Trypanosoma evansi

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Trypanosoma evansi
Parasite140104-fig2 Surra (Trypanosoma evansi infection) in a Tunisian dog.png
Trypanosoma evansi in blood
Scientific classification OOjs UI icon edit-ltr.svg
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]

Contents

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

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

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

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

Trypanocide resistance

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

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]

Related Research Articles

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African trypanosomiasis, also known as African sleeping sickness or simply sleeping sickness, is an insect-borne parasitic infection of humans and other animals. It is caused by the species Trypanosoma brucei. Humans are infected by two types, Trypanosoma brucei gambiense (TbG) and Trypanosoma brucei rhodesiense (TbR). TbG causes over 92% of reported cases. Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.

<span class="mw-page-title-main">Trypanosomatida</span> Flagellate kinetoplastid excavate order

Trypanosomatida is a group of kinetoplastid unicellular organisms distinguished by having only a single flagellum. The name is derived from the Greek trypano (borer) and soma (body) because of the corkscrew-like motion of some trypanosomatid species. All members are exclusively parasitic, found primarily in insects. A few genera have life-cycles involving a secondary host, which may be a vertebrate, invertebrate or plant. These include several species that cause major diseases in humans. Some trypanosomatida are intracellular parasites, with the important exception of Trypanosoma brucei.

<span class="mw-page-title-main">Tsetse fly</span> Genus of disease-spreading insects

Tsetse are large, biting flies that inhabit much of tropical Africa. Tsetse flies include all the species in the genus Glossina, which are placed in their own family, Glossinidae. The tsetse is an obligate parasite, which lives by feeding on the blood of vertebrate animals. Tsetse has been extensively studied because of their role in transmitting disease. They have a pronounced economic impact in sub-Saharan Africa as the biological vectors of trypanosomes, causing human and animal trypanosomiasis.

<span class="mw-page-title-main">Trypanosomiasis</span> Medical condition

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<i>Trypanosoma</i> Genus of parasitic flagellate protist in the Kinetoplastea class

Trypanosoma is a genus of kinetoplastids, a monophyletic group of unicellular parasitic flagellate protozoa. Trypanosoma is part of the phylum Euglenozoa. The name is derived from the Greek trypano- (borer) and soma (body) because of their corkscrew-like motion. Most trypanosomes are heteroxenous and most are transmitted via a vector. The majority of species are transmitted by blood-feeding invertebrates, but there are different mechanisms among the varying species. Trypanosoma equiperdum is spread between horses and other equine species by sexual contact. They are generally found in the intestine of their invertebrate host, but normally occupy the bloodstream or an intracellular environment in the vertebrate host.

<i>Trypanosoma brucei</i> Species of protozoan parasite

Trypanosoma brucei is a species of parasitic kinetoplastid belonging to the genus Trypanosoma that is present in sub-Saharan Africa. Unlike other protozoan parasites that normally infect blood and tissue cells, it is exclusively extracellular and inhabits the blood plasma and body fluids. It causes deadly vector-borne diseases: African trypanosomiasis or sleeping sickness in humans, and animal trypanosomiasis or nagana in cattle and horses. It is a species complex grouped into three subspecies: T. b. brucei, T. b. gambiense and T. b. rhodesiense. The first is a parasite of non-human mammals and causes nagana, while the latter two are zoonotic infecting both humans and animals and cause African trypanosomiasis.

<span class="mw-page-title-main">Surra</span> Parasitic disease of animals

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<span class="mw-page-title-main">Animal trypanosomiasis</span> Parasitic disease of vertebrates

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<i>Trypanosoma cruzi</i> Species of parasitic euglenoids (protozoans)

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<i>Trypanosoma congolense</i> Protozoan parasite, cause of nagana

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<span class="mw-page-title-main">Variant surface glycoprotein</span>

Variant surface glycoprotein (VSG) is a ~60kDa protein which densely packs the cell surface of protozoan parasites belonging to the genus Trypanosoma. This genus is notable for their cell surface proteins. They were first isolated from Trypanosoma brucei in 1975 by George Cross. VSG allows the trypanosomatid parasites to evade the mammalian host's immune system by extensive antigenic variation. They form a 12–15 nm surface coat. VSG dimers make up ~90% of all cell surface protein and ~10% of total cell protein. For this reason, these proteins are highly immunogenic and an immune response raised against a specific VSG coat will rapidly kill trypanosomes expressing this variant. However, with each cell division there is a possibility that the progeny will switch expression to change the VSG that is being expressed. VSG has no prescribed biochemical activity.

