Strongyloidiasis - Causes and Pathogenesis

Causes of Strongyloidiasis

The cause of strongyloidiasis is Strongyloides stercoralis (intestinal eel) - a small dioecious nematode, belongs to the type Nemathelminthes, class Nematoda, order Rhabditida, family Strongyloididae. In the development cycle of S. stercoralis, the following stages are distinguished: free-living and parasitic sexually mature individual, egg, rhabditiform larva, filariform larva (invasive stage). Development occurs without an intermediate host.

Mature parasitic females are 2.2 mm long and 0.03-0.04 mm wide and have a colorless thread-like body tapering toward the anterior end and a conical tail. Free-living females are somewhat smaller: 1 mm long and about 0.06 mm wide. Free-living and parasitic males are the same size (0.07 mm long and 0.04-0.05 mm wide).

The development cycle of S. stercoralis is complex, several variants are possible. In the first variant of development, sexually mature helminths parasitize in the host organism (human), the larvae develop in the environment. In the second variant, sexually mature forms are formed in the environment, reproduction and development of all stages of the helminth occur without the participation of a warm-blooded host. In the third variant, the larvae, without leaving the host organism, transform into sexually mature forms. Thus, the parasitic and free-living generations of this helminth alternate.

In the human body, sexually mature worms parasitize in the upper sections of the small intestine, sometimes in the bile and pancreatic ducts, but most often in the Lieberkühn crypts, where females lay up to 40 eggs daily (about 0.05x0.03 mm in size), from which rhabditiform larvae emerge and enter the environment with feces. The larvae are 0.25x0.016 mm in size, have a conically pointed posterior end of the body, and an esophagus with double expansion (rhabditiform esophagus). Under unfavorable environmental conditions, the rhabditiform larvae molt and after 3-4 days turn into filariform larvae (invasive stage), which are somewhat larger in size (0.5x0.017 mm), have a slightly split posterior end of the body, and a very thin esophagus. The larvae are able to move in the soil. The larvae actively penetrate the human body through the skin or are passively carried in through the mouth with contaminated vegetables, fruits, and water. In all types of infection, the filariform larvae migrate through the host's body, like the larvae of the roundworm. The females penetrate the intestinal mucosa and begin to lay eggs 17-28 days after infection. In the case of S. stercoralis invasion, the pathogenic effect is due to the strong sensitizing property of their antigens, especially at the stage of larval migration. At the same time, the parasites cause a partial immune response to superinvasion, which limits their spread beyond the small intestine.

Under favorable environmental conditions (temperature and soil moisture), rhabditiform larvae give rise to a sexually mature generation (females and males). When temperature and humidity change, and nutritional deficiencies occur, rhabditiform larvae turn into filariform larvae that infect the host, and the worms switch to a parasitic lifestyle.

If rhabditiform larvae remain in the intestine for more than 24 hours (in the presence of diverticula, constipation), they transform into invasive filariform larvae, which have the ability to immediately penetrate the intestinal mucosa or skin of the perianal region. The phenomenon of self-infection (autosuperinvasion) causes the long-term course of strongyloidiasis (sometimes tens of years) and high intensity of invasion.

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Pathogenesis of strongyloidiasis

In the early stages, pathological changes in tissues and organs along the migration routes of larvae are caused by sensitization of the body by the products of helminth metabolism and their mechanical impact. Parasitism of females and larvae causes an inflammatory reaction in the gastrointestinal tract. During migration, larvae can enter the liver, lungs, kidneys and other organs and tissues, where granulomas, dystrophic changes and microabscesses develop. In immunodeficiency states caused by long-term use of glucocorticoids or cytostatics, HIV infection, hyperinvasion and disseminated strongyloidiasis occur. S. stercoralis parasitize the host organism for many years. A long-term asymptomatic course of intestinal invasion is possible, which can quickly reactivate when cellular immunity is suppressed.