Trypanosoma brucei

Lore & Background

The parasite was discovered in 1894 by Sir David Bruce, who was appointed by the Royal Army Medical Corps to investigate nagana in South Africa. On 27 October 1894, Bruce and his wife Mary Elizabeth Bruce moved to Ubombo Hill, where the disease was most prevalent. On the sixth day of investigation, Bruce identified parasites from the blood of diseased cows, initially noting them as a kind of filaria, but by the end of the year established they were protozoan and the cause of nagana. The scientific name was created in 1899 by British zoologists Henry George Plimmer and John Rose Bradford as Trypanosoma brucii due to a printer's error.

Human sleeping sickness was first described medically by John Atkins in 1734, and Thomas Masterman Winterbottom gave a clearer description in 1803, noting swollen posterior cervical lymph nodes (Winterbottom's sign). The first human trypanosome was found by Robert Michael Forde in 1901 in Gambia, and identified as a protozoan by Joseph Everett Dutton, who proposed the name Trypanosoma gambiense. Another human trypanosome (now T. brucei rhodesiense) was discovered by John William Watson Stephens and Harold Benjamin Fantham in 1910.

The Royal Society constituted a Sleeping Sickness Commission in 1902 to investigate an epidemic in Uganda. David Bruce led the second commission, and by August 1903 established that the disease was transmitted by the tsetse fly Glossina palpalis. Friedrich Karl Kleine discovered in 1909 that the parasite had developmental stages in tsetse flies, and Muriel Robertson established between 1911 and 1912 how ingested trypanosomes reach the salivary glands.

Reader's Guide

Trypanosoma brucei is significant as the causative agent of African trypanosomiasis (sleeping sickness) in humans and nagana in animals, diseases that have caused major epidemics in sub-Saharan Africa. The parasite is transmitted by tsetse flies (Glossina) and undergoes complex morphological changes during its life cycle. Its mammalian bloodstream forms feature variant surface glycoproteins that undergo remarkable antigenic variation, enabling persistent evasion of host adaptive immunity and leading to chronic infection. T. brucei is one of only a few pathogens known to cross the blood-brain barrier. The parasite is a species complex grouped into five subspecies: T. b. brucei, T. b. equiperdum, T. b. evansi, T. b. gambiense, and T. b. rhodesiense. The first causes nagana in non-human mammals, while the latter two are zoonotic and cause African trypanosomiasis. Genetic analyses reveal that T. b. equiperdum and T. b. evansi evolved from parasites similar to T. b. brucei. There is an urgent need for new drug therapies, as current treatments can have severe side effects and can prove fatal.

Did You Know?

• The parasite was discovered in 1894 by Sir David Bruce, after whom it was named in 1899.
• It is exclusively extracellular, inhabiting blood plasma and body fluids, unlike other protozoan parasites.
• The subspecies T. b. equiperdum and T. b. evansi have lost kinetoplast DNA and are not historically regarded as T. brucei subspecies.