Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease, transmitted by the tsetse fly.
HAT affects 36 countries in sub-Saharan Africa, where tsetse flies are found, with approximately 7,000 reported cases per year (Source: WHO). 98% of HAT cases are caused by the parasite Trypanosoma brucei gambiense, while the remaining cases are caused by Trypanosoma brucei rhodesiense. Further information is available from the WHO (http://www.who.int/mediacentre/factsheets/fs259/en/) and CDC (http://www.cdc.gov/parasites/sleepingsickness/). This page gives an overview of the transmission dynamics for modellers who are new to modelling trypanosomiasis. At the bottom of the page are some questions about HAT which modelling can help address, as well as some relevant modelling papers.
Causal agent: Trypanosoma brucei gambiense or Trypanosoma brucei
Vector: tsetse flies
During the primary stage of Trypanosoma infection, parasites can be found in the blood, lymph, and subcutaneous tissues. The symptoms of this stage include fever, headaches, joint pain, and itching.
During the secondary stage of infection, also called the neurological phase, parasites cross the blood-brain barrier to infect the brain and central nervous system. Symptoms of this stage include behavior changes, sensory disturbances, lack of coordination, confusion, and disturbances of the sleep cycle. Without treatment, the majority of cases will die.
T.b. gambiense causes a more chronic form of sleeping sickness, and it may be months or years before symptoms appear. T.b. rhodesiense, however, causes an acute form of sleeping sickness, with symptoms developing a few weeks or months after infection.
The global burden of disease has been mapped by the WHO (http://www.who.int/csr/resources/publications/CSR_ISR_2000_1tryps/en/).
The Trypanosoma parasites (T.b. gambiense and T.b. rhodesiense) are transmitted between tsetse flies (Glossina), humans, and animals.
Tsetse flies take blood meals from humans or animals every two to three days. Flies infected with Trypanosoma will inject the parasites into the human or animal that they are feeding on. The parasite undergoes several developmental stages within the mammalian host. Trypanosomes present in an infected human or animal can then be ingested by an uninfected tsetse fly taking its blood meal on the infected host. The trypanosomes will then undergo several more developmental stages within the fly, and eventually reach the salivary glands of the infected tsetse fly. The newly infected tsetse fly will then transmit trypanosomes to its next host during the next blood meal, thus repeating the cycle of infection and transmission.
There are many different species and subspecies of tsetse that transmit trypanosomes, each with varying preferences for feeding on humans or animals. The Morsitans group tends to be found in savannah environments (e.g. G. morsitans sub-morsitans, G. pallidipes, G. synnertoni, and G. austeni). The Palpalis group is typically found in Riverine environments (e.g. G. palpalis palpalis, G. fuscipes fuscipes, G. tachinoides and G. palpalis gambiensis). The Fusca group is found in the forest (e.g. G. fusca fusca, G. brevipalpis, G. longipennis, and G. medicorum). (Source: Fevre et al. 2006 http://www.sciencedirect.com/science/article/pii/S0065308X05610056)
Vector control to reduce tsetse population size: insecticide, traps, sterilized insect technique, paratransgenesis.
Diagnosis and treatment of humans to reduce Trypanosoma reservoir: serological tests can screen human blood for the presence of trypanosomes. If infection is confirmed, staging can be performed with a lumbar puncture to determine if trypanosomes are present in the CNS fluid. The drugs used for treatment depend on the stage of infection, are toxic, and many must be administered intravenously.
The costs and benefits of different approaches to controlling HAT have not yet been examined. Relevant health economic questions that can be answered through modelling are included below.
Can HAT be eliminated by 2020?
What is the optimal combination of interventions to eliminate HAT?
How could new developments in interventions facilitate or speed up the elimination of HAT?