The general name for liver diseases characterized by dystrophic changes in the liver parenchyma in the absence of pronounced signs of inflammation. Depending on the etiological factors, their strength and duration of exposure, fatty degeneration - fatty hepatosis, amyloid degeneration - liver amyloidosis and other types of degeneration may predominate.
FATTY HEPATOSIS (FATTY DYSTROPHY, LIVER STEATOSIS)
A disease characterized by the accumulation of triglycerides in hepatocytes and disruption of basic liver functions. There are acute fatty hepatosis (toxic liver degeneration) and chronic fatty hepatosis, the latter is much more common than the former. In conditions of intensification of livestock farming, fatty hepatosis is the most common disease in highly productive cows, fattening livestock, including sheep. Pigs, fur-bearing animals, dogs, and zoo animals often get sick. Toxic liver dystrophy is more common in pigs.
Etiology. Fatty hepatosis is registered as primary, and more often as secondary concomitant disease. The causes of primary hepatosis include feeding low-quality, spoiled feed. Toxins of pathogenic fungi, products of protein rotting, and rancid fats are especially dangerous for the liver. The disease occurs when feeding livestock low-quality stillage, spent grain, pulp, kitchen waste, fish, meat and bone meal, feed yeast, rancid fats, concentrated and roughage, affected by toxicogenic fungi (Fusarium, Aspergillus, Penicillium, Stachybotris).
Liver dystrophy is caused by lupine alkaloids, potato solanine, and cotton meal goesipol. The possibility of liver damage by pesticides, nitrates and nitrites, urea and others cannot be ruled out. chemicals. Reason fatty liver disease There may be a deficiency of selenium in the feed. As a concomitant disease, hepatosis develops in obesity, ketosis, diabetes mellitus, cachexia and many other diseases, which are based on metabolic disorders and the functions of endocrine organs. Liver dystrophy is often a consequence of infectious and invasive diseases, chronic diseases of the gastrointestinal tract, kidneys and other organs.
Pathogenesis. The mechanism of development of fatty hepatosis consists of two main pathogenetic aspects: increased intake of fatty acids and their precursors into the liver, increased synthesis of triglycerides in hepatocytes and decreased rate of their removal from the liver.
Fatty hepatosis occurs in cases where the supply of fatty acids exceeds the ability of hepatocytes to metabolize and secrete them into the blood as triglycerides. This can be observed in obesity, increased lipolysis in adipose tissue during ketosis, diabetes mellitus, and fasting.
Intensive synthesis of fatty acids and triglycerides in the liver is observed with excessive consumption of fats and carbohydrates and overfeeding of animals. Suppression of fatty acid synthesis in the liver leads to increased formation of triglycerides. Along with this, the formation of lipoproteins in the liver, the main transport form of triglycerides from liver cells, is inhibited. The entry of hepatotropic poisons into the body inhibits the synthesis of apoprotein, a protein that is part of lipoproteins, and the transport of triglycerides is inhibited, so they accumulate in hepatocytes.
Due to the accumulation of fat in hepatocytes, proliferation of stellate endothelial cells occurs, other liver tissues are involved in the pathological process, necrosis and autolysis of cells occurs, which is most pronounced in acute toxic liver dystrophy. Dystrophy, necrosis and autolysis of liver cells lead to disruption of bile formation and excretion, protein-forming, carbohydrate-synthesizing, barrier to other functions of the liver. This is accompanied by indigestion, metabolism, accumulation of toxic metabolic products in the body, etc.
Symptoms. Acute fatty hepatosis develops quickly, it clinical manifestation characterized by signs of general intoxication and jaundice.
Sick animals are severely depressed, indifferent to others, body temperature can increase by 0.5-1°C, but does not stay at this level for long. Appetite is absent or reduced. The liver is often enlarged, soft, and slightly painful. Toxic effects on the brain due to the accumulation of ammonia, amines, phenols and other toxic substances in the body often lead to hepatic coma.
In cows, acute liver dystrophy appears at the time of calving or during the first 2-4 days after it. The animal refuses food, has difficulty getting up, lies down, sharp tachycardia, rapid breathing, and atony of the forestomach are observed.
In sheep, symptoms of the disease often begin to appear 2-4 weeks before lambing. The sheep refuses to feed, the pupils are dilated and motionless, the animal moves in a circle, falls to the ground, and after some time a coma occurs. The temperature is subnormal, fever is an exception.
Piglets experience anorexia, torpor, loss of strength, vomiting, diarrhea, general muscle weakness, sometimes convulsions, often scaly or nodular skin rash. In acute hepatosis, animals can die in a very short time or after 1-2 weeks. The mortality rate reaches 90%.
With chronic hepatosis, the symptoms are mild. Depression, general weakness, decreased appetite, and dyspeptic symptoms are observed. The liver is moderately enlarged, with a smooth surface, painful on palpation and percussion. Yellowness of the mucous membranes does not appear or is very slight. Body temperature is normal.
In the blood with acute and chronic fatty hepatosis, a decrease in glucose content is noted (in cows below 2.22 mmol/l), an increase in pyruvic acid (above 193 µmol/l), lactic acid (above 1.44 mmol/l), bilirubin (more than 10.3 µmol/l), cholesterol (more than 3.9 mmol/l). In case of toxic liver dystrophy, an increase in the activity of AST, ALT, and LDH is established. In the case of concomitant hepatosis, characteristic signs of the underlying disease are noted.
Pathomorphological changes. In acute fatty hepatosis, the liver is sharply enlarged, yellow or lemon-yellow in color, brittle or flabby, the pattern on the cut is smoothed. Chronic fatty hepatosis is often characterized by an enlarged liver, its edges are rounded, the organ has a motley mosaic pattern (brown-red areas alternate with gray or yellow). The predominance of fatty degeneration gives the liver a fatty appearance, clayey or ocher color. Histological examination reveals degeneration of hepatocytes, mainly in central parts lobes, disorganization in the structure of the liver lobes and the disappearance of their beam structure are observed. In toxic liver dystrophy, necrosis and lysis of hepatocytes and other cells are detected.
Diagnosis and differential diagnosis. Based on the results of clinical, laboratory, pathological and morphological data, analysis of animal feeding. Acute fatty hepatosis must be distinguished from acute hepatitis. In acute hepatitis, the spleen is enlarged; in hepatosis, it is normal. This sign allows you to confidently differentiate chronic hepatosis from cirrhosis of the liver.
Forecast. Acute fatty hepatosis is accompanied by severe liver failure and often leads to the death of animals. In chronic hepatosis, if the causes are eliminated and appropriate treatment is applied, the disease ends in recovery. Acute fatty hepatosis can turn into chronic, and the latter into cirrhosis of the liver.
Treatment. Eliminate the causes of the disease. The diets of ruminants include hay, grass cuttings or flour, oatmeal, barley meal, root vegetables; carnivores and omnivores are given fresh skim milk, cottage cheese, good-quality lean meat, fish, oatmeal and other cereals, and bran mash. The diets are supplemented with the introduction vitamin preparations.
Lipotropic, vitamin and choleretic drugs are mainly used as medications. Lipotropic agents include choline chloride, methionine, lipoic acid, lipomide, etc. Choline chloride and methionine release methyl groups, which prevent global infiltration and liver degeneration. Choline chloride is part of lecithin, which is involved in fat transport. It is prescribed orally in cattle: cattle and horses - 4-10 g, sheep - 1-2 g. Oral doses of methionine: cattle and horses - 3-20 g, pigs - 2-4 g, sheep - 0 .5-2 g, dogs - 0.5-1 g. The course of treatment is up to 30 days. Lipoic acid and lipomide have biochemical properties similar to B vitamins. Bile formation and bile secretion are stimulated by the use of magnesium sulfate orally in a dose of 50-70 g, as well as holagol, allohol, etc.
Prevention is based on avoiding the use of bad feed containing high concentrations of pesticides, nitrates, nitrites, etc. Premixes and additives are introduced. Carry out measures to prevent diseases of metabolism and endocrine organs.
LIVER AMYLOID - AMYLOIDOSIS HEPATIS
A chronic disease characterized by extracellular deposition in the tissue of the liver and other organs of a dense protein-saccharide complex - amyloid.
Amyloid is a complex of globulins and polysaccharides that changes color with iodine. Liver amyloid usually occurs in combination with amyloid deposition in the kidneys, spleen, intestines and other organs. The disease is more common in horses and has been reported in cattle and other animals.
Etiology. The disease is often caused by purulent chronic processes in the bones, skin, internal organs (arthritis, osteomyelitis, ulcers, tumors, pleurisy, bronchopneumonia, mastitis, endometritis, etc.). The disease often appears in horses that produce immune serums. Cachexia is in most cases accompanied by liver amyloidosis, although renal amyloidosis is not detected.
Pathogenesis. The waste products of microbes and the breakdown of tissue proteins cause disruption of protein metabolism and the deposition of amyloid on the walls of blood vessels in the liver, kidneys, spleen, and intestines. In the liver, this process begins in the peripheral parts of the hepatic lobules, then spreads to the entire lobule. The hepatic beams atrophy, continuous homogeneous areas of amyloid masses with compressed intralobular capillaries are formed. Due to impaired blood supply, tissue trophism decreases, hepatocyte degeneration and functional liver failure occur.
Symptoms. The most characteristic signs are pallor of the mucous membranes, enlargement of the liver and spleen (hepatosplenomegaly). The liver is dense, low-painful, accessible parts are even and smooth. Its percussion boundaries are expanded. The spleen is significantly enlarged and thickened. Jaundice is rare and mild. Digestion is disturbed. Protein is often found in urine.
Pathomorphological changes. The weight of the liver in large animals reaches 23 kg or more, its capsule is tense, its edges are rounded. The color is brownish clay, the pattern on the section is unclear. The spleen is enlarged and dense. Amyloid lesions are often found in the kidneys, intestines, and foci of inflammation in joints, bones and other tissues.
Diagnosis and differential diagnosis. They are based on medical history, liver biopsy, and characteristic clinical signs. In differential diagnostic terms, other liver diseases are excluded based on their specific symptoms.
Forecast. The disease can last for years.
Treatment. Animals are treated for the underlying disease. Drugs that normalize metabolism in the liver are used.
Prevention. They promptly eliminate inflammatory processes in organs and tissues.
Hepatosis is the general name for liver diseases characterized by dystrophic changes in the liver parenchyma in the absence of pronounced signs of inflammation.
Depending on the etiological factors, their strength and duration of exposure, fatty degeneration - fatty hepatosis, amyloid degeneration - liver amyloidosis and other types of degeneration may predominate.
Fatty hepatosis (fatty degeneration, liver steatosis) is a disease characterized by the accumulation of triglycerides in hepatocytes and disruption of the basic functions of the liver. There are acute fatty hepatosis (toxic liver degeneration) and chronic fatty hepatosis, which occurs much more often than the first. In conditions of intensification of livestock farming, fatty hepatosis is the most common disease in highly productive cows, fattening livestock, including sheep. Pigs, fur-bearing animals, dogs, and zoo animals often get sick.
