Trichomonosis, a Common Curable STI, and Prostate Carcinogenesis—A Proposed Molecular Mechanism

Trichomonosis, a sexually transmitted infection (STI) caused by the protist Trichomonas vaginalis, has significant public health relevance. The annual incidence is ,8 million women in the United States and 170 million worldwide, with an equal number of infected male partners [1]. Both men and women infected with T. vaginalis are at increased risk for human immunodeficiency virus infection [1]. Recent evidence suggests this STI is associated with increased risk of prostate cancer, the most commonly diagnosed cancer and the second leading cause of cancer death among men in the United States [2]. There is no immunity to T. vaginalis, and a hallmark of this STI agent is persistence. Most T. vaginalis infections in men are asymptomatic, and few are diagnosed and treated; thus, infections persist. In older, pre-antibiotic era studies, T. vaginalis was frequently found in prostate fluid specimens from asymptomatic male partners of women with trichomonosis, leading to the belief that the prostate might serve as the reservoir for trichomonosis in men [3]. Trichomonosis may cause chronic prostatitis, and researchers have identified trichomonads in the prostatic urethra, glandular lumina, submucosa, and stroma [4] and, more recently, in benign hyperplastic prostatic tissue [3]. They also observed foci of nonspecific acute and chronic inflammation, as well as intraepithelial vacuolization, near trichomonads, leading them to propose that trichomonosis might contribute to prostate carcinogenesis [4].