Veterinary problems of fur farming. Abstract hemoturia and wetting of minks Dysuria of fur-bearing animals
As a result of diseases of the skin of fur-bearing animals, the value of the fur skin decreases, and sometimes the value is completely depreciated (more about). That is why the study of these diseases and methods of combating them is so important. And today we invite you to talk about diseases of the fur of wild fur-bearing animals.
Pruritic scabies
The causative agent of scabies
The specific mite of fox scabies has a rounded body, dirty white, light brown in some places. It often infects foxes and arctic foxes on fur farms. The size of the female tick is 0.42 by 0.31 millimeters, the male is 0.24 by 0.18 millimeters. On the ventral side you can see 4 pairs of legs, at the tips of which there are either suckers or long bristles. The jaws of the tick are of the gnawing type.
In nature, foxes become infected with equine mange pathogens. The body of this tick reaches a length of 0.2-0.5 millimeters. On the back there are scaly outgrowths and bristles, which point backwards with their points. The proboscis has a horseshoe shape. The legs are short and thick.
Such mites spend their entire lives, at all stages of development, on the body of their owner. They live in the thickness of the skin and feed on lymph, making winding passages in the epidermis. The female can lay from 20 to 50 eggs at a time, from which larvae will appear in 3-7 days, which will turn into nymphs after a few days. After 2-3 molts, the nymphs become sexually mature ticks. It takes 15-20 days for the full development cycle of the itch mite.
Sources of infection
The source of infection, of course, is sick animals. Infection occurs through direct contact with them or through care items, cages in which sick animals were kept. Under natural conditions, infection can also occur when foxes and wolves eat the corpses of horses that were affected by scabies.
How does itchy scabies occur?
Initially, in foxes and arctic foxes with scabies, the paws, inner thigh area, root of the tail and head are affected. In the future, the process can spread to the entire surface of the body. On the affected areas you can find small nodules that turn into blisters. As a result of scratching, a secretion is released from the affected areas, which, when dried, forms crusts. The fur begins to fall out in places where thick hair- falls down. At the same time, the animal itself loses its appetite, looks sick and may die.
To eliminate the epizootic, it is advisable to destroy sick foxes. Their burrows must be treated with a sharp-smelling acaricidal agent and then buried. Despite the fact that this process is labor-intensive, it is necessary to prevent the spread of scabies.
Treatment of pruritic scabies
Treatment of dogs and caged fur-bearing animals that have become ill with pruritic scabies should be carried out with mite-killing agents, with disinfection of the room where they are kept. However, first you should remove dirt and crusts from the surface of the sick animal’s body, and wash it with warm water. The treatment is long-term. And objects with which the animal came into contact before and during the disease are recommended to be disinfected.
Ironwort or demodicosis
This is the name for scabies, which is caused by mites from the Demodex family. Among fur-bearing animals, foxes and arctic foxes most often suffer from demodicosis.
The causative agent is a tick, has a worm-like shape and very short legs with 2 claws at the ends. The length of the tick can be 0.25-0.3 millimeters.
How does ironworm infection occur?
Infection occurs through contact of a sick animal with a healthy one. At the same time, the presence of defects on the skin due to previous skin diseases increases the risk of infection. For example, the animal already had scabies or eczema. Whereas animals with healthy skin rarely get sick.
The gland in fur-bearing animals can occur either in a scaly or pustular form. Moreover, the scaly form usually turns into pustular. The latter is more malignant and more difficult to treat. Fur completely falls out on the affected areas, folds form on the skin, and lymph begins to ooze from the pustules, which forms crusts when it dries. The lesion is complicated by secondary infection. Due to severe intoxication, the animals die.
In order to determine the presence of this type of mite, a deep scraping of the skin is taken from the affected areas, or even better, from the contents of the pustules.
Treatment of the iron worm
By analogy with ironworm in dogs, which can become infected from sick animals, the best treatment is considered to be the intravenous administration of a 1% solution of trypansinia or methylene blue at a dose of 0.01 grams per 1 kilogram of live weight, repeated 2-3 times per week in between. At the same time, it is necessary to rub finely dispersed sulfur into the skin affected by the tick, use 4-carbon chloride, Peruvian balsam, and iodine.
To prevent and eliminate sources of infection, animals suspected of the disease are isolated and treated. And all objects with which they came into contact are disinfected.
Prevention of diseases of fur-bearing animals is achieved by carrying out specific and non-specific measures. Nonspecific prevention of internal diseases involves the following measures: a) control over the keeping of fur-bearing animals at all stages of the production cycle; b) control over feeding and watering of fur-bearing animals; c) veterinary and sanitary examination of feed at all stages - from its entry into the farm to feeding; d) control over feed storage; e) control over the preparation of the feed mixture and its consumption; f) group diet therapy and pharmacoprophylaxis.
The shad is a cover of a gable roof, in which the cages are arranged in two rows, with the door inward, with a central feeding passage. Houses for minks are hung on the side of the feeding passage, and for foxes and arctic foxes they are inserted inside the cage for the period of reproduction and raising of young animals before jigging.
Before whelping, the females’ houses are washed, burned with a blowtorch and filled with dry soft hay or oat straw or thin packaging shavings for insulation. Do not use coarse, moldy or damp straw or hay, as well as barley straw and chaff, which can pierce the very delicate and thin skin of newborn puppies. The litter is checked at least once every 10 days; damp, contaminated or covered with frost, replace them with fresh ones.
