Bacterial vaginosis: a sexually enhanced disease

Sir: Ever since the notorious experiments by Gardner and Dukes ¹ and later on by Criswell et al., ² by which they accomplished to induce bacterial vaginosis (BV) experimentally by inoculating volunteering women with vaginal fluid from BV patients either with high inocula of pure culture Gardnerella vaginalis — the microorganism that could be recovered at a high rate from the urethra in male partners of BV-positive women—BV has been deemed a putatively sexually transmitted disease (STD) with G. vaginalis as the infectious disease agent fitting a traditional STD transmissibility model. From subsequent studies however, a large deal of controversy around this issue has arisen, as BV epidemiology apparently not only shares several features with traditionally defined STDs, ³ but also striking dissimilarities. ⁴

The most intriguing observation in this respect certainly comes from the prevention paradox in BV epidemiology. If BV were expected to act as a genuine STD - as seems to be indicated on one hand by the very consistent association with a multitudiny of sexual behaviour-related characteristics - then proper partner treatment and consistent condom use would be expected to serve as effective means in BV control. However, this is not quite the case. Six subsequent randomized controlled trials failed to document any benefit from partner treatment with antibiotics, a consistent observation that cannot be downplayed by the natural history of BV, as has been suggested, ³ since such bias is contravened by proper randomization. With regard to condom use as a means of preventing BV, it may be acknowledged that six cross-sectional studies^5–10 were equivocal, whereas longitudinal and cohort studies on the other hand are more in line with each other towards a beneficial effect of condom use vis-á-vis BV acquisition,^11–14 although overall the observed effects tend to be very moderate with an average relative risk reduction of merely 20%.

Hence, despite the close relationship with sexual behaviour, it may be inferred that BV differs from true STDs though the lack of evidence in support of simple male-female transmission of a known infectious disease agent, which is also lack of evidence in support of an STD causal pathway according to the Hill causality criterion of experiment and intervention. ¹⁵

Accordingly, while BV epidemiology has challenged the traditional STD transmissibility model in many ways, an alternative infectious disease model emerges, in which BV may be referred to as a sexually enhanced rather than a sexually transmitted disease. This model would basically entail that disease susceptibility is altered through sexual contact allowing opportunistic bacteria to arrive on the scene, rather than pathogens being transmitted. In BV, it appears indeed as if sexual contact sets the scene for anaerobic overgrowth of bacteria already present in the vagina or rectum, which in turn most likely relates to the temporarily antagonizing effect of sexual contact on the persistence of hydrogen peroxide-producing lactobacilli.

Effective control of the vaginal environment has been postulated to depend on the presence of hydrogen peroxide-producing lactobacilli in the early 90s, and this hypothesis has been unequivocally corroborated ever since. Hawes et al. ¹¹ were then the first to document in a longitudinal study that acquisition of BV was indeed strongly associated with a lack or loss of hydrogen peroxide-producing lactobacilli. Eventually, Vallor et al. ¹⁶ showed in yet another longitudinal study that sexual contact and frequency of intercourse in particular emerged as a strong determinant to the loss of colonization with hydrogen peroxide-producing lactobacilli. Hence, the observations on the antagonizing effect of sexual contact on the persistence of hydrogen peroxide-producing lactobacilli and the concomitant observations on the acquisition of BV in relation to vaginal lactobacilli seems to fit rather well the infectious disease model of BV as a sexually enhanced disease, rather than that of an STD. The concept of sexually enhanced diseases is presumably not confined to BV, and other infectious diseases such as (recurrent) urinary tract infection seem to be in line with this model too.