Epidemiology

Over 170 million new cases of trichomoniasis occur yearly, the majority in resource-limited settings. Prevalence and incidence rates are likely underestimated, as most men and up to 30% of women are asymptomatic. Diagnostic accuracy using wet mount microscopy, the mainstay of diagnosis, is less sensitive than previously assumed. While the disease is easily treated, sequelae of untreated infection remain a significant cause of morbidity due to high reinfection rates from untreated partners, underrecognition of asymptomatic cases, and insensitive diagnostics.

From 5 to 8 million cases of trichomoniasis occur each year in the USA. A population-based study conducted in 2005 showed a prevalence of 2.8% in women, 1.7% in men, and an overall prevalence of 2.3%. The incidence of trichomoniasis is highest among females with multiple sexual partners and in groups with the highest rates of other sexually transmitted infections. 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 10¹ to 10⁵ or more protozoa/mL. T. vaginalis is pear shaped and exhibits characteristic twitching motility in wet mount (Fig. 276-1). Reproduction is by binary fission. It exists only as vegetative cells; cyst forms have not been described. T. vaginalis damages host cells and tissues by a number of mechanisms. Adhesion molecules allow attachment of T. vaginalis to host cells, and hydrolases, proteases, and cytotoxic molecules act to destroy or impair the integrity of host cells. Parasite-specific antibodies and lymphocyte priming occur in response to infection, but durable protective immunity does not occur.

Figure 276-1 Trichomonas vaginalis trophozoites stained with Giemsa (left) and iron hematoxylin (right).

(From the Centers for Disease Control and Prevention: Laboratory identification of parasites of public health concern. Trichomoniasis (website). www.dpd.cdc.gov/dpdx/HTML/ImageLibrary/Trichomoniasis_il.htm. Accessed August 30, 2010.)

Clinical Manifestations

The incubation period