Morphology and etiology of trematodosis in livestock animals
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Morphology of trematodes and economic damage from fascioliasis
Fascioliasis is a dangerous helminthic disease of sheep, goats, cattle, and other mammals, including humans. The causative agents are leaf-shaped flukes (trematodes) that parasitize in the bile ducts of the liver. The infection follows a chronic or acute course, causing severe metabolic disorders and systemic damage to the liver. Productivity in infected livestock animals decreases sharply, the quality of meat and wool deteriorates, mortality is possible, and affected livers are culled in large quantities during veterinary-sanitary meat inspection.
- Decrease in milk yield in cows — 25—40%
- Size of the common liver fluke — 2–3 cm in length, 1 cm in width
- Size of the giant liver fluke — up to 7.5 cm in length
- Development of larvae in the mollusk — 2–3 months
- Maturation of the parasite in the livestock organism — 2.5–4 months
- Lifespan of flukes in the liver — several years
| Productivity indicator | Decrease in productivity |
|---|---|
| Milk yield in cows | 25—40% |
Trematodes are a class of leaf-shaped flatworms (biohelminths) ranging in size from 0.1 mm to 10–15 cm. Their body is covered with a dermo-muscular sac containing internal organs. Located at the anterior end of the body is an oral sucker with a mouth opening, followed by a pharynx and an elongated esophagus. The intestine consists of two blind-ending trunks; there is no anal opening, so food remains are expelled through the mouth. To attach to the host's tissues, the parasite uses a ventral sucker on its ventral surface.
The excretory system consists of a network of tubules with an excretory pore at the posterior part of the body. The nervous system consists of subesophageal ganglia and branching nerve trunks. With the exception of certain orders, trematodes are hermaphrodites with a complex reproductive system. The male apparatus includes two testes, vasa deferentia, and a common duct within a muscular bursa. The female apparatus consists of an ootype (where fertilization and egg formation occur), an ovary, a seminal receptacle, and vitelline glands that provide the eggs with nutritional material.
The disease is caused by two species of trematodes: the common liver fluke (2–3 cm long and 1 cm wide) and the giant liver fluke. The giant liver fluke is distinguished by its larger size (up to 7.5 cm long, with an elongated body shape and parallel edges), as well as by its specific developmental cycle and pathogenicity.
Fasciola life cycle and dynamics of livestock infection
Fasciola develop via an alternation of hosts. Sexually mature individuals (maritae) in the bile ducts of the liver release a huge number of eggs, which pass with bile into the intestine and are excreted into the external environment. The first intermediate hosts are mollusks: for the common liver fluke, it is the dwarf pond snail, and for the giant one, it is the ear pond snail. In the development of certain other trematode species, additional hosts such as fish, amphibians, insects, or mollusks may be involved.
- Development of the miracidium: under favorable conditions, a ciliated larva 0.15 mm in length, which swims actively in water, forms within the egg over 2 weeks.
- Parasitism in the mollusk: the miracidium penetrates the body of the dwarf pond snail, sheds its cilia, migrates to the liver, and transforms into a mother sporocyst. Through asexual reproduction, rediae are formed from it, followed by hundreds of cercariae with suckers and a tail appendage. This stage takes 2–3 months.
- Formation of the adolescent: cercariae exit the mollusk into the water, shed their tails, and encyst on plants or the water surface, forming a dense protective shell.
- Ingestion: livestock animals become infected by consuming grass, fresh hay, or at watering places from contaminated water bodies. In the intestine, the cyst wall is destroyed.
- Migration to the liver: young flukes penetrate the bile ducts in two ways: by piercing the intestinal wall and liver capsule with development in the parenchyma over several weeks, or hematogenously — through the intestinal and portal veins.
The primary infection of animals occurs via the ingestion of adolescents formed from eggs laid in the spring. The dwarf pond snail is widespread in pastures and often congregates near watering places. The peak of cercariae release from mollusks occurs in late summer and autumn. Considering that the maturation of the fluke in the organism of the definitive host takes from 2.5 to 4 months, the first parasite eggs are detected in livestock feces in late autumn, and their mass shedding occurs in December — January. Adult flukes are capable of living for several years in the liver of ruminants.
