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PubMed2004

[Transferability of vanA gene from vancomycin-resistant Enterococcus faecalis in the digestive tract of specific pathogen-free mice].

We evaluated the transferability of vanA gene from vancomycin-resistant Enterococcus faecalis (VREF) to vancomycin-sensitive E. faecalis (VSEF) in vitro and in vivo. In vitro conjugal transfer experiment by filter mating, the vanA gene of VREF was transferable at the high frequency to VSEF and a mutant strain which cured vanA gene of VREF. In vivo studies in the digestive tract of specific pathogen-free mice pretreated with oral antibiotics, transconjugants were also detected from the feces of a mouse at the lower frequency. However, the colonization of transconjugants was transient. The vanA gene in the donor and the transconjugant strain was confirmed by using a polymerase chain reaction method. These results suggest that VSEF colonizing in the human digestive tract might be developed to VREF by transferring of the vanA gene.

Animals↗

PubMed2004

Chairside sensor for rapid monitoring of Enterococcus faecalis activity.

In this study, optical spectroscopy was used to monitor a chromogenic, enzyme-substrate reaction for the rapid identification of Enterococcus faecalis. The detection system, comprising a miniature spectrophotometer and an accompanying data acquisition system, was placed in an incubator. During testing, a 3-ml test sample was placed in a cuvette within the spectrophotometer. This permitted online, real-time, and remote analysis of spectral signature needed to monitor the bacteria. It was observed that the absorption peak intensity increased conspicuously 3.5 h after inoculation and through the entire period of testing. A linear-regression analysis demonstrated a significant correlation between the increase in absorption peak intensity at 610 nm (r = 0.9389) and 653 nm (r = 0.9387) with the formation of colony-forming units. Optical spectroscopy-based sensing systems can pave the way for rapid, nonlaboratory-based approaches to monitor microbial status quantitatively and qualitatively from clinical samples.

Biosensing Techniques↗

PubMed2005

Gelatinase is important for translocation of Enterococcus faecalis across polarized human enterocyte-like T84 cells.

Previously, in our laboratory, we established a two-chamber system to study translocation of Enterococcus faecalis across monolayers of polarized human colon carcinoma-derived T84 cells. By using the same system in the present study, we now show that disruption of gelE of strain OG1RF, which also has a polar effect on the cotranscribed sprE, as well as disruption of its regulatory system (fsrA, fsrB, and fsrC) resulted in a loss of detectable translocation by E. faecalis OG1RF; these mutants lost gelatinase (GelE) and serine protease (SprE) production by standard assay. A gelE deletion mutant of OG1RF (GelE- SprE+) also showed that significantly reduced translocation and complementation with the gelE gene (pTEX5438) in trans restored gelatinase and translocation, demonstrating that gelatinase is important for E. faecalis translocation. Complementation of fsrA, fsrB, and fsrC mutants with all three fsr genes also resulted in production of gelatinase and translocation. Furthermore, introduction of fsr genes into two non-gelatinase-producing E. faecalis isolates, the well-characterized laboratory strain JH2-2 and a human-derived fecal isolate, TX1322 (both of which have gelE but not fsrA or fsrB, are gelatinase negative, and do not translocate), resulted in gelatinase production by these strains and restored translocation across T84 monolayers, while transformation with pTEX5438 (gelE) showed little or no translocation and no detectable gelatinase, confirming the importance of both fsr and gelatinase for E. faecalis translocation. The importance of gelatinase production was also corroborated among 20 E. faecalis human isolates (7 fecal, 7 endocarditis, and 6 urine isolates), which showed translocation by all gelatinase-positive isolates but little to no translocation for gelatinase nonproducers. These results indicate that gelatinase is important for the successful in vitro translocation of E. faecalis across human enterocyte-like T84 cells.

Bacterial Proteins↗

PubMed2004

Tissue-specific adherent Enterococcus faecalis strains that show highly efficient adhesion to human bladder carcinoma T24 cells also adhere to extracellular matrix proteins.

