In Vitro Activity of Ampicillin or Vancomycin Combined with Gentamicin or Streptomycin Against Enterococci

Harwick, Herbert J.; Kalmanson, George M.; Guze, Lucien B.

doi:10.1128/aac.4.4.383

Cited by 75 publications

(36 citation statements)

References 10 publications

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“…Strains of E. faecalis exhibit low-level resistance to aminoglycosides (3) and to lincomycin and clindamycin (10); they exhibit an intermediate level of resistance to penicillins and cephalosporins (15). In addition, most clinical isolates exhibit tolerance to the bactericidal effects of cell wall-active agents (7,12). Alarming trends in recent years include the emergence of strains with high-level resistance to aminglycosides (11), the appearance of 3-lactamase-producing isolates (14), and the discovery of strains that are resistant to vancomycin (19).…”

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confidence: 99%

Antimicrobial susceptibility changes in Enterococcus faecalis following various penicillin exposure regimens

Hodges

Zighelboim-Daum

Eliopoulos

et al. 1992

Antimicrob Agents Chemother

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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 regimens for penicillin in the treatment of enterococcal infections, when bactericidal synergism cannot be achieved with penicillin-aminoglycoside combinations.

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confidence: 99%

Antimicrobial susceptibility changes in Enterococcus faecalis following various penicillin exposure regimens

Hodges

Zighelboim-Daum

Eliopoulos

et al. 1992

Antimicrob Agents Chemother

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“…Resistance to penicillin killing (in the absence of ,B-lactamase) is a trait that distinguishes enterococci from other streptococci that commonly cause endocarditis, e.g., the viridans group streptococci (8,16). Although several studies have documented the resistance of enterococci to killing by ,f-lactams (11,23) and one previous study found enterococci resistant to killing by vancomycin (6) (14), another study of S. bovis did not reveal defective killing with ,Blactams (11).…”

Section: Discussionmentioning

confidence: 99%

Defective killing of enterococci: a common property of antimicrobial agents acting on the cell wall

Krogstad¹,

Pargwette²

1980

Antimicrob Agents Chemother

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We tested the ability of antimicrobial agents that act on the cell wall to kill enterococci and found defective killing (a minimal bactericidal concentration/ minimal inhibitory concentration ratio of -32) with both ,8-lactams (penicillin G and cephalothin) and non-,B-lactams (vancomycin, cycloserine, and bacitracin We thawed these cultures and subcultured them first on blood agar plates and then on nutrient agar slants (Remel), which were used to inoculate overnight cultures for both the identification and susceptibility studies. These isolates were initially identified as enterococci by growth in 6.5% salt broth and by the hydrolysis of esculin in the presence of 40% bile (4, 11). Subsequent identification was performed by the methods of Facklam (4) and Gross et al. (5).We studied 10 viridans group streptococci and 9 Streptococcus bovis strains that had been isolated from blood cultures during the same time period and stored similarly at -70°C. We also tested four S. bovis isolates kindly provided by Robert C. Moellering, Jr. These strains had been initially identified by alpha hemolysis with negative tests for the hydrolysis of sodium hippurate (1) and esculin (viridans group streptococci) or by the hydrolysis of esculin in the presence of bile and failure to grow in 6.5% salt broth (S. bovis).The group D precipitin reaction was determined with group D antiserum (Difco) by the method of Rantz and Randall (12), with group D antigen (Difco) as a positive control. We used 40-ml overnight cultures in Todd-Hewitt broth (Difco) and lysozyme treatment (5 mg/ml for 4 h at 3700) (21) for bile-esculin-positive strains that failed to react with the group D antiserum after the Rantz and Randall procedure (one S. bovis isolate).We used commercially prepared bile-esculin medium, 6.5% salt broth, arginine decarboxylase medium, and litmus milk (Remel). Potassium tellurite (Difco), 2,3,5-triphenyltetrazolium (Sigma) agar, 2% starch agar, and heart infusion broths for acid production from carbohydrates were prepared by the method of Facklam (4). Carbohydrates tested were D-sorbitol, Dmannitol, D-melibiose, L-arabinose (Sigma), and Dglycerol (Difco). Broth for acid production from sodium pyruvate (Sigma) was prepared as described by Gross et al. (5). Todd-Hewitt broth was used to grow overnight cultures for the identification tests, MuellerHinton broth (Difco) was used to grow the inocula for susceptibility testing, and sheep blood agar plates (Remel) were used to subculture tubes without visible growth in the tube dilution studies of antimicrobial susceptibility.Antimicrobial agents. The antimicrobial agents used were penicillin G (Pfizer), cephalothin (Lilly), vancomycin (Lilly), cycloserine (Sigma), and bacitracin (Sigma