Fasciola eggs are extremely sensitive to drying, decay, as well as to the effects of high and low temperatures. This is important to consider when carrying out preventive measures on pastures and watering sites.
Fascioliasis: symptoms, treatment, and prevention
The pathogenic effect of flukes begins during the period when larvae migrate from the intestine to the bile ducts of the liver. Adult parasites, while moving through the bile ducts, injure tissues and block them when present in large numbers. The waste products of the helminths exert a pronounced toxic effect on the liver tissue and the organism as a whole. The disease in sheep and goats follows an acute or chronic course, with the acute phase caused by the simultaneous intake of a large quantity of adolescents and accompanied by acute hepatitis.
In the acute form in sheep, pallor of the conjunctiva, depression of appetite, bloody diarrhea, tympany, constipation, dyspnea, and tachycardia are observed. Chronic fascioliasis manifests 1–2 months after infection: the animals become weak, lose weight, the coat falls out, and edema of the eyelids, submandibular region, and chest develops. In cattle, the infestation is more frequently observed in young animals under 2 years of age and proceeds chronically with less pronounced symptoms. Upon necropsy of dead animals, dilated bile ducts filled with thick, dirty-brown bile containing a large number of flukes are discovered.
The diagnosis is made comprehensively based on symptoms, epizootiological data, pathological autopsy, and helminthoovoscopy. To detect the pathogen during the life of the animal, the method of fecal sedimentation is used. Fasciola eggs have a slightly visible operculum, and their content consists of an egg cell surrounded by a mass of yolk cells.
- Body temperature of sheep in acute form — 41.2–41.6 °C
- Frequency of pasture rotation — every 22.5 months.
- Dehelminthization period in the stable — after 3 months.
- Concentration of copper sulfate — 1:5000
- Application rate of molluscicide — 10 l per 1 m²
| Preparation | Sheep | Cattle |
|---|---|---|
| Bithionol | 70–200 mg/kg | 50–70 mg/kg |
| Hexachlorophene | 300–500 mg/kg | — |
| Niclofan | 3–8 mg/kg (oral), 1 mg/kg (i/m) | — |
| Nitroxynil | 10–12.5 mg/kg (s/c) | — |
| Sulfen | 30–100 mg/kg | 15–30 mg/kg |
Prevention of fascioliasis includes the destruction of sexually mature helminths in the organism of animals, larval stages, and intermediate hosts — the dwarf pond snail. Preventive dehelminthization is carried out at least twice a year; it is advisable to perform treatment 3 months after moving livestock to stable housing. Hay from infested pastures is fed during the second half of the stabling period, and all newly arriving animals are examined during the quarantine period and treated if necessary.
It is forbidden to graze livestock on low-lying and swampy areas, and to provide water from stagnant reservoirs, swamps, and small ponds. After chemical treatment of the territory with an aqueous solution of copper sulfate, grazing of animals on these pastures is strictly prohibited for several days.
Dicrocoeliasis: pathogen characteristics and life cycle
Dicrocoeliasis is a widespread helminthiasis parasitizing the bile ducts and gallbladder of more than 70 species of domestic and wild mammals, as well as humans. Ruminants are primarily affected: sheep, goats, cattle">cattle, buffaloes, camels, and deer. The pathogen has a lancet-shaped body up to 1 cm long and 1.5–2 mm wide, with closely spaced oral and ventral suckers.
The development of the parasite occurs with the participation of intermediate hosts — various species of land snails and additional hosts — ants. Eggs with developed miracidia are excreted with bile and feces into the environment, where they are ingested by snails. In the snail's body, the miracidium emerges from the egg, penetrates the connective tissue of the liver, sheds its cilia, and turns into a mother sporocyst, which disintegrates into daughter sporocysts that form cercariae.
- Cercariae from the snail's liver are carried by blood into its respiratory cavity, where they become enveloped in sticky mucus.
