SLEEPING SICKNESS

also called African trypanosomiasis infection from the flagellate protozoan Trypanosoma brucei gambiense or the closely related subspecies T. brucei rhodesiense, transmitted by the tsetse fly. Sleeping sickness is characterized by fever, inflammation of the lymph nodes, and involvement of the brain and spinal cord leading to profound lethargy, frequently ending in death. Infections with T. brucei gambiense occur in an area extending from the west coast of Africa eastward to the East African lakes and southward to the Congo River basin. Cases caused by T. brucei rhodesiense are limited to the highlands of central East Africa. The vast majority of human infections result from inoculation with the trypanosome by tsetse flies as they suck human blood. The flies have become infected while feeding on the blood of people or other mammals already infected. Usually 12 to 15 days elapse before such a fly becomes infective toward humans. During this time the trypanosomes multiply by binary division in the midgut of the fly, then migrate to the salivary glands, and pass out of the fly's proboscis in droplets of saliva during the fly's bloodsucking. After an incubation period in humans lasting one to two weeks, the trypanosomes are found in significant numbers in the circulating blood. Next the lymph nodes and spleen are invaded, becoming swollen, soft, and tender. The marked enlargement of the lymph nodes at the back of the neck (known as Winterbottom's sign) is a common sign of the disease. Irregular fever and delayed sensation to pain are also characteristic symptoms at this stage. In the more severe Rhodesian, or East African, form of sleeping sickness, the toxemia becomes so profound that the patient soon dies. In the Gambian, or West African, type, by contrast, the trypanosomes proceed to invade the brain and spinal cord. The resulting neurological symptoms include severe headache, mental dullness and apathy, a weary shuffling gait, tremors, spastic or flaccid paralysis, chorea, and a profound sleepiness that develops during a meal or when the patient is standing or walking. These symptoms are followed by increasing emaciation, coma, and death. The Gambian form of sleeping sickness usually causes death in two or three years, but in some Africans a tolerance to the infection develops, and the patient may continue to live for many years as a carrier of the parasites. The earlier sleeping sickness is diagnosed and treated, the greater are the chances for recovery. Suramin is effective for early stages of either form, and eflornithine is also used for the Gambian type; pentamidine has been used as an alternative. For later stages involving the central nervous system, the Gambian form may be treated with eflornithine or melarsoprol. The latter is the drug of choice for the late-stage Rhodesian form, with suramin plus tryparsamide, a synthetic arsenical, as an alternative, but all treatment of T. brucei rhodesiense infection is useless once the fulminating toxemic stage has developed. Sleeping sickness is still prevalent in parts of sub-Saharan Africa, and some regions that are heavily infested with tsetse flies are virtually uninhabitable because of the risks posed by the disease. Heroic efforts have been made to control sleeping sickness, including (1) isolation and proper treatment of all infected persons, including large numbers of asymptomatic chronic carriers, (2) protection of humans from bites of tsetse flies by the use of insecticides and by maintaining extensive clearings around villages and residence compounds, (3) prophylactic doses of suramin or of diamidine compounds once every 60 to 90 days for persons who must enter the jungle, so that they will not become infected from tsetse fly bites, and (4) occasional removal of entire villages from endemic to disease-free zones. Some have suggested that entire populations of wild animals be exterminated, since they tend to become reservoirs of the disease.