Bovine fascioliasis: review of the disease and treatment methods. Fascioliasis (fasciola, liver fluke, giant fluke) Diagnosis, treatment and prevention of fascioliasis in cattle

The development of fascioliasis in humans mainly occurs in the liver and bile ducts; less often, the helminth affects the pancreas.

The structure of the fluke is branched and includes:

• sucking apparatus;
• small esophagus;
• two branches of the intestine;
• ventral sucker;
• ovaries;
• testes;
• yellowworts;
• uterus

For the next stage of development, they require warm freshwater water. The optimal temperature is considered to be 22 C, at 10 C development stops, and 30 C is lethal for fluke eggs.

Under favorable conditions, after 9-18 days, larvae emerge from the eggs and are capable of moving independently. The next stage in development is the intermediate host - a freshwater snail; this phase is obligatory for the liver fluke and lasts 30 -70 days. After maturation, the larva again enters the water, but in a special protective shell.

Attaching to the stems and leaves of plants or simply being on the surface of the water, Fasciola hepatica awaits its prey.

Causes of illness in humans. Pathogen

Therefore, residents of remote settlements, who often consume untreated water, are at greater risk of infection.

Fascioliasis: symptoms and development of the disease

The chronic phase of the disease is characterized by: significant damage to liver tissue, susceptibility to infection by third-party microflora (as a result of abscesses), liver fibrosis.

Incubation period

Early stage of the disease

The acute stage of development of fascioliasis occurs precisely during the period of migration of larvae through the liver tissue and is determined by the main symptoms:

• allergies and itching;
• weakness;
• elevated temperature;
• abdominal pain;
• headache;
• nausea;
• subcostal pain on the right side;
• jaundice (initially the whites of the eyes and oral mucosa turn yellow);
• significant enlargement of the liver;
• increased heart rate;
• Quincke's edema;
• chest pain;
• high blood pressure.

Concomitant diseases, general blood test indicators:

• increased ESR;
• leukocytosis (up to 20-50 * 109/l);
• eosinophilia is about 80-85%.

After the liver fluke has reached the bile ducts, in many patients any signs of the disease completely disappear. In rare cases, carriers of this helminth experience pain in the right hypochondrium and periodic signs of jaundice.

Sometimes migrating, Fasciola hepatica can enter other internal organs: lungs, kidneys, eyes, brain, or end up under the skin. In these cases, the disease process occurs with various individual complications.

Chronic phase

The transition of the disease to the chronic stage lasts approximately 3 months after infection. All symptoms and painful manifestations at this stage are associated with harmful changes in the biliary tract and liver. The chronic stage occurs with such manifestations as:

• hepatomegaly – enlarged liver;
• periodic pain in the right hypochondrium and abdominal area;
• nausea;
• bowel dysfunction;
• decreased appetite;
• signs of cholestasis.

A general blood test reveals subtle anemia and a slight increase in eosinophils (up to 10%).

In the advanced phase of the disease, a biochemical blood test reveals:

• changes in the protein spectrum of the blood;
• increase in gamma globulin levels;
• high enzyme activity (GGTP, AST, ALT, alkaline phosphatase);
• increased bilirubin levels.

Without timely and step-by-step treatment, many complications of fascioliasis can develop.

Long-term invasion in humans causes:

1. Cirrhosis of the liver.
2. Hepatitis.
3. Purulent or chronic cholecystitis.
4. Subcutaneous abscesses.
5. Purulent angiocholangitis.
6. Anemia.
7. Liver abscess.
8. Damage to the mammary glands.
9. Lung infection.

Diagnosis of fascioliasis

Identifying the disease at an early stage is quite a difficult task; for this, the patient needs to consult an infectious disease specialist. Diagnosis is based on various data.

1. Epidemiological data including the following facts:

• consumption of water from ponds or other sources that do not meet standards;
• swimming in a polluted stagnant body of water;
• using untreated water for washing food and dishes;
• eating unwashed vegetables and herbs.

2. Clinical data - identifying the presence of the above-described symptoms of the early or chronic stage of the disease.

3. Obtaining laboratory data varies for each phase of the disease.

• At the early stage of invasion by Fasciola hepatica, there is no need to perform coproovoscopy, due to the fact that this helminth begins to lay eggs only after 3-4 months. Therefore, they mainly carry out a comprehensive blood test for various antibodies (ELISA, RNGA, RIF reactions).
• For the chronic phase of the disease, the histological coprogram provides comprehensive answers about the disease. For fascioliasis, stool examination is carried out twice to exclude the possibility of displaying in the analysis false eggs that entered the human body with the consumption of liver from canned food or pates. Sometimes the doctor may prescribe a tomography or ultrasound of the abdominal cavity.

Differential analysis is carried out with various diseases that have similar symptoms: hepatitis, allergic manifestations, various helminthiases, cholecystitis, liver cirrhosis, cholangitis, gastroduodenitis and others.

Treatment of fascioliasis

For each stage of the disease, a specific course of treatment is prescribed. At an early stage of development of the disease, the patient must be hospitalized; in the chronic course of fascioliasis, patients undergo outpatient drug therapy.

