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Background: The nonhuman primate model allows for safety and efficacy testing of topical microbicide products. Goal: The goal of this study was to evaluate the safety and efficacy of vaginal and rectal applications of BufferGel (ReProtect, Inc.). Study Design: The safety of repeated product applications was evaluated by microflora, pH, vaginal colposcopy, and rectal lavage. To test efficacy in preventing chlamydia, infection was documented by culture and nucleic acid amplification tests. Results: Repeated vaginal or rectal applications of BufferGel were not associated with significant changes in microflora. BufferGel use had a transient acidifying effect on vaginal and rectal pH. Colposcopic observations remained relatively normal in all test animals. A slightly increased incidence of epithelial desquamation was noted after rectal product use compared with the control group. BufferGel did not prevent cervical or rectal chlamydial infection. Conclusion: BufferGel has an acceptable safety profile after repeated vaginal and rectal use, but does not prevent chlamydial infection in the macaque models.

An antimicrobial treatment trial of 153 women is performed to evaluate its effect on clinical and laboratory findings in women at risk for endometritis. Antimicrobial therapy decrease in the abnormal clinical findings and histologic endometritis in women without a clinical diagnosis of Pelvic inflammatory disease (PID) prior PID increases the prevalent cervical infection and poses a risk for endometritis.

Bacterial vaginosis diagnosed at 16 to 20 weeks' gestation was significantly associated with preterm delivery in a study in Indonesia. However, vaginosis diagnosed at 28 to 32 weeks' gestation was not associated with premature delivery. A total of 490 women who had prenatal care in three public hospitals participated in the study. The first evaluation took place when the women were 16 to 20 weeks pregnant. They were tested for bacterial vaginosis then and again when they were 28 to 32 weeks pregnant. Socioeconomic status, smoking, alcohol use and other relevant factors also were assessed. At the first evaluation, 17% of the women tested positive for bacterial vaginosis. Their rate of preterm delivery was 20.2% compared to the 11.8% rate of women without vaginosis.

Premature birth causes high rates of neonatal morbidity and mortality. There are multiple causes of preterm birth. This article reviews the evidence linking subclinical infection and premature birth. Although maternal genital tract colonization with specific organisms has been inconsistently associated with preterm birth and/or premature rupture of membranes, some infections have been consistently associated with preterm delivery. The association of histologic chorioamnionitis with prematurity is a consistent finding, but the mechanisms require further study. The relationship between histologic chorioamnionitis infection and the chorioamnionitis of prematurity requires additional research. A varying number of patients in 'idiopathic' preterm labor have positive amniotic fluid cultures (0% to 30%), but it is not clear whether infection preceded labor or occurred as a result of labor. Evidence of subclinical infection as a cause of preterm labor is raised by finding elevated maternal serum C-reactive protein and abnormal amniotic fluid organic acid levels in some patients in preterm labor. Biochemical mechanisms for preterm labor in the setting of infection are suggested by both in vitro and in vivo studies of prostaglandins and their metabolites, endotoxin and cytokines. Some, but by no means all, antibiotic trials conducted to date have reported decreases in prematurity. These results support the hypothesis that premature birth results in part from infection caused by genital tract bacteria. In the next few years, research efforts must be prioritized to determine the role of infection and the appropriate prevention of this cause of prematurity. (Am J Obstet Gynecol 1992; 166: 1515-28.)

Certain types of bacteria, such as lactobacilli, streptococci, and pneumococci, can produce hydrogen peroxide (H2O2), which becomes highly toxic in the presence of the enzyme peroxidase and a halide group (a chemical compound with a halogen, such as chlorine, bromine or iodine). In addition to eliminating surrounding bacteria, fungi, viruses, sperm, and tumor cells, these H2O2-producing bacteria can also be self-destructive in the presence of peroxidase and a halide. Peroxidase is produced by certain types of white blood cells, saliva, cow's milk, and uterine fluid. H2O2-producing Lactobacillus bacteria (LB+) are normally present in the vagina. One study reported that the vaginas of 96 percent of normal women had LB+, whereas only 4 percent of normal women had Lactobacilli that did not generate H2O2. Among women with bacterial vaginosis, or vaginal infection with Gardnerella vaginalis, only six percent had LB+ in the vagina, whereas 36 percent had non-H2O2-producing Lactobacilli. These studies suggest that LB+ may help to prevent the overgrowth of Gardnerella vaginalis. The effects of LB+ on G. vaginalis were assessed in 21 women, including 11 with bacterial vaginosis. High levels of LB+ were toxic to G. vaginalis, and the effectiveness of LB+ was enhanced by myeloperoxidase and chloride. Further observations suggest that the toxicity resulted from H2O2. In addition, the toxic effects of LB+ and chloride could be produced by adding H2O2 combined with iodide, bromide, or thiocyanate. LB+ combined with myeloperoxidase and chloride prevented its own growth. Seventeen of 21 women had sufficient levels of vaginal peroxidase. These findings suggest that LB+ may help to control the growth of bacteria within the vagina. (Consumer Summary produced by Reliance Medical Information, Inc.)