Posted August 2012
Trichomoniasis is a common STI caused by Trichomonas vaginalis (T. vaginalis), a protozoa transmitted primarily through sexual contact. It may cause asymptomatic infection of long duration, even in individuals who have not been sexually active for extended periods of time. Trichomoniasis may coexist with other infections which cause non-gonococcal urethritis (NGU) or vaginitis syndromes, especially non-chlamydial NGU and bacterial vaginosis (BV).
T. vaginalis prevalence is generally higher among women than men. A recent study found that the prevalence of trichomoniasis in non-HIV-infected persons was 10.1% among women vs 2.0% among men.1 While studies have shown a 10% to 20% prevalence of trichomoniasis in HIV-infected women,2-4 it is not known whether the prevalence, incidence, or clinical course of the disease differs compared with non-HIV-infected women. Data regarding the prevalence of T. vaginalis in men who have sex with men (MSM) are lacking. Trichomoniasis has been associated with increased risk of acquisition and transmission of HIV.5
Trichomoniasis also has been associated with complications of pregnancy, including premature rupture of membranes and preterm birth; however, treatment with metronidazole during pregnancy has not been shown to prevent prematurity.6
II. SCREENING FOR TRICHOMONIASIS
Clinicians should screen all sexually active HIV-infected women for trichomoniasis at baseline and at least annually. (AIII)
Screening sexually active HIV-infected women for trichomoniasis is recommended because 1) treatment has been shown to reduce HIV shedding,7,8 and 2) potential complications related to upper genital tract infections in untreated women can be prevented.9-15
See Section IV: Diagnosis for discussion of diagnostic tests that could be used for screening.
Trichomoniasis may or may not be symptomatic. In women, symptomatic trichomoniasis is more common and may include lower genital tract, urethral, and/or vulvar irritation. Trichomoniasis is classically associated with a diffuse, malodorous greenish-yellow, frothy discharge and punctuate petechia on the cervix (strawberry cervix). When the discharge is malodorous, it may be an indication of concomitant BV. Vaginal wall inflammation is common (40% to 75%) with trichomoniasis, but T. vaginalis is not an invasive organism and does not cause systemic symptoms. Symptoms also can include dysuria and dyspareunia.
In men, asymptomatic and self-limited infection is common. When symptomatic, men present with urethral irritation and NGU symptoms that may be relatively mild.
T. vaginalis does not appear to infect oral and rectal sites.16
Clinicians should confirm the clinical diagnosis of trichomoniasis with laboratory testing. (AI) Confirmatory testing may include the following:
- Wet mount
- Trichomonas culture
- Nucleic acid tests (NATs)
- Point-of-care tests, such as rapid antigen test or nucleic acid probe test
Clinicians should confirm the diagnosis of trichomoniasis when it is detected with the conventional Pap smear. (AI)
Clinicians should screen for other STIs when a patient presents with trichomoniasis. (AII)
Because trichomoniasis symptoms are nonspecific, clinical diagnosis must be confirmed by laboratory testing. Several methods are approved for diagnosing trichomoniasis. In women, the most common method is wet mount, which has a sensitivity of 60% to 70% (sensitivity is much lower in men). If microscopy is not available, a NAT or culture may be used based on local availability.
The rapid antigen test and nucleic acid probe test are considered point-of-care tests with results available within 10 minutes and 45 minutes, respectively. Each test has a sensitivity of >83% and a specificity of >97%. However, false-positive results are more likely to occur with point-of-care tests than with those requiring vaginal wet preparation.
Trichomonas culture is another sensitive and highly specific laboratory diagnostic method. Culture is recommended for women if trichomoniasis is clinically suspected but trichomonads are not observed with microscopy.