Etiology. Fatty hepatosis is registered as a primary, and more often as a secondary concomitant disease. The causes of primary hepatosis include feeding poor quality, spoiled feed. Toxins of pathogenic fungi, protein rotting products, and rancid fats are especially dangerous for the liver. Hepatosis occurs when feeding animals with low-quality fish meal, meat and bone meal, feed yeast, rancid fats, spoiled meat, fish, etc.
Liver dystrophy is caused by lupine alkaloids, potato solanine, and cotton meal gossypol. The possibility of liver damage from nitrates, nitrites, pesticides and other mineral fertilizers, which are contained in food products in increased quantities, cannot be ruled out. The cause of fatty hepatosis may be a lack of selenium in feed, as well as a deficiency of essential acids, microelements and vitamins in the diet. In dogs, the most pressing deficiency in the diet is sulfur-containing amino acids - methionine, cystine, lysine, tryptophan, vitamins A, E, group B, selenium and zinc. Also in dogs, a common cause of fatty hepatosis is the administration of large doses of ivomec or cydectin.
As a concomitant disease, hepatosis develops in obesity, ketosis, diabetes mellitus, poisoning, cachexia and many other diseases based on metabolic disorders and dysfunction of endocrine organs.
In cats, in addition to obesity and diabetes, fatty liver disease can lead to anorexia, ulcerative colitis and drug therapy(catecholamines, steroids and corticosteroids), pregnancy and lactation. Stress may be one of the contributing factors.
Liver dystrophy is often a consequence of infectious and invasive diseases, chronic diseases of the gastrointestinal tract, kidneys, uterus, heart and other organs.
Pathogenesis. Fatty hepatosis develops with intense synthesis of triglycerides in the liver and the inability of hepatocytes to secrete them into the blood. The main pathogenetic role in this case is played by the excessive intake of fatty acids and toxins into the liver. Under the influence of toxic products, the synthesis of apoprotein protein, which is part of lipoproteins, is inhibited. Lipoproteins are the main transport form of triglycerides. It is in the composition of lipoproteins that triglycerides are secreted by hepatocytes into the blood. The accumulation of fat in the liver parenchyma is accompanied by a violation of its basic functions, necrosis and lysis of hepatocytes. Dystrophy, necrosis and autolysis of liver cells leads to disruption of bile formation and bile excretion, protein-forming, carbohydrate-synthesizing, barrier and other functions of the liver. This is accompanied by indigestion, metabolism, accumulation of toxic metabolic products in the body, etc.
Symptoms. Acute fatty hepatosis develops quickly, its clinical manifestation is characterized by signs of general intoxication and jaundice. Sick dogs are severely depressed, indifferent to others, body temperature may increase slightly by 0.5-1°C, but does not stay at this level for long. Appetite is absent or reduced. The liver is often enlarged, soft, and slightly painful. Toxic effects on the brain due to the accumulation of ammonia, amines, phenols and other toxic substances in the body often lead to hepatic coma.
The piglets experience anorexia, numbness, and loss of strength; vomiting, diarrhea, general muscle weakness, sometimes cramps, often a scaly or nodular skin rash. In acute hepatosis, animals can die in a very short time or after 1-2 weeks. The mortality rate reaches 90%.
In cows, acute liver dystrophy appears at the time of calving or during the first 2-4 days after it. The animal refuses food, has difficulty getting up, lies down, there is a sharp tachycardia, rapid breathing, and atony of the proventriculus.
In sheep, symptoms of the disease often begin to appear 2-4 weeks before lambing. The sheep refuses to feed, the pupils are dilated and motionless, the animal moves in a circle, falls to the ground, and after some time a comatose state sets in. The temperature is subnormal, fever is an exception.
In dogs, acute fatty hepatosis is accompanied by depression, parenchymal jaundice, and decreased or absent appetite. The temperature at the onset of the disease can increase by 0.5-1.0? C. Flatulence, persistent diarrhea and constipation, sometimes colic are noted, and with severe toxicosis - hepatic coma. The liver is enlarged, soft in consistency, not painful, the spleen is not enlarged.
In cats, the main symptom remains a sluggish appetite for a long time, sometimes the animal completely refuses food. The liver is enlarged, jaundice appears at a late stage of the disease with the development of renal failure.
With chronic hepatosis, the symptoms are mild. Depression, general weakness, and loss of appetite are observed. The liver is moderately enlarged, with a smooth surface, painful on palpation and percussion. Yellowness of the mucous membranes and skin does not appear or is very slight. Body temperature is normal.
In the blood during acute and chronic hepatosis, a decrease in glucose content is noted (in cows below 2.22 mmol/l), an increase in bilirubin (more than 10.3 µmol/l), cholesterol (more than 3.9 mmol/l). In case of toxic liver dystrophy, an increase in the activity of AST, ALT, and LDH is established. In the case of concomitant hepatosis, characteristic signs of the underlying disease are noted.
Course and prognosis. Acute fatty hepatosis is accompanied by severe liver failure and often leads to the death of the animal. In chronic hepatosis, if the causes are eliminated and appropriate treatment is applied, the disease ends in recovery. Acute fatty hepatosis can turn into chronic, and the latter into cirrhosis of the liver.
Pathomorphological changes. In acute fatty hepatosis, the liver is sharply enlarged, yellow or lemon-yellow in color, brittle or flabby, the pattern on the cut is smoothed. Chronic fatty hepatosis is often characterized by an enlarged liver, its edges are rounded, the organ has a motley mosaic pattern (brown-red areas alternate with gray or yellow). The predominance of fatty degeneration gives the liver a fatty appearance, clayey or ocher color. In dogs, the liver is often uniformly yellow, sometimes orange.
Histological examination reveals degeneration of hepatocytes, mainly in the central parts of the lobes, disorganization in the structure of the liver lobes, and the disappearance of their beam structure are observed. In toxic liver dystrophy, necrosis and lysis of hepatocytes and other cells are detected. Cell nuclei are reduced in volume, irregular in shape, located centrally, protoplasm is filled with fat drops of various sizes. Interlobular connective tissue without pronounced changes. The spleen is not enlarged.
The diagnosis is made on the basis of anamnesis, clinical signs, blood biochemistry, scatology, and urine examination. Acute fatty hepatosis must be distinguished from acute hepatitis. In acute hepatitis, the spleen is enlarged. But with hepatosis it is normal. The same sign allows one to confidently differentiate chronic hepatosis from cirrhosis of the liver.
Treatment. Eliminate the causes of the disease. The diets of ruminants include hay, grass cuttings or flour, oatmeal, barley meal, root vegetables; carnivores and omnivores are given skim milk, cottage cheese, good-quality lean meat, fish, oatmeal and other cereals, and bran mash. Diets are supplemented with the introduction of vitamin preparations. Dogs and cats with hepatosis are given food rich in L-carnitine, which activates fat metabolism in hepatocytes. Vigosin can be used as a source of L-carnitine and magnesium sulfate.
Lipotropic, vitamin and choleretic drugs are mainly used as medications. Lipotropic agents include choline chloride, methionine, lipoic acid, lipomide, lipostabil forte, essentiale, Liv-52, vitamin U, etc. Choline chloride and methionine release methyl groups, which prevent fatty infiltration and liver degeneration. Choline chloride is also part of lecithin, which is involved in fat transport. It is prescribed orally in doses: 4-10g for cattle and horses, 2-4g for pigs, 0.5-2g for sheep, 0.5-1g for dogs. The course of treatment is up to 30 days. Oral doses of methionine are indicated for cattle and horses from 3 to 20 g, for pigs - 2-4 g, for sheep - 0.5-1 g.
Vitamin U (the active form of methionine) is administered orally in doses (mg/kg): piglets - 10, sows - 3-5, cattle - 2-3. The approximate therapeutic and prophylactic daily dose of lipoic acid and lipomide is 0.5-1.0 mg/kg of animal weight. The course of treatment is 30 days. The hepatoprotectors hepabene and karsil, silitarin (legalon) and silybin, used in medicine, deserve attention.
Bile formation and bile excretion are stimulated by the use of magnesium sulfate orally in a dose of 50-70 g for large animals, 5-10 g for pigs, 3-5 g for sheep, daily dose should be divided into 2 doses. Cholagol, allohol and others are also prescribed. Dosages of allachol: large animals - 30 mg/kg, pigs and sheep - 50, small animals - 70 mg/kg.
Dogs and cats are prescribed sorbents and probiotics. Cats that refuse to eat are force-fed. Corn silk and immortelle flowers are used as phytotherapeutic agents.
Prevention. Good quality feeding. Use of sorbents for poisoning. Regularly giving probiotics. Providing animals with the necessary amount of carbohydrates, complete protein, selenium, zinc and other microelements, water- and fat-soluble vitamins. For carnivores, avoid foods with a high fat content.
All toxic medications are strictly dosed and used together with hepatoprotectors. Carry out preventive measures against infectious and invasive diseases.
Liver amyloidosis is a chronic disease characterized by the deposition of a dense protein-saccharide complex, amyloid, in the intercellular tissues of the liver and other organs. Liver amyloidosis usually occurs in combination with amyloid deposition in the kidneys, spleen, intestines and other organs. The disease is more common in horses than in cattle and other animal species.
Etiology. The disease is often caused by purulent chronic processes in the bones, skin, internal organs (arthritis, ostiomyelitis, ulcers, tumors, pleurisy, bronchopneumonia, mastitis, endometritis). The disease often appears in horses that produce hyperimmune serums. Cachexia is in most cases accompanied by liver amyloidosis, although renal amyloidosis is not detected.
Pathogenesis. The waste products of microbes and the breakdown of tissue proteins cause metabolic disorders and the deposition of amyloid on the walls of blood vessels in the liver, kidneys, spleen, and intestines. In the liver, this process begins in the peripheral parts of the hepatic lobules, then spreads to the entire lobule. The hepatic beams atrophy, continuous homogeneous areas of amyloid masses with compressed intralobular capillaries are formed. Due to impaired blood supply, tissue trophism decreases, hepatocyte degeneration and functional liver failure occur.
Symptoms. The most characteristic signs are pallor of the mucous membranes, emaciation, enlargement of the liver and spleen (hepatosplenomegaly). The liver is dense, low-painful, accessible parts are even and smooth. The percussion boundaries of the liver are expanded. The spleen is significantly enlarged and thickened. Jaundice is rare and not intense. Digestion is disturbed. Protein is often found in urine.
Pathological changes. The weight of the liver in large animals reaches 23 kg or more, its capsule is tense, its edges are rounded. The color is brownish-clayey, the pattern on the section is unclear. The spleen is enlarged and dense. Amyloid lesions are often found in the kidneys, intestines, and foci of inflammation in joints, bones and other tissues.
Diagnosis. Based on medical history, liver biopsy, and characteristic clinical signs. IN differential diagnosis exclude other liver diseases based on the absence of symptoms specific to them.
Forecast. The disease can last for years. The prognosis is unfavorable.
Treatment. Treated for the underlying disease. They apply the means.
Normalizing metabolism in the liver (sirepar, progepar, heptral).
Prevention. Timely elimination of purulent-inflammatory processes in organs and tissues.
Colostral toxicosis is an acute disease of newborns, characterized by diarrhea and general toxicosis. Calves are most often affected, but it can also occur in young animals of other species.
