BASICS OF MEDICAL BIOLOGY - 2012

Phylum Roundworms (Nemathelminthes)

Main characteristics of the phylum: 1) the body is unsegmented, cylindrical or spindle-shaped, and round in cross-section; 2) they possess a primary body cavity filled with pressurized fluid (the fluid Functions as a hydrostatic Skeleton and transports nutrients); 3) unlike Flatworms, most Roundworms are dioecious; 4) circulatory and respiratory systems are absent; 5) the excretory system is either of the protonephridial type or represented by modified dermal glands; 6) unlike flatworms, the Digestive System features a third (posterior) section ending in an anus.

All roundworms that parasitize humans belong to the Class Nematoda.

Class Nematoda

Integument and locomotory apparatus. The Skin-muscular sac is formed by the cuticle, hypodermis, and musculature. The cuticle has a complex ten-layered Structure AND FUNCTIONS as an external skeleton to which Muscles attach, providing protection against mechanical and Chemical factors; it is insensitive to digestive juices. Beneath the cuticle lies the hypodermis, forming four cords that project deeply into the body cavity. Underneath the hypodermis is a single layer of longitudinal muscles divided by the hypodermal cords. Nematode movements are limited, occurring exclusively in the dorsal plane. Inside the skin-muscular sac lies the primary body cavity (pseudocoelom), which contains coelomic fluid and Internal Organs. A distinctive feature of this cavity is that it is not lined with mesodermal epithelium. The coelomic fluid is under high pressure, providing support for the muscular sac (hydrostatic skeleton). In some nematodes, it is toxic.

Digestive system is a tube beginning with the Mouth and ending with the anus. The mouth is located at the anterior end of the body and is surrounded by several cuticular outgrowths—Lips (2–6)—or takes the form of a buccal capsule with cuticular Teeth or plates. Anterior, middle, and posterior sections of the digestive tube are distinguished. The anterior and posterior sections are of ectodermal origin, while the middle section is endodermal. The posterior section terminates in the anus, which opens on the ventral side of the posterior end of the body.

Circulatory and respiratory systems are absent.

Excretory system is represented by 1–2 unicellular dermal glands. Outgrowths extend from the gland in the form of two lateral canals lying within the lateral hypodermal cords. Posteriorly, the canals end blindly, while in the anterior part they merge into a single unpaired canal that opens to the outside via an excretory pore situated behind the lips. The excretory function is also performed by specialized phagocytic Cells located along the excretory canals.

Nervous system consists of a circumoesophageal nerve ring from which nerve trunks extend—dorsal, ventral, and 4 lateral. The trunks are interconnected by commissures. Sense Organs are poorly developed.

Reproductive System. Reproduction is exclusively sexual. Nematodes are typically dioecious. Reproductive organs have a tubular structure. In males, the reproductive system is unpaired: Testis, vas deferens, ejaculatory duct (opening into the hindgut), and copulatory organ (spicules). The FEMALE REPRODUCTIVE SYSTEM is paired: Ovaries (producing ova), oviducts, and uteri, which merge to form an unpaired Vagina (opening to the outside at the anterior end of the body). In some species, the female possesses only a single reproductive tube. Nematodes exhibit Sexual Dimorphism, with males and females differing in external features. Males are smaller, and the posterior end of the body in some of them is curved toward the ventral side.

Life cycle is simpler than that of flatworms: the transformation of one larval form into another is generally absent. Most nematodes are geohelminths with direct development, lacking intermediate hosts. Fertilized eggs begin to develop in the Uterus, but the final Formation of the larva occurs only in the external environment without the involvement of an intermediate host. Larval development requires specific conditions: warmth, moisture, and free oxygen. The Development of other nematode species (biohelminths) occurs with the participation of an intermediate host. The larvae of many nematodes are characterized by migration within the host's body. Some nematode species are viviparous, meaning the egg develops to the larval stage within the female's reproductive tracts, and live larvae emerge from the female's body.

Medical significance. Many Representatives of the class Nematoda are human parasites. Diseases caused by roundworms (nematodes) are called nematodiases.

Large roundworm (Ascaris lumbricoides) is the CAUSATIVE AGENT OF ascariasis.

Geographical distribution is ubiquitous.

Localization: Small Intestine.

Morphology. Ascarids are yellow with a pinkish tint. The elongated spindle-shaped body is covered with a tough, glossy cuticle and tapers toward both ends. Females reach up to 40 cm in length, and males 15–25 cm. The posterior end of the female is conically pointed; in the anterior third of the body, There is a annular constriction where the external genital opening is located on the ventral side. The posterior end of the male is curved toward the ventral side. The mouth is surrounded by three cuticular lips—one dorsal and two ventral—bearing pairs of sensitive papillae. Longitudinal lateral lines, housing the canals of the excretory system, are visible on the lateral surfaces (Fig. 2.28).

Eggs can be fertilized or unfertilized. Fertilized eggs are round or oval, measuring 60–70×40–50 µm, and are yellow-brown in color. The outer protein coat is tuberculated, the middle one is glossy, and the inner one is fibrous, thick, smooth, and colorless. Inside the egg is a dark germ Cell. The protein coat may be absent. Unfertilized eggs are oval or irregular in shape and larger, measuring 80×55 µm. The entire cavity of the egg is filled with yolk cells.

Life cycle. Ascaris is a geohelminth parasitizing the human small intestine. It lacks specialized attachment organs, maintaining its position in the intestinal lumen through continuous movement against the food flow. It feeds on chyme. The female lays up to 240,000 eggs per day. These are not infectious. Excreted into the external environment with the feces of an infected person, the eggs develop under favorable conditions (free oxygen, warmth, moisture). In soil at an optimal moisture level and a Temperature of +24–25°C, a motile larva develops inside the egg in approximately 24 days, making it infectious. Humans become infected by swallowing infectious eggs. Eggs are introduced into the mouth via unwashed vegetables, fruits, and dirty hands. In the intestine, a larva hatches from the egg, penetrates the intestinal mucosa and Blood Vessels, and migrates through The Human Body via the bloodstream. Migration pathway: intestine – Liver – right Heart – Lungs. Free oxygen is essential for the development of ascarid larvae. They rupture blood capillaries and subsequently penetrate the alveoli, where they grow and molt twice. Next, they enter the bronchioles, Bronchi, Trachea, Larynx, and Oral Cavity. Swallowed again with saliva, the larvae re-enter the small intestine and develop into sexually mature forms. Migration takes about two weeks. The total duration of ascarid development from infection to sexual maturity is 70–75 days. The lifespan of adult ascarids in the human intestine is about a year.

