FAQS
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Definition
of the disease
Human
African trypanosomiasis, known as sleeping sickness,
is a vector-borne parasitic disease. Trypanosoma,
the parasites concerned, are protozoa transmitted to
humans by tsetse flies (glossina). Tsetse flies
live in Africa, and they are found in vegetation by
rivers and lakes, gallery-forests and vast stretches
of wooded savannah.
Another
human form of trypanosomiasis (Human American Trypanosomiasis)
occurs in the Americas and is known as Chagas disease.
- Sleeping sickness occurs only in sub-Saharan Africa,
in regions where tsetse flies are endemic. For reasons
as yet unknown, 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 them 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.
- It develops in foci whose size can range from a
village to an entire region. Within a given focus,
the intensity of the disease can vary considerably
from one village to the next.
Human
African trypanosomiasis takes two forms, depending on
the parasite involved:
- Trypanosoma brucei gambiense (T.b. gambiense) is
found in central and West Africa. It causes chronic
infection, which does not mean benign. 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 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.
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Animal
trypanosomiasis
Other
sub-species of the parasite cause animal trypanosomiasis,
which are pathogenic to animals and are often different
from those that cause the disease in humans. Animals
can carry parasites, especially T.b. rhodesiense; domestic
and wild animals are a major reservoir. They can also
be infected with T. b. gambiense, though the precise
role of this reservoir is not well known. 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, decimation of cattle and abandonment of
fertile land where the disease is rife.
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Major
epidemics
There
have been three severe epidemics in Africa over the
last century: one between 1896 and 1906, mostly in Uganda
and the Congo Basin, one in 1920 in several African
countries, and one that began in 1970 and is still in
progress. The 1920 epidemic was arrested due to mobile
teams systematically screening millions of people at
risk. The disease had practically disappeared between
1960 and 1965. After that success, screening and effective
surveillance were relaxed, and the disease has reappeared
in endemic form in several foci over the last thirty
years.
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Transmission
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 with T.b. gambiense.
- Mother-to-child infection: the trypanosome can
cross the placenta and infect the fetus, causing abortion
and perinatal death.
- Accidental infections can occur in laboratories,
for example, through the handling of blood of an infected
person, although this is fairly rare.
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Symptoms
The
early phase entails bouts of fever, headaches, pains
in the joints and itching. The second, known as the
neurological phase, begins when the parasite crosses
the blood-brain barrier and infests the central nervous
system. This is when the characteristic signs and symptoms
of the disease appear: confusion, sensory disturbances
and poor coordination. Disturbance of the sleep cycle,
which gives the disease its name, is the most important
feature. Without treatment, the disease is fatal. If
the patient does not receive treatment before the onset
of the second phase, neurological damage is irreversible
even after treatment.
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Prevalence
Sleeping
sickness threatens over 60 million people in 36 countries
of sub-Saharan Africa. Only 3 to 4 million people at
risk are under surveillance, with regular examination
or access to a health centre that can provide screening.
Detection
of the disease calls for major human and material resources,
such as well-equipped health centres and qualified staff.
Because such resources are lacking, most people with
sleeping sickness die before they can ever be diagnosed.
- Almost 45 000 cases were reported in 1999, but
the World Health Organization (WHO) estimates that
the number of people affected is ten times greater.
The 45 000 case figure shows not the true situation
but rather the lack of screening in many foci. The
real number of cases seems to be between 300 000 and
500 000. Reported cases in recent years are from countries
where surveillance coverage is no more than 5%.
- In certain villages of many provinces of Angola,
the Democratic Republic of Congo and southern Sudan,
the prevalence is between 20% and 50%. Sleeping sickness
has become the first or second greatest cause of mortality,
ahead of HIV/AIDS, in those provinces.
Countries
are placed in four categories in terms of prevalence.
In each country the spatial distribution of the disease
is very diverse; it is found in foci and micro-foci.
- Countries where there is an epidemic of the disease,
in terms of very high cumulated prevalence and high
transmission: Angola, Democratic Republic of Congo
and Sudan;
- Highly endemic countries, where prevalence is moderate
but increase is certain: Cameroon, Central African
Republic, Chad, Congo, Côte d'Ivoire, Guinea, Mozambique,
Uganda and United Republic of Tanzania.
- Countries where the endemic level is low: Benin,
Burkina Faso, Equatorial Guinea, Gabon, Kenya, Mali,
Togo and Zambia;
- Countries whose present status is not clear: Botswana,
Burundi, Ethiopia, Liberia, Namibia, Nigeria, Rwanda,
Senegal and Sierra-Leone.
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Diagnosis
There
are three stages to case management:
- Screening is the initial sorting of people who
might be infected. This involves checking for clinical
signs or the use of serological tests.
- 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 examination of cerebro-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 makes treatment
difficult. Diagnosis must be made as early as possible
in order to preclude the onset of irreversible neurological
disorders and prevent transmission. Case detection is
difficult and requires major human, technical and material
resources. Since the disease is rife in rural areas
among poor people with little access to health facilities,
this problem is all the more difficult.
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Treatment
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.
First
phase treatments
- Suramine: discovered in 1921, it is used in treatment of
the initial phase of T.b. rhodesiense. There are certain
undesirable effects, especially on the digestive tract.
- Pentamidine: discovered in 1941, it is used in treatment of
the initial phase of T.b. gambiense sleeping sickness.
In spite of a few undesirable effects, it is well
tolerated by patients. Future production is guaranteed
by an agreement between WHO and Aventis.
Second
phase treatments
Melarsoprol: discovered in 1949, it is at present the
only drug available on the market to treat the advanced
stage of sleeping sickness, no matter which parasite
is the cause. It is the last arsenical derivative in
existence. The undesired effects are drastic; they include
reactive encephalopathy (an hyperacute neurological
complication of an allergic nature) - often fatal -
in 3% to 10% of cases; those who survive the encephalopathy
suffer serious neurological sequelae. Furthermore, there
is considerable resistance to the drug, rising to 30%
in parts of central Africa.
Eflornithine: this molecule, which was registered in 1990,
is the alternative to melarsoprol treatment. It is effective
only against T.b. gambiense. The regimen is strict and
hard to apply. Production ceased in 1999. Last year,
the company Aventis gave the licence to WHO, which has
undertaken several initiatives to seek a new source
of production.
In
short, most drugs are old, difficult to administer in
poor conditions and by no means always successful. Early
diagnosis of the disease, which would guarantee low-risk
treatment on an outpatient basis, can rarely be achieved.
It is absolutely necessary that a new producer continues
the production and the marketing of Eflornithine, the
only currently available medicine which can treat the
neurological phase of T.b. gambiense.
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The
Role of the World Health Organization
Faced
with this resurgence of sleeping sickness, WHO coordinates
activities in endemic countries and mobilizes a wide
range of partners for this purpose. The Programme for
Surveillance and Control of African Trypanosomiasis
(PSCAT) includes national control programmes, nongovernmental
organizations (NGOs), donor countries, private foundations,
regional institutions, research centres and universities.
The
objectives of PSCAT are:
- Coordination of the sleeping sickness control network
to ensure that field activities are sustainable;
- Strengthening of existing surveillance systems;
- Development of the network for study of treatment
and drug resistance;
- Promotion of inter-agency collaboration for example
with the FAO;
- Development of the information system and training
activities.
Source:
WHO
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