Medical care during the acute phase

Therefore, the patient is prescribed symptomatic and pathogenetic treatment aimed at relieving pain and acute manifestations of infection.

For this purpose the following are assigned:

• choleretic;
• hepatoprotective;
• sorbents;
• probiotics;
• if signs of hepatitis appear, prednisolone is prescribed;
• antispasmodics;
• for inflammation, antibacterial medications are prescribed;
• antihistamines.

After the obvious signs of the disease subside, anthelmintic drugs are prescribed.

Rest is required during the course of therapy. And the treatment process itself is strictly controlled by the attending physician.

Therapy in the chronic stage

For treatment in the advanced stage of fascioliasis, antispasmodics and physiotherapy are used. When pain syndromes are not expressed, choleretic drugs are used. Chloxyl and drugs aimed at general strengthening of the body are also used for therapy. In the presence of concomitant bacterial inflammation of the biliary tract, antibiotics are prescribed.

After 3-4 months after treatment, the patient must undergo control stool tests for the presence of fascioli eggs and duodenal contents. These studies are also repeated for 6, 12 and 24 months.

Prevention

To avoid infection with liver fluke, a number of measures are taken:

1. Eliminate the possibility of untreated water from stagnant bodies of water entering the body by simply boiling. If there is no way to limit the likelihood of infection in this way, then it is necessary to at least strain the water through a cloth.
2. Eat only clean herbs and vegetables that have been washed with disinfectants or doused with boiling water.
3. Veterinary preventive measures are carried out aimed at reducing the incidence of disease in livestock, involving the use of fresh hay (harvesting period no later than 6 months) and the fight against various mollusks in reservoirs near grazing animals.
4. Provide identification and timely treatment of illness in humans and animals.

In most cases, with timely consultation with a doctor, fascioliasis can be completely cured. But it is better to avoid this disease, because you just need to use the simplest rules of food hygiene.

Fascioliasis- an animal disease caused by trematodes: Fasciola hepatica and, less commonly, Fasciola gigantica, belonging to the family Fasciolidae. This disease is expressed in acute or more often in chronic inflammation of the liver, as well as bile ducts and is accompanied by general intoxication and eating disorder. Fascioliasis often takes the form of enzootic disease.

Fascioliasis mostly affects sheep, goats, cattle, camels, donkeys, and much less often pigs, horses, rabbits, reindeer, hares, squirrels, beavers, and nutria. Sometimes fascioliasis occurs in people.

Mostly sheep die from fascioliasis, especially at a young age. Severe forms of the disease are also observed in cattle. The disease usually has a stationary spread, mainly in damp, swampy and flooded areas.

Economic damage from fascioliasis mainly consists of the following points:

1) mass death of livestock during an enzootic;

2) significant weight loss due to exhaustion of animals during the chronic course of the disease;

3) a decrease in milk yield in cattle suffering from fascioliasis for years by an average of 10%, and in case of severe infestations by 20% or more;

4) rejection of affected livers of slaughter animals.

Fasciolas feed on blood from the capillaries of the host tissues.

The nervous system consists of nerve ganglia located under the pharynx; trunks extend from them to various parts of the body.

Their common vas deferens is enclosed in a skin-muscular sac - the genital bursa. In its cavity there are the seminal vesicle and the penis - the cirrus, which opens with the external genital opening on the ventral side in front of the abdominal sucker.

Fasciola are hermaphrodites. They can both self-fertilize and cross-fertilize. Spermatozoa move through the uterine canal and enter the ootype, where their mutual assimilation with egg cells occurs.

Fasciola gigantea is found in the southern and southeastern regions of the European part of the USSR.

Fascioliasis: development fasciol. Fasciola vulgaris lives in the bile ducts of the liver of animals (in cattle, fasciolae are often found in the lungs), where it secretes a huge number of eggs (hundreds of thousands). From the liver, eggs pass through the bile duct along with bile into the intestines, and from there, mixed with feces, they are thrown out.

Oval-shaped, golden-yellow in color, fasciola eggs are covered on the outside with a smooth shell consisting of four layers. They are 0.12 - 0.15 mm in length and 0.07 - 0.08 mm in width. At one of the poles of the egg there is a cap. In the external environment, at a favorable temperature (from 15 to 30°), an embryo develops in the egg - miracidia. In the presence of oxygen, moisture and light, the latter hatches from the egg after 10 - 25 days (at a pH in the range of 5 - 7.7) and begins to float freely in liquid (small puddles, ditches, ponds, rivers). In the dark, miracidia do not emerge from the eggs and can remain in them for a long time (up to 8 months).

The body of the miracdia (embryo hatched from an egg) is densely covered with cilia and reaches 0.19 mm in length and 0.026 mm in width. The embryo can survive in water for no more than 40 hours. It is sensitive to various chemicals. For its further development, an intermediate host is necessary - the small truncated pond snail - Limnaea truncatula (In 1952, the truncated pond snail was transferred to the genus Galba.)

