lus sp. in the vagina are replaced with high concentrations of characteristic sets of aerobic and anaerobic bacteria. 8,9 Positive amniotic fluid cultures were reported in 20-30% of women with preterm labor. 10 In two other studies, it is predicted that anywhere from 10-41% of women have Bacterial Vaginosis and 50% of those are asymptomatic. 9,11 There is still debate about how these microbes arise within the uterus. Some argue that the microbes ascend through the dilated cervix after the parturial process has initiated as a result of a change in the uteroplacental endocrine interface. Others argue that the microbes ascend to the deciduas, membranes and amniotic fluid primarily through the vagina and initiate inflammatory response in the deciduas, membranes and fetus. A third and most valid theory is that the micro organisms responsible are present in the endometrium before conception and initiate a sub clinical infection of the deciduas , chorioamnion, and fetus weeks or even months before the preterm labor. 10 This last theory fits best with the prostaglandin pathway. The sub clinical or clinical infections caused by the microbes have the same result of producing proinflammatory cytokines and other immunomodulatory proteins. 9,10 These cytokines stimulate prostaglandin synthesis, advancing the evolution of events that lead to cervical ripening, membrane weakening and eventual membrane rupture. In discussing prediction and prevention indices, it is important to keep in mind that Premature delivery is an end-stage symptom of a multi-factorial disease. Pre-tem labor is one of the last symptoms in a cascade of biochemical events that lead to preterm delivery. The most appropriate way to end preterm delivery would be to prevent the causes that initiate the cascade that ends in pre-term labor. 12 Another issue to restate is that there is a lack of understanding of the pathogenesis of preterm birth. The effectiveness of the pre...
