Updated: Dec 06, 2018
  • Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor: Michael Stuart Bronze, MD  more...
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Trichomoniasis is a sexually transmitted infection (STI) caused by the motile parasitic protozoan Trichomonas vaginalis. It is one of the most common STIs, both in the United States and worldwide. [1, 2]

The high prevalence of T vaginalis infection worldwide and the frequency of coinfection with other STIs make trichomoniasis a compelling public health concern. Notably, research has shown that infection with T vaginalis increases the risk of HIV transmission in both men and women. [1, 3] Trichomoniasis is also associated with adverse pregnancy outcomes, infertility, postoperative infections, and cervical neoplasia. [4]

Humans are the only known host of T vaginalis. Transmission occurs predominantly via sexual intercourse. The organism is most commonly isolated from vaginal secretions in women and urethral secretions in men. It has not been isolated from oral sites, and rectal prevalence appears to be low in men who have sex with men. [5]

Women with trichomoniasis may be asymptomatic or may experience various symptoms, including a frothy yellow-green vaginal discharge and vulvar irritation. Men with trichomoniasis may experience nongonococcal urethritis but are frequently asymptomatic. [6]

Trichomoniasis is thought to be widely underdiagnosed due to a variety of factors, including a lack of routine testing, [2] the low sensitivity of a commonly used diagnostic technique (wet mount microscopy), [6, 7, 8] and nonspecific symptomatology. Self-diagnosis and self-treatment or diagnosis by practitioners without adequate laboratory testing may also contribute to misdiagnosis.

Testing is recommended for T vaginalis in all women seeking care for vaginal discharge and screening for T vaginalis in women at high risk of STI. [9]

Sex partners of infected women should also be treated. Both patient and partner should abstain from sex until pharmacological treatment has been completed and they have no symptoms. Infected women who are sexually active have a high rate of reinfection; thus, rescreening at 3 months post treatment should be considered. [9] Currently, no data are available on rescreening men.

Oral metronidazole (Flagyl) remains the treatment of choice for trichomoniasis. In cases in which the first-line agent is ineffective, other nitroimidazoles or high doses of metronidazole may be used. Topical metronidazole and other antimicrobials are not efficacious and should not be used to treat trichomoniasis.



T vaginalis is approximately the size of a white blood cell (WBC)—about 10-20 μm long and 2-14 μm wide—though its size may vary with physical conditions (see the image below). It has 4 flagella projecting from the anterior portion of the cell and 1 flagellum extending backward to the middle of the organism, forming an undulating membrane. An axostyle, a rigid structure, extends from the posterior aspect of the organism. [10, 11]

Trichomonas vaginalis. (A) Two trophozoites of T v Trichomonas vaginalis. (A) Two trophozoites of T vaginalis obtained from in vitro culture, stained with Giemsa. (B) Trophozoite of T vaginalis in vaginal smear, stained with Giemsa. Images courtesy of Centers for Disease Control and Prevention.

In women, T vaginalis is isolated from the vagina, cervix, urethra, bladder, and Bartholin and Skene glands. In men, the organism is found in the anterior urethra, external genitalia, prostate, epididymis, and semen (see the image below). It resides both in the lumen and on the mucosal surfaces of the urogenital tract. [11] The flagella allow the trophozoite to move around vaginal and urethral tissues.

Life cycle of Trichomonas vaginalis. T vaginalis t Life cycle of Trichomonas vaginalis. T vaginalis trophozoite resides in female lower genital tract and in male urethra and prostate (1), where it replicates by binary fission (2). The parasite does not appear to have a cyst form and does not survive well in the external environment. T vaginalis is transmitted among humans, the only known host, primarily via sexual intercourse (3). Image courtesy of Centers for Disease Control and Prevention.

