Trichomoniasis

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Trichomoniasis

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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]

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.

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]

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]

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]

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]

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.

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]

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.

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Darvin Scott Smith, MD, MSc, DTM&H Adjunct Associate Clinical Professor, Department of Microbiology and Immunology, Stanford University School of Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Permanente Medical Group

Darvin Scott Smith, MD, MSc, DTM&H is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine

Disclosure: Nothing to disclose.

Natalia Ramos, MD, MPH Clinical Assistant Professor, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Judith C Brillman, MD Professor Emerita, Emergency Medicine Department, University of New Mexico School of Medicine

Judith C Brillman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Association of Women Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Benjamin W Friedman, MD Staff Physician, Department of Emergency Medicine, Jacobi/Montefiore Medical Centers

Benjamin W Friedman, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George’s University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Ashir Kumar, MD, MBBS, FAAP Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS, FAAP is a member of the following medical societies: American Association of Physicians of Indian Origin and Infectious Diseases Society of America

Disclosure: Nothing to disclose

Mark L Plaster, MD, JD Executive Editor, Emergency Physicians Monthly

Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

Binita R Shah, MD, FAAP, Professor of Clinical Pediatrics and Emergency Medicine, SUNY Health Sciences Center at Brooklyn; Director of Pediatric Emergency Medicine, Departments of Emergency Medicine and Pediatrics, Kings County Hospital Center

Binita R Shah, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children’s Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Robert W Tolan Jr, MD Chief, Division of Allergy, Immunology and Infectious Diseases, The Children’s Hospital at Saint Peter’s University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

R Gentry Wilkerson, MD Assistant Professor, Director of Research, Emergency Medicine Residency Program, University of South Florida College of Medicine, Tampa General Hospital

R Gentry Wilkerson, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Renee Wilson, MD, Clinical Assistant Instructor, Department of Emergency Medicine, SUNY-Downstate and Kings County Hospital

Renee Wilson, MD is a member of the following medical societies: Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Jeffrey M Zaks, MD Clinical Associate Professor of Medicine, Wayne State University School of Medicine; Vice President, Medical Affairs, Chief Medical Officer, Department of Internal Medicine, Providence Hospital

Jeffrey M Zaks, MD is a member of the following medical societies: American College of Cardiology, American College of Healthcare Executives, American College of Physician Executives, and American Medical Association

Disclosure: Nothing to disclose.

Acknowledgments

The authors wish to thank Amy Cai, MD, for the video and for sharing patient samples and insights.

Trichomoniasis

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