Procyclins themselves are chained surface glycoproteins with repeating segments of either glu-pro (EP) or gly-pro-glu-glu-thr (GPEET). For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the Quantitative Buffy Coat (QBC) technique. PLoS Volume 4 Issue 2 e4493. Certain protease-resistant early epimastigote coat proteins have been identified in Trypanosoma Congolese (Non-human Mammalian Trypanosomiasis), but these protease-resistant surface (PRS) molecules have not been found in any other form of Trypanosome and are assumed to be a species specific variant. For an overview including prevention, control, and treatment visit Fenn, K. Matthews, K.R. The parasites get into the bloodstream by entering lymphatic or blood vessels. Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College. The kinetoplast is closely associated with the flagellum of the trypanosome and is believed to be an essential part of the regulation of flagellar motility as the parasite enters different stages of its life cycles. [Trypanosoma brucei gambiense] [Trypanosoma brucei rhodesiense]. This trypomastigote travels quickly through the proventriculus of the fly until it reaches the fly’s salivary gland. EP-2 procyclins are found in large numbers throughout every procyclic stage. The Lancet 390 (10110), pp. Recall that rhodosiense infection is far more acute and severe and can quickly lead to death while gambiense is a more chronic and more actively employing the use of antigenic variation. GPEET-procyclin coats typically last until about the 4th or 5th day of infection before higher concentrations of EP-procyclin molecules are found within them. Further analysis of the trypanosome genome has shown that there are upwards of 1500 “silent” VSG genes that are not associated with the polycistronic ES. Volume 9 p.124-141 a)Procyclic form in fly midgut. While it is feeding on blood, metacyclic trypomastigotes are transmitted to the skin from the salivary glands of the fly. 3. f) metacyclic trypanosome in salivary gland, prepared for host inoculation. Volume 22 No. These advantageous VSG coats are only found within the metacyclic stages of the trypanosomes life cycle which exist only in the salivary gland of the Tsetse fly and in the mammalian host bloodstream. Irregardless the mechanism, the stumpy forms quickly transform into the procyclic stage where the trypanosomes attach to the cells of the ectoperitrophic space and begin to transform into a more motile form that travels along the proventriculus of the fly midgut, known as a late procyclic form or a trypomastigote (mastigo- v. whip in greek. Two subspecies that are morphologically indistinguishable cause distinct disease patterns in humans: T. b. gambiense, causing chronic African trypanosomiasis (“West African sleeping sickness”) and T. b. rhodesiense, causing acute African trypanosomiasis (“East African sleeping sickness”). 8. After a few weeks with rhodensiensis and after as much as a couple of years with gambiensis, evidence of increased immune response in tissues other than the blood begins to appear, signaling their infection. 11 p.614-621 Major Surface Glycoproteins of Insect Forms of Trypanosoma brucei Are Not Essential for Cyclical Transmission by Tsetse 2009. The only known vector for each is the tsetse fly (Glossina spp.). The cell biology of Trypanosoma brucei differentiation. The third subspecies T. b. brucei is a parasite primarily of cattle and occasionally other animals, and under normal conditions does not infect humans. Trypanosoma Brucei. Severe ataxic dyskinesia eventually sets in and the patient can lose the ability to coordinate their actions at all. Procyclic trypanosomes with large numbers of GPEET-procyclin and low levels of EP-procyclins are marked as “early stage Procyclic”. In this environment most pathogens would be susceptible to not only the damaging effects of the innate immune response (inflammation, leukocytes, etc) but also the adaptive immune response (antibodies, killer T cells, etc.). The kinetoplast (originally attached to the flagella) is transferred within the cell which causes the trypomastigote change into the long epimastigote form. Volume 116 No. Protists of the genus trypanosoma are a fairly typical eukaryotic flagellates with fully intact and functional organelles including mitochondria and nuclei (which is atypical of most obligate parasites). The trypanosome itself is digesting the cells of the lymphatic system systematically and causing the body to respond harshly. Trends in Genetics. The course of infection is much more acute and rapid with T. b. rhodesiense than T. b. gambiense, and both infections are almost invariably fatal without treatment. Roditi, I. Lehane, M.J. Interactions between trypanosomes and tsetse flies. Subspecies gambiense is a much more chronic form of the disease with cyclical infective patterns marked by a rapid change in the VSG coat of the parasite. Upon the site of metacyclic trypanosome injection, one of the first sign of trypanosome infection that occurs in the rhodosiense subspecies is the presence of deep lesions as the trypanosome tears its way through the capillary beds of the human skin and proceeds to infect larger and more favorable blood vessels. ~150 of these silent genes are found in the telomeres of tightly packed 80-100kb minichromosomes. In T. brucei short epimastigotes, cell surface proteins consist mainly of an alanine-rich protein (BARP). The life cycle of trypanosoma parasite starts in the tsetse fly with ingestion of trypomastigotes in a blood meal from humans or any reservoir host. The transfer of the kinetoplast and its overall function are also not well understood, but it is known that relocating the kinetoplast is essential to the production of long epimastigotes. 517-520 Here, the parasite undergoes development in the insect before being transmitted when the fly is … As the stumpy forms develop, they lose the ability to reproduce entirely and instead lie near the surface capillary beds to infect the blood meal of a potential insect vector. Eventually in the most devastating periods of the disease, personality changes in the form of anger and depression can onset followed soon after by incapacitation of basic reasoning or mental processing. Krafsur, K. "Tsetse flies: Genetics, evolution, and role as vectors" Infection, Genetics and Evolution 2009. The metacyclic trypanosome requires the reacquisition of the VSG coat to survive the immune response of the human host. Kennedy, P.G.E. As stated earlier, there must be a distinction in the type of African trypanosomiasis as the rhodosiense subspecies and the gambiense subspecies cause different symptoms altogether. Even from as early a stage in the fly infection as the transfer of the stumpy infective form, the VSG coat that surrounds the trypanosome is shed off completely and is replaced with a midgut protease resistant coat of a particular group of proteins known as procyclins. Rapid tests for T. b. gambiense are used for the screening of whole blood for control/elimination  ; performance is variable depending on endemicity. Studer, E. Hemphill, A. Fragoso, C. Butikofer, P. Brun,R. A wet preparation should be examined for the motile trypanosomes, and in addition a blood smear (thin or thick) should be fixed, stained with Giemsa (or Field), and examined. The Centers for Disease Control and Prevention (CDC) cannot attest to the accuracy of a non-federal website. 2003. As the fly portion of the trypanosome life cycle comes to a close, the short epimastigotes begin to produce large numbers of metacyclic trypanosomes in the salivary glands of Glossina. Time taken to reach the infective stag in tsetse fly is 20 to 21 days. Ecologically, T. brucei is an obligate parasite and requires the presence of a host cell to function. Human African trypanosomiasis. In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission, leave the midgut, and transform into epimastigotes. As the fly takes in a blood meal from a human host, there are two major forms of T. brucei: the slender (normal) forms and the stumpy (non-replicating) forms. In the case of the rhodosiensis, the effects of such an acute attack could cause the body to overrespond in its attempts to rescue the body and possibly lead to edema, pancarditis and congestive heart failure. These symptoms will persist for a few days and then, while the lymph node is draining from the infection, the trypanosome will pass through into the lymph node and begin infection of the lymphatic system. 2008. Before transmission to the human host, the trypanosome gathers the previously mentioned variable surface glycoprotein (VSG) coat. It is possible that these multiple BARP forms are used by the epimastigote to promote adhesion to the salivary gland cells, but it is not currently known. Volume 21 It is known to have affected up to 36 sub-Saharan countries with an estimated 300,000 new infections each year.