African trypanosomiasis pathophysiology: Difference between revisions
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===Transmission=== | ===Transmission=== | ||
Infection is usually transmitted via the tsetse fly bite to the human host. | |||
===Reservoir=== | ===Reservoir=== |
Revision as of 22:15, 27 June 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Pilar Almonacid
Pathophysiology
Two subspecies of Trypanosoma brucei. that are morphologically indistinguishable is responsible for African trypanosomiasis. They 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.)
Stages of infection
- 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.
Transmission
Infection is usually transmitted via the tsetse fly bite to the human host.
Reservoir
- Humans are the main reservoir for Trypanosoma brucei gambiense, but this species can also be found in animals.
- Wild animals are the main reservoir of T. b. rhodesiense.
Human cycle
- 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, the microbe transforms into bloodstream trypomastigotes
- They are carried to other sites throughout the body, reach other blood 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.
Tsetse fly cycle
- 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.
Infective stage of the parasite
- Metacyclic trypomastigotes