CastellanellaChalmers 1918 non Pacheco & Rodrigues 1930
DuttonellaChalmers 1918
HaematomonasMitrophanow 1883
SchizotrypanumChagas 1909
TrypanozoonLühe 1906
Trypanosoma is agenus ofkinetoplastids (class Trypanosomatidae[1]), amonophyletic[2] group of unicellularparasiticflagellateprotozoa. Trypanosoma is part of the phylumEuglenozoa.[3] The name is derived from theAncient Greektrypano- (borer) andsoma (body) because of their corkscrew-like motion. Most trypanosomes areheteroxenous (requiring more than one obligatory host to complete life cycle) and most are transmitted via avector. The majority of species are transmitted by blood-feedinginvertebrates, but there are different mechanisms among the varying species.Trypanosoma equiperdum is spread between horses and otherequine species by sexual contact. They are generally found in theintestine of their invertebrate host, but normally occupy thebloodstream or anintracellular environment in the vertebrate host.
The mitochondrial genome of theTrypanosoma, as well as of other kinetoplastids, known as thekinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort ofproteins for organisation duringcell division.
A number of different methods demonstrate that the traditionalTrypanosoma genus is not monophyletic, with the biflagellateBodonida nested within. The American and African trypanosomes constitute distinct clades, implying that the major human disease agentsT. cruzi (cause of Chagas' disease) andT. brucei (cause of African sleeping sickness) are not closely related to each other.[9]
Phylogenetic analyses suggest an ancient split between a branch containing allSalivarian trypanosomes and a branch containing all non-Salivarian lineages. The latter branch in turn splits into a clade containing bird, reptilian and theStercorarian trypanosomes infecting mammals, and a clade with a branch of fish trypanosomes and a branch of reptilian or amphibian lineages.[10]
The ancestor of modern trypanosomes absorbed agreen alga around one billion years ago and co-opted some of its genetic material. This has resulted in modern trypanosomes such asT. brucei containing essential genes for the breakdown of sugars that are most closely related to plants. This difference may be used as the target of therapies.[16]
The relationships between the species have not been worked out to date. It has been suggested thatT. evansi arose from a clone ofT. equiperdum which lost its maxicircles.[17] It has also been proposed thatT. evansi should be classified as a subspecies ofT. brucei.[18]
It has been shown thatT. equiperdum has emerged at least once in Eastern Africa andT. evansi at two independent occasions in Western Africa.[19]
T. evansi, which causes one form of the diseasesurra in certain animals including camels[20] (a single case report of human infection in 2005 in India[21] was successfully treated withsuramin[22])
Two different types of trypanosomes exist, and their life cycles are different, the salivarian species and the stercorarian species.[citation needed]
Stercorarian trypanosomes infect insects, most often thetriatomid kissing bug, by developing in the posterior gut followed by release into the feces and subsequent depositing on the skin of the vertebrate host. The organism then penetrates and can disseminate throughout the body. Insects become infected when taking a blood meal.[citation needed]
Salivarian trypanosomes develop in the anterior gut of insects, most importantly theTsetse fly, and infective organisms are inoculated into the host by the insect bite before it feeds.[citation needed]
As trypanosomes progress through their life cycle they undergo a series of morphological changes as is typical oftrypanosomatids. The life cycle often consists of thetrypomastigote form in the vertebrate host and the trypomastigote orpromastigote form in the gut of the invertebrate host. Intracellular lifecycle stages are normally found in theamastigote form. The trypomastigote morphology is unique to species in the genusTrypanosoma.[citation needed]
Evidence has been obtained for meiosis inT. cruzi, and for genetic exchange.[25]T. brucei is able to undergomeiosis within thesalivary glands of itstsetse fly host, and meiosis is considered to be an intrinsic part of theT. brucei developmental cycle.[26][27] An adaptive benefit of meiosis forT. crucei andT. brucei may be therecombinational repair ofDNA damages that are acquired in the hostile environment of their respective hosts.[28]
^Hamilton PB, Stevens JR, Gaunt MW, Gidley J, Gibson WC (2004). "Trypanosomes are monophyletic: evidence from genes for glyceraldehyde phosphate dehydrogenase and small subunit ribosomal RNA".Int. J. Parasitol.34 (12):1393–404.doi:10.1016/j.ijpara.2004.08.011.PMID15542100.