The ability of Enterococcus faecalis clinical isolates to adhere to immobilized extracellular matrixes (ECMs) coating the walls of microtiter plates was examined by microscopy. The ECMs consisted of fibronectin, laminin, collagen types I, II, IV, and V, fibrinogen, and lactoferrin. With the exception of fibrinogen, each isolate showed a different level of adherence to each of the ECMs. No significant level of adherence to fibrinogen was observed for any isolate. The tissue-specific adhesive strains AS11, AS12, AS14, AS15, HT11, and HT12, which showed highly efficient adherence to human bladder carcinoma T24 cells and human bladder epithelial cells, showed strong adherence to fibronectin, laminin, and collagen type I, II, IV, and V ECMs, and the levels were greater than 10(4) cells/mm2 of well surface coated by ECM. None of the isolates that showed little adherence to human bladder carcinoma T24 cells showed efficient adherence to all the ECMs. The levels of adherence of gelatinase-producing isolates to the collagens were lower than the levels of adherence of gelatinase-negative isolates. When tissue-specific adhesive strains that adhered strongly to each ECM were preincubated with fibronectin, the adherence of the strains to fibronectin was inhibited, but the adherence of the strains to collagen type IV was not inhibited. Likewise, preincubation with collagen type IV inhibited adherence to collagen type IV but not adherence to fibronectin. All of the E. faecalis isolates were shown to carry the ace gene by PCR analysis performed with specific primers for collagen binding domain A of ace. The ace gene encodes Ace (adhesin of collagen from enterococci). The prtF gene of group A streptococci, which encodes the fibronectin binding protein of group A streptococci, was not detected in the tissue-specific adhesive strains by Southern analysis performed with the prtF probe of the Streptococcus pyogenes JRS4 strain. Mutants with altered collagen binding were isolated by insertion of Tn916 into the chromosome of tissue-specific adhesive strain AS14. The number of mutant adhesive bacterial cells that adhered to collagen and also to laminin was 1 or 2 orders lower than the number observed for the wild-type strain, but the level of adherence to fibronectin remained the same as that of the wild-type strain.

ATP-Binding Cassette Transporters↗

PubMed1995

Physical mapping of the conjugative bacteriocin plasmid pPD1 of Enterococcus faecalis and identification of the determinant related to the pheromone response.

The pheromone-responding conjugative bacteriocin plasmid pPD1 (59 kb) of Enterococcus faecalis was mapped physically by using a relational clone approach, and transposon analysis with Tn917 (Emr) or Tn916 (Tcr) facilitated the location of the bacteriocin-related genes in a segment of about 6.7 kb. Tn917 insertions within a 3-kb region resulted in constitutive clumping. The nucleotide sequence of the region that included the insertions giving rise to constitutive clumping was determined. The region of pPD1 spanned about 8 kb and was found to contain a number of open reading frames, some of which were named on the basis of homologies with two other pheromone-responding plasmids, pAD1 and pCF10. The genes were arranged in the sequence repB-repA-traC-traB-traA-ipd-traE-traF- orfY-sea-1 with all but repB and traA oriented in the same (left-to-right) direction. traC and traB corresponded, respectively, to traC and traB of pAD1 and to prgY and prgZ of pCF10.

Amino Acid Sequence↗

PubMed1994

The Enterococcus faecalis extracellular metalloendopeptidase (EC 3.4.24.30; coccolysin) inactivates human endothelin at bonds involving hydrophobic amino acid residues.

The extracellular metalloendopeptidase (EC 3.4.24.30; coccolysin) from Enterococcus faecalis (Strain OG1-10) inactivates human endothelin-1 by hydrolyzing the peptide primarily at the Ser5-Leu6 and the His16-Leu17 bonds and the human big endothelin at several bonds involving hydrophobic amino acid residues. The big endothelin fragment 22-38 was also hydrolyzed at a high rate. The degradation of endothelin by coccolysin resembles the peptidolytic processing of endothelin by thermolysin. Because E. faecalis is associated with a large number of infectious diseases, it is possible that the manifestation of inflammatory conditions in the presence of this organism is related to the coccolysin-catalyzed inactivation of endothelin.