Etiology and pathogenesis. The main reason for calves is feeding straw, hay, silage, haylage or other feed affected by toxic fungi (mycotoxicosis) to dry and calving cows (heifers). Possible reason- toxicosis that occurs when pesticides and other toxic substances penetrate into the fetus and colostrum. As well as mastitis pathogens and their toxins.
The pathogenesis of this disease is similar to toxic dyspepsia. The central link in the pathogenesis of colostrum toxicosis is fermentopathy due to inhibition by toxins digestive enzymes with subsequent development of toxicosis.
Symptoms. The disease begins after the first drinking of colostrum on the 1st-2nd day after birth. Manifestations of the disease increase quickly: loss of appetite, uncontrollable diarrhea, liquid feces, severe depression to the point of coma, sunken eyes. Body temperature is within normal limits or below it. Reserve alkalinity is reduced.
Pathological changes are uncharacteristic. The mucous membrane of the abomasum and small intestine is swollen with pinpoint hemorrhages. The liver, kidneys and heart muscle are in the stage of protein-fatty degeneration. The spleen is not enlarged.
Diagnosis. Established on the basis of clinical signs, results of mycological and toxicological studies of feed, colostrum (milk), and rennet contents. It is necessary to differentiate the disease from toxic dyspepsia of a different etiology, bacterial, viral and other diseases.
Course and prognosis. The disease is fleeting. The prognosis is cautious and unfavorable.
Treatment. Calves are prescribed a strict diet using a decoction of flaxseed and rice. Oak bark, oatmeal jelly, yarrow infusion, horse sorrel and others medicinal herbs. Instead of two regular feedings, young animals are given a 0.5-1% solution of table salt or the above-mentioned decoctions.
The volume of the first portion of colostrum for a calf after fasting does not exceed 0.25 - 0.5 liters, but as recovery progresses it is gradually increased. Sick calves are fed 4 times a day. To suppress secondary microflora, antimicrobial drugs are prescribed orally 2-3 times a day, the course is 3-7 days. Antibiotics are prescribed after determining the sensitivity of the pathogenic intestinal microflora to them. Farmazin is administered orally at 1 ml/kg 2 times a day, ampiox, oksikan (calves, lambs 8-15 mg/kg, piglets 10-20 mg/kg 2 times a day).
To prevent dysbiosis, probiotics are prescribed (vetom, lactobacterin, bificol). To normalize water-electrolyte metabolism and acid-base balance, a 1% sodium chloride solution is prescribed orally (calves 2-4 liters per day); subcutaneous, intravenous or intraperitoneal alkaline solution of Chappot (equal volumes of 0.9% sodium chloride solution and 1.3% sodium bicarbonate solution, 5% glucose solution), Ringer-Locke solution and other salt mixtures.
To eliminate acidosis, 40-50 ml of 6-7% sodium bicarbonate solution is injected subcutaneously; the injection is repeated as it resolves. To relieve toxicosis, adsorbents are used orally 2-3 times a day: activated carbon, lignin (50-100 g for calves), enterosorbent (0.1 g/kg), polysorb VP (200 mg/kg for calves, 50-100 for piglets).
Hemodez (calves 50-100 ml), polyglucin (calves on the 1st day 10-15 ml/kg, on the 2-3rd day 5-7 ml/kg) are administered intravenously. To restore enzymatic processes in gastrointestinal tract prescribed orally 2-3 times: natural gastric juice, trypsin (0.1-0.3 mg/kg), enteroform (0.1-0.15 g/kg), lysozyme or lysosubtilin. The means of stimulating therapy include glucose-citrate blood, lactoglobulin, and dosm. The greatest attention is paid to the use of adsorbents and antitoxic drugs.
Russian Academy of Agricultural Sciences
State scientific institution
North Caucasus Research Institute
Livestock
FATTY LIVER
IN DAIRY COWS
(Toolkit)
Krasnodar 2012
UDC 636.22/.28.034:616.36
SKNIIZH
Reviewers:Kozlovsky Vsevolod Yurievich, Doctor of Biological Sciences, professor of quarrels, head. Department of Animal Science and Technology for Processing Livestock Products of the Velikolukskaya State Agricultural Academy;
Zolotukhin Sergey Nikolaevich, Doctor of Biological Sciences, Professor, Dean of the Faculty of Veterinary Medicine, Ulyanovsk State Agricultural Academy.
The brochure provides a description of a currently widespread disease - fatty liver in dairy cows, in a fully developed form necessary for its study by students and mastery by veterinary specialists. This description presents for the first time: a precise definition of the disease and the form of its manifestation; the main factors and conditions for the occurrence and development of the pathogenesis of the disease; symptoms and pathological changes; diagnosis and prognosis. The relevance of this work is that in the section “treatment of the disease” the author describes a new developed and implemented method for the treatment and prevention of hepatosis in animals (patent for invention) using an injectable hepatoprotective drug.
The manual was reviewed and approved at a meeting of the Academic Council of the State Scientific Institution SKNIIZH, protocol No. 6 of September 10. 2012.
© Russian Agricultural Academy © State Scientific Institution SKNIIZH
Definition Forms Etiology Pathogenesis Symptoms Pathological and anatomical changes Diagnosis Prognosis Treatment Literature usedDEFINITION
Fatty liver is a disease characterized by changes in the trophism and morphology of hepatocytes due to impaired energy metabolism in the body and infiltration of liver tissue with lipids.FORMS According to the course, acute, subacute and chronic are distinguished. According to its occurrence, it can be genetically determined (or dependent) and infectious-toxic in origin. Depending on the cause that caused fatty degeneration, it manifests itself as atrophy or hypertrophy of the liver.
There are simple hypertrophic obesity and degenerative-dystrophic fatty liver.
ETIOLOGY
Predisposing factors in the occurrence of fatty liver disease, both in adult cattle and in young animals, may be general weakening of the body and metabolic disorders, stagnation of blood in the venous system, overwork and hypothermia. However, fatty liver does not develop in all animals exposed to such effects, but depends on the adaptive and protective mechanisms of the body.
Various factors that reduce the body's resistance contribute to the disease: hypovitaminosis, mineral starvation, physical inactivity, irregular feeding, as well as prolonged protein overfeeding and dehydration.
Fatty liver syndrome constantly develops with ketosis and maternity paresis. Fatty liver degeneration in cows, as a secondary process, is observed with dystonia of the proventriculus, abomasum and intestines.
The following aggravating reasons, in combination with genetic pathology and the predisposition of the liver to dystrophy, as well as low adaptive ability, include the use of hormonal drugs for separation of the placenta, for the fruitful insemination of cows and/or mating of heifers under the age of 18 months, as well as intensive fattening of replacement young stock.
Degenerative fatty liver and necrobiosis of liver cells with rapid decay and autolysis of the organ parenchyma can occur due to intoxication with spoiled silage (butyric acid), poisons of plant (alkaloids, lupine) and mineral (phosphorus, arsenic, mercury) origin, as well as with increased use in feeding cattle residues from technical feed processing (potato stillage, brewer's grains, beet pulp, molasses). Fatty infiltration of the liver especially progresses with a deficiency of methionine, cystine, choline and tocopherol in the diet, when animals are deprived of active exercise.
PATHOGENESIS
Until now, the pathogenesis has been poorly understood; only one thing was clear: the occurrence of the disease is facilitated by a violation of fat metabolism.Dystrophic changes in the liver parenchyma in initial stage The development of the process is accompanied by swelling of the liver cells, disruption of the beam structure of the lobules and a general increase in liver volume. Subsequently, if the process becomes progressive, due to the disintegration and resorption of a large number of parenchymal cells, the volume of the liver decreases, and signs of fatty liver atrophy develop. In severe cases, cells that have undergone decay can gradually be replaced by fibrinous connective tissue, and then the so-called cirrhosis of the liver develops.
The accumulation in the body of toxic products of autolysis (lysis itself) of the liver parenchyma leads to severe damage to the heart (dystrophic processes), kidneys and central nervous system. Hemorrhages appear on the mucous and serous surfaces, the functioning of the digestive organs deteriorates, and parenchymal jaundice and hemolytic anemia may develop.
Next step toxic substances on liver cells causes dystrophic changes in them. In this case, the liver cells swell, compressing the bile ducts and portal vessels. The death of the affected cells is accompanied by nodular regeneration of the surviving remnants of the lobules and the growth of connective tissue elements in their place. Growing nodular regenerates compress the surrounding tissue, especially thin-walled veins, capillaries, lymphatic slits and bile ducts, which leads to a decrease in the blood supply to unaffected cells. At the same time, the formation of connective tissue partitions between the portal fields and the center of the lobules is enhanced. When toxins enter the liver through the portal vein, the process spreads along the periphery of the lobules. As a result of their compaction and wrinkling, the liver gradually decreases in volume - atrophic cirrhosis occurs.
With hypertrophic changes, the liver significantly enlarges as a result of intense neoplasm processes connective tissue not only inside the lobules, but also outside them. Most often, this process occurs when toxins enter through the hepatic artery. As a result of organ hypertrophy, blood flow slows down, blood stagnation occurs in the portal vein system, which leads to the occurrence of a catarrhal process in the biliary tract and gastrointestinal tract. Venous stagnation of blood in the portal system of the liver and the vessels of the mesentery causes a change in the physical colloidal and buffer state of the blood, which leads to increased permeability and fragility of peripheral blood vessels. The death of many hepatocytes leads to disruption of the protein-synthesizing function of the liver. As a result, the amount of albumin, prothrombin, fibrinogen and many enzymes in the blood serum decreases and the fraction of gamma globulins increases. Violation of the neutralizing function of the liver leads to the development of intoxication in the body and a decrease in the body’s natural resistance to various infections. Due to liver failure and autointoxication, parenchymal or obstructive jaundice can develop.
The occurrence in such cases of dystrophic lesions of the liver, as well as other organs and tissues, complicates the course of concomitant diseases and can cause death.
Another pathogenesis is associated with the intensity of lipid metabolism in the liver in cows before calving and in the early phase of lactation, leading to the accumulation of lipids in the liver due to excessive mobilization of fat reserves. The amount of fat reserves and the ability to use them under conditions of dominant lactation is considered as the main pathogenetic factor in the development of genetically determined fatty liver degeneration in cows.
Intensive selection of dairy cattle to increase milk yield has led to the fact that the genetic potential of productivity in early period lactation exceeds the animal's ability to consume a sufficient amount of feed, which forms a state of negative energy balance. If during the period of deep pregnancy the expenditure of energy and plastic substances in cows is determined by the rate of fetal growth, then in the new calving period - by the activity of biosynthesis and secretion of milk components on the one hand, and by inadequate exogenous intake nutrients and energy - on the other. At the same time, the intensive use of fat and protein reserves to cover the resulting deficiency is accompanied by the so-called “milking” of animals and a number of significant changes in lipid metabolism, which determine the subsequent productivity and health of highly productive cows. Excessive deposition of lipids (mainly triacylglycerols) in the parenchymal cells of the liver disrupts its functions, such as gluconeogenesis, glycogen synthesis, fatty acid oxidation, etc., and predisposes animals to a number of diseases - ketosis in the first place.
