African sleeping sickness Essay

African sleeping sickness


Human African Trypanosomiasis, known as sleeping sickness, is a vector-borne parasitic disease. Trypanosoma which are the parasites are protozoa transmitted to humans by tsetse flies. Tsetse flies live in Africa, and they are found in vegetation by rivers and lakes, gallery-forests and vast stretches of wooded savannah.


Sleeping sickness occurs only in sub-Saharan Africa, in regions where tsetse flies are endemic. There are many regions where tsetse flies are found, but sleeping sickness is not. The rural populations that live in such environments and depend on the flies for agriculture, fishing, animal husbandry or hunting are the most exposed – along with their livestock – to the bite of the tsetse fly. Sleeping sickness affects remote and rural areas where health systems are least effective, or non-existent. It spreads with socio-economic problems such as political instability, displacement of populations, war, and poverty.


Human African trypanosomiasis takes two forms, depending on the parasite involved: Trypanosoma brucei gambiense (T.b. gambiense) is found in central and West Africa. A person can be infected for months or even years without obvious symptoms of the disease emerging. When symptoms do emerge, the disease is already at an advanced stage.


Trypanosoma brucei rhodesiense (T.b. rhodesiense) is found in southern and east Africa. It causes an acute infection that emerges after a few weeks. It is more virulent than the other strain and develops more rapidly, which means that it is more quickly detected clinically.


The disease was first seen in the fourteenth century. A writer named Ibn Khaldoun described in a book he wrote “History of the Berbers” that a Sultan from Mali got a disease that killed him. The description made of the disease has the same symptoms and disorders as this African sleeping sickness (Domergue, 1981).


The distribution of African trypanosomiasis is completely linked to the range of its vector, the tsetse fly.  Due to the tsetse fly’s climatic restrictions, the disease is restricted between the 14th latitude north and the 29th latitude south on the African continent (Molyneux 1983).  According to the World Health Organization in 2001, countries, where the disease is currently epidemic, include Angola, the Democratic Republic of the Congo, Uganda & Sudan.

Countries with high levels of this disease are Cameroon, Congo, Cote d’Ivoire, Central African Republic, Guinea, Mozambique, Tanzania, & Chad.  African sleeping sickness can also be found in low endemic levels in Benin, Burkina-Faso, Gabon, Ghana, Equatorial Guinea, Kenya, Mali, Nigeria, Togo, & Zambia.  Because of poor disease surveillance and reporting, epidemiological information in Burundi, Botswana, Ethiopia, Liberia, Namibia, Rwanda, Senegal, & Sierra-Leone is poorly understood.


Sleeping sickness is a daily threat to more than 60 million men, women and children in 36 countries of sub-Saharan Africa, 22 of which are among the least developed countries in the world. However, only 3 to 4 million of these people are under surveillance and the 45,000 cases reported in 1999 do not reflect the reality of the situation, but simply show the absence of case detection. The estimated number of people thought to have the disease is between 300,000 and 500,000. In Uganda, two-thirds of all deaths are caused by sleeping sickness. Most people with sleeping sickness die before they can ever be diagnosed (WHO, 2001).


The disease is transmitted with the bite of the tsetse fly. At first, the trypanosomes multiply in the blood, and that process can last for years. In a mother-to-child infection, the trypanosome can cross the placenta and infect the fetus, causing abortion and prenatal death.


After a person is bitten by an infected fly, symptoms such as a red painful swelling develop at the site of the fly bite. From this site of injection, the parasite invades the bloodstream causing episodes of fever, headache, sweating, and enlargement of the lymph nodes. Parasites then invade the central nervous system where they produce the symptoms typical of sleeping sickness. Then the parasites invade the brain, causing first behavioral changes such as fear and mood swings followed by headache, fever, and weakness. Death may occur within 6 months from cardiac failure. Gambiense-infected people develop drowsiness during the day, but insomnia at night. Sleep becomes uncontrollable as the disease progresses until the patient becomes exhausted (Ford, 1979).


Risk factors include living in those parts of Africa where the disease is found and being bitten by tsetse flies. The incidence is extremely low in the U.S. and is only found in travelers from those areas.