Ascaris eggs are resistant to adverse environmental conditions and can remain viable for up to 6 years or more. They are resilient against various chemical agents but quickly perish under METABOLISM/18.html">The Influence of high temperatures. A temperature of +60°C kills them within 1–2 minutes, and +70°C destroys them in a matter of seconds. Flies and cockroaches play a certain role in the dissemination of eggs as mechanical vectors.

Pathogenic action. Ascariasis is a geohelminthiasis and an anthroponosis. The sole source of infection is an infected human. The transmission mechanism of the causative agent is fecal-oral.

The pulmonary stage of ascariasis is characterized by a cough, chest pain, and fever, often accompanied by urticaria, lasting up to 2 weeks.

The intestinal stage of ascariasis manifests as headaches, abdominal pain, dyspeptic disorders, mechanical damage to the intestinal wall, and The formation of abnormal intestinal Reflexes due to constant irritation of the intestinal walls. Ascarids absorb nutrients, contributing to hypovitaminosis and bodily exhaustion.

Complications of ascariasis may include intestinal obstruction. Cases of extraintestinal (atypical) localization of ascarids, associated with their high mobility, have been described. Most commonly, ascarids penetrate the liver, causing abscesses and obstructive jaundice due to the blockage of the Bile ducts. Instances of ascarids detected in the frontal sinuses, tympanic cavity, larynx, and other sites have also been reported.

Fig. 64. Internal Structure of an ascarid:

a - female; b - male; 1 - lips; 2 - nerve ring; 3 - Pharynx; 4 - phagocytic cells; 5 - Esophagus; 6 - midgut; 7 - lateral hypodermal cord with excretory canal; 8 - oviduct; 9 - uterus; 10 - Ovary; 11 - vagina; 12 - ventral hypodermal cord; 13 - vas deferens; 14 - testis; 15 - ejaculatory duct.

Fig. 65. Scheme of Ascaris larva migration in the human body.

Laboratory Diagnostics. Detection of larvae in sputum (larvoscopy) during the pulmonary stage of the disease; fecal ovoscopy (eggs may be absent in feces if only males or young ascarids parasitize the intestine), serological tests.

Prevention. Personal: wash hands before eating. Vegetables and berries consumed raw should be subjected to heat Treatment. To do this, thoroughly wash plant products first with clean cold Water, then dip them for 2-3 s in boiling water or for 8-10 s in hot water (70-76° C), and subsequently rinse with cold water. This ensures that vegetables, berries, fruits, and other greens are completely decontaminated from the eggs of ascarids, whipworms, and other geohelminths. Public: sanitary maintenance of populated areas, protection of soil from fecal contamination, and control of flies and cockroaches. Kitchen gardens and berry patches should not be fertilized with fresh human feces and pig excrement. Fertilizing gardens with feces is permissible only after composting them for one year (at least). Although the pig ascarid does not parasitize the human intestine, larval migration can occur within the human body and cause a morbid condition.

Whipworm (Trichocephalus trichiurus) - the causative agent of trichuriasis.

Geographical distribution - ubiquitous.

Localization - cecum, upper PARTS OF THE Large Intestine.

Morphology. The whipworm is 3-5 cm long. The anterior part of the body is narrowed and resembles a thread or Hair (hence the name), containing a long esophagus. All other organs are located in the posterior, widened part of the body. In males, the posterior end of the body is spirally coiled.

The eggs are yellowish-brown, measuring 50-54 x 22-23 µm, with a finely granular content. In shape, they resemble a lemon or a barrel with light plug-like structures at the poles.

Fig. 66. Whipworm (Trichocephalus trichiurus):

a - female; b - male; 1 - anterior end; 2 - posterior end.

Life cycle. The whipworm is a geohelminth and a strict human parasite. The source of infection is a person sick with trichuriasis. The transmission mechanism is fecal-oral. Whipworm eggs are discharged into the environment with the patient's feces. A larva develops inside the egg, reaching invasive maturity at a temperature of 25-30° C in approximately 25-30 days. Infection occurs by swallowing invasive eggs with unwashed vegetables, berries, fruits, or water. Under the action of gastric juice, the egg membranes dissolve, releasing larvae which, unlike ascarid larvae, do not migrate. They penetrate the villi of the small intestine and develop there for three to ten days. The villus is destroyed, and the larvae re-enter the intestinal lumen, descend, and attach to the wall of the cecum or large intestine. With its anterior thread-like end, the parasite deeply penetrates the intestinal wall, seemingly stitching through it, and feeds on blood (hematophagous) and Cells of the intestinal wall. 1-1.5 months after infection, the female begins to lay eggs. The lifespan of the whipworm is 5-6 years, and the female lays about 60 thousand eggs daily.

Pathogenic action. Trichuriasis is a geohelminthiasis and anthroponosis accompanied by paroxysmal lower abdominal pain, especially on the right side, loss of appetite, digestive disorders, dizziness, and epileptiform seizures in children. Blood tests show eosinophilia. Whipworms can cause inflammation of the vermiform Appendix. When treating trichuriasis, it must be borne in mind that drugs administered into the intestinal lumen have no effect on the whipworm, as it is a hematophage and does not feed on intestinal contents.

Laboratory diagnostics. Detection of eggs in the feces of an infected person.

Prevention. Personal: do not consume unwashed vegetables, berries, and fruits; wash hands after using the toilet; protect food from flies and cockroaches, which are mechanical vectors of helminth eggs. Public: health education; avoid fertilizing kitchen gardens with uncomposted human feces; construction of toilets according to Sanitary and hygienic standards; control of flies and cockroaches.

Old World hookworm (Ancylostoma duodenale) - the causative agent of ancylostomiasis.

Geographical distribution - predominantly in countries with subtropical and tropical climates; found in the South Caucasus and Central Asia. In temperate and even cold climates, foci of ancylostomiasis can occur in mines where relatively high temperature and humidity are constantly maintained.

Localization - duodenum.

Morphology. Small reddish parasites. The HEAD end is curved toward the ventral side (hence the name hookworm). The length of the female is 10-18 mm, and the male is 8-10 mm. In males, the posterior end is expanded into a bell-shaped copulatory bursa. A buccal capsule with 4 teeth is located at the head end, into which the ducts of two glands open. The secretion of these glands prevents blood clotting. With the capsule, the hookworm grasps an area of the intestinal mucosa and, attaching to it, feeds on blood (hematophage).

The egg is similar in shape to an ascarid egg, but the shell is smooth, thin, and transparent, measuring 66 x 38 µm. It is at the stage of 4-8 spherical blastomeres.