A PCR assay for detection of gonorrhea and chlamydial infection (Amplicor; Roche Diagnostic) has been modified for T. vaginalis detection in vaginal or endocervical swabs and in urine from women and men; sensitivity ranges from 88% to 97% and specificity from 98% to 99%.17 The APTIMA T. vaginalis Analyte Specific Reagents (Gen-Probe) also can detect T. vaginalis, with sensitivity and specificity ranges from 74% to 98% and 87% to 98%, respectively.18-20 However, this assay is approved for testing endocervical/vaginal swabs and urine from females only. This test is not approved for use with male specimens.
For men, in whom wet preparation is not sensitive, urine, semen, or urethral swab cultures may be performed. However, NATs (i.e., PCR or transcription-mediated amplification [TMA]) have superior sensitivity for T. vaginalis diagnosis in men.17-20
The sensitivity of a Pap test for T. vaginalis diagnosis is poor. Liquid-based Pap test has improved sensitivity compared with conventional Pap test; however, false-positive tests occur and clinicians should confirm the diagnosis of trichomoniasis.21 In settings where wet mount is the only test available, it may be reasonable to consider empiric treatment, due to the low sensitivity of wet mount.
Clinicians should not use topical antimicrobials (metronidazole gel) to treat trichomoniasis. (AI)
Clinicians should consider rescreening sexually active HIV-infected women 3 months after completion of therapy. (BIII)
Metronidazole and tinidazole both have high cure rates (90% to 95% and 86% to 100%, respectively), and high-level resistance is rare. The alternative regimen (metronidazole 500 mg PO twice daily for 7 days) may be more effective in HIV-infected women than the 2 g single dose22 but may result in lower adherence to treatment. Patients allergic to nitroimidazoles, such as metronidazole and tinidazole, can be managed by metronidazole desensitization in consultation with a specialist.23-25
Metronidazole gel and other topical regimens have been shown to have unacceptably low cure rates (<50% for metronidazole) and are not recommended for treatment of T. vaginalis.
Rescreening after 3 months of therapy should be considered for sexually active women.14,26,27 The most common cause of recurrent or persistent symptoms is reinfection by untreated sex partners (see Section VI. Management of Partners). Evaluation for other infections also should be considered.
If single-dose metronidazole treatment failure occurs and reinfection is excluded, the patient can be treated with tinidazole or the alternative 7-day metronidazole regimen. If failure occurs with either tinidazole or the 7-day metronidazole regimen, treatment with metronidazole or tinidazole at 2 g orally for 5 days can be considered. Persistent treatment failure should be discussed with a specialist, and susceptibility testing by the CDC should be considered (telephone: 1-404-718-4141; website: www.cdc.gov/std).
VI. MANAGEMENT OF PARTNERS
Clinicians should consider both HIV and STI exposures to partners when HIV-infected patients present with a new STI. Clinicians should also assess for the presence of other STIs (see Management of STIs in HIV-Infected Patients). (AIII)
A. Management of HIV Exposure in Partners
When HIV-infected patients present with a new STI, clinicians should offer assistance with notifying partners of both the potential HIV and STI exposures or should refer patients to other sources for partner notification assistance (Partner Services in New York State or CNAP in New York City). Partners without confirmed HIV infection should undergo HIV testing at baseline, 1, 3, and 6 months. Confirmatory testing according to New York State regulations must be performed to confirm HIV diagnoses.
Clinicians must report confirmed cases of HIV according to New York State Public Health Law (for more information about required reporting, see www.health.ny.gov/diseases/aids/regulations/index.htm).
Clinicians should educate patients with non-HIV-infected partners or partners of unknown HIV status to be vigilant for any post-exposure acute HIV symptoms in their partners, such as febrile illness accompanied by rash, lymphadenopathy, myalgias, and/or sore throat (see Diagnosis and Management of Acute HIV Infection). (AIII)
Partners who present within 36 hours of an HIV exposure should be evaluated as soon as possible for initiation of post-exposure prophylaxis therapy (see HIV Prophylaxis Following Non-Occupational Exposure Including Sexual Assault). (AII)
Presentation of a new STI in HIV-infected patients suggests exposure of both HIV and the STI to their partners. In this case, offering HIV non-occupational post-exposure prophylaxis (nPEP) to partners is usually not an option because the period prior to STI symptom onset is usually longer than the 36-hour window for initiating HIV nPEP. Therefore, sequential HIV testing of partners without confirmed HIV infection should be performed for early identification of potential HIV acquisition. However, if a patient with an HIV exposure does present within 36 hours, evaluation for nPEP should occur (see HIV Prophylaxis Following Non-Occupational Exposure Including Sexual Assault).