For prevention, Pentamidine injections protect against Gambiense but have not yet been demonstrated as effective against Rhodesiense. Insect control could help prevent the spread of sleeping sickness. Wearing long sleeve shirts and avoiding areas that are filled with bugs will also help reduce the risk of getting bit.


Sleeping sickness also has major impacts on economic and social roles in Africa. Sleeping sickness has a major impact on the development of rural areas by decreasing the labor force and hampering production and work capacity. It remains a major obstacle to the development of entire regions. In countries such as Angola, the Democratic Republic of Congo or Sudan, the operational capacity to respond to the epidemic situation is largely surpassed and in certain endemic areas, the observed prevalence is huge. In numerous provinces in these countries, prevalence greater than 20% has been reported. Other sub-species of the parasite cause animal trypanosomiasis. The two human and animal forms of the disease remain a major obstacle to the development of rural regions of sub-Saharan Africa: human loss, the decimation of cattle and abandonment of fertile land where the disease is rife.


If the disease is diagnosed early, the chances of cure are high. The type of treatment depends on the phase of the disease: initial or neurological. Success in the latter phase depends on having a drug that can cross the blood-brain barrier to reach the parasite. Four drugs have been used until now.


There are three stages to case management, and the first is screening is the initial sorting of people who might be infected. This involves checking for clinical signs or the use of serological tests. The diagnosis shows whether the parasite is present. The only sign, one that has been known for centuries, is swollen cervical glands. Phase diagnosis shows the state of progression of the disease. It entails an examination of cerebra-spinal fluid obtained by lumbar puncture and is used to determine the course of treatment.


The long, asymptomatic first phase of T.b. gambiense sleeping sickness is one of the factors that make treatment difficult. The diagnosis must be made as early as possible in order to prevent the beginning of irreversible neurological disorders and prevent transmission. Case detection is difficult and requires major human, technical and material resources. Since the disease is widespread in rural areas among poor people with little access to health facilities, this problem is all the more difficult.


Unless treated, African trypanosomiasis is a fatal illness, and the treatment is costly. The drug used to treat the early signs of the disease is also used to kill a parasite that affects some people with the disease of AIDS. This has increased its price. The drug used in more severe Sleeping Sickness infections is a poison that can kill up to ten percent of the patients who use it (Anonymous, 2001). A safer medicine had stopped being produced recently. However, the W.H.O. negotiated an agreement with a drug company to provide all the medicines to treat sleeping sickness free of charge.


Sleeping sickness experts say more people in Africa should be examined for the disease. They also say that leaders of affected countries must improve national health care systems to prevent the disease.




  • Anonymous. African Trypanosomiasis. The Journal of Tropical Medicine and International Health 2001. Volume 65: 330-361.
  • D. Domergue, ‘La lutte contre la trypanosomiase en Côte d’Ivoire, 1900-1945,’ Journal of African History, v. 22 (1981), pp. 63-72.
  • Kobayashi, A., Tizard, I. & Woo, P.T.K. 1975. Studies on the anemia in experimental African Trypanosomiasis. The pathogenesis of the anemia in calves infected with Trypanosoma congolense. American Journal of Tropical Med. Hyg. 25: 401-407.
  • John Ford, ‘Ideas Which Have Influenced Attempts to Solve the Problems of African Trypanosomiasis,’ Social Science and Medicine, v. 13B (1979), pp.




  • Despommier DD, Gwadz RW, Hotez PJ Parasitic Disease (3rd Edition) New York: Springer-Verlag, 1995.  196.


  • Smith DH, Pepin J, Stich A. Human African trypanosomiasis: an emerging public health crisis. Brit Med Bull 1998; 54: 341-355


  • Dumas M, Boa FY Human African Trypanosomiasis.  Hand Book of Clinical Neurology: Microbial Disease Vol 8 (52), 339.


  • Molyneux DH and Ashford RW. The Biology of Trypanosoma and Leishmania, Parasites of Man and Domestic Animal.  New York: Taylor and Francis Inc, 1983.  p.129.


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