The body of the pond snail is covered on the outside with an ovoid or spindle-shaped shell. The shell is curled to the right; its last whorl is noticeably expanded. The small pond snail is up to 10 mm in height and 5 mm in width. It usually lives at a depth of 10 - 40 cm in holes with water, small ponds, spring streams, puddles with a muddy bottom, overgrown with grass. Pond snails reproduce in water, laying a significant number of eggs on plant stems, stones and other objects. Young pond snails emerge from the eggs after 8-10 days. The latter can withstand low temperatures well (they can overwinter under ice) and drying out, burrowing into wet silt or attaching to grass stems. For some time (up to two months), mollusks can be stored even in dry sand.

In addition to the small pond snail, other species of mollusks of the genus Limnaea can be intermediate hosts of fasciolae; Thus, it has been experimentally established that in Armenia they are young forms of Limnaea peregra, Limnaea ovata, Galba palustris, Limnaea stragnalis, Radix lagotis.

Miracidium, swimming in the water, encounters a mollusk, into whose body it actively penetrates. Having then entered the liver of the pond snail, the miracidium sheds its ciliated cover and turns into a sac-shaped sporocyst (length 0.15 mm); it contains germ cells. Gradually increasing in size, these cells, after 15-30 days, form redia - oblong formations equipped with a mouth, pharynx and a blind intestine. When the sporocyst increases (up to 0.5 - 0.7 mm) and the redia reach 0.26 mm in length, they break through the shell of the sporocyst and come out of it, remaining in the organs of the mollusk.

From one sporocyst, through asexual division (parthenogony), 5 to 15 redia are formed, each of which can produce a new generation of larvae (daughter redia). The redia continue to grow, increase to 1 mm in length and after 35 - 40 days form up to 15 - 20 cercariae, equipped with two suckers, a long tail and a branched intestine (they are similar in shape to tadpoles). The period of development from the miracidium to the cercarium in the body of the mollusk is estimated at 50 - 80 days.

Having reached a certain age, the cercariae leave the mollusk’s body through its mouth and begin to swim in the water using their tail. Cercariae are up to 0.28 - 0.3 mm in length and up to a maximum of 0.23 mm in width. On the dorsal and ventral sides they bear cutaneous cystogenic glands. The number of cercariae in one infected mollusk can reach 600 - 800. They usually emerge from the mollusk within several weeks.

Thus, the complete development of the fasciola embryo is presented in the following form: in the external environment - 1) egg, 2) miracidium; then in the mollusk - 3) sporocyst, 4) redia and of these 5) cercariae. The full development cycle from egg to cercaria takes from 70 to 100 days.

The Adolescaria cyst is thick and consists of two membranes. It contains a mobile fasciola embryo with well-defined oral and abdominal suckers, a branched intestine and an excretory bladder.

In infested pastures, animals ingest Adolescaria when they drink water from puddles, ponds and ditches or eat grass. In the intestine of the animal, the shell of the adolescarii dissolves and the embryos, with the help of the secretion of the “penetration glands,” enter the bile ducts of the liver and there develop into sexually mature forms of fascioli.

Fascioli penetrate the bile ducts in two ways. Some of the larvae penetrate the intestinal mucosa, into the intestinal veins and move through the portal vein to the liver. Once in vessels with a small diameter, young fascioli cannot move further; they drill through the vascular wall, then into the liver tissue and after a few weeks penetrate into the bile ducts. Another part of the larvae passes through the intestinal wall into the abdominal cavity, and then through the liver capsule into the bile ducts.

In small laboratory animals (rabbits), fasciolas reach sexual maturity after 2 months.

The development cycle of giant fasciola is similar to that of common fasciola. In the conditions of the Armenian SSR, the intermediate host for this fasciola is the mollusk Limnaea limosa (P.K. Svadzhyan). The development of miracidia to the cercariae stage in the intermediate host lasts 41 - 60 days (at a temperature of 19 - 29.5°). Other species of mollusks of the genus Limnaea (L. peregra, L. ovata, L. truncatula) can also be intermediate hosts.

It takes more than 3 months for Fasciola gianta to develop in sheep and cattle.

It is assumed that in early spring animals do not become infected with fascioliasis. Thus, in the central regions of the European part of the USSR, laboratory tests do not find fasciola eggs in young animals (lambs, calves) that were on pasture from spring to October. During the summer months, during random autopsies, sexually mature fasciolae are also not recorded in the liver of young animals. Some of the fasciolae embryos can, however, overwinter in the body of the small pond snail. Such embryos, as they mature, leave the body of the mollusk in June and are capable of infecting animals. Adolescaria are persistent and do not die for a long time at - 4° (- 6°). For example, in the conditions of the Moscow region, some adolescarii can survive until spring. At normal summer-autumn temperatures, they can be stored in moist hay and water for 5 months or more.

Infection with fascioliasis occurs in the summer (from the second half of June) and, moreover, is most intense in the last months of the animals’ stay on the pasture. By this time, the number of mollusks on the latter increases significantly, and many cercariae and adolescariae appear in the reservoirs, which have managed to develop and reproduce in the intermediate host over the summer.

