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PubMedDate not supplied

High-level gentamicin-resistant enterococci: in vitro activity of double and triple combinations of antimicrobial drugs.

The ability of double and triple combinations of antimicrobials with different mechanisms of action, such as teicoplanin, meropenem, gentamicin and sparfloxacin, to achieve synergisms was investigated in vitro on some moderate-level gentamicin-resistant (MLGR: 8 < or = MIC < or = 256 mg/l) and high-level gentamicin-resistant (HLGR: MIC > 500 mg/l) enterococci. On MLGR strains, a constant synergistic effect was achieved by a combination of teicoplanin with gentamicin or with meropenem, while generally addition, sometimes close to synergism, was exhibited by gentamicin-meropenem, gentamicin-sparfloxacin and teicoplanin-sparfloxacin associations. Triple combinations of teicoplanin, meropenem and gentamicin, or teicoplanin, sparfloxacin and gentamicin, always showed a remarkable advantage in terms of synergism over double combinations. On HLGR enterococci, the only double association showing an additive effect, sometimes close to synergism, was teicoplanin plus meropenem, while the triple combination of teicoplanin with gentamicin and meropenem always showed a marked synergistic effect. An effect very close to synergism was also shown by the combination of teicoplanin with sparfloxacin and gentamicin.

Anti-Bacterial Agents↗
PubMedDate not supplied

The comparative in vitro activity of clinafloxacin and other antimicrobials against vancomycin-susceptible and vancomycin-resistant enterococci.

The susceptibilities of 50 unique vancomycin-susceptible (n = 15) and vancomycin-resistant (n = 35) enterococci to 6 antimicrobials were compared. Teicoplanin was consistently the most active agent for all strains. Ampicillin and imipenem were active primarily for vancomycin-sensitive Enterococcus faecalis. Clinafloxacin and ciprofloxacin showed poorer activity compared to prior studies, suggesting that the emergence of quinolone resistance is now occurring in enterococci.

Ampicillin↗
PubMed1978

Plasmid-mediated resistance to antibiotic synergism in enterococci.

Mating experiments have shown that high-level resistance (minimal inhibitory concentration greater than 2,000 microgram/ml) to streptomycin and kanamycin, and resistance to penicillin-streptomycin and penicillin-kanamycin synergism are transferable by conjugation from resistant clinical isolates of enterococci to a sensitive recipient strain. Cesium chloride-ethidium bromide ultracentrifugation revealed a satellite (plasmid) band in resistant clinical isolates and the transconjugant strains but not in the sensitive recipient. Examination of these satellite bands by agarose gel electrophoresis and electron microscopy demonstrated a common plasmid with a weight of 45 megadaltons. Novobiocin treatment of a resistant clinical isolate produced simultaneous loss of high-level resistance to streptomycin and kanamycin, and of resistance to penicillin-aminoglycoside synergism. These results suggest that (a) high-level resistance to streptomycin and kanamycin among some clinical isolates of enterococci is associated with a 45 megadalton plasmid, and (b) the same plasmid is also responsible for the resistance to penicillin-aminoglycoside synergism observed in these strains.

Aminoglycosides↗
PubMed2005

Pathogenesis of implant infections by enterococci.

Enterococci are commensals of human and animal intestinal tract that have emerged in the last decades as a major cause of nosocomial infections of bloodstream, urinary tract and in infected surgical sites. Enterococcus faecalis is responsible for ca. 80% of all enterococcal infections while Enterococcus faecium accounts for most of the others; among the most relevant risk factors for development of enterococcal infections is the presence of implanted devices. The pathogenesis of such infections is poorly understood, but several virulence factors have been proposed. Among them, the ability to form biofilm has recently been shown to be one of the most prominent features of this microorganism, allowing colonization of inert and biological surfaces, while protecting against antimicrobial substances, and mediating adhesion and invasion of host cells and survival within professional phagocytes. Biofilm formation has been shown to be particularly important in the development of prosthetic valve enterococcal endocarditis and stent occlusion. Enterococci are also able to express other surface factors that may support colonization of both inert and biological surfaces, and that may be involved in the invasion of, and survival within, the host cell.

