Literature review > Issue_4 

Wiesenfeld et al. found a strong link between bacterial vaginosis (BV) and chlamydia and gonorrhea in an STD clinic population. On the other hand, women with H2O2 producing lactobacilli had a low risk for chlamydia. Yudin et al. in a rather similar study also from an STD clinic setting found that BV with polymorphonuclear leukocytes (PMNs) predicts plasma cell endometritis among women with no symptoms and signs suggesting frank PID. Not surprisingly, absence of vaginal PMNs suggests absence of PID. These authors used multiple exclusion criteria suggesting that there may have been a significant selection bias present.

Utilizing vaginal wet mount findings in the diagnosis of cervicitis or upper genital tract infection is really not big time news. The Swedish investigators showed the association between vaginal PMNs and proven PID already back in the 1960's. Similarly, busy ER or gynecology outpatient clinic physicians rely on the high negative predictive value of finding heavy lactobacillus flora in the absence of a high number of PMNs in order to rule out PID.

The high prevalence of BV makes BV a major risk factor for other STIs. However, it is still not yet known whether BV actually causes an increase in susceptibility to other STIs or whether the association simply is a marker for risk taking behavior. Substantial evidence links BV and adverse pregnancy outcome. It is however, disturbing that most treatment trials of systemic or topical treatment of BV have produced disappointing results. Intervention studies of BV treatment in pregnancy have been marginally successful in so called high risk populations only. Similarly, evidence links BV and PID, but again, the plausible biological mechanism for this observation is not known.

Unfortunately, neither of the studies reviewed provide answers or explanations to the most burning questions regarding BV and reproductive health. Does BV simply eliminate protective factors produced by lactobacilli such as H2O2 or lactic acid? Does BV induce inflammatory cytokines that may increase susceptibility of target cells to chlamydia or gonorrhea or both? Does BV simply degrade cervicovaginal defense mechanisms by producing proteases? Does BV change the vaginal or cervical immune response? Does any change in the immune factors facilitate ascension of vaginal microorganisms into the upper genital tract? What are the specific virulence factors induced by BV?

Thus, although solid evidence links BV with many STIs such as HIV, HSV-2, N. gonorrhoeae, C. trachomatis, urinary tract infection, PID, and NGU in men, the biological basis remains to be defined and understood. One disturbing fact is also that BV does not induce inflammatory response in the vagina as determined by colposcopic, cytologic or histopathologic criteria. In addition, most BV is not associated with the presence of PMNs. Does this mean that BV simply is a secondary marker of another major virulence factor? Recent evidence suggests that production of high levels of nitric oxide (NO) in response to primary chlamydial infection may down-regulate the T-cell response and leave the host susceptible to repeat chlamydial infection and PID. Thus, high NO production in some individuals may lead to suppression of the T-cell response and reduction in cytokine production important for the clearance of chlamydial infection. How BV fits into this scenario of NO dependant T-cell regulation remains to be seen.

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