Isosporiasis pathophysiology: Difference between revisions
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== Pathophysiology== | == Pathophysiology== | ||
[[Image:Isospora_LifeCycle.gif|left|frame|Life cycle of Isospora belli]] | [[Image:Isospora_LifeCycle.gif|left|frame|Life cycle of Isospora belli]] | ||
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Revision as of 20:04, 4 October 2012
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Isosporiasis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Isosporiasis pathophysiology On the Web |
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American Roentgen Ray Society Images of Isosporiasis pathophysiology |
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Risk calculators and risk factors for Isosporiasis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
At time of excretion, the immature oocyst contains usually one sporoblast (more rarely two) 1. In further maturation after excretion, the sporoblast divides in two (the oocyst now contains two sporoblasts); the sporoblasts secrete a cyst wall, thus becoming sporocysts; and the sporocysts divide twice to produce four sporozoites each 2. Infection occurs by ingestion of sporocysts-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate schizogony 3. Upon rupture of the schizonts, the merozoites are released, invade new epithelial cells, and continue the cycle of asexual multiplication 4. Trophozoites develop into schizonts which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes 5. Fertilization results in the development of oocysts that are excreted in the stool 1. Isospora belli infects both humans and animals.