Biofilms↗
PubMed1996

Vancomycin-resistant enterococci.

OBJECTIVE: To review vancomycin resistance in enterococci (Enterococcus faecalis and Enterococcus faecium) with respect to history, epidemiology, mechanism of resistance, and management. DATA SOURCES: A MEDLINE, IDIS, and current journal search of English-language articles on vancomycin-resistant enterococci (VRE) published between 1982 and 1994 was conducted. STUDY SELECTION: Studies and reports pertaining to vancomycin-resistant E. faecalis and E. faecium were evaluated. Case reports, cohort, epidemiologic, in vitro and in vivo studies were evaluated. DATA EXTRACTION: Reports in which vancomycin minimum inhibitory concentrations were 32 micrograms/mL or more were evaluated. DATA SYNTHESIS: Large outbreaks of VRE infection have occurred as a result of nosocomial spread. Such outbreaks have required intensive infection control procedures to limit the spread of VRE. Vancomycin resistance in E. faecalis and E. faecium has been subdivided into phenotypes, VanA and VanB. The mechanism of vancomycin resistance is caused by the production of depsipeptide D-Ala-D-Lac, which replaces D-Ala-D-Ala in the peptidoglycan pathway, thereby preventing the binding of vancomycin to D-Ala-D-Ala in the peptidoglycan cell wall. The vanA gene is associated with a transpositional element (Tn1546) that can be transferred via conjugation while most data suggest that vanB has an endogenous origin. Education, aggressive infection control practices. surveillance programs, and appropriate use of vancomycin are necessary to respond to the VRE problem. CONCLUSIONS: The prevalence of VRE has increased significantly in recent years and has become a worldwide problem. Several factors, such as prior exposure to vancomycin and antibotics (e.g., cephalosporins, antianaerobic agents), physical location in the hospital, immunosuppression, prolonged hospital stay, and VRE gastrointestinal colonization are associated with VRE infection and colonization. Antibiotic treatment of serious VRE infection depends on the phenotype. Optimal treatment of the VanA phenotype is unknown; the VanB phenotype may be treated with teicoplanin and an aminoglycoside.

Animals↗
PubMed2006

Systemic inflammatory response syndrome in adult patients with nosocomial bloodstream infections due to enterococci.

BACKGROUND: Enterococci are the third leading cause of nosocomial bloodstream infection (BSI). Vancomycin resistant enterococci are common and provide treatment challenges; however questions remain about VRE's pathogenicity and its direct clinical impact. This study analyzed the inflammatory response of Enterococcal BSI, contrasting infections from vancomycin-resistant and vancomycin-susceptible isolates. METHODS: We performed a historical cohort study on 50 adults with enterococcal BSI to evaluate the associated systemic inflammatory response syndrome (SIRS) and mortality. We examined SIRS scores 2 days prior through 14 days after the first positive blood culture. Vancomycin resistant (n = 17) and susceptible infections (n = 33) were compared. Variables significant in univariate analysis were entered into a logistic regression model to determine the affect on mortality. RESULTS: 60% of BSI were caused by E. faecalis and 34% by E. faecium. 34% of the isolates were vancomycin resistant. Mean APACHE II (A2) score on the day of BSI was 16. Appropriate antimicrobials were begun within 24 hours in 52%. Septic shock occurred in 62% and severe sepsis in an additional 18%. Incidence of organ failure was as follows: respiratory 42%, renal 48%, hematologic 44%, hepatic 26%. Crude mortality was 48%. Progression to septic shock was associated with death (OR 14.9, p < .001). There was no difference in A2 scores on days -2, -1 and 0 between the VRE and VSE groups. Maximal SIR (severe sepsis, septic shock or death) was seen on day 2 for VSE BSI vs. day 8 for VRE. No significant difference was noted in the incidence of organ failure, 7-day or overall mortality between the two groups. Univariate analysis revealed that AP2>18 at BSI onset, and respiratory, cardiovascular, renal, hematologic and hepatic failure were associated with death, but time to appropriate therapy >24 hours, age, and infection due to VRE were not. Multivariate analysis revealed that hematologic (OR 8.4, p = .025) and cardiovascular failure (OR 7.5, p = 032) independently predicted death. CONCLUSION: In patients with enterococcal BSI, (1) the incidence of septic shock and organ failure is high, (2) patients with VRE BSI are not more acutely ill prior to infection than those with VSE BSI, and (3) the development of hematologic or cardiovascular failure independently predicts death.

