permeability impairment in Enterococcus faecalis.

Enterococci are intrinsically resistant to low levels of aminoglycosides. We previously selected in vitro and in vivo Enterococcus faecalis with intermediate-level resistance to gentamicin that did not abolish synergism with a cell-wall-active agent (E. Aslangul et al., Antimicrob. Agents Chemother. 49:4144-4148, 2005). The aim of this study was to investigate the mechanism of resistance to gentamicin in the 1688-G3 third-step mutant (MIC, 512 microg/ml) of E. faecalis JH2-2. No mutations were found in the genes for L6 ribosomal protein and the four copies of 16S rRNA. Production of a known aminoglycoside-modifying enzyme was unlikely due to the distinct resistance phenotype and absence of the corresponding genes. Efflux was also unlikely since ethidium bromide MICs were similar for JH2-2 and 1688-G3 and since the pump inhibitors reserpine and verapamil had no effect on gentamicin resistance in both strains. To study gentamicin accumulation, we developed a nonisotopic method based on a fluorescent polarization immunoassay. Impaired gentamicin accumulation was observed in 1688-G3 compared to JH2-2 and was only partially reversible by the N,N'-dicyclohexylcarbodiimide (DCCD) uncoupler agent. The lower sensitivity of 1688-G3 to DCCD suggested alteration of the FoF1-ATPase. However, no mutations were detected in the structural genes (atp) for the Fo channel and no difference in transcript levels of atpB and atpE was found between 1688-G3 and JH2-2. Our data are compatible with acquisition of intermediate-level gentamicin resistance by uptake impairment in E. faecalis.

Adenosine Triphosphate↗

PubMed1995

Enterococcus faecalis colonisation and endocarditis in five intensive care patients as late sequelae of selective decontamination.

OBJECTIVE: To describe Enterococcus faecalis colonisation and endocarditis in 5 intensive care patients after treatment with selective decontamination (SDD). SETTING: Intensive care unit (ICU) in a general hospital. PATIENTS: The patients were admitted to the ICU because of adult respiratory distress syndrome, polytrauma (2 patients), abdominal aortic surgery and gastrointestinal surgery. Because these patients needed mechanical ventilation they received systemic cefotaxime and SDD (polymyxin E, amphotericin B and norfloxacin). RESULTS: Colonisation with E. faecalis was documented in all patients. Intravascular catheter-related infection with E. faecalis occurred in 4 patients. None of the patients received antibiotics active against, E. faecalis, because body temperature normalised after catheter removal. In the course of his ICU stay one patient died. Autopsy showed E. faecalis endocarditis. The other 4 patients recovered from their primary illness, but had to be readmitted after several months because of E. faecalis endocarditis. One of these patients died. One patient recovered of endocarditis, but one year later valve surgery was necessary. The other 2 patients needed acute valve replacement. The latter 3 patients survived. CONCLUSION: We observed 5 patients with E. faecalis endocarditis as a late and severe sequela of SDD during their ICU stay.

Aged↗

PubMedDate not supplied

Efficacy of propolis as an intracanal medicament against Enterococcus faecalis.

This study sought to compare the antibacterial efficacy of three commonly used intracanal medicaments with propolis against Enterococcus faecalis. This study utilized 180 freshly extracted single-rooted intact human permanent teeth with a single root canal. After root canal preparations and sterilization, canals were contaminated with E. faecalis and incubated at 37 degrees C (+/- 1.0 degrees C) for seven days. The teeth were divided randomly into six groups. To determine bacterial growth on blood agar, microbiological samples were carried out with sterile paper points to evaluate results at 48 hours and at ten days. All data were analyzed statistically with t-test, Mann Whitney, Kruskal Wallis, and one-way ANOVA tests. This study revealed that propolis had good in vitro antibacterial activity against E. faecalis in the root canals, suggesting that it could be used as an alternative intracanal medicament.

Analysis of Variance↗

PubMed1987

Enterococcus faecalis hemolysin-bacteriocin plasmids belong to the same incompatibility group.

Plasmid pair coexistence was studied both among nine Enterococcus faecalis hemolysin-bacteriocin (Hly-Bcn) plasmids, including pJH2, pAD1, pAM gamma 1, and pIP964, and between pIP964 and five R plasmids. Some of the Hly-Bcn plasmids used were derivatives encoding resistance to erythromycin or tetracycline. The Hly-Bcn plasmids were incompatible with each other; 40 to 100% displacement was observed bilaterally for eight pairs and unilaterally for one pair. In contrast, pIP964 stably coexisted with each of the R plasmids. Entry exclusion was associated with incompatibility for most of the Hly-Bcn plasmids. The nine Hly-Bcn plasmids harbored by E. faecalis form a distinct incompatibility (Inc) group, designated IncHly.

Bacteriocins↗

PubMed2005

Differences in the Enterococcus faecalis lsa locus that influence susceptibility to quinupristin-dalfopristin and clindamycin.

