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 in females is 5-28 days. Symptoms may begin or exacerbate with menses. Most infected women eventually develop symptoms, although up to one third remain asymptomatic. Common signs and symptoms include a copious malodorous gray, frothy vaginal discharge, vulvovaginal irritation, dysuria, and dyspareunia. Physical examination may reveal a frothy discharge with vaginal erythema and cervical hemorrhages (“strawberry cervix”). The discharge usually has a pH of >4.5. Abdominal discomfort is unusual and should prompt evaluation for pelvic inflammatory disease (Chapter 114).

Most infections in males are asymptomatic. Symptomatic males usually have dysuria and scant urethral discharge. Trichomonads occasionally cause epididymitis, prostatic involvement, and superficial penile ulceration. Infection is often self-limited, spontaneously resolving in 36% of men. Trichomonas has been implicated as a cause of recurrent or relapsing urethritis and can be isolated in 3-20% of men with nongonococcal urethritis. Treatment failures with standard therapy for gonorrhea and Chlamydia are frequently treated with antitrichomonal therapy.

Diagnosis

Trichomonads may be recognized in vaginal secretions by using the wet mount technique. This technique has been estimated to have a sensitivity of 60-70%; studies using more sensitive assays with nucleic acid probes and polymerase chain reaction (PCR) have suggested that this is closer to 35-60%. Although Trichomonas is sometimes seen on Pap smears and urine, these methods are not considered reliable tests for disease. Wet mount examination of material obtained by platinum loop from the anterior urethra may reveal the organism in 50-90% of infected men. Microscopic examination of urine sediment after prostatic massage is also useful in infected men. Culture of the organism is the gold standard for detection, and commercial culture media are available. Enzyme-linked immunosorbent assay and direct fluorescent antigen testing of vaginal secretions are more sensitive than wet mount testing but less sensitive than culture for detection of T. vaginalis infection. In women, DNA immunoblot and PCR testing of vaginal secretions have similar sensitivity and specificity to culture. In men, these methods appear to be more sensitive at detection of infection than culture. Nucleic acid amplification testing (NAAT) and immunologic diagnostic kits for diagnosis of Trichomonas alone and in combination with other gynecologic diseases such as Candida and Gardnerella have been evaluated by multiple studies and have been found to be accurate and easy to use. At least 2 point-of-care kits for rapid testing, Affirm VP III (BD Diagnostic Systems, Sparks, MD) and OSOM Trichomonas Rapid Test (Genzyme Diagnostics, Cambridge, MA), have received approval by the U.S. Food and Drug Administration (FDA). Conventional and multiplex PCR assays for clinical use have been developed, and preliminary testing results are promising. Patients with T. vaginalis should be screened for other sexually transmitted infections, including Chlamydia and gonorrhea.

Complications

Untreated trichomoniasis has been associated with pelvic inflammatory disease, premature delivery, low birthweight, tubal infertility, and vaginal cuff cellulitis. T. vaginalis infection increases the risk of acquisition and transmission of HIV. Trichomonas-induced inflammation of the genital mucosa recruits greater numbers of CD4⁺ cells in the epithelium and provides more direct access to the bloodstream for HIV. In HIV-infected individuals, trichomoniasis is associated with a higher viral load in cervical secretions and semen as well as higher levels of infected lymphocytes in urogenital fluids. HIV-1 shedding in vaginal fluids is decreased by treatment of trichomoniasis.

Treatment

In the USA, metronidazole and tinidazole are used; in other countries ornidazole is also used. Both metronidazole (single-dose regimen of 2 g orally as a single dose for adolescent and adults; alternative regimen, 500 mg orally bid for 7 days) and tinidazole (single 2 g dose orally in adolescents and adults) are used as first-line treatment. For children infected prior to adolescence, the recommended regimen is metronidazole 15 mg/kg/day divided in 3 doses orally for 7 days; tinidazole is not approved for dosing in younger children. Topical metronidazole gel is not efficacious when used as the sole therapy for T. vaginalis infection, but it may decrease symptoms in individuals with severe infection when used in conjunction with oral therapy. Sexual partners should be treated simultaneously to prevent reinfection. Multiple head-to-head trials comparing the efficacy between single-dose/short courses of metronidazole and single-dose tinidazole have shown either noninferiority or superior efficacy for tinidazole. A Cochrane meta-analysis demonstrated that single dose tinidazole was superior compared to short-course metronidazole in clinical efficacy and parasitologic cure rates and had significantly fewer side effects. Tinidazole is more expensive than metronidazole and is generally reserved for treatment failures or metronidazole intolerance.

Treatment failures have been reported with metronidazole, although poor response can usually be overcome by higher doses of drugs. Second-line treatment recommendations include either a 7-day course of metronidazole 500 mg twice daily or a single dose of tinidazole. If this treatment fails, either metronidazole or tinidazole at 2 g daily for 5 days is recommended. Further treatment failure should be referred to an infectious diseases specialist and may require susceptibility testing, which is available from the Centers for Disease Control and Prevention. Metronidazole has not been shown to be teratogenic during pregnancy in humans but is currently classified as a category C drug. At least 2 prospective studies showed an association between premature births or low birth weight with metronidazole treatment of asymptomatic T. vaginalis infection in pregnancy. Further studies are needed to confirm these findings. Treatment of symptomatic trichomoniasis in pregnancy should be weighed against possible risks, while treatment of asymptomatic disease should be delayed as much as possible to near term.

Prevention

Prevention of T. vaginalis infection is best accomplished by treatment of all sexual partners of an infected person and by programs aimed at prevention of all sexually transmitted infections (Chapter 114). No vaccine is available, and drug prophylaxis is not recommended.