The physiological and genetic predisposition of highly productive cows to the pathological mobilization of their own body’s reserves for dairy products, in turn, leads not only to excessive fatty, but subsequently protein and toxic liver degeneration.
Recent studies of the behavior of the lability of VFA concentrations in the blood and in the rumen as the main sources of energy for ruminants, depending on its motor function, have shown that at the end of pregnancy and the beginning of lactation, the functional capacity of the rumen is significantly reduced, and the indicators of the live body weight of cows at the beginning lactation had negative dynamics. This circumstance explained the main physiological reason functional interruptions in the activity of the rumen - the leading proventriculus in ruminants. The physiological essence of this phenomenon lies in the fact that in the last stages of pregnancy there is not only an intensive increase in the weight and size of the fetus, but no less in the pregnant uterus of the cow there is also amniotic fluid, which together exert physical compression on the rumen, and thus most limit his full motor skills. Now, based on these data, we can make a reasonable conclusion that the energy deficit in the early period of lactation is not associated with a lack of feed consumed, but with insufficient (slow) rumen function, which already begins to appear two months before calving. At the same time, at the beginning of lactation in highly productive cows, tissue reserves provide almost half of the energy costs for the formation of milk components; according to some sources, more than 300 g of protein and up to 1000 g of fat are consumed per day. According to other observations, high milk yield in cows was ensured, in addition to feed energy, by mobilizing 2 kg of body fat per day, that is, metabolic processes in adipose tissue during this lactation period are aimed at mobilizing fatty acids.
According to some information, during the early period of lactation, cows consume up to 60 kg of tissue lipids. At the same time, intensive mobilization of reserve lipids, in addition to a positive effect when pronounced, also has its negative aspects: it can inhibit feed consumption, inhibit the fat-synthesizing function of the mammary gland, predispose cows to ketosis, while the efficiency of using the energy of reserve lipids is lower than energy from feed. Thus, the amount and utilization of body fat in cows are critical factors for optimizing their milk production, feed intake, reproduction and health.
In this regard, the main functions of the liver are disrupted:
bile formation and excretion, synthesis of proteins, urea and glycogen, neutralization of toxins, etc. This disease is caused by a change in the species composition of rumen microorganisms and causes insufficient or excessive fermentation of fiber, protein breakdown and self-poisoning with decay products. This disease is accompanied by a decrease in live weight, milk yield, joint pain, changes in the state of the nervous and cardiovascular systems, digestive and metabolic disorders and leads to general toxicosis.
In the chronic course of the disease, along with dystrophic changes in the liver, liver cirrhosis is possible.
SYMPTOMS
A genetically determined form of fatty liver degeneration in cows is detected using percussion along the enlarged boundaries of hepatic dullness. Diagnostic measurement of percussion boundaries is carried out along a horizontal line according to Aliyev. At the same time, it should also be noted that hepatic changes occur with concomitant changes in forestomach motility (detected by the generally accepted method of auscultation), general exhaustion (by visual examination) and metabolic disorders (by biochemical analysis blood and biopsied liver samples).The boundaries of the area of hepatic dullness with fatty liver hypertrophy will be localized in the following aisles: in the 1st month of lactation from the 13th rib to the 9th rib; in the 2nd month of lactation from the 12th rib to the 9th rib; at 6-9 months of lactation from 11 to 8 ribs; 10-12 months after calving from the 10th rib to the 8th rib. In addition, the shape of the percussion boundaries, depending on the calving period, will also change during the course of the reproductive cycle and will be in the form of a half-petal (lancet) smoothly turning into an elongated rhombus, and then turning into an irregular quadrangle. The presented data on the topographic location of the liver throughout the reproductive cycle are explained primarily by the biochemical indicators of lipid metabolism in the liver and blood, as well as the stages of pregnancy according to the period of gestation. Depending on the duration of pregnancy and the position of the fetus, the topography of the borders of the liver will change in the following sequence: at the 1st month of pregnancy, the borders will be from the 12th rib to the 9th rib;
at 4-7 months of pregnancy - from 11 to 8 ribs; at 8-9 months - from the 10th rib to the 8th rib.
Of the general symptoms for acute forms of genetically determined liver dystrophy and toxic pathology, general depression is noted, muscle weakness, sharp progressive weight loss, against the background of decreased productivity, a decrease in appetite (belching and chewing gum), disorders of the proventriculus (hypotension and atony) and gastrointestinal tract (diarrhea followed by constipation) are characteristic. Body temperature is normal or slightly reduced. On palpation and percussion, the liver area is painful in some cases, and in most cases an increase in the posterior percussion border is noted. Sometimes yellowness or cyanosis is detected on the mucous membranes and sclera of the eyes, in other cases hemorrhages are detected varying degrees(from spot to extensive) and a tendency to anemia (plastic, hemolytic).
An admixture of protein, an increased amount of urobilin and indican (a breakdown product of proteins), and sometimes bile pigments are found in the urine. In the sediment, along with organized elements of renal origin, crystals of leucine and tyrosine are often found, indicating a violation of the protein-forming function of the liver.
In the acute toxic form and rapidly increasing symptoms of intoxication against the background of cardiovascular failure, death can occur.
In case of chronic fatty liver degeneration clinical symptoms less pronounced. In such animals, nonspecific general symptoms come to the fore: exhaustion or sometimes emaciation does not progress, and general obesity of the animal, atony and hypotension of the forestomach, stagnation of feed mass in the book, slowdown of intestinal motility, decreased productivity and reproduction (reproduction) are also recorded. Jaundice syndrome may not exist. Mild hemorrhages of the mucous membranes, sclera, and sometimes trophic ulcers and erosions on the skin are noted. With hypertrophic fatty liver, the percussion border is increased. In atrophic it is reduced. The course of the disease is feverless, body temperature often drops to the minimum normal limits.
An increased content of globulins, residual nitrogen, ammonia, urea, and serum transaminase is found in the blood of patients. At the same time, the content of albumin, fibrinogen and glucose in the blood serum is significantly reduced. Hypoplastic anemia (impaired bone marrow hematopoiesis) and decreased blood clotting (slow ESR) are noted.
PATHOLOGICAL AND ANATOMICAL CHANGES
The pathological and anatomical clinical picture of genetically determined fatty (as well as toxic) liver degeneration is confirmed as a result of repeated forced slaughter and autopsy. An autopsy must be performed no earlier than 2 hours after death. In this case, the liver at autopsy is found to be yellow or gray-yellow (clayey) in color, and feels moderately dense or loose to the touch.At hypertrophic form the liver is significantly increased in volume compared to the norm, its edges are rounded, the capsule is tense, the pattern of the lobular structure is smoothed. In most cases, when palpating the liver, some areas are crushed in the hand or areas of disintegrated liver tissue of varying sizes are found. In rare cases, the size of the liver is unchanged or reduced, while the consistency is moderately dense. Clay-colored buds with a smeared, loosened surface of the cortical layer are often found. During the autopsy, the vast majority of blood is uncoagulated and in small volumes. The mucous membranes of the intestines are diffusely or in some areas inflamed, bright red, swollen, sometimes covered with viscous transparent mucus, in places with noticeable small hemorrhages. In severe cases, erosions and ulcers are noticeable on the mucous membranes.
During autopsies of dead animals and forced slaughter of such animals, along with liver pathology, thinning of the rumen walls is also revealed. This circumstance, in turn, explains the impaired function of the rumen, which arose as a result of compression of the proventriculus by the fetus in last month pregnancy
DIAGNOSIS
The diagnosis is made based on the results of a clinical examination - the percussion method reveals enlarged boundaries of hepatic dullness (graph 1), and the auscultation method reveals hypotension and atony of the scar. At the same time, subclinical blood parameters indicate increased levels of ketone bodies and decreased levels of glucose and hemoglobin. Anamnestic information for the genetically determined form of fatty liver degeneration states the predominant retirement of cows in the first month after calving. And for all animals characteristic feature is rapid weight loss. Biochemical analysis in the blood establishes high concentrations of non-esterified fatty acids (NEFA) and low betalipoproteins (VLDL - very low density lipoproteins), and in biopsied liver samples a high degree of infiltration of liver tissue with lipids is determined, mainly due to the triacylglycerol fraction.Graph 1. Liver dimensions along the horizontal line in cows by months after calving (cm) Photo 1. Picture of fatty liver during histological examination The diagnosis is confirmed by the results of a comprehensive pathological autopsy of dead and forced slaughtered animals, as well as histological examination (photo 1) of selected liver samples . Methods of toxicological analysis exclude the causes of toxic fatty degeneration in feed in intravital biological and pathological material.
FORECAST
The acute form lasts from 4 to 7 days, the subacute form lasts from seven days to three weeks, and without active pathogenetic therapy can lead to the death of the animal or forced slaughter and departure of highly productive cows from the herd. The chronic course of liver lipidosis does not lead to death in ruminants, but without therapeutic measures they can become the object of culling for productivity and reproductive ability. Recently, new cows, even with subclinical fatty liver, have an increased service period. Since lipid liver causes a delay in normal estrus after calving at the beginning of cyclic ovarian activity, this increases the number of inseminations before fertilization. The immediate reasons for this are a lack of glucose produced in the liver and a violation of the metabolism of sex steroids - a process that occurs directly in the liver. In this context, one can find an explanation for why reproductive function tends to be more frequently impaired when cows are highly productive. In these cases, there is severe carbohydrate (glucose) deficiency and excessive mobilization of lipids, which can disrupt liver functions, primarily glucose-synthesizing and steroid-metabolizing. When the concentration of glucose in the blood is low, its availability to peripheral tissues decreases and the hypothalamic-pituitary-gonadal connections necessary for reproductive function are disrupted. On the other hand, lipid liver cells, due to reduced functional activity, cannot provide the necessary metabolism and/or catabolism of sex steroids, which leads to impaired reproductive function.TREATMENT
Treatment should first of all be directed against the underlying disease and the cause that caused fatty liver degeneration. Due to the fact that the etiology of fatty liver has a wide range of causes, factors and conditions for their occurrence, treatment must be comprehensive. Complex treatment includes:dietary regimen, pathogenetic and symptomatic therapy, which, in turn, has an effect on the harmful agent, is aimed at removing toxic metabolic products from the body, combating dehydration, and restoring the normal functioning of all systems and organs. A correctly established diagnosis is no less important, since the symptom of liver dysfunction is accompanied by a large list of diseases of various etiologies and pathologies.
Poor quality, toxic or suspected toxic feed is excluded from the diet, and silage production is reduced. The feeding regimen should be 5–6 times. Easily digestible carbohydrate and good-quality feeds are introduced into the diet (grass, carrots, vegetables, herbs, meadow hay, grass flour, root vegetables, fresh skim milk) and provide the animals with a constant watering hole, accordingly reducing the nutritional value of protein feeds. To bind toxins and absorb excess gases, milk, aqueous suspensions of activated or charcoal are injected inside through a probe.