B. Management of T. vaginalis Exposure in Sex Partners
All recent and current sex partners of patients with acute, persistent, or recurrent trichomoniasis should be treated or referred for treatment regardless of symptoms. (AII)
To prevent serial reinfection and curtail further transmission, sex partners of patients with a diagnosis of symptomatic or asymptomatic trichomoniasis should be treated or referred for treatment, even if clinical symptoms are not present in the contact. In one study, T. vaginalis was found in over 73% of the male partners of women with trichomoniasis.28 In a contact with clinical symptoms, other NGU or vaginitis co-pathogens in addition to T. vaginalis should be excluded. Non-chlamydial NGU and BV are the most common coexisting syndromes in men and women, respectively.
1. Bachmann LH, Hobbs MM, Seña AC, et al. Trichomonas vaginalis genital infections: progress and challenges. Clin Infect Dis 2011;53(Suppl 3):S160-S172. [PubMed]
2. Laga M, Manoka A, Kivuvu M, et al. Non-ulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: Results from a cohort study. AIDS 1993;7:95-102. [PubMed]
3. Cu-Uvin S, Ko H, Jamieson DJ, et al. for the HIV Epidemiology Research Study Group. Prevalence, incidence, and persistence or recurrence of trichomoniasis among human immunodeficiency virus (HIV)-positive and HIV-negative women at high risk for HIV infection. Clin Infect Dis 2002;34:1406-1411. [PubMed]
4. Muzny A, Rivers CA, Austin EL, et al. Trichomonas vaginalis infection among women receiving gynaecological care at an Alabama HIV Clinic. Sex Transm Infect 2013 Feb 28. [Epub ahead of print] [PubMed]
5. Helfgott A, Eriksen N, Bundrick CM, et al. Vaginal infections in human immunodeficiency virus-infected women. Am J Obstet Gynecol 2000;183:347-355. [PubMed]
6. Klebanoff MA, Carey JC, Hauth JC, et al. Failure of metronidazole to prevent preterm delivery among pregnant women with asymptomatic Trichomonas vaginalis infection. N Engl J Med 2001;345:487-493. [PubMed]
7. Tuomala RE, O‘Driscoll PT, Bremer JW, et al. Cell-associated genital tract virus and vertical transmission of human immunodeficiency virus type 1 in antiretroviral-experienced women. J Infect Dis 2003;187:375-384. [PubMed]
8. Wang CC, Mcclelland RS, Reilly M, et al. The effect of treatment of vaginal infections on shedding of human immunodeficiency virus type 1. J Infect Dis 2001;183:1017-1022. [PubMed]
9. Centers for Disease Control and Prevention. Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents. MMWR 2009;58(No. RR-4). [PubMed]
10. Van Der PB, Kwok C, Pierre-Louis B, et al. Trichomonas vaginalis infection and human immunodeficiency virus acquisition in African women. J Infect Dis 2008;197:548554. [PubMed]
11. Moodley P, Wilkinson D, Connolly C, et al. Influence of HIV-1 coinfection on effective management of abnormal vaginal discharge. Sex Transm Dis 2003;30:1-5. [PubMed]
12. Moodley P, Wilkinson D, Connolly C, et al. Trichomonas vaginalis is associated with pelvic inflammatory disease in women infected with human immunodeficiency virus. Clin Infect Dis 2002;34:519-522. [PubMed]
13. McClelland RS, Sangare L, Hassan WM, et al. Infection with Trichomonas vaginalis increases the risk of HIV-1 acquisition. J Infect Dis 2007;195:698-702. [PubMed]
