To study the role of infection in prematurity, we studied the demographic and obstetrical characteristics, chorioamnionic cultures, and placental histologic features of women who delivered prematurely and compared these findings with those in women who delivered at term. Microorganisms were isolated from the area between the chorion and the amnion (chorioamnion) in 23 of 38 placentas (61 percent) from women with preterm labor who delivered before 37 weeks' gestation and in 12 (21 percent) of 56 placentas from women without preterm labor who delivered at term (odds ratio, 5.6; 95 percent confidence interval, 2.1 to 15.6). The most frequent isolates from the placentas of those whose infants were delivered prematurely were Ureaplasma urealyticum (47 percent) and Gardnerella vaginalis (26 percent). The recovery of any organism from the chorioamnion was strongly associated with histologic chorioamnionitis (odds ratio, 7.2; 95 percent confidence interval, 2.7 to 19.5) and with bacterial vaginosis (odds ratio, 3.2; 95 percent confidence interval, 1.1 to 6.6). When multiple logistic regression was used to control for demographic and obstetrical variables, premature delivery was still related to the recovery of organisms from the chorioamnion (odds ratio, 3.8; 95 percent confidence interval, 1.5 to 9.9) and with chorioamnionitis (odds ratio, 5.0; 95 percent confidence interval, 1.6 to 15.3). The proportion of placentas with evidence of infection was highest among those who delivered at the lowest gestational age. We conclude that infection of the chorioamnion is strongly related to histologic chorioamnionitis and may be a cause of premature birth.

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Antepartum bacterial vaginosis in pregnancy has been related to premature delivery, the recovery of microorganisms from amniotic fluid of women in premature labor with intact membranes, to histologic chorioamnionitis and to the recovery of microorganisms from the placenta or membranes. Microorganisms associated with bacterial vaginosis are commonly recovered from the amniotic fluid and chorioamnion of patients who deliver prematurely. In addition, bacterial vaginosis is associated with maternal infectious morbidity during labor and in the postpartum period. Very little is known of the pathophysiologic mechanisms by which bacterial vaginosis may cause preterm labor and/or premature rupture of the membranes. However, it is of interest to speculate on possible mechanisms. The high concentration of potentially pathogenic microorganisms in the vagina and cervix of pregnant women with bacterial vaginosis may increase the possibility of an ascending infection via the cervix, decidua, fetal membranes, maternal placenta, and amniotic fluid. Some of the bacteria associated with bacterial vaginosis such as Bacteroides sp. are particularly virulent. Certain bacteria produce enzymes that potentially could affect the fetal membranes or maternal deciduae. Bacteroides sp. and group B streptococcus produce proteases. Protease enzymes reduce the chorioamniotic membrane strength in vitro. It is even possible that a high concentration of bacteria in the lower genital tract could produce enough proteases to weaken the fetal membrane strength causing premature rupture of the membranes. Bacterial lipases could also produce tissue injury. Schwarz et al. demonstrated that lysosomes within fetal membrane cells contain phospholipase A2 in high concentrations. Phospholipase A2 is a precursor of prostaglandin synthesis and the destruction of lysosomes within deciduae or chorioamnion cells may induce prostaglandin synthesis resulting in uterine contractions. Bejar et al. found a high rate of phospholipase A2 production by Bacteroides sp., anaerobic streptococci, Fusobacterium sp., and G. vaginalis. Benett et al. demonstrated that bacterial products of group B streptococci, viridans streptococci, Escherichia coli and Bacteroides fragilis but not of Lactobacillus sp. increase the synthesis of prostaglandins in the membranes. Thus, selected bacteria, including some closely related to bacterial vaginosis may play a role in the initiation of uterine contractions by stimulating prostaglandin synthesis. In an alternative mechanism, either the release of prostaglandin in the membrane or uterine contraction could cause microbreaks of the membrane that allow bacterial colonization of the membrane.(ABSTRACT TRUNCATED AT 400 WORDS)

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