Trichomonas vaginalis infection: can we afford to do nothing?

For more than a century following its initial description in 1836, Trichomonas vaginalis was considered to be either a harmless vaginal colonizer or simply a minor nuisance [1]. This view may have been sustained by the observation that women with trichomoniasis vaginalis were usually either asymptomatic or had only mild symptoms. More recently, it has been recognized that T. vaginalis infection may be associated with a range of adverse reproductive health outcomes, including preterm birth [2– 4], cervical neoplasia [5, 6], posthysterectomy infection [7], atypical pelvic inflammatory disease [8, 9], and infertility [10]. Perhaps most concerning, in the context of the global HIV-1 epidemic, is the emerging recognition that T. vaginalis infection may increase women’s susceptibility to HIV-1 infection. Two prospective analyses, both conducted in populations of female sex workers, have demonstrated significant associations between trichomoniasis vaginalis and HIV-1 acquisition [11, 12]. Several additional longitudinal studies have suggested that trichomoniasis vaginalis increases a woman’s risk of acquiring HIV-1 by 1.2–2.4-fold [13–18], although these findings were not statistically significant. Of note, the majority of studies have been underpowered to demonstrate an association of this magnitude. While there is continued debate about the causal linkage between T. vaginalis infection and obstetrical, gynecological, and infectious complications, it is generally recognized that the incidence of this sexually transmitted infection (STI) has reached epidemic levels throughout much of the world. In 1999, the World Health Organization (WHO) estimated the global incidence of T. vaginalis infection to be 173 million cases annually, making this the most common nonviral STI [19]. The greatest burden of disease was observed in less developed regions, but a high incidence was also found in North America (8 million cases annually) and western Europe (11 million cases annually). In response to evidence that T. vaginalis infection is highly prevalent and may lead to serious complications, there have been numerous calls for control strategies, including screening, centralized reporting, treatment, and partner notification [20 –23]. Two articles in this issue of the Journal of Infectious Diseases provide additional evidence supporting the need to reconsider public health responses for control of trichomoniasis vaginalis [24, 25]. In the first article, Van Der Pol et al. [24] report findings from a nested casecontrol study conducted in a general population cohort of women recruited in Uganda and Zimbabwe. A total of 213 HIV-1 seroconverters were compared to 419 women who remained HIV-1 seronegative throughout the follow-up period. Polymerase chain reaction (PCR) analysis detected T. vaginalis at the visit prior to HIV-1 acquisition in 24 seroconverters (11.3%) and at the matched visit in 19 nonseroconverters (4.5%) (odds ratio, 2.41; 95% confidence interval [CI], 1.28 – 4.53). These findings remained statistically significant in analyses that adjusted for individual-level demographic, behavioral, and biological confounding factors, as well as for primary sex partner– associated risk. Two features of this study were unique in comparison to prior prospective studies that have demonstrated significant associations between T. vaginalis infection and HIV-1 acquisition [11, 12]. First, these findings were from a general population cohort, confirming that the association is not restricted to high-risk women. Second, this study used PCR for detection of T. vaginalis. The increased sensitivity of this technique, compared with that of Received 19 October 2007; accepted 19 October 2007; electronically published 5 February 2008. Potential conflicts of interest: none reported. Financial support: National Institutes of Health (grant K23AI52480). Reprints or correspondence: Dr. R. Scott McClelland, International AIDS Research and Training Program, University of Washington, Box 359909, 325 Ninth Ave., Seattle, WA 98104 ([email protected]). The Journal of Infectious Diseases 2008; 197:487–9 © 2008 by the Infectious Diseases Society of America. All rights reserved. 0022-1899/2008/19704-0001$15.00 DOI: 10.1086/526498 E D I T O R I A L C O M M E N T A R Y