In rainy years, mass infection of animals with fascioliasis is often observed even in places where there are no puddles and swamps; on the contrary, in dry years, when these small bodies of water dry up, the spread of fascioliasis sharply decreases.

High infestation of fascioliasis is observed especially where animals are kept for a long time on the same wet pastures. Staying in the same area, infected cattle excrete Fasciola eggs along with their feces, pollute the pastures more and more, and after some time they are infested again. It should be borne in mind that in the body of a pond snail, 100 - 150 dercariae can develop from one miracidium, so the presence in a herd of even a small number of animals infected with fasciolae poses a serious danger.

In winter, animals (in the central and northern zones) are not infected with fascioliasis. In summer, when kept in stalls, such an infestation can occur when animals are fed grass cut on low-lying pastures, since there may be attached adolescaria on it.

Fascioliasis: pathogenesis and pathological changes with fascioliasis. The pathogenic effect of fasciolae on animals consists mainly of nutritional disorders, poisoning by toxins and poisonous waste products of fasciolae, hydremia, the introduction of microbes from the intestines to other organs and tissues, etc.

The enlarged fascioli move from the liver tissue into the bile ducts and clog them; the consequence of this is stagnation of bile and jaundice (obstructive jaundice).

Young fascioli, migrating from the intestines to the liver and bile ducts, bring there various bacteria (from the Coli group, etc.). By multiplying in the bile ducts, these microbes aggravate the intoxication of the body and can contribute to the development of various infections. Due to the introduction of pathogenic bacteria by fasciola larvae, ulcers often form in the liver and other organs.

Fascioliasis: pathological changes with fascioliasis in the liver depend on the degree of invasion by fasciolae. If it becomes widespread, acute inflammation of the organ is observed first, which can be enlarged and hyperemic. It shows foci and in them dark red cords up to 2 - 5 mm in length, coagulated blood and very small fascioli, visible only under a magnifying glass after appropriate treatment of the liver. The number of young fasciolae reaches 1000 or more. Small hemorrhages and sometimes fibrinous films are visible on the serous surface. With severe invasion, peritonitis is detected, and sometimes heavy bleeding (up to 2 - 3 liters) into the abdominal cavity. The mucous membranes are matte pale.

After some time (2 - 3 months), chronic inflammation of the liver develops; it becomes dense, and the bile ducts expand; they contain a large amount of muco-bloody fluid and many fascioli. In place of the destroyed liver tissue, cicatricial grayish-white strands appear. The mucous membrane of the bile ducts is thickened due to the increased development of connective tissue. The walls of the bile ducts become hard (calcified) and their inner surface becomes rough. They appear on the stove in the form of dense strands running in different directions. Dilated bile ducts are filled with dirty-brown fluid, fascioli, and sometimes they contain purulent masses mixed with blood.

The liver parenchyma becomes discolored; its edges are sometimes rounded. Typically, a severely affected liver increases in weight by 2 to 3 times (especially in cattle).

In cases of mild invasion, changes in the bile ducts from the surface of the liver are little noticeable; when palpating the organ, it is possible to detect thickened bile ducts, in which, upon incision, fascioli are found. Most often, fascioliasis is accompanied by chronic catarrhal inflammation of the bile ducts and interstitial inflammation of the liver. With significant calcification of the bile ducts, the fascioli present in them die or move to other, less altered areas. In a severely affected organ, fascioli are often not found, and their presence is evidenced only by calcified bile ducts.

With intensive infestation, sharp emaciation and hydremia are observed in sheep and cattle. In such animals, the muscles are saturated with serous fluid and are flabby; the meat is watery, grayish in color. A transparent transudate accumulates in the abdominal and chest cavities, as well as in the cardiac membrane.

In cattle, fascioli, in addition to the liver, are often found in the lungs (up to 20%). The latter have a normal color on the surface; in places, sharply limited dense nodes the size of a walnut to a chicken egg are noticeable on them. The contents of such a node consist of a semi-liquid mass of dark brown color, 1 - 2 fascioli, living or in the stage of decay. The entire mass is surrounded by a connective tissue capsule, often calcified.

In pregnant animals with fascioliasis, intrauterine infection of the fetus can occur (intrauterine invasion). However, the latter is not significant in the epizootology of fascioliasis.

The primary disease of animals with fascioliasis occurs in late summer and autumn, and its chronic form can be observed throughout the year.

In sheep and goats, fascioliasis occurs in acute or chronic form. The acute form of fascioliasis occurs only in autumn. The initial stage of the disease is characterized by fever (often visible). Patients are depressed, quickly get tired, lag behind the herd, lose appetite; in the liver area they have an increased area of ​​dullness and increased sensitivity. Then anemia quickly develops, the number of red blood cells decreases (to 3 - 4 million), and the percentage of hemoglobin drops sharply. The mucous membranes are pale.

