ABSTRACT
PATHOGENESIS It is generally accepted that E. histolytica invades tissue and causes clinical disease through a well-defined sequence of events that starts with the ingestion of the infectious cyst form of the parasite from fecally contaminated food or water (11-14). Excystation of the amoebic trophozoites occurs in the intestinal lumen. The trophozoites adhere to the colonic mucus and epithelial cells through interaction of a Gal/GalNac inhibitable lectin with host Gal/GalNac-containing glycoconjugates (12,14,15). Secretion of proteolytic enzymes by the parasite may aid disruption of the intestinal mucus and epithelial barrier and facilitate tissue penetration (10). The trophozoite kills host epithelial and immune cells at points of invasion, causing the characteristic flask-shaped colonic ulcers for which it is known. Ingestion of the apoptotic corpse by the amoeba rapidly follows. Finally, E. histolytica resists the host’s immune response and survives to cause prolonged extraintestinal infection such as amoebic liver abscesses.
