Trypanosoma Brucei - Sleeping Sickness
Sleeping sickness, African trypanosomiasis, is a deadly blood disease caused by two variates of Trypanosoma
brucei and transmitted by tsetse fly. Trypanosoma brucei rhodesiense causes East African
trypanosomiasis. 1000 new T. b. rhodesiense infections are reported to World Health Organization annually.
Trypanosoma brucei gambiense causes West African trypanosomiasis (also known as Gambian sleeping
sickness). More than 12 000 new infections are reported to the WHO each year. The two subspecies do not
overlap in geographic distribution. They infect humans and tsetse flies (Glossina genus) in the
woodlands, savannah and the dense vegetation between Kalahari and Sahara deserts. Less than 1 % of tsetse flies
carry the parasite. T.b. rhodesiense is found in eastern and southeastern Africa. Over 95 % of the
T.b. rhodesiense infections occur in Malawi, Tanzania, Uganda, and Zambia. T.b. gambiense is
found predominately in central Africa and in some areas of West Africa. Over 95 % of the T.b. gambiense
infections occur in Angola, Central African Republic, Chad, northern Uganda, Sudan, Republic of the Congo and
Democratic Republic of the Congo.
Trypanosoma brucei needs two hosts to live and reproduce. Its life cycle starts, when
an infected tsetse fly bites human skin. While it is feeding on blood, metacyclic trypomastigotes are transmitted
to the skin from the salivary glands of the fly. The parasites get into the bloodstream by entering lymphatic or
blood vessels. They travel in different body fluids (such as blood, lymphatic or spinal fluid), transform into
bloodstream trypomastigotes and multiply by binary fission. The disease can be spread by another tsetse fly that
drinks the infected blood. Inside the fly the life cycle takes about three weeks. Ingested bloodstream
trypomastigotes transform into procyclic trypomastigotes in the fly's midgut and multiply. They transform into
epimastigotes, migrate to the salivary glands, then transform into metacyclic trypomastigotes and multiply once
again by binary fission.
Trypanosoma brucei is not killed by the immune system because it has a glycoprotein (VSG) coating. The
coating makes its cell membrane very thick and hard to recognize. It also changes frequently its structure to
always keep ahead of the immune response. T. b. rhodesiense and T. b. gambiense are
indistinguishable under a microscope. A trypomastigote is 14 to 33 µm long and has a tiny kinetoplast located at
the posterior end, a centrally located nucleus, an undulating membrane, and a flagellum. Trypomastigotes are the
only stage found in patients. Humans are the main host for T. b., but it is sometimes found in
East African trypanosomiasis is more acute and progresses quicker than West African trypanosomiasis.
Symptoms can be minor in the beginning but usually become apparent within the first months of the
infection. African trypanosomiasis has three symptomatic stages, the last one being the most dangerous eventually
leading to death, if left untreated.
1. In 1–3 weeks after the bite a chancre (a red sore skin lesion) can develop on the bite area.
2. Several weeks or months later Trypanosoma parasites in the blood, spinal and lymphatic fluid
(hemolymphatic stage) can cause:
- cardiac dysfunction
- pruritus (itching)
- muscle or joint pain
- skin rash
- splenomegaly (enlargement of the spleen)
- swelling of the lymph nodes (most prominently in the back of the neck and in the groin), hands and
- thrombocytopenia (low level of platelets, thrombocytes)
- weight loss.
3. The disease reaches its final stage when the parasites get through the blood-brain barrier entering the
brain. The central nervous system involvement can occur as early as within a month in some cases. This
meningoencephalitic stage (inflammation of the central nervous system) causes (in addition to the above second
stage symptoms) some of the following symptoms:
- confusion and abnormal behaviour
- death (within months or years)
- insomnia (sleeping troubles)
- personality changes
- somnolence (extreme fatigue).
Your health care provider does the diagnosis by examining blood, lymph node or tissue aspirates
(fluid suction), bone marrow, chancre or cerebrospinal fluid under a microscope.
Treatment is based on symptoms and laboratory results. The drug choice depends on the infecting
species and the stage of infection. Pentamidine isethionate and suramin are usually used for treating the
hemolymphatic stage of West and East African Trypanosomiasis, respectively. Melarsoprol is used for late disease
with central nervous system involvement (infections by T.b. gambiense or T. b. rhodiense).
Hospitalization for initial treatment is often necessary. Periodic follow-ups that include a spinal tap are
required for two years.
Tsetse flies are common only in rural Africa, not in urban cities. Areas of heavy infestation (endemic areas)
should be avoided. Tsetse flies are attracted to bright colours, very dark colours and moving
vehicles. Check for tsetse flies before entering the car. Tsetse flies are day biters. They can bite through thin
clothing and the bite is usually very painful. Permethrin-impregnated clothing and use of DEET repellent
(spray) can reduce the risk of getting bitten. Wear long-sleeved shirts and pants made of medium-weight material in
neutral colours that blend in with the background environment. Avoid thickets because during the hottest period of
the day tsetse fly rests in bushes. Use insect repellent. Even though insect repellents are not effective against
flies, they are effective in preventing other insects (such as malaria-carrying Anopheles mosquitoes) from biting.
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