Life cycle. The hookworm is a geohelminth, a parasite exclusively of humans. Fertilized eggs are excreted into the external environment with the feces of an infected person. At a favorable temperature (25-27 °C), rhabditiform larvae hatch from the eggs within a day. They are non-invasive and characterized by the presence of two esophageal bulbs. The larvae molt twice. During the second molt, the cuticle detaches but is not shed, and the larva remains as if inside a sheath. Simultaneously, the esophagus reorganizes into a cylindrical shape, and the rhabditiform larva transforms into a filariform larva. Filariform larvae are invasive. They concentrate mainly in the upper soil layers and can also climb moisture-laden plant stems. Infection occurs in two ways: 1) through the skin upon contact of bare body areas with soil contaminated with invasive hookworm larvae (when a person walks barefoot or lies on the ground; in mines), and 2) through the mouth with vegetables or water contaminated with hookworm larvae. Larvae that have penetrated the human body through the skin undergo migration, sequentially passing into the right side of The Heart, pulmonary Arteries, alveoli, bronchioles, bronchi, trachea, and pharynx, where they are swallowed with saliva and enter the esophagus, Stomach, and duodenum, becoming sexually mature. They live in the intestine for 5-6 years. If the larva enters the human body through the mouth, migration generally does not occur. It is believed that oral infection is less common. The main route of infection is the active penetration of larvae through the skin. The source of infection is a person sick with ancylostomiasis. Those most frequently affected are people in constant contact with the soil: tea plantation workers, gardeners, ditchdiggers, and miners.

Fig. 67. Hookworm (Ancylostoma duodenale):

a - female; b - male; c - anterior end (cuticular teeth are visible in the buccal capsule).

Pathogenic effect. Ancylostomiasis is a geohelminthiasis and anthroponosis characterized by a chronic course, progressive weakness, headache, weight loss, iron deficiency chloranemia, and edema. The pathogenic effect of hookworms is caused by blood loss—which serves as their food source—and intoxication by the parasite's Metabolic waste products.

Laboratory diagnostics. Detection of eggs in feces and duodenal contents.

Prevention. Individual: in ancylostomiasis endemic areas, do not walk barefoot or lie unclothed on the ground. Avoid consuming unwashed garden produce and strictly follow personal hygiene rules. Public: detection and treatment of infected individuals; to prevent the Introduction of hookworms into mines, coprological examinations for helminth eggs are performed on all workers hired for underground labor; infected individuals are reassigned to surface work until completely cleared of hookworms; if larvae are detected in mines, the rock is treated with table salt. There are no endemic foci of ancylostomiasis in the mines of Ukraine.

New World hookworm (Necator americanus) is the causative agent of necatoriasis, which is clinically indistinguishable from ancylostomiasis. Consequently, these conditions are grouped together under ancylostomiasis. Necator is prevalent in tropical and subtropical climates, primarily in Asia and South America. Morphologically and biologically, it is very similar to Ancylostoma, though slightly smaller: females measure 8-13 mm in length, and males 5-10 mm. Instead of teeth, the buccal cavity contains two sharp cutting plates. The eggs are morphologically identical to those of the Old World hookworm. Diagnosis is performed as for ancylostomiasis. Prevention is the same as for ancylostomiasis.

Pinworm (Enterobius vermicularis) is the causative agent of enterobiasis.

Geographic distribution: ubiquitous.

Localization. Lower section of the small intestine and initial section of the large intestine.

Morphology. The pinworm is a small, white nematode. Females are about 10 mm long, and males 2-5 mm. The posterior end of the male is curved toward the ventral side, while in the female, it is awl-shaped and pointed. The anterior end features a cuticular Swelling called a vesicle, which surrounds the oral opening and assists in anchoring the helminth to the intestinal walls. A spherical swelling, the bulb, is located in the posterior part of the esophagus. The intestine is a straight tube. The reproductive system has a typical nematode structure.

Pinworm eggs are colorless, asymmetric (one side convex, the other flat), with a smooth, transparent shell. Their size is 50-60 x 20-30 µm. A larva can be observed inside the egg.

Life cycle. The pinworm is exclusively a human parasite. Pinworms attach to the intestinal wall using the bulb and vesicle. Males die after fertilizing the females. The female does not lay eggs within the intestine. The fertilized female migrates down toward the anal opening—chiefly at night when sphincter tone relaxes—emerges, and deposits between 10,000 and 15,000 eggs onto the perianal skin. Optimal conditions for egg development are a temperature of 34-36°C and high humidity (70-90%). Pinworm eggs become infectious within 4-6 hours. As the females crawl about, they cause skin irritation, leading to intense itching. During Sleep, patients with enterobiasis scratch the itchy areas. The eggs get onto their fingers, accumulating particularly under the fingernails, and are also scattered across bed linen. From the hands, they can be transferred to the mouth by the patient (especially in children with a habit of nail-biting). This results in reinfection (autoinfection). The egg is the infectious stage. The swallowed eggs hatch into larvae, which develop into mature forms in the intestine. No larval migration occurs. The lifespan of a pinworm is about 1 month. If no new infection occurs during this period, spontaneous recovery is possible. The pinworm is a contact helminth. The sole source of infection is a person suffering from enterobiasis. Unlike other helminthiases, a patient with enterobiasis poses an immediate epidemiological hazard.

Pathogenic effect. Enterobiasis is a contact helminthiasis and anthroponosis accompanied by nocturnal perianal itching. Gastrointestinal and nervous system disorders are observed - 234 -

such as nausea, loss of appetite, abdominal pain, and occasionally headaches, insomnia, and seizures in children. If pinworms penetrate the vermiform appendix, they can cause appendicitis. Pinworms may also contribute to the development of perineal fissures, dermatitis, and eczema, and can crawl into the vagina, causing vulvovaginitis.

Laboratory diagnostics. Detection of eggs in scrapings from the perianal skin folds. Adult pinworms that have emerged may occasionally be visible in the feces.

Prophylaxis. Strict adherence to personal hygiene rules and maintaining cleanliness in living quarters. It is especially important to instill hygienic habits in children, monitor the cleanliness of their hands and Nails, and keep their nails trimmed short. Infected children are advised to wear snug underwear at night, which must be washed in the morning and ironed damp with a hot iron. Community prophylaxis involves mass screening of children, particularly in organized childcare settings, followed by deworming. Wet cleaning should be performed in indoor spaces. Toys must be treated periodically with boiling water. Sanitary and educational outreach and raising the medical literacy of the population are of great importance.

