African trypanosomiasis

African trypanosomiasis

African trypanosomiasis

Trypanosoma gambiense and Trypanosoma rhodesiene are causative agents of the African typanosomiasis, transmitted by insect bites. The vector for both is the tsetse fly.


The trypomastigotes spread from the skin through the blood to the lymph node and the brain. The typical somnolence (sleeping sickness) usually progresses to coma as a result of demyelinating encephalitis. In acute form, cyclical fever spike (approximately every 2 weeks) occurs that is related to antigenic variation. As antibody mediated agglutination and lysis of the trypomastigotes occurs, the fever subsides. With a few remains of antigenic variants new fever spike occurs and the cycle repeats itself over a long period.


T.burceigambiense is limited to tropical west and central Africa, correlating with the range of the tsetse fly vector. The tsetse flies transmitting T.b. gambiense prefer shaded stream banks for reproduction and proximity to human dwellings. People who work in such areas are at greatest risk of infection. An animal reservoir has not been proved for this infection.


T.burceirhodeseinse is found primarily in East Africa, especially the cattle-raising countries, where tsetse flies breed in the brush rather than along stream banks. T.b. rhodeseines also differs from T.b. gambiense in that domestic animal hosts (cattle and sheep) and wild game animals act as reservoir hosts. This transmission and vector cycle makes the organism more difficult to control than T.b. gambiense.

Clinical features

Although both species cause sleeping sickness, the progress of the disease is different. T.gambiense induced disease runs a low-grade chronic course over a few years. One of the earliest signs of disease is an occasional ulcer at the site of the fly bite. As reproduction of organisms continues, the lymph nodes are invaded, and fever, myalgia, arthralgia, and lymph node enlargement results. Swelling of the posterior cervical lymph nodes is characteristic of Gambian sleeping sickness and is called winterbottom’s sign.

Chronic disease progresses to CNS involvement with lethargy, tremors, meningoencephalitis, mental retardation, and general deterioration. In the final stages, convulsions, hemiplegia, and incontinence occur. The patient becomes difficult to arouse or obtain a response from, eventually progressing to a comatose state. Death is the result of CNS damage and other infections, such as pneumonia.

In T.rhodesiense, the disease caused is a more acute, rapidly progressive disease that is usually fatal. This more virulent organism also develops in greater numbers in the blood. Lymphadenopathy is uncommon, and early in the infection, CNS invasion occurs, resulting in lethargy, anorexia, and mental disturbance. The chronic stages described for T.gambiense are not often seen, because in addition to rapid CNS disease, the organism produces kidney damage and myocarditis, leading to death.


Both the humoral and cellular immunity involve in these infections. The immune responses of the host to the presence of these parasites, however, is faced with antigenic variation, in which organisms that have changed their antigenic identity can escape the host immune response and initiate another disease process with increased level of parasitemia.


Examination of thin and thick films, in concentrated anticoagulated blood preparations, and in aspiration from lymph nodes and concentrated spinal fluid. Methods for concentrating parasites in blood may be helpful approaches including centrifugation of heparinized samples and an ion–exchange chromatography. Levels of parasitosis vary widely, and several attempts to visualize the organism over a number of days may be necessary.



The same treatment protocol is applied for these parasites. For the acute stages of the disease the drug of choice is suramin with pentamidine as an alternative. In chronic disease with CNS involvement, the drug of choice is melarsoprol. Alternatives include trypars amide combined with suramin.


• Control of breeding sites of tsetse flies and use of insecticides.

• Treatment of human cases to reduce transmission to flies.

• Avoiding insect bite by wearing protective clothing & use of screen, bed netting and insect repellants.


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