Trichomonas vaginalis, HIV, and African-Americans. (Synopsis).(Statistical Data Included)

Trichomonas vaginalis may be emerging as one of the most important cofactors in amplifying HIV transmission, particularly in African-American communities of the United States. In a person co-infected with HIV, the pathology induced by T. vaginalis infection can increase HIV shedding. Trichomonas infection may also act to expand the portal of entry for HIV in an HIV-negative person. Studies from Africa have suggested that T. vaginalis infection may increase the rate of HIV transmission by approximately twofold. Available data indicate that T. vaginalis is highly prevalent among African-Americans in major urban centers of the United States and is often the most common sexually transmitted infection in black women. Even if T. vaginalis increases the risk of HIV transmission by a small amount, this could translate into an important amplifying effect since Trichomonas is so common. Substantial HIV transmission may be attributable to T. vaginalis in African-American communities of the United States.

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Trichomonas vaginalis is a protozoan parasite transmitted principally through vaginal intercourse. Infection with the organism, while frequently asymptomatic, can cause vaginitis in women and urethritis in men. Despite a relative paucity of studies on the prevalence and incidence of trichomoniasis, recent publications suggest that T. vaginalis is one of the most common sexually transmitted infections (STIs) in the United States, with an estimated 5 million new cases occurring annually (1). Although the organism appears to be highly prevalent and has a widespread geographic distribution, Trichomonas has not been the focus of intensive study nor of active control programs. This neglect is likely a function of the relatively mild nature of the disease (2), the lack of effect on fertility, and the historic absence of association with adverse birth outcomes (although recent data suggest a possible causal role in low birth weight and prematurity [3]). However, Trichomonas may play a critical and underrecognized role in amplifying HIV transmission (4). We present the rationale to support the hypothesis that T. vaginalis may be an important cofactor in promoting the spread of HIV and, in some circumstances, may have a major impact on the epidemic dynamics of HIV in African-American communities.

Biologic Rationale

Expanding the Portals of Entry and Exit

T. vaginalis infection typically elicits an aggressive local cellular immune response with inflammation of the vaginal epithelium and exocervix in women and the urethra of men (5). This inflammatory response induces a large infiltration of leukocytes, including HIV target cells such as CD4+ bearing lymphocytes and macrophages to which HIV can bind and gain access (6,7). In addition, T. vaginalis can frequently cause punctate mucosal hemorrhages (8). In an HIV-negative person, both the leukocyte infiltration and genital lesions induced by Trichomonas may enlarge the portal of entry for HIV by increasing the number of target cells for the virus and allowing direct viral access to the bloodstream through open lesions. Similarly, in an HIV-infected person the hemorrhages and inflammation can increase the level of virus-laden body fluids, the numbers of HIV-infected lymphocytes and macrophages present in the genital contact area, or both. The resulting increase of both free virus and virus-infected leukocytes can expand the portal of exit, thereby heightening the probability of HIV exposure and transmission to an uninfected partner. Increased cervical shedding of HIV has been shown to be associated with cervical inflammation (9), and substantially increased urethral viral loads have been documented in men with Trichomonas infection (10). In addition, T. vaginalis has the capacity to degrade secretory leukocyte protease inhibitor, a product known to block HIV cell attachment; this phenomenon may also promote HIV transmission (11). Moreover, since most patients with Trichomonas infection are asymptomatic or mildly symptomatic (12), they are likely to continue to remain sexually active in spite of infection. Studies suggest that approximately 50%-70% of persons with T. vaginalis have subclinical infection (12).

Empiric Evidence Implicating Trichomonas in HIV Transmission

Data from studies conducted in Africa have shown an association between Trichomonas and HIV infection, suggesting a two- to threefold increase in HIV transmission (4,13,14). A cross-sectional study conducted among 1,209 female sex workers in the Ivory Coast found an association between HIV and Trichomonas infection in bivariate analysis (crude odds ratio 1.8, 95% confidence intervals 1.3, 2.7). In another cross-sectional study performed in Tanzania among 359 women admitted to a hospital for gynecologic conditions, Trichomonas was more common in women with HIV infection in multivariate analysis (odds ratio 2.96, no confidence intervals provided, p<0.001). While such cross-sectional studies are limited by the issue of temporal …