During pregnancy and lactation, outside work is prohibited on the farm. The condition of newborn puppies is judged by their squeaks. If a multi-voiced squeak is heard in the nest, and the female is restless and drags the puppy around the cage, then you need to immediately open and inspect the nest and the newborns. When inspecting the nest, count the number of puppies and pay attention to their condition and size. If the puppies are weak, they should be given a 2% solution of ascorbic acid with glucose and thiamine (1-2 times a day) for 2-3 days. Puppies from females that do not have milk or lack maternal instinct should be removed and placed with others. Part of the offspring from females with multiple births is also added (8 puppies are left at the mink, 6-7 at the foxes). For adoptive mothers, they choose dairy females who have puppies of the same age as the adopted ones or slightly younger. The puppies must be placed either directly into the nest (when the female is outside the house) or at the entrance to the house. The female, hearing the squeak of the puppies, carries them into the nest herself. Females who do not have enough milk to feed their offspring should increase the supply of dairy feeds, such as muscle meat, liver, milk, and vegetables. In some females, on the contrary, there is a large influx of milk, the mammary glands swell, and therefore the puppies cannot latch on. In this case, it is recommended to reduce the amount of food for the females and exclude milk from the diet for several days, and the female foxes should be milked. When puppies start eating food, you need to be especially careful about its quality and cleanliness in the house. By this time, the female eats the puppies’ feces and the house is clean. When the female stops eating the puppies' feces, the house becomes dirty, since puppies, such as minks, do not leave it at 30-35 days of age. Therefore, along with the bedding, the bottom of the house is sprinkled with sawdust. The bedding should be regularly changed to fresh one, and the inserted wooden bottoms of the houses should be washed with hot water and a disinfectant solution every two days. The bottom is washed with the mixture, and with the onset of hot days the litter is removed.
Feeding of fur-bearing animals should be organized so that the diet contains all nutrients in sufficient quantities and in the required ratio. The need for nutrients in animals varies according to the seasons of the year and biological periods. Rationing is carried out by metabolic energy, expressed in kilocalories, and by digestible protein. Along with this, the standards indicate the percentage (by calorie content) of feed: meat and fish, dairy, grain, vegetable group, yeast, fish oil. When rationing, air temperature is also taken into account (at -30 ° C the norm should be increased by 10-15%), the fatness and size of the animals. The metabolic energy requirement of an adult mink is 250-300 kcal; it needs 8.5-11.5 g/100 kcal of digestible protein (25-28 g per day, and 30 g during lactation). The meat and fish group in the diet of minks and arctic foxes should be 65-75%, foxes - 55-65%; grains, respectively, 15-25 and 25-30%; milk - 5% for mink, 10% for arctic fox in certain periods and 5-15% for fox; vegetables - 2-3% for mink and fox and 3-5% for arctic fox; fish oil - 3% for mink and 1.5-3% for fox, 2% for arctic fox; yeast - 3% for mink and 4-5% for fox and arctic fox.
The diet is per serving, that is, per 100 kcal. When analyzing diets, in addition to protein content, attention is paid to the content of individual amino acids, especially methionine, cystine and tryptophan, fat, which is the cheapest and most concentrated source of energy, and carbohydrates. The fat content of the diet can range from 2.5 to 5.7 g per 100 kcal of metabolizable energy. Enriching the diets of minks and arctic foxes in summer with fat up to 5-5.7 g/100 kcal has a beneficial effect on the growth of animals and does not reduce the quality of their skin. A moderate amount of fat (4.5 g/100 kcal) has a positive effect on the reproductive ability of animals. During the period of preparation for the rut and pregnancy (December-April), the fat rate is slightly reduced in order to prevent females from becoming obese. The same is done 2 months before slaughter, while simultaneously increasing the amount of carbohydrates and improving the quality of the skins. The optimal amount of carbohydrates in the diets of minks is 15-25%, in the diets of foxes and arctic foxes - 20-25% of the metabolic energy of the feed. Their number can be increased for the latter to 40-45% from 4 months of age to slaughter. During lactation, carbohydrates should make up no more than 30% of metabolic energy. The maximum amount of grain for minks is 15 g, for foxes and arctic foxes - 20 g/100 kcal. The calcium requirement of young animals and lactating female fur-bearing animals is 0.15-0.25, phosphorus - 0.12-0.18 g/100 kcal of feed. The optimal ratio between them in the diet is 1:1-1.7:1. The animals' need for these macroelements is met by feeding 5-7 g of freshly ground bone per 100 kcal of metabolic energy. The need for table salt is 0.2-0.3% of the weight of raw feed, and it is provided by meat and fish feed. During lactation, it is advisable to add 0.2-0.3 g of table salt per 100 kcal of diet to porridge.
Fur-bearing animals are sensitive to vitamin deficiency. The most vitamins are found in liver, milk, yeast, fortified with fish oil. To provide animals with vitamins, multivitamin preparations are used: Pushnovit-1 (for the main herd) and Pushnovit-2 (for young animals). The norm of furshnovit for a mink is 1 g, for a fox and arctic fox - 2 g per day. This amount provides the animals’ need for vitamins B1, B2, B12, E, C and 50% for vitamins B6, Bc. If your diet includes fish, yeast and, especially, liver, then a deficiency of the last three vitamins does not occur.
