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Trypanosoma evansi

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Trypanosoma evansi
Trypanosoma evansi in blood
Trypanosoma evansi in blood
Scientific classification Edit this classification
Domain: Eukaryota
Phylum: Euglenozoa
Class: Kinetoplastea
Order: Trypanosomatida
Family: Trypanosomatidae
Genus: Trypanosoma
Species:
T. evansi
Binomial name
Trypanosoma evansi
(Steel) Chauvrat, 1896
Synonyms[1]

Trypanosoma brucei evansi

Trypanosoma evansi is a parasitic species of excavate trypanosome in the genus Trypanosoma that is one cause of surra in animals.[2] Discovered by Griffith Evans in 1880 at Dera Ismail Khan (British India), it is the first known trypanosome that causes infection. It is a common parasite in India and Iran[3] and causes acute disease in camels and horses, and chronic disease in cattle and buffalo. In Pakistan, it has been found to be the most prevalent trypanosome species in donkeys. It is now established to infect other mammals, including humans.[4][5]

It has been proposed that T. evansi is—like T. equiperdum—a derivative of T. brucei.[6] Due to the loss of part of the mitochondrial (kinetoplast) DNA T. evansi is not capable of infecting tsetse flies, the usual invertebrate vectors of trypanosomes, and establishing the subsequent life-stages.[7][8] Due to its mechanical transmission T. evansi shows a very broad vector specificity including members of the genera Tabanus, Stomoxys, Haematopota, Chrysops and Lyperosia.[9] It rarely causes disease in humans,[10] but human infections are common.[4] Haemoglobin plays a role in trypanolytic host defense against T. evansi.[4]

History

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T. evansi was a parasite that caused severe, often fatal, infection in mammals such as horses, donkeys, cattle and camels. In India, where it was prevalent from ancient times, the disease was known as surra.[11] Under the British rule, it caused serious impediment to the British Army, as their horses were infected. In August 1880, Griffith Evans of the Royal Army Service Corps was deployed to investigate the case at army base in Dera Ismail Khan (now in Pakistan). He immediately recognised worm-like parasites from the blood samples of all diseased horses. He reported in 1881:

When I first saw it [the parasite) I thought for a moment it was some form of spirillum [a kind of bacteria], but the next instant convinced me it was not... It has an apparently round body, when it is fresh and active, which tapers in front to a neck ending in a blunt head, and behind it has a tapering tail from which there extends a long slender lash [this now known as the flagella, and is located towards the anterior end, not at the "tail"], so fine that it can seldom be seen... I came to the conclusion that it has two fin-like papillae on each side, one near where the neck commences and another near where the tail begins [now understood to be one undulating membrane, not two, formed by a flagellum].[12]

Griffith experimentally showed that the parasite was the causative pathogen of surra by infecting healthy horses using infected blood.[13] However, the medical authority in British India rejected the idea that the parasite could cause of such disease. Timothy Richards Lewis, Special Assistant to the Sanitary Commissioner, confirmed the parasite but not the connection with the disease. Lewis had discovered a trypanosome (later named Trypanosoma lewisi) of rats in 1878 (reported in 1879).[14] He was convinced that the trypanosome was harmless because he discovered them from only healthy rats. He and David Douglas Cunningham (Professor of Physiology in the Medical College, Calcutta, and Surgeon-General of India), in response to Griffith's observations, officially stated that "no microbe found in the living blood of any animal was pathogenic."[13] It was later recorded in Nature: "Official opinion was strongly against him [Griffith]."[15][16]

Griffith's discovery was independently established. In 1885, J. H. Steel reported from British Burma (now Myanmar) the same parasites he identified from the blood samples of military transport mules. The similarity of the disease and the parasites to those described by Griffith immediately became obvious.[17] However, Steel mistakenly recognised the parasite was as a type of spirochaete bacteria and named it Spirochaeta evansi, in honour of the discoverer.[18] Edgar Crookshank at King's College London correctly identified it as a kind of protozoan renaming it as Haematonomas evansi, but quickly changed it to Trichomonas evansi in 1885. In 1896, French veterinarian J. Chauvrat gave the correct description and the name Trypanosoma evansi.[19] The parasite was then established as the first trypanosome that caused disease (trypanosomiasis).[20]

