Epidemiology

The epidemiology of African sleeping sickness is far from being fully understood (Jordan 1986). A com­plex epidemiology makes it most difficult to analyze and predict, thereby necessitating analysis of the total context of the disease pattern.

The focal nature of sleeping sickness means that the ecological settings in which it occurs are of vital importance for understanding its epidemiology. Seemingly impossible to destroy, many historical foci tend to flare up in spite of concentrated efforts since the 1930s on the part of surveillance and pre­vention personnel (Duggan 1970; Janssens, personal communication). This means that very often the vil­lages and regions that were affected decades ago remain problem areas today. The disease involves humans, parasites, tsetse flies, wild and domesti­cated animals, and the ecological setting that they share. Although foci remain at varying levels of endemicity, increasing population movements have complicated the epidemiology (Lucasse 1964; Ruppol and Libala 1977). Moreover, disease incidence is not necessarily related to fly density. Research has shown that a small number of flies with good human-fly contact can sustain an endemic, even as epidemic, incidence.

The average life-span of tsetse flies is 1 to 6 months, during which they require shade, humidity, and a temperature range between 20^o and 30^oC. Tsetse spe­cies have varying food preferences, ranging from the blood of wild and domestic animals to that of humans, but they require a daily blood meal, thereby making a single fly potentially highly infective.

Gambiense sleeping sickness is classically a dis­ease of the frontier of human environment, where human-created habitat meets sylvan biotope. Hu­mans are the principal reservoir of T. b. gambiense, and they maintain the typical endemic cycle of the disease. It is now known, however, that some ani­mals, including domestic pigs, cattle, sheep, and even chickens, can act as reservoirs. The key to understanding the gambiense form is its chronicity and the fact that there are usually very low numbers of parasites present in the lymph and other tissue fluids. Gambiense disease can be maintained by a mere handful of peridomestic flies—that is, those that have invaded bush or cultivations near human settlements. This is known as close human—fly con­tact. Cultivation practices such as the introduction ofbanana groves, shade trees, new crops like tobacco and Iantana hedges, or the creation of new farms can provide fresh ecological niches into which tsetse flies may spread, introducing sleeping sickness through peridomestic transmission.

Riverine G. palpalis are most commonly found near the low-level brush bordering smaller water­ways and pools; during dry seasons, when humans and flies are brought together through their shared need for water, the flies become particularly infec­tive. Activities such as fishing, bathing, water collec­tion, and travel bring humans into daily contact with the insects, and in this way an endemic level of the disease can be maintained over long periods. Other common foci for the disease are sacred groves, which are often small clearings in the forest where the high humidity allows the flies to venture farther from water sources.

The virulent rhodesiense form of the disease is a true zoonosis maintained in wild animal reservoirs in the eastern African savannas. In the case of T. b. gambiense, humans are probably the normal mam­malian hosts, with wild and domestic animals as adventitious hosts, whereas in the case of T. b. rhodesiense the usual mammalian hosts are wild ungulates, with humans as adventitious hosts.

The wild and domestic animal reservoir of trypanosomes is an important factor in the epide­miology and history of sleeping sickness. The paleogenesis of human trypanosomiasis has been much studied, and it is well established that the trypanosomiases are ancient in Africa. Indeed, it is conjectured that the presence of sleeping sickness may explain why the ungulate herds of the African savanna have survived human predators for so long; the wild-animal reservoir of trypanosomes firmly restricted the boundaries of early human settlement (McNeill 1977). Although the wild ungulate herds became trypo-tolerant, with few ex­ceptions domestic cattle still succumb to the dis­ease, and the vast majority of research and funding has been aimed at solving the problem of animal - not human - sleeping sickness.

In evolutionary terms, the presence of trypano­somes in Africa may perhaps have precluded the development of some ground-dwelling faunas, thus encouraging certain more resistant primates, includ­ing the early ancestors of humankind, to fill the empty ecological niches (Lambrecht 1964). If so, then humans were exposed to the possibility of trypanosomal infection at the time of their very re­mote origin. The parasites are, on the whole, poorly adapted to humans, which accounts for the variety of clinical symptoms and ever-changing epidemio­logical patterns. The fact that the parasitism of hu­man beings is still evolving helps us to understand the unpredictable nature of the disease. A perfectly adapted parasite does not kill its host - at least in the short run.