Pushnovit does not contain vitamins A and K, so they are prescribed additionally if necessary. The requirement of minks for retinol is 250 IU per 1 kg of body weight, foxes - 100 IU. During the period of preparation for the rut, pregnancy and lactation, the need increases by 2.5-3 times. In practical conditions, the need of animals for vitamins is determined by the calorie content of their diets. For 100 kcal of feed you need: 150-250 IU of retinol; 30-50 IU cholecalciferol; 2-5 mg tocopherol; 0.1-0.18 thiamine; 0.1-0.25 riboflavin; 0.45-1.20 niacin; 0.36-1.20 pantothenic acid; 0.18-0.27 pyridoxine; 0.02-0.09 folic acid; 10-20 choline; 10-20 mg of ascorbic acid; 1.5-2.5 mcg of cyanocobalamin and 4-6 mcg of biotin. It should also be taken into account that tocopherol and retinol are destroyed by fat oxidation products, thiamine - by the enzyme thiaminase, contained in many freshwater (carp, crucian carp, perch, etc.) and sea (capelin, sardine, anchovy, sprat, sprat, herring) fish. To prevent B and hypovitaminosis, it is recommended to exclude fish containing thiaminase from the diet for 1-2 days every week. These days, mink are given 2-2.5 mg of thiamine, and foxes and arctic foxes - 4-5 mg.
Foxes are very sensitive to a lack of ascorbic acid. If it is deficient during pregnancy, puppies are born with signs of red feet: the paws are thickened, hemorrhages appear on the paw pads, in place of which scabs form after 1-2 days. To treat sick dogs, 1 ml of a 2% solution of ascorbic acid is injected twice a day through the mouth with a pipette.
High water quality is important in the prevention of diseases of fur-bearing animals. It should contain no more than 1 g of dry matter. The chloride content should not exceed 350 mg/l; sulfates - 500, iron - 0.3, manganese - 0.1, copper - 5, zinc - 5, aluminum - 0.5 mg/l. Water hardness, due to the total concentration of calcium and magnesium salts, does not exceed 10 mEq (1 mEq of hardness corresponds to the content of 20.04 mg of calcium and 12.16 mg of magnesium in 1 liter of water). The pH value of good quality water is 6.5-8.5. The total bacterial contamination of water should not exceed 100 thousand microorganisms in 1 liter, the coli index should not be more than 3, and the coli titer should not be less than 300 ml.
Veterinary and sanitary examination includes organoleptic and laboratory assessment of the quality of feed supplied to the farm, and daily organoleptic assessment of all feed that are ingredients of the diet, immediately before preparing the feed mixture. All feed, upon receipt, is examined in the animal farm or zonal laboratory. Meat and fish feeds are examined for general bacterial contamination, the peroxide and acid numbers, the presence of aldehydes, chlorides, heavy metal salts, amino-ammonium nitrogen (AAA) content are determined, plant feeds are examined for the content of mycotoxins and chemical poisons.
For physiologically justified feeding of fur-bearing animals, only good-quality raw food is suitable. The good quality of feed is determined by the following indicators: a) infection (invasiveness), b) toxicity, c) freshness. The food is considered to be of good quality if the listed indicators meet certain standards.
If a particular feed has lost its quality and without special treatment can cause illness or death of animals, then it is classified as conditionally suitable or of poor quality. Conditionally suitable food is considered to be food that has only partially lost its quality and can be used in limited quantities after special processing. Poor quality food is unsuitable for feeding animals, even when boiled.
Among benign food, one should distinguish impeccable quality, or dietary, that is, food that, when used in accordance with physiologically based standards, does not cause pathology in animals (meat, offal, fish, cheese, etc.), potentially dangerous and food in initial stage of damage. Potentially dangerous benign feeds are characterized by imperfect technology for their production and methods sanitary assessment, rapid spoilage during storage (silkworm pupa, fish meal, milk replacer, yeast, fish waste, meat and offal of marine animals, cake). More often, feed deteriorates through contamination with microorganisms and their toxins, oxidation and decay, and the presence of toxic substances. Feeding such food in limited quantities. Feed in the initial stage of spoilage takes an intermediate place between dietary and conditionally suitable. They are not allowed to be stored for a long time.
In fur farms, the quality of feed is determined using organoleptic methods daily, immediately before preparing the feed mixture; infection - periodically in regional laboratories; toxicity and freshness - in farm laboratories. If the quality of the feed cannot be determined using laboratory and organoleptic methods, then a bioassay is performed.
Breeding animals are fed only high-quality food. As a rule, poor-quality food is not given to animals, but sometimes, subject to compliance with veterinary and sanitary requirements, it is used to feed slaughter animals, monitoring the health of the animals.
Tested feed is stored. Before storing in the refrigerator, food from the meat and fish group is sorted by quality and variety and, accordingly, is stored in separate chambers. By-products and other types of feed are stored in stacks at a distance of 0.5 m from the walls, wall batteries and 0.1 m from the floor, leaving 1.2 m wide passages between the stacks. It is better to store by-products and fish in briquettes, which are placed in containers. Frozen meat and offal are loaded into the refrigerator at the rate of 600-800 kg, fish - 450 kg, lamb - 300 kg per 1 m3 of chamber volume. The foreman records the date the chamber was loaded with food, its quantity, quality and shelf life, which depends on the air temperature in the chamber: at -2 ° C - about 4 months, at -18 ° C - 5-6 months. Fish feed is stored at a temperature no higher than -18 ° C. Meat and fish feed is checked every week. One of the refrigerator chambers is adapted for storing eggs, vegetables, and fruits at a temperature of about 0 ° C. To protect meat and fish feed from rodents, the chamber doors are lined with iron, the cracks in the walls and floor are covered with a metal mesh with cement, and the ventilation holes are covered with mesh. If rodents are detected, mechanical traps are placed in the chambers and chemicals are used to kill the rodents.
