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At least 1,243 records · Page 69Linked to original sources
PubMed1983

Ceftazidime therapy of infections caused by Enterobacteriaceae and Pseudomonas aeruginosa.

Sixteen patients with serious Gram-negative bacillary infections were treated with intravenous ceftazidime, 2 g every 8 h. The majority of patients had bacteraemia or pneumonitis or both. Ten patients were cured and six improved. Seven of ten patients infected with Pseudomonas aeruginosa were cured, and three improved. No adverse reactions occurred. Four strains of Ps. aeruginosa became resistant to ceftazidime in patients who were cured or improved clinically. Ceftazidime is effective as single drug therapy for serious Gram-negative infections, including those due to Ps. aeruginosa.

Adult↗
PubMed1985

Determination of molecular hydrogen in investigations of the susceptibility of Enterobacteriaceae to ampicillin.

One hundred and five enterobacterial isolates from urinary tract infections were examined for ampicillin-susceptibility by measurement of molecular hydrogen production with a palladium metal oxide semi-conductor (Pd-MOS sensor). Eighty-one per cent of hydrogen producing strains could be placed in the same susceptibility groups as recorded by disc-diffusion tests. However, it was harder to separate susceptible from intermediate types than to determine resistance. In all but five strains the hydrogen production allowed determination of viability within 5 h.

Ampicillin↗
PubMed1985

Inability of gentamicin and fosfomycin to eliminate intracellular Enterobacteriaceae.

The ability of gentamicin and fosfomycin to kill Salmonella typhimurium and Escherichia coli in a HeLa cell culture system was investigated. Antibiotic activity against extracellular, cell membrane-attached and intracellular bacteria were determined. Both gentamicin and fosfomycin had the same low ability to kill intracellular bacteria. The efficacy of fosfomycin against extracellular bacteria was also low, whereas gentamicin rapidly killed such bacteria. These observations show that intracellular enterobacteria are protected from the bactericidal activity of gentamicin and fosfomycin.

Anti-Bacterial Agents↗
PubMed1985

Mezlocillin, ceftizoxime, and amikacin alone and in combination against six Enterobacteriaceae in a neutropenic site in rabbits.

Closed-space, locally neutropaenic infection sites were simulated in rabbits by implanting subcutaneous semipermeable chambers inoculated with 5 X 10(4) cfu/ml of Escherichia coli (one strain), Citrobacter diversus (one strain), Klebsiella pneumoniae (two strains) or Serratia marcescens (two strains). Four hours after inoculation, treatment was begun with amikacin (15 mg/kg), mezlocillin (100 mg/kg), or ceftizoxime (50 mg/kg) alone or in two-drug combinations. Antibiotics were given intramuscularly every 6 h for 16 doses. Chambers were sampled for bacterial counts at the start of therapy, and 20, 44, and 92 h thereafter. Blood and chamber antibiotic levels were determined during the treatment course. In-vivo results were compared to in-vitro tests of inhibition, killing and synergism. Ceftizoxime alone was successful in vivo (greater than 6 log reduction in count) against the three strains of klebsiella and citrobacter, mezlocillin against one serratia strain, and amikacin alone against none of the strains. The best in-vitro correlation was with the minimum inhibitory concentration (MIC) at a high (10(8] inoculum for the beta-lactams and with the anaerobic MIC for amikacin. Among combinations, amikacin plus mezlocillin alone was successful against the three strains of klebsiella and serratia, but neither amikacin nor mezlocillin added to ceftizoxime were more successful than ceftizoxime alone. In-vitro chequerboard synergism was not predictive of in-vivo success. Mezlocillin alone was inactivated in vivo by all the strains except Ser. marcescens, and the E. coli strain inactivated both mezlocillin and ceftizoxime alone and in combination.

Agranulocytosis↗
PubMed1986

Genetic and biochemical basis of resistance of Enterobacteriaceae to beta-lactam antibiotics.

Resistance to beta-lactam drugs is usually determined by genes mediating the production of beta-lactamases. These genes can be located on resistance plasmids or on the chromosome. Resistance to drugs which have been available for many years is mostly transposable. Although the origin of these genes is not known, it is possible to draw a hypothetical flow diagram of the evolution of resistance genes in general. The mechanism of resistance although mediated in Gram-negative bacteria mostly by beta-lactamases cannot be simply described as the hydrolytic function of the enzyme. It is a complex interaction involving the affinity of the drug for the target and the lactamase, the amount of drug in the periplasmic space, the amount of enzyme and the number of lethal target sites. Usually one of these factors is predominant.

