African sleeping sickness has apparently been endemic in some parts of Africa for a very long time. The first historical note of this disease comes from the Arabian historian Ibn Khaldun, who described how in 1374 A.D. Sultan Mari Djata of Mali died of an illness which, according to the description, is at least compatible with this disease. The disease was observed and described in 1803 by the English doctor Thomas Masterman Winterbottom, who was working in Sierra Leone. He was struck by the frequent occurrence of swollen cervical lymph nodes in sick persons. Slave-traders also knew about this and avoided buying people with cervical lymphadenopathy.

In 1843 David Gruby in Paris discovered a parasite in the blood of a frog and proposed the name "trypanosome" ("Trypanosoma sanguinis"). In 1881 Griffith Evans, a veterinary surgeon in India, found trypanosomes in the blood of sick camels and horses. These animals died of a serious disease, known locally as "surra". The surra parasite was later given the name "Trypanosoma evansi". The next major step was taken by the British army medical officer Dr. David Bruce, famous because of his work on brucellosis. After the elucidation of Malta fever in 1884, he was transferred to South Africa. In 1895 Bruce, working in Zululand, discovered that trypanosomes were responsible for a cattle disease (nagana). The parasite species was subsequently named after him (Trypanosoma brucei brucei). Bruce also suspected that the disease was transmitted by tsetse flies and thought that there was a reservoir in antelopes. After the Boer War (1899) he continued his investigation in 1903-1906 in, among other places, Uganda. The next breakthrough with respect to the aetiology of human trypanosomiasis came in 1901, when Dr. Forde discovered a motile parasite in the blood of a sick captain of a river boat in Gambia. He was unable to identify the parasite and the patient was repatriated to England. In 1902 the parasite was identified as a trypanosome by Dutton in Liverpool. Because of the patient’s origin, the Italian researcher Aldo Castellani gave the parasite the name T. gambiense. In 1903 Castellani found trypanosomes in the cerebrospinal fluid of persons who had died of East African sleeping sickness, but did not initially recognize their significance. In 1909-1910 Trypanosoma rhodesiense (after the former Rhodesia) was described by Stephens and Fantham. The taxonomy has subsequently been slightly modified. Three subspecies of Trypanosoma brucei are now described: Trypanosoma brucei brucei (not pathogenic for man), Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense.

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Apart from the great rinderpest or cattle plague (viral) and nagana epidemics in South Africa at the end of the nineteenth century, there were also epidemics of human trypanosomiasis. It is possible that the great epidemics since then have arisen through the conflict between two different ecosystems (the natural one with its original vegetation, fauna and vectors and the artificial human ecosystem with its animals, exploitations and cultivations). From 1896 to 1906 there was a major epidemic in the Congo with more than 500,000 fatalities. Another epidemic raged around Lake Victoria and killed two thirds of the local population (between 1900 and 1920 about 250,000 people died of what was probably a T.b. rhodesiense epidemic). Between 1924 and 1926 trypanosomiasis was a major cause of death in Central Cameroon. In the 1980s there was a flare-up in Uganda with many thousands of cases. After an initial phase of decline in the 20th century, the disease (principally T. b. gambiense) has now regained its former range (Congo, Sudan, Uganda, Angola).

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The connection between the terrible rinderpest epidemic and sleeping sickness has been rather extensively investigated. Rural East Africa and the Sahel before 1887 were dominated by vast grasslands with enormous numbers of cattle. Grazing maintained the grassland biotopes. In 1887 rinderpest was introduced into the continent for the first time via Eritrea. The indigenous fauna had no resistance. This viral disease, related to measles and distemper, had an enormous mortality rate in cattle and in wild (cloven-hoofed) animals. The epidemic spread with lightning speed, resulting in the collapse of practically all cattle stock (for example: Botswana 1891: 400,000 head of cattle; only 20,000 in 1892). The grasslands quickly disappeared and the resulting bush with its thorn bushes and small trees was ideal for tsetse flies resulting in an increase in sleeping sickness. The wild animal stock recovered more quickly than the domestic cattle. An alternative hypothesis states that after the massive die-off of cattle, livestock restocking occurred. The large-scale movement of these cattle could be linked to the introduction of the disease in new areas.