Preventive disinfection of refrigeration chambers is carried out as they are emptied, but at least once a year, with a 2% hot solution of sodium hydroxide, hypochlorine solution or clarified bleach containing 2% active chlorine, at the rate of 1 liter per 1 m2 at exposure 1 h.
Before preparing the feed mixture, meat and fish products are defrosted either in the air or in baths with cold water, or under the shower. Mandatory rule is the complete defrosting of offal, since they should be sorted by quality and belonging to a particular type of meat. By-products obtained from the slaughter of pigs can cause Aujeszky's disease in foxes, arctic foxes, minks, ferrets and sables, so they are boiled for 30 minutes. By-products from sheep infected with scrapie, when fed raw, can be a source of encephalopathy in minks. Therefore, they should always be cooked at 110-120 ° C for 3.5 hours.
Benign by-products of large cattle and horses are fed to fur-bearing animals raw, offal in the initial stage of spoilage is pre-washed with water or a 5-10% solution of potassium permanganate.
Conditionally suitable by-products are fed after boiling at 110-120 ° C for 3.5 hours, and poor-quality by-products are boiled or processed into meat and bone meal, after which they can only be fed to slaughter animals.
Grain feed is the main source of carbohydrates for animals. More often, porridge is cooked for animals from coarsely ground grains of wheat, barley, oats or animal feed. Sometimes the grain is extruded. The quality of grain feed decreases primarily due to rancidity. Grain lipids are hydrolyzed to form fatty acids, peroxide compounds, aldehydes, ketones and hydroxy acids, vitamins and amino acids are destroyed.
The quality of grain is determined by sensory and laboratory methods. The fresh, benign grain has a specific odor, a smooth glossy surface and a typical color, does not contain seeds of poisonous and harmful herbs, smut, horns, metal impurities, and is not infected or damaged by grain pests. The acidity of such grain is less than 3.5 °. Conditionally suitable grain is dull, covered with dark spots, bitter in taste, with a musty odor, its acidity is from 3.5 to 9.5 °. Low-quality grain is dark gray, covered with mold, tastes bitter, has a musty - putrid smell, contains impurities of smut and horns of more than 0.05%, its acidity is more than 9.5 °. In addition to good quality in terms of freshness, the grain is examined for toxicity (using a skin test on rabbits) and infection, and impurities of chemical and biological poisons are also determined.
Dairy products for animals include milk (whole and combined) and cheese, which, in terms of their effect on the body, are considered dietary foods. Milk may have high acidity and high bacterial contamination, so it is fed after heat treatment. Cheese is examined by color, smell, consistency and taste. A good-quality cheese of white color, slightly crumbly consistency with a specific pleasant smell and taste. Conditionally suitable cheese is white-yellow-gray in color, crumbly or slightly viscous consistency, sour in taste, and has the smell of acetone. It is used, like condensed milk, after boiling.
Yeast is used as an essential component of diets for fur-bearing animals of all types: baker's, brewer's and feed yeast (hydrolyzed, protein-vitamin concentrate). Benign hydrolyzed yeast is added to the feed mixture without pre-treatment, and baker's and brewer's yeast are boiled for 2-3 minutes before feeding to prevent fermentation of the feed, which causes dilation of the stomach. You cannot cook yeast with other foods, as long-term heat treatment destroys the vitamins. Baker's and brewer's yeast are tested organoleptically. They must have a characteristic color and consistency, and be free of foreign odors and mold.
After the crushed and disinfected feed enters the mixer, vitamins, microelements and other pharmacological preparations are added to the feed mixture, which are pre-dissolved in water or vegetable oil and mixed with the feed for 10-15 minutes. The temperature of the prepared feed mixture should be 10-12 ° C in summer, +20-25 ° C in winter, the smell is specific, without sour or putrefactive impurities. All components of the feed mixture must be well ground and evenly mixed so that the mixture is homogeneous. Its consistency is viscous, the mixture does not crumble when distributed, but also does not be sticky. In winter, feed mixtures are prepared thicker than in summer. The pH value of the feed mixture should be 5.6-6.0.
From each prepared feed mixture, the doctor takes a control sample weighing at least 100 g, which is stored in the refrigerator for 7 days. After organoleptic evaluation, the finished feed mixture is distributed to the animals within 1 hour after preparation. If the mixture, after being delivered to the farm, has fermented (began to “come up” like dough) or has acquired a sour or other unusual odor, then it is not distributed to animals. A high-quality feed mixture is laid out in winter and spring on food shelves, placed on the cage door, and in the summer - on top of the cage. They control the consumption of the mixture by animals. Its remains are collected before the next distribution, and for puppies during the suckling period - 2-3 hours after distribution.
In addition to organoleptic evaluation, the feed mixture is monitored twice a month using laboratory testing. The most informative indicators are the pH value of the mixture, total bacterial contamination, the content of amino-ammonium nitrogen, volatile fatty acids, fat, protein, vitamins A, B], VG, and sometimes calcium, phosphorus and chlorides.
The pH value of the feed mixture should be in the range of 5.6-6.0. The closer the pH is to alkaline, the lower the sanitary quality of the mixture. A particularly negative effect of the alkaline feed mixture manifests itself during the period of intensive growth of young minks: urocystitis, pyelonephritis and urolithiasis occur in puppies. To reduce the pH value, phosphoric and acetic acids are currently used.