Fig. 67. Pinworm (Enterobius vermicularis):

a - female; b - male; 1 - mouth; 2 - vesicle; 3 - esophagus; 4 - bulb; 5 - midgut; 6 - vaginal opening; 7-9 - parts of the reproductive system; 10 - anus.

Strongyloides (Strongyloides stercoralis) is the causative agent of strongyloidiasis. Geographical distribution: predominantly in tropical and subtropical countries, but also found in the temperate zone. Localization: small intestine.

Morphology. Sexually mature specimens are colorless and translucent: the female is 2-3 mm long, and the male is 0.7 mm long. The anterior end of the body is evenly tapered, and the posterior end is pointed. The buccal capsule is short, with four weakly defined lips.

Life cycle. The strongyloides is a geohelminth that parasitizes exclusively in humans. Its life cycle involves the alternation of free-living and parasitic generations. Rhabditiform larvae hatch from eggs in the human intestine and are passed into the external environment with the feces. Subsequent development of rhabditiform larvae can follow two pathways: 1) if a rhabditiform (non-infective) larva encounters unfavorable conditions in the soil, it molts and rapidly transforms into a filariform (infective) larva, which actively penetrates human skin and migrates through the right side of the heart, lungs, respiratory tract, and pharynx, and is then swallowed to reach the intestine. During migration (which lasts 17-21 days), the larvae develop into sexually mature forms. Fertilization can occur in the lungs and in the intestine; 2) if rhabditiform larvae encounter favorable conditions in the external environment (warmth, moisture, oxygen), they develop into males and females of the free-living generation, which live in the soil and feed on decomposing organic matter. Rhabditiform larvae hatch from the eggs laid by the female and, under favorable conditions, develop into sexually mature individuals once again. Under unfavorable conditions, the rhabditiform larvae of the free-living generation transform into filariform larvae capable of infecting humans and initiating the parasitic generation; 3) a third developmental pathway exists—autoinfection, or internal intestinal infection (development of parasites within the human intestine without emerging into the external environment). Rhabditiform larvae retained in the intestine transform into filariform larvae, penetrate the intestinal wall and subsequently the lumen of blood vessels, and begin a new developmental cycle. The source of infection is a person suffering from strongyloidiasis. Modes of transmission are the same as in hookworm infection. People who work with soil are most commonly infected. Epidemics of strongyloidiasis in mines have been described.

Pathogenic effect. Strongyloidiasis is a geohelminthiasis and anthroponosis characterized by impaired digestive function, pronounced toxic-allergic effects, mechanical tissue damage during larval migration, and lesions of the small intestinal mucosa that predispose to secondary infection. Inflammatory skin lesions may occur As a result of larval penetration through the skin.

Laboratory diagnostics. Detection of larvae (larvoscopy) in feces, which must be fresh and still warm.

Prophylaxis is the same as for hookworm infections.

Trichinella (Trichinella spiralis) is the causative agent of trichinosis. Trichinella larvae were first discovered in 1835 by James Paget, an English medical student (later a renowned English surgeon), in the muscles of a human cadaver.

Geographical distribution. Found on all continents except Australia and Antarctica.

Localization. Mature adults inhabit the wall of the small intestine, while larvae reside in striated skeletal muscles.

Morphology. Small, thread-like worms. The female is 3–4 mm long, and the male is 1.4–1.6 mm long (Fig. 2.33). A stylet is located in the buccal capsule. Trichinella females are viviparous.

Life cycle. Trichinella is a biohelminth parasitizing humans and numerous mammals. The host Organism serves as both the definitive and intermediate host simultaneously. Infection occurs via the alimentary route when consuming meat containing Trichinella larvae. Under the action of gastric juice, the meat and the wall of the capsule surrounding the larvae are digested. The larvae are released from the capsules, penetrate the mucous membrane of the small intestine, and develop into mature adult forms. The adults embed their anterior ends under the epithelium, while their posterior ends lie between the villi. In the intestine of humans and animals, adult Trichinella parasitize for a short period (no more than 42–56 days in humans). During this time, starting from the 4th day post-infection, the female produces up to 2,000 larvae (0.1 mm). Young Trichinella are carried by Lymph and blood streams to all organs and Tissues (migrating), but they settle exclusively in skeletal muscles. Most commonly affected are the Diaphragm, intercostal, masticatory, deltoid, and calf muscles. The larvae penetrate beneath the sarcolemma of the Muscle fiber, grow, and coil spirally. On the 20th–23rd day after infection, a thin Connective Tissue capsule forms around the spirally coiled larva and the adjacent area of sarcoplasm.

In the encysted state, larvae remain viable and infective for a very long period (virtually for the remainder of the host's life). Occasionally, a single capsule contains multiple larvae. Gradually, the capsule wall thickens and becomes impregnated with calcium salts (calcified).

Fig. 68. Trichinella (Trichinella spiralis):

a — female; b — male; c — encysted larva in a muscle fiber; d — main Circulation pathway of Trichinella in synanthropic foci.

For the larvae to develop into mature adults, they must enter the gastrointestinal tract of another host. This occurs when the meat of an infected animal is consumed by an animal of the same or a different species—for instance, if a rat is eaten by another rat or a pig. In The life cycle of Trichinella, humans act as a biological dead end, since upon human death the parasites are not transmitted to other hosts and perish. Humans become infected by consuming infected pork, pork products (sausage, ham, lard with meat streaks), or the meat of wild animals (wild boar, bear, badger, nutria, etc.).

Fig. 70. Encysted Trichinella larva in a human cadaver.

Fig. 71. Encysted Trichinella larvae in a compressed muscle squash preparation from pork.

Trichinosis is a zoonotic disease with natural foci. The circulation of Trichinella in natural foci is maintained through trophic links among numerous mammalian species, predominantly carnivores (wolves, foxes, etc.), as they feed on meat. In populated areas, synanthropic foci of trichinosis can form if anti-trichinosis regulations are violated. Within synanthropic foci, Trichinella circulate between domestic animals (pigs, dogs, cats) and synanthropic rodents (rats, mice). The spread of Trichinella is facilitated by free-range pig farming and the feeding of raw offal or carcasses of hunted game to domestic animals.

Pathogenic effect. Human cases often occur in groups or family outbreaks linked to a shared source of infection. The period of intestinal invasion corresponds to the incubation period of the disease, though heavy infections may be accompanied by abdominal pain and digestive disorders. During the migration phase, primary clinical symptoms appear: periorbital and facial edema, muscle pain, fever, and high eosinophilia (up to 40%). Severe infections can lead to complications such as damage to the myocardium, lungs, and Brain.

