Trichomonas vaginalis

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A Microbial Biorealm page on the genus Trichomonas vaginalis



Higher order taxa

Eukaryota; Parabasalidea;Trichomonada;Trichomonadida;Trichomonadidae; NCBI


NCBI: Taxonomy

Trichomonas vaginalis

Description and significance

Trichomonas vaginalis is a parasitic, flagellated protozoan, which causes trichomoniasis by infecting the urogenital tract of both females and males. Trichomoniasis is the most prevalent nonviral sexually transmitted disease. According to the WHO, there are about 170 million cases annually worldwide.5 In North America, there are more than 8 million new cases yearly and in the United States there are about 5 million new cases annually.7

Genome structure

The T. vaginalis genome is the first parabasalid genome to be described. Its genome is about 160 megabases in size with at least 65% of repeats and transposable elements. A core set of ~60,000 protein-coding genes were identified, which means T. vaginalis has one of the highest coding capacities among eukaryotes. Introns were found in 65 genes, transfer RNAs were found for all twenty amino acids, and about 250 ribosomal DNA were identified in this genome. There are six chromosomes in T. vaginalis. An interesting discovery was that the transcription machinery of this eukaryote appeared more metazoan than protozoan. The genome also showed there are 152 cases of possible prokaryote-to-eukaryote lateral gene transfer. The genome helped with the discovery of unknown metabolic pathways, clarification of pathogenic mechanisms, and identification of unknown functions of organelles in T. vaginalis which is discussed in the other sections.1

Cell structure and metabolism

Trichomonas vaginalis varies in size and shape, with an average length of 10μm and width of 7μm. The appearance of this protozoan is altered by physiochemical conditions. In a pure culture, the shape is more uniform such as pear-shaped or oval. As a parasite, it appears more amoeboid when attached to the vaginal epithelial cells. It has five flagella—four of which are in the anterior and the other flagellum is incorporated within the undulating membrane. The flagella and the undulating membrane contribute to its motility. Under unfavorable growth conditions, the trichomonad can round up and internalize its flagella. The cytoskeleton is made of tubulin and actin fibers. The nucleus, surrounded by a porous nuclear envelop, is located at its anterior end. A thin hyaline, rod-like structure called the axostyle begins at the nucleus and bisects the protozoan longitudinally. It protrudes through the posterior portion of the protozoan, ending in a sharp point. The axostyle helps anchor the protozoan to the vaginal epithelial cells. T. vaginalis exists as a trophozite and lacks a cystic stage. An interesting structure of this trichomonad is its hydrogenosome which plays an important part in metabolism.5

The main energy source of T. vaginalis comes from fermentative carbohydrate metabolism under both anaerobic and aerobic conditions. The products include acetate, lactate, malate, glycerol, CO2, and H2 (under anaerobic condition). The metabolism occurs in the cytoplasm where glucose is converted to phosphoenolpyruvate and then to pyruvate, and in the double-membraned hydrogenosome. The hydrogenosome is the site of fermentative oxidation of pyruvate. It also produces ATP by substrate-level phosphorylation, produces hydrogen, and processes half of the carbohydrates of the cell. The metabolism of T. vaginalis closely resembles that of anaerobic bacteria than aerobic bacteria. The trichomonad can adapt its metabolism according to available carbon sources. It has high maintenance energy, using up to half of its carbon on maintaining internal homeostasis. This is crucial because the vaginal environment constantly changes with respect to pH, hormones, and nutrient supply. If there is a limiting source of carbon, T. vaginalis can use amino acid metabolism to sustain growth and survival.5 It is the first eukaryote known to lack an apparent glycosylphosphatidylinositol (GPI)-anchor biosynthesis pathway.1


T. vaginalis invades the human urogenital mucosa where it induces inflammation. There are many mechanisms which are thought to be responsible for successful colonization: binding to and degradation of components from mucus and extracellular matrix proteins, binding to host cells including vaginal epithelial cells and immune cells, phagocytosis of vaginal bacteria and host cells, and endocytosis of host proteins. The T. vaginalis surface proteins play a role in these activities too.2 The parasite also serves as vectors for spread of other organisms, carrying pathogens attached to their surface into the fallopian tubes.7

Trichomoniasis is more common in women than men because men have asymptomatic infections. For women, the symptoms are thin frothy, green-yellow vaginal discharge, vulvovaginal irritation, vaginal soreness, and redness of the vagina.8 Women also have a higher prevalence of invasive cervical cancer when they have trichomoniasis. During pregnancy, there is an increased risk of preterm and low weight babies. Men have non-gonoccocal urethritis and chronic prostatitis. This infection has been found to be associated with prostate cancer. In both sexes, there is a higher susceptibility to HIV and infertility. Treatment of this disease in HIV-infected individuals can cause a decrease in HIV transmission also.7

This STD is diagnosed by using microscopic examination of the discharge, which is fast, inexpensive, and gives immediate identification of organisms. Pap smears can also be used. However, both of these methods have low sensitivity to the parasite. PCR is a better method of testing for this infection but it is expensive and restricted to the research setting only.7

In the United States, there is only one available treatment for trichomoniasis—metronidazole. It is very effective with cure rates of greater than 90%. However, there are some side effects like nausea, vomiting, metallic taste and gastrointestinal upset. There are reports of metronidazole-resistant strains of T. vaginalis so another possible treatment could be tinidazole which is available outside of the US.7