The total bacterial contamination should not exceed 1 million microbes per 1 g, the content of amino-ammonium nitrogen is less than 40 mg per 100 g (in a conditionally suitable mixture - 61-80), volatile fatty acids - up to 8.4 mg KOH per 100 g of mixture ( in conditionally suitable - 14.1-19.6), chloride content is not more than 0.4% by weight of the feed mixture.
In exceptional situations, the finished feed mixture is examined for the presence of pathogens of infectious diseases, the content of botulinum toxins, mercury compounds, nitrites, mycotoxins, etc. The material for the study should be control samples of the feed mixture.
Group diet therapy is one of the most important elements in the system of preventing diseases of fur-bearing animals. To do this, dietary feed is selected and reserved, which is pre-tested organoleptically and by laboratory methods, and stored in separate refrigerators with the lowest temperature. These foods include: meat, offal, especially liver, fish, milk, cheese, herbs, fruits. Group diet therapy is carried out primarily during the most intense physiological periods - during the rut, pregnancy, lactation, during the period of intensive growth and fur formation - taking into account the results of medical examination of the livestock. In addition, it can be carried out periodically for the purpose of prevention and treatment of liver diseases, urolithiasis, gastroenteritis, etc. (raw liver is added to the feed mixture at 5-8 g per 100 kcal of feed, hydrolysin, glucose, lipotropic drugs, vitamins B, tocopherol).
In addition to vitamins, iron salts, cobalt and copper, antibacterial drugs are sometimes used for pharmacotherapy, since increased microbial contamination of feed (more than 1 million microbes per 1 g of feed) negatively affects the hematopoietic and enzyme systems of fur-bearing animals and their reproductive function.
Prevention. Fish containing TMAO is introduced, on the recommendation of domestic researchers, into the diet of adult animals in an amount of no more than 35% (25-28 g per 100 kcal of feed), and for young animals - no more than 50% of the calorie content of the meat and fish group of feeds. To exclude the occurrence of anemia, ferroglucin is injected or ferroanemine is added to the feed." If this cannot be done, then the level of raw pollock in the diet is reduced to 12-15 g per 100 kcal (up to 20% of the total weight of the feed).
Ferroanemine and ferroglucin have an effect even with daily feeding of fish containing TMAO. Other ferrous preparations - sulfate, glycerophosphate or iron lactate have a preventive effect only when added to a feed mixture that does not contain fish with TMAO. Usually such feedings are arranged every 2 days. The dosages of all drugs are calculated based on the concentration of iron.
Ferroglucin (a compound of iron with low molecular weight dextran, containing 50-75 mg of ferric iron in 1 ml) is administered intramuscularly at a dose of 1-2 ml up to 3 times a year in cases where animals are forced to feed TMAO-containing fish and there is no way to boil it excess or add ferroanemine to it. If the level of such fish in the diet exceeds 35% (of the amount of animal protein), the first injection of ferro-glucin is given to mink puppies in early July; if it reaches 50% or more, the second - at the end of August; if more than 30%, the third - to the minks of the main herd in December (1 ml is administered).
It is less labor-intensive to use another drug, ferro-anemine, which has an anti-anemic effect when added to feed, since it does not combine with TMAO. Easily absorbed
from the intestine and accumulates in the liver in an amount that ensures normal hematopoietic function. The drug is fed, mixed with food, after diluting it with water 3-10 times, at a dose of 20 mg of iron per mink every other day in courses of 4 months; from July to October and from December to March.
In some countries, it is recommended to feed large quantities of spleen and blood of farm animals (up to 3-8 and 12-14% of the weight of the feed mixture, respectively). Everywhere abroad, the antianemic drug Chemax (iron glutamate) is introduced into the feed at a dose of 0.5 g per mink per day.
If the amount of fish with TMAO in the diet exceeds the recommended standards and it is not possible to periodically replace it or combine it with ferroanemine supplements, then the excess fish should be boiled for 30-40 minutes at 90-100 °C. With each successive formation of the herd, females and their puppies that suffer from anemia or with low reproduction are culled. With this selection from year to year, it is possible to increase the resistance of mink herds to anemia and adapt to feeding with similar fish. Lactation wasting is a disease of lactating females, mainly minks, characterized by emaciation, weakness, agalactia and high mortality.
Etiology. The disease develops as a result of inadequate (in terms of a number of ingredients) and insufficient (in terms of level) feeding of females during periods of preparation for reproduction, pregnancy and lactation. The absence of table salt additives in the feed is of great importance during lactation. The disease is facilitated by the practice, which has taken root in many farms, of keeping the breeding herd from the beginning of preparation for breeding to whelping in a condition of below average fatness (due to a decrease in the level of feeding). As a result, nutrient reserves in the body of females are prematurely depleted during lactation. Exhaustion can occur very quickly, since the costs of the mother's body during this period are very large. Thus, the female Arctic fox secretes up to 19% of her body weight in milk every day.
Pathogenesis. It is based on dehydration of the animal's body due to a large loss of salt in milk. At the end of the lactation period, in females poorly prepared for reproduction, nutrient reserves run out, followed by the development of hypoproteinemia, hypoalbuminemia, the activity of amylase and nonspecific resistance factors (complement, lysozyme, beta-lysines) decreases, and the activity of some enzymes (LDH, ALT) increases. Milk production stops and the sick animal may die.
