Trypanosoma evansi | |
---|---|
Trypanosoma evansi in blood | |
Scientific 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]
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]
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]
Suramin is recommended. [29] Isometamidium chloride is ineffective. [29]
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]
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]
African trypanosomiasis is an insect-borne parasitic infection of humans and other animals.
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.
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 pronounced economic and public health impacts in sub-Saharan Africa as the biological vectors of trypanosomes, causing human and animal trypanosomiasis.
Trypanosomiasis or trypanosomosis is the name of several diseases in vertebrates caused by parasitic protozoan trypanosomes of the genus Trypanosoma. In humans this includes African trypanosomiasis and Chagas disease. A number of other diseases occur in other animals.
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.
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.
Τrypanosoma equiperdum is a species of kinetoplastid parasites that causes Dourine or covering sickness in horses and other animals in the family equidae. T. equiperdum is the only known trypanosome that is not spread by an insect vector. There has been substantial controversy surrounding whether T. equiperdum should be considered a unique species, or a strain of T. evansi or T. brucei. T. equiperdum is unique in that its kinetoplast, the network of connected rings that make up its mitochondrial DNA, consists of thousands of "minicircles" that are identical in sequence.
Surra is a disease of vertebrate animals. The disease is caused by protozoan trypanosomes, specifically Trypanosoma evansi, of several species which infect the blood of the vertebrate host, causing fever, weakness, and lethargy which lead to weight loss and anemia. In some animals the disease is fatal unless treated.
Major-General Sir David Bruce, was a Scottish pathologist and microbiologist who made some of the key contributions in tropical medicine. In 1887, he discovered a bacterium, now called Brucella, that caused what was known as Malta fever. In 1894, he discovered a protozoan parasite, named Trypanosoma brucei, as the causative pathogen of nagana.
Animal trypanosomiasis, also known as nagana and nagana pest, or sleeping sickness, is a disease of vertebrates. The disease is caused by trypanosomes of several species in the genus Trypanosoma such as T. brucei. T. vivax causes nagana mainly in West Africa, although it has spread to South America. The trypanosomes infect the blood of the vertebrate host, causing fever, weakness, and lethargy, which lead to weight loss and anemia; in some animals the disease is fatal unless treated. The trypanosomes are transmitted by tsetse flies.
Trypanosoma cruzi is a species of parasitic euglenoids. Among the protozoa, the trypanosomes characteristically bore tissue in another organism and feed on blood (primarily) and also lymph. This behaviour causes disease or the likelihood of disease that varies with the organism: Chagas disease in humans, dourine and surra in horses, and a brucellosis-like disease in cattle. Parasites need a host body and the haematophagous insect triatomine is the major vector in accord with a mechanism of infection. The triatomine likes the nests of vertebrate animals for shelter, where it bites and sucks blood for food. Individual triatomines infected with protozoa from other contact with animals transmit trypanosomes when the triatomine deposits its faeces on the host's skin surface and then bites. Penetration of the infected faeces is further facilitated by the scratching of the bite area by the human or animal host.
Trypanosoma congolense is a species of trypanosomes and is the major pathogen responsible for the disease nagana in cattle and other animals including sheep, pigs, goats, horses and camels, dogs, as well as laboratory mice. It is the most common cause of nagana in east Africa, but is also a major cause of nagana in west Africa. This parasite is spread by tsetse flies. In its mammalian host, Trypanosoma congolense only lives in blood vessels, and causes in particular anaemia.
Trypanosoma rangeli is a species of hemoflagellate excavate parasites of the genus Trypanosoma. Although infecting a variety of mammalian species in a wide geographical area in Central and South America, this parasite is considered non-pathogenic to these hosts. T. rangeli is transmitted by bite of infected triatomine bugs of the Reduviidae family, commonly known as barbeiro, winchuka(vinchuca), chinche, pito ou chupão.
A Trypanosomiasis vaccine is a vaccine against trypanosomiasis. No effective vaccine currently exists, but development of a vaccine is the subject of current research.
Wendy Gibson is Professor of Protozoology at University of Bristol, specialising in trypanosomes and molecular parasitology.
Fexinidazole is a medication used to treat African trypanosomiasis caused by Trypanosoma brucei gambiense. It is effective against both first and second stage disease. Also a potential new treatment for Chagas disease, a neglected tropical disease that affects millions of people worldwide. It is taken by mouth.
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.
A trypanotolerant organism is one which is relatively less affected by trypanosome infestation.
Griffith Evans was a Welsh physician and veterinary pathologist who was the first to determine that a trypanosome parasite was responsible for surra disease in horses while serving in British India. Described as "the man who first saw a pathogenic trypanosome", he identified the causal organism as a haematozoon in 1880 which was given the species name Trypanosoma evansi after him.
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.
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