PubMed · 1726204
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R N Jones. 1991. Microbiological conclusions.. https://doi.org/10.2165/00003495-199100423-00006
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Previous reports documenting the essentially identical spectra of activity of ceftizoxime, cefotaxime, and ceftriaxone prompted our hospital formulary committee to replace the latter two drugs with ceftizoxime on the basis of cost differences. However, we subsequently observed that every one of 60 isolates of Streptococcus pneumoniae tested was less susceptible to ceftizoxime than to either cefotaxime or ceftriaxone. The difference between minimal inhibitory concentrations (MICs) was greatest for strains moderately or fully resistant to penicillin, which at our institution represent approximately 32% of all isolates of S. pneumoniae. Ten isolates with cefotaxime and ceftriaxone MICs of 2.0-6.0 micrograms/mL had ceftizoxime MICs of > or = 256 micrograms/mL. Time-kill kinetic studies assessing bactericidal activity confirmed the diminished activity of ceftizoxime against penicillin-resistant isolates of S. pneumoniae. Ceftizoxime should not be used to treat proven or suspected pneumococcal infection in areas where resistance to penicillin is prevalent.
The presence of human granulocytes and monocytes increased the activity of cefetamet against non-ingested Staphylococcus aureus. During ingestion of S. aureus by granulocytes, the activity of cefetamet was equal to that found in the absence of cells. Enhanced activity of cefetamet 30 mg/L was observed during ingestion of S. aureus by monocytes. The effect of cefetamet on S. aureus ingested by granulocytes was much less than that on bacteria in a liquid medium, the maximum growth inhibition (ERmax) being 0.15 and 0.90 log/h, respectively. The concentration at which 50% of the maximum effect was achieved (EC50) was 19.7 mg/L under both conditions. Cefetamet was also more active against S. aureus ingested by monocytes than against bacteria in medium (ERmax 0.97 and 0.77 log/h, respectively). The EC50 under both conditions was 9.7 mg/L. The granulocyte-associated concentration of cefetamet was about on third of that in medium, whereas the monocyte-associated concentration was about two thirds of that in medium. The low intracellular activity of cefetamet against S. aureus ingested by granulocytes is explained primarily by the minimal intracellular growth of bacteria.
A selective HPLC method is described for the determination of cefpodoxime levels in plasma and sinus mucosa. Sample preparation included solid-phase extraction with a C8 cartridge. Cefpodoxime and cefaclor (internal standard) were eluted with methanol and analyzed on an optimised system consisting of a C18 stationary phase and a ternary mobile phase (0.05 M acetate buffer pH 3.8-methanol-acetonitrile, 87:103, v/v) monitored at 235 nm. Linearity and both between- and within-day reproducibility were assessed for plasma and sinus mucosa samples. Inter-assay coefficients of variation were lower than 13.6% (n = 10) for plasma (0.2 micrograms/ml) and lower than 12.4% (n = 5) for sinus mucosa (0.25 micrograms/g). The quantification limit was 0.05 micrograms/ml for plasma and 0.13 micrograms/g for tissue. The method was used to study the diffusion of cefpodoxime in sinus mucosa.