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
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]
Trypanosoma evansitrypanocide 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]
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.
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,
S2CID222586223