Trypanosoma evansi

Trypanosoma evansi
	Trypanosoma evansi
Systematics
without rank:	Euglenozoa
without rank:	Kinetoplastea
without rank:	Metakinetoplastina
without rank:	Trypanosomatida
Genre :	Trypanosomes ( Trypanosoma )
Type :	Trypanosoma evansi
Scientific name
	Trypanosoma evansi
	( Steel , 1885) Balbiani , 1888

Trypanosoma evansi is a type of single-celled parasites of the genus of trypanosome known as pathogens of Surra , an animal epidemic , especially in horses and camels occurs in North Africa, the Middle East, Asia and Latin America. The parasite is usually through bites of brakes transferred; however, the parasite does not multiply in the insect. The Mal de Caderas pathogen,originally called Trypanosoma equinum , an epidemic in horses in South America, is now included in the Trypanosoma evansi species. A case of aperson sufferingfrom Trypanosoma evansi has been describedin India; humans are usually resistant to this pathogen.

Discovery and Description

Trypanosoma evansi was discovered in 1880 by the British veterinarian Griffith Evans (1835–1935) in India in horses suffering from the surra. According to Evans, the species was erroneously called Spirochaete evansi by the veterinarian JH Steel on the assumption that it was bacteria from the group of spirochetes . In 1888 this was corrected to the name Trypanosoma evansi , which is valid today . The discovery of Trypanosoma evansi was the first case in which a parasite from the genus Trypanosomes was detected as a pathogen.

The unicellular organism has a single flagellum , which runs on the cell surface under an undulating membrane to the front end of the cell and becomes a free-floating flagellate there. The cells also have a small kinetoplast, a collection of deoxyribonucleic acid within a large mitochondrion ; the kinetoplast is absent in some isolates. The parasite only occurs in a trypomastigote cell shape up to 33 µm long. The parasite cannot be distinguished microscopically from Trypanosoma brucei or Trypanosoma equiperdum .

The species Trypanosoma evansi is currently classified in the subgenus Trypanozoon . With Trypanosoma equinum a separate species was described originally in South America as a causative agent of Mal de Caderas described or cross paralysis in horses. This species is now regarded as a form of Trypanosoma evansi .

According to molecular studies, all representatives of the subgenus Trypanozoon , which includes Trypanosoma evansi , Trypanosoma equiperdum and the three subspecies of Trypanosoma brucei, are very similar. Trypanosoma evansi. differs from Trypanosoma brucei. practically only due to the complete absence of the kDNA maxicircles . the mitochondrial DNA found in many copies in the kinetoplast . This difference is the reason why Trypanosoma evansi cannot reproduce in tsetse flies. Genes encoded by mitochondrial DNA , including cytochromes, are essential for the oxidative energy metabolism that Trypanosoma brucei needs for reproduction in tsetse flies. In mammals, trypanosomes are limited to glycolysis for energy production. Detailed molecular studies came to the conclusion that Trypanosoma evansi is not monophyletic , but rather represents a group of multiple spontaneous mutations of Trypanosoma brucei ; from this it was deduced that classification as a separate species was not justified. It has been proposed to classify the parasites as a subspecies of Trypanosoma brucei with the designation Trypanosoma brucei evansi .

Distribution and host animals

Trypanosoma evansi occurs in North Africa, the Near and Middle East, Asia, and Latin America. In addition to horses and camels, cattle, buffalo, deer, the Asian elephant and tiger are named as natural hosts. The most important vector are horseflies , but calf sticks also contribute to its spread. In South America, vampire bats are also involved in the transmission; these can also serve as reservoir hosts in which the parasite reproduces in the blood. In South America, the Capybara is also considered a game reserve.

In India, a single confirmed case of a person suffering from Trypanosoma evansi infection has been described. Detailed analyzes showed that the patient had mutations in both alleles of the ApoLI gene. The ApoLI protein encoded by this gene is an apoprotein that is responsible for human serum resistance to many trypanosomes. After this case, it was found in the local population that apparently a larger number of people had contact with the parasite, but without falling ill.

Life cycle

Trypanosoma evansi has a simple life cycle for trypanosomes; reproduction takes place exclusively in mammals, there is no change in shape as with other trypanosomes. The transmission by blood-sucking insects takes place purely mechanically through cells of the last blood meal on an infected mammal that remained in the mouthpiece of the horsefly. After being bitten by a vector that had recently ingested a meal of blood from an infected animal, trypanosomes enter the mammal's tissue and from there into the lymphatic system and into the bloodstream, where they multiply by splitting longitudinally.