- Mucous clumps (100–200 or more cercariae in each) are pushed out by the respiratory movements of the snail and stick to plants (development in the snail takes 3–6 months).
- The mucous clumps on plants are eaten by ants, in whose bodies the cercariae emerge from the mucus and penetrate from the intestine into the abdominal cavity.
- In the ant's abdominal cavity, the cercariae lose their tail, encyst, and after 1–2 months turn into invasive metacercariae.
Epizootiology, symptoms, and prevention of dicrocoeliasis
Livestock become infected with dicrocoeliasis on pastures by ingesting ants infected with metacercariae along with the grass. The parasite, having entered the ant's nervous system, causes spasm of the insect's mandibles: the lethargic ants hold firmly to the plants and do not react to external stimuli. After the ant is digested in the animal's digestive tract, young helminths penetrate the liver through the common bile duct. The main peak of infection occurs in spring and autumn; lethargic ants on the grass are easy to detect in the morning and evening, and in early spring — throughout the day. Parasite eggs and larvae successfully overwinter in snails and ants in the environment.
- Duration of parasite development in the liver — 1.5–3 months
- Size of Dicrocoelium eggs — 0.038–0.045 × 0.02–0.03 mm
- Number of scolex suckers in tapeworms — 2–4 pcs.
- Body length of cestodes — from a few mm to 10 m
The pathological process is localized in the bile ducts of the liver. With high intensity of infestation, chronic catarrhal inflammation of the bile ducts and miliary cirrhosis of the liver develop. Mild infestation is asymptomatic. In severe cases of the disease, the following are observed:
- depressed state and digestive disorders (diarrhea alternating with constipation);
- loss of coat quality: hair brittleness, appearance of bald patches;
- edema in the chest and brisket area.
Antemortem diagnosis is performed by fecal ovoscopy. Dicrocoelium eggs are small, dark brown, asymmetric, with a thick shell, contain a miracidium, and have an operculum at one of the poles. Postmortem diagnosis is based on the discovery of helminths during a liver necropsy.
Pastures located in river valleys and floodplains are the most dangerous for livestock infestation. When infested areas are identified, grazing of livestock on them is ceased, or the method of fencing (isolating) anthills is applied.
Prevention of dicrocoeliasis requires a comprehensive approach and includes the following measures:
- planned deworming of adult livestock;
- helminthological survey of pastures by inspecting the herbage and assessing the infection of mollusks and ants;
- transfer of young animals to stall-and-paddock housing;
- measures to reduce the population of intermediate hosts.
General morphology and development of cestodes
Cestodes (class of tapeworms) in the sexually mature stage parasitize in the digestive organs of vertebrates. Representatives of two orders are of the greatest veterinary importance: cyclophyllideans (true tapeworms) and diphyllobothriideans (broad tapeworms). The body of the parasite is flattened in the dorsoventral direction and consists of three main parts: the head (scolex), an unsegmented neck, and a ribbon-like body (strobila) containing from one to several thousand segments (proglottids).
The attachment organs differ depending on the taxonomic affiliation of the parasite:
- In cyclophyllideans: the scolex is rounded, equipped with 2–4 muscular suckers (sometimes with hooks) and often a muscular rostellum with one or more rows of hooks;
- In diphyllobothriideans: the scolex is elongated, having two or four sucking slits (bothria).
The neck serves as the growth zone: new segments are formed at its base, gradually pushing older ones toward the posterior end of the body. The outer covering is represented by a tegument (cuticle, basal membrane, sub-tegument). The digestive system is absent in cestodes — the absorption of nutrients occurs through the entire surface of the body.
The development of the reproductive system in the strobila proceeds sequentially: from asexual young segments near the neck — to male, then to hermaphroditic and mature ones. In mature segments, all organs degenerate, leaving only the uterus filled with fertilized eggs.
Mature segments detach and are released into the external environment with the host's feces either singly or as fragments of the strobila. Cyclophyllidean eggs are released upon the rupture of the segment in the intestine or in the external environment, whereas in diphyllobothriideans, they are excreted through an independent uterine pore.
