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Trypanosomes
Trypanosoma cruzi parasites
Scientific classification
Domain: Eukaryota
Kingdom: Excavata
Phylum: Euglenozoa
Subphylum: Mastigophora
Class: Kinetoplastea
Order: Trypanosomatida
Genera

Blastocrithidia
Crithidia
Endotrypanum
Herpetomonas
Leishmania
Leptomonas
Phytomonas
Trypanosoma
Wallaceina

Trypanosomes are a group of kinetoplastid protozoa distinguished by having only a single flagellum. All members are exclusively parasitic, found primarily in insects.[1] A few genera have life-cycles involving a secondary host, which may be a vertebrate or a plant. These include several species that cause major diseases in humans.[2]

The most important trypanosomal diseases are trypanosomiasis (African Sleeping Sickness and South American Chagas Disease); these are caused by species of Trypanosoma. The Leishmaniases are a set of trypanosomal diseases caused by various species of Leishmania.

Contents

Life Cycle and Morphology

A variety of different forms appear in the life-cycles of trypanosomes, distinguished mainly by the position of the flagellum:

Amastigote (leishmanial) - reduced or absent flagellum. Occurs in life cycles of some speices and is definitive in genus Leishmania. The tiny Lesihmania amastigoes may be the smallest eukaryotic cells. The flagellum is very short, projecting only slightly beyond the flagellar pocket.

Promastigote (leptomonad) - flagellum anterior of nucleus, free from cell body. The kinetosome and kinetoplast are located in front of the nucleus, near the anterior end of the body. The promastigote form is found in the life cycles of several species while they are in their insect hosts.

Epimastigote (crithidial) - flagellum anterior of nucleus, connected by a short undulating membrane. Here the kinetoplast and kinetosome are still located between the nucleus and the anterior end, but a short undulating membrane lies along the proximal part of the flagellum. The genera Crithidia and Blastocrithidia both parasites of insects, exhibit this form during their life cycles.

Opisthomastigote (herpetomonad) - flagellum posterior of nucleus, passing through a long groove in the cell.

Trypomastigote (trypanosomal) - flagellum posterior of nucleus, connected by a long undulating membrane. This stage is characteristic of the Trypanosoma species in the bloodstream as well as infective metacyclic stages in the tsetse fly vector. In trypomastigotes the inetoplast and kinetosome are near the posterior end of the body, and the flagellum runs along the surface, usually continuing as a free whip anterior to the body. The flagellar membrane is closely applied to the body surface, and, and when the flagellum beats, this area of the pellicle is pulled up into a fold; the fold and flagellum constitute the undulating membrane. In a typical bloodstream a simple mitochondrion with or without tubular cristae runs anteriorly from the kinetoplast. In the insect stage, the mitochondrion is much larger and more complex, with lamellar cristae.

Most trypanosomes have at least amastigote and promastigote stages. Trypanosoma appears in all five forms, with the trypanosomal stage occurring in the vertebrate host. Trypanosoma brucei sub-species have two forms in the bloodstream of a vertebrate host, the rapidly dividing long-slender form and the non-dividing short stumpy form. The short stumpy parasites are adapted for uptake into the tsetse fly vector, and are non-proliferative in comparison with the slender forms.

The stages that occur only in the insect are the Promastigote and Epimastigote. All species of Trypanosomatidae have a single nucleus and are either elongated with a single flagellum or rounded with a very short, nonprotruding flagellum. Many members of the family are heteroxenous: During one stage of their lives they live in the blood and/or fixed tissues of all vertebrate classes. And during other stages they live in the intestine of bloodsucking invertebrates. These parasites usually must contain blood, thus call them hemoflagellates.

Transmission

Unique to the African trypanosome Trypansoma brucei is the expression of a variable surface glycoprotein (VSG) coat on the cell surface, which undergoes constant variation in order to evade the humoral immune system (antibody response). It is thought that recombination via double-stranded DNA breaks from a repertoire of about 100 complete VSG genes, and a large number of VSG-related sequences, is responsible for the vast diversity of the parasite.[3] This recombination would retain effectiveness in immune evasion by maintaining diversity.

The acidocalcisome organelle was first identified in trypanosomes. [4]

A notable characteristic of trypanosomes is that they are able to perform Trans-splicing.

Research and Disease Control

Trypanosoma is transmitted by tsetse fly, in the anterior station development. T. brucei locates in the posterior section of the midgut of the insect, where it multiplies the trypomastigote form. They then migrate farther forward into the espophagus, pharynx, and hypopharynx and enter the salivary glands. Once in the salivary glands they transform into epimastigotes and attach to host cells or lie free in the lumen. After, several asexual generations they transform into metacycylic trypomastigoes, which are small and stumpy and lack a free flageullum. Only metacyclic trypomastigotes are infective to a vertebrae host.