To stimulate peristalsis and intestinal secretion, Carlsbad salt is recommended in small doses. For severe pain in the liver area, use atropine, belladonna extract, analgin, and warming the liver area with incandescent lamps. In a complex of therapeutic measures to normalize liver function and relieve intoxication, glucose (20% - 300 ml) with ascorbic acid (5% ml per cow), insulin (200 units per cow), cardiac drugs, and also vitamins K, B1. If necessary, symptomatic therapy is carried out in parallel with the use of antidotes and antioxidants. For 2-3 weeks after clinical recovery (restoration of appetite, disappearance of intoxication), the animals are kept on a gentle diet with the introduction of the best hay, carrots, and fresh skim milk. Methionine and vitamins are also given.
Other known generally accepted methods and drugs used to provide medical care for hepatic diseases, include: glucose, hemodez, methionine, tocopherol, analgin, urotropine and choleretic agents.
Despite the fact that in veterinary practice widely, depending on the conditions and prevailing situations in a particular case, approaches complex treatment, set out above, using simultaneously various schemes, methods and means, consisting of several drugs. The issues of treatment and prevention of hepatic disorders still remain an urgent problem in the safety of animals, including adult cattle, since, firstly, it is not always possible to independently determine the cause without laboratory analysis, and also to eliminate and prevent manifestation of dystrophy and liver dysfunction. Secondly, the results of subclinical research of biological material and examination of feed are received by the treating doctor, unfortunately, as a rule, late.
Thirdly, the action of the recommended drugs is aimed at eliminating toxins from the body, bile from the patient’s liver, and relieving pain, which, in turn, do not fully restore impaired liver function and structural changes in liver cells.
In connection with the problems raised above and based on the requirements for treatment and prevention, when creating and using new environmentally friendly drugs from natural and natural remedies, a new drug “Antitox” has now been proposed, which has an antiseptic and anti-inflammatory effect, improves and restores lipid-carbohydrate (energy) metabolism, tissue regeneration, is a good antidote and antioxidant, and above all, is not an antagonist of drugs used in complex regimens for the treatment and/or prevention of hepatosis, including vaccines.
The advantage of the proposed drug and the method of its use is that it allows, using the liver percussion method, to more quickly monitor the clinical state of its size, since the results of subclinical (laboratory) analysis, and even more so histological examination, as production practice shows, are received in farming in at least 7-14 days.
The advantage of the drug is that it consists of amino acids from the liver tissue of clinically healthy animals, obtained by hydrolytic means, and therefore its entry into the body by injection allows the drug to be selectively directed to the liver, since the body has a genetically corrected dependence in the use of ingredients obtained from similar fabrics. When hydrolytic cleavage of the protein structures of the liver extract occurs, long polypeptide chains of the protein are broken down into amino acids. During the process of cleavage, the protein loses its species specificity, colloidal properties and no longer has primary toxicity or antigenic and anaphylactic properties. However, amino acids retain their belonging to liver tissue.
The injection method for the treatment and prevention of hepatosis, including fatty degeneration in cows, is used due to the fact that in case of liver disease, the intake of the therapeutic and prophylactic agent together with the feed and its absorption will be ineffective due to the digestive characteristics of ruminant animals, in addition A sick animal usually has no appetite. As for the digestive characteristics of ruminant animals (cows, sheep, goats, camels, etc.), a solution of a therapeutic and prophylactic agent containing amino acids, including essential ones, that enters the digestive system can be used by microorganisms and the animal’s body itself as nutritional components, in addition, it is impossible to accurately control the dose of the drug entering the body together with the feed.
Injection of a solution of liver hydrolyzate promotes faster and better diffusion (penetration) into the liver than when taken together with food, as a result of which regenerative processes and binding of toxic substances are more actively carried out.
Therapeutic and preventive effectiveness is achieved directly by administering the hepatoprotective agent “Antitox” by injection subcutaneously, intramuscularly or intravenously once a day. For therapeutic purposes, fresh cows with a live weight of 350-550 kg, in which hepatic changes occur with concomitant changes in forestomach motility, general exhaustion and metabolic disorders, the dose of the drug is 20.0 ml, with 0.5 doses administered subcutaneously and 0.5 doses intramuscularly. simultaneously for 5-6 days in a row. In case of maternity paresis and “critical animals”, with obvious signs of staleness, and in order to avoid death, the drug is administered daily intravenously in a dose of 100-200 ml, diluted 1:1 with 40% glucose, until the threat of forced slaughter is eliminated, and then scheme for fresh cows. For the purpose of prevention - dry cows weighing 350-550 kg in a dose of 10.0-20.0 ml with an interval of 7 days, a total of 5-7 injections.
The hepatoprotective drug “Antitox” can be successfully used not only for the treatment of fatty liver, but also for other types of hepatic disorders.
BIBLIOGRAPHY
1. Dushkin E.V. Indicators of lipid-carbohydrate metabolism and fatty acid composition of milk fat by phases of the reproductive cycle in Yaroslavl cows: Abstract of the dissertation of the candidate of biological sciences. – Borovsk:VNIIFBP agricultural animals, – 1993. – 25 S.
2. Dushkin E.V., Trofimushkina E.A. Changes in the content of ketone bodies in the blood of Yaroslavl cows depending on the level of feeding during the new calving period // Veterinary Science of Kuban. - Krasnodar. – 2007. – No. 1. – pp. 20-21.
3. Dushkin E.V. Percussion diagnosis of liver lipidosis in cows and its treatment with the drug “Antitox” // Scientific and Practical Congress “Current Problems of Veterinary Medicine”. – St. Petersburg, – 2007. – P. 90-93.
4. Dushkin E.V. Physiological and biochemical substantiation of the lability of lipid-carbohydrate metabolism and its correction in cattle: Abstract of the dissertation of a doctor of biological sciences. – Orel: Orel State Agrarian University, – 2009. – 37 P.
5. Dushkin E.V. Liver lipidosis and ketonemia // Veterinary medicine of Kuban. - Krasnodar. – 2007. – No. 5. – P. 25.
6. Baird G.D. Primary ketosis in high-producing dairy cows; Clinical and subclinical disorders, treatment, prevention, and outlook // Journal of Dairy Science. – 1982. – Vol. 65. – N1. – R. 43-47.
7. Dushkin E.V. Dependence of milk production and liver condition after calving // Animal husbandry technology. - Volgograd. – 2008. – No. 3 (3). – P. 36-8. Dushkin E.V., Firsov V.I. Technological and physiological-biochemical causes of fatty liver // Materials of the international scientific and practical conference “Agrarian Forum - 2008”. – Sumy: Sumy national. agricultural, university. – 2008. – P. 83-84.
9. Sharabrin I.G. Internal non-contagious diseases of farm animals: – M.: “Kolos”, – 1976. – S.
10. Dushkin E.V., Paraponov S.B., Mundyak I.G. Hepatic disorders are curable // Animal husbandry of Russia. – 2008. – No. 1. – pp. 42-43.
11. Sharabrin I.G., Alikaev V.A., Zamarin L.G. Internal non-communicable diseases of farm animals:
– M.: Agropromizdat, – 1985. – P. 348-404.
12. Khokhrin S.N. Feeding farm animals: – M.: Kolos, – 2004. – 692 p.
13. Dushkin E.V. Fatty liver degeneration and methods of its improvement in cattle // Agro-industrial complex market. - Volgograd. – 2008. – No. 1 (52). – pp. 92-93.
14. Dushkin E.V. On the relationship between mammary gland function and fatty liver in highly productive cows // Agricultural biology. Animal biology series. - Moscow. – 2010. – No. 2. – P. 18-24.
15. Dushkin E.V. Features of adaptation of lipid metabolism in ruminants // Effective animal husbandry. - Krasnodar. – 2007. – No. 12 (25). – pp. 15-16.
16. Dushkin E.V., Paraponov S.B., Mundyak I.G. Breast function and fatty liver. // Agrarian expert. – 2008. – No. 6. – P. 38-40.
17. Denisov N.I. Ways to increase the use of feed energy by productive animals // Physiology and biochemistry of energy nutrition of agricultural animals. Scientific works of VNIIFBP of agricultural animals. – Borovsk, – 1975. – No. 14. – pp. 20-30.
18. Dmitrochenko A.P. The importance of balanced feeding in the intensification of livestock production. – L.: Knowledge, – 1974. – P. 67-71.
19. Dushkin E.V. The content of total lipids and triglycerides in the liver depending on the level of feeding in fresh-calving Yaroslavl cows // Abstract journal. Dairy and beef cattle breeding. – 1989. – No. 10. – P. 1.
20. Nadalyak E.A., Reshetov V.V. Energy metabolism in lactating cows // Animal husbandry. – 1978. – No. 1. – pp. 53-56.
21. Oll Yu.K. On the regulation of energy nutrition for cattle // Physiology and biochemistry of energy nutrition for agricultural animals. Scientific works of VNIIFBP of farm animals. – Borovsk: VNIIFBP agricultural. animals, – 1975. – No. 14. – P. 98Broster W.H. Experiments on the nutrition of the dairy heifer; 8. Effect on milk production of level of feeding at 2 stages of lactation // Journal of Agricultural Science. – 1969. –Vol. 72. – N2. – P. 229-245.
23. Broster W.H., Foot A.S., Lene C. The effect of the plane of nutrition in gestation on the amount and range of milk produced in the first lactation by cattle // L. Tierphysiol. Tiernernahr. Futtermittelk. – 1970. – Vol. 26. – N2. – P. 112-120.
24. Reid I.M., Roborts C.I. Fatty liver in dairy cows // In Practice – 1982. – N4. – P. 164-169.
25. Reshetov V.V., Nadalyak E.A. Energy metabolism and productivity of cows with increasing concentration of metabolic energy in the diet // Scientific. tr. VNIIFBiP agricultural
animals. – Borovsk: VNIIFBP agricultural. animals, - 1979. - T.
21. P. 3-11.
26. Dushkin E.V. The degree of lipid infiltration in the liver during the new calving period and problems of the reproductive cycle // Materials of the international scientific and practical conference “Current problems of animal reproduction”. – Dubrovitsy-Bykovo, – 2007. – P. 182-184.
27. Dushkin E.V. Milk production and liver condition after calving based on the results of using the drug “Antitox” // Zootechnics. – 2008. – No. 7. – pp. 21-22.
28. Dushkin E.V. Testing a new drug “Antitox” for fatty liver hypertrophy in fresh cows // Veterinary Science of Kuban. – 2008. – No. 1. – pp. 12-13.
29. Dushkin E.V. Physiology of lactation and problems of liver pathology // Collection of scientific papers of the international scientific and practical conference “Scientific principles of increasing the productivity of farm animals”. – Krasnodar: SKNIIZH, – 2008. – Part 1. – P. 112-114.
30. Dushkin E.V. Antitox – testing a new drug // Veterinary medicine of farm animals. – 2010.
– No. 10. – pp. 45-46.
31. Dushkin E.V., Dushkin V.V., Eremenko V.I. Motor function of the rumen and the level of VFA in cows according to the phases of the reproductive cycle // Collection of scientific papers of the 4th international scientific and practical conference “Scientific principles of increasing the productivity of farm animals”. – Krasnodar: SKNIIZH, – 2011. – Part 2. – P. 108-109.
