sleeping sickness


sleeping sickness
1. Also called African sleeping sickness, African trypanosomiasis. a generally fatal disease, common in parts of Africa, characterized by fever, wasting, and progressive lethargy: caused by a parasitic protozoan, Trypanosoma gambiense or T. rhodesiense, that is carried by a tsetse fly, Glossina palpalis.
2. Also called epidemic encephalitis, lethargic encephalitis. a viral disease affecting the brain, characterized by apathy, sleepiness, extreme muscular weakness, and impairment of vision.
[1870-75]

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Protozoal disease transmitted by the bite of the tsetse fly.

Two forms, caused by different species of the genus Trypanosoma, occur in separate regions in Africa. The parasite enters the bloodstream and invades the lymph nodes and spleen, which become swollen, soft, and tender. Irregular fever and delayed pain sensation develop. In the Rhodesian form, the patient soon dies of massive toxemia. The Gambian type progresses to brain and spinal cord invasion, causing severe headache, mental and physical fatigue, spastic or flaccid paralysis, chorea, and profound sleepiness, followed over two or three years by emaciation, coma, and death. Some patients develop a tolerance but still carry the trypanosomes. The earlier drug treatment begins, the greater the chance of recovery. Sleeping sickness is still prevalent in parts of Africa despite efforts to control it.

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Introduction
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.

Infection and disease course
      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.

Diagnosis and treatment
      The earlier sleeping sickness is diagnosed and treated, the greater are the chances for recovery. Diagnosis is made by microscopic examination of blood and lymph for the presence of trypanosomes and of cerebrospinal fluid for increased levels of white blood cells. Information obtained from these tests is then used to determine the stage of disease and course of treatment.

       suramin is effective for early stages of either form of sleeping sickness. eflornithine is used for the early stages of the Gambian type, with pentamidine used as an alternative. For later stages involving the central nervous system, the Gambian form is treated with eflornithine, which replaced the highly toxic and less-effective organoarsenic agent melarsoprol. Suramin plus tryparsamide, a synthetic arsenical, may be used as an alternative to eflornithine. All treatment of T. brucei rhodesiense infection is useless once the fulminating toxemic stage has developed. Researchers have been investigating eflornithine-based combination therapies for Gambian sleeping sickness. The most effective combination has been eflornithine used in conjunction with nifurtimox, an agent used to treat Chagas' disease.

Prevention
      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.

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Universalium. 2010.

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