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Cervical morphology in pregnancy, bacterial vaginosis and the risk of preterm delivery

Recent advances in neonatal care have resulted in increased survival of preterm infants, including those born at the very margins of viability, albeit without a reduction in the incidence of cerebral palsy. On the other hand, modern obstetric services have not reduced the incidence of preterm delivery in the last 50 years. Bacterial vaginosis (BV) is a state of abnormal vaginal ecology in which the normal and protective lactobacilli-dominated flora is transformed by an overgrowth of vaginal anerobes and varying degrees of depletion of the lactobacilli population. The stimuli that initiate this transformation are unknown. Bacterial vaginosis is associated with subclinical intrauterine infection and confers a 2±7-fold increase in the risk of preterm delivery and mid-trimester pregnancy wastage. Previously, the causes of a third of all preterm births were unknown and classified as idiopathic. Today, subclinical intrauterine infection is recognized to play a key role in the pathogenesis of labor and delivery in 30±40% of preterm births. Decidual activation and fetal host response results in the release of pro-inflammatory cytokines, including IL-1, IL-6 and TNF-b. These cytokines do not only drive the process of preterm labor but are now recognized as playing a crucial role in the pathogenesis of the longterm neurological and pulmonary morbidity previously attributed to biological immaturity. The most widely accepted route of intrauterine infection in pregnancy is the ascent of lower genital tract organisms, although pre-existing endometrial colonization and/or inflammation is probably more plausible. The BV-related micro-organisms involved are usually atypical Mycoplasmas (M. hominis and Ureaplasma urealyticum). They are non-pyrogenic, very rarely evoke systemic symptoms and as such evade routine microbiological and clinical detection. The traditional use of demographic data to predict spontaneous preterm delivery has been unsuccessful because of its low sensitivity and specificity. Preterm labor/delivery is a syndrome produced by a wide variety of disease conditions operating through different pathways and mechanisms. Modern obstetrics, having failed in its search for reliable predictors of preterm delivery, falls back on a reactive strategy to arrest a process that is driven by an irreversible cascade mechanism. Consequently, none of the currently available interventions such as tocolysis, antibiotic therapy, bed rest and cervical cerclage have been proven beyond reasonable doubt to halt the process of preterm labor, prevent preterm delivery and reduce neonatal morbidity and mortality. In the long term, the causes of preterm labor will inevitably produce changes in the cervix as a final common pathway. One manifestation of such a change is cervical effacement, which may be detectable sonographically as cervical shortening. The competent cervix provides a mechanical resistance against preterm delivery. However, the cervix itself may become a target for cellular and biochemical modulation during pregnancy. The mucous plug provides a layer of mechanical and immunological protection against the ascent of lower vaginal organisms. The crucial question is whether these protective functions of the cervix correlate with its length; whether a shorter cervix is necessarily weaker in strength, altered in constitution and deficient in the quantity and/or quality of the mucous plug? A short cervical length , 25 mm (10th centile) clearly identifies a group of women at high risk of preterm delivery, but how might BV affect cervical length and morphology in pregnancy? Organisms associated with bacterial vaginosis may possess lipopolysaccharides (endotoxin), produce Phospholipases A2 and C all of which may induce prostaglandin synthesis. Prostaglandins can induce myometrial contractility and extra-cellular matrix changes in the cervix associated with cervical ripening. Other virulence factors such as collagenases, mucinases and sialidases produced by BV organisms may exert potentially lytic effects on the ground substance on the cervix. Therefore, it is plausible that these bioactive agents may act synergistically on the cervix to produce changes that lead to effacement and dilatation. Although BV is associated with preterm delivery, it is unknown whether this association is causal, and at present, there is no direct in-vivo evidence that BV shortens the cervix. In this issue of the journal Surbeck et al. makes this important connection and links BV with changes in cervical length and morphology in women admitted into hospital with preterm labor. Their findings are of great clinical interest and merit closer observation. What readers may find intriguing is the lack of correlation between the short cervix demonstrated in the BV-positive group and the occurrence of preterm delivery. The reasons for this paradox may well lie in the design and execution of the study. Surbeck et al. defined preterm labor as $ 3 painful contractions in 20 min with or without cervical effacement and dilatation but did not state whether cervical assessment was performed digitally or sonographically and over two time points, since a snapshot will not define the process of effacement, dilatation or indeed labor. Where digital examination was performed, was a lubricant used? Gels and antiseptic solutions may influence the accuracy of the diagnosis of BV by Gram stain. The same question