32. Dushkin E.V., Podlesny N.V., Eremenko V.I. Results of using liver hydrolyzate in cattle // Materials of the V International scientific conference dedicated to the 50th anniversary of VNIIFBP “Current problems of biology in animal husbandry.” – Borovsk: VNIIFBP agricultural. animals, – 2010. – P. 157-158.
33. Ovcharenko E.V., Ilchenko M.D., Medvedev I.K.
The function of milk formation and the state of tissue depots of the body depending on the level of energy consumed at the beginning of lactation in highly productive cows // Scientific. tr. “Physiology and biochemistry of agricultural energy nutrition. animals." – Borovsk: VNIFBP agricultural. animals, – 1975. – T. 14. – P. 193-204.
34. Islamova N.I. Blood lipids and their use by the mammary gland in connection with the level of fat secretion in cows' milk: Abstract of the dissertation of a candidate of biological sciences. – Borovsk: VNIIFBP agricultural. animals, - 1968. - 19 S.
35. Chapman M.J., Forgez P. Lipid transport systems:
some recent aspects in swine, cattale and trout during development // Reproduction nutrition development. – 1985. – Vol. 25. – N16. – P. 217-226.
36. Matyushchenko P.V. Metabolism of lipids in the adipose tissue of dry and fresh cows: Abstract of the dissertation of a candidate of biological sciences. – Borovsk: VNIIFBP agricultural. animals, – 1996. – 21 p.
37. Emery R.S. Deposition, secretion, transportation and oxidation of the fat in ruminants // Journal of Animal Science. – 1979. – Vol. 48. – P. 1530-1537.
38. Vernon R.Y., Cleg R.A., Flint D.D. Adaptations of adipose metabolism and number of insulin receptors // Comparative Biochemistry Physiological – 1985. – Vol. 81B. – P. 909-913.
39. Smirnov A.M., Konopelko Ya.P., Postnikov V.S.
Clinical diagnosis of internal non-communicable diseases of farm animals. – L.: Kolos, – 1981. – S.
40. Aliev A.A. Liver biopsy // Operative methods for studying farm animals. – L.: Science, – 1974. – P. 233-236.
41. Dushkin E.V. Profile of total lipids and triacylglycerols in the liver by phases of the reproductive cycle // Scientific journal. Proceedings of the Kuban State Agrarian University. – 2007. – No. 4 (8). – pp. 78-80.
42. Dushkin E.V. Topography of the liver of cows by phases of the reproductive cycle // XX Congress of the Physiological Society named after. I.P. Pavlova. – Moscow, – 2007. – P. 218.
43. Dushkin E.V. Features of changes in NEFA and beta-lipoproteins in the blood depending on different levels feeding and the associated lipid content in the liver of fresh cows of the Yaroslavl breed // Abstract journal. Dairy and beef cattle breeding. – 1990.– No. 3.– P. 4.
44. Dushkin E.V., Matyushchenko P.V., Eremenko V.I. Dynamics of VFA in the blood according to the phases of the reproductive cycle // Bulletin of Sumy NAU. Series "Veterinary Medicine". - Sumy. – 2006. – No. 7 (17). – pp. 33-36.
45. Dushkin E.V. The condition of the liver of cows according to the phases of the reproductive cycle and during its fatty infiltration during the milking period at different levels of feeding // Veterinary Science of Kuban. - Krasnodar. – 2006. – No. 6. – P. 21.
46. Reid I.M., Collins R.A., Treacher R.J. Organelle changes in the liver cells of dairy cows around the time of calving // Journal comparative pathological. – 1981. – Vol. 190. – P.
47. Dushkin E.V., Mundyak I.G. Fatty liver in cows after calving and problems during the service period // Mixed feed. – 2008. – No. 7. – P. 77.
48. Mazur A., Gueux E., Chilliard Y. Evolution des lipides et lipoproteines plasmatiques chez la vache // Reprod. Nutr. Develop. – 1986.– V. 26. – P. 357-358.
49. Mazur A., Rayssiguier Y., Gueux E. Importance de la steatose hepatiques chez la vache laitiere presentant des troubles metaboliquis en debut lactation // 15th World Buiatrics Congress, Plama de Mallorca. – 1988. – P. 252.
50. Reid I.M. Incidence and severity of fatty liver in dairy cows // Veterinary Research. – 1980. – Vol. 107. – P. 281-284.
51. Reid I.M., Collins R.A., Baird G.D. Lipid production rates and the pathogenesis of fatty liver in fasted cows // Journal of Agricultural Science. – 1979. – Vol. 93. – P. 253-256.
52. Reid I.M., Roberts C.J., Treacher R.J. Effect of body conditijn at calving on tissue mobilization // Anim. Prod. – 1986.
– V. 43. – P. 7-15.
53. Baird G.D. Lactation, pregnancy and metabolic disorder in the ruminant // Proceedings Nutrition Society. – 1981. – Vol.
40. – N1. – P. 115-120.
54. Dushkin E.V. Indicators of liver lipidosis and service period depending on different levels of feeding // Abstracts of reports of the international scientific and practical conference. "Problems of intensification of production of livestock products." – Zhodino, – 2008. – P. 190-191.
55. Dushkin E.V. The problem of hepatic disorders and approaches to their elimination with the complex drug “Antitox” // Collection of scientific papers of the XIV International Scientific and Practical Conference “Modern problems of intensification of pork production”. – Ulyanovsk, – 2007. – T. 3. – P. 207-211.
56. Dushkin E.V., Dushkin D.V. New in the treatment of dyspepsia // Materials of the scientific conference of the Sumy Agricultural Institute: Ways to increase productivity and quality of agricultural products. – Sumy: Sumy Agricultural Institute, – 1993. – P. 109.
57. Antipov V.A., Menshenin V.V., Turchenko A.N.
Effective veterinary technologies to increase the reproduction, safety and productivity of animals (guidelines). – Krasnodar, – 2005. – P. 1, 42-43.
58. Dushkin E.V. Method for the treatment and prevention of hepatosis in animals // Patent for invention No. 2385728. Application No. 2008113942/13. Priority of invention 04/09/08. Application publication date 10.20.2009. Registered in the State Register of Inventions of the Russian Federation on 04/10/10. Published 04/10/10. - Bull. – No. 10.
59. Antipov V.A., Urazaev D.I., Kuzmirova E.V.
The use of beta-carotene preparations in animal husbandry and veterinary medicine. – Krasnodar: KubGAU, – 2001.
60. Topuria L.Yu. Environmentally safe medicines in veterinary medicine // Izv. OSAU. – Orenburg:
OSAU, – 2004. – T. 4. – P. 121-122.
Similar works:
« ST. PETERSBURG STATE FORESTRY ACADEMY NAMED AFTER S. M. KIROV DEPARTMENT OF FORESTRY FORESTRY TAXATION AND FOREST MANAGEMENT INDEPENDENT WORK OF STUDENTS Guidelines for training certified specialists in the specialty 080502 Economics and management at an enterprise (forestry farming and forestry..."
“Federal Agency for Agriculture Federal State Educational Institution of Higher Professional Education Michurinsk State Agrarian University Department of Technology of Production and Processing of Livestock Products Methodological instructions for conducting laboratory and practical classes in the discipline “Technology of primary processing of livestock products” for 5th year students of the Technological Institute of specialty 310700 – animal science Approved...”
“MINISTRY OF AGRICULTURE OF THE RUSSIAN FEDERATION State University of Land Management Department of Land Use and Land Cadastre LAND CADASTRE Guidelines for writing and formatting theses (thesis projects) Faculty - Land Cadastre Specialty - 3 1 1 0 0 0 Land Cadastre Moscow 2001 UDC 333 .34 Prepared and recommended for printing by the Department of Land Use and Land Cadastre of the State University of Land Management (protocol No. 2..."
"MINISTRY OF AGRICULTURE OF THE RUSSIAN FEDERATION FEDERAL STATE EDUCATIONAL INSTITUTION OF HIGHER PROFESSIONAL EDUCATION ALTAI STATE AGRICULTURAL UNIVERSITY E.G. Paramonov, A.P. Simonenko BASICS OF AGROFORESTRY Tutorial Barnaul Publishing house AGAU 2007 UDC 634.0.2.(635.91) Fundamentals of agroforestry: textbook / E.G. Paramonov, A.P. Simonenko. Barnaul: Publishing house AGAU, 2007. 224 p. The educational publication contains the main provisions revealing...”
“PHARMACOLOGY AND THERAPY UDC 619.6:616.2:636.42/.46 METHODOLOGICAL MANUAL for the diagnosis, prevention and treatment of respiratory diseases in piglets Voronezh-2010 Methodological manual developed by the All-Russian Research Veterinary Institute of Pathology, Pharmacology and Therapy of the Russian Agricultural Academy (A.G. Shakhov, L. Yu. Sashnina, D.V. Fedosov,...”
“LABOR AND EMPLOYMENT AGENCY OF THE KRASNOYARSK REGION Methodological manual FIRST STEPS OF AN ENTREPRENEUR Krasnoyarsk 2011 Methodological manual First steps of an entrepreneur, intended for unemployed citizens starting their own business, beginning and existing entrepreneurs. The methodological manual provides information on the interaction of entrepreneurs with territorial bodies of federal executive authorities and other institutions related to the organization and management...”
"DONETSK STATE MEDICAL UNIVERSITY. M. GORKY DEPARTMENT OF SOCIAL MEDICINE, HEALTH ORGANIZATION AND HISTORY OF MEDICINE METHODOLOGICAL INSTRUCTIONS on social medicine, organization and economics of health care for 6th year students of the medical and preventive department (module 1: USE OF A COMPLEX OF STATISTICAL METHODS TO ASSESS THE STATE OF HEALTH POPULATION AND ACTIVITIES OF MEDICAL INSTITUTIONS. TREATMENT ORGANIZATION -PREVENTIVE CARE AT DIFFERENT LEVELS AND...”
"KUBAN STATE AGRICULTURAL UNIVERSITY Faculty of Management Department of State and Municipal Administration METHODOLOGICAL RECOMMENDATIONS for the introduction of public-private partnerships in the economy of the agro-industrial complex of the Krasnodar region for students of economic specialties Krasnodar 2012 1 Methodological instructions..."
"MINISTRY OF EDUCATION AND SCIENCE OF THE RUSSIAN FEDERATION federal state budgetary educational institution of higher professional education ULYANOVSK STATE TECHNICAL UNIVERSITY M. A. Ryabova ANALYSIS OF FINANCIAL REPORTING Educational and practical manual for students of specialty 08010965 Accounting, analysis and audit and bachelor's degree ditch direction Economics majoring in Accounting, analysis and audit of full-time and part-time departments of Ulyanovsk UlSTU 2011 UDC 657..."
« State Agrarian University N.E. Borisenko, O.V. Kronewald VETERINARY AND SANITARY CONTROL OF THE PRE-SLAUGHTER CONDITION OF ANIMALS, METHOD OF VETERINARY AND SANITARY INSPECTION OF SLAUGHTER PRODUCTS AND DETERMINATION OF THE SPECIES OF MEAT Educational and methodological manual for laboratory and practical classes and independent work for students and..."
