Toxic degeneration of the liver is characterized by severe toxicosis, fatty degeneration and necrosis of liver cells. Sucker piglets suffer from this disease, along with weaners and gilts, in autumn and winter. At the same time, significant mortality is observed from December to January. In various industrial complexes, this pathology is observed in absolutely all periods of the year.
Etiology in animals
Toxic dystrophy of the liver develops mainly in those farms in which pigs and calves are fed biological inferior feed for a long time and kept in conditions that are characterized by an unsatisfactory microclimate. The main cause of toxic dystrophy of this organ is intoxication, which is caused by feeding spoiled and mold-affected feed to animals, as well as products that contain alkaloids along with saponins andmineral poisons.
The disease is very often recorded in areas that are characterized by a deficiency of assimilable forms of selenium in soils. The cause of toxic liver dystrophy in animals can be a violation of the protein and carbohydrate ratio in the diet, along with a lack of methionine, cystine, choline, and, in addition, vitamin E. In this case, a large number of underoxidized products are formed that are very toxic to the body. The disease also appears with unsystematic and prolonged use of antibiotics related to the tetracycline series, and the use of other antibacterial drugs is also a factor in its development.
Toxic substances that come with food and are formed in the body against the background of indigestion and the intermediate metabolic process, after absorption penetrate the liver. Already in the body, depending on the dosage and duration of their intake, various processes appear, for example, the activity of oxidative enzymes may decrease, a sharp drop in glycogen levels is noted, and at the same time, fatty infiltrations develop and the breakdown of liver cells is recorded, and subsequently - liver necrosis.
Fatty infiltrations in combination with organ necrosis especially progress in the presence of a deficiency in the diet of cystine, methionine, choline and tocopherol, including. The absence or deficiency of these lipotropic factors leads to the fact that the newly formed fatty acid is not involved in the synthesis of phospholipids, but is deposited in the liver in the form of triglycerides. Tothe same process of deposition of fat in this organ leads to a decrease in the level of oxidation as a result of a decrease in lipolytic activity. Next, find out what factors influence the appearance of this disease in animals.
Causes of illness in calves and piglets
Pigs suffer from this disease mainly along with gilts and calves during the period of weaning and fattening. In industrial complexes that specialize in fattening livestock, on farms and farms where nutritional rules are violated (toxic feed is introduced in large quantities), the disease spreads massively, causing significant economic damage due to the forced slaughter of animals and death.
Toxic liver dystrophy in calves and pigs can be formed as a result of other diseases (infectious, gastroenteritis of various origins, sepsis), while there is an increased process of absorption of toxic products into the blood.
Symptoms
In suckling piglets, the disease is most often acute and may be characterized by signs of agitation, rapid heart rate and shortness of breath. Animals are in a state of depression. Body temperature sometimes rises to 40.8 degrees, and then drops and becomes subnormal. With toxic liver dystrophy in piglets, yellowness of the mucous membranes and skin is sometimes possible along with vomiting, and constipation is replaced by diarrhea.
Against the background of all this, animals receive a large amount of bilirubin into the blood and oliguria is formed. In urine with highspecific gravity contains bilirubin, urobilin and protein. Against the background of insufficiency of the activity of the heart in toxic liver dystrophy in pigs and calves, blue ears, skin and abdomen are observed. This form of the disease is most often fatal.
Subacute and chronic form of the course of the disease is recorded mainly among weaned piglets, and it is characterized by less pronounced signs. There may be depression of the general condition along with loss of appetite, sometimes vomiting and diarrhea. The temperature may be within normal limits or low. Jaundice of the mucous membranes and skin in a chronic course is rarely observed.
Diagnosis
The disease is determined on the basis of anamnestic information, the dynamics of the development of clinical symptoms, on the result of laboratory tests of feed, urine, blood and pathological changes in parenchymal organs.
Anatomical change largely depends on the ethnological factor. At an early stage in the development of the disease, the liver in animals is slightly enlarged, it has a flabby texture and has a yellow color. With the development of necrosis of the parenchyma, flabbiness with wrinkling of the organ is more pronounced, while the shade is clayey or red. Degenerative changes in the heart muscle and kidneys are noted. The organ can be swollen, loosened, hyperemic, sometimes with hemorrhages, and the mucous membrane of the digestive system is covered with a viscous secret. Observe erosion and ulceration.