^Leadbeater, B.S.C & McCready, S.M.M. (2000).The Flagellates. Unity, diversity and evolution. Ed.: Barry S. C. Leadbeater and J. C. Green Taylor and Francis, London, p. 12.
^Valentin, G. 1841. Ueber ein Entozoon im Blute vonSalmo fario.Müller's Archiv, p. 435.
^Gruby, D. 1843. Recherches et observations sur une nouvelle espéce d'haematozoaire,Trypanosoma sanguinis.Comptes Rendus de l'Académie des Sciences, 17: 1134–1136,[1].
^Environmental kinetoplastid-like 18S rRNA sequences and phylogenetic relationships among Trypanosomatidae: Paraphyly of the genus Trypanosoma. Helen Piontkivska and Austin L. Hughes, Molecular and Biochemical Parasitology, November 2005, Volume 144, Issue 1, Pages 94–99,doi:10.1016/j.molbiopara.2005.08.007
^The molecular phylogeny of trypanosomes: evidence for an early divergence of the Salivaria. Jochen Haag, Colm O'hUigin and Peter Overath, Molecular and Biochemical Parasitology, 1 March 1998, Volume 91, Issue 1, Pages 37–49,doi:10.1016/S0166-6851(97)00185-0
^"salivarian". Retrieved8 March 2019 – via The Free Dictionary.
^Sex and evolution in trypanosomes. Wendy Gibson, International Journal for Parasitology, 1 May 2001, Volume 31, Issues 5–6, Pages 643–647,doi:10.1016/S0020-7519(01)00138-2
^abDihydrofolate reductases within the genus Trypanosoma. J.J. Jaffe, J.J. McCormack Jr and W.E. Gutteridge, Experimental Parasitology, 1969, Volume 25, Pages 311–318,doi:10.1016/0014-4894(69)90076-9
^Brun R, Hecker H, Lun ZR (1998)Trypanosoma evansi andT. equiperdum: distribution, biology, treatment and phylogenetic relationship (a review). Vet Parasitol 79(2):95-107
^Carnes J, Anupama A, Balmer O, Jackson A, Lewis M, Brown R, Cestari I, Desquesnes M, Gendrin C, Hertz-Fowler C, Imamura H, Ivens A, Kořený L, Lai DH, MacLeod A, McDermott SM, Merritt C, Monnerat S, Moon W, Myler P, Phan I, Ramasamy G, Sivam D, Lun ZR, Lukeš J, Stuart K, Schnaufer A (2015) Genome and phylogenetic analyses ofTrypanosoma evansi reveal extensive similarity toT. brucei and multiple independent origins for dyskinetoplasty. PLoS Negl Trop Dis 9(1):e3404. doi: 10.1371/journal.pntd.0003404
^Cuypers B, Van den Broeck F, Van Reet N, Meehan CJ, Cauchard J, Wilkes JM, Claes F, Goddeeris B, Birhanu H, Dujardin JC, Laukens K, Büscher P, Deborggraeve S (2017) Genome-wide SNP analysis reveals distinct origins ofTrypanosoma evansi andTrypanosoma equiperdum. Genome Biol Evol doi: 10.1093/gbe/evx102
^World Health, Organization (2005). "A new form of human trypanosomiasis in India. Description of the first human case in the world caused by Trypanosoma evansi".Wkly. Epidemiol. Rec.80 (7):62–3.PMID15771199.
^Joshi PP, Chaudhari A, Shegokar VR, et al. (2006). "Treatment and follow-up of the first case of human trypanosomiasis caused by Trypanosoma evansi in India".Trans. R. Soc. Trop. Med. Hyg.100 (10):989–91.doi:10.1016/j.trstmh.2005.11.003.PMID16455122.