Anti-Bacterial Agents↗
PubMed1986

Antibacterial properties of imipenem with special reference to the activity against methicillin-resistant staphylococci, cefotaxime-resistant Enterobacteriaceae and Pseudomonas aeruginosa.

Imipenem was examined with standardized agar dilution procedures against a wide range of bacteria. Geometric mean MICs against the genera Escherichia, Klebsiella, Enterobacter, Citrobacter and Serratia were 0.1-0.4 mg/l, and Proteus and Providencia spp. were inhibited by 0.25-4 mg/l. Acinetobacter calcoaceticus var. anitratum strains were inhibited by concentrations ranging from 0.12-0.5 mg/l. Methicillin-susceptible staphylococci were highly susceptible to the drug (MICs: less than or equal to 0.03 mg/l) and enterococci were inhibited by 0.25-16 mg/l. Most of the multi-resistant JK corynebacteria were resistant to imipenem. Imipenem was more active than any other beta-lactam against methicillin-resistant staphylococci; this was also demonstrated in a population analysis. Imipenem-resistant minorities in populations, however, were also observed. Cefotaxime-resistant and -intermediate Enterobacter and Citrobacter strains were inhibited by concentrations of 0.5 mg/l or less. No third-generation cephalosporin nor any other beta-lactam showed similarly high activity against these groups of organisms. Among 20 ceftazidime-resistant and 20 ceftazidime-susceptible isolates of Pseudomonas aeruginosa, no strain was resistant and only five ceftazidime-resistant strains were intermediately susceptible (MIC, 8 mg/l) to imipenem.

Anti-Bacterial Agents↗
PubMed1991

Phenotypic characterization of quinolone-resistant mutants of Enterobacteriaceae selected from wild type, gyrA type and multiply-resistant (marA) type strains.

The NCTC type strains of Escherichia coli, Enterobacter cloacae, Serratia marcescens and Klebsiella pneumoniae were exposed to 3, 5 and 10 x MIC of nalidixic acid, enoxacin, ciprofloxacin, PD 117596 and PD 127391. From each strain a mutant with a high MIC of quinolones alone (gyrA) and a mutant with intermediate resistance to quinolones, some beta-lactams, chloramphenicol and tetracycline (multiply resistant, m-r) were selected on agar containing antibiotics. The gyrA mutants required a higher concentration of quinolone to inhibit DNA synthesis by 50% but quinolone uptake kinetics and outer membrane profile were the same as the wild type. The m-r mutants had similar DNA synthesis IC50 as the wild type, decreased quinolone uptake kinetics and had decreased expression of an OMP of approximately 40 kD. The gyrA and m-r mutants were then exposed to 3, 5 and 10 x MIC of the same quinolones and new mutants (F2) selected. The F2 mutants from the gyrA mutants displayed a further increase in quinolone MIC; the F2 mutants from the m-r mutants had several phenotypes: high quinolone MICs with cross resistance to other agents, high quinolone resistance alone, or intermediate quinolone resistance alone. Most F2 mutants had MICs above the recommended breakpoint concentrations for quinolones. The F2 mutants often had altered biochemical profiles (API 20E), however, only in the case of E. cloacae did this affect speciation with the strains being identified as Rhanella aquatalis.

Anti-Infective Agents↗
PubMed1991

A comparison of methods used for measuring the accumulation of quinolones by Enterobacteriaceae, Pseudomonas aeruginosa and Staphylococcus aureus.

Accumulation of norfloxacin by Escherichia coli was studied with a range of published procedures that used either radioactively-labelled norfloxacin (14C and 3H) or the natural fluorescence of the quinolone for detection. All methods except bioassay generated comparable data. A method involving the detection of fluorescence was found to be the method of choice. This method was used to study the accumulation kinetics of ciprofloxacin, lomefloxacin, fleroxacin, norfloxacin, and enoxacin by several species of Gram-negative bacteria, and a Staphylococcus aureus strain. Saturation and efflux kinetics were also studied. There was no saturation at a concentration of norfloxacin less than 50 mg/L. Norfloxacin efflux was minimal during the uptake assay as the samples were withdrawn into ice-cold buffer; however, when the cells were sampled into buffer at 37 degrees C, up to 50% of cell-associated quinolone effluxed within 5 min.

Anti-Infective Agents↗