Adult↗
PubMed2006

Synergistic effect of [10]-gingerol and aminoglycosides against vancomycin-resistant enterococci (VRE).

An extract from ginger (root of Zingiber officinale) reduced the minimum inhibitory concentrations (MICs) of aminoglycosides in vancomycin-resistant enterococci (VRE). The effective compound was isolated and identified as [10]-gingerol. In the presence of [10]-gingerol at 1/10 concentration of its own MIC, the MIC of arbekacin was lowered by 1/32 to 1/16. [10]-Gingerol also reduced the MICs of other aminoglycosides, and of bacitracin and polymixin B, but not of other antimicrobial agents tested. Because [10]-gingerol reduced the MICs of several aminoglycosides both in strains possessing or lacking aminoglycoside-modification enzymes, it seems that the effect of [10]-gingerol is not related to these enzymes, which mainly confer bacterial resistance against aminoglycosides. It seemed that a detergent-like effect of [10]-gingerol potentiated the antimicrobial activity of the aminoglycosides. In fact, some detergents such as sodium dodecyl sulfate (SDS) and Triton X-100 reduced the MICs of aminoglycosides, bacitracin and polymixin B in VRE. Since the intrinsic resistance to aminoglycosides in enterococci is due to low level of entry of the drugs into the cells, increase in the membrane permeability caused by [10]-gingerol will enhance the influx of aminoglycosides into enterococcal cells.

Acetyltransferases↗
PubMed2002

In vitro assessment of urinary isolates of ampicillin-resistant enterococci.

OBJECTIVE: Susceptibility and minimum inhibitory concentration (MIC) studies of ampicillin-resistant enterococci (ARE) were performed with vancomycin, ciprofloxacin, and trovafloxacin. Ampicillin MICs were determined to make comparisons with achievable urinary concentrations of ampicillin. DESIGN: From July 1998 to April 1999, all enterococci isolated from urinary specimens were tested for susceptibility to ampicillin by disk diffusion. For all ARE, vancomycin, ciprofloxacin, and trovafloxacin susceptibilities were determined by use of either disk diffusion or the E-test. Ampicillin MICs were determined for these isolates by liquid agar microdilution testing. ARE were identified to the species level on the basis of biochemical reactions. SETTING: The study was performed at a university-affiliated tertiary care hospital. OUTCOME MEASURES: In vitro susceptibility studies and MIC determinations were performed in accordance with the National Committee for Clinical Laboratory Standards. RESULTS: A total of 310 urine samples were culture positive for enterococcus. Thirty (9.7%) unduplicated isolates were resistant to ampicillin. Of these, nine ARE isolates (30%) were also vancomycin resistant, whereas only 2 ampicillin-susceptible isolates were vancomycin resistant (p < 0.05). All ARE were resistant to ciprofloxacin, and 29 (96.7%) were resistant to trovafloxacin. Nine (30%), 18 (60%), and 3 (10%) isolates had an ampicillin MIC of 128, 256, and 512 micrograms/mL, respectively. Ampicillin MICs did not differ significantly between vancomycin-susceptible and -resistant isolates (p = 0.963). Twenty-seven isolates (90%) were identified as Enterococcus faecium; the other 3 were either Enterococcus avium or Enterococcus raffinosus. CONCLUSIONS: Ampicillin resistance is associated with resistance to vancomycin. Most ARE are resistant to fluoroquinolone antibiotics such as ciprofloxacin and trovafloxacin. Ampicillin MICs for ARE found in these urinary specimens were all within 1 dilution of 256 micrograms/mL, a concentration achievable in the urine with higher doses of oral amoxicillin or intravenous ampicillin. Additional studies are needed to assess the clinical implications of these data.

Adult↗
PubMed2004

Susceptibility patterns of enterococci causing infections.