Individual evidence

↑ ^a ^b A. Schnaufer, GJ Domingo, K. Stuart: Natural and induced dyskinetoplastic trypanosomatids: how to live without mitochondrial DNA. In: Int J Parasitol. 32 (9), 2002 Aug, pp. 1071-1084. PMID 12117490
^ W. Gibson: Resolution of the species problem in African trypanosomes. In: Int J Parasitol. 37 (8-9), 2007 Jul, pp. 829-838. PMID 17451719 .
↑ DH Lai, H. Hashimi, ZR Lun, FJ Ayala, J. Lukes: Adaptations of Trypanosoma brucei to gradual loss of kinetoplast DNA: Trypanosoma equiperdum and Trypanosoma evansi are petite mutants of T. brucei. In: Proc Natl Acad Sci USA . 105 (6), 2008 Feb 12, pp. 1999-2004. PMID 18245376
↑ B. Vanhollebeke, P. Truc, P. Poelvoorde, A. Pays, PP Joshi, R. Katti, JG Jannin, E. Pays: Human Trypanosoma evansi infection linked to a lack of apolipoprotein LI. In: N Engl J Med . 355 (26), 2006 Dec 28, pp. 2752-2756. PMID 17192540 .
↑ E. Pays, B. Vanhollebeke, L. Vanhamme, F. Paturiaux-Hanocq, DP Nolan, D. Pérez-Morga: The trypanolytic factor of human serum. In: Nat Rev Microbiol . 4 (6), 2006 Jun, pp. 477-486. PMID 16710327
↑ VR Shegokar, RM Powar, PP Joshi, A. Bhargava, VS Dani, R. Katti, VR Zare, VD Khanande, J. Jannin, P. Truc: Short report: Human trypanosomiasis caused by Trypanosoma evansi in a village in India: preliminary serological survey of the local population. In: Am J Trop Med Hyg. 75 (5), 2006 Nov, pp. 869-870. PMID 17123979 .

literature

Ian Maudlin, PH Holmes, Michael A. Miles (Eds.): The Trypanosomiases . CABI Publishing, Wallingford 2004, ISBN 0-85199-475-X .
R. Brun, H. Hecker, ZR Lun: Trypanosoma evansi and T. equiperdum: distribution, biology, treatment and phylogenetic relationship (a review). In: Vet Parasitol. 79 (2), 1998 Oct, pp. 95-107. PMID 9806490

[Schnaufer-1] A. Schnaufer, GJ Domingo, K. Stuart: Natural and induced dyskinetoplastic trypanosomatids: how to live without mitochondrial DNA. In: Int J Parasitol. 32 (9), 2002 Aug, pp. 1071-1084. PMID 12117490

[Gibson-2] W. Gibson: Resolution of the species problem in African trypanosomes. In: Int J Parasitol. 37 (8-9), 2007 Jul, pp. 829-838. PMID 17451719 .

[3] DH Lai, H. Hashimi, ZR Lun, FJ Ayala, J. Lukes: Adaptations of Trypanosoma brucei to gradual loss of kinetoplast DNA: Trypanosoma equiperdum and Trypanosoma evansi are petite mutants of T. brucei. In: Proc Natl Acad Sci USA . 105 (6), 2008 Feb 12, pp. 1999-2004. PMID 18245376

[4] B. Vanhollebeke, P. Truc, P. Poelvoorde, A. Pays, PP Joshi, R. Katti, JG Jannin, E. Pays: Human Trypanosoma evansi infection linked to a lack of apolipoprotein LI. In: N Engl J Med . 355 (26), 2006 Dec 28, pp. 2752-2756. PMID 17192540 .

[5] E. Pays, B. Vanhollebeke, L. Vanhamme, F. Paturiaux-Hanocq, DP Nolan, D. Pérez-Morga: The trypanolytic factor of human serum. In: Nat Rev Microbiol . 4 (6), 2006 Jun, pp. 477-486. PMID 16710327

[6] VR Shegokar, RM Powar, PP Joshi, A. Bhargava, VS Dani, R. Katti, VR Zare, VD Khanande, J. Jannin, P. Truc: Short report: Human trypanosomiasis caused by Trypanosoma evansi in a village in India: preliminary serological survey of the local population. In: Am J Trop Med Hyg. 75 (5), 2006 Nov, pp. 869-870. PMID 17123979 .