Chronic form of fascioliasis. If the infected animal does not die soon, after 1 - 2 months its anemia increases, the mucous membranes turn pale, the hair becomes dry and falls out easily, especially on the sides and chest. Then cold swelling appears on the eyelids, in the intermaxillary space, on the chest, and lower abdomen. Jaundice is minor. Sheep eat poorly, lose a lot of weight, their milk becomes thin, and lambs suck poorly from sick mothers. In some sheep, nervous phenomena are observed that resemble in their form a false whirlwind, and miscarriages in the last period of pregnancy. Ultimately, the affected animals die from exhaustion.

When sheep are less intensively infected, the disease becomes protracted. Sick sheep that have overwintered in the spring on the pasture get better, but when they are switched to stabling, they lose weight again. Such chronicles spread fascioliasis infestation. With a single invasion, clinical signs are mild or absent. Such carriers of fasciolae also contribute to the dispersion of invasion.

Fascioliasis is especially severe in sheep when there is a lack of vitamins (vitamin A) and calcium salts in the feed.

Fascioliasis: diagnosis. The acute form is accurately diagnosed only by helminthological autopsy when small-sized fascioli and massive hemorrhages are detected in the liver parenchyma, and blood or fluid is found in the abdominal cavity. Due to the similarity of clinical signs of fascioliasis and some other diseases, the diagnosis must be confirmed by examining feces (sheep, goats and cattle) using the method of serial drains. Feces are taken from the animal's rectum in an amount of about 50 g. By this method, fascioliasis eggs are found in a maximum of 60% of sheep and 30 - 40% of cattle infected with fascioliasis.

Fasciola eggs have an operculum. The latter becomes clearly visible when a few drops of caustic potassium solution are added to the preparation. The egg contains large numbers of yolk cells, filling its entire cavity.

An accurate diagnosis of fascioliasis is established only by the presence of clinical signs confirmed by the detection of eggs in feces, or during autopsy of dead animals, when a large number of fascioli are found in the liver. Animals that do not have a clinical picture and only single eggs are found during scatological studies are considered fasciocarriers.

N.N. Komaritsyn (1952) observed bilirubinemia (up to 19 mg%) and urobilinuria in cattle with fascioliasis. Since the urine of cows always contains urobilin (in various levels), therefore, if fascioliasis is suspected, it is recommended to additionally examine the blood to determine the presence of bilirubinemia.

Fasciolosis in animals can be detected by checking slaughtered animals at meat inspection stations and slaughter sites.

Immunobiological methods for diagnosing fascioliasis (ophthalmic reaction, intradermal reactions and complement fixation) are not yet widely used.

It has been established that during intradermal tuberculinization of cattle infected with fascioliasis, positive and questionable reactions can be observed in adult animals free from tuberculosis (reactions are often observed with secondary administration of tuberculin). An eye test with tuberculin in such animals gives a negative result in 90% of cases. During the pathological and histological examination of these animals (positive and questionable reacting to tuberculin), no tuberculous changes were found in 99.3% of cases (A. I. Uteshev).

According to K. A. Popova and A. I. Uteshev, in farms unfavorable for fascioliasis (with infestation from 70 to 90%), the number of animals responding to intradermal tuberculinization reached 7 - 37%. After double deworming (with an interval of 21/2 months) in fascioliasis animals that react to an intradermal test with tuberculin, the reactions disappear in 51 - 56% of cases, and in a significant part of the livestock, positive reactions turn into questionable ones. Along with this, in some animals that did not respond to intradermal administration of tuberculin during the first study, after double deworming (after 21/2 months), positive intradermal reactions appear. In order to avoid diagnostic errors in farms that are unfavorable for fascioliasis, it is necessary to deworm cattle 4 - 5 months before a scheduled examination for tuberculosis.

Fascioliasis: treatment. Sheep and goats with fasciolosis are treated with carbon tetrachloride, and cattle with hexachloroethane-fasciolin (formerly known as hexachloroethane). Carbon tetrachloride is not used in cattle.

When taken orally, carbon tetrachloride is absorbed in the small intestine and reaches primarily the liver. Initially, it affects the central nervous system (weakens cardiac activity), and later on the liver. Even small (therapeutic) doses cause partial degeneration of liver cells. This process is reversible, and after a few days they are restored to normal. Large doses of the drug, especially with frequent repeated administrations, cause fatty degeneration and necrosis of the liver tissue. In some sheep, after the administration of carbon tetrachloride in the blood, the concentration of calcium decreases and the content of bilirubin increases 2-4 times (accumulation of guanidine). Lack of ionized calcium increases vascular porosity.

During mass deworming of sheep with carbon tetrachloride, isolated cases of death of animals are observed, and in some farms there is a significant waste of them.

Such cases of death of sheep and their illnesses are recorded mainly in the central and northern regions of the Soviet Union, especially in September and October in dry years and in March and April in the spring. In the southern zones, such complications in sheep are rare. Thus, in the Stavropol Territory in 1940, during mass deworming of sheep (400 thousand heads were treated) against hemonchosis using large doses. (8 - 10 ml) carbon tetrachloride toxicosis in sheep has been observed.