Enterococci are among the common organisms associated with hospital-acquired infections. We examined in vitro activities of different antibiotics to 103 enterococcal isolates. Minimal inhibitory concentrations (MICs) of penicillin G, ampicillin, gentamicin, ciprofloxacin, ofloxacin, levofloxacin, grepafloxacin, trovafloxacin and gemifloxacin were determined by broth microdilution testing method. Among the isolates 71 (69%) were identified as E. faecalis and 32 (31%) as E. faecium. While over 75% of E. faecium isolates were resistant to penicillin and ampicillin, approximately 25% of E. faecalis isolates were resistant to penicillin and ampicillin. None of the E. faecalis and E. faecium isolates were resistant to vancomycin. While 17 (52%) of E. faecium isolates exhibited high-level gentamicin resistance (HLGR), high level streptomycin resistance (HLSR) was detected in 24 (74%) of the isolates. In contrast, HLGR and HLSR rates for E. faecalis were 14 (20%) and 22 (31%), respectively. Both HLGR and HLSR were detected with higher frequency in ampicillin resistant isolates. Among fluoroquinolones, gemifloxacin and trovafloxacin were the most potent antibiotics tested. There was no increase in MIC90 values of the fluoroquinolones in ampicillin resistant isolates in comparison with ampicillin susceptible isolates. Our data suggest newer fluoroquinolones would be good alternative agents to use especially for combination drug therapy where enterococci with ampicillin resistance and HLAR are prevalent.

Anti-Bacterial Agents↗
PubMedDate not supplied

Genetic relatedness of high-level aminoglycoside-resistant enterococci isolated from poultry carcasses.

Approximately 46% (75/162) or poultry enterococci collected between 1999 and 2000 exhibited high-level resistance to gentamicin (minimum inhibitory concentration [MIC] > or = 500 microg/ml), kanamycin (MIC > or = 500 microg/ml), or streptomycin (MIC > or = 1000 microg/ml). Forty-one percent of the isolates were resistant to kanamycin (n = 67), whereas 23% and 19% were resistant to genramicin (n = 37) and streptomycin (n = 31), respectively. The predominant species identified was Enterococcus faecium (n = 105), followed by Enterococcus faecalis (n = 40) and Enterococcus durans (n = 8). Using polymerase chain reaction, the isolates were examined for the presence of 10 aminoglycoside resistance genes [ant(6)-Ia, ant(9)-Ia, ant(4')-Ia, aph(3')-IIIa, aph(2")-Ib, aph(2")-Ic, aph(2")-Id, aac(6')-Ie-aph(2")-Ia, and aac(6')-Ii]. Five aminoglycoside resistance genes were detected, most frequently aac(6')-Ii and ant(6)-Ia from E. faecium. Seven E. faecalis isolates resistant to gentamicin, kanamycin, or streptomycin were negative for all genes tested, indicating that additional resistance genes may exist. Phylogenetic analysis revealed that the isolates were genetically different with little clonality. These data indicate that enterococci from poultry are diverse and contain potentially unidentified aminoglycoside resistance genes.

Aminoglycosides↗
PubMed1996

Emerging resistance to antimicrobial agents in gram-positive bacteria. Enterococci, staphylococci and nonpneumococcal streptococci.

Staphylococci (Staphylococcus aureus and coagulase-negative Staphylococcus species) and enterococci are the aetiological organisms in 47 to 52% of nosocomial blood stream infections and approximately 30% of all nosocomial infections in the US. In European intensive care units, almost half of all infections are attributed to staphylococci. The streptococci have also become increasingly important because of the modified virulence of Streptococcus pyogenes strains, and the emerging role of the viridans group streptococci as a cause of potentially fatal bacteraemia in the neutropenic host. Resistance to available antimicrobial agents is increasing and includes, in particular, resistance to the glycopeptides (vancomycin and teicoplanin) amongst enterococci, resistance to penicillinase-resistant penicillins (oxacillin and methicillin) and fluoroquinolones (ciprofloxacin and ofloxacin) amongst staphylococci, and resistance to penicillin and some other beta-lactams amongst viridans group streptococci. New compounds for effective therapy of infection with antimicrobial-resistant Gram-positive species are needed urgently. To this end, the streptogramin combinations [quinupristin/dalfopristin (RP 59500; Synercid)], everninomycin derivatives (SCH 27899), oxazolidinones (U-100572, U-100766) and several newer fluoroquinolones (clinafloxacin, DU 6859a, grepafloxacin, levofloxacin, sparfloxacin, trovafloxacin) are under rapid development and clinical investigation.