14. Kissinger P, Secor WE, Leichliter JS, et al. Early repeated infections with Trichomonas vaginalis among HIV-positive and HIV-negative women. Clin Infect Dis 2008;46:994-999. [PubMed]
15. Kissinger P, Amedee A, Clark RA, et al. Trichomonas vaginalis treatment reduces vaginal HIV-1 shedding. Sex Transm Dis 2009;36:11-16. [PubMed]
16. Francis SC, Kent CK, Klausner JD, et al. Prevalence of rectal Trichomonas vaginalis and Mycoplasma genitalium in male patients at the San Francisco STD clinic, 2005–2006. Sex Transm Dis 2008;35:797-800. [PubMed]
17. Van Der PB, Kraft CS, Williams JA. Use of an adaptation of a commercially available PCR assay aimed at diagnosis of chlamydia and gonorrhea to detect Trichomonas vaginalis in urogenital specimens. J Clin Microbiol 2006;44:366-373. [PubMed]
18. Hardick A, Hardick J, Wood BJ, et al. Comparison between the Gen-Probe transcription-mediated amplification Trichomonas vaginalis research assay and real-time PCR for Trichomonas vaginalis detection using a Roche LightCycler instrument with female self-obtained vaginal swab samples and male urine samples. J Clin Microbiol 2006;44:4197-4199. [PubMed]
19. Huppert JS, Mortensen JE, Reed JL, et al. Rapid antigen testing compares favorably with transcription-mediated amplification assay for the detection of Trichomonas vaginalis in young women. Clin Infect Dis 2007;45:194-198. [PubMed]
20. Nye MB, Schwebke JR, Body BA. Comparison of APTIMA Trichomonas vaginalis transcription-mediated amplification to wet mount microscopy, culture, and polymerase chain reaction for diagnosis of trichomoniasis in men and women. Am J Obstet Gynecol 2009;200:188-197. [PubMed]
21. Lara-Torre E, Pinkerton JS. Accuracy of detection of Trichomonas vaginalis organisms on a liquid-based papanicolaou smear. Am J Obstet Gynecol 2003;188:354-356. [PubMed]
22. Kissinger P, Mena L, Levison J, et al. A randomized treatment trial: Single versus 7-day dose of metronidazole for the treatment of Trichomonas vaginalis among HIV-infected women. J Acquir Immune Defic Syndr 2010;55:565-571. [PubMed]
23. Pearlman MD, Yashar C, Ernst S, et al. An incremental dosing protocol for women with severe vaginal trichomoniasis and adverse reaction to metronidazole. Am J Obstet Gynecol 1996;174:934-936. [PubMed]
24. Kurohara ML, Kwong FK, Lebherz TB, et al. Metronidazole hypersensitivity and oral desensitization. J Allergy Clin Immunol 1991;88:279-280. [PubMed]
25. Helms DJ, Mosure DJ, Secor WE, et al. Management of Trichomonas vaginalis in women with suspected metronidazole hypersensitivity. Am J Obstet Gynecol 2008;198:370-377. [PubMed]
26. Peterman TA, Tian LH, Metcalf CA, et al. High incidence of new sexually transmitted infections in the year following a sexually transmitted infection: A case for rescreening. Ann Intern Med 2006;145:564-572. [PubMed]
27. Niccolai LM, Kopicko JJ, Kassie A, et al. Incidence and predictors of reinfection with Trichomonas vaginalis in HIV-infected women. Sex Transm Dis 2000;27:284-288. [PubMed]
28. Hobbs MM, Lapple DM, Lawing LF, et al. Methods for detection of Trichomonas vaginalis in the male partners of infected women: Implications for control of trichomoniasis. J Clin Microbiol 2006;44:3994-3999. Epub 2006 Sep 13. [PubMed]