Trichomonas vaginalis, an anaerobic, parasitic flagellated protozoan, is the causative agent of trichomoniasis, and is the most common pathogenic protozoan infection of humans in industrialized countries.[1] The WHO has estimated that 180 million infections are acquired annually worldwide. The estimates for North America alone are between 5 and 8 million new infections each year, with an estimated rate of asymptomatic cases as high as 50%.[2]
Protein function
T. vaginalis also has many enzymes that catalyze a number of reactions making the organism relevant to the study of protein function. T. vaginalis lacks mitochondria and other necessary enzymes and cytochromes to conduct oxidative phosphorylation. T. vaginalis obtains nutrients by transport through the cell membrane and by phagocytosis. The organism is able to maintain energy requirements by the use of a small amount of enzymes to provide energy via glycolysis of glucose to glycerol and succinate in the cytoplasm, followed by further conversion of pyruvate and malate to hydrogen and acetate in an organelle called the hydrogenosome.[3]
Morphology
The T. vaginalis trophozoite is oval as well as flagellated. Five flagella arise near the cytosome; four of these immediately extend outside the cell together, while the fifth flagellum wraps backwards along the surface of the organism. The functionality of the fifth flagellum is not known. In addition, a conspicuous barb-like axostyle projects opposite the four-flagella bundle; the axostyle may be used for attachment to surfaces and may also cause the tissue damage noted in trichomoniasis infections.[4]
While T. vaginalis does not have a cyst form, organisms can survive for up to 24 hours in urine, semen, or even water samples. Combined with an ability to persist on fomites with a moist surface for 1 to 2 hours, T. vaginalis is among the most durable protozoan trophozites.
Clinical
Pap smear, showing infestation by Trichomonas vaginalis. Papanicolau stain, 400x.
Trichomoniasis is a sexually transmitted disease which can occur in females (males rarely exhibit symptoms of a T. vaginalis infection) if the normal acidity of the vagina is shifted from a healthy, semi-acidic pH (3.8 - 4.2) to a much more basic one (5 - 6) that is conducive to T. vaginalis growth. Some of the symptoms of T. vaginalis include: preterm delivery, low birth weight, and increased mortality as well as predisposing to HIV infection, AIDS, and cervical cancer.[5] T. vaginalis has also been reported in the urinary tract, fallopian tubes, and pelvis and can cause pneumonia, bronchitis, and oral lesions. Other symptoms include inflammation with increasing number of organisms, greenish-yellow frothy vaginal secretions and itching. Condoms are effective at preventing infection.
Classically, with a pap smear, infected individuals have a transparent "halo" around their superficial cell nucleus. It is also is rarely detected by studying discharge or with a pap smear because of their low sensitivity. T. vaginalis was traditioinally diagnosed via a wet mount, in which "corkscrew" motility was observed. Currently, the most common method of diagnosis is via overnight culture,[6][7] with a sensitivity range of 75-95%.[8] Newer methods, such as rapid antigen testing and transcription-mediated amplification, have even greater sensitivity, but are not in widespread use.[8] The presence of T. vaginalis can also be diagnosed by PCR, using the primers L23861 Fw and Rev.[9]
Infection is treated and cured with metronidazole or tinidazole, and should be prescribed to any sexual partner(s) as well because they may potentially be asymptomatic carriers.[10]
Genome Sequencing
Jane Carlton led a project to sequence the Trichomonas vaginalis genome which found that the genome was much larger than was expected.[1] [2]
References
- ^ Soper D (2004). "Trichomoniasis: under control or undercontrolled?". Am J Obstet Gynecol 190 (1): 281–90. doi:10.1016/j.ajog.2003.08.023. PMID 14749674.
- ^ Hook E (1999). "Trichomonas vaginalis--no longer a minor STD". Sex Transm Dis 26 (7): 388–9. doi:10.1097/00007435-199908000-00004. PMID 10458631.
- ^ Upcroft P, Upcroft J (2001). "Drug targets and mechanisms of resistance in the anaerobic protozoa". Clin Microbiol Rev 14 (1): 150–64. doi:10.1128/CMR.14.1.150-164.2001. PMID 11148007.
- ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0838585299.
- ^ Schwebke J, Burgess D (2004). "Trichomoniasis". Clin Microbiol Rev 17 (4): 794–803, table of contents. doi:10.1128/CMR.17.4.794-803.2004. PMID 15489349.
- ^ Ohlemeyer CL, et al (1998). "Diagnosis of Trichomonas vaginalis in adolescent females: InPouch TV culture versus wet-mount microscopy". Journal of Adolescent Health 22: 205-208. PMID 9502007.
- ^ Sood S, et al (2007). "InPouch TV culture for detection of Trichomonas vaginalis.". Indian J Med Res 125: 567-571. PMID 17598943.
- ^ a b Huppert JS; Mortensen JE, Reed JL, Kahn JA, Rich KD, Miller WC, Hobbs M (Jul 15). "Rapid antigen testing compares favorably with transcription-mediated amplification assay for the detection of Trichomonas vaginalis in young women.". Clinical Infectious Diseases 45 (2): 194-198. doi:10.1086/518851. PMID 17578778.
- ^ Schrirm, J. et al (2007). "Trichomonas vaginalis detection using real-time TaqMan PCR". Journal of Microbiological methods 68: 243–247. doi:10.1016/j.mimet.2006.08.002. PMID 17005275.
- ^ Cudmore S, Delgaty K, Hayward-McClelland S, Petrin D, Garber G (2004). "Treatment of infections caused by metronidazole-resistant Trichomonas vaginalis". Clin Microbiol Rev 17 (4): 783–93, table of contents. doi:10.1128/CMR.17.4.783-793.2004. PMID 15489348.
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