
With that, a new paper, Promiscuity in mice is associated with increased vaginal bacterial diversity:
Differences in the number of sexual partners (i.e., mating system) have the potential to exert a strong influence on the bacterial communities present in reproductive structures like the vagina. Because this structure serves as a conduit for gametes, bacteria present there may have a pronounced, direct effect on host reproductive success. As a first step towards the identification of the relationship between sexual behavior and potentially pathogenic bacterial communities inhabiting vital reproductive structures, as well as their potential effects on fitness, I sought to quantify differences in bacterial diversity in a promiscuous and monogamous mammal species. To accomplish this, I used two sympatric species ofPeromyscus rodents—Peromyscus californicus and Peromyscus maniculatus that differ with regard to the number of sexual partners per individual to test the hypothesis that bacterial diversity should be greater in the promiscuous P. maniculatus relative to the monogamous P. californicus. As predicted, phylogenetically controlled and operational taxonomic unit-based indices of bacterial diversity indicated that diversity is greater in the promiscuous species. These results provide important new insights into the effects of mating system on bacterial diversity in free-living vertebrates, and may suggest a potential cost of promiscuity.

There are some studies of metagenomics of bacterial communities in humans. But to my knowledge it doesn’t look like there are any which have attempted to correlate number of sexual partners to diversity of vaginal flora. This is possible very important as a long term issue. The evolutionary biologist Paul Ewald has been reporting that there is a connection between history of infection and many late in life diseases, such as cancers. Mike Snyder had Stanford has been tracking his own biomarkers in extensive detail for several years, and has indicated that his own onset of Type II Diabetes was probably triggered by an earlier infection. These inferences were only possible because of his extremely rich personal data set, part of a broader project in his laboratory. But, it might give us a window into the more precise individual etiologies of diseases.
Citation: Naturwissenschaften. 2011 Nov;98(11):951-60. Epub 2011 Oct 1
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