We have previously shown that the Enterococcus faecalis lsa gene, encoding the putative ABC protein Lsa, influences resistance to quinupristin-dalfopristin (Q-D) and clindamycin (CLI). We have now found that, while cloned lsa from E. faecalis strain V583 (lsa(V)) fully restored resistance to Q-D, CLI, and dalfopristin (DAL) lost by the OG1 lsa disruption mutant TX5332 and also caused increased MICs for Lactococcus lactis LM2301, cloned lsa from OG1 (lsa(OG)) did not cause any increase in MICs for either species. Sequencing of ca. 2 kb of these two lsa alleles found differences between lsa(OG) and lsa(V) in the upstream region as well as in the 5' and 3' halves of the lsa gene. To investigate the reason for the phenotypic differences expressed by the two cloned loci, 5' half plus 3' half hybrid constructs were created. When introduced into both TX5332 and L. lactis, cloned lsa(V5)(')(OG3)(') conferred increases in MICs of Q-D, CLI, and DAL similar to those of cloned lsa(V) while cloned lsa(OG5)(')(V3)(') showed a moderate increase in MICs relative to those of lsa(OG), indicating that both halves of the locus can influence resistance expression. After site-directed mutagenesis of the cloned lsa alleles at positions -131 and -133 (relative to the putative Lsa start codon ATG), which converted two A's of lsa(V) to the G and T of lsa(OG) and vice versa, MIC testing showed that mutagenized lsa(OG) (lsa(OG-M)) was strongly influenced by these changes in terms of conferring increased MICs of Q-D, CLI, and DAL relative to lsa(OG) while the phenotype of mutagenized lsa(V) (lsa(V-M)) was less influenced, with moderately decreased MICs, primarily to CLI, relative to lsa(V). In conclusion, this study found that changes in different regions of the E. faecalis lsa locus influence the ability of cloned lsa to confer resistance to Q-D, CLI, and DAL.

ATP-Binding Cassette Transporters↗

PubMed1996

Penicillin-binding protein 5 as an inhibitory target of cefozopran in Enterococcus faecalis.

The concentration of cefozopran which inhibits binding of [14C]benzylpenicillin to penicillin-binding protein (PBP) 5 of Enterococcus faecalis TN2OO5 by 50% was 11 mg/L, and its MIC was 12.5 mg/L. Ceftazidime and cefmenoxime, which were inactive at 100 mg/L, showed no affinity for PBP 5 at this concentration. Ampicillin, benzylpenicillin and imipenem showed higher affinity for PBPs 3/4 and PBP 5 than cefozopran, and their MICs were lower than that of cefozopran. No correlation between MICs of the test compounds and the affinity for PBP 1, 2 or 6 was found. These results suggest that cefozopran exhibits antimicrobial activity against E. faecalis TN2OO5 by binding to PBP 5.

Anti-Bacterial Agents↗

PubMed1998

Evidence of nosocomial infection in Japan caused by high-level gentamicin-resistant Enterococcus faecalis and identification of the pheromone-responsive conjugative plasmid encoding gentamicin resistance.

A total of 1,799 Enterococcus faecalis isolates were isolated from inpatients of Gunma University Hospital, Gunma, Japan, between 1992 and 1996. Four hundred thirty-two (22.3%) of the 1,799 isolates had high-level gentamicin resistance. Eighty-one of the 432 isolates were classified and were placed into four groups (group A through group D) with respect to the EcoRI restriction endonuclease profiles of the plasmid DNAs isolated from these strains. The 81 isolates were isolated from 36 patients. For 35 of the 36 patients, the same gentamicin-resistant isolates were isolated from the same or different specimens isolated from the same patient at different times during the hospitalization. For one other patient, two different groups of the isolates were isolated from the same specimen. Groups A, B, C, and D were isolated from 5, 14, 12, and 6 patients, respectively. The strains had multiple-drug resistance. The restriction endonuclease digestion patterns of the E. faecalis chromosomal DNAs isolated from isolates in the same group were also identical. The patients who had been infected with the gentamicin-resistant isolates from each group were geographically clustered on a ward(s). These results suggest that the isolates in each group were derived from a common source and had spread in the ward. The gentamicin-resistant isolates exhibited a clumping response upon exposure to pheromone (E. faecalis FA2-2 culture filtrate). The gentamicin resistance transferred at a high frequency to the recipient E. faecalis isolates by broth mating, and the pheromone-responsive plasmids encoding the gentamicin resistance were identified in these isolates.

Conjugation, Genetic↗

PubMed2006

Primer sensitivity: can it influence the results in Enterococcus faecalis prevalence studies?