“Educational institution Vitebsk Order of the Badge of Honor State Academy of Veterinary Medicine M.V. Bazylev Development of job descriptions for managers and specialists of agricultural enterprises Educational and methodological manual for students of the Faculty of Veterinary Medicine full-time and correspondence forms training, students of FPK and PC Vitebsk Educational Institution VGAVM 2007 UDC 631.158: 658.3 - 05 BBK 65.9 (2) 32 R 17 Reviewers: Bezborodkin N.S., candidate of veterinary sciences, associate professor; Aleksin M.M., candidate...”
“Ministry of Agriculture of the Russian Federation Federal State Educational Institution of Higher Professional Education Ural State Academy of Veterinary Medicine A.A. Belookov Basic lectures on the course Fundamentals of biotechnology for processing agricultural products Troitsk, 2006 UDC 631. 147 (075) BBK 65. 9 (2) B 44 Reviewers: Doctor of Agricultural Sciences, Professor of the UGAVM. A.M. Monastyrev Doctor of Agricultural Sciences, Professor of the Bashkir Scientific Research Institute of Agricultural Sciences. A.G. Fenchenko Candidate of Agricultural Sciences,...”
“Ministry of Agriculture of the Russian Federation Federal State Budgetary Educational Institution of Higher Professional Education BURYAT STATE AGRICULTURAL ACADEMY IM. V.R. FILIPPOVA FACULTY OF VETERINARY MEDICINE _ Department of Therapy and Clinical Diagnostics Guidelines for completing course work in the discipline Clinical diagnostics with radiology for 3rd year students of the Faculty of Veterinary Medicine (specialty 111200.65 - veterinary medicine and 111900.62 - veterinary and sanitary examination). N.V. Mantatova, Ph.D. vet. Sciences, Associate Professor Ulan-Ude 2012..."
“MINISTRY OF AGRICULTURE OF THE RUSSIAN FEDERATION Federal State Educational Institution of Higher Professional Education Altai State Agrarian University N.E. Borisenko, O.V. Kronewald VETERINARY AND SANITARY EXAMINATION OF PRODUCTS OF FORCED SLAUGHTER OF ANIMALS, WHEN DETECTING DISEASES AND CHANGES ARISING IN THE PROCESS OF MEAT STORAGE Educational and methodological manual for laboratory practical classes and independent work for students and students of the department...”
« State Agrarian University N.I. Vladimirov, L.N. Cheremnyakova, V.G. Lunitsyn, A.P. Kosarev, A.S. Popelyaev FEEDING FARM ANIMALS Textbook Barnaul Publishing House AGAU 2008 1 UDC 636.04 Reviewer - Doctor of Agricultural Sciences, Professor of the Department of Veterinary Genetics and Private Animal Science of the Institute of Veterinary..."
“UDC 582 (075.8) BBK 28.5я73 F 64 Recommended as an educational and methodological aid by the editorial publishing department of the Vitebsk Order of the Badge of Honor State Academy of Veterinary Medicine dated 02/03/2012 (protocol No. 1) Authors: Dr. Agricultural Sciences. sciences, prof. N.P.Lukashevich, Art. teachers I.I. Shimko, I.V. Kovaleva, Ph.D. agricultural Sciences, Associate Professor T.M. Shloma Reviewers: Ph.D. agricultural Sciences, Associate Professor L.M. Linnik, Ph.D. agricultural Sciences, Associate Professor L.A. Troublemaker F 64 Phytocenology. Taxonomy. Ecology: teacher of met. allowance /...”
“Ministry of Agriculture of the Russian Federation Department of Personnel Policy and Education State Unitary Enterprise Michurinsk State Agrarian University Department of Tractors and Agricultural Machines Guidelines for the study of potato harvesting machines in the discipline Mechanization, electrification and automation of agricultural production, section Agricultural machines for students of agronomic specialties. Approved by the Methodological Commission of Agronomic...”
“MINISTRY OF AGRICULTURE OF THE RUSSIAN FEDERATION Federal State Budgetary Educational Institution of Higher Professional Education Saratov State Agrarian University named after N.I. Vavilova Landscape Science Guidelines for conducting practical classes and completing coursework in specialties 120301 - Land Management and 120302 - Land Cadastre Landscape Science: Guidelines for conducting practical classes and completing coursework..."
“Ministry of Agriculture of the Russian Federation Federal State Budgetary Educational Institution of Higher Professional Education Oryol State Agrarian University Pavlovskaya N.E., Gagarina I.N., Gorkova I.V., Gavrilova A.Yu. METHODOLOGICAL INSTRUCTIONS FOR COMPLETING THE DIPLOMA THESIS For full-time students in the field of preparation Biotechnology Compiled by: Candidate of Agricultural Sciences, Associate Professor of the Department of Biotechnology Gagarina I.N., Senior Lecturer of the Department of Biotechnology Gagarina A.Yu...."
This disease is characterized by the accumulation of fat in the liver of cows, associated with metabolic disorders.
Active selection of high-yielding cattle has led to a decrease in genetic potential: increased productivity at the beginning of lactation exceeds the cow’s ability to consume sufficient feed. This leads to an imbalance in energy balance.
Forms of liver dystrophy
The disease steatosis can be genetically determined (dependent) and infectious-toxic, manifesting itself in the form of atrophy or hypertrophy of the organ. There are three stages of pathology:
- acute (4-7 days);
- subacute (7-21 days);
- chronic.
Causes of fatty liver
Fatty infiltration of the liver in cattle occurs as a result of too active activity of this organ when it strives to process a lot of fat. Fat mobilization occurs as a result of negative energy balance. Destroyed lipids return to the liver and become toxic, causing dystrophy.
The cause of the acute form is the infectious-toxic state of the animal’s body. The cause of the genetically determined form is a disorder of lipid-carbohydrate metabolism, which usually manifests itself before calving or in the first weeks after calving. Liver lipidosis is more common at the beginning of lactation in highly nourished and productive cows, since their tissue mobilization of fat is intense, and their consumption functions are slow; in this case, subcutaneous lipid reserves are consumed more.
Predisposing factors for fatty liver degeneration in cattle of any age:
- weakening of the body;
- changes in metabolic rates;
- stagnation of blood in the veins;
- hypovitaminosis;
- mineral starvation;
- overwork;
- protein overfeeding;
- excess beet pulp, potato stillage and other waste in feed;
- hypothermia;
- the use of hormonal drugs after calving, during insemination or early mating);
- intensive fattening of young animals;
- deficiency in the diet of methionine, choline, cystine, tocopherol;
- dehydration.
Moreover, the likelihood of developing dystrophy depends on the adaptive and protective ability of the body. The condition is also guaranteed in case of ketosis and maternity paresis. Fatty liver degeneration can become a secondary process in dystonia of the proventriculus, intestines and abomasum.
Degenerative obesity and rapid necrobiosis of liver cells with autolysis of the liver parenchyma can provoke intoxication with bad silage, alkaloids and lupine, mineral fertilizers and chemicals - phosphorus, mercury, arsenic.
Symptoms
- Decrease in milk yield;
- Suppressed appetite;
- General exhaustion;
- Changes in proventriculus peristalsis (hypotension and atony);
- Diarrhea alternating with constipation;
- Cases of milk fever, ketosis, mastitis, etc.;
- Declining birth rate;
- Muscle weakness;
- Tendency to anemia (plastic and hemolytic forms);
- The acute toxic form can cause the death of the animal.
Blood tests (biochemical) show increased fatty acid concentrations, non-esterified (NEFA) levels (free fatty acids) and increased ketones.
There is always an admixture of protein in the urine, increased urobilin and indican, and possible bile pigments. Crystals of leucine and tyrosine are found in the sediment - signs of liver dysfunction.
The disease can also be identified using the percussion method, with the determination of the enlarged boundaries of hepatic dullness; the area is determined by horizontal measurement according to Aliyev.
The boundaries of fatty liver hypertrophy are localized:
- 1 month of lactation: 13 - 9 ribs;
- 2-5 months: 12 - 9 ribs;
- 6-9 months after calving: 11 - 8 ribs;
- 10-12 months 10 - 8 ribs.
The shape of the percussion boundaries will also change over time, being determined in the form of a half-petal transforming into an elongated rhombus, and an unequal quadrangle. This is explained by special biochemical indicators of fat metabolism]. The topography of the liver borders changes depending on the duration of pregnancy (it is important to take into account the position of the fetus).
- 1-3 months of pregnancy: 12 - 9 ribs;
- 4-7 months: 11 - 8 ribs;
- 8-9 months: 10 - 8 ribs.
Body temperature is usually normal or slightly reduced. On the mucous membranes and sclera of the eyes, yellowness or blueness, hemorrhages are possible.
In a chronic course, the signs of dystrophy are weakly expressed. Noted:
- mild exhaustion without progress, general obesity is more common;
- atony and hypotension of the forestomach;
- stagnation of food in the book;
- weak intestinal motility;
- low body temperature
- deterioration in milk yield and reproduction;
- decline in bone marrow hematopoiesis;
- decreased blood clotting.
Jaundice syndrome is often absent, but trophic ulcers on the skin are possible. Hypertrophic fatty liver is accompanied by an increase in the percussion border. Atrophic - decrease.
The blood contains a lot of globulins, nitrogen residues, ammonia and urea, and serum transaminase is also detected. The content of albumin, glucose and fibrinogen is reduced.
Pathogenesis
In infectious-toxic obesity, the toxin or pathogen penetrates the bile or blood into the liver. The pathology is based on a complex disorder of fat metabolism in the liver cells, leading to the development of dystrophic changes in the organ.
The lack of methionine, cystine, tocopherol and choline suppresses the synthesis of phospholipids; fatty acids, deposited in the liver, are transformed into triacylglycerols. In this case, several important functions are disrupted at once: gluconeogenesis, bile formation, lipogenesis, the activity of enzymes involved in oxidative processes is reduced, the barrier function of the liver, the synthesis of glycogen and plasma proteins are weakened.
The liver undergoes the following changes:
- in the initial stage, swelling of the liver cells and disruption of the structure of the lobules occurs; the liver increases in volume;
- with progression, due to the breakdown of parenchymal cells, the liver loses volume; fatty liver atrophy appears;
- Severe cases lead to cell breakdown and are replaced by fibrinous tissue, causing cirrhosis of the liver.
Toxic autolysis products cause severe damage to the heart (dystrophy), kidneys and central nervous system.
Cure prognosis
Spicy and subacute forms active therapy can lead to the death of cattle or the loss of highly productive females from the herd. The chronic course does not lead to death, but reduces productivity, requiring culling of the animal.
Treatment of fatty liver in cattle
Without treatment, the mortality rate can be as high as 25 percent. To prevent death, the introduction of the hepatoprotector “Antitox” is required. The drug has antiseptic and anti-inflammatory effects. It has been proven that it can restore lipid-carbohydrate metabolism and liver tissue, being an antidote and antioxidant. The drug consists of proteins from the liver tissue of healthy cattle. If the rules of administration are followed, this drug enters the liver.