Current Research

  • One fairly recent study wanted to investigate if the presence of T. vaginalis (TV) is linked with an increased risk of coinfection with Chlamydia trachomatis (CT) and/or Neisseria gonorrhoeae (NG) in female patients submitted to the Emergency Department (ED) with symptoms consistent with a sexually transmitted disease (STD). These researchers found that there was a strong negative association between the presence of TV and coinfection with CT and/or NG. The presence of T. vaginalis actually made it less likely to have a coinfection with these two diseases. Based on these results, they concluded that T. vaginalis cannot be used as a reliable marker for Chlamydia and gonorrhea. Therefore, emergency physicians will continue to treat the high-risk patients and call back the lower-risk patients with positive test results for treatment instead of confidently treating all the infections at once.8

  • Besides being transmitted sexually, there have been cases of nonsexual transmission of trichomoniasis such as contaminated douche nozzles, specula, toilet seats, or swimming pool water. The role of public swimming pools in spreading the disease is controversial yet there is little research done. The viability of T. vaginalis in samples of water was reexamined by Pereira-Neves and Benchimol. They concluded that T. vaginalis remains viable and infective in swimming pool water samples for several hours. The survival time is dependent on the cytotoxicity of the strain. The possible transmission of trichomoniasis in public swimming pools may be low.4

  • T. vaginalis infections are usually diagnosed using direct microscopic examination and selective culture media such as Diamond’s medium. These two methods are equally sensitive but they are inefficient in detecting low numbers of parasites, defective parasites or organisms not surviving the transfer to culture medium. In previous studies, T. vaginalis PCR was shown to be more sensitive than culture and direct microscopic examination. However PCR products are more labor intensive and expensive. The goal of this research was to develop a sensitive real-time PCR for the detection of T. vaginalis in gential swabs using TaqMan technology. The results show that the real-time PCR is much more sensitive than the culture and direct microscopy, and the specificity and positive predictive value are also very high (99.9% and 95%). Therefore, it should be the method of choice for the diagnosis of T. vaginalis infections in women with vaginal discharge and men with non-gonococcal urethitis. Compared to the regular PCR, the real-time PCR is easy to perform, less labor-intensive, and takes only a few hours.6

  • Jasmonates are small lipids produced in plants which function as stress hormones. They are selectively cytotoxic against cancer cells. One of the naturally occurring jasmonates, methyl jasmonate has direct mitochondriotoxic effects which suggest that mitochondria are target organelles of jasmonates. The study wanted to analyze whether jasmonates can damage cells without mitochondria like a human parasitic flagellates i.e. T. vaginalis. The researchers found that methyl jasmonate induces non-apoptotic death of the amitochondriate T. vaginalis parasite by fragmentation and DNA condensation. It induces cell cycle block at the G2/M phase which is similar to the effect of metronidazole. It was also found to be cytotoxic towards a metronidazole-resistant strain of T. vaginalis; thus it can be effective for the treatment of nidazole-refractory trichomoniasis. This discovery is important for the treatment because there has been an increased number of metronidazole-resistant trichomoniasis. Besides demonstrating the potential of using methyl jasmonate as a treatment, the study shows that methyl jasmonate can act via a mithochondria-independent mechanism, which is helpful in the research of cancer. 3


1. Carlton, J.M., Hirt, R.P., Silva, J.C., Delcher, A.L., Schatz, M., Zhao, Q., Wortman, J.R., Bidwell, S.L., Alsmark, C.M., and Besteiro, S. 2007. Draft genome sequence of the sexually transmitted pathogen Trichomonas vaginalis. Science, v. 315, p. 207-211.

2. Hirt, R.P., Noel, C.J., Sicheritz-Ponten, T., Tachezy, J., and Fion, P-L. 2007. Trichomonas vaginalis surface proteins: a view from the genome. Trends in Parasitology, v. 23, p. 540-547.

3. Ofer, K., Gold, D., and Flescher, E. 2008. Methyl jasmonate induces cell cycle block and cell death in the amitochondriate parasite Trichomonas vaginalis. International Journal for Parasitology, v. 38, p. 959-968.

4. Pereira-Neves, A. and Benchimol, M. 2008. Trichomonas vaginalis: In vitro survival in swimming pool water samples. Experimental Parasitology, v. 118, p. 438-441.

5. Petrin, D., Delgaty, K., Bhatt, R., and Garber, G. 1998. Clinical and microbiological aspects of Trichomonas vaginalis. Clinical Microbiology Review, v. 11, p. 300-317.

6. Schirm, J., Bos, P.A.J., Roozeboom-Roelfsema, I.K., Luijt, D.S., and Möller, L.V. 2007. Trichomonas vaginalis detection using real-time TaqMan PCR. Journal of Microbiological Methods, v. 68, p. 243-247.

7. Soper, D. 2004. Trichomoniasis: Under control or undercontrolled? American Journal of Obstetrics and Gynecology, v. 190, p. 281-290.

8. White, M.J., Sadalla, J.K., Springer, S.R., and Counselman, F.L. 2005. Is the presence of Trichomonas vaginalis a reliable predictor of coinfection with Chlamydia trachomatis and/or Neisseria gonorrhoeae in female ED patients? American Journal of Emergency Medicine, v. 23, p. 127-130.

Edited by student of Emily Lilly at University of Massachusetts Dartmouth.

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