Trypanosome parasites experience differentiation in their life cycles in response to changes in temperature, availability of nutrients, and immune system defense. These changes occur so the parasites can readily adapt to new environments. In previous studies, it was discovered that cycling between the mammalian host and the insect vector, trypanosomes express different types of stage specific surface coat proteins including VSGs and PARPs, that allow them to evade the immune systems of both species. The morphology of Trypansoma brucei is known to be pleomorphic, meaning that more than two structural forms exist in its life cycle. The forms range from slender forms to stumpy forms. Previous studies also determined that bloodstream trypanosomes can be induced to differentiate by cis-aconitate or citrate, intermediates in the Krebs cycle, and that temperature reduction from 37 °C to 20 °C induced hypersensitivity of stumpy forms to the Kerbs cycle intermediates. The researchers in this paper wanted to know what type of molecule was sending a differentiation signal when the parasite was exposed to CCA.

Recently researchers have discovered additional surface coat proteins called PAD proteins, and concluded that PAD proteins are the molecules responsible for the differentiation signal in the specifically the Trypanosome brucei. PAD proteins are identified as “proteins associated with differentiation”, where PAD1 was expressed on the cellular surface of the stumpy forms and PAD2 proteins expressed in the slender forms. Four key points about PAD proteins are: (1) PAD proteins are expressed on the surfaces of stumpy forms but not slender forms; (2) PAD protein is expressed at the same time as differentiation of the parasite in the bloodstream ; (3) PAD2 is expressed during cold temperatures; and (4) concentrations lowering PAD protein expression causes reduced differentiation capability and response to CCA (Dean et al., 2009). Based on past experiments and research a clearer understanding of how the trypanosomes differentiate between stumpy, slender, and procyclic forms, and the exact molecules associated with the stumpy and procyclic forms, PAD1 and PAD2 respectively, is understood.

References

  1. ^ Podlipaev S (May 2001). "The more insect trypanosomatids under study-the more diverse Trypanosomatidae appears". Int. J. Parasitol. 31 (5-6): 648–52. doi:10.1016/S0020-7519(01)00139-4. PMID 11334958.  
  2. ^ Simpson AG, Stevens JR, Lukes J (April 2006). "The evolution and diversity of kinetoplastid flagellates". Trends Parasitol. 22 (4): 168–74. doi:10.1016/j.pt.2006.02.006. PMID 16504583.  
  3. ^ Taylor JE, Rudenko G (November 2006). "Switching trypanosome coats: what's in the wardrobe?". Trends Genet. 22 (11): 614–20. doi:10.1016/j.tig.2006.08.003. PMID 16908087.  
  4. ^ http://www.nature.com/nrmicro/journal/v3/n3/full/nrmicro1097.html Nature Reviews Microbiology 3, 251-261 (March 2005) | doi:10.1038/nrmicro1097 Acidocalcisomes? Conserved from bacteria to man? Roberto Docampo, Wanderley de Souza, Kildare Miranda, Peter Rohloff Silvia N. J. Moreno

5. Butikofer, P., Stefan R., Monika B., and Isabel Roditi. 1997. GPEET procyclin is the major surface protein of procyclic culture forms of Trypanosoma brucei brucei strain 427. Biochemistry Journal 326: 415-423.

6. Dean, S., R. Marchetti, K. Kirk, and K. R. Matthews. 2009. A surface transporter family conveys the trypanosome differentiation signal. Nature 459: 213-217.

7. Engstler, M. and M. Boshart. 2009. Cold shock and regulation of surface protein trafficking convey sensitization to induces of stage differentiation in Trypanosoma brucei. Genes and Development 18: 2798-2811.

8. Hofer, A., D. Steverding, A. Chabes, R. Brun. and L. Thelander. 2001. Trypanosoma brucei CTP synthetase: a new target for treatment of African sleeping sickness. Proceedings of the National Academy of Sciences 98: 6412-6416.

9. Janovy, J, and L.S. Roberts 2005. Foundations of Parasitology, 7th ed. McGraw Hill, New York, NY, pp.61-69.

10. Buscher. 2002. Treatment of Human African trypanosomiasis- present situation and needs for research and development. The Lancet Infectious: Diseases 2: 437-440.

11. Matthews, K. R. 2005. The developmental cell biology of Trypanosoma brucei. Journal of Cell Science 118: 283-290.

12. Matthews, K. R., and K. Gull. 1994. Evidence for an interplay between cell cycle progression and the initiation of differentiation between life cycle forms of African trypanosomes. Journal of Cell Biology 125, 1147-1156.

13. Morrison. L.J., Marcello, L., and R. McCulloch. 2009. Antigenic variation in the African trypansome: molecular mechanisms and phenotypic complexity. Cellular Microbiology 10: 1-37.

14. Seed, J.R., and M.A. Wenck. 2003. Role of the long slender to short stumpy transition in the life cycle of the African trypanosomes. Kinetoplastid Biology and Disease 2: 1-8.

15. Shandan, S. 2009. Microbiology: Signals for change. Nature 459: 175.

16. Sherwin, T., and K. Gull. 1989. The cell division cycle of Trypanosoma brucei brucei: Timing of Event markers and cytoskeletal modulators. Philosphical transactions of the royal society: Biological Sciences (B) 323: 573-588.

17. World Health Organization. Online: African trypanosomiasis. August 2006. http://www.who.int/mediacentre/factsheets/fs259/en/.

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