eMedicine Specialties > Emergency Medicine > Infectious Diseases

Trichomoniasis

Author: R Gentry Wilkerson, MD, Clinical Assistant Professor, Department of Emergency Medicine, State University of New York-Downstate; Attending Physician, Department of Emergency Medicine, Kings County Hospital
Coauthor(s): 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; Benjamin W Friedman, MD, Staff Physician, Department of Emergency Medicine, Jacobi/Montefiore Medical Centers; Judith C Brillman, MD, Professor, Department of Emergency Medicine, Assistant Dean, Graduate Medical Education, University of New Mexico School of Medicine
Contributor Information and Disclosures

Updated: Oct 22, 2009

Introduction

Background

Trichomoniasis is a nonreportable sexually transmitted disease (STD) caused by the parasite Trichomonas vaginalis. Humans are the only known host with the trophozoite transmitted via coitus. Transmission via fomites has been reported. The organisms are usually pyriform in shape, although they may take an amoeboid shape after attachment to the vaginal epithelium.

Life cycle of <I>Trichomonas vaginalis.</I><I>T v...

Life cycle of Trichomonas vaginalis.T vaginalis resides in the female lower genital tract and the 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, its only known host, primarily by sexual intercourse (3). Image courtesy of the Centers for Disease Control and Prevention.

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Life cycle of <I>Trichomonas vaginalis.</I><I>T v...

Life cycle of Trichomonas vaginalis.T vaginalis resides in the female lower genital tract and the 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, its only known host, primarily by sexual intercourse (3). Image courtesy of the Centers for Disease Control and Prevention.


The individual organism is 10-20 m m long and 2-14 m m wide. Four flagella project from the anterior portion of the cell and one flagellum extends backwards to the middle of the organism, forming an undulating membrane. An axostyle extends from the posterior aspect of the organism.1

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Trichomonas vaginalis on a saline wet mount at 40X on the microscope. Several motile parasites transit through the field, surrounded by white blood cells and squamous epithelial cells.

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<I>Trichomonas vaginalis</I> on a saline wet moun...

Trichomonas vaginalis on a saline wet mount at 40X on the microscope. Several motile parasites transit through the field, surrounded by white blood cells and squamous epithelial cells.


<i>Trichomonas vaginalis.</i> A, Two trophozoites...

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

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<i>Trichomonas vaginalis.</i> A, Two trophozoites...

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


Pathophysiology

T vaginalis principally infects the squamous epithelium of the genital tract. Incubation time is generally between 4 and 28 days.2,3 Infection may persist for long periods in females but generally persists less than 10 days in males. Anecdotal evidence suggests that asymptomatic infection may persist for months or even years in women.4

Infection produces immunity that at best is only partially protective. There is evidence of lymphocyte priming as shown by the presence of antigen-specific peripheral blood mononuclear cells.2 An antibody response locally and in serum has also been detected. Despite the interaction that the human immune system has with T vaginalis, there is little evidence that it prevents infection. One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in HIV women.5 Another study showed that human immunodeficiency virus (HIV) seropositivity does not alter the rate of infection in males.6

Frequency

United States

  • An estimated 7.4 million new cases of trichomoniasis occur per year in the United States.7
  • The prevalence in adolescents is reported to be 2.3%8 and 3.1% in women aged 14-49 years9 .  
  • The reported prevalence in inner-city STD clinics approaches 25%.2 Other high-risk populations have very high prevalence rates reported. In two samples of female prison inmates, the prevalence was 31.2-46.9%.10,11
  • Exact numbers are difficult to obtain, as the infection is not nationally reportable, and many infections are asymptomatic. Prevalence is also typically underestimated due to the poor sensitivity of diagnostic tests.

International

The World Health Organization estimates that the burden of trichomonal infection is 174 million cases. 12

Mortality/Morbidity

  • In females, vaginitis is the most common manifestation of infection. Other complications include infection of the adnexa, endometrium, and Skene and Bartholin glands.
  • Males are usually asymptomatic. When symptoms are present, they usually manifest as urethritis. Up to 11% of nongonococcal urethritis cases in men are caused by T vaginalis.13 Other complications include infection of the prostate, foreskin, glans, and epididymis.
  • T vaginalis has been found in the bronchoalveolar lavage fluid taken from patients with Pneumocystis pneumonia14 and acute respiratory distress syndrome.15 In this setting, the organism appears amoeboid, without the presence of flagella.
  • Trichomonal sinus disease has been reported in a previously healthy adolescent following multiple trauma who had previously engaged in oral-to-genital sexual activity.
  • Infection with T vaginalis is a marker of high-risk sexual behavior. Co-infection with other STDs is common. In one study of adolescents that had a diagnosis of at least one STD, there was almost a 9-fold increase in the likelihood of T vaginalis infection in the ensuing 3 months.16
  • Infection with T vaginalis may increase the rate of infection or reactivation with human papillomavirus, although it may shorten the duration of infection.17
  • Trichomoniasis predisposes one to infection with HIV. Infection with HIV increases one's infectiveness for transmitting T vaginalis.
    • Cheeson et al estimates that 747 new HIV cases a year in women alone are a result of the facilitative effects of T vaginalis on the transmission of the HIV virus.18
    • Symptomatic males with T vaginalis and HIV had significantly higher numbers of HIV RNA particles in their seminal fluid.
    • Treatment of trichomoniasis has been shown to decrease the rate of viral shedding in HIV patients.19,20
  • The Vaginal Infections and Prematurity (VIP) Study showed infection with T vaginalis resulted in an increased risk of low birth weight, preterm delivery, and preterm delivery of a low birth weight baby.21
  • The National Institute of Child Health and Human Development Maternal Fetal Medicine Units Network presented data that suggested that metronidazole treatment of asymptomatic carriers of T vaginalis increased risk of preterm birth.22,23 This is a controversial conclusion, as the study design did not accurately reflect clinical practice. The investigators used 4 doses of 2 g metronidazole in the treatment of infection, which is significantly higher than what is standard practice. The women included in the study were between 16 and 23 weeks gestational age, suggesting a significant delay in treatment.
  • A more recent study by Mann et al24 showed no increased risk of preterm birth with the use of metronidazole for the treatment of trichomoniasis. 
  • Increased risk of pelvic inflammatory disease (PID) has been shown in HIV-positive women.25
  • Increased risk of posthysterectomy infection including cuff cellulitis, cuff abscess, and wound infection has been documented.26
  • An association with cervical intra-epithelial neoplasia has been shown.27
  • In males, there is a risk of epididymitis, prostatitis, and decreased sperm cell motility.28
  • Systemic immune response was demonstrated in pregnant women infected with T vaginalis. A significant increase in granulocyte-macrophage colony-stimulating factor and C-reactive protein was noted.29