Amino Acid Sequence↗

PubMed2000

Enterococcus faecalis conjugative plasmid pAM373: complete nucleotide sequence and genetic analyses of sex pheromone response.

pAM373 is a 36.7 kb conjugative plasmid in Enterococcus faecalis that encodes a response to a peptide sex pheromone, cAM373, secreted by plasmid-free (recipient) strains of enterococci. It was identified over 15 years ago as one of five plasmids in E. faecalis strain RC73 and was of interest because a related pheromone activity could be detected in culture supernatants of Staphylococcus aureus and Streptococcus gordonii. Because of increased clinical concern relating to the possibility of mobilizing vancomycin resistance determinants from enterococci, where they are becoming common, into pathogens such as S. aureus, efforts were initiated to characterize pAM373 further. The results of a complete nucleotide sequence determination of pAM373, as well as a genetic analysis of key genes related to regulation of the pheromone response, are reported here. With regard to determinants related to conjugation, the plasmid has a structural organization similar to other known pheromone-responsive plasmids such as pAD1, pCF10 and pPD1; however, there are several unique features. Although there are significant homologues relating to a pheromone-binding surface protein (TraC) and a negatively regulating protein (TraA), there is an absence of a determinant equivalent to traB of pAD1 (reduces endogenous pheromone) and a determinant for surface-exclusion protein. The precursor structure of the inhibitor peptide iAM373 was identified, and its determinant (iam373) was found to be about 500 nt upstream of an apparent transcription terminator t1. Tn917-lac insertion analyses provided interesting insights into aspects of control of the pheromone response and showed that, although the traA product is sensitive to pheromone, it appears to act differently from the traA homologue of pAD1.

Adhesins, Bacterial↗

PubMed2002

Transfer origins in the conjugative Enterococcus faecalis plasmids pAD1 and pAM373: identification of the pAD1 nic site, a specific relaxase and a possible TraG-like protein.

The Enterococcus faecalis conjugative plasmids pAD1 and pAM373 encode a mating response to the peptide sex pheromones cAD1 and cAM373 respectively. Sequence determination of both plasmids has recently been completed with strong similarity evident over many of the structural genes related to conjugation. pAD1 has two origins of transfer, with oriT1 being located within the repA determinant, whereas the more efficiently utilized oriT2 is located between orf53 and orf57, two genes found in the present study to be essential for conjugation. We have found a similarly located oriT to be present in pAM373. oriT2 corresponds to about 285 bp based on its ability to facilitate mobilization by pAD1 when ligated to the shuttle vector pAM401; however, it was not mobilized by pAM373. In contrast, a similarly ligated fragment containing the oriT of pAM373 did not facilitate mobilization by pAD1 but was efficiently mobilized by pAM373. The oriT sites of the two plasmids each contained a homologous large inverted repeat (spanning about 140 bp) adjacent to a series of non-homologous short (6 bp) direct repeats. A hybrid construction containing the inverted repeat of pAM373 and direct repeats of pAD1 was mobilized efficiently by pAD1 but not by pAM373, indicating a significantly greater degree of specificity is associated with the direct repeats. Mutational (deletion) analyses of the pAD1 oriT2 inverted repeat structure suggested its importance in facilitating transfer or perhaps ligation of the ends of the newly transferred DNA strand. Analyses showed that Orf57 (to be called TraX) is the relaxase, which was found to induce a specific nick in the large inverted repeat inside oriT; the protein also facilitated site-specific recombination between two oriT2 sites. Orf53 (to be called TraW) exhibits certain structural similarities to TraG-like proteins, although there is little overall homology.

