More than 66 million women, men and children in 36 countries of sub-Saharan Africa suffer from human African trypanosomiasis (HAT). There are two
forms of African sleeping sickness, caused by two different parasites:
Trypanosoma brucei gambiense , which causes a chronic infection lasting years and affecting countries of western and central Africa
Trypanosoma brucei rhodesiense , which causes acute illness lasting several weeks in countries of eastern and southern Africa
When untreated, trypanosomiasis gives no respite from suffering and ultimately ends in death.
The parasite that causes sleeping sickness is called the trypanosome. It is transmitted to humans through the bite of a tsetse fly of the genus
Human trypanosomiasis is therefore a vector-borne parasitic disease. The vector is found only in Africa, between the fifteenth parallels north and
south. Its favoured habitat is the vegetation along watercourses and lakes, forest edges and gallery forests, extending to vast areas of scrub
The tsetse fly feeds on the blood of animals and humans. Once inoculated by an infected fly, the trypanosomes proliferate and gradually invade all the
organs of the host. Most of the parasites are effectively destroyed by the host's natural defences, but some trypanosomes manage to evade the immune
system by modifying their surface membrane, a process known as antigenic variation. The trypanosome can express thousands of variants, multiplying
with each new surface change.
At first, the main clinical signs of human trypanosomiasis are high fever, weakness and headache, joint pains and pruritus (itching). Gradually, the
immune defence mechanisms and the patient's resistance are exhausted. As the parasite develops in the lymph and blood of the patient, the initial
symptoms become more pronounced and other manifestations such as anaemia, cardiovascular and endocrine disorders, abortion, oedema and kidney
In advanced stages of disease, the parasite invades the central nervous system. The patient's behaviour changes; they can no longer concentrate and
become indifferent to their environment. Sudden and unpredictable mood changes become increasingly frequent, giving rise to lethargy with bouts of
aggressiveness. Patients are overcome by such extreme torpor that eating, speaking, walking or even opening the eyes call for an unsurmountable
effort. At night they suffer insomnia and during the day are exhausted by periods of sleep-like unconsciousness. Finally, patients fall into a deep
coma and die.
Sleeping sickness was first described in the fourteenth century in what is now the country of Mali. For a long time, though they did not know its
origin, caravanners recognized the signs of sleeping sickness that had often been observed in travels to southern kingdoms. It was only at the
beginning of this century that the extent of destruction caused by sleeping sickness was recognized, and that millions were affected by an epidemic
that left half a million dead. During the same period, the parasite and its tsetse fly vector were discovered and initial treatment methods were
found. At that time the disease ravaged all of east, west, and south Africa, irrespective of the colonial administration. The human reservoir of the
parasite was vast and transmission rapid. As the spread of the disease had to be stopped, control campaigns were organized, health services mobilized
and administrative structures formed. Prevention campaigns employing the drug pentamidine covered entire populations, each person receiving one
injection. At the time it was thought (wrongly) that a low dose of this drug protected each individual from sleeping sickness for six months.
Additionally, agronol prevention, consisting of methodically clearing undergrowth from villages, water sources, paths, and bridges, dispersed the
tsetse fly by destroying its natural habitat.
By the start of African independence, the disease was reduced to a few sporadic cases. It had taken half a century to bring down the incidence of
sleeping sickness. But in many newly independent countries the human and financial resources were not available to keep up the effort to control and
monitor the disease. This explains new outbreaks which have been reported in the last 30 years in old foci and in other areas previously
In recent years the results of scientific and technical research produced new tools and improved field control strategies:
1902 Ford and Dutton, two English physicians working in The Gambia, identified one causative agent of trypanosomiasis, a parasite which they named
Trypanosoma brucei gambiense .
1903 Castellani working in Uganda observed the parasite in the cerebrospinal fluid of one of his patients. In the same year, the tsetse fly was
recognized by David Bruce as being the vector of the parasite.
1906 Ayres Kopke introduced an arsenic compound, Atoxyl, for the treatment of the disease.
1920 Jamot, a colonel in the French army working on trypanosomiasis control, observed that in the Ubangi river loop more than half of all deaths were
due to sleeping sickness. The major epidemics early in the century claimed hundreds of thousands of lives. Entire populations were affected, and
indeed Jamot reported that a whole ethnic group had been wiped out in northern Congo.
1924 Tryparsamide, a drug still based on arsenic but less toxic than Atoxyl, was used on a wide scale in Belgian Congo and Cameroon.
1930 A headline stated: "Our doctors have vanquished the tsetse fly!"
1932 700 patients became blind after receiving the wrong dose of Atoxyl. In response to this disaster, Professor Friedheim, a Swiss physician and
chemist, developed the drug melarsoprol, the bold concept of which was a single product containing a highly toxic arsenic-based molecule and its
1960 Melarsoprol was used systematically in cases where there was involvement of the central nervous system.
1984 The World Health Organization (WHO) launched a programme to control trypanosomiasis.
1993 WHO developed the central African initiative, a major project for regional approach to Sleeping Sickness in ten countries: Angola, Cameroon,
Central African Republic, Congo, Gabon, Equatorial Guinea, Uganda, Sudan, Chad and Zaire.
Social and economic changes coupled with political disorder occurring in many African countries are allowing a resurgence of trypanosomiasis. This
systematic medical surveillance is interrupted
there are certain changes to the environment
populations are displaced
In about twenty African countries, trypanosomiasis is one of the major public health problems. These epidemics sorely test individuals and families
and disrupt the local economy. They are a serious handicap to populations and countries striving for lasting social and economic development. The
farmers, shepherds, herdsmen and hunters of the rural community are most exposed to sleeping sickness, though occasional visitors such as merchants,
travellers and tourists are also at risk.
It is estimated that today over 66 million people living in rural areas are at risk from the bite of the fly. If the entire population exposed to
sleeping sickness could be under medical surveillance, the number of cases detected would undoubtedly reach the order of 250,000 to 300,000. Since
this is a disease of rural areas, many sufferers go undiagnosed and untreated and die in their villages. Today, only one-tenth of the population at
risk is under medical surveillance, and each year an average of 25,000 new cases are identified. Two-thirds of such cases are at the advance stage of
the disease, when the nervous system is involved. Treatment with melarsoprol - still the only drug available - exposes almost 10% of them to serious
risk, especially of arsenic encephalopathy, of which almost a thousand people die each year. For untreated cases of trypanosomiasis, death is certain.
It is estimated that every year, some 250,000 to 300,000 women, people die for lack of diagnosis and treatment.
Of the 36 countries in which trypanosomiasis is endemic, 22 are actively involved in the WHO programme. The most effective approach for controlling
sleeping sickness has three parts:
Mobile medical surveillance of the population at risk by specialized staff using the most effective diagnostic tools (serology and parasitology)
available. Patients are sent to specific referral centres for determination of the stage of the disease and treatment, and for post-therapeutic
Fixed post medical surveillance delivered at dispensaries, health centres or hospitals where blood samples are taken and analyzed at reference
centres. All patients or suspected cases are sent to special centres for confirmation of diagnosis, determination of the stage of the disease and
treatment, and for post-therapeutic follow-up
Vector (Glossina ) control using screens and traps: simple, cheap and ecologically acceptable methods.