Human African Trypanosomosis (HAT) is caused by a protozoan parasite, Trypanosoma brucei and is transmitted by the bite of tsetse flies (Glossina species). The disease is found in 36 sub-Saharan countries and exists in two clinical forms due to T. brucei gambiense and T. b. rhodesiense which so far are geographically separated. The clinical presentation of T. b. rhodesiense is more acute; the T. b. gambiense form is chronic, with months to years elapsing before the appearance of obvious signs or symptoms. Sleeping sickness is fatal if untreated.
Pentamidine and suramin are used for treatment of the early stage of the disease. For the late stage melarsoprol (an organo-arsenical) is the first line drug, eflornithine and nifurtimox are alternatives for refractory cases. The available drugs are old, expensive and toxic. Since 1995, the rate of treatment failures with melarsoprol, the most important drug, was observed to have increased to over 20% in some areas. The disease with all its symptoms and the long period of hospitalisation required for treatment creates social and economic burden for the families and the national health budget of the countries affected.
By the 1960’s the disease had been brought under control by active surveillance and vector control. But since the 1970’s a dramatic resurgence of sleeping sickness was noted in many countries. It is estimated that 60 million people are at risk, but only 5 million of them are under active surveillance or have access to health centres. Prevalence is estimated at 400’000, the number of new cases at 60’000 and the mortality at 40’000 per annum. In countries like Angola, DR Congo, Sudan and Uganda the disease is considered epidemic due to a high prevalence and transmission level. Today, Eastern Africa has dropped back to the status of 1930.
Transmission of African trypanosomosis is enhanced by increased contact between Glossina and humans. Population movements play an important role in the spread of the disease. Wars and civil unrest cause migration of infected people thus introducing the parasite to areas which were under control. Examples are the focus in north-western Uganda, the Kajo-Kaji focus in southern Sudan and several foci in Angola and Tanzania, all of which became reactivated during the civil wars that affected those countries. Migration does not only promote the distribution of sleeping sickness it also increase the danger that the two forms of sleeping sickness will eventually overlap. In Uganda there is the risk of both clinical forms overlapping and being transmitted by the same Glossina species.
The Eastern Africa Network for Trypanosomosis (EANETT) was founded in 1999 and started to operate in 2001. EANETT is the first network for trypanosomosis in the region. Founding members were national institutions involved in trypanosomosis and tsetse research and control in Uganda, Kenya, Sudan and Tanzania. These countries are all affected by animal trypanosomosis (Nagana) and human trypanosomosis (sleeping sickness). T.b.gambiense is found in Southern Sudan and Northern Uganda, T.b.rhodesiense is endemic in Southeastern Uganda and in various foci in Tanzania. The network aims at establishing collaboration in research, training and control of trypanosomosis, links for exchange of information and technologies through workshops, technical exchange visits, MSc and PhD programmes, and an annual conference.
The network is based on bilateral collaborations between the Swiss Tropical Institute and the African partners involved (contacts with LIRI, formerly EATRO, Uganda date back to 1970 and with KETRI to the early 90’s). KETRI and LIRI have collaborated since the establishment of KETRI in the late 70’s.