Amino Acid Sequence↗

PubMed1999

Characterization of dihydrofolate reductase genes from trimethoprim-susceptible and trimethoprim-resistant strains of Enterococcus faecalis.

Enterococci are usually susceptible in vitro to trimethoprim; however, high-level resistance (HLR) (MICs, >1,024 microg/ml) has been reported. We studied Enterococcus faecalis DEL, for which the trimethoprim MIC was >1,024 microg/ml. No transfer of resistance was achieved by broth or filter matings. Two different genes that conferred trimethoprim resistance when they were cloned in Escherichia coli (MICs, 128 and >1,024 microg/ml) were studied. One gene that coded for a polypeptide of 165 amino acids (MIC, 128 microg/ml for E. coli) was identical to dfr homologs that we cloned from a trimethoprim-susceptible E. faecalis strain, and it is presumed to be the intrinsic E. faecalis dfr gene (which causes resistance in E. coli when cloned in multiple copies); this gene was designated dfrE. The nucleotide sequence 5' to this dfr gene showed similarity to thymidylate synthetase genes, suggesting that the dfr and thy genes from E. faecalis are located in tandem. The E. faecalis gene that conferred HLR to trimethoprim in E. coli, designated dfrF, codes for a predicted polypeptide of 165 amino acids with 38 to 64% similarity with other dihydrofolate reductases from gram-positive and gram-negative organisms. The nucleotide sequence 5' to dfrF did not show similarity to the thy sequences. A DNA probe for dfrF hybridized under high-stringency conditions only to colony lysates of enterococci for which the trimethoprim MIC was >1,024 microg/ml; there was no hybridization to plasmid DNA from the strain of origin. To confirm that this gene causes trimethoprim resistance in enterococci, we cloned it into the integrative vector pAT113 and electroporated it into RH110 (E. faecalis OG1RF::Tn916DeltaEm) (trimethoprim MIC, 0.5 microg/ml), which resulted in RH110 derivatives for which the trimethoprim MIC was >1, 024 microg/ml. These results indicate that dfrF is an acquired but probably chromosomally located gene which is responsible for in vitro HLR to trimethoprim in E. faecalis.

Amino Acid Sequence↗

PubMed1998

Serological diagnosis of experimental Enterococcus faecalis endocarditis.

A modified rat model of endocarditis with catheterization for 2 days was established in female Lewis rats using different inocula of Enterococcus faecalis (strain no. EF 19) in order to measure IgG antibodies in serum during the course of infection. Increasing the inocula intravenously resulted in an increase in the CFU/g vegetation and the CFU/g spleen, the ID50 being about 10 CFU/ml and the ID90 about 1x10(2) CFU/ml. The lowest bacterial inoculum infecting 100% of the rats was 3x10(3) CFU/ml, and for further investigations we used this inoculum size. Rats were sacrificed on day 2, 5, 7, 9, 11 and 28 after infection. The CFU/g vegetation and the CFU/g spleen increased until day 7 and then decreased. Serum samples were collected from 129 rats at different times after challenge. Three different ELISA systems were established to measure the IgG antibody responses: E. faecalis sonicate ELISA (a pool of four sonicates of strain no. EF 10, EF 11, EF 19 and EF 48), E. faecalis whole cell ELISA (strain no. EF 19) and E. faecalis purified cell wall ELISA (strain no. EF 19). An IgG antibody response was detected already on day 2, and except for a minor decrease on day 6/7 the antibody response continued to increase until day 14 (whole cell ELISA and sonicate ELISA) and day 21 (purified cell wall ELISA) when a plateau was reached. Significant increases in IgG antibody responses (p<0.05) were found between groups of rats from days 0-2, 2-8/9 and 8/9-14 in the E. faecalis whole cell and sonicate ELISAs and from days 0-2, 2-10/11 and 10/11-21 in the E. faecalis purified cell wall ELISA. In conclusion, we established a model of endocarditis in rats with catheterization for 2 days and were able to demonstrate an increase in IgG antibodies during the course of infection.

