Modified peptidoglycan transpeptidase activity in a carbenicillin-resistant mutant of Pseudomonas aeruginosa 18s. (1/301)

A carbenicillin-resistant mutant of Pseudomonas aeruginosa 18s was found to possess peptidoglycan transpeptidase activity significantly more resistant to inhibition by benzyl penicillin, ampicillin, carbenicillin, and cephaloridine than that of the parent strain. The mutant was more resistant than the parent strain to all of the beta-lactam antibiotics tested, and 50% inhibition values for these compounds against membrane-bound model transpeptidase activity paralleled this increase. The resistance of the mutant to kanamycin, streptomycin, and chloramphenicol was unchanged.  (+info)

Bacteriologic cure of experimental Pseudomonas keratitis. (2/301)

Two long-term therapy trials with high concentrations of antibiotic were carried out to determine the duration of therapy required to achieve bacteriologic cure of experimental Pseudomonas keratitis in guinea pigs. In the first study, corneas still contained Pseudomonas after 4 days of continual topical therapy with either tobramycin 400 mg/ml, amikacin 250 mg/ml, ticarcillin 400 mg/ml, or carbenicillin 400 mg/ml. In an 11-day trial of topical therapy with tobramycin 20 mg/ml, 34 of 36 corneas grew no Pseudomonas after 6 or more days of therapy. The bacteriologic response to therapy in this model occurred in two phases. About 99.9% or more of the organisms in the cornea were killed in the first 24 hr of therapy. The numbers of bacteria remaining in the cornea declined gradually over the next several days until the corneas were sterile. Optimal antibiotic therapy may include two stages: initial intensive therapy with high concentrations of antibiotic applied frequently to achieve a large rapid decrease in numbers of organisms in the cornea, followed by prolonged, less intensive therapy to eradicate organisms and prevent relapse.  (+info)

Stability of gentamicin in serum. (3/301)

Patients' sera were divided into three portions when the initial gentamicin level was determined and were stored at -20, 4, and 25 degrees C in plastic or glass tubes. Gentamicin levels were repeated after 1 and 2 days of storage at the respective temperatures. There was no significant difference in gentamicin levels among portions, except those from a patient in renal failure with high serum concentrations of carbenicillin.  (+info)

Proposed ticarcillin disk control values for Escherichia coli and Pseudomonas aeruginosa: multicenter cooperative study. (4/301)

In a multicenter cooperative controlled study, individual test, accuracy, and precision control values were determined for 75-mug ticarcillin disks with Escherichia coli ATCC 25922 and Pseudomonas aeruginosa ATCC 27853.  (+info)

An explanation for the apparent host specificity of Pseudomonas plasmid R91 expression. (5/301)

Pseudomonas aeruginosa strain 9169 has been reported to contain a plasmid that expresses resistance to carbenicillin (Cb), kanamycin (Km), and tetracycline (Tc) in Escherichia coli but resistance only to Cb in certain Pseudomonas recipients. The triply resistant plasmid in E. coli belonged to incompatibility (Inc) group P or P-1, whereas the singly resistant plasmid in P. aeruginosa was compatible with IncP-1 plasmids and other plasmids of established Inc specificity but incompatible with plasmid pSR1 that is here used to define a new Pseudomonas Inc group P-10. Additional physical and genetic studies showed that strain 9169 contained not one but two plasmids: IncP-1 plasmid R91a, determining the Cb Km Tc phenotype, and IncP-10 plasmid R91, determining Cb that differed in molecular weight and in EcoRI and BamHI restriction endonuclease recognition sites. Plasmid multiplicity rather than host effects on plasmid gene expression can account for differences in the phenotype of strain 9169 transconjugants to E. coli and P. aeruginosa.  (+info)

Susceptibility of the anaerobic bacteria, group D streptococci, Enterobacteriaceae, and Pseudomonas to semisynthetic penicillins: carbenicillin, piperacillin, and ticarcillin. (6/301)

Sodium piperacillin T-1220, a new semisynthetic penicillin, was tested in vitro against 297 clinical isolates of anaerobic bacteria and 669 aerobic bacteria by the conventional agar dilution method and compared with carbenicillin and ticarcillin. At a 100-mug/ml concentration the three drugs showed comparable effectiveness against the anaerobes tested. However, at 20 mug/ml, piperacillin was the most effective drug against Bacteroides fragilis, peptostreptococci, and group D streptococci. At this drug concentration only 48% of the B. fragilis strains exhibited susceptibility to carbenicillin only, 64% exhibited susceptibility to ticarcillin but 90% exhibited susceptibility to piperacillin. Similar findings were observed with peptostreptococci and group D streptococci. On a weight basis piperacillin was statistically shown to be the most effective antibiotic of the three tested against these anaerobes. At 20 mug/ml, piperacillin exhibited a statistically significant difference (P < 0.01) over carbenicillin and ticarcillin for Serratia marcescens, Escherichia coli, Klebsiella species, Klebsiella pneumoniae, Pseudomonas isolates, and Citrobacter diversus. At both 20- and 100-mug/ml concentrations, piperacillin appeared to be the most effective (calculated P < 0.01) upon Klebsiella species, K. pneumoniae, S. marcescens, and C. freundii in activity over ticarcillin and carbenicillin.  (+info)

BL-P1654: a bacteriostatic penicillin? (7/301)

In tube dilution studies, large discrepancies between inhibitory and bactericidal concentrations of BL-P1654 against Pseudomonas were observed. To explain these discrepancies which were not observed with carbenicillin, the kinetics of bacterial killing by these two penicillins were evaluated and compared. The kinetics of bacterial killing by both antimicrobial agents were characteristic of a penicillin, with killing initiating simultaneously with growth. Kill curves revealed the presence of a small number of cells resistant to BL-P1654 which were not detectable macroscopically. Studies on microbial resistance also showed the presence of a small but consistent number of cells resistant to BL-P1654 over a broad range of concentrations above its minimal inhibitory concentration. This pattern of resistance was not observed with carbenicillin. Thus, the discrepancies between inhibitory and bactericidal concentrations of BL-P1654 were not due to any unusual bacteriostatic activity but rather due to a small number of resistant cells whose presence could be detected only by sensitive subculturing techniques.  (+info)

Mechanism of intestinal absorption of an orally active beta-lactam prodrug: uptake and transport of carindacillin in Caco-2 cells. (8/301)

Absorption characteristics of carindacillin (CIPC) were investigated using Caco-2 cells, and the results were compared with those of its parent drug, carbenicillin (CBPC). Uptake of CBPC was not affected by the metabolic inhibitor or the change in extracellular pH. CBPC appeared to be taken up into Caco-2 cells by passive diffusion. In contrast, the uptake of CIPC was greater at lower extracellular pH and was inhibited in the presence of carbonyl cyanide p-(trifluoromethoxy)phenyl hydrazone, a protonophore. Also, transport of CIPC through Caco-2 cell monolayer was energy and temperature dependent. Moreover, the uptake and transport of CIPC were significantly inhibited in the presence of various monocarboxylic acids, which are the substrates of the monocarboxylic acid transport system(s), whereas the substrates of the oligopeptide transporter had no effect on the uptake or transport of CIPC. These results suggested that the absorption of CIPC may be mediated by the monocarboxylic acid transport system(s), not by the oligopeptide transporter. Furthermore, the uptake and transport of CIPC were approximately 40-fold greater than those of CBPC. Therefore, it is likely that the participation of a carrier-mediated transport in the absorption of CIPC may significantly contribute to the improved absorption of the prodrug over the parent drug.  (+info)

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