No abstract

The bactericidal action of chloramphenicol against six Haemophilus influenzae type b isolates and six Escherichia coli K-1 isolates was compared. Cells were grown in antibiotic-free medium into the late-stationary and mid-exponential phases of growth, and inocula of 105 to 106 cells per ml were added to fresh media containing 1 or 10 ,ug of chloramphenicol per ml for H. influenzae isolates, 80 MATERIALS AND METHODS Isolates. Six H. influenzae type b strains and six E. coli K-1 strains were isolated from cerebrospinal fluid of infants and neonates, respectively. Isolates were identified by standard techniques (9). Serogrouping was done by a latex agglutination method (11) for H. influenzae and counterimmunoelectrophoresis (6) for E. coli or centrifuged culture supematants after overnight growth in Mueller-Hinton broth (MHB) with or without 3% supplement C (Difco Laboratories) at 37°C and pH 7.2.Chloramphenicol. Ten milligrams of chloramphenicol standard powder (1,000 ,ug/ml) was dissolved in 0.2 ml of sterile ethanol, and 9.8 ml of MHB was added to make a stock solution of 1,000 p.g/ml. Serial dilutions of the stock solution were made in MHB with or without supplement C (3%; Difco) to achieve the final concentrations of chloramphenicol for the MICs, MBCs, and kill curves.Quantitation of bacteria. Quantitation of bacteria was done by evenly spreading 0.1-ml samples from

Thirty-four infants and children ranging in age from 2.5 to 180 months (mean, 40

Three consecutive doses of 75 mg of cefoxitin per kg were given intravenously every 6 h (225 mg/kg), in addition to penicillin or ampicillin, to 24 patients on days 4 and 5 and 9 and 10 of therapy for meningitis. Haemophilus influenzae b was isolated from cerebrospinal fluid (CSF) of 21 patients, Streptococcus pneumoniae from 2 patients, and Neisseria meningitidis from 1 patient. The median minimal inhibitory and bactericidal concentrations of cefoxitin for 16 isolates of H. influenzae b were 0.312 and 0.625 micrograms/ml, respectively. Sixteen of 18 isolates of H. influenzae b and S. pneumoniae were killed by 2.5 micrograms of cefoxitin per ml. Mean levels in CSF peaked at 1 h at 6 and 4.9 micrograms/ml on days 5 and 10, respectively. CSF levels on days 5 and 10 were greater than or equal to twice the median minimal inhibitory and bactericidal concentration in 20 and 18 patients, respectively. However, bacterial levels in CSF were greater than or equal to 2.5 micrograms/ml in only 11 of 23 patients on days 5 and 10. No significant adverse effects were found. These data indicate that at this dosage, cefoxitin may not reach levels in the CSF required for killing all susceptible strains of H. influenzae b and S. pneumoniae.