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The pathogenesis is dependent mainly on host susceptibility and immune status, in addition to the diet rich in carbohydrates, steroids, protein malnutrition and pregnancy.

However, the conditions of neutral or alkaline pH, a low pO2, and nutrients from bacteria associated with influencing the development of the amoeba.

the pathogenesis is also dependent on the environment, the amount, virulence and resistance to phagocytic capacity the parasites.

The invasiveness of a strain is related to their phagocytic capacity (erythrophagocytosis), production of collagenase and a cytotoxic protein immunogenicity, resistance to the host inflammatory response and its ability of cell lysis after contact with the host cell. Furthermore, the adhesive strength is given by Lecithin, there is also a pore-forming protein (amebaporo), which alters the cell membrane, subsequently producing intestinal cytolysis, attracting neutrophils that release toxic, causing an inflammatory reaction that continues until destruction of the mucosa, which subsequently leads to ulcer.

The PMN, is with the amoeba, and is phagocytosed, but when he tries to phagocytose amebaporo is released so the white blood cell is destroyed (kiss of death).

The amoeba reaches the lumen of the intestine, starts to crawl by the epithelial cells, and can feed on detritus and can lead to injury, to ulcers.

Therefore, broken cells and reaches the submucosa of the intestine, and can begin to multiply, while the submucosa now has the largest endowment of SI cells (MALT) Peyer's patches, but the grace that has the E. histolytica is that it has strategies to evade the SI in this way can cause an abscess (ameboma) and can penetrate the submucosa and reach the capillaries and thus reach Via Porta and subsequently to the liver, and this is the most serious condition of the disease.