Trichinosis with severe complications can be fatal.

Laboratory diagnostics. The diagnosis is established based on the clinical signs mentioned above and confirmed by: 1) detecting Trichinella larvae in the meat suspected of causing the infection; 2) immunological tests. In rare cases, a muscle biopsy is performed to confirm the diagnosis (a surgeon excises a Muscle tissue sample measuring 3 × 1.5 cm).

Prevention. Individual prevention involves avoiding the consumption of meat that has not undergone veterinary and sanitary inspection. Thermal Processing of trichinotic meat is ineffective because Trichinella deep within pieces of meat remain viable and capable of causing infection. Public Prevention includes veterinary and sanitary inspection of pork and game susceptible to trichinosis (wild boar, badger, bear, nutria), proper disposal of infected meat, keeping pigs in well-maintained housing facilities, and sanitary education.

Guineaworm (Dracunculus medinensis) is the causative agent of dracunculiasis.

Geographical distribution. Iraq, India, tropical Africa, and several other countries. A focus of dracunculiasis previously existed in Bukhara, Central Asia, but was successfully eradicated between 1923 and 1932 thanks to the research and practical efforts of L. M. Isaev (1886–1964).

Localization. Subcutaneous tissue, typically near the JOINTS OF THE lower extremities.

Morphology. One of the largest human nematodes. The body shape is thread-like. Females reach a length of 30 to 150 cm with a thickness of 1–1.7 mm. Males are smaller, measuring 12–29 mm in length and 0.4 mm in thickness. Viviparous. The external genital opening is closed, so the larvae escape through a rupture of the uterus and cuticle at the anterior end.

Fig. 72. Guineaworm (Dracunculus medinensis).

Life cycle. The guinea worm is a biohelminth. Its life cycle involves a change of hosts. The definitive host is a human, though domestic and wild animals (horses, dogs, monkeys, etc.) may also serve as hosts, while the intermediate host is the freshwater copepod Cyclops. Only fertilized females are found in the subcutaneous tissue (copulation occurs at earlier Stages of the parasite's development). Residing in the subcutaneous tissue of the definitive host, the guinea worm forms a cord-like ridge, at the end of which a blister develops. Upon rupture of the blister, the anterior end of the worm protrudes through the resulting wound. When the blister is washed with water, the worm's uterus bursts, and the released larvae (microfilariae) are discharged into the water. Further larval development occurs when they enter a body of water and are swallowed by a copepod. Humans become infected by ingesting copepods carrying microfilariae when drinking raw, unfiltered water. The invasive stage is the microfilarial larva. In the human stomach, the copepod is digested, and the guinea worm microfilariae penetrate the intestinal wall and migrate to the subcutaneous tissue. The developmental cycle of the guinea worm was discovered by the Russian zoologist and traveler A.P. Fedchenko (1868).

Pathogenic action and diagnosis. Dracunculiasis manifests as itching and induration at the site of the parasite's localization. When localized near joints, the patient becomes unable to walk. The ulcers are painful and may also be complicated by secondary infections. In the late phase of the disease, prior to the appearance of ulcers, diagnosis can be established by the presence of clearly visible tortuous ridges beneath the skin at the sites of the parasite's localization.

Prevention. Personal: in endemic foci of dracunculiasis, avoid drinking raw, unfiltered water. Public: detection and treatment of infected individuals; draining of water bodies where infected copepods may reside; elimination of copepods in open water bodies; health education.

Filariae (Filaria) are the causative agents of filariasis. This group unites thread-like nematodes (from the Greek filus, meaning thread), which are prevalent in tropical and subtropical regions. Females give birth to live larvae, known as microfilariae. The transmission mechanism is vector-borne, with blood-sucking dipteran insects acting as vectors. Filariae include Wuchereria bancrofti, Brugia malayi, Onchocerca volvulus, and Loa loa.

Wuchereria bancrofti is the causative agent of bancroftian filariasis.

Geographical distribution. Asia (China, Japan, countries of the Indochinese Peninsula, India, Sri Lanka, the Philippines, Indonesia), as well as certain countries in Africa and South America.

Localization. Adult nematodes parasitize The Lymphatic system and connective tissue, while the larvae inhabit the Circulatory system.

Morphology. Sexually mature individuals are thread-like and milky-white in color. The female measures about 80-100 mm, and the male about 40 mm. The female is viviparous.

Life cycle. The definitive host is exclusively human, while the intermediate host and vector are mosquitoes of the genera Anopheles, Culex, Aedes, and Mansonia. In the Lymphatic vessels and nodes of the definitive host, males and females typically intertwine, forming a tangle. Females produce microfilariae that migrate from the lymphatic system into the circulatory system. During the day, the larvae reside in large blood vessels (such as the aorta and carotid artery) and the vessels of internal organs or muscles, whereas at night they move into peripheral blood vessels. Consequently, these larvae are referred to as nocturnal microfilariae (Microfilaria nocturna). This daily migration is explained by the synchronization of the parasite's and the vector's cycles. The vectors (mosquitoes) feed on humans primarily during nighttime hours. Along with the infected person's blood, the larvae enter the mosquito's stomach. From the digestive tract, they migrate to the thoracic muscles and subsequently to the proboscis. The duration of the developmental cycle within the mosquito ranges from 8 to 35 days, depending on temperature conditions. At the moment of a mosquito bite, the microfilariae rupture the Sheath of the proboscis, land on the skin, and actively penetrate it. Thereafter, they are transported to specific sections of the lymphatic system, where they develop into sexually mature forms. Their lifespan in the human body is approximately 17 years.

Pathogenic action. Bancroftian filariasis is a vector-borne biohelminthiasis and anthroponosis. By aggregating into tangles, Wuchereria can obstruct the lumen of lymphatic vessels, disrupting normal lymph circulation. As a result, the volume of the affected organ increases dramatically, sometimes reaching enormous proportions. Due to this condition, filariasis is commonly known as elephantiasis (Fig. 2.39). The lower extremities, genitalia, and Mammary Glands are most frequently affected. Occasionally, the disease is complicated by secondary bacterial infections.

Laboratory diagnosis. The sample for examination is blood, which is drawn at night. Microfilariae are detected under a Microscope. Immunological tests are also utilized.

Prevention. Personal: protection against mosquito bites. Public: detection and treatment of infected individuals, eradication of mosquitoes at all Selection/3.html">Stages of development using insecticides, agrotechnical measures for environmental sanitation, and health education.