Human cases

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The first human case was reported from Maharashtra, India, in 2005. In 2004, a 45-year-old cattle farmer from Seoni village was hospitalised due to severe fever and disturbed neurological behaviours. Serological, microscopic, and DNA (PCR) test indicated that he was infected with T. evansi.[4][21] The clinical case was confirmed by the World Health Organization.[22] Normally, humans have natural trypanolytic protein called apolipoprotein L1 (APOL1) that kills different species of trypanosomes during infection. The individual was diagnosed to lack APOL1.[23] Serological survey in 2006 in the same region revealed that the infection was already prevalent; 5 to 22% of the population, based on different tests, were found to be positive for T. evansi.[24][25] Outside India, the first human cases were reported from Egypt in 2011.[26][27] A single case was reported from Vietnam in 2016 in which an infected 38-year-old woman had normal APOL1, indicating that lack of APOL1 is not the primary reason for human infectivity.[25][28]

Treatment

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Suramin is recommended.[29] Isometamidium chloride is ineffective.[29]

Trypanocide resistance

[edit]

Trypanosoma evansi trypanocide resistance is widespread.[4] Diminazene aceturate is often ineffective for bovine, equine, porcine, and elephant use in Thailand.[4] Quinapyramine is not recommended for cattle use due to its tendency to produce cross-resistance with both diminazene aceturate and isometamidium chloride.[4] Quinapyramine is recommended for equine and camel use only.[4] For the Philippines blanket treatment of all affected livestock is recommended, while biannual treatment of an individual village's livestock might be more financially realistic but risks developing resistance.[4]

Range

[edit]

Trypanosoma evansi is rapidly expanding its geographic range.[29] It was historically restricted to Africa but for centuries it has been found in North-East Africa, South Asia, most of East Asia and Latin America.[29] It was first detected in the Canary Islands in 1997 and since 2010 has been imported into Europe, in Germany, France and mainland Spain.[29]

