Abnormal vaginal flora as a biological risk factor for acquisition of HIV infection and sexually transmitted diseases.

The role that the vaginal flora plays in protecting the host from sexually transmitted infections (STIs), including HIV infection, is becoming increasingly appreciated. Significant alterations in the microbiological environment of the vag-inal ecosystem, such as those that occur in bacterial vaginosis (BV), appear to be a biological risk factor for the acquisition and transmission of STIs/HIV, and, therefore , BV has tremendous public health implications. BV occurs in 20%–25% of women in the general population and in 40%–50% of women attending STI clinics [1, 2]. An estimated 3 million symptomatic cases of BV, as well as an equal number of asymp-tomatic cases, occur in the United States annually [3]. BV is characterized by dramatic changes in the vaginal flora, from an environment in which lactobacilli are predominant to one in which there is a marked decrease in the number of lac-tobacilli, particularly those that produce H 2 O 2 [4–6]. In BV, there are large numbers of anaerobic and facultative anaero-bic organisms, the majority of which are normally found in the vagina in small amounts [6]. Changes in the vaginal flora are not all or none but comprise a spectrum of patterns [7]. Therefore, we are presently unable to attribute BV to a single pathogenic organism, and this limitation greatly hampers our diagnostic and treatment strategies. Lactobacilli become the predominant inhabitant of the vagina at the time of puberty and are believed to be the key defense of the vaginal flora [8]. In vitro, lactobacilli produce various potential microbial toxins, including H 2 O 2 and more poorly defined bacteriocins [8, 9]. Lacto-bacilli that produce H 2 O 2 have been shown in vitro to inhibit various microorganisms , including Gardnerella vaginalis, an-aerobes, Neisseria gonorrhoeae, and HIV [10–14]. Other means by which lactoba-cilli may play a protective role within the vaginal ecosystem include competition for epithelial cell attachment sites and stimulation of the local immune system [15, 16]. Additionally, lactobacilli maintain the acidity of the vagina through the production of lactic acid as a metabolic by-product. The acidic pH, normally !4.5, is inhospitable to many bacteria. The pH of the vagina becomes more alkaline as the flora shifts toward the population present in BV [17]. The pathogenesis of BV is poorly understood. Epidemiological correlates of BV include a history of STIs, increased numbers of sex partners, a new sex partner within the month preceding symptom onset, and douching [1, 18–21]. …