Aetiology of preterm labour: bacterial vaginosis
Article first published online: 19 DEC 2006
BJOG: An International Journal of Obstetrics & Gynaecology
Special Issue: Reducing the Burden of Prematurity: New Advances and Practical Challenges
Volume 113, Issue Supplement s3, pages 46–51, December 2006
How to Cite
Guaschino, S., De Seta, F., Piccoli, M., Maso, G. and Alberico, S. (2006), Aetiology of preterm labour: bacterial vaginosis. BJOG: An International Journal of Obstetrics & Gynaecology, 113: 46–51. doi: 10.1111/j.1471-0528.2006.01122.x
- Issue published online: 19 DEC 2006
- Article first published online: 19 DEC 2006
- Accepted 8 September 2006.
- bacterial vaginosis;
- immune response;
- preterm birth;
- vaginal pH
Bacterial vaginosis (BV) is a common condition characterised by a polymicrobial disorder, with an overgrowth of several anaerobic or facultative bacteria and with a reduction or absence of lactobacillus colonisation. The prevalence of BV ranges from 4 to 64%, depending on the racial, geographic and clinical characteristics of the study population. In asymptomatic women, the prevalence varies from 12 to 25%, and similar percentages are observed in pregnant women. Although BV is associated with several adverse outcomes, such as upper genital tract infections, pelvic inflammatory disease, endometritis, preterm birth and low birthweight, many basic questions regarding the pathogenesis of BV remain unanswered. Mucosal immune system activation may represent a critical determinant of adverse consequences associated with BV. An unequal risk for BV acquisition and\or recurrence could derive from different mucosal immune host abilities and\or capability of invading microbes to produce factors that inactivate the local immune response. BV is associated with a two-fold increased risk of preterm birth, with the greatest risk when BV is present before 16 weeks of gestation (odds ratio = 7.55). This may indicate a critical period during early gestation when BV-related organisms can gain access to the upper genital tract and set the stage for spontaneous preterm labour later in gestation. The results of treatment trials for pregnant women with BV have been heterogeneous, with anywhere from an 80% reduction to a two-fold increase in preterm birth among women who received treatment. For this reason, in current clinical practice significant controversy surrounds determining not only who and when to screen but also who and how to treat. Recent evidence shows that individual genetic backgrounds can affect chemokine production. This is an interesting area for future research and could lead to trials of treatment only for women genetically predisposed to preterm birth.