Schistosomiasis: causes and pathogenesis

Causes of schistosomiasis

Schistosomiasis is caused by schistosomes, which are of the Plathelminthes type, the Trematoda class, the Schistosomatidae family. Five species of schistosomes: Schistosoma mansoni, Schistosoma haematobium, Schistosoma japonicum, Schistosoma intercalation and Schistosoma mekongi - causative agents of helminthiosis in man. Schistosomes differ from all other members of the Trematoda class in that they are dioecious and differ in sexual dimorphism. The body of mature sexually schistosomes is elongated, cylindrical, covered with cuticle. There are suckers located close to each other - oral and abdominal. The body of the female is longer and thinner than that of the male. Along the body of the male there is a special copulatory groove (gyneco-form canal) in which the male retains the female. The male and female are almost always together. The external surface of the male is covered with spines or tubercles, the female spines are present only at the anterior end of the body, the rest of the surface is smooth. Schistosomes live in the smallest venous vessels of the final host, man and some animals, feed on blood through the digestive tube and partially adsorb the liquid part through the cuticle. In the uterus of S. Haematobium there are simultaneously no more than 20-30 eggs. The female S. Japonicum possesses the greatest reproductive capacity. For a day laying from 500 to 3500 eggs. The larva in the egg of the schistosome, deposited in the small veins of the host, ripens in the tissues for 5-12 days. Migration of eggs from blood vessels is due to the presence of a spike, proteolytic activity of secretions of larvae, and also under the influence of contractile movements of the muscular layer of the walls of the vessels, intestine and bladder. In the environment eggs fall into the urine (S. Haematobium) or feces (S. Mansoni, etc.). Further development occurs in water, where the shell of eggs is destroyed; out of them come miracidia. The cycle of development of schistosomes is associated with the change of host. Their intermediate host is freshwater mollusks, in the body of which miracidia during 4-6 weeks pass a complex process of forming cercariae (a generation of invasive larvae capable of penetrating into the organism of the final host). After penetrating the human body, the larvae lose the caudal appendage. Life expectancy of miracidium - up to 24 hours, cercariae - up to 2-3 days. Sexually mature individuals with schistosomes - 5-8 years.

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Pathogenesis of schistosomiasis

Schistosomes do not multiply in the body of the final host, so their number may increase only due to reinfusion. The pathogenic influence of parasites begins from the moment of penetration of cercariae through the skin. The secrets of the glands of migrating larvae, the decay products of some of them are strong antigens that cause the reactions of GNT and HRT. Clinically, it manifests itself as a transient papular itchy rash and is known as cervical hepatitis (scabies swimmers). Larvae that have lost the tail appendage (schistosomes), penetrating into the peripheral lymphatic and venous vessels, migrate and enter the right heart, into the lungs, then reach the vessels of the liver, where they develop and mature to adults. Sexually mature females and males mate and migrate into vessels of permanent localization - into the system of mesenteric veins (intestinal varieties of schistosomes) or the bladder and small pelvis - S. Haematobium. Four to six weeks after infection, during the completion of the migration of schistosomes and the beginning of egg laying by ripe females, the allergic reactions that underlie the acute ("toxemic") phase of the disease, also called Katayama's disease, sharply increase. By the nature of clinical manifestations, this phase resembles serum sickness. More often it is observed with S. Japonicum invasion , much less often after infection with S. Mansoni and other pathogens.

Of the total number of eggs of schistosomes deposited by females in small venous vessels. Feeding the walls of the intestine or urinary bladder, the environment does not get more than 50%: the rest is retained in the tissues of the affected organs or blood flow is recorded in other organs. The basis of pathological changes in the chronic period of the disease is a set of inflammatory changes around the eggs of schistosomes (the formation of a specific cellular infiltrate - granuloma, followed by fibrosis and calcification). T-lymphocytes, macrophages, and eosinophils are involved in the formation of granulomas around eggs. Initially, the process is reversible, but with the deposition of collagen and the development of fibrosis, morphological changes in tissues become irreversible. The granulomatous reaction and fibrosis cause blood flow disorders in the organ wall, which causes secondary dystrophic changes in the mucosa, the formation of ulcers. As a result of constant and prolonged stimulation of tissues by parasite eggs, the products of the vital activity of larvae in them and their decay may also be hyperplasia and metaplasia of the epithelium of the mucosa. In the bladder, in 85% of cases, the underlying site of lesions associated with the deposition of S. Haematobium eggs is the submucosal layer: the muscular layer is less affected. In the ureters, on the contrary, deeply located layers are more often affected. Since the causative agent of intestinal schistosomiasis of S. Mansoni is localized in the veins of the hemorrhoidal plexus and in the inferior mesenteric vein, and in the same place the deposited eggs accumulate, the main pathological changes develop mainly in the distal parts of the colon. S. Japonicum, unlike other species, lays not single eggs, but groups, and they are more rapidly subjected to calcification. With all forms of schistosomiasis, eggs are introduced into other organs, especially the liver and lungs. The most severe liver damage leading to cirrhosis develops in Japanese and intestinal schistosomiasis (with S. Mansoni invasion - tubular-infertile fibrosis of Simmers). The ingress of eggs into the lungs leads to the development of obstructive-destructive arteritis, arteriovenous anastomoses - as a result, hypertension of the small circulation circulates, which causes the formation of a "pulmonary" heart. Chasing the eggs with schistosomes (more often with S.japonicum invasion ) in the dorsal and brain.

Symptoms of schistosomiasis largely depend on the intensity of infestation, i.e. In the final analysis, on the number of eggs laid by the female parasites and their accumulation in the affected tissues. At the same time, the size of the granule around the eggs, the severity of fibrosis in the tissues of the organs depend on the characteristics of the host's immune response, in particular on the level of production of antibodies, immune complexes, activity of suppressor T-lymphocytes, macrophages. Of definite importance are genetic factors, which, for example, affect the development of tubular-infertile fibrosis in the liver. Mature schistosomes are immune to the effects of immunity factors. An important role in this is played by the phenomenon of antigenic mimicry, which is characteristic of these parasites. Schistosomiasis can be a factor in carcinogenesis, as evidenced by the fact that tumors of the genitourinary system and colon are relatively common in the foci of this helminthiosis. Tumor growth in schistosomiasis is explained by the development of fibrosis in the organs, metaplasia of the epithelium, immunosuppression, as well as the synergism of the action of schistosomes, exogenous and endogenous carcinogens.