Use of Continuous Culture to Model the Establishment of Bacterial Vaginosis

Abstract

Bacterial vaginosis (BV) is the most common vaginal tract infection seen among women of childbearing age in primary health care in the United States. It is a polymicrobial syndrome characterized by an alteration in the composition of the vaginal microflora. During BV, the lactobacilli that are usually dominant in the healthy vagina are replaced by an overgrowth of Gardnerella vaginalis and anaerobic bacteria; however, the cause 9f this shift in the vaginal tract ecology is currently not well understood. In previous studies conducted in this laboratory a bacterium of vaginal origin, Enterococcus faecium 62-6, was isolated and found to produce a bacteriocin antagonistic to the growth of vaginal lactobacilli. Our hypothesis is that the introduction of an exogenous bacterium like E. faecium 62-6 into the vaginal tract via sexual transmission could cause a decline in the Lactobacillus populations, thus paving the way for the establishment of bacteria associated with BV. Using continuous culture to model the vaginal environment, the aim of this study was to determine whether the introduction of E. faecium 62-6 to an established population of lactobacilli would cause the lactobacilli to decline in concentration and to determine if this decline correlated with bacteriocin production. Enterococcus faecium 62-6 was found to cause a decrease in the concentration of the sensitive Lactobacillus strain tested due to bacteriocin production; however, the decrease was followed by an increase in concentration due to the development of resistant strains. The concentration of the resistant strain, L. casei 62-5, decreased by 2 IOglO cfu/ml in the presence of E. faecium 62-6, and then stabilized. This decrease did not correlate with bacteriocin production. The growth of the other resistant strain, L. acidophilus 46-1, was unaffected by E. faecium 62-6 and its high concentration of 10 log 10 cfu/ml did not allow E. faecium 62-6 to establish at normal levels (9.6 log 10 cfu/ml) or to produce bacteriocin. These results do not support our hypothesis that bacteriocin production may be one mechanism leading to the decline in concentration of the vaginal lactobacilli and the establishment of BV.

With honors.