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Biomedical subjects

M D Kitzis

Publications and source records attributed to M D Kitzis.

96 records · Page 6Linked to original sources

Penetration of cefoxitin into cerebrospinal fluid of dogs with and without experimental meningitis.

The penetration of cefoxitin into the cerebrospinal fluid (CSF) after slow intravenous infusion of 50-100 mg/kg over 1 hr was studied in normal dogs and in dogs with meningitis experimentally induced by intrathecal injection of 10(9) Staphylococcus aureus. With healthy dogs the peak CSF concentration of 1 microgram of cefoxitin/ml was found to correspond with a serum level of 120 micrograms/ml. With administration of probenecid the CSF level was 1.5 micrograms of cefoxitin/ml. Doubling the dose from 50 to 100 mg/kg resulted in a CSF concentration of 2 micrograms of cefoxitin/ml. In the CSF of animals with meningitis, a peak concentration of 10 micrograms of cefoxitin/ml was obtained 90 min after the start of the infusion, and 5 micrograms/ml was still present at 240 min. The peak level in CSF of animals with meningitis was about 10% of the simultaneous level in serum.

Animals↗

Recovery period and the exposure of bacteria to subminimal inhibitory concentrations of antibiotics.

The minimal antbiotic concentration (MAC) refers to the lowest concentration of drug that results in a detectable effect on bacteria (e.g., inhibition of growth, change in morphology, and delay in recovery to normal growth in drug-free medium). Strains of Escherichia coli and Staphylococcus aureus were subjected to a range of subminimal inhibitory concentrations of four drugs-ampicillin, gentamicin, rosaramicin, and tetracycline. Inhibition curves (percentage of normal growth vs. concentration of drug) were related to the period of recovery before resumption of normal growth, which was chosen to express MAC value. In both E. coli and S. aureus, the longest delay in recovery of normal growth was observed with rosaramicin. Ampicillin resulted in a delay in recovery only with S. aureus.

Ampicillin↗

Plasmid-mediated beta-lactamase (TEM-7) involved in resistance to ceftazidime and aztreonam.

TEM-7, a novel TEM-type beta-lactamase (pI 5.41) encoded on a plasmid of approximately 85 kilobases, was found in a clinical isolate of Citrobacter freundii. Strains containing this enzyme exhibited decreased susceptibility to ceftazidime (64-fold) and aztreonam (16-fold) but not to other third-generation cephalosporins. Addition of a beta-lactamase inhibitor--clavulanic acid, sulbactam, or YTR 830--restored normal susceptibility to associated compounds such as ampicillin, piperacillin, ceftazidime, and aztreonam. DNA-DNA hybridization of an intragenic probe of TEM-1 occurred with a 19-kilobase EcoRI fragment of the plasmid encoding TEM-7. A TEM-2 derivative, TEM-201, with characteristics similar to those of TEM-7 was selected spontaneously in the presence of ceftazidime in vitro.

Aztreonam↗

[Activity of sulbactam and clavulanic acid, alone and combined, on Acinetobacter calcoaceticus].

Sulbactam and clavulanic acid, both beta-lactamase inhibitors, were studied alone or associated on 85 isolates of Acinetobacter calcoaceticus. When sulbactam was tested alone the minimal inhibitory concentration (MIC) was less than 2 micrograms/ml with the carbenicillin-sensitive strains of A. Calcoaceticus and between 8 to 16 micrograms/ml with the carbenicillin-resistant strains. In the presence of clavulanic acid (5 or 10 micrograms/ml) the MIC of sulbactam on all the carbenicillin-resistant strains decreased to less than 4 micrograms/ml.

Acinetobacter↗