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We evaluated moxalactam in 62 patients with puerperal or postabortal genital infections. In all patients, the initial dose was 6 g/day. In 84% of patients, we found anaerobes in genital specimens. Of aerobic isolates, only enterococci were resistant. Among anaerobes tested, only two isolates (a Clostridium leptum and a Bacteroides disiens) had minimal inhibitory concentrations of greater than or equal to microgram/ml. Good clinical responses occurred in 56 of 62 (90%). Moxalactam was well tolerated with little local irritation and minimal hepatic, renal, or hematological abnormalities.

A randomized comparison of ceftazidime versus clindamycin-tobramycin was performed for the treatment of obstetrical and gynecological infections. Entry criteria were an oral temperature of greater than or equal to 38 degrees C and a clinical diagnosis of endometritis, salpingitis, or pelvic cellulitis after hysterectomy. All patients with endometritis had cultures of intrauterine material obtained via a transcervical single-lumen catheter. The patients with pelvic cellulitis had material from the vaginal apex aspirated for culture, and all patients with salpingitis had a culdocentesis for culture of intraperitoneal material. Of 38 patients who received ceftazidime, 34 had endometritis after cesarean section, 3 had endometritis after abortion, and 1 had pelvic cellulitis. Of 39 patients who received clindamycin-tobramycin, 35 had endometritis after cesarean section, 3 had salpingitis, and 1 had pelvic cellulitis. The most common bacterial isolates were Lactobacillus sp., Bacteroides bivius, Escherichia coli, other gram-negative aerobic bacilli, group B streptococci, and other aerobic streptococci. Bacteremia occurred in 9.0% of the patients. Of the patients receiving clindamycin-tobramycin and ceftazidime, 34 (87.2%) and 34 (89.5%), respectively, responded to therapy. All the clinical failures occurred in patients with endometritis after cesarean section. Clinical failures had persistent fever despite 3 or more days of treatment. One of the patients receiving clindamycin-tobramycin developed an urticarial rash after her infection had resolved. No patient in either group developed diarrhea. In these small groups of patients, there were no significant differences in cure rate, side effects, or length of hospital stay.

Ceftazidime in the breast milk of 11 puerperal women were determined by bioassay. Each patient received 2 g of ceftazidime intravenously every 8 h for 5 days. The mean (+/- standard deviation) ceftazidime concentrations in the milk were: 3.8 +/- 2.0 (before the next dose), 5.2 +/- 3.0 (1 h after), and 4.5 +/- 1.7 micrograms/ml (3 h after). Ceftazidime was excreted in breast milk at relatively constant levels between days 2 and 4 of therapy.

Amniotic fluid (AF) was collected via a transcervical, intrauterine catheter from 52 patients with clinical intra-amniotic infection (IAI) and from 52 matched, uninfected controls. The AF was cultured for Mycoplasma hominis and Ureaplasma urealyticum as well as for aerobic and anaerobic bacteria. Eighteen (35%) patients with IAI and four (8%) controls had M. hominis in AF (P < 0.001). Twenty-six (50%) patients with IAI and 26 (50%) control patients had U. urealyticum in AF (difference not significant). In the AF specimens of patients with IAI, 15 (83%) of the 18 with M. hominis also contained 102 colony-forming units (cfu) of a high-virulence bacterial isolate/ml (P < 0.05). Within the limitations of the experimental design, U. urealyticum in AF is not associated with clinical IAI, whereas, with qualitative cultures, M. hominis in AF is. However, in IAI, M. hominis is isolated most commonly from the AF of patients with 102 cfu of a high-virulence bacterial isolate/ml.