Abstract
The mechanism of pathogenesis of amebic lesions has not been elucidated yet. Proteolytic secretions by Entamoeba histolytica, which are supposed to produce cellular damage of the tissues, have never been convincingly demonstrated. On the basis of experimental observations described herein, a new theory of the pathogenesis of amebic lesions is proposed. It is based on the assump tion that the cytolitic activity of E. histolytica is not due to lytic secretions but to the effect of digestive endoenzymes of the ameba, liberated upon its death and desintegration. The ameba, while alive and migrating in the tissue, does not harm healthy cells but feeds on cellular debris and cells undergoing necrosis. When a trophozoite arrives at a focus of cell decay, it starts to feed and reproduce, forming an amebic colony which grows until all available necrotic cells have been consumed. At this point a part of the colony dies and the digestive endoenzymes of the dead amebae damage the surrounding tissue cells, providing food for the remaining amebae which continue reproducing. In this manner a labile equilibrium is established between dying and reproduc ing amebae, which leads to enlargement of the amebic abscess. Eventually the small abscess drains into the intestinal lumen, returning the amebae to their original habitat. The production of les ion s in acute and chronic intestinal amebiasis, and of amebic abscess of the liver by this mechanism is discussed in detail.Comments
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