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Trichomonas vaginalis

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Trichomonas vaginalis
T. vaginalis phase contrast microscopy
Scientific classification
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T. vaginalis
Binomial name
Trichomonas vaginalis
(Donné 1836)

Trichomonas vaginalis is an anaerobic, flagellated protozoan, a form of microorganism. The parasitic microorganism is the causative agent of trichomoniasis, and is the most common pathogenic protozoan infection of humans in industrialized countries.[1] Infection rates between men and women are the same with women showing symptoms while infections in men are usually asymptomatic. Transmission takes place directly because the trophozoite does not have a cyst. The WHO has estimated that 180 million cases of infection 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] Usually treatment consists of metronidazole and tinidazole.[3]

Clinical

Pap smear, showing infestation by Trichomonas vaginalis. Papanicolaou stain, 400x.

Trichomoniasis is a sexually transmitted infection which can occur in females if the normal acidity of the vagina is shifted from a healthy, semi-acidic pH (3.8 - 4.2) to a much more basic or alkaline one (5 - 6) that is conducive to T. vaginalis growth. Males rarely exhibit symptoms of a T. vaginalis infection. Some of the symptoms of T. vaginalis in females include: preterm delivery, low birth weight, and increased mortality as well as predisposing to HIV infection, AIDS, and cervical cancer.[4] 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 reducing, but not wholly preventing, transmission.[5] Ten percent of those infected will present with a "strawberry" cervix or vagina on examination.[citation needed]

Classically, with a pap smear, infected individuals have a transparent "halo" around their superficial cell nucleus. It is also rarely detected by studying discharge or with a pap smear because of their low sensitivity. T. vaginalis was traditionally 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 primers specific for GENBANK/L23861.[9][10]

Recent research also suggests a link between T. vaginalis infection in males and subsequent aggressive prostate cancer.[11]

Infection is treated and cured with metronidazole or tinidazole, and should be prescribed to any sexual partner(s) as well because they may be asymptomatic carriers.[12]

Morphology

The T. vaginalis trophozoite is oval as well as flagellated. It is slightly larger than a white blood cell, measuring 9 X 7 μm. Five flagella arise near the cytostome; 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.[13]

While T. vaginalis does not have a cyst form, organisms can survive for up to 24 hours in urine, semen, or even water samples. It has an ability to persist on fomites with a moist surface for 1 to 2 hours.

Protein function

T. vaginalis has many enzymes that catalyze many chemical 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.[14]

Adherence

One of the hallmark features of Trichomonas vaginalis are the adherence factors that allow cervicovaginal epithelium colonization in women. The adherence that this organism illustrates is specific to vaginal epithelial cells (VECs) being pH, time and temperature dependent. A variety of virulence factors mediate this process some of which are the microtubules, microfilaments, adhesins (4), and cysteine proteinases. The adhesins are four Trichomonad enzymes called AP65, AP51, AP33, and AP23 that mediate the interaction of the parasite to the receptor molecules on VECs.[15] Cysteine proteinases may be another virulence factor because not only do these 30 kDa proteins bind to host cell surfaces but also may degrade extracellular matrix proteins like hemoglobin, fibronectin or collagen IV.[16]

Genome sequencing and statistics

The T. vaginalis genome was found to be approximately 160 megabases in size[17] – ten times larger than predicted from earlier gel-based chromosome sizing [18] (The human genome is ~3.5 gigabases by comparison.[19]) As much as two-thirds of the T. vaginalis sequence consists of repetitive and transposable elements, reflecting a massive, evolutionarily-recent expansion of the genome. The total number of predicted protein-coding genes is ~98,000, which includes ~38,000 'repeat' genes (virus-like, transposon-like, retrotransposon-like, and unclassified repeats, all with high copy number and low polymorphism). Approximately 26,000 of the protein-coding genes have been classed as 'evidence-supported' (similar either to known proteins, or to ESTs), while the remainder have no known function. These extraordinary genome statistics are likely to change downward as the genome sequence, currently very fragmented due to the difficulty of ordering repetitive DNA, is assembled into chromosomes, and as more transcription data (ESTs, microarrays) accumulate. But it appears that the gene number of the single-celled parasite T. vaginalis is, at minimum, on par with that of its host H. sapiens.

In late 2007 TrichDB.org was launched as a free, public genomic data repository and retrieval service devoted to genome-scale trichomonad data. The site currently contains all of the T. vaginalis sequence project data, several EST libraries, and tools for data mining and display. TrichDB is part of the NIH/NIAID-funded EupathDB functional genomics database project.[20]

Increased susceptibility to HIV

The damage caused by Trichomonas vaginalis to the vaginal endometrium increases the woman's susceptibility to an infection by the HIV virus. Since, the parasite not only causes inflammation in the area, it also causes lysis of epithelial cells and RBCs in the area leading to genital inflammation and the leakiness seen in this very important protective barrier. Having Trichomonas vaginalis also may increase the chances of the infected woman passing on the HIV virus to her sex partner(s).

