A combination of historical, geographical, and epidemiological studies has given sufficient insight into the ecology of sleeping sickness to enable the main factors influencing the development and spread of an epidemic to be traced.The evidence shows that in West Africa sleeping sickness is not primarily a disease of the forest, where tsetse flies are most abundant, but belongs essentially to the dry country in the north of the savanna woodland zone, where the earliest occurrences and severest outbreaks have been located.The first mention of sleeping sickness comes from the upper Niger and dates back to the 14th century. By the beginning of the present century intense though localised epidemics were devastating parts of the Mossi, Grounsi and Lobi country of the upper Volta rivers. At this time the disease was unknown on the coast and of sporadic occurrence only in the forest. A severe trans-Volta epidemic covering 60,000 square miles, developed between 1924 and 1940, but was confined to the north of the inland savanna zone with nothing comparable in the forest.The epidemic spread in three principal ways : (1) Outwards from original foci of infection because of the dynamic nature of the disease. This produced a concentration of infection around headwaters, a feature characteristic of advanced epidemics. (2) Through the agency of travellers, originally from north to south but subsequently in both directions : a rapid method of spread producing linear distribution of infection along trade routes. The tempo was greatly increased on the pacification and development of West Africa after 1900. (3) A gradual southward shift in the main epidemic zone appears to be resulting from a long-term change in the African climate which is combining with man's activities to produce a southerly extension of xerophytic vegetation types and a regression of forest.The most important spread was that caused by the trading caravans, more especially the cola traders, who have been coming down to the cola-nut areas in the Ashanti forest from the big markets on the Niger and Upper Volta since the 11th century. The caravans were formerly very large, up to one or two thousand strong, and were frequently made up of Mossi and Grounsi from the territory that was so
heavily infected by the beginning of the present century. It is certain that a continuous introduction of infection would have been taking place into the forest ever since trypanosomiasis was prevalent in the north, that is for 100 years at least. And infection has been known in the forest for about that period, yet always to a mild degree, never reaching epidemic form. It has been sought for, because conditions in the forest, with the vector Glossina palpalis in contact with every village and path, appeared to be ideal for the transmission of infection and this drew the particular attention of the early workers from 1908 onwards. But the most that could be found was a threatened epidemic in north-west Ashanti, very significantly centering on the big cola markets which formed the termini for the northern traders.This historical evidence and the reasoning from epidemiology lead to the conclusion that conditions in the forest are not conducive to the development of epidemic sleeping sickness and that the low state of endemicity found there is maintained by the constant introduction of infection from the true epidemic areas in northern savanna.From this conclusion arises a practical point of the greatest importance. If the sources from which infection is introduced into the forest could be eliminated the disease there should eventually die out and the tsetse, from the human point of view, would be harmless. Tsetse control in the forest may prove difficult and expensive, and if it is attempted by clearing this might end in the literal destruction of the forest. Such measures would be hard to justify, so many other factors of possibly greater importance than trypanosomiasis are involved, both the intrinsic value of a forest for its products and the wider value through its influence on climate, soil and water.In formulating a plan for the control of sleeping sickness, the habits of both vectors, human as well as insect, should be considered. The tsetse plays a major role in the development of the high infection rates characterising the epidemic outbreaks in northern savanna ; the human vector distributes infection from these sources along trade routes and into the forest. The elimination of the disease at its source, in true epidemic centres, which can be most effectively accomplished by eradication of the tsetse, will check the distribution of infections to the secondary areas of lighter infection which could then be cleared up by quite minor control measures or might even disappear spontaneously.This plan is now in operation in the Gold Coast. The validity of the arguments on which it was based is being shown by the results that are already apparent : the high rates of reduction in the epidemic areas and the pronounced lowering of infection in neighbouring, uncontrolled areas, more particularly in the forest region of north-west Ashanti where it is entered by a trade route coming from the previously heavily infected country.
Mathematical modelling and control of African animal trypanosomosis with interacting populations in West Africa—Could biting flies be important in main taining the disease endemicity?
