Comparative in vitro activity of cefepime (BMY 28142) against multiresistant nosocomial isolates ofPseudomonas aeruginosa

Voutsinas, D.; Mavroudis, Th.; Avlamis, Athina; Giamarellou, Helen

doi:10.1007/bf01963783

Cited by 5 publications

(2 citation statements)

References 12 publications

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“…25 (2) 1993al. 1990Fuchs et al 1986a,b;Giamarellou et al 1987;Kessler et al 1985;Khan et al 1984;King et al 1990;Kropec & Daschner 1989;Masuyoshi et al 1989;Neu et al 1986;Norden & Neiderriter 1987;Rolston et al 1986;Steele et al 1985;Tomatsu et al 1986;Tsuji et al 1985;Van Landuyt et al 1986;Voutsinas et al 1989;Vuye & Pijck 1985). Cefepime has anaerobic activity similar to ceftazidime, and is not active against Bacteroides fragilis or Clostridium dijJicile .…”

Section: Spectrum Of Activitymentioning

confidence: 95%

Cefepime Clinical Pharmacokinetics

Okamoto

Nakahiro

Chin

et al. 1993

Clinical Pharmacokinetics

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Cefepime is a new parenteral cephalosporin with antimicrobial activity similar to third-generation cephalosporins. It acts against the Enterobacteriaceae family, and Pseudomonas aeruginosa, but maintains Gram-positive activity similar to that of first- or second-generation cephalosporins. Cefepime has in vitro activity against many bacterial isolates resistant to ceftazidime and cefotaxime, is stable against chromosomally mediated beta-lactamases, demonstrates lower affinity for these enzymes and shows a high resistance to enzymatic hydrolysis. Clinical uses thus far include treatment of lower respiratory tract, intra-abdominal and urinary tract infections, skin and soft tissue infections and for prophylaxis in biliary tract and prostate surgery. Pharmacokinetic studies indicate that cefepime exhibits linear pharmacokinetic behaviour. Pharmacokinetic variables are not significantly different between single- and multiple-dose administration, indicating a lack of drug accumulation in patients with normal renal function. Cefepime is not highly bound to plasma proteins, with binding values of approximately 16 to 19%. The drug is widely distributed in various biological tissues and fluids. The primary route of elimination is from the kidneys, with over 80% of the drug recovered in the urine as unchanged drug in patients with normal renal function. Total drug clearance and renal clearance are similar to creatinine clearance, and glomerular filtration is thought to be the primary mechanism of renal excretion. The elimination half-life is approximately 2 to 2.5 h in patients. Cefepime is removed by haemodialysis (over 3h) and peritoneal dialysis (over 72h) to an appreciable extent, with 40 to 68% and 26% of the drug removed, respectively. Overall, cefepime is well tolerated by patients and no significant drug interactions have been reported to date.

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Section: Spectrum Of Activitymentioning

confidence: 95%

Cefepime Clinical Pharmacokinetics

Okamoto

Nakahiro

Chin

et al. 1993

Clinical Pharmacokinetics

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“…There are numerous reports describing a high incidence of P. aeruginosa strains resistant to a variety of antimicrobial agents (2,11,15). New quinolones generally show potent antibacterial activities against P. aeruginosa strains (6), but the number of resistant clinical isolates has increased with the wide usage of these drugs in clinical practice (7,9,12).…”

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Occurrence of the nfxB type mutation in clinical isolates of Pseudomonas aeruginosa

Jakics

Iyobe

Hirai

et al. 1992

Antimicrob Agents Chemother

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Seven spontaneous norfloxacin (NFLX)-resistant mutants obtained in vitro from 20 NFIX-susceptible clinical isolates and 3 NFLX-resistant clinical isolates of Pseudomonas aeruginosa were transformed with the pNF111 plasmid, whose BamHIl fragment is responsible for conferring susceptibility to NFLX, by complementing the nfxB mutation. The resulting patterns of MICs of NFLX, i lactams, aminoglycosides, and chloramphenicol and the observed increased accumulation of NFLX were consistent with the occurrence of the nfxB type mutation in these clinical isolates.Because of the increasing number of infections caused by Pseudomonas aeruginosa, the accurate determination of resistance patterns associated with this organism has become an essential step in chemotherapy. There are numerous reports describing a high incidence of P. aeruginosa strains resistant to a variety of antimicrobial agents (2,11,15). New quinolones generally show potent antibacterial activities against P. aeruginosa strains (6), but the number of resistant clinical isolates has increased with the wide usage of these drugs in clinical practice (7,9,12).Bacterial resistance to quinolones is due to chromosomal mutations that involve alterations in DNA gyrase and in the bacterial outer membrane. In P. aeruginosa, several established types of mutations are responsible for norfloxacin (NFLX) resistance. These mutation types, designated nfrA, nfxB, nfxC, and nalB, have been well characterized previously (4, 5, 13).In our preliminary study, the chromosomal localization of the nffxB mutation in clinical isolates of P. aeruginosa was established (5). A wild-type DNA fragment complementing the nfxB mutation was cloned (10). Recently, NFLX-resistant mutants derived from NFLX-susceptible clinical isolates and NFLX-resistant clinical isolates were tested in order to determine whether the observed nfxB resistance phenotype is complementable by using the constructed recombinant plasmid; the results are presented in this paper. P. aeruginosa strains were isolated and characterized by the Clinical

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Combination effect of SCE-2787 and cefepime with aminoglycosides on nosocomial gram-negative bacteria

et al. 1991

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The in vitro activity of cefepime and SCE-2787, two new parenteral cephalosporins, and the combination effect with tobramycin and gentamicin against nosocomial gram-negative rods was studied using checkerboard agar dilution technique. Cefepime showed excellent in-vitro activity against Klebsiella pneumoniae, Enterobacter cloacae, Serratia marcescens and Proteus vulgaris (MIC90 0.03-0.125 mg/l) and good to moderate activity against Acinetobacter anitratus, Pseudomonas aeruginosa and Pseudomonas cepacia (MIC90 4-16 mg/l). SCE-2787 had an excellent activity against Citrobacter spp. (MIC90 0.125 mg/l) and a very good activity against A. anitratus, P. aeruginosa and P. vulgaris (MIC90 1-2 mg/l). Pseudomonas maltophilia was not inhibited at therapeutically achievable concentrations (MIC90 64 mg/l). On average, 14-28% of the strains were inhibited by synergistic SCE-2787 aminoglycoside-combinations, whereas only 8.6% were inhibited by a synergistic effect of the combination with cefepime and gentamicin. No antagonism occurred with any of the combinations.

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Comparative in vitro activity of cefepime (BMY 28142) against multiresistant nosocomial isolates ofPseudomonas aeruginosa

Cited by 5 publications

References 12 publications

Cefepime Clinical Pharmacokinetics

Cefepime Clinical Pharmacokinetics

Occurrence of the nfxB type mutation in clinical isolates of Pseudomonas aeruginosa

Combination effect of SCE-2787 and cefepime with aminoglycosides on nosocomial gram-negative bacteria

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