See also

References

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  2. ^ Hook EW (1999). "Trichomonas vaginalis--no longer a minor STD". Sexually transmitted diseases. 26 (7): 388–9. doi:10.1097/00007435-199908000-00004. PMID 10458631. {{cite journal}}: Unknown parameter |month= ignored (help)
  3. ^ The STI Clinic http://www.thesticlinic.com/trichomonas-vaginalis.aspx
  4. ^ Schwebke JR, Burgess D (2004). "Trichomoniasis". Clinical microbiology reviews. 17 (4): 794–803, table of contents. doi:10.1128/CMR.17.4.794-803.2004. PMC 523559. PMID 15489349. {{cite journal}}: Unknown parameter |month= ignored (help)
  5. ^ "Trichomoniasis - CDC Fact Sheet". Centers for Disease Control and Prevention. 2007-12-17. Retrieved 2010-06-11.
  6. ^ Ohlemeyer CL, Hornberger LL, Lynch DA, Swierkosz EM (1998). "Diagnosis of Trichomonas vaginalis in adolescent females: InPouch TV culture versus wet-mount microscopy". The Journal of adolescent health : official publication of the Society for Adolescent Medicine. 22 (3): 205–8. PMID 9502007. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. ^ Sood S; et al. (2007). "InPouch TV culture for detection of Trichomonas vaginalis". Indian J Med Res. 125 (4): 567–571. PMID 17598943. {{cite journal}}: Explicit use of et al. in: |author= (help)
  8. ^ a b Huppert JS (July 15, 2007). "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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  9. ^ Schirm J, Bos PA, Roozeboom-Roelfsema IK, Luijt DS, Möller LV (2007). "Trichomonas vaginalis detection using real-time TaqMan PCR". Journal of microbiological methods. 68 (2): 243–7. doi:10.1016/j.mimet.2006.08.002. PMID 17005275. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ http://www.ncbi.nlm.nih.gov/nuccore/496275
  11. ^ JR Stark, G Judson, JF Alderete, V Mundodi, AS Kucknoor, EL Giovannucci, EA Platz, S Sutcliffe, K Fall, T Kurth, J Ma, MJ Stampfer, LA Mucci (9 September 2009). "Prospective Study of Trichomonas vaginalis Infection and Prostate Cancer Incidence and Mortality: Physicians' Health Study". Journal of the National Cancer Institute. 101 (20): 1406–11. doi:10.1093/jnci/djp306. PMC 2765259. PMID 19741211.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Cudmore SL, Delgaty KL, Hayward-McClelland SF, Petrin DP, Garber GE (2004). "Treatment of infections caused by metronidazole-resistant Trichomonas vaginalis". Clinical microbiology reviews. 17 (4): 783–93, table of contents. doi:10.1128/CMR.17.4.783-793.2004. PMC 523556. PMID 15489348. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0838585299. {{cite book}}: |author= has generic name (help)
  14. ^ Upcroft P, Upcroft JA (2001). "Drug targets and mechanisms of resistance in the anaerobic protozoa". Clinical microbiology reviews. 14 (1): 150–64. doi:10.1128/CMR.14.1.150-164.2001. PMC 88967. PMID 11148007. {{cite journal}}: Unknown parameter |month= ignored (help)
  15. ^ Arroyo R, Engbring J., Alderete JF (2006). "Molecular basis of host epithelial cell recognition by Trichomonas vaginalis". Molecular Microbiology. 6 (7): 853–862. doi:10.1111/j.1365-2958.1992.tb01536.x. PMID 1602965. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  16. ^ Mendoza-Lopez MR; et al. (2000). "CP30, a Cysteine Proteinase Involved in Trichomonas vaginalis Cytoadherence". Infection and Immunity. 68 (9): 4907–12. doi:0019-9567/00/$04.00+0. PMC 101697. PMID 10948104. {{cite journal}}: Check |doi= value (help); Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)
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  19. ^ Zimmer, C. (2007). "Jurassic Genome". Science. 315 (5817): 1358–1359. doi:10.1126/science.315.5817.1358. PMID 17347424.
  20. ^ Aurrecoechea C, Brestelli J, Brunk BP; et al. (2008). "GiardiaDB and TrichDB: integrated genomic resources for the eukaryotic protist pathogens Giardia lamblia and Trichomonas vaginalis". Nucleic Acids Research. 37 (Database issue): D526–30. doi:10.1093/nar/gkn631. PMC 2686445. PMID 18824479. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)