During infection with T vaginalis, jerky motile trichomonads may be observed on wet mount microscopy. T vaginalis destroys epithelial cells by direct cell contact and by release of cytotoxic substances. It also binds to host plasma proteins, thereby preventing recognition by the alternative complement pathway and by host proteinases. [1] During infection, the vaginal pH increases, as does the number of polymorphonuclear leukocytes (PMNs). PMNs, a type of white blood cell, are the predominant host defense mechanism. These cells respond to chemotactic substances released by trichomonads. There is also evidence that lymphocyte priming occurs, as shown by the presence of antigen-specific peripheral blood mononuclear cells. [11] An antibody response has been detected both locally and in serum. However, infection produces an immunity that is only partially protective, at best.

Despite the interaction the human immune system has with T vaginalis, there is little evidence that a healthy immune system prevents infection. One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in HIV-infected women. [12] Another study showed that HIV seropositivity did not alter the rate of infection in males. [13]

Symptoms of trichomoniasis typically occur after an incubation period of 4-28 days. [11, 14] Infection may persist for long periods in women but generally persists for fewer than 10 days in males. Anecdotal evidence suggests that asymptomatic infection may persist for months or even years in women. [15]



The risk of acquiring T vaginalis infection is based on the type of sexual activity. Women who engage in higher-risk sexual activity are at a greater risk of infection. Risk factors for T vaginalis infection include:

  • New or multiple partners

  • A history of STIs

  • Current STIs

  • Sexual contact with an infected partner

  • Exchanging sex for money or drugs

  • Using injection drugs

  • Not using barrier contraception (eg, because of oral contraceptives)

In a study that considered risk factors for prevalent trichomoniasis, drug use in the preceding 30 days was the one most strongly associated with infection and with incident infection (new infection observed during the study). [16] The most significant risk factor was sexual activity in the preceding 30 days (with 1 or more partners). Women with 1 or more sexual partners in the preceding 30 days were 4 times more likely to have T vaginalis infection. [16]



United States statistics

Trichomoniasis is one of the most common STIs in the United States, with a prevalence estimated at 8 million cases annually. [17, 18, 19, 20] Exact numbers are difficult to obtain because the infection is not nationally reportable and many infections are asymptomatic. Prevalence is also thought to be underestimated due to the low sensitivity of diagnostic tests, particularly the commonly used wet mount technique.

Research done among high-risk populations shows that the prevalence varies widely. The prevalence of T vaginalis infection at STI clinics ranges from 15% to 54%. [21] The reported prevalence from a different study done among inner-city STI clinics approached 25%. [11] In 2 samples of female prison inmates, the prevalence was 31.2-46.9%. [22, 23] In men, trichomoniasis accounts for 10-21% of urethritis cases not attributable to gonorrheal or chlamydial infection. [21] Multiple studies have found that T vaginalis infection is less prevalent in men than in women. [24, 25, 26]

International statistics

Estimates of the worldwide prevalence of trichomoniasis range from 170-180 million cases annually. The World Health Organization estimates the worldwide incidence of trichomonas infection at over 170 million cases annually. [27]

The incidence of trichomoniasis in Europe is similar to that in the United States. In Africa, the prevalence of trichomoniasis may be much higher. The prevalence of vaginal T vaginalis infection was estimated to be 11-25% among African study populations. [28, 29, 30]

Age-related demographics

Trichomoniasis is an STI. As such, it is typically found in sexually active adolescents and adults. In female adolescents, trichomoniasis is more common than gonorrhea; this is particularly disconcerting in that it increases susceptibility to other infections. [31]

Vertical transmission of T vaginalis during birth is possible and may persist up to 1 year. From 2-17% of female offspring of infected women acquire infection. [32]

Unlike other STIs, trichomoniasis generally becomes more common with age and lifetime number of sexual partners. [33] The National Longitudinal Study of Adolescent Health Study [34] found a prevalence of 2.3% among adolescents aged 18-24 years and 4% among adults 25 years and older. A prevalence of 3.1% in females aged 14-49 years was observed based on a nationally representative sample of women in the National Health and Nutrition Examination Survey (NHANES) 2001-2004 study. [33]

In a study of men attending an STI clinic in Denver, the prevalence of trichomonal infection was 0.8% in men younger than 30 years and 5.1% in men 30 years and older. The increase in prevalence was thought to be due to age-related enlargement of the prostate gland. [24]

