Vaginal biofilms and bacterial vaginosis: of mice and women.

“What is bacterial vaginosis, anyway? Why can’t we treat it very well? What does a biofilm have to do with it? I thought those were involved in prosthetic device infections! Isn’t there an animal model for this condition that can help us answer these questions, whose importance I personally doubt, as there is for any respectable disease?” In this issue of the Journal, Hymes and colleagues present data that speak to several of these questions, which, despite the interlocutor’s skepticism above, seriously affect women’s (and men’s, as it turns out) health. These investigators report a novel finding that might explain why the vaginal biofilm associated with bacterial vaginosis appears to be so tenacious, and how it might be disrupted. Most investigators would agree that a vaginal microbiome dominated by specific species of Lactobacillus—namely, Lactobacillus crispatus and Lactobacillus jensenii—optimizes the likelihood of several desirable outcomes. These outcomes include healthy pregnancy and delivery, absence of upper genital tract infection, lack of abnormal vaginal symptoms, and reduced risk for acquiring several sexually transmitted pathogens, including human immunodeficiency virus. When these species of Lactobacillus are replaced by a diverse mix of copious numbers of anaerobic bacteria, the vaginal pH increases (above the optimal range, which is ≤4.5), and bacterial vaginosis results, if this disruption proceeds to the point where clinical or Gram stain criteria are fulfilled. Among the most important adverse outcomes that have consistently been linked to bacterial vaginosis are elevated risk of HIV acquisition [1], preterm delivery [2], and pelvic inflammatory disease [3]. In a recent, prospective cohort study of HIV-serodiscordant heterosexual couples in which the female partner had HIV infection at enrollment, bacterial vaginosis that occurred during follow-up was associated with an increased risk of HIV acquisition among the male sex partners of these women [4]. It would seem intuitively simple to treat the anaerobic abundance that defines bacterial vaginosis, but this approach has proved to be difficult. In fact, relief from antibiotic therapy of bacterial vaginosis—metronidazole or clindamycin, given topically or orally—is often shortlived, and the overwhelming majority of affected women are subject to recurrence in the next several months unless ongoing antibiotic therapy (typically, biweekly vaginal metronidazole gel) is used as a suppressive approach [5]. Most investigators believe that in addition to a reduction in the bacterial vaginosis–associated bacterial concentrations, adequate repletion of the desirable Lactobacillus species must be established and sustained to fully “heal” the vaginal microenvironment. Critically, the initial event leading to the shift of the anaerobic predominance that characterizes bacterial vaginosis is unknown, although data suggest that sexual activity likely contributes—at least in some women [6]. Numerous studies conducted over the past 3 decades have substantiated the association of Gardnerella vaginalis with bacterial vaginosis. However, with use of more-sensitive detection methods, including bacterium-specific polymerase chain reaction, G. vaginalis can be detected in women who have no signs of bacterial vaginosis or, indeed, any other vaginal infection. In fact, G. vaginalis is estimated to colonize approximately 50%–70% of women whose vaginal fluid is characterized as normal on the basis of the Nugent score [7]. These observations have led some to suggest that G. vaginalis may act synergistically with other anaerobic bacteria to cause bacterial vaginosis [8]. The role of biofilms in potentiating the tenacityof bacterial vaginosis has emerged Received and accepted 22 January 2013; electronically published 19 February 2013. Correspondence: Jeanne M. Marrazzo, MD, MPH, Harborview Medical Center, Division of Infectious Diseases, 325 Ninth Ave, Mailbox 359932, Seattle, WA 98104 ( jmm2@uw. edu). The Journal of Infectious Diseases 2013;207:1481–3 © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/infdis/jit050