Bacterial vaginosis (BV) is the most common cause of vaginal discharge in the U.S. It is associated with adverse outcomes including preterm birth, pelvic inflammatory disease, and increased risk of acquisition and transmission of sexually transmitted infections (STIs), including HIV. Microbiologically, BV is characterized by depletion of lactobacilli that comprise the normal vaginal flora and increases in facultative (Gardnerella vaginalis; GV) and strict anaerobes.

Three out of four Amsel criteria are necessary for the clinical diagnosis of BV and include (1) homogeneous, thin, grayish-white vaginal discharge, (2) vaginal pH \>4.5, (3) positive whiff-amine test, and (4) clue cells present on a wet mount of vaginal fluid. BV diagnosis, however, is based most rigorously on Nugent scoring of a Gram stain of vaginal secretions. Optimal vaginal flora, indicative of a predominance of lactobacilli, is represented by a Nugent score of 0-3. Abnormal vaginal flora includes not only what is currently defined as BV (Nugent score 7-10) but also what is referred to as intermediate flora (Nugent score 4-6). For reasons not well understood, BV is very common among women who have sex with women (WSW), perhaps more so than among heterosexual women. Risks for prevalent BV among WSW have included higher numbers of lifetime female sexual partners, shared use of vaginally inserted sex toys, and oral-anal sex. In addition, WSW in monogamous sexual partnerships have a high concordance for the presence or absence of BV. These data support the hypothesis that BV is sexually transmitted.

It is well accepted that BV is caused by a synergistic relationship between a large number of microorganisms including GV and other anaerobics (i.e. BV-associated bacteria; BVAB) however the trigger which initiates these alterations is debated. It is unknown whether BV results from acquisition of GV as the "founder" organism which subsequently leads to the complex changes in the vaginal microbiota associated with BV or whether BV is transmitted as a polymicrobial consortium. GV, as a facultative anaerobe, may be better able to tolerate the high oxidation-reduction (redox) potential of the healthy vaginal microbiome, unlike strict anaerobes. Similar to facultative anaerobes involved in the initiation of oral disease, it is possible that GV, through its metabolic pathways and ability to form a biofilm (perhaps influenced by specific oligotypes), creates a lower redox potential in the vaginal microbiome. This alteration would then cause a marked decrease in lactobacilli and an increase in other BVAB that are normally present in very low concentrations, leading to the BV syndrome. Determining the exact etiology of the agent(s) causing a shift from optimal to abnormal vaginal flora and BV is vital for appropriate treatment and prevention of adverse outcomes. With increasing use of molecular methods, identification of vaginal microorganisms (some uncultivable) to the species level in women with BV has become more feasible. This study will seek to further investigate BV pathogenesis. We hypothesize that sexual exposure to Gardnerella vaginalis is the inciting event leading to the complex changes in vaginal flora associated with BV. If Gardnerella vaginalis is the initial insult, then its appearance and establishment in the vaginal microbiome will be seen in women who develop incident BV prior to increases in other BV-associated bacteria.

Only African American women will be enrolled in this protocol as differences in the composition of vaginal microbial communities of women with and without BV of different racial and ethnic groups have been noted which could confound the results of this study.