Sex-related demographics

Symptomatic trichomoniasis is more common in women than in men. Trichomoniasis infection in men tends to be less clinically apparent. However, women can also frequently be asymptomatic carriers. The NHANES 2001-2004 study conducted on a nationally representative sample of women aged 14-49 years found that 85% of women found to have trichomoniasis reported no symptoms. [33]

The reported incidence of trichomoniasis among men in various populations has ranged from 2.8-17%. [24, 25] This incidence may be underestimated, depending on the method of detection and the site of specimen collection. The use of multiple sites in the genitourinary tract (urine, urethral swab, and semen) in male patients has been shown to increase sensitivity. [35]

In one study, T vaginalis was detected in 72% of male sexual partners of women with trichomoniasis. [36] Of these, 77% patients were asymptomatic.

Race-related demographics

In the National Longitudinal Study of Adolescent Health Study, significant differences in the prevalence of trichomoniasis among adolescents were noted by race: white, 1.2%; Asian, 1.8%; Latino, 2.1%; Native American, 4.1%; and African American, 6.9%. [34] Considerable differences were also observed in the national NHANES 2001-2004 study conducted among women ages 14-49: non-Hispanic whites, 1.2%; Mexican Americans, 1.5%; and non-Hispanic blacks, 13.5%. [33]

Evidence suggests that T vaginalis infection likely increases HIV transmission. Thus, the observed higher prevalence of T vaginalis infection among African American women is cause for great concern. Control of T vaginalis may represent an important means of slowing HIV transmission, particularly among African Americans. [37]



Recommended metronidazole therapy regimens have produced a 90-95% cure rate in randomized clinical trials. [9] The recommended tinidazole regimens have produced cure rates of 86-100%. [9] Cure rates may be even higher with concurrent treatment of a patient’s sexual partners.

Recurrent infections are common in sexually active patients. One study found that 17% of sexually active patients with T vaginalis infection were reinfected at 3-month follow-up. [38]

T vaginalis infection is strongly associated with the presence of other STIs, including gonorrhea, [39] chlamydia, and sexually transmitted viruses. T vaginalis infection increases the susceptibility to other viruses, including herpes, human papillomavirus (HPV), and HIV. [31] Persons with trichomoniasis are twice as likely to develop HIV infection as the general population. [29] There are 2 explanations for the association between T vaginalis and HIV, as follows:

  • Disruption of the epithelial monolayer leads to increased passage of the HIV virus

  • T vaginalis induces immune activation, specifically lymphocyte activation and replication and cytokine production, leading to increased viral replication in HIV-infected cells

Pregnant women with T vaginalis infection are more likely than uninfected women to deliver preterm or to have other adverse pregnancy outcomes, including low birth weight, premature rupture of membranes, and intrauterine infection. [1] Respiratory or genital infection in the newborn may also occur. [6] T vaginalis infection may also increase the vertical transmission of HIV due to a disruption of the vaginal mucosa.

One study reported a higher risk of pelvic inflammatory disease (PID) in women with trichomoniasis. [40] Other studies have reported a 1.9-fold risk of tubal infertility in women with trichomoniasis. [41] Trichomoniasis may also play a role in cervical neoplasia and postoperative infections. [4]


Patient Education

Education concerning STI treatment and prevention is vital (see Prevention). Because T vaginalis infection is strongly associated with the presence of other STIs (gonorrhea, [39] chlamydia, and sexually transmitted viruses such as HIV), providers should provide appropriate counseling, testing, and treatment.

Upon diagnosis of trichomoniasis, healthcare providers should discuss treatment, including the adverse effects and interactions encountered with metronidazole and other nitroimidazole drugs, and should address the treatment of sexual partners. Persons with trichomoniasis who notify partners of their infection help disrupt the transmission of trichomoniasis and other STIs. [6] Providers should also discuss methods of preventing T vaginalis reinfection. It may be important to explain that the infection may have been longstanding and not due to a recent sexual encounter. Lastly, the US Centers for Disease Control and Prevention (CDC) advises providers to consider rescreening sexually active women at 3 months after the completion of treatment. [9]

For additional patient education resources, see the CDC’s Fact Sheet.