[Trypanosoma brucei gambiense] [Trypanosoma brucei rhodesiense]
Protozoan 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 body fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission . 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 fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s 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.
T. b. 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.
Infection occurs 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. gambiens.
Trypansoma brucei ssp. in thick blood smear stained with Giemsa.
The two Trypanosoma brucei subspecies that cause African trypanosomiasis, T. b. gambiense and T. b. rhodesiense, are indistinguishable morphologically. A typical trypomastigote has a small kinetoplast located at the posterior end, a centrally located nucleus, an undulating membrane, and a flagellum running along the undulating membrane, leaving the body at the anterior end. Trypomastigotes are the only stage found in patients. Trypanosomes range in length from 14 to 33 &m.
Figure A: Trypansoma brucei ssp. in a thick blood smear stained with Giemsa.
Figure B: Trypansoma brucei ssp. in a thick blood smear stained with Giemsa.
Figure C: Trypansoma brucei ssp. in a thick blood smear stained with Giemsa.
Trypansoma brucei ssp. in thin blood smears stained with Giemsa.
Figure A: Trypanosoma brucei ssp. in a thin blood smear stained with Giemsa.
Figure B: Trypanosoma brucei ssp. in a thin blood smear stained with Giemsa.
Figure C: Trypomastigotes of T. brucei ssp. in a blood smear stained with Giemsa.
Figure D: Trypomastigotes of T. brucei ssp. in a blood smear stained with Giemsa.
Trypansoma brucei ssp. in thin blood smears stained with Wright-Giemsa.
Figure A: Trypanosoma brucei ssp. in a thin blood smear stained with Wright-Giemsa.
Figure B: Trypanosoma brucei ssp. in a thin blood smear stained with Wright-Giemsa.
Figure C: Trypanosoma brucei ssp. in a thin blood smear stained with Wright-Giemsa.
Figure D: Trypanosoma brucei ssp. in a thin blood smear stained with Wright-Giemsa.
Figure E: Trypanosoma brucei in a thin blood smear stained with Wright-Giemsa.
Figure F: Trypanosoma brucei ssp. in a thin blood smear stained with Wright-Giemsa.
Trypanosoma brucei ssp. in thin blood smear, beginning to divide.
Figure A: Trypanosoma brucei ssp. in a thin blood smear stained with Giemsa. The trypomastigote is beginning to divide; dividing forms are seen in African trypanosomes, but not in American trypanosomes.
The diagnosis 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.
The CDC currently does not offer any serologic or molecular tests for African trypanosomiasis.
Treatment information for African trypanosomiasis can be found at: https://www.cdc.gov/parasites/sleepingsickness/health_professionals/index.html#tx
DPDx is an education resource designed for health professionals and laboratory scientists. For an overview including prevention and control visit www.cdc.gov/parasites/.
- Page last reviewed: December 31, 2017
- Page last updated: December 31, 2017
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