Zaporozhyan state medical university departement of infectious diseases

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Biogelmintiasis behave to the 3-th group. Their agents pass the cycle of 

development with changing of 2—3 hosts. Last host is final (definitive), in him a 

helmint becomes adult. Other hosts the larval stages parasitize in which -  

intermediate. Contamination biogelmintiasis can take place per oral or 

percutaneous by a way. For example, at schistosomiasis,  larvae actively inculcated 

in a skin or at a bite insects (mosquitoes, horse-flies).  

Pathogeny. The feature of pathogeny of helminthisms is impossibility of 

exciter to propagate oneself in the organism of man. Intensity of invasion is 

determined the amount of eggs (larvae) of helmint, gettings in an organism. 

Intensity of invasion is determined by expressed of clinical displays illness. For the 

organism of man the most expressed pathogenic properties are possessed by the 

larval stages of helmints. In pathogeny of helminthisms select two stages: sharp  

and chronic (from a few months to many years). 

Clinical presentation. Acute stage (from a few days to 2—3 months) 

characterize migration of larvae and toxic and allergic reactions. Toxic substances 

(enzymes, proteins, metabolites) have antigen and sensibilizating properties. An 

inflammatory reaction develops on the ways of their migration. Acute stage are 

characterize fever, pains in muscles and joints, general intoxication, eruption, 

edemata, «volatile» infiltrates in lungs, hypereosinophilia. Organic damage of 

different organs develop therefore: myocarditis, hepatitis, pneumonia, 

encephalopathy. At a massive invasion the necrotic damage of internals organs are 

possible.  In a chronic phase clinical presentation are determined localization of 

parasite and conditioned the local damage of mucous membranes. For example, 

Ankylostoma and Cestode injure the mucous membrane of intestine, Opistorchis - 

biliation ways, Schistosoma - colon and urination ways, Echinococcus cyst is a 

general bilious channel and cause a subhepatic icterus. Consuming nutritives 

helmints are instrumental in development of hypotrophy, albuminous failure, 

hypovitaminosis. At helminthisms development autoimmune reactions, reducing 

resistance to the bacterial and viral infections. After the release of organism from a 

parasite circulation of specific antibodies is halted within the limits of 1 year. 

Diagnostics. Helminthisms haven’t specific clinical symptoms. Laboratory 

diagnostics has an important value.  

A research purpose is an exposure of eggs, larvae, helmints of adult or their 

fragments (segments). They can be visible macroscopically (for example, 

ascarides, segments of tapeworm et cetera). 

For finding out helmints probe feces, urine, duodenal content, sputum, 

scrape from a perianal folds, blood, biopsy tissues.  For diagnostics of tissue 

helminthisms use serum methods (RDGA, RCK, elisa and other). Additional 

instrumental methods used (endoskopy, ultrasonoscope, CT, MRT). 

Treatment. For treatment of helminthisms use antihelminthic chemo 

preparation. Depending on the type of helminthism and possibility of side effects 

treatment is conducted ambulatory or in permanent establishment. On testimonies a 

chemotherapy is combined with the use of antihistaminic and antihelminthic and 

anti-inflammatory preparations, sometimes steroids. 

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NEMATODOSES 

 

ASCARIDOSIS (syn. - ascariasis, lumbricosis) is the anthroponotic 

geohelmintosis, belongs to nematodosis. 

Etiology. Human Ascarides (Ascaris lumbricoides) are the agent of 

ascaridosis. Grown-up individuals are fusiform. The female length is 20-40 sm., 

male – 15-25 sm. Each female lays about 200 000 eggs daily, which are not 

invasion but getting into the soil with excrements at the optimal temperature ( +24-

30° C), humidity and aeration in 12-14 days, became matur up to invasion stage, 

which may cause the disease of a man. At the temperature lower then 12°C 

development doesn’t occur, but vitability of the eggs and developing larvas are 

preserved.  

Epidemiology.  Man ill with ascaridosis is the source of invasion. 

Mechanism of infection is fecaly-oral, which is realized by alimentary way. The 

ascaride eggs excreted by invasion sources together wich feces get to the external 

medium, became mature in the soil, contaminate vegetables, berries, fruits and 

hands, articles of daily use, which become the factors of invasion transmission. 

The contamination takes place at swallowing of mature eggs, that why the patients 

ill with ascaridosis  can't be the source of invasion for people at everyday contact. 

At present time the great danger for spreading of Ascaridosis have the private plats 

of cultivated lands, where sometimes not purified human feces are used for 

fertilizing soil. 

Pathogenesis. From mature eggs swallowed by man, in small intestine the 

larvas go out, penetrate into intestine wall and bloody capillaries, then by blood 

migrate into liver, lungs and other organs. Early (migrate) phase of pathogenesis 

begins, which means sensabilisation by products of Ascarides larvas metabolism 

and traumatisation of tissues during their migration. During larvas migration 

inflammatory cellular infiltrates with great amount of eosinophiles (in liver, lungs) 

are formed, which may have clinical manifestation or develope asymptomatic. In 

lungs larvas get into the alveoles and bronchioles, move along the small and large 

bronchus, with the help of ciliary epithelium to stomatopharynx, where swallowing 

of larvas together with sputum takes place. The larvas getting into intestine become 

pubertal during 70-75 days. The late phase of pathogenesis (intestinal) depends on 

parasiting of mature helminth in the intestinum tenue lumen and is characterised 

with mechanical affection of mucose membrane and also with toxic action of 

helminth metabolism products on different organs and tissues and first of all on 

nervous system. Ascorides don’t fix itself in intestinum. But are kept, leaning with 

its ends against intestine wall. That`s why they can descend and ascend along the 

intestine, to penetrate into stomack and then through esophagus into throat, in 

respiratory tract and even into frontal sinus.  

Symptomes and course. The clinical manifestation of ascaridosis depend 

on parasites localization and intensity of invasion. Ascaridosis in clinical 

manifistation has two phases – early (migratory) and late (intestinal). The first 

phase coincides with larvas migration period, the second phase depends on 

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