Cross Infection↗
PubMed1991

Enterococci in milk and milk products.

Enterococci are widely distributed in nature. They gain entry into milk and milk products through the water supply, equipment, and insanitary and unhygienic conditions of production and handling. They have been incriminated as direct or indirect agents of disease. The evidence concerning their involvement is only circumstantial. These reports are also disputed as the disease symptoms have not been experimentally induced in animal models. However, there is sufficient evidence to indicate that prolific growth of enterococci in foods may lead to formation of clinically significant levels of pressor amines. These amines are very thermostable and therefore remain active even after heat processing, which eliminates all viable streptococci. These pressor amines may be involved in the onset of migraine attacks and produce hypersensitive crises in psychiatric patients who are being treated with monoamine oxidase inhibitors for depression.

Amines↗
PubMed1986

Enterocin typing of enterococci isolated from dried infant foods.

One hundred and fifty enterococcal isolates recovered from 16 market samples of infant foods and 35 from other sources were characterized and subjected to enterocin typing with 18 indicator strains. Among 150 enterococcal isolates, 114 (76%) were able to be typed by the indicator strains. Although 24 enterocin patterns were observed with these enterococci, the most prevalent types were X-9, 224, and 65-603. Occurrence of pattern X-9 either singly or in combination with many other types was most frequent. Many of the enterocin patterns in enterococcal isolates were recovered from samples of dairy water supply and hand washings of personnel working in a dairy plant that manufactured infant food; this suggests the possibility of these as sources of contamination. Enterocin typing of enterococci could prove useful in epidemiological studies.

Animals↗
PubMed2004

Nosocomial infection with vancomycin-dependent enterococci.

We report three patients infected with unique strains of vancomycin-dependent enterococci. Two were first infected by genetically identical strains of vancomycin-resistant enterococci (VRE). All three patients had much greater exposure to vancomycin and third-generation cephalosporins than did two control groups (patients infected with VRE and hospitalized patients without enterococcal infections). While antimicrobial pressure promotes nosocomial colonization by VRE, prolonged exposure to vancomycin may foster the transition from vancomycin resistance to dependence.

Anti-Bacterial Agents↗
PubMed2005

Prevalence and molecular epidemiology of vancomycin-resistant enterococci (VRE) strains isolated from animals and humans in Korea.

BACKGROUND: To assess the possibility of VRE transmission from animals to humans, we studied the prevalence of vancomycin-resistant enterococci (VRE) in farm animals, raw chicken meat, and healthy people. We then determined the molecular relatedness of VRE isolates between animals and humans in Korea. METHODS: We aimed to isolate VRE from 150 enterococci specimens of farm animals, 15 raw chicken meat samples, and stools from 200 healthy people. Species differentiation was done with conventional biochemical tests. Vancomycin resistance genotyping was done by polymerase chain reaction (PCR). Using the agar dilution method, antimicrobial susceptibility was tested for 8 antimicrobials and pulsed-field gel electrophoresis (PFGE) was done to evaluate the molecular relatedness of VRE isolates. RESULTS: The prevalence of VRE was 14.7% (22/150) in farm animal specimens, 1% (2/200) in healthy people, and 60% (9/15) in raw chicken meat. Of 22 animal VRE isolates, 1 vanA E. faecium, 15 vanC1 E. gallinarum, and 6 vanC2 E. casseliflavus were identified. All of the 9 VRE from raw chicken meat and all of the 20 clinical VRE strains were vanA E. faecium. However, in healthy people, only 2 vanC2 E. casseliflavus were isolated. These showed low-level resistance to vancomycin and susceptibility to teicoplanin. However, 9 VRE strains from raw chicken meat had high-level resistance to vancomycin (MIC(50,90): >128 microg/mL), teicoplanin (MIC(50,90): >128 microg/mL), ampicillin (MIC(50,90): >128 nicrog/mL), erythromycin (MIC(50.90): >128 microg/mL), and tetracycline (MIC(50/90): 128/>128 microg/mL). CONCLUSION: This study demonstrated little evidence of VRE colonization in healthy people despite high recovery of VRE among raw chicken meat. It is suggested that there is little evidence of VRE transmission from animals to healthy people. However, we assumed that there exists the possibility of VRE contamination during the processing of chicken meat.

