| dc.description.abstract | 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 | en_US |