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The Sleeping Sickness Commission was a medical project established by the British Royal Society to investigate the outbreak of African sleeping sickness or African trypanosomiasis in Africa at the turn of the 20th century. The outbreak of the disease started in 1900 in Uganda, which was at the time a protectorate of the British Empire. The initial team in 1902 consisted of Aldo Castellani and George Carmichael Low, both from the London School of Hygiene and Tropical Medicine, and Cuthbert Christy, a medical officer on duty in Bombay, India. From 1903, David Bruce of the Royal Army Medical Corps and David Nunes Nabarro of the University College Hospital took over the leadership. The commission established that species of blood protozoan called Trypanosoma brucei, named after Bruce, was the causative parasite of sleeping sickness.

<span class="mw-page-title-main">Griffith Evans (bacteriologist)</span> Welsh veterinary pathologist (1835–1935)

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Keith Roland Matthews,, , is a British cell biologist and parasitologist, currently Professor of Parasite Biology in the School of Biological Sciences at the University of Edinburgh. His research focuses on African trypanosomes, which cause human sleeping sickness and the equivalent cattle disease nagana.

References

  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.
    This review cites this research.
    Rjeibi MR, Ben Hamida T, Dalgatova Z, Mahjoub T, Rejeb A, Dridi W, Gharbi M (2015). "First report of surra (Trypanosoma evansi infection) in a Tunisian dog". Parasite . 22: 3. doi:10.1051/parasite/2015004. PMC   4318485 . PMID   25654368. S2CID   14728034. Open Access logo PLoS transparent.svg
  3. ↑ Sazmand A, Joachim A (2017). "Parasitic diseases of camels in Iran (1931-2017) - a literature review". Parasite . 24. EDP Sciences: 21. doi:10.1051/parasite/2017024. ISSN   1776-1042. PMC   5479402 . PMID   28617666. S2CID   13783061. Open Access logo PLoS transparent.svg
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    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.
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    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). Elsevier BV: 13–17. doi:10.1016/j.rvsc.2011.08.011. ISSN   0034-5288. PMID   21940025. S2CID   26549677. Association for Veterinary Teaching and Research Work (AVTRW).
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  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). Nature Portfolio: 775–786. doi:10.1038/nrmicro2221. ISSN   1740-1526. 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, Faculty Opinions Ltd, 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). Cell Press: 482–490. doi:10.1016/j.pt.2009.07.007. ISSN   1471-4922. PMID   19748317. S2CID   8166416.
    These reviews cite this research.
    Lai DH, Hashimi H, Lun ZR, Ayala FJ, Lukes J (February 2008). "Adaptations of Trypanosoma brucei to gradual loss of kinetoplast DNA: Trypanosoma equiperdum and Trypanosoma evansi are petite mutants of T. brucei". Proceedings of the National Academy of Sciences of the United States of America . 105 (6): 1999–2004. Bibcode:2008PNAS..105.1999L. doi: 10.1073/pnas.0711799105 . PMC   2538871 . PMID   18245376. S2CID   25105010.
  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 . PMID   16505565.
  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. 1 2 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 D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (1879). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 109–114. doi:10.1242/jcs.s2-19.73.109. 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. ISSN   0007-1447. 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. 1 2 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.
    This review cites this research.
    Haridy FM, El-Metwally MT, Khalil HH, Morsy TA (April 2011). "Trypanosoma evansi in dromedary camel: with a case report of zoonosis in greater Cairo, Egypt". Journal of the Egyptian Society of Parasitology . 41 (1): 65–76. PMID   21634243. S2CID   11613056.
  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. 1 2 3 4 5
    This review is cited by De Rycker et al., 2022, Melfi et al., 2023, Hofer 2023:
    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. Frontiers Media SA: 828111. doi: 10.3389/fvets.2022.828111 . ISSN   2297-1769. PMC   8959112 . PMID   35356785. S2CID   247245582.
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