Animals↗
PubMed2006

Vancomycin-resistant enterococci: colonization, infection, detection, and treatment.

Vancomycin-resistant enterococci (VRE) are becoming a major concern in medical practice. Their increased prevalence and their ability to transfer vancomycin resistance to other bacteria (including methicillin-resistant Staphylococcus aureus) have made them a subject of close scrutiny and intense investigation. Colonization is usually acquired by susceptible hosts in an environment with a high rate of patient colonization with VRE (eg, intensive care units, oncology units). Vancomycin-resistant enterococci can survive in the environment for prolonged periods (>1 week), can contaminate almost any surface, and can be passed from one patient to another by health care workers. Whether VRE colonization leads to infection depends on the health status of the patient. Whereas immunocompetent patients colonized with VRE are at low risk for infection, weakened hosts (patients with hematologic disorders, transplant recipients, or severely ill patients) have an increased likelihood of developing infection following colonization. Quinupristin-dalfopristin and linezolid are among the anti-infective agents that have recently become available to treat infection caused by VRE. Other antimicrobials are currently under development. Molecular techniques such as polymerase chain reaction and standard culture studies are being used to detect VRE colonization, infection, and outbreaks.

Colony Count, Microbial↗
PubMed2004

Occurrence and behavior of Enterobacteriaceae and enterococci in mediterranean dry sausages during ripening in a Pilot-Scale chamber.

The occurrence and evolution of Enterobacteriaceae, coliforms, Escherichia coli, and enterococci in 252 samples of six types of Mediterranean dry-ripened sausages during maturation was investigated. The changes of the pH values were also recorded. Samples were analyzed in three steps of the ripening process: fresh product, first drying stage, and finished product. In all six sausages, Enterobacteriaceae, coliforms, and E. coli counts were characterized by high initial concentrations that significantly decreased during ripening. However, the initial counts of enterococci remained stable throughout the experiments in all sausages types. The average pH values of finished sausages ranged from 4.54 to 5.31.

Animals↗
PubMed2005

Contribution of enterococci to the spread of antibiotic resistance in the production chain of swine meat commodities.

Thirty-six samples, including fecal specimens, dry feedstuffs, raw and processed pork meat products, and dry fermented sausages, were collected from two production chains of swine meat commodities and analyzed for the presence of 11 antibiotic resistance (AR) genes. Specific PCR assays carried out on DNA extracted directly from the samples revealed a high incidence of the genes tet(K) (80.5%), ermB (66.7%), and tet(M) (66.7%). Feces and feedstuffs gave the largest number of positive amplifications. To elucidate the contribution of enterococci to the occurrence and spread of AR, 146 resistant enterococci were isolated, and their identity, genetic fingerprints, and AR gene profiles were determined by means of molecular techniques. Enterococcus faecalis and Enterococcus faecium were the predominant isolated species (43.8 and 38.4%, respectively); Other Enterococcus species identified were E. durans (8.9%), E. hirae (2.7%), E. gallinarum (2.1%), E. mundtii (2.1%), and E. casseliflavus (2.1%). A number of isolates displayed a complex AR gene profile comprising up to four different resistance determinants. The genes tet(M) and ermB were highly diffused, being present in 86.9 and 84.9%, respectively, of the isolates. The application of amplified fragment length polymorphism fingerprinting was particularly valuable to monitor the resistant enterococcal isolates along the production chain and to individuate steps in which contamination might occur. In fact, isolates of E. faecalis and E. faecium showing the same amplified fragment length polymorphism profile and AR gene pattern were detected in samples taken at different steps of the food chain suggesting three cases of bacterial clonal spread.

Animals↗