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Asymptomatic bacterial vaginosis: is it time to treat?

Ronald S. Gibbs, MD In the last 30 years, there has been a fascinating evolution in our understanding of the condition now known as bacterial vaginosis (BV). Previously called "nonspecific vaginitis," "Gardnerella vaginalis vaginitis," and "Haemophilus vaginalis vaginitis," this very common condition results from the replacement of normal peroxiclase-producing lactobacilli in the vagina with a mix of anaerobes, genital mycoplasmas, and G vaginalis and a several log increase in total bacterial colony count. Causing abnormal vaginal discharge and odor in symptomatic women, BV has been recognized as being asymptomatic in approximately one-half of the women who experience it. Usually diagnosed by the presence of an elevated pH, a homogenous milky or creamy discharge, amine odor, and the presence of "clue cells" on microscopy, BV is also diagnosed by Gram stain in which there is an absence or decrease of lactobacilli and the presence of other organisms that cause the condition. Nugent et al' developed a quantitative score to assess these changes that are seen on Gram stain, and the "Nugent criteria" have been used widely in research settings for the diagnosis of BV. Whether symptomatic or asymptomatic, BV has been associated strongly with both obstetric complications, which include preterm birth and amnionitis,5 and gynecologic complications, which include postoperative infections and the acquisition of human immunodeficiency virus and other sexually transmitted diseases (STDs).6 There is good biologic plausibility as to the reason that BV causes these complications. Specifically, BV organisms may cause ascending infection and often are isolated in upper genital tract specimens from patients with these obstetric complications. BV may predispose to STDs because the lack of peroxidase-producing lactobacilli may allow infection with STDs, or the local cytokine production in the lower genital tract of women with BV may facilitate the acquisition of STDs. In this issue of the Journal, Schwebke and Desmond' report a randomized trial of the treatment of asymptomatic BV in women who attended an STD clinic to determine whether this intervention would prevent the acquisition of new STDs. The intervention consisted of a 5-day treatment course of intravaginal metronidazole gel followed by biweekly application in a preventative phase for 6 months. The authors found that, compared with the observational group, those women in the metronidazole gel group had a significantly longer time to the development of an STD, with the difference being driven by the significant difference in the number of Chlamydia trachomatis infections. This novel and interesting study has considerable scientific merit; but like all trials, it also has its limitations and raises other important questions. For example, no placebo was used, and no measure of compliance was reported. In addition, there was premature cessation of the study with less than three-fourths of the patients in the sample size analysis actually enrolled. Next, the results may not be generalizable to women who are at low risk for STDs. Further, it appears that the protective effect from the recurrence of BV (authors' Table II) and the protective effect from the new STD acquisition (authors' Figure II) was limited to the first 3-4 months of the 6-month trial. It is unclear whether this limited period of efficacy was due to decreasing compliance or other reasons. Finally, there was not a uniform decrease in all STDs over time. Data are not given for specific STDs at the end of the 6-month trial; however, at 12 months after enrollment, the treatment group actually haAa nearly 3-fold increase in the rate of new Neisseria gonorrhoeae infections (22.9% vs 8.3%). Although not statistically significant, this difference is a cause for concern. What, then, are the clinical messages of this timely and provocative study?

First, both this study and that of Sobel et al demonstrate the significant but limited benefit of metronidazole gel prophylaxis for the recurrence of BV. It is clear that we need better approaches to prevent BV, particularly in view of its high recurrence rate and frequent symptomatic occurrences among many women. Second, although the authors suggest that "consideration should be given to routine treatment of women with asymptomatic BV," my interpretation is less enthusiastic. There are too many limitations and unanswered questions in this small, nonblinded study among high-risk women to warrant such a broad change of practice now. We do not know, for example, whether any benefit would be seen among low-risk women. Then, even among women in an STD clinic setting, there are reasons for caution. With the period of efficacy apparently being limited to just a few months, the practical aspects of this approach are limited severely for women who are at risk over a long period of time. Further, the nearly 3-fold increase in N gonorrhoeae infections 6 months after the trial is a cause for concern. Perhaps a different regimen might have been effective for a longer period of time. Studies regarding intervention for asymptomatic BV to prevent preterm birth have notably led to discordant results,' owing perhaps to differences in the risk of the population or the exact regimen that was used. There is a good rationale for intervention studies in asymptomatic women with BV to prevent obstetric and gynecologic complications. We must develop effective preventative interventions. However, the benefit of routine treatment in high- or low-risk nonpregnant women with asymptomatic BV to prevent the acquisition of STDs has not been demonstrated sufficiently over any extended period of time, and the routine treatment of nonpregnant women with asymptomatic BV presently should not become part of practice. The 2006 Centers for Disease Control and Prevention STD guidelines note that currently the established benefits of therapy for BV in nonpregnant women are to relieve symptoms of infection and reduce the risk of infection after abortion or hysterectomy.3

From the Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Denver, CO. Reprints: Ronald S. Gibbs, MD, University of Colorado at Denver and Health Sciences Center, Department of Obstetrics and Gynecology, 4200 East 9th Ave, B198, Denver, CO 80262; ronald.gibbs@uchsc.edu 0002-9378/free Q 2007 Mosby, Inc. All rights reserved. doi: 10.1016/j.ajog.2007.04.001
REFERENCES 1. Eschenbach DA. History and review of bacterial vaginosis. Am J Obstet Gynecol 1993;169:441-5. 2. Allsworth JE, Peipert JF. Prevalence of bacterial vaginosis: 2001-2004 national health and nutrition examination survey data. Obstet Gynecol 2007;109:114-20. 3. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines. MMWR Morb Mortal Wkly Rep 2006;55:49-52. 4. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of Gram stain interpretation. J Clin Microbiol 1991;29:297-301. 5. Klein LL, Gibbs RS. Use of microbial cultures and antibiotics in the prevention of infectionassociated preterm birth. Am J Obstet Gynecol 2004;190:1493-502. 6. Taha TE, Hoover DR, Dallabetta GA, et al. Bacterial vaginosis and disturbances of vaginal flora: association with increased acquisition of HIV. AIDS 1998;12:1699-706. 7. Schwebke JR, Desmond, R. A randomized trial of metronidazole in asymptomatic BV to

prevent acquisition of STDs. Am J Obstet Gynecol 2007;196:517-8. 8. Sobel J, Ferris D, Schwebke JR, et al. Suppressive maintenance antibacterial therapy with 0.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis. Am J Obstet Gynecol 2006;194:1283-9.

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