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“…However, with penicillin and aminoglycoside resistance rates increasing vanconiycin is now often used to treat enterococcal infections. VRE were extremely rare before 1988 with just two isolates (MIC greatern than 100 m g/mL) documented in the previous two decades (16,17). In 1988, VRE began to emerge as a clinical concern, with the description of 55 clinical isolates of VRE (seven Enterococcus faecalis and 48 E faecium) (MICs greater than 64 m g/mL) from 22 British patients with renal impairment (18).…”

Section: Discussionmentioning

confidence: 99%

Low Prevalence of VRE Gastrointestinal Colonization of Hospitalized Patients in Manitoba Tertiary Care and Community Hospitals

Zhanel

Harding

Rosser

et al. 2000

Canadian Journal of Infectious Diseases and Medical Microbiolog

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OBJECTIVE:To determine the prevalence of vancomycin-resistant enterococci (VRE) bowel colonization in hospitalized patients in Manitoba who had stool specimens collected for Clostridium difficile toxin and/or culture testing. DESIGN: Two tertiary care and five community hospitals in Winnipeg and three rural Manitoba community hospitals participated in this study. From January 1 to December 31, 1997 stool specimens, one per patient, submitted to hospital microbiology laboratories for C difficile toxin and/or culture testing were screened for VRE on colistin-nalidixic acidvancomycin (6 m g/mL) (CNAV) agar plates. The study was divided into six, eight-week intervals. Stool specimens received in the first two weeks of each eight week interval were screened for VRE. MAIN RESULTS: A total of 1408 stool specimens were submitted over the 48-week study period. Sixty-seven (4.8%) patients with VRE colonization of their lower gastrointestinal tract were identified. Three of the 67 (4.5%) VRE isolates were Enterococcus faecium, with the remaining 64 (95.5%) were Enterococcus gallinarum. The three vancomycin-resistant E faecium (VREF) (from two different Winnipeg hospitals) demonstrated the vanA genotype, and were resistant to vancomycin, teicoplanin and ampicillin. All three VREF isolates also demonstrated high level resistance to both gentamicin and streptomycin but were susceptible to quinuprisitin/dalfopristin and LY333328. CONCLUSION: VRE colonization in hospitalized patients in Manitoba is infrequent and most commonly due to E gallinarum. The prevalence of VREF colonization in the patients studied was 0.2% (three of 1408). Key Words: Manitoba; Prevalence; Vancomycin-resistant enterococciPour le résumé, voir page suivante V ancomycin-resistant Enterococcus faecium (VREF) accounts for up to 65% of E faecium isolates in hospitalized patients across the United States and is endemic in many North American tertiary care institutions (1,2). The management of these infections presents a significant clinical challenge because species of the genus Enterococcus, and in particular E faecium, are frequently resistant to several antimicrobial agents (3). High level penicillin resistance, high level aminoglycoside resistance and most recently vancomycin resistance are emerging as significant concerns in the treatment of enterococcal infections. This has prompted the development and evaluation of new antimicrobial agents such as quinupristin/dalfopristin and LY333328, a glycopeptide, which may offer activity against enterococci resistant to conventional therapy (2).VREF is not endemic in Manitoba hospitals, and infection with VREF is extremely rare (4). However, the prevalence of VREF lower gastrointestinal tract (GIT) carriage, which frequently precedes infection (5,6), is presently unknown for patients hospitalized in Manitoba. To determine whether the lack of VREF endemnicity correlated with an absence of lower GIT colonization, we assessed lower GIT carriage of VREF for patients hospitalized in 10 Manitoba hospitals from January 1...

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In Vitro Activity of Ampicillin or Vancomycin Combined with Gentamicin or Streptomycin Against Enterococci

Cited by 75 publications

References 10 publications

Antimicrobial susceptibility changes in Enterococcus faecalis following various penicillin exposure regimens

Antimicrobial susceptibility changes in Enterococcus faecalis following various penicillin exposure regimens

Defective killing of enterococci: a common property of antimicrobial agents acting on the cell wall

Low Prevalence of VRE Gastrointestinal Colonization of Hospitalized Patients in Manitoba Tertiary Care and Community Hospitals

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