Amoebiasis - Causes and pathogenesis

Causes of amebiasis

The causes of amebiasis are Entamoeba histolytica, which is attributed to the half-kingdom of Protozoa, the subtype of Sarcodina, the class of Rhizopoda, the order of Amoeba, the family of Entamoebidae.

The life cycle of E. Histolytica includes two stages - vegetative (trophozoite) and resting stage (cyst). The shallow vegetative form (luminal form, or forma minuta) has sizes from 7 to 25 microns. The division of the cytoplasm into ecto- and endoplasm is poorly expressed. This non-pathogenic, commensal form lives in the lumen of the human colon, feeds on bacteria through endocytosis, is mobile, propagates vegetatively. Tissue form (20-25 microns) is found in the affected tissues and organs of the host. It has an oval nucleus, a well-expressed vitreous ectoplasm and granular endoplasm, is very mobile, forms broad, blunt pseudopodia. A large vegetative form (forma magna) is formed from a tissue form. Body gray, round, large (up to 60 μm or more when moving), ectoplasm light, granular, cloudy, dark and endoplasma; digestive vacuoles contain phagocytized erythrocytes. It is because of this that it is also called "erythrophage". As you move through the large intestine, amoeba turn into pre-cystic stages, and then into cysts. Cysts of round or oval shape (10-15 microns) with a smooth two-contour shell. Immature cysts contain one or two nuclei, mature - four nuclei with karyosomes.

Cysts are resistant to environmental factors: at a temperature of 20 ° C they remain viable in the soil for several days, in winter conditions (-20 ° C) - up to 3 months. Because of the resistance to disinfectants (chlorine, ozone) in the concentrations used at water treatment plants, viable cysts can be found in drinking water. High temperatures for them are fatal, with drying and heating the cysts quickly die. Vegetative forms in the external environment are unstable and have no epidemiological significance.

When a person is infected, amoeba cysts with water or with food fall into the mouth. And then into the intestines. In the distal parts of the small intestine, under the action of intestinal enzymes, the cyst shell dissolves. Of the mature cysts, four meta-cyst mononuclear amoebas emerge, which in turn are divided in two every two hours. As a result of subsequent divisions, they turn into vegetative luminal stages (see above). It is known about the presence in the population of two species of amoebas: the potentially pathogenic strains of E. Histolytica and the non-pathogenic E. Dispar, which are the same morphologically, can only be distinguished by DNA analysis.

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Pathogenesis of amebiasis

The reason why E. Histolytica passes from a luminal state to tissue parasitism, is not fully understood. It is believed that the main virulence factor in E. Histolytica is cysteine proteinase, which is absent in E. Dispar. In the development of invasive forms of amoebiasis, factors such as the intensity of infestation, changes in the physico-chemical environment of intestinal contents, immunodeficiency, starvation, stress, etc., are important. They note the relatively frequent development of invasive forms in women during pregnancy and lactation, in persons infected HIV. Probably, amoebae pass to tissue parasitism with the acquisition of properties characteristic of other pathogenic microorganisms, such as adhesiveness, invasiveness, the ability to act on the protective mechanisms of the host, etc. It has been established that trophozoites attach to epithelial cells due to a specific lectin-galactose-N-acetylgalactosamine.

E. Histolytica found hemolysins, proteases, in some strains - hyaluronidase, which can play a significant role in the destruction of the epithelial barrier by amoebae. Trophozoites of the parasite are able to cause a contact lysis of non-neutrophilic leukocytes with the release of mono-oxidants that enhance the process of tissue melting. Amoebas have an inhibitory effect on monocytes and macrophages, which contributes to their survival. They are able to specifically block the production of IL intestinal cells (IL-1beta, IL-8), cleaved complement (C ₃ ), IgA, IgG, thus affecting the inflammatory processes at the site of introduction of the parasite. Under the influence of cytolysins and proteolytic enzymes amoeb damage to the mucosa and adjacent layers of the intestinal wall. The primary manifestation of amebiasis is the formation of small areas of necrosis in the mucosa of the colon, which progress to ulceration. Synchronicities in the development of ulcers do not occur. Ulcers not only increase in the periphery (due to the submucosal layer), but also deep into the muscular and even serous membrane lining the walls of the large intestine. Deep necrotic process leads to the appearance of adhesions of the peritoneum and can cause perforated peritonitis. Amoebic ulcers are more often localized in the region of the cecum. Further in descending order of the defeat rate, follow the straight and sigmoid colon, appendix and terminal site of the ileum. In general, due to the fact that bowel damage is segmental and usually spreads slowly, the intoxication syndrome is poorly expressed. Typical amebic ulcers are sharply delimited from surrounding tissues, have uneven edges. At the bottom of the ulcer are necrotic masses consisting of fibrin and containing trophozoites of amoebas. Inflammatory reaction is weakly expressed. Necrotic process in the center, undercut and elevated edges of the ulcer, reactive hyperemia and hemorrhagic changes around it are the most typical features of ulceration in intestinal amebiasis. Due to the regenerative process leading to the restoration of the defect through the proliferation of fibrous tissue, strictures and stenosis of the intestine may occur. With chronic amoebiasis in the wall of the intestine, amoeba is sometimes formed - a tumor-like growth, located mainly in the ascending, blind or rectum. Amoeboma consists of fibroblasts. Collagen and cellular elements and contains a relatively small number of amoebas.

As a result of the penetration of amoebas into the blood vessels of the intestinal wall, they are transferred to the blood stream with other blood vessels, where foci of lesions appear in the form of abscesses. Most often abscesses are formed in the liver, less often in the lungs, brain, kidneys, pancreas. Their contents are gelatinous, yellowish in color, in large abscesses pus has a red-brown color. Single abscesses are more often located in the right lobe of the liver, closer to the diaphragm or lower surface of the organ. In large abscesses, the outer zone consists of a relatively healthy tissue containing trophozoites of amoebas and fibrin. When a chronic abscess is usually a thick capsule, the contents are yellowish, with putrefactive odor. Due to the breakthrough of the abscess of the liver under the diaphragm, after purging it, purulent pleurisy develops. In mild abscesses, in most cases, they are localized in the lower or middle lobe of the right lung.