the basic mechanisms involved in the production of focal lytic lesions include complex multifactorial processes in which lectins facilitate adhesion, proteases degrade extracellular matrix components, porins help nourish the parasite and may also kill incoming polymorphonuclear leukocytes and macrophages, and motility is used by the parasite to invade deeper layers of the colon. In addition, E. histolytica has developed mechanisms to modulate the immune response during acute infection. Nevertheless, much still needs to be unraveled to understand how this microscopic parasite has earned its well-deserved histolytic name.
Entamoeba histolytica normally eats bacteria by phagocytosis and digests them using enzymes targeted to the food vacuoles. If the amoeba comes in contact with epithelium, the same process is triggered but the epithelium cannot be ingested so the enzymes end up outside the amoeba, where they kill the host cell the amoeba is attached to. The amoeba on its own would not cause too much damage, but neutrophils etc are attracted to the location of the amoeba and these are also killed by the amoeba. The enzymes inside the neutrophils are released when they lyse and these cause more damage to the epithelium, which attracts more cells - it almost becomes a chain reaction amplifying the initial damage caused by E. histolytica. So most of the damage is probably caused by the host response to the initial damage rather than being caused the amoeba itself.
I'm absolute convinced watch Dr Clark stated regarding that relationship E histolytica-host is critical to trigger or not epithelium damage..and much more when many cases are due to confections...I mean not all damages are originated by the parasite itself
That is why only few clinical cases are described in healthy carriers