Infection occurs when the amoeba cysts with food or water enter the digestive canal. Cysts easily overcome the acid barrier of the stomach, in the small intestine, their membrane is dissolved by enzymes and four amoeba metacysts come out from each cyst , from which vegetative forms of amoeba form through transverse division. The latter intensively multiply in the upper part of the colon and for a long time can be in its lumen, without causing significant damage to the macroorganism . Intestinal dysbiosis, various diseases, intoxications, injuries, hypothermia can contribute to the development of the infectious process.

Several factors are distinguished for the pathogenic effect of dysenteric amoeba on the mucous membrane of the colon: 

1) mechanical action – the active promotion of the pathogen in the intestinal wall tissue due to pseudopodia, 

2) the isolation of proteolytic enzymes, 

3) the pathogenic effect of a specific cytolytic substance, 

4) the effect of the pathogenic intestinal flora, which enhances the invasive properties of amoebas. After penetration of the luminal forms of the amoeba into the crypts of the blind and ascending part of the colon, it multiplies and turns into tissue. Under the influence of its proteolytic enzymes and other toxic substances, cytolysis of epithelial cells, necrotization, and fusion of certain sections of the mucosa and muscle layer of the intestinal wall occur . This leads to the formation in the submucosal layer of microabscesses, which, breaking into the intestinal lumen, turn into ulcers with saped edges. In this case, not only the mucous and muscle layers of the intestinal wall are often affected, but also serous. In addition to the blind and ascending, the rectum and sigmoid colon are often affected. Absorption of decay products of necrotic tissues is the cause of general intoxication, which in patients with amoebiasis is much less than with other intestinal infections. Along with this, a specific protein component with pronounced antigenic properties is pathogenic for the body, which is the cause of allergic and paraallergic manifestations. Morphological changes are characterized by small erosions, a large number of round ulcers, the opening of which is much narrower, the deeper the part is located (the shape of an inverted funnel). Between ulcers, noticeable areas of normal mucosa. The size of ulcers is different – from a few millimeters to 2 cm. The bottom of the ulcers is covered with purulent layers, the edges are sap, surrounded by a zone of hyperemia. In the case of a long and severe course of amoebiasis, ulcers can merge in the submucosal layer, forming extensive ulcerative defects with irregularly shaped edges. The latter can penetrate or perforate, their healing occurs by scarring with the formation of constrictions (strictures), which leads to stenosis of the intestinal area or even to its obstruction. In rare cases, mucosal exfoliation is possible. A severe long course of amoebiasis causes the formation of cysts, polyps, amoeba. Deep ulcers lead to a violation of the integrity of the blood vessels, which is the cause of intestinal bleeding, as well as the penetration of vegetative forms of amoeba into the blood system. As a result, the pathogen enters the liver, where individual or multiple abscesses may form. Sometimes the hematogenous spread of the pathogen causes the formation of abscesses in other organs (lungs, brain, spleen, kidneys, etc.).