Antitox must be injected (subcutaneously, intramuscularly) once a day. Newly born cows (350-550 kg) with general wasting required dose medications - 20.0-40.0 ml, with simultaneous administration of half the dose subcutaneously and half intramuscularly for 5 days in a row. The presence of maternity paresis and signs of retention Antitox is administered intravenously every day, 100-200 ml, mixing it 1: 1 with 40% glucose. The injections last until the threat of slaughter is eliminated, then you can switch to the usual scheme.
Also, your veterinarian, adhering to a comprehensive classical approach to the treatment of fatty liver, may recommend the use of glucose, hemodez, methionine, tocopherol, analgin, methenamine and choleretic agents.
Treatment accumulates against the cause that caused pathological condition. Comprehensive treatment includes:
- diet;
- therapy with hepatoprotectors and supportive drugs aimed at removing toxic products and correcting dehydration;
- improving the quality of feed;
- reduction of silage rates;
- transfer to 5-6 meals a day.
The diet should include grass, vegetables and root vegetables, meadow hay, grass meal, skim milk. Regular watering is important.
To neutralize toxic products and gases, it is recommended to introduce milk and an activated carbon solution through the probe. It is also necessary to give the animal Carlsbad salt, which normalizes peristalsis.
For pain in the liver, atropine, belladonna, and analgesics are used. Intravenous administration of glucose (20% - 300 ml) with ascorbic acid (5% - 2 ml), subcutaneous insulin (200 units), cardiac drugs is practiced. Additionally, vitamins K and B1 are given.
After recovery, you need to maintain a gentle diet with good hay, carrots, vitamins, methionine and skim milk.
Please note that the disease requires the administration of drugs by injection; if the drugs are given with food, they will not work, since there is no guarantee that the animal will eat the whole food, plus the peculiarities should be taken into account digestive system Cattle. Injections of a hydrolyzate solution facilitate immediate delivery of the drug to the liver.
Prevention
Careful attention to the condition of cows before calving will prevent excessive fat breakdown and fatty liver degeneration. It is important to maintain a diet during pregnancy and after childbirth, monitor the room temperature and water regime.
Glucose supplementation is considered a preventative measure to minimize liver stress. For preventive purposes, you can administer Antitox to animals. Requires 5 injections of 10.0-20.0 ml. at weekly intervals.
Use: in veterinary medicine, namely for the treatment of hepatosis in cows. The essence of the invention is that the biologically active substance Erakond is administered intramuscularly to animals, which is a preparation of plant origin, including a condensed plant extract, for example grass or alfalfa hay, containing soluble metal salts, mg/kg of plant mass: Mo 8.0; Ba 10.0; Pb 20.0; U 1.0; Cz 0.5; Zn 200.0; Fe 300.0; Sn 40.0 according to the following scheme: intramuscularly 20% solution in a dose of 55 ml per head once a day daily for three days and after a five-day break - again, orally 10% solution in a dose of 220 ml per head once a day every day and after a five-day break - again. 1 table
The invention relates to veterinary medicine and can be used for the treatment of hepatosis in cows. Toxic liver dystrophy hepatosis (Dystrophia hepatioxica Hepatosis) is characterized by dystrophic liver damage without a pronounced mesenchymal cell reaction, accompanied by symptoms of general toxicosis. The disease mainly affects lactating cows, gilts and calves during the weaning and fattening period. The most common and immediate cause of the disease is the accumulation on a farm or eating on a pasture of grain infected with toxic fungi, spoiled silage, stillage, pulp, mixed feed, and poisonous plants. The disease can also occur when animals eat mineral fertilizers and feed treated with herbicides, or overdose of urea in cattle. Symptoms of liver dystrophy are noted in cattle with ketosis. The disease is promoted by various factors that reduce the body's resistance: hypovitaminosis, mineral starvation, physical inactivity, irregular feeding, gastrointestinal infections. Diagnosis is usually made on the basis of history, clinical presentation, and autopsy. When treating hepatosis, toxic or suspected toxic foods are excluded from the animals’ diet. Prescribe a diet of easily digestible, good-quality feed and reduce the amount of concentrates accordingly. For sick cattle, the rumen is washed with warm water, deep cleansing enemas are given and laxatives are given. To bind toxins and absorb excess gases, milk, aqueous suspensions of activated or charcoal are injected inside through a probe. To stimulate intestinal peristalsis and secretory function, Carlsbad salt, sodium or magnesium sulfate are indicated in small doses. When intoxication develops, glucose with ascorbic acid and cardiac medications are administered intravenously. For 2-3 weeks after clinical recovery, animals are kept on a gentle diet. Methionine and vitamins are also prescribed (see Veterinary formulation with the basics of therapy and prevention. M. Agropromizdat, 1988, pp. 167-169). For the treatment of the liver, cyanocobalaminum (Cyanocabalaminum) vitamin B 12 (Vitaminum B 12), which has a high biological activity and has a beneficial effect on liver function. Close to it are oxycobalamin (Oxycobalaminum) and cobamamidum (Cobamamidum). Vitohepatum, Surepar, Calcii chloridum, and Kalii arotas are also used. Ascorbic acid (Acidum ascoridum) can be isolated from products of plant origin. It is found in rose hips, cabbage, lemon, orange, horseradish, fruits, berries, pine needles (see M.D. Mashkovsky, Medicines. M. Medicine, 1989, part 2, p. 130). Glucose (Glucosum) can be isolated as a drug that stimulates metabolic processes. When hypertonic (10-40%) solutions are injected into a vein, metabolic processes increase and the antitoxic function of the liver improves. The liver participates to one degree or another in all metabolic processes. Therefore, when its function is disrupted, the regulation of metabolic reactions changes, the biochemical parameters of the blood change, and the activity of cellular and humoral resistance factors of the animal body decreases. The drugs considered for the treatment of toxic liver dystrophy are either not effective enough, or their use leads to changes in the morphological composition of the blood. The proposed method for treating cow hepatosis is implemented as follows. The Troitsk Veterinary Institute, together with the collective farm "Southern Ural" of the Troitsky district of the Chelyabinsk region, conducted a scientific and production experiment. Five groups of cows were selected according to the principle of analogues, ten cows in each group. In cows of groups 1, 2, 3 (experimental) and group 4 (control), hepatosis was established based on clinical signs, biochemical blood tests and a test with copper sulfate according to V.S. Postnikov. Cows of group 5 are healthy (control). In the blood of cows with impaired liver function (groups 1-4), the level of carotene (0.32 0.04-0.390.04 mg%), glucose (37.86 2.13-39,962.38 mg%), phosphorus was reduced (3.10.13-3.94 0.19 mg%), calcium (8.9 0.33-9.460.41 mg%), sodium (252.320.02-312.14.46 mg%), potassium ( 14.41.25-15.9213.6 mg%), reserve alkalinity (30.08 1.11-37.643.13 vol% CO 3) and increased total protein content (9.030.31-10.01.2 g% ), copper (122.8 7.12-144.6 2.71 μg%). At the same time, these indicators in healthy cows of group 5 were within normal limits. In cows with hepatosis, in contrast to healthy animals, the following changes were noted: slightly depressed general condition, hairline tousled, matte, skin elasticity is reduced. Appetite is reduced, chewing gum is sluggish and short. Hypo- or atony of the scar, an increase in the area of hepatic dullness, and pain on palpation of the liver were noted. The test with copper sulfate according to V.S. Postnikov was negative (-) in group 5, positive (++) and sharply positive (+++) in the remaining groups. The cows of the experimental groups were administered Erakond according to a certain scheme. Medicine eracond is an aqueous extract of alfalfa grass (hay), obtained by treatment with an extractant containing a mixture of microelements, mg/kg of plant mass: Mo 8.0; Ba 10.0; Pb 20.0; Co 1.05; V 1.0; Cz 0.5; Zn 200.0; Fe 300.0; Sn 40.0. The method of obtaining and the composition of erakonda is as follows. Prepare a solution of microelement salts based on distilled water steam condensate, including Mo 8.0 mg, Ba 10.0 mg, Pb 20.0 mg, Co 1.05 mg, V 1.0 mg, Cz 0.5 mg, Zn 200, 0 mg, Fe 300.0 mg, Sn 40.0 mg. Alfalfa grass (hay) is crushed and placed in an autoclave, filled with the prepared solution in a ratio of 1:5, the autoclave is sealed, heated to a temperature of 120 o C and kept for 10 minutes. The autoclave is depressurized, the primary extract is poured into a storage container, and the raffinate remaining in the autoclave is again filled with the extracting mixture in the same ratio and heated to a temperature of 180 o C, held for 10 minutes. The secondary extract is poured into a storage container and mixed with the primary extract. The resulting mixture is evaporated until numerous bubbles appear on the surface of the mirror. Then the extract is filtered through a cotton-gauze filter. The resulting filtrate is placed on a baking sheet covered with plastic film and continued to evaporate in a drying cabinet at a temperature of 60 o C until a plasticizing mass is formed over the entire thickness of the extract poured onto the baking sheet. The resulting mass is formed into a lump for further use or storage. A sterile 10-20% aqueous solution of Erakond in distilled water was prepared from the plasticizing mass. The solution was filtered through several layers of gauze and used immediately after preparation (it is possible to ampulate the solution for long-term storage). In group 1, intravenously 2 times with an interval of 1 day (10% solution at a dose of 110 ml per 1 head) and again after a 5-day break. In the second group, intramuscularly (20% aqueous solution, 55 ml per 1 cow, 1 time per day) and in the third group orally (10% aqueous solution, 220 ml per 1 head, 1 time per day) daily for 3 days and after a 5-day break again. Subsequent blood tests showed that in the blood of cows of the experimental groups the content of carotene (0.450.07-0.500.05 mg%), glucose (48.32.08-52.52.34 mg%), phosphorus (5.28 0. 68-6.36 0.41 mg%), calcium (9,580.32-10,040.27 mg%), sodium (322.46.82-331,211.93 mg%), potassium (17,261.63-18,800.90 mg %), total protein (6.8 0.27-7.281.02 g%), the level of reserve alkalinity (46.861.07-50.362.19 vol% CO 2), while the condition of animals in group 4 worsened. The level of these indicators in the blood of healthy cows of group 5 decreased slightly, but continued to remain within normal limits, except for the carotene content (0.26–0.07 mg%). During the experiment, it was found that effective ways of using Erakonda are intramuscular and oral administration (see table). Thus, the results obtained show that under the influence of Erakonda, the clinical status of cows with hepatosis significantly improved and the functional state of the liver normalized. At the same time, no changes in the morphological composition of the blood under the influence of eracond were detected. Animal digestion was normalized. The tenderness of the liver upon palpation disappeared.
Claim
METHOD FOR TREATING HEPATOSIS OF COWS, including administering biologically active substance, characterized in that the biologically active substance is a plant extract of alfalfa obtained by treatment with an extractant containing a mixture of microelements, mg/kg of plant mass: Mo - 8; Ba - 10.0; Pb - 20; Co - 1.05; V - 1; Cz - 0.5; Zn - 200; Fe - 300; Sn - 40, which is administered as a 20% aqueous solution intramuscularly at a dose of 55 ml per cow once a day for three days, after a five-day break the course is repeated or administered in the form of a 10% aqueous solution at a dose of 220 ml per cow once a day for three days, and after a five-day break the course is repeated.