Treatment
BeforeAbove all, it is important to eliminate the cause of the disease. With the development of acute toxic liver dystrophy, the stomach and intestines are washed with warm water or a solution of potassium permanganate using a probe and an enema. Inside, 100 grams of castor oil are introduced, 50 - sunflower, 30 - hemp and 100 - linseed. A hunger diet is prescribed for twelve hours. Further, sick animals are fed dietary feed (we are talking about milk, skim milk, oatmeal jelly, liquid cereals from oatmeal and barley groats, yogurt).
In addition, an acidophilic broth culture (from 20 to 40 milliliters) is prescribed twice for five to seven days. Hydrolysin is injected subcutaneously, and lipotropic components in the form of choline chloride, tocopherol acetate and methionine are administered orally. In the future, animals are transferred to a diet of carbohydrate feed with the necessary amount of protein, vitamins, amino acids and mineral ingredients.
Glucose solution
At the beginning of the development of toxic liver dystrophy, subcutaneous injection of a ten percent glucose solution at a dosage of 20 to 50 milliliters is effective, in addition, sodium selenite is used in an amount of 0.2 milligrams per kilo of animal weight and intramuscular injection of calcium gluconate. The drugs are used twice a day, in the absence of glucose, milk with sugar, hay infusion, jelly and porridge can be given inside. If necessary, heart drugs are prescribed.
Prevention
As part of prevention, it is important to constantly monitor the nutritional value of products,sanitary quality of feed, and at the same time the conditions of keeping calves and pigs. The composition of the diet must include, according to the existing standards for each age category, essential amino acids in the form of lysine, methionine, cystine, as well as a set of minerals and various vitamins. Any feed must be regularly examined for toxicity.
In disadvantaged farms, for prevention, intramuscular injection of a 0.1% solution of sodium selenite is recommended (once twenty-five days before farrowing at the rate of 0.1 milligram per kilo of animal weight).
Calf autopsy protocol
According to the calf autopsy protocol, with toxic liver dystrophy, a sick animal has fatty degeneration and cell necrosis. The organ, as a rule, is enlarged in volume, the capsule is unevenly colored and tense, and against the general background there are foci of a yellowish color of a flabby consistency, which are easily destroyed by pressure. Portal lymph nodes without any changes. The gallbladder is filled with moderately thick bile, and its mucous membrane is velvety, the patency of the excretory ducts is not impaired. Based on the autopsy data, it can be concluded that the death of the animal was due to toxic liver dystrophy.
Features of pathology
The pathological anatomy of toxic liver dystrophy varies depending on the periods of the disease. In total, the disease takes about three weeks. In the early daysthe organ is enlarged and flabby. It takes on a yellow color. Then the capsule becomes wrinkled. Liver tissue is usually clay-like. Microscopically, in the first days of the disease, fatty degeneration of hepatocytes is noted, which is quickly replaced by necrosis and autolytic decay with the formation of fat-protein detritus, in which there are crystals of tyrosine and leucine.
Progressing, the necrotic change captures all sections of the lobules by the end of the second week of the disease. Only on their periphery remains a narrow strip of hepatocytes. These changes in the organ characterize the stage of yellow dystrophy. In the third week of the disease, the liver may decrease in size and become red. This is due to the fact that the fat-protein detritus of the lobules undergoes the process of phagocytosis and is resorbed.
Macro preparation
Macropreparation of toxic liver dystrophy is a slide on which an object is located, prepared for research under a microscope. From above, this object is usually covered with a thin cover glass. The size of the slides is 25 by 75 millimeters, and their thickness is standardized, which greatly facilitates the storage and handling of instruments.
Conclusion
Thus, the disease involves massive progressive necrosis. As a rule, this is, first of all, an acute, much less often chronic pathological condition, which in animals is characterized by massive necrosis of the organ and its insufficiency. The disease develops most often with exogenous andendogenous intoxications. It is also encountered in viral hepatitis as an expression of its malignant form. In pathogenesis, importance is attached to the hepatotoxic effects of the virus. Allergic factors sometimes play a role.
