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Trichomoniasis 

Trichomoniasis
Chapter:
Trichomoniasis
Author(s):

Sharon Hillier

DOI:
10.1093/med/9780199204854.003.070813_update_001

Update:

Pathogenesis—genomic studies of adhesions and other proteins.

Treatment of pregnant women—unresolved concerns about safety of metronidazole.

Updated on 31 May 2012. The previous version of this content can be found here.
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Essentials

Trichomonas vaginalis is a sexually transmitted protozoan pathogen that may cause more than one-half of all curable sexually transmitted genital infections worldwide. Women with trichomoniasis are often asymptomatic, but they may develop vaginal malodour, discharge, erythema, or itching, and their male or female sexual partners may also be infected, although urethritis in men is less likely to cause symptoms. Women with trichomoniasis have an increased risk of HIV acquisition, HIV shedding, pelvic inflammatory disease, and preterm birth. For diagnosis, rapid antigen detection, culture, and polymerase chain reaction (PCR) methods have advantages over conventional microscopy, but are more expensive. Oral metronidazole is usually an effective treatment, with both sexual partners needing to be treated to prevent reinfection.

Acknowledgement: The editors acknowledge the inclusion of material from Dr J P Ackers’ chapter in the previous edition of the Oxford Textbook of Medicine.

Introduction

Trichomoniasis is an infection of the human urogenital tract caused by the protozoan Trichomonas vaginalis. There are about 170 million new cases each year, making it the world’s commonest nonviral sexually transmitted infection and, according to the World Health Organization (WHO), it accounts for more than one-half of all curable sexually transmitted infections worldwide. Pregnant women who have trichomoniasis are at increased risk of preterm delivery as well as HIV acquisition and shedding.

Historical perspective

T. vaginalis was first described in 1836. In the preantibiotic era, it was considered a frequent unwanted outcome of sexual activity associated with symptoms but with few adverse health outcomes. With diagnosis and treatment, this infection has become less prevalent in wealthier countries but has remained highly prevalent in the developing world.

Aetiology, genetics, pathogenesis, and pathology

Although there are more than 100 species of this protozoan, only T. vaginalis parasitizes the human genital tract. In vitro, T. vaginalis has a well-defined, contact-mediated, cytotoxic effect, but its relationship to pathogenesis in vivo is unknown. It activates complement and attracts neutrophils, which may kill the parasite but, in large numbers, may also contribute to the pathology. The organism produces several proteolytic enzymes which degrade genital tract mucins. Several potential T. vaginalis adhesions have been identified but, apart from its surface lipophosphoglycan, there is little evidence supporting a role in adhesion. Availability of the T. vaginalis genome sequence has allowed wider search for surface, soluble, and secreted proteins involved in host–parasite interactions. In women, T. vaginalis may be found in the vagina and the exterior cervix in over 95% of infections, but is recovered from the endocervix in 13%. The urethra and Skene’s glands are also commonly infected. In men, the urethra is the most common site of infection but the organism has also been recovered from epididymal aspirates. Dissemination beyond the lower urogenital tract is extremely rare even in severely immunocompromised patients.

Trichomoniasis in women was previously regarded as unpleasant but harmless; however, epidemiological studies have now linked it with a modest increase in the risk of heterosexual HIV transmission, and with complications in pregnancy.

Epidemiology

Understanding the epidemiology of trichomoniasis has been limited by the variability in the sensitivity and accuracy of diagnostic methods used. Although it is often difficult to isolate the organism from male contacts of infected women, epidemiological evidence suggests that T. vaginalis is transmitted almost exclusively by sexual intercourse, both during heterosexual intercourse and in sexual activity between female sexual partners. Although the organism can survive for many hours at room temperature if kept damp, there is only limited evidence that this pathogen is transmitted among household members in the absence of sexual exposure. A very small proportion of female babies of infected mothers will become infected during birth, but this infection is transient and trichomoniasis discovered in a child should immediately raise the suspicion of sexual abuse.

