Hydatidous echinococcosis: causes and pathogenesis

Causes of hydatidid echinococcosis

The cause of echinococcosis is hydatidosis - Echinococcus granulosus, which is classed as Plathelminthes, class Cestoda. The Taeniidae family. Sexually mature E. Granulosus is a belt helminth of white color 3-5 mm in length. It consists of a head with four suckers and a double crown of hooks, from the cervix and 2-6 segments. The last segment is filled with a uterus containing eggs (oncospheres), which possess invasive ability and do not need ripening in the environment. Sexually mature helminth parasitizes in the small intestine of the final host - carnivorous animals (dogs, wolves, lynxes, cats, etc.). Mature segments with feces get into the environment. Eggs are highly resistant in the external environment, in winter they remain viable up to 6 months.

The larval stage is a bubble filled with a liquid. The wall of the echinococcal cyst (larvocysts) consists of the inner germinal (germinative) and external (cuticular) membranes. As a result of the reaction of the host tissues around the echinococcal cyst, a dense fibrous membrane forms. From the embryonic layer, brood capsules are formed, in which scolexes develop. Mature scolexes are removed from the capsules and float freely in the liquid, forming the so-called hydatid sand. In the thickness of the embryonic shell of the scolex, daughter blisters are formed; breaking away, they also freely swim in the liquid. In the cavity of the daughter can form grandiose blisters, and they all contain brood capsules. The larvocyst grows in the tissues of the intermediate host (sheep, cattle, moose, reindeer, pigs, rabbits, etc.). Man, finding himself in the role of intermediate host, in the life cycle of this parasite becomes a biological dead end.

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Pathogenesis of hydatidid echinococcosis

Because of the hematogenous pathway, the oncospheres of echinococcus can be entered into any organ, but most often echinococcal cysts are located in the liver (30-75%) and lungs (15-20%), much less often in the central nervous system (2-3%), spleen , pancreas, heart, in tubular bones and kidneys (up to 1%). The transformation of the oncosphere into a larvocyst in an invaded person lasts about 5 months; during this time it reaches a diameter of 5-20 mm. The pathological effect of echinococcus is due to mechanical and sensitizing factors. In most patients, the only organ is affected by a single solitary cyst, but multiple echinococcosis can develop. The parasite has a number of adaptive mechanisms that ensure its long-term development in the body of the intermediate host. These include the loss of the larvocystic portion of the receptors during the formation of the hyaline membrane, the production of immunosuppressors. Protein mimicry due to the inclusion of host proteins in its shell. Cysts vary in size from 1 to 20 cm (or more) in diameter. Echinococcal cyst grows slowly over a number of years, moving the tissues of the affected organs, where dystrophic changes gradually develop, sclerosis of the stroma and atrophy of the parenchyma. In 5-15% of patients, compression of the bile ducts with calcified intrahepatic cysts is noted. In the lung tissue around the dead parasite there are atelectasises, foci of pneumosclerosis, bronchiectasis. Cysts that damage bones gradually destroy the structure of bone tissue, which leads to pathological fractures. With prolonged course of hydatidosis of echinococcosis, suppuration and rupture of echinococcal cysts can occur. When the cyst is opened (spontaneously or as a result of damage to its walls), severe allergic reactions to antigens that form part of the fluid develop: the release of multiple scolexes leads to dissemination of the pathogen.