N.I. Sereda established experimentally that the introduction of carbon tetrachloride into the body of cattle and sheep at a dose of 0.015 per 1 kg of live weight is accompanied by an increase in the percentage of guanidine and bilirubin in the blood, while simultaneously reducing ionized calcium and sugar. Since ionized calcium salts neutralize free bilirubin and guanidine, N.I. Sereda considers the accumulation of bilirubin and guanidine in the body to be the cause of hypocalcemia.

Toxicoses after the use of therapeutic doses of carbon tetrachloride are observed in sheep with calcium deficiency: it causes hypocalcemia and often death in such animals. By subcutaneous or intramuscular injection of 5 ml of a 5% solution of calcium glucopate, as well as feeding 1 - 2 weeks before the introduction of carbon tetrachloride pea straw, meat and bone meal, bran and other feeds rich in calcium salts and vitamins, toxicosis and hypocalcemia can be prevented.

Some sheep, after using carbon tetrachloride, experience slight illness: general depression, poor appetite, increased body temperature. Usually these phenomena last 1 - 3 days and disappear.

Severe toxicosis is accompanied by the following clinical picture. The sheep lie down and fall behind the herd; their body temperature rises to 40, and sometimes to 41°, general depression, atony of the rumen and forestomach are observed; peristalsis is weakened; later, tympany of the rumen and intestines develops, convulsions occur, and cardiac activity weakens; When pressure is applied to the abdomen, the sheep will experience pain.
Some sheep in the last stages of pregnancy sometimes have abortions. Death usually occurs 18 - 24 and less often 36 - 48 hours after giving carbon tetrachloride.

When opening dead and slaughtered sheep, a picture of hemorrhagic inflammation of the gastrointestinal tract is found. In sheep slaughtered early (12 to 18 hours after carbon tetrachloride was given), pronounced pathological changes occur only in the rumen (hemorrhagic inflammation).

Mostly adult sheep and, in a smaller percentage, young animals die from toxicosis. The state of their nutritional status does not play a role (emaciated sheep, those with good and above-average nutritional status, die), nor does the technique of introducing carbon tetrachloride (through the mouth or directly into the rumen). After the administration of carbon tetrachloride, sheep infected and not infected with fascioliasis become ill and die.

Long-term use of even small doses of carbon tetrachloride leads to cirrhosis of the liver. A sheep tolerates a large single dose of this drug more easily than several divided doses. That is why you cannot resort to repeated dewormings, following one after another.
When toxicosis has already occurred, the administration of calcium preparations (chalk, etc.) by mouth does not have an effect, since calcium salts are slowly absorbed. In such cases, sheep are given fresh milk orally and a 5% calcium chloride solution is injected intramuscularly.

Carbon tetrachloride has a laxative effect and a significant percentage of treated sheep pass semi-liquid faeces the next day.

In the absence of carbon tetrachloride in sheep and goats, fasciolin can be used, the effectiveness of which is much lower. Fasciolin is prescribed to sheep and goats at a dose of 0.2 - 0.4 g per 1 kg of live weight in the form of an emulsion, suspension or powder. Suspensions are prepared with bentonite (a special type of clay) in the ratio: 9 parts fasciolin and 1 part dry bentonite with the addition of 15 parts water to the well-pounded mixture. The appropriate dose is administered from a bottle or tube.

The dose of fasciolin for cattle is the same (0.2 - 0.4 per 1 kg of live weight). It is administered to emaciated animals in two doses of 0.1 per 1 kg of live weight, with a two to three day interval. In some animals, fasciolin can cause tympany, so one day before deworming and for 3 days after it, cattle should not be given easily fermentable and protein-rich feed. In the first days (1 - 2 days) after deworming, some cows reduce their milk yield.

Difluorotetrachloroethane-freon 112 (F-112) at a dose of 0.1 - 0.2 g per 1 kg of live weight gives almost complete liberation of sheep from fascioli. This Soviet drug is injected directly into the scar through the skin (N.V. Demidov).

Fascioliasis: preventive measures. Fascioliasis is a disease common to all types of farm animals. To successfully eliminate it, a complex set of preventive measures is required, consisting of preventing contamination of pastures and water bodies by Fasciola embryos, protecting animals from infection, improving the health of infested animals, neutralizing manure, land reclamation, etc.

In areas where fascioliasis is stationary, planned deworming is carried out simultaneously in the entire area (in a group of village councils, on collective farms, subsidiary farms), treating all animals in the locality, regardless of their ownership (including animals for individual use) so that the recovery There are no livestock infected with fascioliasis left in the territory. To take into account the effectiveness of the measures, 10 - 15 days after winter deworming, feces are examined selectively (from 10 - 20% of dewormed animals) using the method of successive drains.

Biothermal neutralization of manure for fascioliasis is a very important preventive measure in the fight against fascioliasis and other helminthiases. All livestock farms must have manure storage facilities where all manure must be transported. Where there are no manure storage facilities, manure can be stored in areas inaccessible to animals. First, the manure is piled loosely in small piles (up to 1 m3) to ensure free access of air to all its layers. As the temperature in the heap rises, it is compacted and covered with a new layer of manure. They do this for several months, putting the manure in piles before transporting it to the field.

