African trypanosomiasis pathophysiology: Difference between revisions
| Line 11: | Line 11: | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
'''1'''. Inside the host, they transform into bloodstream trypomastigotes '''2''', are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission '''3'''. 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 ('''4''','''5'''). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission '''6''', leave the midgut, and transform into epimastigotes '''7'''. The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission '''8'''. 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. | |||
[[Image:Life cycle--trypanosomiasis.gif|frame|center|Life cycle of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense]] | [[Image:Life cycle--trypanosomiasis.gif|frame|center|Life cycle of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense]] | ||
Revision as of 14:37, 30 August 2012
|
African trypanosomiasis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
African trypanosomiasis pathophysiology On the Web |
|
American Roentgen Ray Society Images of African trypanosomiasis pathophysiology |
|
Risk calculators and risk factors for African trypanosomiasis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Pilar Almonacid
Overview
Pathophysiology
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.)
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. gambiense.
Microscopic Pathology
1. Inside the host, they transform into bloodstream trypomastigotes 2, are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission 3. 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 (4,5). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission 6, leave the midgut, and transform into epimastigotes 7. The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission 8. 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.
