Simian Model for Infection-Associated Preterm Labor

Abstract

Preterm labor that results in premature birth is the most common cause of perinatal mortality, accounting for 80% of perinatal deaths which are not attributable to congenital malformations. There is now considerable evidence to suggest that cytokines participate in the pathogenesis of infection-associated preterm labor. To examine the temporal and quantitative relationships between intra-amniotic infection and preterm labor, the authors developed a simian model involving chronically catheterized rhesus monkeys (Macaca mulatta) with timed gestations. Bacterial vaginosis, previously associated with preterm labor and intra-amniotic infection in women, was identified by Gram stain criteria in 8 of 31 monkeys (26%), a prevalence similar to that reported in women, and was likewise associated with increased intravaginal concentrations of Gardnerella vaginalis, Mobiluncus spp., and anaerobes. Following intra-amniotic infection, increases in prostaglandin E2 (PGE2) and PGF2α concentrations in amniotic fluid occur in parallel with increases in cytokine concentrations in amniotic fluid and precede increases in uterine contractility. The presence of a single fetus, the hormonal control of parturition, and hemochorial placentation with an abundant amniotic fluid cavity all approximate the human situation. Ideally, prevention of prematurity should be directed toward identification and eradication of the offending microorganism while it is still confined to the lower genital tract, as has been demonstrated for certain lower genital tract infections.