What is African Sleeping sickness?
African trypanosomiasis, commonly called sleeping sickness, is caused by two protozoan parasites that are morphologically similar but cause dramatically different diseases. East African sleeping sickness is caused by the parasite Trypanosoma brucei rhodesiense,whereas West African sleeping sickness, also known as Gambian sleeping sickness, is caused by Trypanosoma brucei gambiense. Both diseases are transmitted by tsetse flies (one third of the population of Africa lives in tsetse fly-infested areas). Sleeping sickness newly infects about 20,000 to 25,000 people each year and causes about 55,000 deaths each year. Each day, about 100 people die of the disease.
East African Sleeping Sickness. East African sleeping sickness is an acute disease that typically leads to death within weeks or months if not treated. The initial bite leaves a distinctive sore spot called a chancre. Symptoms, which appear one to four weeks after infection, may include swollen lymph nodes, irritability, fever, severe headache, fatigue, muscle and joint pain, and a skin rash. During the second stage of the disease, the parasite crosses the blood-brain barrier and attacks the central nervous system. Neurological complications include slurred speech, confusion, and difficulty with walking.
West African Sleeping Sickness. Like East African sleeping sickness, West African (Gambian) sleeping sickness is a serious disease that is fatal if not treated. However, it is a chronic disease in which symptoms may not appear for months to years after the initial infection. Initial symptoms include swollen lymph nodes, swelling of face and hands, skin rash, fever, severe headaches, muscle and joint pain, and fatigue. Weight loss is common as the disease progresses. Neurological impairment occurs during the second stage in which the victim can experience personality changes, slurred speech, changes in sleep patterns, progressive confusion, difficulty with walking, and seizures.
Sleeping sickness has a profound impact on the health of a large portion of sub-Saharan Africa. Furthermore, the economic impact of sleeping sickness is significant owing to the dramatic reduction in the labor force and resulting decrease in economic productivity. This in turn has countless added direct and indirect impacts on the quality of life of people in affected countries. The economic impact is further increased because sleeping sickness can reduce cattle production 20-40% in areas where the disease is epidemic. It is estimated that cattle-production losses alone amount to $2.7 billion each year.
How do people contract Sleeping Sickness?
Seven species of tsetse flies in the genus Glossinaact as vectors of the disease to humans. The cycle begins when a fly bites an infected mammal and ingests the parasites. The protozoans multiply and develop over a series of weeks within the gut and salivary glands of the fly. When the fly bites another human or other animal host, the mature forms of the parasite enter the host, settling in the blood and spinal fluid. Humans can also contract West African sleeping sickness through maternal transfer, blood transfusion, or by organ transplant. Once a fly is infected, it remains able to transmit trypanosomiasis to humans throughout its one- to six-month life span.
What is the geographic distribution of Sleeping Sickness?
Sleeping sickness occurs in sub-Saharan Africa. The disease is at, or is approaching epidemic levels in Angola, the Democratic Republic of Congo, Uganda, Sudan, Cameroon, Cote d'Ivoire, Central African Republic, Guinea, Mozambique, Tanzania, and Chad.
The East African form is concentrated in rural woodland and savanna areas in Eastern and Central African countries. Wild game mammals are the primary reservoir for the disease. Humans contract it when they travel outside the villages, for example, going into the countryside to collect firewood or monitor livestock. The level of occurrence varies in different localities.
In contrast, West African sleeping sickness has a much wider range in Western and Central Africa; it is found in forests, near dense shrubs, and by rivers and watering holes. Humans and other animals are the primary reservoir. This disease organism is concentrated close to settlements where humans contact it during daily activities. This pattern of distribution, and the fact that West African sleeping sickness only requires a small vector population to maintain high levels of the trypanosome in a local population, make this form of sleeping sickness particularly difficult to eradicate locally.
Since 1967, there have only been 21 documented instances of Americans traveling to Africa and contracting East African sleeping sickness. Even fewer American travelers have contracted West African sleeping sickness. In sub-Saharan Africa, however, health officials estimate that currently 60 million people in 36 countries are at risk of acquiring sleeping sickness. This represents the third major epidemic of sleeping sickness in Africa since the early 1900s, when the parasites and vector were first identified. One of these epidemics killed 500,000 people. Control programs were implemented around 1920 and gradually the disease was reduced or eradicated within much of its range by 1960. Unfortunately, over the past thirty years, war and the resulting breakdown in public health infrastructure in many countries have disrupted control programs, and the disease is showing a resurgence. For example, the rate of infection in several villages in Sudan rose from 0.3% in 1988 to 19.3% in 1997. In the Democratic Republic of the Congo, where 70% of reported cases occur, the prevalence of sleeping sickness has nearly reached that of AIDS. In 1999, 40,000 to 45,000 cases of sleeping sickness were reported in Africa, but it is estimated that from 300,000 to 500,000 people have the disease. It has been nearly impossible to estimate the incidence of West African sleeping sickness because reported cases come only from screening centers and hospitals, which tend to be located far from the rural areas where the disease is most prevalent.
