Treatment of Vaginal Infections to Prevent Preterm Birth: A Meta-Analysis

Abstract

Introduction Approximately 10% of all pregnancies in the United States end in preterm birth, but this 10% accounts for approximately 70% of the perinatal deaths and half of the long-term neurologic morbidity. A majority of morbidity and mortality is concentrated in those infants delivered at less than 32 weeks gestation and birth weight ,1500 g. Intrauterine infection has been found to play a major role in preterm birth and is thought to be responsible for preterm birth in up to 40% of cases. The most common pathway of intrauterine infection and resultant amniotic infection is thought to be the ascending route from the cervix and vagina. Intrauterine infection may occur early in pregnancy or even before pregnancy and remain asymptomatic and undetected for months until preterm labor or premature rupture of membranes (PROM) occurs. When membranes and amniotic fluid were cultured from women undergoing cesarean delivery with and without labor at various gestational ages, there was an inverse association between positive cultures and gestational age, suggesting that microbial colonization is more frequent among spontaneous preterm births at lower gestational ages. It is likely that maternal and fetal signals in response to infection are what initiate preterm labor after silent chorioamnionitis. An active inflammatory response occurs in women with positive chorioamniotic membrane cultures as shown by high concentrations of tumor necrosis factor alpha and interleukin-6 in amniotic fluid. In vivo studies in women have linked increased expression of proinflammatory cytokines in vaginal secretions, amniotic fluid, and maternal and fetal blood with adverse pregnancy outcomes. Correspondence: Mark A. Klebanoff, MD, DESPR, NICHD, NIH, 6100 Bldg, Room 7B05, Bethesda, MD 20892. E-mail: mk90h@nih.gov