Cyclophyllidean eggs are fairly uniform in their morphology, oval, round, or spherical in shape, covered with an extremely delicate transparent shell, through which the oncosphere inside is clearly visible, consisting of a thick radially striated membrane, inside which lies an embryo with six embryonic hooks, surrounded by its own tightly fitting membrane. In representatives of the diphyllobothriidean order, eggs have an operculum similar to the eggs of trematodes.
All cestodes are biohelminths, and their development occurs with the participation of one (cyclophyllideans) or two (diphyllobothriideans) intermediate hosts. In the body of intermediate hosts, the larvae of various cestodes have diverse structures. The main types of these larvae are:
- In cyclophyllideans: cysticercus, cysticercoid, coenurus, hydatid cyst, alveolar cyst, strobilocercus, and tetrathyridium.
- In diphyllobothriideans: procercoid and plerocercoid.
Cysticercus is a bladder-like formation filled with fluid and surrounded by an outer connective tissue capsule. Inside the bladder, there is one scolex with a rostellum, suckers, and chitinous hooks.
A bladder filled with fluid that contains not one, but multiple scolices arranged in groups on the inner lining is called a coenurus.
The hydatid cyst (larvocyst of Echinococcus) is a single-chambered bladder of complex structure filled with fluid. The inner germinal membrane can produce brood capsules with the simultaneous formation of germinal scolices and secondary (daughter) bladders within them. In the body of the intermediate host, Echinococcus takes on various morphological modifications.
The alveolar cyst (larvocyst of Alveococcus) is a conglomerate of small irregular-shaped vesicles in which germinal scolices can be seen as small dots. In some cestodes, the microscopic larvocyst has an expanded anterior part with an invaginated scolex and a posterior part in the form of a tail appendage.
The strobilocercus is characterized by the presence of a well-defined scolex armed with large hooks, with a long pseudo-segmented strobila extending from it, ending at the posterior end in a small vesicle filled with fluid.
A tetrathyridium is an invaginated (like the finger of a glove) unarmed scolex with four suckers and a relatively long tail appendage without a caudal vesicle.
A procercoid is the larval stage of diphyllobothriideans; the body is elongated, with a depression at the anterior end and a spherical appendage with embryonic hooks at the posterior end.
Plerocercoid is a larval stage of tapeworms, reaching 1 m in length, with bothria located at the anterior end of the body.
Bovine cysticercosis is caused by the larval stage of a cestode that parasitizes the human intestine. Cysticerci are localized in the intermuscular connective tissue of skeletal muscles, the heart, the tongue, and less frequently in the tissues of parenchymal organs.
Pathogen. A fully developed cysticercus is grayish-white in color, transversely oval in shape, 5-15 mm long and 3-8 mm wide. A large scolex, 1.52 mm in diameter, equipped with four suckers, is located on its inner membrane. The sexually mature stage of T reaches 10 m (or more) in length and 12—14 mm in width. The scolex is unarmed.
Intermediate host - livestock animal">cattle, yak, zebu.
Biology of the pathogen. From the intestine of an infested human, mature proglottids are excreted into the external environment with feces. Infection of intermediate hosts occurs when they ingest oncospheres and, in some cases, Taeniarhynchus proglottids.
In the intestine of cattle, the embryo emerges from the egg and, with the help of six hooks, penetrates into the intestinal capillaries, and subsequently, it can be carried via the bloodstream to any organ, where an invasive cysticercus forms after 4.5 months. Cysticerci develop primarily in the intermuscular connective tissue. In individual cases, they reach invasiveness in the subcutaneous tissue, adipose tissue, brain, liver, lungs, heart, and in the eyes of cattle.
Humans become infected with taeniarhynchosis by consuming cattle meat, or by eating dishes made from raw or insufficiently cooked meat (stroganina, shashlik, basturma, beefsteak, etc.). When cysticerci enter the human digestive tract, under the influence of gastric juice and bile, they evert the scolex, which attaches to the wall of the upper part of the small intestine with the help of suckers. Subsequently, the parasite grows. From the moment cysticerci enter the human intestine until the formation of a sexually mature cestode, an average of 3 months passes. The lifespan of Taeniarhynchus is more than 10 years.