Race

  • In an analysis of the National Longitudinal Study of Adolescent Health (Add Health), Miller et al8 presented the prevalence of trichomoniasis among adolescents. Significant differences were noted among races: white, 1.2%; Latino, 2.1%; black, 6.9%; Asian, 1.8%; and Native American, 4.1%.
  • Differences were also reported by Sutton et al9 in their study of women aged 14-49 years: non-Hispanic whites, 1.2%; Mexican Americans, 1.5% and non-Hispanic blacks 13.5%.

Sex

  • Trichomoniasis is more common in women than in men.
  • The incidence in males has been reported in varying populations to be between 2.8 and 17%.30,31 This may be underestimated due to the method of detection and the site of specimen collection. Use of multiple sites of the genitourinary tract (urine, urethral swab, and semen) in males has been shown to increase sensitivity.32
  • T vaginalis was detected in 72% of male sexual partners of women with trichomoniasis.33

Age

  • 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.34
  • Unlike other STDs, the incidence of trichomoniasis increases with age.
    • The Add Health Study8 found that the prevalence among adolescents aged 18-24 years was 2.3%. For adults 25 years and older, the prevalence was 4%.
    • In a study by Joyner et al30 of 454 men attending an STD clinic in Denver, the prevalence in men younger than 30 years was 0.8% and, for men 30 years and older, the prevalence increased to 5.1%. This difference was thought to be due to age-related enlargement of the prostate gland.

Clinical

History

  • Nearly half of infected women and almost all infected males are asymptomatic.3,35
  • Presenting signs and symptoms may include vaginal or urethral discharge, odor, irritation, itch, dysuria, abdominal pain, and dyspareunia.2,29
  • One third of asymptomatic women become symptomatic within 6 months.3
  • Males are divided into 3 groups: asymptomatic carrier state, acute trichomoniasis, and mild symptomatic disease.3

Physical

  • Vaginal discharge is found in 42% of infected women.2
    • The discharge is classically described as thin and frothy; however, this is only seen in about 10% of patients.2
    • The discharge is often yellow. Sometimes, it is thick enough to be confused with candidiasis.
  • Abnormal vaginal odor was found in 50% of infected women.2
  • Edema or erythema was found in 22-37% of infected women.2
  • Vaginal pH is often elevated (>4.5).36
  • Colpitis macularis (strawberry cervix) is the finding of punctate hemorrhages and occasionally vesicles or papules on the cervix. It is the most specific clinical sign for the diagnosis of trichomoniasis. Without colposcopy, it is seen in less than 5% of cases. With the use of colposcopy, it is seen in nearly half.37
  • In males, if symptomatic, there is usually only scant, thin discharge.
  • The clinician's ability to accurately diagnose T vaginalis infection based on physical findings alone was shown in one study to have a positive predictive value of only 47%.38

Causes

Trichomoniasis is caused by the flagellated protozoan Trichomonas vaginalis.

  • Risk factors for T vaginalis include the following:
    • Infection with other STDs, especially gonorrhea
    • Four or more lifetime sex partners
    • Sexual contact with an infected partner
    • Not using barrier contraception
    • Trading sex for money or drugs

More on Trichomoniasis

Overview: Trichomoniasis
Differential Diagnoses & Workup: Trichomoniasis
Treatment & Medication: Trichomoniasis
Follow-up: Trichomoniasis
Multimedia: Trichomoniasis
References
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Further Reading

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Keywords

trichomoniasis, trichomonas, STD, sexually transmitted disease, Trichomonas vaginalis, T vaginalis, vaginitis, urethritis, infection of the adnexa, infection of the endometrium, infection of the Skene glands, infection of the Bartholin glands, nongonococcal urethritis, infection of the prostate, infection of the foreskin, infection of the glans, infection of the epididymis, cervicitis, pelvic inflammatory disease

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Contributor Information and Disclosures

Author

R Gentry Wilkerson, MD, Clinical Assistant Professor, Department of Emergency Medicine, State University of New York-Downstate; Attending Physician, Department of Emergency Medicine, Kings County Hospital
R Gentry Wilkerson, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

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.

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.

Judith C Brillman, MD, Professor, Department of Emergency Medicine, Assistant Dean, Graduate Medical Education, 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.

Medical Editor

Theodore J Gaeta, DO, MPH, FACEP, Clinical Associate Professor, Department of Emergency Medicine, Joan and Sanford Weill Medical College at Cornell University; 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
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

 
 
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