Animals↗

PubMed2004

Sonicated extract of Enterococcus faecalis induces irreversible cell cycle arrest in phytohemagglutinin-activated human lymphocytes.

The purpose of this study was to examine whether the sonicated extract of Enterococcus faecalis (SEF) alters the cell cycle transition of lymphocytes and thus regulates the fate of the arrested cells. Human lymphocytes were activated by phytohemagglutinin in the presence or absence of SEF, and cell cycle was assessed by flow cytometry. Seventy-two hours after activation with phytohemagglutinin, cells were activated from G0/G1 to S (6.1%) and G2/M (3.8%) phases of the cell cycle. In contrast, pretreatment with SEF resulted in 90.5% of cells remaining in G0/G1, and cell cycle progression to the S and G2/M phases was consequently inhibited. Caspase assay demonstrated that SEF-treated cells exhibited significantly increased apoptosis (56.7%) compared with phytohemagglutinin alone (28.1%). We propose that if this irreversible cell cycle arrest induced by E. faecalis occurs in vivo, it may result in local immunosuppression and contribute to the pathogenesis of endodontic failure. Our findings that E. faecalis can inhibit lymphocyte responses may be of particular relevance to the pathogenesis of endodontic failure. Although the immunologic mechanism involved in the pathogenesis of persistent periapical lesion is not clearly defined, it is reasonable to predict that the altered immune reaction may be linked to the immunosuppressive potential of E. faecalis or other oral bacteria.

Apoptosis↗

PubMed1999

Two-step acquisition of resistance to the teicoplanin-gentamicin combination by VanB-type Enterococcus faecalis in vitro and in experimental endocarditis.

The activity of vancomycin and teicoplanin combined with gentamicin was investigated in vitro against strains of Enterococcus faecalis resistant to vancomycin and susceptible to teicoplanin (VanB type) and against mutants that had acquired resistance to teicoplanin by three different mechanisms. In vitro, gentamicin selected mutants with two- to sixfold increases in the level of resistance to this antibiotic at frequencies of 10(-6) to 10(-7). Teicoplanin selected teicoplanin-resistant mutants at similar frequencies. Both mutations were required to abolish the activity of the gentamicin-teicoplanin combination. As expected, simultaneous acquisition of the two types of mutations was not observed. In therapy with gentamicin or teicoplanin alone, each selected mutants in three of seven rabbits with aortic endocarditis due to VanB-type E. faecalis BM4275. The vancomycin-gentamicin combination selected mutants that were resistant to gentamicin and to the combination. In contrast, the teicoplanin-gentamicin regimen prevented the emergence of mutants resistant to one or both components of the combination. These results suggest that two mutations are also required to suppress the in vivo activity of the teicoplanin-gentamicin combination.

Animals↗

PubMed1996

Brodimoprim synergy against Enterococcus faecalis evaluated in vitro.

Combinations of either brodimoprim or trimethoprim plus either carbenicillin, gentamicin, ciprofloxacin or rifampicin showed synergy at sub-inhibitory concentrations against both Enterococcus faecalis NCTC 5957 and 775. Brodimoprim alone and in combination showed greater antibacterial activity against both strains of E. faecalis than trimethoprim. MBCs of brodimoprim and trimethoprim were 14.4 and 25.6 mg/L for E. faecalis NCTC 5957 and 7.2 and 12.8 mg/L for E. faecalis NCTC 775. Combinations of either brodimoprim or trimethoprim plus the other antibacterial agents, except gentamicin and dibromopropamidine isethionate, were bactericidal at achievable plasma concentrations. Viable count determinations of cultures of both test organisms in the presence of 3/4 of the MIC of each of the four antibiotics and the two antifolates alone and combinations of each antibiotic with either brodimoprim or trimethoprim indicated that only the combinations prevented recovery and regrowth of the cultures over 24 h. The ATP released from cultures of both strains of E. faecalis treated with brodimoprim and trimethoprim at the same concentrations was approximately 1.5 times greater with brodimoprim than with trimethoprim. Combinations of 3/4 of the MIC of each of the antibiotics in combination with 3/4 of the MIC of brodimoprim against cultures of both strains of E. faecalis resulted in greater release of ATP than occurred with equivalent trimethoprim combinations. It is postulated that the increased activities observed with the brodimoprim combinations resulted from an effect of brodimoprim on the bacterial cell permeability control. These results indicate that both brodimoprim and trimethoprim offer potential benefits for use with either carbenicillin, gentamicin, ciprofloxacin or rifampicin for the treatment of E. faecalis infections.

