|
Distribution
36 countries in sub-Saharan Africa:
7 countries: disease is highly endemic.
4 countries: disease is endemic.
12 countries: disease has moderate endemicity
13 countries: epidemiological status is poorly understood. |
Causative agent
| Protozoan parasites of the genus Trypanosoma, which enter the blood-stream via the bite of bloodfeeding tsetse flies (Glossina spp.). Trypanosoma brucei rhodesiense occurs mainly in east and southern Africa. T.b. gambiense mainly in west and central Africa. A third subspecies, T.b. brucei is responsible for the cattle disease but does not infect humans. |
Transmission
| Via the bite of bloodsucking male and female tsetse flies that transfer the parasites from human to human. Cattle and other wild mammals act as reservoir hosts of the parasites. Tsetse flies can acquire parasites by feeding on these animals, or on an infected person. Inside the human host, trypanosomes multiply and invade most tissues. |
Symptoms
| Infection leads to malaise, lassitude and irregular fevers. Early symptoms, which include fever and enlarged lymph glands and spleen, are more severe and acute in T.b. rhodesiense infections. Early signs are followed by a range of symptoms including headache, anaemia, joint pains and swollen tissues; advanced symptoms include neurological and endocrine disorders. |
As the parasites invade the central nervous system, mental deterioration begins, leading to coma and death. T.b rhodesiense infection is usually acute, causing severe symptoms and death within a few days or weeks. T.b. gambiense infections tend to progress more slowly (over several years) and are less severe.
Prevention and control
| Control relies mainly on systematic surveillance of at-risk populations, coupled with treatment of infected people. In addition, reduction of tsetse fly numbers plays a significant role, especially against the rhodesiense form of the disease. In the past, this has involved extensive clearance of bush to destroy tsetse fly breeding and resting sites, and widespread application of insecticides. More recently, efficient traps and screens have been developed that, usually with community participation, can keep tsetse populations at low levels in a cost-effective manner. |
Treatment has always been difficult, especially when the disease has reached an advanced stage with central nervous system involvement, as few effective drugs are available.
Pentamidine is not effective against late-stage disease and some parasite strains are resistant to it.
Suramin has to be administered intravenously and can have adverse side-effects.
Melarsoprol, an arsenical drug developed over 50 years ago, is used against late-stage disease, but often induces serious - sometimes fatal - side-effects.
A new drug, eflornithine, originally developed as an anticancer agent, has shown promising results against the gambiense form and new treatment regimes have been discovered that should halve the cost of treatment. |
Print
Add Feedback