Symptoms In the second half of lactation, females experience loss of appetite, anemic mucous membranes, exhaustion and immobility, narrowing of the palpebral fissure, and tarry feces (in small quantities). Then comes coma and death. Multi-litter females are susceptible to the disease: those with 5 puppies or more. Puppies from sick females are not fed, lethargic, cold, stunted in growth and most often die
from colds. They are often found near the corpse of a female, when they lick the remains of her tears, which may also indicate salt deficiency.
Diagnosis. Diagnosis is based on the seasonality of the disease, analysis of the fatness and multiple births of females, inadequate diets and low levels of feeding, and lack of table salt in the diet. The effectiveness of treating many patients using saline solutions is taken into account.
Treatment. First of all, large volumes of saline sodium chloride solution are administered (30-40 ml subcutaneously or intraperitoneally). At the same time, symptomatic agents are used: glucose, camphor, hydrolysine, vitamins B, C, A, etc. Instead of saline solution, Ringer's fluid (10-20 ml per mink) or an electrolyte solution (sodium chloride - 4.5) can be administered in the same dose g, sodium bicarbonate - 6.5, glucose - 100 g, water - up to 1 l). Treat until recovery. Dietary feeding is useful: raw cattle liver, meat, fish, cottage cheese, skim milk, yeast, greens.
Prevention. During the lactation period, animals are fed ad libitum, trying to maximize the level of dietary feed in the diet: whole fish, pulpy by-products, liver, yeast, and dairy products. The food is also enriched with vitamins and always table salt (0.5-1 g per small animal) so that the total level of chlorides does not exceed 0.4% of the weight of the food (to avoid salt poisoning). They ensure that the females have complete food intake. In order for puppies to consume food earlier and more, the food mixture is thoroughly crushed (passed through a meat grinder with fine grids and through a paste maker), its consistency should be pasty. 1-2 weeks before weaning, it is also useful to add protein hydrolysates to the feed - aminopeptide-2 or hydrolysin L-103. For puppies up to 25 days of age, the hydrolyzate is drunk from a pipette in doses from a few drops to 1-3 ml, for older puppies - 0.5-3 ml, for adult minks - 5-10, for foxes and arctic foxes - 10-20 ml. Hydrolysates continue to be given with food for another 5-10 days after weaning (weaning) of puppies from females.
During the lactation period, animals should be provided with plenty of drinking water. If the water intake is insufficient, females stop milk production and the body may become dehydrated, which contributes to the development of lactation exhaustion. Table salt begins to be given after whelping is completed on the farm and is stopped 2 weeks after the young are dropped off.
DISEASES OF THE URINARY SYSTEM
Dysuria(wetting) is a common disease accompanied by urinary dysfunction due to a deep metabolic disorder. Found in fur-bearing animals
of all types and causes great damage to farms as a result of damage to the quality of skins and death of animals. Known abroad as “wet belly”.
Sable puppies of post-weaning age with identical signs develop diaper rash, unjustifiably called wetting. Diaper rash occurs from the third ten days of May in cases where no measures are taken to improve the ventilation of the houses (wooden covers and bottoms are not removed). The course of the disease is often benign. However, sables, like other animals, can also suffer from typical dysuria.
Etiology and pathogenesis. Primary dysuria occurs when there is an excess content of fat and calcium in the feed and a lack of carbohydrates. As a result, metabolism is disrupted and poorly soluble soaps are formed, which reduce the surface tension of urine. Therefore, urine is not released in a stream, but in drops, spreading over the stomach, absorbed by the hair and irritating the skin. Along with overloading the diet with fat, the use of feed with oxidized fat is of great importance in the etiology of the disease. However, in both cases, similar mechanisms of disease development are involved - a deficiency of many vitamins (due to large waste or oxidation), which allows us to consider dysuria as one of the forms of manifestation of hepatosis, polyhypovitaminosis and feed intoxication.
Secondary dysuria occurs when animals are fed conditionally suitable and low-quality feed (infected with Proteus, Escherichia, etc.), with urocystitis and urolithiasis, urethral cysts, stress, biotin deficiency, salmonellosis, posterior girdle paresis and other diseases.
Symptoms In sick animals, urine is excreted almost continuously. Due to constant moisture, the skin in the abdomen, perineum and inner surface of the pelvic limbs becomes macerated and inflamed, the hair becomes wet and acquires a yellow-brown color. Animals emit a sharp, unpleasant odor. They lose weight and lose their appetite. At a late stage of the disease, thickening and ulceration of the skin, often inflammation of the prepuce, paresis of the pelvic limbs, exhaustion and death are noted. With secondary dysuria, signs of the main one are added
When sables have diaper rash, wet hair is found in the abdomen and the inner surface of the pelvic limbs. Later, the skin in these areas becomes red and slightly swollen. The epidermis is rejected, and small weeping foci are found, which are sometimes covered with purulent exudate. The animals are losing weight. When moving, they move their pelvic limbs and hunch over. Very often, sick puppies run only on their front legs, and imitate movement with their rear legs raised. In some years, a large number of puppies become ill. The illness usually lasts 2 weeks.
Diagnosis. Installed according to characteristic features
Treatment. Sick animals are injected with a mixture of vitamins
group B, glucose, aminopeptide, hexamethylene-tetramine, sulfamonomethoxine and other antimicrobial agents are given orally, 5-10 drops of Eleutherococcus tincture. Locally, the wound or skin is treated with a 3% solution of hydrogen peroxide, septone-x, penicillin solution and dusted with fine powder (chlortetracycline).
