Chemotherapy of @entity1 XXXX .

@entity1 @entity7246 @entity5747 @entity25 @entity16 @entity3177 @entity772 @entity16580 @entity281 @entity7341 @entity26922 @entity3494 @entity204 @entity7247 @entity238 @entity11747
@entity1 @entity7247 or @entity25 is resurgent [1,2]. The disease is caused by subspecies of the parasitic haemoflagellate, @entity3177 . Infection starts with the bite of an infected tsetse @entity238 (Glossina spp.). Parasites move from the site of @entity281 to the draining lymphatic vessels and blood stream. The parasites proliferate within the bloodstream and later invade other tissues including the central nervous system. Once they have established themselves within the CNS, a progressive @entity16 . @entity772 precedes @entity204 during this late phase. Two forms of the disease are recognised, one caused by @entity3177 rhodesiense, endemic in Eastern and Southern Africa, in which parasites rapidly invade the CNS causing @entity204 within weeks if untreated. T. b. gambiense, originally described in West Africa, but also widespread in Central Africa, proliferates more slowly and can take several years before establishing a CNS-involved @entity281 . Many countries are in the midst of epidemics caused by gambiense-type parasites. Four drugs have been licensed to treat the disease [3]; two of them, @entity7341 and @entity5747 , are used prior to CNS involvement. The @entity3494 -based drug, @entity26922 is used once parasites are established in the CNS. The fourth, @entity11747 , is effective against late stage disease caused by T. b. gambiense, but is ineffective against T. b. rhodesiense. Another drug, @entity16580 is licensed for South American @entity7246 but also been used in trials against @entity26922 -refractory late sage disease. This review focuses on what is known about modes of action of current drugs and discusses targets for future drug development.
