NEW CONCEPTS REGARDING THE PATHOGENESIS OF AMEBIASIS

Our understanding of the pathogenesis of amebiasis has progressed sign ificantly since Dr. Braude's description of the major clinical syndrom es of amebic liver abscess. His hypothesis that invasive amebic strain s must be resistant to complement-mediated lysis has been confirmed. W e have also shown that Entamoeba histolytica activates complement by a unique mechanism, i.e., cleavage of C3 by an extracellular cysteine p roteinase. Cysteine proteinases are important virulence factors encode d by at least three genes; one gene, acp1, is unique to invasive strai ns. The amebic cysteine proteinases are homologous to proteinases rele ased by transformed cells and may represent a common mechanism of tiss ue invasion. The initial division of Entamoeba into invasive E. histol ytica and noninvasive Entamoeba dispar by isoenzymes has been supporte d by genetic differences between amebae. Thus, a model of pathogenesis differentiating between two separate species of Entamoeba best explai ns the epidemiology, clinical syndromes, and pathology of amebiasis.