Prevention. Do not allow excess fat in the diet. Only benign fats are fed. In the autumn and winter-spring periods, the fat content should not exceed 4.5 g, and in the summer - 5.5 g per 100 kcal of feed. A sufficient amount of carbohydrate feed is introduced into the diet - boiled potatoes, cabbage, carrots, etc. Otherwise, the prevention of primary dysuria is the same as for hepatosis, polyhypovitaminosis and intoxication. It is necessary that the diets contain a sufficient amount of vitamin E and that the animals are given plenty of water. To prevent diaper rash in sables, the wooden lids of the houses should be kept open from about mid-May. With the onset of warm nights, it is necessary to remove the wooden bottoms from the houses, leaving only the mesh ones.
Hematuria is a symptom complex of various diseases characterized by the presence of blood in the urine. It is registered everywhere in fur farms, and people get sick especially often.
arctic foxes, foxes, minks.
Etiology. The reasons for the appearance of blood in the urine include: acute feed intoxication, vitamin E deficiency, hereditary muscular dystrophy, inflammation of the urinary tract and urolithiasis (urocystitis, pyelonephritis, urolithiasis), external irritants (sharp forceful catching, mating), tumors in the genitourinary system , and in newborn fox and arctic fox puppies - hemorrhagic diathesis(red feet, hypovitaminosis C).
Symptoms In animals, the urine is brightly bloody or contains an admixture of blood. In many cases it turns brown. Depending on the etiology, other signs may develop - loss of appetite, depression, diarrhea, abortion, anemia of visible areas of the mucous membranes and skin, frequent and painful urination, increased bladder volume (determined by palpation) and bloody-purulent discharge. In newborn puppies, swelling and si-
the niceness of the paw crumbs.
Diagnosis. The symptoms of the disease are characteristic, but it is necessary to establish the underlying cause of its occurrence. Thus, with vitamin E deficiency, a significant number of animals become ill. Urine is usually brown in color. Skeletal and cardiac muscles are pale, dystrophic, subcutaneous fat is yellow or anemic.
The seasonality of the disease is not clearly expressed. A high percentage of empty females, analysis of diets and feed indicate an overload of diets with fat or the use of oxidized fat with insufficient supply of vitamin E. With feed intoxication, along with bloody urine, many or most animals exhibit other symptoms - loss of appetite and diarrhea, and the amount In patients with these signs, the increase does not gradually, but quickly.
Urocystitis and urolithiasis are characterized by strict seasonality (mainly July - August), mainly male mink puppies are affected, and the disease, despite some coverage of the population, still remains sporadic and subsides by autumn. External stimuli (forcible taking of an animal, mating) are characterized by hemorrhages in the organs of the urinary system, which, in case of delayed emptying Bladder gives urine a brown color. This disease usually occurs only during the rutting period in isolated cases. Male foxes and arctic foxes are most often affected.
In the case of tumors, the incidence is generally single. Red paws are observed in puppies under 5 days of age. Hereditary muscular dystrophy differentiated using pathohistological studies for the presence of different diameters of myofibrils in a cross section of skeletal muscles, degenerative processes and phagocytosis of myofibrils, basophilia of their sarcoplasm, etc.
Prevention. The main cause of the disease is eliminated, most often vitamin E deficiency and feed intoxication.
Urocystitis And urolithiasis(urolithiasis) is a disease predominantly of minks, characterized by inflammation of the organs of the urinary system or the formation of stones in them. Most often it is recorded in male mink puppies, which differ from females in having greater growth energy.
Etiology. The disease has not been fully studied. It is assumed that the infectious factor plays a leading role in its etiology. After using antimicrobial agents at the onset of the disease, quite satisfactory results are obtained. After infection with staphylococcus in a significant part of the minks, this microbe is found in all layers of the stone, which also indicates the infectious etiology of the disease.
Vitamin A deficiency, if possible at all, is not decisive in the etiology of urolithiasis. This is confirmed by the excess content of retinol in the liver of dead animals and unsuccessful attempts to experimentally reproduce urolithiasis in two generations of minks deprived of vitamin A. A deficiency of vitamin B6 is most likely of more significant importance.
Factors predisposing and contributing to the disease may be intensive metabolism (transition period
puppies for independent food, pregnancy and lactation in females), metabolic disorders (mainly salt and nucleotide) and acid-base balance, physico-chemical state of protective colloids that maintain salts in a dissolved state, functional activity of the parathyroid glands, as well as stiffness water, excessive feeding of bones (calcium salts), slightly acidic or alkaline reaction of the feed, low sanitary quality of feed due to bacterial contamination, the presence of foreign toxic substances and products of their spoilage.
Among the microorganisms with urocystitis and urolithiasis, Proteus, Escherichia, staphylococci and streptococci are most often isolated. They are considered the leading cause of the development of the disease (in the presence of the listed predisposing and contributing factors).
It is possible that in some cases urocystitis not only ends with urolithiasis, but is also the result of urolithiasis, since mechanical damage the walls of the bladder culminate in inflammation. Stones can get stuck in the ureters and cause blockage and, as a result, the development of hydronephrosis
or pyelonephritis.
