Vaginal Microbiome in Preterm Rupture of Membranes

There is good evidence for an association between reduced Lactobacillus spp relative abundance in the maternal vaginal microbiota and risk of PPROM, which, mechanistically, is mediated through untimely activation of inflammatory cascades in the gestational tissues (Fig. 3). Cases of PPROM appear to be divisible into 2 groups: those that are linked to vaginal dysbiosis, and those that have other causes. Women who have prior excisional cervical surgery are probably at high risk of PPROM through mechanical factors and will do well with cervical cerclage if they have a short cervix, although choice of suture material may affect outcomes. In most cases of PPROM linked to vaginal dysbiosis, reduced Lactobacillus spp relative abundance develops close to the time of membrane rupture, although dysbiosis at any gestational age increases the risk. The event of PPROM itself may change the vaginal microbiota in some women through direct effects of amniotic fluid; however, antibiotic therapy appears to have a greater effect. In women with Lactobacillus spp deletion at the time of PPROM, antibiotics may have a beneficial effect on bacterial load, but antibiotics appear to damage optimal vaginal microbiota communities by selectively targeting Lactobacillus spp Both chorioamnionitis and early-onset neonatal sepsis, which are risk factors for developmental delay, cerebral palsy, and a range of other adverse neonatal outcomes, are increased where the vaginal microbiota are Lactobacillus spp depleted close to the time of delivery. It is now time to reconsider the role of antibiotic therapy in PPROM, and to develop strategies to allow targeted rather than universal therapy. Many studies have identified a role for L crispatus as protective against PTB, which opens the way for preventative strategies involving live therapeutics.