Brugia malayi is the causative agent of brugian filariasis. In its Structure and Life cycle, it is similar to W. bancrofti. It differs by having a slightly smaller size: females reach up to 55 mm, and males measure 20-23 mm. They are viviparous.

Geographical distribution. More restricted, occurring exclusively in Asian countries (Indonesia, India, Vietnam, etc.).

Localization. Adult nematodes parasitize the lymphatic system and connective tissue, while the larvae inhabit the circulatory system.

Life cycle. The definitive host is humans, though cats, dogs, and monkeys may also serve as hosts. Intermediate hosts are the same species of mosquitoes as those for Wuchereria, most frequently mosquitoes of the genus Mansonia. The larvae are also detected in peripheral blood at night, though differing slightly in timing.

Laboratory diagnosis. Detection of microfilariae in peripheral blood. Blood is collected in the evening and at night. Immunological tests are employed.

Prevention. The same as for bancroftian filariasis.

Fig. 73. Elephantiasis caused by Wuchereria bancrofti.

Onchocerca volvulus is the causative agent of onchocerciasis. Onchocerciasis represents a major medical and socio-economic challenge for many countries worldwide. In Africa alone, approximately 20 million people suffer from onchocerciasis, of whom 1-2% become blind as a result of the infection.

Geographical distribution. Prevalent in countries of Africa and Central America (Mexico, Guatemala).

Localization: skin, subcutaneous tissue, Lymph Nodes, and visual organs.

Morphophysiological characteristics. The body is thread-like, white, and tapered at both ends. Females reach up to 50 cm in length, whereas males are considerably smaller, measuring 2.5-4 cm. Females give birth to tiny larvae (microfilariae) up to 0.03 mm in length.

Life cycle. The definitive host is humans, and the intermediate host is blackflies of the genus Simulium. When feeding on an infected person, blackflies ingest microfilariae into their stomach. Under favorable conditions, the microfilariae become infective within 6 days. When blackflies bite a human, the infective larvae penetrate the skin, migrate into the lymphatic system, then into the subcutaneous tissue and beneath muscle aponeuroses, where they develop into sexually mature individuals. Parasitizing the human body, the female gives birth to microfilariae, which accumulate in the skin. The source of infection is a person suffering from onchocerciasis. The invasive stage is the microfilaria.

Pathogenic action. Onchocerciasis is a vector-borne biohelminthiasis. The symptoms depend on the localization of parasite nodules and the intensity of the infection. A patient typically has 1-3 nodules (onchocercomas), though the number can reach up to 50, ranging in size from a pea to a pigeon's egg. A severe complication is ocular Damage caused by onchocercal larvae, frequently resulting in complete blindness. American onchocerciasis generally exhibits a more malignant course than the African variant: blindness occurs more frequently, and due to nodule positioning in the periost, perforation of the cranial bones and nervous system disorders are possible. Microfilarial parasitism leads to lymph stasis and ulceration. Metabolic products of the parasites cause systemic allergic reactions. Treatment is surgical.

Laboratory diagnostics. If clinical diagnosis through physical examination proves difficult, biopsy and histological examination of the nodule are performed.

Prevention. Individual protection involves avoiding blackfly bites. Community-wide measures include detecting and treating infected individuals, and eliminating blackflies in their breeding sites—most commonly rapid, rocky mountain streams—along with public health education.

Fig. 74. Life Cycle of Onchocerca volvulus:

a - definitive host (human): top right - male and female parasites; b - section of a subcutaneous nodule with onchocerci; 2 - microfilariae from the subcutaneous connective tissue; 3 — microfilariae in the blood; b - intermediate host (blackfly Simulium damnosum); 4 - infective larvae from the mouthparts of the intermediate host.

Loa loa is the causative agent of loiasis.

Geographical distribution - equatorial Africa, tropical rainforest zone.

Localization. Adult filariae parasitize the subcutaneous connective tissue and subserosal layers, migrating at a speed of 12.5 mm per minute, and are particularly often observed beneath the conjunctiva of the eye. From there, they can move into the vitreous body, deep into the Orbit, and return to the anterior chamber of the eye. The parasite is clearly visible in the eye to the naked eye, and its movements are rapid.

Morphology. The body is thread-like, translucent, white or yellowish, covered with numerous rounded protuberances. The male is 30 mm long and 0.43 mm thick, while the female reaches 50-70 mm in length and 0.50 mm in thickness.

Life cycle. The definitive host includes humans and monkeys; the intermediate hosts are deer flies of the genus Chrysops. Fertilized females give birth to microfilariae, which travel via the lymphatic and blood vessels to the lung capillaries and, within a few weeks, systematically migrate into peripheral blood vessels. This species exhibits diurnal periodicity, hence the name Microfilaria diurna. This is due to the biological traits of deer flies, which display daytime activity. Deer flies become infected by biting an infected person. Within 7-10 days inside the fly, the larvae migrate to its head. When the fly bites a healthy person, the microfilariae pass onto the skin and rapidly penetrate its deeper layers.

Pathogenic action. Loiasis is a vector-borne biohelminthiasis. The parasite's impact on the human body is both toxic and mechanical. An early and persistent symptom is the sudden development of dense edema of the skin and subcutaneous tissue (known as Calabar swelling).

Laboratory diagnostics. Microscopic blood examination, immunological tests.

Prevention. Personal protection includes preventing deer fly bites. Public measures involve identifying and treating infected individuals, controlling deer fly populations, and health education.

Animal ascarid larvae are the causative agents of cutaneous and visceral larva migrans syndromes. The larvae of certain animal ascarids, which migrate within their obligate hosts, are capable of similar migration in the human body; however, in this abnormal host, they cannot complete their full developmental cycle. The clinical syndrome resulting from this phenomenon is known as larva migrans, which manifests in cutaneous and visceral forms.

In humans, larval toxocariasis is the most common form, caused by ascarid larvae of the genus Toxocara: Toxocara canis and T. mystax. T. canis parasitizes the intestine of canids (dogs, wolves, foxes, arctic foxes), while T. mystax parasitizes felids (domestic cats, wild felines), which serve as their obligate hosts. Humans act as a accidental host, in which these helminths persist only in the larval stage. Infection occurs when infective eggs enter the gastrointestinal tract. Eggs are primarily introduced into the mouth via contaminated hands—most commonly in children playing in soil—as well as through unwashed vegetables and fruit. The larvae hatch and migrate through various organs and tissues, where they encyst and remain viable for several years. Eventually, they become surrounded by granulomas, then fibrous tissue, and die. Migration can persist for up to 10 years (based on primate experiments).

