One of the most devastating health crises in modern Africa is African sleeping sickness, or trypanosomiasis. The disease is caused by one of several parasites: Trypanosoma brucei gambiense, which affects countries in central and western Africa, and Trypanosoma brucei rhodesiense, which affect countries in central and southern Africa. The parasite is transferred to mammals by the bite of the tsetse fly; untreated, the disease is always fatal.
While noted in literature as early as the fourteenth century by Ibn Khaldoun in his History of the Berbers , the extent of the destruction of the disease was not noted until the early twentieth century.
The spread of trypanosomiasis cannot be viewed in isolation as a mere example of disease evolution; instead, the disease must be examined within a historical context, and the effects that human activity has contributed to the emergence of the disease as a major health concern in the twentieth century.
The type of parasite that causes sleeping sickness is known as a trypanosome; these parasites have a unique ability to evade attempts by the human immune system to combat the intruder. Evolutionary parasitologists are not in agreement as to the mechanisms by which the parasite evades its hosts, but a large body of evidence suggests that mammals are able to develop resistance to trypanosomes.
It is widely believed that wild game animals, such as antelope and deer, are the reservoirs for the parasites that cause trypanosomiasis; areas that are prone to epidemics of sleeping sickness tend to be those that are near dry, savannah-like areas. Humans come into contact with the tsetse fly when they encroach upon the natural habitats for the insect. In addition, livestock are equally prone to infection after tsetse bites, and can serve as secondary parasitic reservoirs.
The rinderpest epidemic of 1896, itself a manifestation of an unintended side effect by the introduction of European cattle into Africa by colonialists, had a secondary, more far-reaching result: indigenous wild and domesticated animals with trypanosome resistance were wiped out . As a result, the cattle that were imported to replace the herds destroyed by rinderpest did not have resistance to trypanosomiasis, and this lack of immunity created an environment ripe for the rise of trypanosomiasis.
A number of additional colonial behaviors contributed to the spread of trypanosomiasis. The demands for products such as rubber created coerced labor forces that traveled to unpopulated areas in the effort to gather rubber; these activities not only enabled the disease to migrate, but caused trypanosome variants to move as well. Trypanosomes with different antigen properties can cause illness in mammals that have developed antibodies to a slightly different version; this “antigenic switching” is one of the ways that trypanosomes “fool” the immune system.
Forced resettlement was another loathsome hallmark of colonial rule; there are numerous instances of entire tribes being relocated (along with their livestock) to areas that more completely fit the desires of the colonialists. The unexpected result of the migration of large groups of people and animals to distant lands is, again, the scattering of trypanosome variants.
Population declines in many agricultural and pastoral regions have contributed to the spread of trypanosomiasis. As an area becomes depopulated, the habitat reverts back to bush country; this, of course, is the natural habitat of the tsetse fly. Giblin cites a number of colonialist-inspired actions that have caused depopulation in rural regions: intense labor conscription during World War I by the British and Germans, famines that were the direct result of ill-conceived water-control projects, such as dams and canals, and the disruption caused by German and British troop movements.
A harmonious balance between competing populations- humans, livestock, wild animals, tsetse flies, and trypanosomes – existed in the pre-colonial era. The modern emergence of trypanosomiasis is not simply a matter of parasitic evolution, but a result of a disharmony within the ecosystems.
Some researchers, such as Giblin and Ford, argue that the primary responsibility for the spread of trypanosomiasis was the inadvertent actions of European colonialists. Such an approach is not without historical precedents; for example, the travel of bubonic plague in fourteenth-century European merchant vessels from Asia, the spread of smallpox in the New World by European conquerors, and the introduction of syphilis to the Old World by the same Europeans upon their return to Europe all involved the interplay of history and disease pathology.
However, Giblin discounts the incredible mutative abilities of trypanosomes in his examination of the increase in the incidence of trypanosomiasis; these organisms have a sophisticated mechanism of survival that have, until this point, defied the best minds of modern medicine. While the role of Europeans in the spread of trypanosomiasis cannot be overlooked, the primary cause of the spread of the disease is the biochemical nature of the organism itself.
Giblin also fails to acknowledge the role of data collection and reporting in his analysis of African health statistics. Part of the rise in reported trypanosomiasis cases could be due to the fact that improvement in reporting systems may simply mean that more cases are being reported; it is very likely that rural cases may not have been properly documented in the past.
In addition, Giblin neglects to consider sociological aspects of the disease; in particular, the socio-economic status of the victims of African sleeping sickness was not discussed. The disease strikes a highly disproportional number of the rural poor, and the plight of disadvantaged groups has generally been ignored in the past. A statement by the Center for Disease Control reinforces this point:
African sleeping sickness is a low-priority rural disease. Effective, sustainable control is unlikely until traditional uses of land change and socioeconomic conditions improve in rural Africa. The primary approach to control is treatment with drugs that are expensive and not readily available.
Giblin, meanwhile, argues, “alternative approaches based upon historical African experience may actually be the most feasible options in trypanosomiasis control.” This statement suggests an impractical, Pollyanna-esque return to an ancient pastoral society; the likelihood of recreating the harmonious balance (if, indeed, it ever existed) between the populations in the models of John Ford and James Giblin simply may not be possible.