Search

To compare the efficacy and safety of meropenem with cefotaxime for the treatment of infants and children with bacterial meningitis.Infants and children with strongly suspected or documented bacterial meningitis were randomly assigned in a prospective multicenter study to receive either meropenem or cefotaxime. Patients were assessed at the end of therapy and at 5 to 7 weeks and 5 to 7 months after the end of treatment for the presence of neurologic and sensory neural sequelae.A total of 258 children were randomized to either treatment group. A further 8 patients with suspected pneumococcal meningitis were treated with meropenem without randomization. Of the randomized patients 154 were fully evaluable, 79 in the meropenem group and 75 in the cefotaxime group. At the end of treatment there were no significant differences in clinical outcome between the two treatment groups. Clinical cure with or without sequelae was achieved in 97 and 96% of the meropenem- and cefotaxime-treated patients, respectively. At the end of treatment and at 5 to 7 weeks, 46 and 54% of meropenem patients were cured with no sequelae, respectively. Corresponding results for cefotaxime patients were 56 and 58%. All pathogens were eradicated. In total 37 patients had seizures during treatment, 15 (12%) in the meropenem and 22 (17%) in the cefotaxime group. None of the seizures was considered to be drug-related.This trial shows that meropenem is suitable therapy for bacterial meningitis in infants and children and that it offers an efficacy and safety profile similar to that of cefotaxime.

Three Carcinoembryonic Antigen (CEA) gene family members: CEA, Non-specific cross-reactive antigen 50/90 (NCA) and biliary glycoprotein (BGP) were expressed in the colon carcinoma cell lines LS174T and HT29. The CEA, NCA50/90 and four alternatively spliced BGP transcripts (BGP a-d) were identified. The molecular weights of the mature glycoproteins were: CEA, 180kD; NCA50/90, 70-100 kD; BGP, 85, 120 and 140 kD. Pulse chase experiments demonstrated that CEA first appears as a 165 kD high mannose precursor which is trimmed to a 160 kD intermediate and finally transformed into the mature 180 kD glycoprotein. The precursor form of NCA had a molecular weight of 50 kD. CEA and NCA50/90, but not BGP, were linked to the cell membrane via glycosyl phosphatidyl inositol and could be released from the intact tumor cells by glycosyl phosphatidyl inositol-specific phospholipase C. CEA on isolated membranes and in cell lysates, but not on intact cells, was also cleaved by fresh human serum or purified glycosyl phosphatidyl inositol-specific phospholipase D.

Between August 1977 and January 1979, 16 children (7 males and 9 females) ranging in age from 5 to 38 months (mean age 18 months) were treated with trimethoprim-sulfamethoxazole (TMP-SMX) (40 mg/kg SMX per 24 hours) for otitis media caused by beta-lactamase strains of ampicillin-resistant Haemophilus influenzae. Fourteen patients had failed after antecedent ten-day courses of ampicillin (9 patients) or amoxicillin (5 patients) therapy. The remaining two patients received only five days of ampicillin before changing to TMP-SMX. Six of the isolates were nontypable, 3 were type B, 5 isolates were Haemophilus parainfluenzae, and 2 strains were unavailable for typing. Of 13 strains tested, 10 had a minimal inhibitory concentration (MIC) in excess of 3.12 microgram/ml of ampicillin; the remaining 3 had an MIC of3.12 microgram/ml. All 13 isolates were susceptible to 0.19 microgram/ml TMP-SMX. Five of 16 children were symptomatic (irritable; fever of38.2 C); within three days of starting TMP-SMX treatment, they became asymptomatic. Fifteen of 16 patients (93%) responded favorably after ten days of TMP-SMX. Only one patient had H influenzae resistant to ampicillin (12.5 microgram/ml) and sensitive to TMP-SMX (0.19 microgram/ml) isolated from the middle ear at the end of ten days of TMP-SMX. At the end of TMP-SMX therapy, middle ear effusions were noted in ten patients; the fluid was sterile in the four patients who had a second tympanocentesis. There were two recurrences within one month of TMP-SMX therapy. No adverse clinical reactions were noted.

Infusions of 50 mg of sulbactam per kg per day and 400 mg of ampicillin per kg per day in divided doses to infants and children with bacterial meningitis produced levels in cerebrospinal fluid approximately one-third those in serum. Concentrations in cerebrospinal fluid of 5.5 micrograms of sulbactam per ml and 16.0 micrograms of ampicillin per ml declined within a few days of therapy to 1.9 microgram of sulbactam per ml and 5.2 micrograms of ampicillin per ml.

It is generally believed that Haemophilus influenzae is not commonly a causative agent of otitis media in children older than 5 years of age. We recently studied cases of 58 children, aged from 5 to 9 years, who had acute otitis media. Haemophilus species were the causative agents in 36% of cases. This high incidence of Haemophilus isolation from the middle ear exudate of these children has important therapeutic implications; antibiotics effective against H influenzae should be employed when dealing with otitis media in this older age group.

The MICs for 41 Neisseria gonorrhoeae strains from patients receiving spectinomycin treatment were determined by the agar dilution method and compared with the zones of inhibition produced by disks containing 100 micrograms of spectinomycin. Our data demonstrated a good correlation between the two methods. Moreover, a zone of inhibition of less than or equal to 15 mm was a good predictor of clinical treatment failures with spectinomycin.