BACKGROUND/OBJECTIVE: Recent polymerase chain reaction (PCR)-based studies have shown significant variability in the prevalence of Enterococcus faecalis cases with nonhealing endodontic infections. This variability may be, at least in part, due to the differences in sensitivities of the primers used. The purpose of this study was to compare the sensitivity of 3 sets of PCR primers which have been reported in the endodontic literature. METHODS: The 3 primers sets used were: group 1) tuf gene-based primers with genus-level specificity; and groups 2 and 3) 16S rDNA-based primers that were E. faecalis specific. Three strains of E. faecalis at concentrations of 10(2)-10(8) cells/mL were included in this study. RESULTS: The PCR amplification of E. faecalis strains with the 3 primer pairs showed that group 1 primers consistently had the highest sensitivity, followed by group 2 and group 3 (P<.0001). CONCLUSION: A tuf-based PCR identification assay followed by direct sequencing would yield accurate and consistent prevalence rates of E. faecalis in endodontic infections.

Bacterial Proteins↗

PubMed2002

Biochemical and genetic characterization of the two-peptide bacteriocin enterocin 1071 produced by Enterococcus faecalis FAIR-E 309.

The structural genes for the two-peptide bacteriocin enterocin 1071 (Ent1071) in Enterococcus faecalis FAIR-E 309 were cloned. DNA sequence analysis showed that the enterocin 1071A (Ent1071A) peptide of strain FAIR-E 309 differed by two amino acids from the Ent1071A reported for E. faecalis BFE 1071 (E. Balla, L. M. T. Dicks, M. Du Toit, M. J. van der Merwe, and W. H. Holzapfel, Appl. Environ. Microbiol. 66:1298-1304, 2000), while the Ent1071B gene encoded identical peptides in these strains. However, resequencing of ent1071A from E. faecalis BFE 1071 showed that the Ent1071A peptide sequence reported previously was incorrect in two amino acids. Also, ent1071B in E. faecalis FAIR-E 309 encoded a prepeptide that was three amino acids shorter than that previously reported for E. faecalis BFE 1071 Ent1071B. A presumptive immunity gene (eni1071) was located downstream of the bacteriocin structural genes. This gene was cloned into the heterologous host E. faecalis ATCC 19433 and was shown to confer immunity. A truncated ABC transporter gene was located upstream of the Ent1071 structural genes.

Amino Acid Sequence↗

PubMedDate not supplied

Aerosol transmission of arthropathic and amyloidogenic Enterococcus faecalis.

One-day-old brown layer chicks were exposed to an aerosol of an arthropathic and amyloidogenic Enterococcus faecalis strain alone or after being subjected to treatment with formaldehyde gas (100-200 ppm). Four-day-old chicks were also treated with the same aerosol but after treatment with a Newcastle disease vaccine virus (NDVV) aerosol or intramuscular injection with methylprednisolon at day 1. The same E. faecalis strain was inoculated intramuscularly in day-old chicks as positive control. Bacteremia with time showed that 24 hr after the aerosol the day-old exposed chicks had the highest rate of positive blood cultures (70%-80%). Lower numbers of bacteremic birds at this point in time were found in the chicks treated with E. faecalis aerosol at day 4 (3/10 in the methylprednisolon-treated group and 0/10 in the NDVV-treated group) and the E. faecalis intramuscular-injected group at day 1 (2/10). Formaldehyde gas treatment did not favor the occurrence of bacteremia. NDVV aerosol exposure or injection with corticosteroids did not favor the occurrence of bacteremia 24 hr after E. faecalis aerosol exposure at day 4 either, although 66 days after aerosol, one bird (1/14) treated with NDVV showed bacteremia. A few bacteremic birds were found 10 days after aerosol in the NDVV- and methylprednisolon-treated groups, whereas at 14 days after aerosol, one bacteremic bird was seen in the group subjected to E. faecalis aerosol at day 1, indicating the occurrence of chronic bacteremia. In contrast to the E. faecalis intramuscular-inoculated birds, no joint pathology was seen in the aerosol-exposed groups in spite of the occurrence of chronic bacteremia.

Aerosols↗

PubMed2001

Sequence of the 50-kb conjugative multiresistance plasmid pRE25 from Enterococcus faecalis RE25.

The complete 50,237-bp DNA sequence of the conjugative and mobilizing multiresistance plasmid pRE25 from Enterococcus faecalis RE25 was determined. The plasmid had 58 putative open reading frames, 5 of which encode resistance to 12 antimicrobials. Chloramphenicol acetyltransferase and the 23S RNA methylase are identical to gene products of the broad-host-range plasmid pIP501 from Streptococcus agalactiae. In addition, a 30.5-kb segment is almost identical to pIP501. Genes encoding an aminoglycoside 6-adenylyltransferase, a streptothricin acetyltransferase, and an aminoglycoside phosphotransferase are arranged in tandem on a 7.4-kb fragment as previously reported in Tn5405 from Staphylococcus aureus and in pJH1 from E. faecalis. One interrupted and five complete IS elements as well as three replication genes were also identified. pRE25 was transferred by conjugation to E. faecalis, Listeria innocua, and Lactococcus lactis by means of a transfer region that appears similar to that of pIP501. It is concluded that pRE25 may contribute to the further spread of antibiotic-resistant microorganisms via food into the human community.

Animals↗