Priorities for the Elimination of Sleeping Sickness

Sleeping sickness describes two diseases, both fatal if left untreated: (i) Gambian sleeping sickness caused by Trypanosoma brucei gambiense, a chronic disease with average infection lasting around 3 years, and (ii) Rhodesian sleeping sickness caused by T. b. rhodesiense, an acute disease with death occurring within weeks of infection. Control of Gambian sleeping sickness is based on case detection and treatment involving serological screening, followed by diagnostic confirmation and staging. In stage I, patients can remain asymptomatic as trypanosomes multiply in tissues and body fluids; in stage II, trypanosomes cross the blood brain barrier, enter the central nervous system and, if left untreated, death follows. Staging is crucial as it defines the treatment that is prescribed; for both forms of disease, stage II involves the use of the highly toxic drug melarsoprol or, in the case of Gambian sleeping sickness, the use of complex and very expensive drug regimes. Case detection of T b. gambiense sleeping sickness is known to be inefficient but could be improved by the identification of parasites using molecular tools that are, as yet, rarely used in the field. Diagnostics are not such a problem in relation to T b. rhodesiense sleeping sickness, but the high level of under-reporting of this disease suggests that current strategies, reliant on self-reporting, are inefficient. Sleeping sickness is one of the 'neglected tropical diseases' that attracts little attention from donors or policymakers. Proper quantification of the burden of sleeping sickness matters, as the primary reason for its 'neglect' is that the true impact of the disease is unknown, largely as a result of under-reporting. Certainly, elimination will not be achieved without vast improvements in field diagnostics for both forms of sleeping sickness especially if there is a hidden reservoir of 'chronic carriers'. Mass screening would be a desirable aim for Gambian sleeping sickness and could be handled on a national scale in the endemic countries perhaps by piggybacking on programmes committed to other diseases. As well as improved diagnostics, the search for non-toxic drugs for stage II treatment should remain a research priority. There is good evidence that thorough active case finding is sufficient to control T b. gambiense sleeping sickness, as there is no significant animal reservoir. Trypanosoma brucei rhodesiense sleeping sickness is a zoonosis and control involves interrupting the fly animal human cycle, so some form of tsetse control and chemotherapy of the animal reservoir must be involved. The restricted application of insecticide to cattle is the most promising, affordable and sustainable technique to have emerged for tsetse control. Animal health providers can aid disease control by treating cattle and, when allied with innovative methods of funding (e.g. public private partnerships) not reliant on the public purse, this approach may prove more sustainable. Sleeping sickness incidence for the 36 endemic countries has shown a steady decline in recent years and we should take advantage of the apparent lull in incidence and aim for elimination. This is feasible in some sleeping sickness foci but must be planned and paid for increasingly by the endemic countries themselves. The control and elimination of T. b. gambiense sleeping sickness may be seen as a public good, as appropriate strategies depend on local health services for surveillance and treatment, but public-private funding mechanisms should not be excluded. It is timely to take up the tools available and invest in new tools - including novel financial instruments - to eliminate this disease from Africa.