References

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  1. ^ Giordani, Federica; Morrison, Liam J.; Rowan, TIM G.; De Koning, Harry P.; Barrett, Michael P. (2016). "The animal trypanosomiases and their chemotherapy: A review". Parasitology. 143 (14): 1862–1889. doi:10.1017/s0031182016001268. PMC 5142301. PMID 27719692.
  2. ^ Aregawi, Weldegebrial G.; Agga, Getahun E.; Abdi, Reta D.; Büscher, Philippe (January 2019). "Systematic review and meta-analysis on the global distribution, host range, and prevalence of Trypanosoma evansi". Parasites & Vectors. 12 (1): 67. doi:10.1186/s13071-019-3311-4. PMC 6357473. PMID 30704516.
  3. ^ Sazmand A, Joachim A (2017). "Parasitic diseases of camels in Iran (1931-2017) - a literature review". Parasite. 24: 21. doi:10.1051/parasite/2017024. PMC 5479402. PMID 28617666. S2CID 13783061.
  4. ^ a b c d e f g h i Desquesnes M, Dargantes A, Lai DH, Lun ZR, Holzmuller P, Jittapalapong S (2013). "Trypanosoma evansi and surra: a review and perspectives on transmission, epidemiology and control, impact, and zoonotic aspects". BioMed Research International. 2013: 321237. doi:10.1155/2013/321237. PMC 3789323. PMID 24151595. S2CID 18573610.
  5. ^ Habila, Nathan; Inuwa, Mairo H.; Aimola, Idowu A.; Udeh, Michael U.; Haruna, Emmanuel (2012). "Pathogenic mechanisms of Trypanosoma evansi infections". Research in Veterinary Science. 93 (1): 13–17. doi:10.1016/j.rvsc.2011.08.011. PMID 21940025. S2CID 26549677.
  6. ^
    Giordani, Federica; Morrison, Liam J.; Rowan, TIM G.; De Koning, Harry P.; Barrett, Michael P. (2016). "The animal trypanosomiases and their chemotherapy: A review". Parasitology. 143 (14): 1862–1889. doi:10.1017/s0031182016001268. PMC 5142301. PMID 27719692.
    Field, Mark C.; Carrington, Mark (2009). "The trypanosome flagellar pocket". Nature Reviews Microbiology. 7 (11): 775–786. doi:10.1038/nrmicro2221. PMID 19806154. S2CID 13783989.
    Engstler, Markus (2008), Faculty Opinions recommendation of Adaptations of Trypanosoma brucei to gradual loss of kinetoplast DNA: Trypanosoma equiperdum and Trypanosoma evansi are petite mutants of T. brucei, doi:10.3410/f.1101182.557184, S2CID 222586223
    This review is cited by Giordani et al., 2016, Baldacchino et al., 2014, Berninger et al., 2017, Antonovics et al., 2017, Auty et al., 2015, Cnops et al., 2014 and others: Desquesnes M, Dargantes A, Lai DH, Lun ZR, Holzmuller P, Jittapalapong S (2013). "Trypanosoma evansi and surra: a review and perspectives on transmission, epidemiology and control, impact, and zoonotic aspects". BioMed Research International. 2013: 321237. doi:10.1155/2013/321237. PMC 3789323. PMID 24151595. S2CID 18573610.
    Tielens, Aloysius G.M.; van Hellemond, Jaap J. (2009). "Surprising variety in energy metabolism within Trypanosomatidae". Trends in Parasitology. 25 (10): 482–490. doi:10.1016/j.pt.2009.07.007. PMID 19748317. S2CID 8166416.
  7. ^ Borst P, Fase-Fowler F, Gibson WC (February 1987). "Kinetoplast DNA of Trypanosoma evansi". Molecular and Biochemical Parasitology. 23 (1): 31–38. doi:10.1016/0166-6851(87)90184-8. PMID 3033499.
  8. ^ Hoare CR (1972). The trypanosomes of the Mammals. Oxford: Blackwell Publishing.
  9. ^ Luckins AG (May 1988). "Trypanosoma evansi in Asia". Parasitology Today. 4 (5): 137–142. doi:10.1016/0169-4758(88)90188-3. PMID 15463067.(and references therein)
  10. ^ Powar RM, Shegokar VR, Joshi PP, Dani VS, Tankhiwale NS, Truc P, et al. (January 2006). "A rare case of human trypanosomiasis caused by Trypanosoma evansi". Indian Journal of Medical Microbiology. 24 (1): 72–74. doi:10.4103/0255-0857.19904 (inactive 1 November 2024). PMID 16505565.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  11. ^ Desquesnes M, Holzmuller P, Lai DH, Dargantes A, Lun ZR, Jittaplapong S (2013). "Trypanosoma evansi and surra: a review and perspectives on origin, history, distribution, taxonomy, morphology, hosts, and pathogenic effects". BioMed Research International. 2013: 194176. doi:10.1155/2013/194176. PMC 3760267. PMID 24024184.
  12. ^ Evans G (1881). "On a Horse Disease in India Known as "Surra," Probably Due to a Hæmatozoon". The Veterinary Journal and Annals of Comparative Pathology. 13 (9): 180–200. doi:10.1016/S2543-3377(17)43154-2.
  13. ^ a b Saygin D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (1918-07-25). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 1–16. doi:10.1080/00034983.1918.11684153. PMC 7052475. PMID 32166015.