How can Sleeping sickness be treated and controlled?
Medicines. Currently, there is neither a vaccine nor a drug available to preventinfection with sleeping sickness. There are drugs available for treatmentof the disease, but at present, the drugs are scarce, difficult to administer, and sometimes dangerous. One of the original drugs developed to combat sleeping sickness, atoxyl, contained arsenic and caused blindness in hundreds of patients in 1932. A drug called melarsoprol was developed to prevent such side effects, but there are very limited supplies remaining. Suramin, pentamidine, and berenil have been used to treat, and sometimes cure, sleeping sickness prior to the onset of neurological symptoms. However, the older drugs need to be replaced with safer, more effective, more affordable compounds. The drug trybizine has tested successfully for East African sleeping sickness in research animals. Research and development of such drugs by the private sector have been minimal because development of drugs intended to treat people in impoverished countries is not considered to be a profitable venture by many pharmaceutical companies. Eflornithine, one of a few anti-trypanosomal drugs developed over the past few decades, has been effective in treating late-stage West African sleeping sickness. Up until very recently it was expensive and therefore not available to many of the impoverished countries where trypanosomiasis is endemic. In March 2001, however, the World Health Organization reached an agreement with Bristol-Myers-Squibb, Dow Chemical, Akorn Manufacturing, and the French-German company Aventis to produce and donate 60,000 doses of eflornithine to help with efforts to combat sleeping sickness. This is an example of how public-private sector collaborations can successfully work in fighting infectious disease.
This description of medicines is given for general information purposes only; contact your health care provider for details on specific treatment options.
The second stage of African trypanosomiasis is particularly difficult to treat; treatment regimens in the second stage fail in 15-30% of cases. The underlying reasons for this are not well understood. In children, physical and neurological problems can occur even after the trypanosome is eliminated from the body. Additional difficulties with treatment of sleeping sickness include drug resistance, limited technical expertise in endemic countries (which limits diagnosis and treatment), and the continually changing range of antigenic expression seen in T. brucei,which makes vaccine development difficult.
Screening. Because of the characteristically long symptom-free periods following initial infection, periodic screening is the key to detecting this disease and establishing reliable estimates of incidence. However, screening has become more focused on high-risk areas. As a result, reported cases under-represent the actual level of incidence. As screening and treatment are decreased or halted in certain areas, the disease intensifies. In 1999, 40,000-45,000 cases were reported. However, only three to four million people were screened out of an estimated 60 million at risk.
Vector Control. Economic and social factors have made continued implementation of effective vector-control strategies difficult. There are successful vector control programs, but they exist in fewer than 2% of the areas where the disease is endemic. Ground spraying of insecticides, aerial spraying, the use of cloth baits (cloth sprayed with insecticide), and the use of live baits (cattle sprayed with insecticide) have all shown some success. Transegenic techniques, such as introducing into tsetse flies (or symbiotic microorganisms living in the flies) foreign genes that will restrict the tsetse flies ability to survive, reproduce, or transmit pathogens, hold great promise.
Since the risk of infection increases with the number of times a person is bitten by the tsetse fly, the best means of protection against the disease involves personal measures. People should, when possible, avoid areas of high infection. Within these areas, they should wear thick, long-sleeved clothing that is khaki or olive colored (tsetse flies are attracted to both bright and dark colors). Bed nets that have solid (not mesh) tops should be used during sleep. People should inspect vehicles before entering them, and they should refrain from riding in the back of open vehicles because tsetse flies are attracted to the dust vehicles kick up. Bushes should be avoided because tsetse flies rest on bushes during hot periods.
Where can you find out more about Sleeping Sickness?
- Allsopp, R. 2001. Options for vector control against trypanosomiasis in Africa. Trends in Parasitology. 17: 15-18.
- Aksoy, S., Maudlin, I., Dale, C., Robinson, A., and O'Neill, S. 2001. Prospects for control of African trypanosomiasis by tsetse vector manipulation. Trends in Parasitology. 17: 29-34.
- Deiser, J., Stich, A., and Burri, C. 2001. New drugs for the treatment of human African trypanosomiasis: research and development. Trends in Parasitology. 17: 42-49.
- Grant, I. 2001. Insecticides for tsetse and trypanosomiasis control: is the environmental risk acceptable? Trends in Parasitology. 17: 10-14.
- Guerrant, R. L., Walker, D. H., and Weller, P. F. (Eds.) 2001. Essentials of Tropical Infectious Diseases. W. B. Saunders, Philadelphia.
- Beaty, B. J., and Marquardt, W. C. (Eds.) 1996. The Biology of Disease Vectors. University of Colorado Press, Niwot, Colorado.
- The Centers for Disease Control, Division of Parasitic Diseases
- The World Health Organization
--Prepared by Susan L. Thomas--
Last updated: March 1, 2002