Microsporidiosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
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Revision as of 18:29, 11 December 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Microbiology
At least 14 microsporidian species have been recognized as human pathogens, spread across eight genera:
- Brachiola
- B. algerae, B. connori, B. vesicularum
- Encephalitozoon
- E. cuniculi, E. hellem, E. intestinalis
- Enterocytozoon
- E. bieneusi
- Microsporidium
- M. ceylonensis, M. africanum
- Nosema
- N. ocularum
- Pleistophora sp.
- Trachipleistophora
- T. hominis, T. anthropophthera
- Vittaforma
- V. corneae.
Life Cycle
- The infective form of microsporidia is the resistant spore and it can survive for an exteneded period of time in the environment.
- The spore extrudes its polar tubule and infects the host cell.
- The spore injects the infective sporoplasm into the eukaryotic host cell through the polar tubule.
- Inside the cell, the sporoplasm undergoes extensive multiplication either by merogony (binary fission) or schizogony (multiple fission).
- This development can occur either in direct contact with the host cell cytoplasm (E. bieneusi) or inside a vacuole called a parasitophorous vacuole (E. intestinalis). Either free in the cytoplasm or inside a parasitophorous vacuole, microsporidia develop by sporogony to mature spores.
- During sporogony, a thick wall is formed around the spore, which provides resistance to adverse environmental conditions. When the spores increase in number and completely fill the host cell cytoplasm, the cell membrane is disrupted and releases the spores to the surroundings.
- These free mature spores can infect new cells thus continuing the cycle.