Anti-Bacterial Agents↗

PubMed1992

Evidence of incorporation of the chromosomal beta-lactamase gene of Enterococcus faecalis CH19 into a transposon derived from staphylococci.

We recently reported the chromosomal location of the staphylococcal beta-lactamase gene in four strains of Enterococcus faecalis. Transfer of this gene from strain CH19 to an enterococcal recipient was accompanied by transfer of numerous other antimicrobial resistance determinants in the absence of detectable plasmid DNA. A restriction map developed by comparing digestions of the regions surrounding the beta-lactamase gene in donor and recipient chromosomes resembles published maps of previously described staphylococcal beta-lactamase transposons, particularly in the area of the structural gene and its downstream region. In addition, DNA sequence analysis of the region immediately downstream of the beta-lactamase gene from both CH19 and its transcipient, CX19, revealed the presence of a 121-bp inverted repeat region found in Tn552 and Tn4002, two previously described staphylococcal beta-lactamase transposons. These results suggest that the chromosomal beta-lactamase gene of E. faecalis CH19 is incorporated into a transposonlike element derived from staphylococci.

Base Sequence↗

PubMed1999

Clinical and molecular epidemiology of hospital Enterococcus faecalis isolates in eastern France.

OBJECTIVE: To report on the occurrence of Enterococcus faecalis hospital isolates obtained during 1 year in hospitals in the Franche-Comté region of France. METHODS: Clinical isolates of E. faecalis of different antibiotic susceptibility phenotypes from hospitalized patients were characterized by pulsed-field gel electrophoresis. Patients with positive cultures were investigated by three case-control studies to identify risk factors for colonization/infection. RESULTS: The crude incidence of colonization/infection was 2.37%, and 4-day and 7-day colonization rates after admission were 10.0% and 6.36%, respectively. The rates of high-level resistance to kanamycin (HLKR) and to gentamicin (HLGR) were 47.1% and 7.1%, respectively. No isolate was resistant to glycopeptides or produced beta-lactamase. The 209 hospital isolates obtained during the study yielded 98 major DNA patterns, of which two were major epidemic patterns including HLKR isolates. No single factor was significantly associated with colonization/infection by HLKR isolates. The length of hospitalization before isolation was associated with colonization by HLGR isolates. CONCLUSIONS: The isolation frequency of E. faecalis strains with acquired resistance to aminoglycoside antibiotics, and the wide dissemination of resistant strains with characteristics that allow them to persist and spread, argue for further large prospective surveys of clinical isolates of E. faecalis in hospitals.

Journal Article↗

PubMed2003

Effectiveness of stannous fluoride and calcium hydroxide against Enterococcus faecalis.

The objective of this study was to evaluate the antimicrobial activity of stannous fluoride, calcium hydroxide, or the two in combination against Enterococcus faecalis. Fifteen Mueller-Hinton agar plates were used to conduct a disc diffusion susceptibility test. The plates were inoculated with E. faecalis. The groups tested were: (a) stannous fluoride (Stanimax); (b) calcium hydroxide; and (c) a combination of stannous fluoride and calcium hydroxide. Three filter paper discs, each soaked with one of the groups, were placed along with an antibiotic control (ampicillin) on each agar plate. The plates were then incubated at 37 degrees C. The zones of inhibition were measured at 24 and 48 h. One-way ANOVA revealed a statistically significant difference (p < 0.05) between the three groups. Stannous fluoride displayed the widest zone (1.7 mm), followed by the combination of stannous fluoride and calcium hydroxide (1.1 mm), whereas calcium hydroxide by itself displayed a minimal zone of inhibition (0.05 mm).

