Trypanosoma brucei is a species complex of parasitic flagellated protozoa that cause African sleeping sickness in humans and nagana in animals.
Biology and Pathogenicity
Members of the Trypanosoma brucei complex are transmitted by tsetse flies (Glossina species) and have a digenetic life cycle involving both insect and mammalian hosts. Three subspecies are recognised: T. b. gambiense, which causes a chronic form of West African sleeping sickness; T. b. rhodesiense, responsible for an acute form in East Africa; and T. b. brucei, which infects livestock but is non-pathogenic to humans. In the mammalian bloodstream the parasites exist as extracellular, spindle‑shaped trypomastigotes with a single flagellum and a kinetoplast rich in mitochondrial DNA. They proliferate in blood and lymph and evade host immunity through antigenic variation by repeatedly switching their variant surface glycoprotein coat. This allows chronic infection and facilitates transmission to tsetse flies when they feed. In the fly midgut, the parasites differentiate into procyclic forms and then migrate to the salivary glands, where they become metacyclic trypomastigotes ready to infect a new vertebrate host. Without treatment the human disease progresses from a haemolymphatic phase with fever, anemia and lymph node enlargement to a meningoencephalitic phase when parasites cross the blood–brain barrier, causing sleep disturbances, neuropsychiatric signs and, ultimately, coma. Control relies on active surveillance, vector control and chemotherapy. Early‑stage infections are treated with pentamidine or suramin, while late‑stage disease requires drugs that cross the blood–brain barrier, such as melarsoprol or eflornithine in combination with nifurtimox.
Disease Manifestations and Control
West African sleeping sickness caused by T. b. gambiense progresses slowly, often over months or years, and accounts for the majority of reported cases. East African sleeping sickness due to T. b. rhodesiense presents acutely with high parasitemia and rapid involvement of the central nervous system. Historical epidemics in the early twentieth century led to millions of deaths, but concerted control efforts combining vector control and mass screening have dramatically reduced incidence. Despite progress, sporadic outbreaks continue to threaten rural communities, particularly where tsetse habitats overlap with human activity and livestock. Research on antigenic variation in T. brucei has provided insight into immune evasion strategies and has informed broader understanding of surface protein switching in pathogens. Efforts to develop vaccines have been hampered by the parasite’s antigenic diversity, but new therapies targeting metabolic pathways, the kinetoplast and cytokinesis are under investigation.
Trypanosoma brucei exemplifies the complex interplay between parasites, vectors and host immunity. Continued surveillance, vector management and improved treatments are essential to sustain progress towards elimination and to protect both human health and livestock productivity in endemic regions.
Related Terms: trypanosomiasis, protozoa, tsetse fly, antigenic variation, kinetoplast