Hydatid echinococcosis - Causes and pathogenesis

Causes of hydatid echinococcosis

The cause of hydatid echinococcosis is Echinococcus granulosus, which belongs to the type Plathelminthes, class Cestoda. family Taeniidae. Mature E. granulosus is a white tapeworm 3-5 mm long. It consists of a head with four suckers and a double crown of hooks, a neck and 2-6 segments. The last segment is filled with a uterus containing eggs (oncospheres), which have invasive ability and do not need to mature in the environment. Mature helminth parasitizes in the small intestine of the final host - carnivores (dogs, wolves, lynxes, cats, etc.). Mature segments enter the environment with feces. Eggs are highly resistant in the external environment, in winter they remain viable for up to 6 months.

The larval stage is a fluid-filled bladder. The wall of the echinococcal cyst (larvocyst) consists of an internal germinal (germinal) and external (cuticular) membrane. As a result of the host tissue reaction, a dense fibrous membrane forms around the echinococcal cyst. Brood capsules are formed from the germinal layer, in which the scolexes develop. Mature scolexes are released from the capsules and float freely in the liquid, forming the so-called hydatid sand. In the thickness of the germinal membrane, daughter bladders are formed from the scolexes; when they break away, they also float freely in the liquid. Granddaughter bladders may form in the cavity of the daughter bladders, and all of them contain brood capsules. The larvocyst grows in the tissues of the intermediate host (sheep, cattle, elk, reindeer, pigs, hares, etc.). A person, finding himself in the role of an intermediate host, becomes a biological dead end in the life cycle of this parasite.

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Pathogenesis of hydatid echinococcosis

Due to the hematogenous route of spread, echinococcus oncospheres can be introduced into any organ, but most often echinococcal cysts are localized in the liver (30-75%) and lungs (15-20%), much less often in the central nervous system (2-3%), spleen, pancreas, heart, tubular bones and kidneys (up to 1%). The transformation of the oncosphere into a larva cyst in an infected 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, a single organ is affected by one solitary cyst, but multiple echinococcosis can also 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 larvae cyst portion of receptors during the formation of the hyaline membrane, the production of immunosuppressants, protein mimicry due to the inclusion of host proteins in their membrane. The size of the cysts varies from 1 to 20 cm (or more) in diameter. The echinococcal cyst grows slowly over a number of years, pushing aside the tissues of the affected organs, where dystrophic changes, stromal sclerosis and parenchyma atrophy gradually develop. In 5-15% of patients, compression of the bile ducts by calcified intrahepatic cysts is noted. Atelectasis, foci of pneumosclerosis, and bronchiectasis occur in the lung tissue around the dead parasite. Cysts affecting the bones gradually destroy the structure of the bone tissue, which leads to pathological fractures. With a long course of hydatid echinococcosis, suppuration and rupture of echinococcal cysts may occur. When a cyst opens (spontaneously or as a result of damage to its walls), strong allergic reactions to antigens contained in the fluid develop: the release of numerous scolexes leads to the dissemination of the pathogen.