[2] Discovered by Griffith Evans in 1880 at Dera Ismail Khan (British India), it is the first known trypanosome that causes infection.

[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.

[4] T. evansi was a parasite that caused severe, often fatal, infection in mammals such as horses, donkeys, cattle and camels.

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].

Timothy Richards Lewis, Special Assistant to the Sanitary Commissioner, confirmed the parasite but not the connection with the disease.

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.

In 1885, J. H. Steel reported from British Burma (now Myanmar) the same parasites he identified from the blood samples of military transport mules.

[17] However, Steel mistakenly recognised the parasite was as a type of spirochaete bacteria and named it Spirochaeta evansi, in honour of the discoverer.

In 2004, a 45-year-old cattle farmer from Seoni village was hospitalised due to severe fever and disturbed neurological behaviours.

[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.