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African trypanosomiasis (sleeping sickness) is a parasitic disease transmitted
by tsetse flies of the genus Glossina and caused
by a group of parasites called trypanosomes.1 West
African trypanosomiasis, also called Gambian sleeping sickness,
is caused by a subspecies of the extracellular flagellate Trypanosoma
brucei known as Trypanosoma brucei gambiense.
East African trypanosomiasis, also called Rhodesian sleeping sickness,
is caused by T brucei rhodesiense. These diseases
exist in Africa wherever the various species of Glossina (ie,
the tsetse fly) are found.
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African trypanosomiasis has a focal distribution but expands
outward during epidemics. About 60 million people live in risk areas
of African trypanosomiasis, and the World Health Organization estimates
a continent-wide prevalence of both forms of African trypanosomiasis
of 300,000 cases; an average of 30,000 new cases of the disease
have been reported annually over the last 10 years, although underreporting
rates are high.1 Thirty-six sub-Saharan countries are
considered endemic for one or the other form of the disease despite
that some of them have reported no cases in the last decade.2 The
Gambian form is currently a major public health problem over vast
areas of Africa from Sudan in the north to northwest Uganda to the
Democratic Republic of the Congo to Angola in the south. This form
represents more than 90% of reported cases.2 The
Rhodesian form continues to present a serious health risk in the Lake
Victoria Basin, particularly in eastern Uganda, and there are small
pockets of disease endemic in other countries of east and central
Africa. A line drawn from north to south through sub-Saharan Africa,
roughly following the Rift Valley, differentiates the distribution
of the 2 diseases with the Gambian form to the west and the Rhodesian
to the east of this notional line.1T brucei
rhodesiense is a zoonotic parasite, and wild and domestic
animals serve as reservoirs. A number of domestic animals species,
including pigs, dogs, goats, sheep, and cattle, may carry human-infective
trypanosome species. For T brucei gambiense, the
nature of animal reservoirs and its role in disease transmission
is somewhat less certain.1
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All members of the T brucei complex share a
common morphology, biochemistry, and life cycle (eFig.
355.1). Infective metacyclic trypomastigotes are inoculated
into subcutaneous tissue of a human or another mammalian host by
a bite from the tsetse fly. They are converted to the pleomorphic
blood forms: long, slender forms (20–40 by 1 μm)
and stumpy forms (15–25 by 3.5 μm). Within
the human host, trypomastigotes multiply in blood, lymph, and extracellular
spaces. The central nervous system eventually is invaded, where
multiplication continues unabated. The tsetse fly is infected with
ingestion of a blood meal. Trypomastigotes differentiate into procyclic
forms in the midgut where they multiply by binary fission and remain
for the next 2 to 3 weeks. Finally, they enter the salivary glands
and transform into infective ...