Trichomoniasis (Trichomonas vaginalis)


Trichomoniasis is caused by the protozoan Trichomonas vaginalis. It is the second most common sexually transmitted infection worldwide. Vulvovaginitis is the symptomatic disease form, but T. vaginalis has been implicated in pelvic inflammatory disease, pregnancy loss, chronic prostatitis, and an increased risk of HIV transmission.

Epidemiology

Over 276 million new cases of trichomoniasis occur annually, making it the most common nonviral sexually transmitted infection globally. Most men and up to 30% of women are asymptomatic. Although the disease is easily treated, sequelae of untreated infection remain a significant cause of morbidity because of high reinfection rates from untreated partners, underrecognition of asymptomatic cases, and insensitive diagnostics.

Trichomoniasis is the most common parasitic infection in the United States, with a total of 3.7 million cases and approximately 1.1 million new infections per year. T. vaginalis is recovered from > 60% of female partners of infected men and 70% of male sexual partners of infected women. Vaginal trichomoniasis is rare until menarche. Its presence in a younger child should raise the possibility of sexual abuse.

Trichomoniasis may be transmitted to neonates during passage through an infected birth canal. Infection in this setting is usually self-limited, but rare cases of neonatal vaginitis and respiratory infection have been reported.

Pathogenesis

T. vaginalis is an anaerobic, flagellated protozoan parasite. Infected vaginal secretions contain 10 1 to 10 5 or more protozoa/mL. T. vaginalis is pear shaped and exhibits characteristic twitching motility in wet mount ( Fig. 310.1 ). Reproduction is by binary fission. It exists only as vegetative cells; cyst forms have not been described. Many types of adhesion molecules allow attachment of T. vaginalis to host cells. Tv lipoglycan is a surface glycoconjugate that binds human galectin-1 and -3 and plays a major role in adhesion, pathogenesis, and immune modulation. In addition, hundreds of putative membrane proteins, BspA proteins, and tetraspanins are involved in cellular attachment. Some of these proteins are contained in exosome vesicles, along with a large concentration of RNA oligonucleotides, which seem to further enhance adhesion. Adhesion is a prerequisite to cytolysis, and once attached the parasite secretes hydrolases, proteases, and cytotoxic molecules that destroy or impair the integrity of host cells. Trichomonas is highly dependent on iron for its growth and metabolism, and cysteine proteinase mRNAs have been shown to interact with other parasite proteins for posttranscriptional regulation in the absence of iron-regulatory proteins, which are present in other eukaryotes. This dependence on iron may partially explain the propensity of T. vaginalis to infect women due to a higher iron state during menses. The T. vaginalis genome is very large, with multiple repetitive sequences and transposable elements making up over 60,000 genes, as well as apparently nonfunctional but transcribed pseudogenes. This unusually large number of genetic elements is thought to have an adaptive function, with differential gene expression occurring in response to differing conditions, giving the organism flexibility for survival.

Fig. 310.1, Trichomonas vaginalis trophozoites stained with Giemsa (A) and iron hematoxylin (B).

Macrophage migration and cytokine production have been shown to be downregulated by the parasite in successful infection. Parasite-specific antibodies and lymphocyte priming occur in response to infection, but durable protective immunity does not occur, possibly also owing to degradation of antibodies by parasitic cysteine proteases.

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