To prevent leaching and leaching of valuable organic substances from the fertilizer, sheds are made over the heaps and stacks, and a dense floor or lining made of a layer of dry straw is laid under them; ditches are dug around the stacks. The embryos of fasciolae and other helminths, found in large quantities in feces, quickly die under the influence of the high temperature developing in the manure, after which the neutralized fertilizer can be transported to the fields.

Fighting shellfish with fascioliasis. In the fight against the intermediate host of fasciola, the small pond snail, drainage (reclamation) of marshy, low-lying pastures is of great importance. Reclamation alone, however, cannot achieve complete destruction of mollusks, since between hummocks, in ditches, there are often small holes and depressions in which pond snails can partially survive and develop. Therefore, pasture drainage is complemented by chemical and biological control of shellfish. Thus, small reservoirs with stagnant water, inhabited by a large number of mollusks, are periodically (1 - 2 times a year) treated with a solution of copper sulfate in a concentration of 1: 5000 in the entire volume of water. Treatment of swamps with low humidity is effective only under the condition of abundant irrigation with the same solution at the rate of at least 5 liters per 1 m2 of area (Panova). To destroy shellfish in water bodies using a biological method, it is recommended to breed geese and ducks, which exterminate pond snails, clearing water basins of them.

Pasture prevention. It is recommended not to graze animals on swampy, low-lying pastures. When farms are forced to use such pastures, animals are kept on them for no more than 11/2 - 2 months and then transferred to other areas that have not been grazed during the current season.

On collective farms, where there are several brigades (settlements), young animals (calves and lambs) after weaning are kept on separate isolated pastures, to which adult cattle are not allowed during the entire grazing season (it is best to transfer young animals for grazing to those brigades where located cattle and sheep farms).

Hay collected from infested pastures is fed to animals after 6 months of storage.

Watering place for fascioliasis. It is best to water animals from automatic drinking bowls or from wells with well-equipped gutters and decks. You can also drink from rivers, but only if there are good approaches to the water, strewn with gravel and sand. Quite often (especially in Ukraine) livestock is kept on dry pastures, and animals become infected with fascioliasis at watering places, when small streams with marshy banks or ponds with unimproved approaches to the banks are used for this purpose.

Planning interventions for fascioliasis. The veterinarian of the veterinary department develops a plan for the recovery of animals from fascioliasis for each collective farm, taking into account all disadvantaged areas, farms, as well as animals belonging to collective farmers. The plan reflects the number of animals (cattle and sheep) to be dewormed at each point, the timing of treatment, the need for anthelmintics, the dates of scatological studies after winter deworming, reclamation work, and pasture prevention. The treatment plan primarily includes farms that are most disadvantaged by fascioliasis.

Unfavorable for fascioliasis are those points in which cases of the disease were observed or in pathoanatomical autopsies (examinations) and scatological studies fasciol carriers were identified. The latter are most fully detected in January - February.

On farms where cattle and sheep are kept on common pastures, the sheep are examined first. When fascioliasis is detected in the latter, the cattle of this point are also considered unfavorable for this invasion.

In rainy years, more research is planned and preventive deworming is carried out in areas that were unfavorable in previous years.

In order to improve measures in the fight against fascioliasis, it is necessary to study the dynamics of fascioliasis invasion in sheep and cattle in different zones, to identify the species composition of mollusks - intermediate hosts, their ecology and the degree of invasion by fascioliasis germs in different periods of the year, to find new effective drugs against fascioliasis, study pasture prevention and methods of improving water bodies.

The issues of intravital diagnosis and the dynamics of development of fasciolae in the body of definitive hosts also require great attention.

Cases of fascioliasis infection in humans are not as common as in animals. However, in history there are known cases of mass invasions among the population. The most famous of them was recorded in Iran, when more than 10 thousand people were infected. At the moment, the disease is periodically recorded in the countries of Africa, South America, and Central Asia. Cases of incidence are not uncommon in European countries, such as France, Portugal, Moldova, Belarus, and Ukraine. Fascioliasis is also registered in some Russian regions.

Causes of fascioliasis

Helminth larvae can get from the gastrointestinal tract to the liver in two ways: hematogenously or through intensive migration through Glisson's capsule. The main pathological disorders appear during the migratory movement of worm larvae through the liver parenchyma. This process lasts more than a month. The main habitat of adult worms is the bile ducts. In some cases, larvae can be localized in places unusual for them: subcutaneous tissues, brain, lungs, pancreas and others.

A significant contribution to the poisoning of the human body is made by helminth waste products. When moving, the worm brings intestinal microflora into the liver, which entails the breakdown of stagnant bile and, as a consequence, the formation of micronecrosis and microabscesses. As a result, the body experiences disturbances in the functioning of various systems (nervous, cardiovascular, reticuloendothelial, respiratory), malfunctions in the gastrointestinal tract occur, and various pathological reflexes arise. A significant deficiency of many vitamins (especially vitamin A) suddenly appears, and allergization processes actively develop.

Over time, the patient's lumen of the common bile duct expands, the duct walls thicken, as a result of which purulent cholangitis can develop.