Toxocariasis is observed primarily in children aged 1.5 to 4 years. Its main symptoms include allergies, urticaria, pulmonary edema, hepatomegaly, and eosinophilia. Various skin rashes and small nodules may also appear. Many infected children exhibit pica (depraved appetite), attempting to eat soil, lime, or chalk. Signs of Central Nervous System involvement are frequently detected, including irritability, sleep and behavioral disorders, as well as encephalitis and meningitis. Ocular toxocariasis is a specific clinical variant affecting the retina, lens, and iris, which can lead to Vision loss. A definitive diagnosis of toxocariasis is established upon detecting larvae in tissue biopsies.

Prevention: protecting gardens, playgrounds, and public parks from animal fecal contamination, screening and treating cats and dogs, and practicing personal hygiene.

Laboratory Diagnostics of Helminthiases

Adult helminths residing inside the host organism continuously produce eggs or larvae. Depending on the parasite's localization, these are either released into the environment or accumulate in the blood, lymph, and other tissues. The detection of specific helminths, their eggs, or larvae forms The basis of the laboratory diagnostics of helminthiases. Eggs or larvae are most commonly excreted into the environment with feces. Therefore, fecal examination, or coprological analysis (from Greek *kopros* — feces), is the most frequently performed Procedure. The main Methods used include helmintoscopy, helminthoovoscopy, and helmintholarvoscopy.

Helmintoscopy is a laboratory diagnostic method based on the detection of intact helminths or their fragments. This is a macroscopic method performed without a microscope, using a magnifying Glass only when necessary. Macroscopic fecal examination is used either to detect helminths expelled after deworming or to identify segments or fragments of tapeworms that periodically detach from the strobila and are excreted with feces.

The technique of helmintoscopic examination is as follows: small portions of feces are mixed with water and examined under good lighting in glass trays with black paper placed underneath; helminths and any suspicious white structures are removed using forceps or a pipette for further study. The successive sedimentation method is more commonly used in helmintoscopy. For this, the entire fecal sample is stirred with water in glass cylinders, allowed to settle for a few minutes, the supernatant is decanted, and the sediment is refilled with water and stirred. This is repeated several times. Once the liquid becomes clear, it is decanted, and the sediment is examined in small portions in a glass tray or Petri dish against a dark Background.

Helminthoovoscopy is a laboratory diagnostic method for detecting helminth eggs in feces.

Direct smear method. A pea-sized sample of feces is placed on a glass slide (6 x 9 cm) in a 50% aqueous glycerol solution, mixed with a wooden applicator stick, large undissolved particles are removed, and the preparation is examined microscopically without a coverslip. Native smears can reveal eggs of all helminth species. However, this method has low sensitivity because when eggs are few in number, they may be missed. More accurate methods rely on concentrating the eggs contained in a sample into a small volume (so-called concentration methods), such as Fülleborn's method, Kalantaryan's method, etc.

Fülleborn's flotation method. This method is based on the flotation of helminth eggs in a saturated sodium chloride solution (specific gravity 1.2). A high porcelain or glass beaker (50-100 ml) is filled with 2.5-5 g of feces, and saturated sodium chloride solution is gradually added while thoroughly mixing the feces. The solution is filled almost to the brim. Wooden sticks, replaced each time, are most convenient for mixing. Large particles floating to the surface are removed, and the mixture is left to stand for 45 minutes. During this time, due to differences in specific gravity, the lighter eggs float and concentrate in the surface film, while large insoluble fecal particles settle to the bottom. Using a wire loop bent at a right angle, the surface film is skimmed, transferred onto a microscope slide, covered with a coverslip, and examined under a microscope. At least four preparations are examined. The loop is sterilized over a spirit lamp. While effective, this method fails to float eggs of trematodes, taeniids, the broad fish tapeworm (due to their greater weight), and unfertilized Ascaris eggs (whose shell is permeable to salts). Therefore, examining both the surface film and the sediment is necessary, which complicates the procedure.

Fig. 75. Eggs of trematodes and cestodes:

1 - Nanophyetus; 2 - cat liver fluke; 3, 4 - lancet liver fluke (immature and mature); 5 - Chinese liver fluke; 6 - lung fluke; 7 - Metagonimus; 8 - Fasciola; 9 - Japanese blood fluke; 10 - urogenital blood fluke; 11 - Manson's blood fluke; 12 - taeniids; 13 - dwarf tapeworm; 14 - broad fish tapeworm.

The Kalantaryan method is a slightly modified version of Fülleborn's method. Instead of a saturated sodium chloride solution, a saturated sodium nitrate solution (specific gravity 1.38) is used. During the examination, eggs of the broad fish tapeworm and unfertilized Ascaris eggs also float to the surface. The disadvantage of this method is that sodium nitrate is more expensive than sodium chloride.

There are also helminthovoscopical Methods based on THE PRINCIPLE OF sedimentation, where eggs settle in a solution whose specific gravity is lower than that of the eggs.

Fig. 76. Nematode eggs:

Ascaris: 1 - fertilized, with a protein coat; 2 - unfertilized, with a protein coat; 3 - fertilized, without a protein coat; 4 - whipworm; 5, 6 - pinworm: freshly passed and with a larva; 7 - hookworms.

Pinworms lay their eggs in the perianal region; therefore, Laboratory Diagnosis of enterobiasis relies on a specific technique known as the perianal tape test (or perianal scraping). A cotton swab tightly wound around a wooden stick and moistened with a 50% aqueous glycerin solution is used to gently scrape the perianal folds. The stick with the swab is then placed in a dry test tube and sent to the laboratory. In the lab, the eggs are washed off the swab using 1-2 drops of a 50% aqueous glycerin solution, and 4 preparations are made on two glass slides. Alternatively, a wooden spatula (such as a cleaned matchstick) moistened with a 50% aqueous glycerin solution or sticky cellophane tape can be used. In addition to pinworm eggs, this method also detects beef tapeworm eggs.

Helmintholarvoscopy is a method used to detect helminth larvae. In certain helminthiases (such as strongyloidiasis), larvae rather than eggs are excreted in the feces, and the Baermann method is employed for their detection. This method is based on the natural tendency of helminth larvae to migrate toward heat. A glass funnel, fitted with a rubber tubing and a pinchcock at its lower, narrow end, is mounted in a laboratory stand. A 5-10 g sample of feces is placed onto a small sieve lined with double-layered gauze. The sieve is then immersed in the funnel, which is filled with warmed water (40–45°C) so that the lower part of the sieve is submerged. The larvae actively migrate out of the feces into the warm water and concentrate in the rubber tubing. After 4 hours, the water from the tubing is drained into a centrifuge tube and centrifuged. The supernatant is discarded, and the sediment is examined microscopically.