Very few studies have been made of genuinely unselected populations; the majority have examined either pregnant women or those attending sexually transmitted disease clinics. Usually cases in women are observed 5 or 10 times more than those in men. T. vaginalis has been reported in 18 to 24% of women attending sexual health clinics in the United States of America and in 3 to 34% of women in four African cities. The epidemiology of this pathogen is less well understood among men, but has been reported in 3 to 20% of men attending sexually transmitted disease clinics. Factors associated with trichomoniasis include coinfection with other sexually transmitted pathogens, past infection with Trichomonas, being unmarried, having more than one sexual partner, and not using condoms.

In several developed countries, there has been a steady decline in the incidence of trichomoniasis in the past few decades, but this has not occurred in less-developed countries nor in deprived inner-city areas in industrialized nations. Human trichomoniasis is becoming a disease of the underprivileged.

Prevention

Because up to one-half of infected individuals are asymptomatic, the only way to reduce the population prevalence of this pathogen is through screening of individuals and providing treatment to individuals and their sexual partners. Several studies have documented improved cure rates in women whose male partners received treatment. Persons who report use of male or female condoms have a reduced incident of recurrent trichomoniasis. There is no effective vaccine against T. vaginalis.

Clinical features

In women, T. vaginalis can infect the vagina, urethra, and the Bartholin’s and Skene’s glands. From 10 to 50% of cases are asymptomatic but acute inflammatory diseases may occur, with copious and malodorous vaginal discharge, vulvovaginal soreness and irritation, dysuria, and dyspareunia. Trichomoniasis is significantly associated with purulent yellow vaginal discharge, vulvar itching, and colpitis macularis (strawberry cervix) detectable by colposcopy, with vulval and vaginal erythema. Vaginal pH is usually elevated and concomitant bacterial vaginosis is common. The discharge fluctuates with time and, if untreated, may disappear spontaneously or persist for months or even years.

Most men with trichomoniasis are asymptomatic, but the parasite is responsible for a small but increasing proportion of cases of nongonococcal urethritis.

Differential diagnosis

In women, vaginal discharge syndromes including bacterial vaginosis, yeast vulvovaginitis, and trichomoniasis should be considered (see Chapter 8.4). Women who present with vaginal discharge, vulvar itching, and/or vaginal malodour may have no infection, or could have any combination of these common vaginal infections. In men, other causes of urethritis should be ruled out.

Criteria for diagnosis

An accurate diagnosis cannot be made based upon signs or symptoms elicited during the clinical evaluation.

Trichomoniasis in women

The most commonly used method for diagnosis is identification of the pathogen in vaginal (not endocervical) secretions examined under the microscope at ×400 magnification. In clinical specimens or culture, T. vaginalis is a motile and round or oval flagellate, 10 to 13 μ‎m long and 8 to 10 μ‎m wide. Fixed and stained, it is about 25% smaller (Fig. 7.8.13.1). Diagnostic features include the jerky motility, undulating membrane, and microtubular rod (axostyle), which runs through the body and projects as a thin spine from the posterior end. In contact with vaginal epithelial cells in vitro, the organism becomes extremely flattened and adherent. The life cycle is simple; no resistant cysts are formed and there are no intermediate or reservoir hosts. Two other trichomonads, T. tenax and Pentatrichomonas hominis, are uncommon and probably harmless human parasites of the mouth and large bowel, respectively. All three species are site specific. Urogenital trichomoniasis is not due to contamination from other sites.

Fig. 7.8.13.1 Trichomonads in vaginal secretions (Giemsa stain).

Fig. 7.8.13.1
Trichomonads in vaginal secretions (Giemsa stain).

(Copyright J P Ackers.)

Microscopy is inexpensive and can be used as a bedside diagnostic test, allowing immediate treatment of infected people. However, its sensitivity is only 65 to 80% and it requires a microscope. Broth culture methods for detection of T. vaginalis have the advantage of greater sensitivity, but require up to 5 days’ incubation. Diamond’s TYM and the very convenient if rather expensive InPouch system are among the best. Rapid antigen tests can be performed within the clinic in a few minutes. Their sensitivity and specificity are equivalent to those of culture, with the advantage of providing results during the clinic visit. The polymerase chain reaction (PCR) has the highest sensitivity and specificity for diagnosis of T. vaginalis but is expensive and requires specialized equipment, limiting its implementation. Specimens for PCR can be obtained less invasively with self-administered tampons.

