New concepts regarding the pathogenesis of amebiasis.

Abstract

Our understanding of the pathogenesis of amebiasis has progressed significantly since Dr. Braude's description of the major clinical syndromes of amebic liver abscess. His hypothesis that invasive amebic strains must be resistant to complement-mediated lysis has been confirmed. We have also shown that Entamoeba histolytica activates complement by a unique mechanism, i.e., cleavage of C3 by an extracellular cysteine proteinase. Cysteine proteinases are important virulence factors encoded by at least three genes; one gene, acp1, is unique to invasive strains. The amebic cysteine proteinases are homologous to proteinases released by transformed cells and may represent a common mechanism of tissue invasion. The initial division of Entamoeba into invasive E. histolytica and noninvasive Entamoeba dispar by isoenzymes has been supported by genetic differences between amebae. Thus, a model of pathogenesis differentiating between two separate species of Entamoeba best explains the epidemiology, clinical syndromes, and pathology of amebiasis.