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.
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 |
| Promastigote (leptomonad) |
- anterior of nucleus, free from cell body |
| Epimastigote (crithidial) |
- anterior of nucleus, connected by a short undulating membrane |
| Opisthomastigote (herpetomonad) |
- posterior of nucleus, passing through a long groove in the cell |
| Trypomastigote (trypanosomal) |
- posterior of nucleus, connected by a long undulating membrane |
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.
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 and host antibodies. It is thought that recombination 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.
References
- ^ Podlipaev S (May 2001). "The more insect trypanosomatids under study-the more diverse Trypanosomatidae appears". Int. J. Parasitol. 31 (5-6): 648–52. PMID 11334958.
- ^ 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.
- ^ 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.
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