Migrating in the liver tissues, helminths destroy not only the bile ducts, but also the parenchyma and capillaries. The passages formed in this way are transformed into fibrous cords after a short time.

Occasionally, individuals of the worm can travel through the circulatory system to the lungs, where they die before reaching the stage of puberty.

Symptoms

The symptoms of the disease are divided into 2 stages of development: acute and chronic. The time during which fascioliasis does not manifest itself in any way (incubation period) can last from 1 week to 2 months.

In the early stages, the disease causes acute allergization in the body. It causes symptoms such as headache, high fever (up to 40°C), loss of appetite, increased fatigue, general malaise, and weakness. Allergic symptoms are expressed in the appearance of a rash on the skin, which is often accompanied by itching. Often they suffer from nausea, vomiting, cough, paroxysmal pain in the abdominal area (often in the right hypochondrium), jaundice, and fever. High eosinophilia and leukocytosis are almost always detected. The liver increases in size, its tissues become denser, and painful sensations appear when pressed. In some cases, at this stage of fascioliasis, symptoms of allergic myocarditis are observed: tachycardia, transient arterial hypertension, muffled heart sounds, chest pain. Respiratory system problems may occur. If in the early phase of the disease there are no various kinds of complications, sensitization manifestations gradually fade, and the number of eosinophils in the blood also decreases.

The acute phase of the disease is followed by the chronic phase. This occurs 3 to 6 months after the pathogen enters the body. At this stage, gastroduodenitis develops (relatively compensated), accompanied by manifestations of cholepathy (in some cases, pancreatopathy). If a secondary infection is added to the above phenomena, cholangiohepatitis or bacterial cholecystocholangitis may occur. All this is complemented by dyspeptic and pain syndromes, as well as disturbances in liver function.

The occurrence and development of obstructive jaundice, liver abscesses, purulent angiocholangitis, and sclerosing cholangitis cannot be ruled out. With a prolonged course of the disease, cirrhotic changes occur in the liver, macrocytic anemia occurs, and stool disorders are observed.

Diagnosing diseases in the early stages (in the acute phase) is quite problematic. The presence of fascioliasis is assumed by careful study of data from epidemiological, anamnestic and clinical studies. The possibility of mass invasion of certain groups of people (geologists, tourists, etc.) is allowed. At the same time, the presence or absence of cases of the disease in a given region is determined.

In each case, differential diagnosis is carried out. Simultaneous studies are being conducted for infection with clonorchiasis, trichinosis, opisthorchiasis, eosinophilic leukemia, viral hepatitis (in the acute stage of fascioliasis), as well as cholangitis, cholecystitis and pancreatitis (in the chronic phase of the disease).

If there are suspicions about the hepatobiliary system for possible complications of a bacterial nature, it is necessary to consult a surgeon.

Treatment of fascioliasis

In case of severe allergic reactions characteristic of the acute stage of fascioliasis, treatment consists of a course of desensitizing therapy: calcium chloride and antihistamines are prescribed. The patient must adhere to a diet. If an infected person develops hepatitis or myocarditis, it is recommended to take prednisolone (30–40 mg per day) for a week. When the symptoms of the acute phase pass, the drug Chloxil is prescribed. The daily dosage is calculated as follows: per 1 kg of a person’s weight, 60 mg of the drug must be taken. The daily dose is drunk in 3 approaches. The course of treatment with Chloxyl is 5 days.

Another drug recommended by WHO is triclabendazole. The dose of the active substance should be 10 mg/kg. The medicine is taken once. In advanced cases, 20 mg/kg is prescribed. This dosage is taken in 2 approaches, the time interval between which should be 12 hours.

If fascioliasis is mild and without complications, praziquantel is recommended. The daily dose of the drug is 75 mg/kg. The medicine is taken in 3 approaches over 1 day.

Treatment of fascioliasis at the chronic stage is carried out using Chloxyl. General strengthening drugs and drugs that relieve cholestasis are also prescribed. In the event of a bacterial bile duct infection, a course of treatment with antibiotics is required.

At the end of the course of therapy, you need to take choleretic agents to cleanse the bile ducts from fragments of dead helminths.

Carrying out preventive measures to prevent cases of fascioliasis is a priority task of modern medicine and veterinary medicine.

To improve the health of hayfields and pastures, veterinary services use various molluscicidal agents designed to reduce the number of intermediate hosts. In regions that act as hotbeds of the disease, it is recommended to reclaim wetlands. For the treatment and prevention of animals, anthelmintic drugs are used, such as fasinex, valbazen, acemidofen, ivomekol plus, vermitan and others. Measures that reduce the possibility of fascioliasis include changing pastures and ensiling feed.

For humans, the main preventive measures are the following:

1. Thorough washing and heat treatment (dousing with boiling water, boiling) herbs, berries, vegetables, fruits.
2. Use well-filtered (preferably boiled) water for drinking.
3. Sanitary education for the population living in areas where this helminthiasis is endemic.

Prognosis of fascioliasis

In most cases, the disease has a prognosis that is favorable for life. Lethal outcomes, which are recorded quite rarely, are most often caused by complications that arise.