  14. ^ Saygin, Didem; Tabib, Tracy; Bittar, Humberto E.T.; Valenzi, Eleanor; Sembrat, John; Chan, Stephen Y.; Rojas, Mauricio; Lafyatis, Robert (2020). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 1–15. doi:10.1177/2045894020908782. PMC 7052475. PMID 32166015.
  15. ^ Saygin D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (1935). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 172–173. doi:10.1038/136172a0. PMC 7052475. PMID 32166015.
  16. ^ Saygin D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (1935). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 942–943. doi:10.1038/136942a0. PMC 7052475. PMID 32166015.
  17. ^ Steel JH, Evans G (3 December 1880). "Report of veterinary surgeon JH Steel, AVD, on his investigation into an obscure and fatal disease among transport mules in British Burma, which he found to be a fever of relapsing type, and probably identical with the disorder first described by Dr. Griffith Evans under the name" Surra", in a report (herewith reprinted)". The Veterinary Journal. London: Punjab Government, Military Department, No. 439-4467. Retrieved 2022-11-23 – via Wellcome Collection.
  18. ^ Hevia JL (2018). "Surra and the Emergence of Tropical Veterinary Medicine in Colonial India". Animal Labor and Colonial Warfare. University of Chicago Press. pp. 218–249. doi:10.7208/chicago/9780226562315.003.0009. ISBN 978-0-226-56228-5.
  19. ^ "Dr. Griffith's Evan's 100th birthday". British Medical Journal. 2 (3893): 313–314. 1935. PMC 2461164.
  20. ^ "Dr. Griffith Evan's Hundredth Birthday". Canadian Medical Association Journal. 33 (4): 430–431. October 1935. PMC 1561448. PMID 20320047.
  21. ^ Joshi PP, Shegokar VR, Powar RM, Herder S, Katti R, Salkar HR, et al. (September 2005). "Human trypanosomiasis caused by Trypanosoma evansi in India: the first case report". The American Journal of Tropical Medicine and Hygiene. 73 (3): 491–495. doi:10.4269/ajtmh.2005.73.491. PMID 16172469.
  22. ^ The World Health Organization (February 2005). "A new form of human trypanosomiasis in India. Description of the first human case in the world caused by Trypanosoma evansi". Relevé Épidémiologique Hebdomadaire. 80 (7): 62–63. PMID 15771199.
  23. ^ Vanhollebeke B, Truc P, Poelvoorde P, Pays A, Joshi PP, Katti R, et al. (December 2006). "Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I". The New England Journal of Medicine. 355 (26): 2752–2756. doi:10.1056/NEJMoa063265. PMID 17192540.
  24. ^ Shegokar VR, Powar RM, Joshi PP, Bhargava A, Dani VS, Katti R, et al. (November 2006). "Short report: Human trypanosomiasis caused by Trypanosoma evansi in a village in India: preliminary serologic survey of the local population". The American Journal of Tropical Medicine and Hygiene. 75 (5): 869–870. doi:10.4269/ajtmh.2006.75.869. PMID 17123979.
  25. ^ a b Aregawi WG, Agga GE, Abdi RD, Büscher P (January 2019). "Systematic review and meta-analysis on the global distribution, host range, and prevalence of Trypanosoma evansi". Parasites & Vectors. 12 (1): 67. doi:10.1186/s13071-019-3311-4. PMC 6357473. PMID 30704516.
  26. ^ Giordani, Federica; Morrison, Liam J.; Rowan, TIM G.; De Koning, Harry P.; Barrett, Michael P. (2016). "The animal trypanosomiases and their chemotherapy: A review". Parasitology. 143 (14): 1862–1889. doi:10.1017/s0031182016001268. PMC 5142301. PMID 27719692.
  27. ^ Radwanska M, Vereecke N, Deleeuw V, Pinto J, Magez S (2018). "Salivarian Trypanosomosis: A Review of Parasites Involved, Their Global Distribution and Their Interaction With the Innate and Adaptive Mammalian Host Immune System". Frontiers in Immunology. 9: 2253. doi:10.3389/fimmu.2018.02253. PMC 6175991. PMID 30333827.
  28. ^ Van Vinh Chau N, Buu Chau L, Desquesnes M, Herder S, Phu Huong Lan N, Campbell JI, et al. (April 2016). "A Clinical and Epidemiological Investigation of the First Reported Human Infection With the Zoonotic Parasite Trypanosoma evansi in Southeast Asia". Clinical Infectious Diseases. 62 (8): 1002–1008. doi:10.1093/cid/ciw052. PMC 4803109. PMID 26908809.
  29. ^ a b c d e Kasozi, Keneth Iceland; MacLeod, Ewan Thomas; Ntulume, Ibrahim; Welburn, Susan Christina (2022). "An Update on African Trypanocide Pharmaceutics and Resistance". Frontiers in Veterinary Science. 9: 828111. doi:10.3389/fvets.2022.828111. PMC 8959112. PMID 35356785. S2CID 247245582.
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