The rate of proglottid discharge remains stable at 6-8 proglottids per day, meaning that in a year, a person suffering from taeniarhynchosis sheds about 2,500 proglottids, or about 440 million oncospheres.
Epizootiological data. The intensity of infestation in cattle is usually low. Calves are more susceptible to cysticercosis than adult livestock animals; intrauterine infection is occasionally observed. Infection of animals occurs under unsanitary conditions of livestock housing, and also if the maintenance staff does not use toilets.
Symptoms of the disease. Clinically, bovine cysticercosis does not manifest.
Diagnosis. Post-mortem diagnosis is based on the detection of cysticerci in cattle carcasses during post-slaughter examination.
Treatment. Panacur (22.2% fenbendazole granulate) at a total dose of 0.05 g/kg of body weight (by active ingredient) and Droncit (praziquantel) at a total dose of 0.01 g/kg (by active ingredient) when applied for 2 consecutive days individually with a small amount of moistened feed.
Porcine cysticercosis is an anthropozoonosis caused by the larval stage of a cestode that parasitizes the human intestine. The cysticerci themselves are localized in pigs in the muscles, heart, brain, eyes, liver, and lungs; in humans, they are located in the brain and eyes.
Porcine cysticercosis: biology of the pathogen, epizootiology, and diagnosis
Cysticercosis is a dangerous helminthiasis in which the larval stages of the tapeworm affect the muscles and internal organs of animals. For pig farms, the disease poses a serious sanitary problem, as the main source of herd infection is humans, who shed parasite eggs into the external environment. The main difficulty in timely detection of infestation lies in the absence of clinical manifestations in the livestock.
The pathogen of the disease is represented by developed cysticerci — transparent vesicles of ellipsoidal shape, localized in the tissues of intermediate hosts.
| Cysticercus parameter | Value |
|---|---|
| Length | 6—20 mm |
| Width | 5—10 mm |
The intermediate hosts of the parasite include the following species:
- pig;
- wild boar;
- bear;
- camel;
- dog;
- cat;
- rabbit;
- hare;
- human.
- Cysticercus development period — 2–4 months
- Lifespan of cysticerci in a pig — 3–6 years
- Appearance of mature proglottids in humans — 2–3 months
The only definitive host of the pathogen is the human, who periodically sheds mature proglottids with feces. Animals become infected by ingesting helminth eggs with feed or water. In the intestine, an oncosphere emerges from the egg, and the ingested embryo penetrates into the blood or lymphatic vessels of the gut and is carried by the bloodstream throughout the body, most often settling in the intermuscular connective tissue, brain, eyes, and internal organs.
A human can act not only as a definitive host but also as an intermediate host of the pork tapeworm. Infection with larvae occurs when swallowing oncospheres with food or through internal self-infection: due to the gag reflex, mature proglottids can enter the stomach from the intestine via antiperistalsis, where eggs are released from the digested proglottids.
The final development of the helminth occurs in the human intestine upon the consumption of undercooked or under-fried meat containing cysticerci. In the gastrointestinal tract, the bladder wall is digested, the scolex evaginates and attaches to the mucous membrane with its hooks. Then, a strobila forms, and after 2–3 months, mature proglottids begin to detach from the parasite, with the lifespan of an adult tapeworm spanning years.
The spread of the infestation on a farm is facilitated by coprophagia, common in pigs and dogs, as well as the absence of sanitary toilets and poor hygiene in the housing conditions. Due to the long lifespan of the helminth, one infested person is capable of contaminating vast territories with tapeworm eggs.
Porcine cysticercosis is asymptomatic. There are no clinical signs of the disease in animals; therefore, the diagnosis is made exclusively post-mortem by detecting cysticerci in the muscles and internal organs during carcass processing or necropsy.
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