Morphology of Helminth Eggs

The identification of helminth eggs takes into account the following features: size, shape, shell structure, and internal Organization.

Trematode Eggs.

1. The egg of Fasciola is oval, yellowish-brown, and enclosed in a thin shell. It measures 130–150 µm in length and 70–90 µm in width. One pole features an operculum, while the opposite pole bears a small, flattened prominence.

2. The egg of Dicrocoelium is asymmetrical and dark brown. It measures 38–45 µm in length and

— 22–33 µm in width. The shell has a thickened wall. An operculum is present at one pole, and two large cells can be distinguished within the egg.

3. The egg of Opisthorchis is grayish-yellow, measuring 26–32 µm in length and 11–15 µm in width. The shell is thin and smooth. One pole is broadened and features a minor shell thickening resembling a tiny spine. The internal content is finely granular.

4. The egg of Paragonimus is golden-brown, oval, with a distinct operculum at one pole. It measures 80–118 µm in length and 48–60 µm in width. The shell is thick.

5. The egg of Schistosoma is oval with a spine located at one pole. It measures 120–150 µm in length and 40–60 µm in width. Eggs of other schistosome species vary in size, but the presence of spines is a consistent diagnostic feature.

Cestode Eggs.

1. The egg of the broad fish tapeworm is oval, grayish-brown, and covered with a thin, double-contoured shell. One pole bears an operculum, and the other has a small protuberance. It measures 68–72 µm in length and 54 µm in width.

2. The egg of the pork tapeworm possesses a very delicate outer membrane that easily disintegrates in the external environment. Inside lies an oncosphere with three pairs of hooks, surrounded by a thick, radially striated brown shell. The egg measures 31–36 µm in length and 20 µm in width.

3. The egg of the beef tapeworm is nearly spherical. There are 1–2 filamentous appendages on the sides of the egg. It measures 30–40 µm in length and 20–30 µm in width. The membrane of the oncosphere is radially striated.

4. The egg of the dwarf tapeworm is ellipsoidal or spherical, with a transparent, colorless shell. Its diameter is 40–50 µm, and the oncosphere measures 29–30 µm. The egg features long, thread-like filaments at the poles.

Nematode Eggs.

1. The Ascaris egg is oval-shaped and dark brown. A fertilized egg is 50-70 µm long and 40-50 µm wide. It is covered by 3 membranes: the outer membrane is bumpy and proteinaceous; the middle one is glossy; and the inner one is fibrous and lipoid in nature. There is clear space at the poles. Unfertilized Ascaris eggs are larger and contain an egg cell inside.

2. The pinworm (Enterobius vermicularis) egg is asymmetrically oval with one flattened side. It is 50-60 µm long and 23-30 µm wide, covered with a thick, colorless membrane. The egg contains a larva inside.

3. The whipworm (Trichuris trichiura) egg is golden-yellow, barrel-shaped, and covered with a thick membrane. It is 50-54 µm long and 22-23 µm wide, featuring plug-like, light-colored structures at the poles.

4. Ancylostomatid eggs are colorless, oval-shaped, with bluntly rounded poles and a thin membrane. The egg contains 2-4 Cleavage stages. It is 56-76 µm long and 34-40 µm wide.

K.I. Skryabin's Doctrine of Deworming and Devastation

K.I. Skryabin was a prominent Russian helminthologist and founder of the USSR school of helminthology. He established the world's first specialized Institute of Helminthology (Moscow), which has borne his name since 1939. He authored a unique 25-volume monograph, "Trematodes of Animals and Man," the first 12 volumes of which were awarded the State Prize (1957). Together with his students, he also created the 25-volume "Essentials of Nematology." He was named a Hero of Socialist Labor in 1958.

K.I. Skryabin developed the fundamental methods for combating helminthiases: the principle of deworming (1925) and the principle of devastation (1944). Anti-helminthic measures comprise both therapeutic and preventive actions. Therapeutic measures are implemented through deworming—the administration of specialized medications (anthelminthics) that rid the human or animal body of helminths. Rational prevention of helminthiases involves not only mass, planned deworming of the population, but also a comprehensive set of measures to protect the environment from contamination with infectious material. The success of these public health efforts largely depends on the public's sanitary awareness, the adoption of hygiene habits in daily life, and a conscious approach to personal prevention.

Devastation is a system of measures aimed at the complete eradication of helminths at all stages of development and in all their habitats (host organism, external environment). Total devastation refers to the complete elimination of specific helminth species in a given territory. An example is the complete eradication of the dracunculiasis pathogen in Uzbekistan (Old Bukhara) under the leadership of L.M. Isaev in 1923-1932.

Partial devastation is not a complete eradication, but rather a sharp reduction in the incidence of certain helminthiases in specific areas. An example is the elimination of an ancylostomiasis focus in a mine.

Current problems of Medical Helminthology in Ukraine

Parasitic diseases are a widespread pathology in Ukraine, infecting approximately 20% of the population annually. The most common human helminthiases include geohelminthiases (ascariasis, trichuriasis) and enterobiasis. Among biohelminthiases, trichinosis and echinococcosis are extremely dangerous. Between 1960 and 1980, 770 cases of trichinosis were recorded in Ukraine, with 37% of local cases originating in Vinnytsia and Khmelnytskyi regions. Domestic pigs served as the primary source of infection. Although anti-helminthic control measures implemented in Ukraine helped achieve a certain decline in the incidence of major helminthiases, the socio-economic instability of the 1990s led to a significant deterioration in the epidemiological situation regarding parasitic diseases. Recently, foci of trichinosis have resurged and are now also registered in southern and central regions where they were previously absent. In addition to domestic pigs, wild boars (in Zakarpattia and Kherson regions) serve as a source of infection. In southern Ukraine, there has been an increase in human echinococcosis, which accounts for 40% of all fatalities caused by parasitoses. Ukraine also harbors natural foci of opisthorchiasis: in the basin of the Dnipro River and its tributaries, infection rates reach 4.3–61.1% among the human population, 0.6–2% among Mollusks, up to 20–60% in fish, and up to 70% in cats. Protecting water bodies and household plots from fecal contamination (with helminth eggs and protozoan cysts) is particularly urgent for the northwestern regions of Ukraine, where the incidence of geohelminthiases is 2 to 4 times higher than the national average. Furthermore, cross-border and domestic migration flows, which have intensified recently, pose a growing threat to the spread of human parasitic diseases.