Analysis of Variance↗

PubMed2006

Heterologous expression of glycopeptide resistance vanHAX gene clusters from soil bacteria in Enterococcus faecalis.

OBJECTIVES: The aim of the study was to determine whether glycopeptide resistance gene clusters from soil bacteria could be heterologously expressed in Enterococcus faecalis and adapt to the new host following exposure to vancomycin. METHODS: The vanHAX clusters from Paenibacillus thiaminolyticus PT-2B1, Paenibacillus apiarius PA-B2B and Amycolatopsis coloradensis DSM 44225 were separately cloned in an appropriately constructed shuttle vector containing the two-component regulatory system (vanRS) of Tn1546. The complete vanA(PT) operon (vanRSHAXY) from P. thiaminolyticus PT-2B1 was cloned in the same shuttle vector lacking enterococcal vanRS. All plasmid constructs were electroporated into E. faecalis JH2-2 and the MICs of vancomycin and teicoplanin were determined for each recombinant strain before and following exposure to sublethal concentrations of vancomycin. RESULTS: The vanHAX clusters from P. thiaminolyticus and P. apiarius conferred high-level vancomycin resistance (MIC > or = 125 mg/L) in E. faecalis JH2-2. In contrast, cloning of the vanHAX cluster from A. coloradensis did not result in a significant increase of vancomycin resistance (MIC = 0.7 mg/L). Resistance to vancomycin was not observed after cloning the complete vanA(PT) operon from P. thiaminolyticus (MIC = 2 mg/L), but this recombinant rapidly adapted to high concentrations of vancomycin (MIC = 500 mg/L) following exposure to sub-lethal concentrations of this antibiotic. CONCLUSION: The results showed that vanA(PT) in P. thiaminolyticus is a possible ancestor of vanA-mediated glycopeptide resistance in enterococci. Experimental evidence supported the hypothesis that enterococci did not acquire glycopeptide resistance directly from glycopeptide-producing organisms such as A. coloradensis.

Actinomycetales↗

PubMed2000

Modulation of efficacies and pharmacokinetics of antibiotics by granulocyte colony-stimulating factor in neutropenic mice with multidrug-resistant Enterococcus faecalis infection.

It has been demonstrated previously that, in non-neutropenic animals, interferon-gamma markedly enhances the efficacies of gentamicin and vancomycin against Enterococcus faecalis resistant to these antibiotics. The aim of our study was to determining whether granulocyte colony-stimulating factor (G-CSF) can be beneficial as an adjunct to gentamicin and vancomycin in the treatment of the same infection in neutropenic mice. After induction of neutropenia by cyclophosphamide, mice were inoculated ip with the organism. The infected animals received sc administrations of G-CSF, antibiotic or a combination of both agents at determined dosing regimens. Infected animals treated with G-CSF alone showed a dose-dependent increase in survival. The inoculum size used in establishing infection affected the effectiveness of the cytokine. Survival was significantly (P: < 0.01) better in the infected animals given gentamicin and vancomycin plus G-CSF than in those given antibiotics or G-CSF alone. The possibility of pharmacokinetic interaction between G-CSF and each of the antibiotics was examined. The cytokine significantly increased the plasma clearance of gentamicin, with a resultant decrease in the area under the concentration-time curve (AUC), while the disposition of vancomycin was not affected. This study suggests that G-CSF may be a useful adjunct to gentamicin and vancomycin for the treatment of multidrug-resistant E. faecalis infection in neutropenic patients.

Animals↗