Trichomoniasis in men

For diagnosis of urethritis due to trichomonas in men, culture or PCR is essential as the sensitivity of microscopy with urethral swab or scrapings, centrifuged urine sediment, or prostatic fluid is only 10 to 20%.

Treatment

The first, and the so-far only effective, drugs are 5-nitroimidazoles. A single 2 g dose of oral metronidazole is most widely used. The alternative is 250 mg three times a day for 7 days. Recurrence occurs in 8 to 20% of women in the first month after therapy. About half the occurrences are attributed to reinfection by the same or a new sexual partner. Women who experience treatment failure are more likely to have isolates of T. vaginalis that show reduced susceptibility to metronidazole in vitro. Single-dose metronidazole may not be adequate to treat these patients. Sexual partners must also be treated. Only the 7-day regimen has been extensively evaluated in men, in whom it appears as effective as in women. In pregnant women, single-dose metronidazole treatment probably achieves parasitological cure but one trial suggested increased risk of preterm and low-birthweight deliveries.

Prognosis

In most women who receive appropriate treatment, symptoms will resolve but they are at increased risk of becoming infected with Trichomonas in the future. Men may spontaneously clear their infections, but unless both sexual partners are treated, reinfection is common.

Areas of uncertainty or controversy

Trichomonisis has been linked with preterm birth, pelvic inflammatory disease (Chapter 8.5), and an increased risk of HIV. However, metronidazole treatment has failed to reduce the risk of preterm delivery or acquisition of HIV. No study has yet documented that accurate diagnosis and treatment of trichomoniasis provides a long-term health benefit for men and women.

Likely developments in the near future

Broader implementation of specific and sensitive screening tests and prospective studies of treatment should reveal whether routine screening and treatment of T. vaginalis reduces morbidity.

Further reading

Gülmezoglu AM, Azhar M (2011). Interventions for trichomoniasis in pregnancy. Cochrane Database Syst Rev, 5, CD000220.Find this resource:

Hobbs MM, et al. (2008). Trichomonas vaginalis and trichomoniasis. In: Holmes KK, et al. (eds) Sexually transmitted diseases, 6th edition, pp. 773–93. McGraw-Hill, New York.Find this resource:

    Honigberg BM (ed) (1989). Trichomonads parasitic in humans. Springer-Verlag, New York.Find this resource:

      Huppert JS, et al. (2007). Rapid antigen testing compares favorably with transcriptase-mediated amplification assay for the detection of Trichomonas vaginalis in young women. Clin Infect Dis, 45, 194–8.Find this resource:

      Johnston VJ, Mabey DC (2008). Global epidemiology and control of Trichomonas vaginalis. Curr Opin Infect Dis, 21, 56–64.Find this resource:

      Kissinger P, et al. (2008). Early repeated infections with Trichomonas vaginalis among HIV-positive and HIV-negative women. Clin Infect Dis, 46, 994–9.Find this resource:

      Klebanoff M, et al. (2001). Failure of metronidazole to prevent preterm delivery among pregnant women with asymptomatic Trichomonas vaginalis infection. New Engl J Med, 345, 487–93.Find this resource:

      Krieger JN (1995). Trichomoniasis in men: old issues and new data. Sex Transm Dis, 22, 83–96.Find this resource:

      Petrin D, et al. (1998). Clinical and microbiological aspects of Trichomonas vaginalis. Clin Microbiol Rev, 11, 300–17.Find this resource:

      Ryan CM, et al. (2011). Trichomonas vaginalis: current understanding of host-parasite interactions. Essays Biochem, 51, 161–75.Find this resource:

      Van der Pol B, et al. (2008). Trichomonas vaginalis infection and human immunodeficiency virus acquisition in African women. J Infect Dis, 197, 548–54.Find this resource: