hemoflagellates belonging to the complex Trypanosoma brucei. Two
subspecies that are morphologically indistinguishable cause distinct
disease patterns in humans: T. b. gambiense causes West African
sleeping sickness and T. b. rhodesiense causes East African
sleeping sickness. (A third member of the complex, T. b. brucei,
under normal conditions does not infect humans.)
During a blood
meal on the mammalian host, an infected tsetse fly (genus Glossina)
injects metacyclic trypomastigotes into skin tissue. The parasites
enter the lymphatic system and pass into the bloodstream
Inside the host, they transform into bloodstream trypomastigotes
are carried to other sites throughout the body, reach other blood fluids
(e.g., lymph, spinal fluid), and continue the replication by binary
The entire life cycle of African Trypanosomes is represented by
extracellular stages. The tsetse fly becomes infected with bloodstream
trypomastigotes when taking a blood meal on an infected mammalian host (
In the flyís midgut, the parasites transform into procyclic
trypomastigotes, multiply by binary fission
leave the midgut, and transform into epimastigotes
The epimastigotes reach the flyís salivary glands and continue
multiplication by binary fission
The cycle in the fly takes approximately 3 weeks. Humans are the main
reservoir for Trypanosoma brucei gambiense, but this species can
also be found in animals. Wild game animals are the main reservoir of
T. b. rhodesiense.
gambiense is found in foci in large areas of West and Central
Africa. The distribution of T. b. rhodesiense is much more
limited, with the species found in East and Southeast Africa.
in 3 stages. A trypanosomal chancre can develop on the site of
inoculation. This is followed by a hemolymphatic stage with symptoms
that include fever, lymphadenopathy, and pruritus. In the
meningoencephalitic stage, invasion of the central nervous system can
cause headaches, somnolence, abnormal behavior, and lead to loss of
consciousness and coma. The course of infection is much more acute with
T. b. rhodesiense than T. b. gambiense.
rests upon demonstrating trypanosomes by microscopic examination of
chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late
stages of infection, cerebrospinal fluid. A wet preparation should be
examined for the motile trypanosomes, and in addition a smear should be
fixed, stained with Giemsa (or Field), and examined. Concentration
techniques can be used prior to microscopic examination. For blood
samples, these include centrifugation followed by examination of the
buffy coat; mini anion-exchange/centrifugation; and the Quantitative
Buffy Coat (QBC) technique. For other samples such as spinal fluid,
concentration techniques include centrifugation followed by examination
of the sediment. Isolation of the parasite by inoculation of rats or
mice is a sensitive method, but its use is limited to T. b.
rhodesiense. Antibody detection has sensitivity and specificity
that are too variable for clinical decisions. In addition, in
infections with T. b. rhodesiense, seroconversion occurs after
the onset of clinical symptoms and thus is of limited use.
20-2002 from the New England Journal of Medicine (Vol. 346,
No. 26, June 27, 2002).
be started as soon as possible and is based on the infected personís
symptoms and laboratory results. The drug regimen depends on the
infecting species and the stage of infection. Pentamidine isethionate*
and suramin (under an investigational New Drug Protocol from the CDC
Drug Service) are the drugs of choice to treat the hemolymphatic stage
of West and East African Trypanosomiasis, respectively. Melarsoprol is
the drug of choice for late disease with central nervous system
involvement (infections by T.b. gambiense or T. b. rhodiense).
* This drug is
approved by the FDA, but considered investigational for this purpose.