Symptoms Massive cases of the disease are observed in rapidly growing puppies, usually in male minks or in adult females during pregnancy and lactation. More often, the disease begins in the summer (June - July) in mink puppies shortly after laying. Isolated cases are possible at any time of the year. Signs of the disease are not clearly expressed - many patients die suddenly. The most consistent symptom is frequent urination. If animals are picked up for vaccination, weighing, transplantation, treatment, then patients notice traces of blood or purulent exudate on the hair around the urethra, swelling in the area of the frontal fusion or the preputial sac. Visible mucous membranes and hairless areas of skin (soles of paws) are anemic, as in white puffiness. In subacute or chronic cases, when urocystitis is accompanied by urolithiasis, sick animals can be detected by less mobility, tense gait, paresis of the pelvic limbs, wetting, and poor appetite. Palpation can determine the presence of stones in the bladder.
Diagnosis. They detect purulent or bloody discharge in the urine, symptoms of dysuria, paresis of the pelvic limbs, anemia of the visible mucous membranes, paw pads, and frequent urination. A group diagnosis is made taking into account the season of the disease and the results of the pathological autopsy.
Treatment. Due to the late detection of sick animals, the effectiveness of treatment is low. Antibacterial agents are prescribed internally - antibiotics (penicillin, neomycin, tetracycline, tetraolean, etc.) mixed with furans and sulfonamide drugs in generally accepted dosages until recovery.
The effectiveness of treatment increases when hexamethylenetetramine is added to these drugs at a dose of 0.1-0.2 g 2 times a day or injections of ribonuclease or deoxyribonuclease at a dose of 5-10 mg in saline every other day. Positive results obtained after the use of cystenal and urodan. Prevention. During the intensive growth of young animals and the reproduction of the main herd, the use of conditionally suitable and, especially, poor-quality feed is avoided, the proportion of potentially dangerous feed that may be contaminated (contaminated) with microorganisms or toxic substances (fish meal, whole milk substitute, hydrolytic yeast, etc.) is limited. . In summer, the feed mixture must be prepared cold, at a temperature of 4 to 12 ° C, which reduces the rate of microflora reproduction. Limit the proportion or exclude from the diet feed with a neutral or alkaline reaction. Agents that lower the pH and prevent the growth of bacteria are added to the feed mixture: apple cider vinegar (1% of the feed in the form of a 1% solution), ortho-phosphoric acid (up to 0.5 g per 100 kcal of feed in terms of pure preparation).
After the first signs of disease or mortality appear, the entire livestock is fed a mixture of compatible antibacterial agents 2 times a day for 7-10 days (see treatment). The course of group therapy is repeated if the incidence begins to increase again. Usually, after 2-3 courses of treatment in the summer, the massive spread of urocystitis and urolithiasis completely stops. Along with the prevention and treatment of urolithiasis, such therapy is very effective against widespread gastrointestinal diseases, which often manifest themselves in the post-weaning period.
In addition to using antibacterial agents, they take care of the completeness of the diet and do not allow the proportion of bone products and nucleic acids(ears, lips, milk, BVK), enriched with vitamins and their sources (greens, nettles, etc.). In the case of an alkaline urine reaction, orthophosphoric or lactic acid and apple cider vinegar are added to the diet. The administration of ammonium chloride, as recommended by some authors, is, in our opinion, inappropriate, since animals may experience a decrease in appetite, poisoning due to an overdose of the drug, and precipitation of calcium salts in the urinary organs after prolonged use with food containing excess calcium.
DISEASES OF THE SKIN
Section and prolapse hair (cutting, self-cutting, flowing) - this is fragility and hair loss due to metabolic disorders, stress and, possibly, hereditary
location. It is observed in all types of fur-bearing animals. In some cases, when only the guard hairs are damaged, they talk about cutting them; when the guard hairs and down hairs are damaged, they talk about cutting them. Etiology. It is not completely clear. It is assumed that the haircut is caused by a deficiency of biotin, sulfur-containing amino acids, B vitamins, and microelements (sulfur, copper, cobalt, magnesium). Poor-quality feed and unsystematic long-term feeding of antimicrobial agents can lead to a deficiency of certain vitamins. Chronic diseases can also cause unsatisfactory keratinization of hair, loss of elasticity and fragility. Sectioning is often observed in the absence of disease, when, with a high protein content in the feed mixture, the growth of guard hairs is excessively accelerated and their strength is lost.
Sectioning and cutting, especially in certain areas of the body (on the tail, sides, rump, belly), can be a consequence of stress, tight spaces or a hereditary predisposition.
Hair loss (hair loss) occurs due to the presence of some of the listed reasons and as a result of a deficiency of unsaturated fatty acids or the use of feed with chemical preservatives. Post-mortem hair flow is observed after self-heating (steaming) of the carcasses of killed animals or skins removed, if they were folded tightly one to one and slowly
were frozen.
When kept together in the same cage, animals can bite each other's hair, which is also due to protein deficiency and other metabolic disorders. In some animals, especially among sables, the habitual cutting or plucking of hair before whelping is sometimes noted, probably as a result
Many defects in the quality of pubescence are in some cases hereditary, and they are very difficult to differentiate. For example, loss of guard and down hair on the abdomen (thinning or fraying) depends on the influence of environmental factors. Thus, the size of the hole in the house and the live weight of the animal are decisive in the appearance of the named anomaly.
One of the pubescence defects of arctic foxes is “samsonism”, or. “cotton fur” (sparse and short covering hair), transmitted to offspring only by females, would seem to confirm its purely hereditary origin. However, cases of the occurrence of Samson's disease in healthy animals, as well as the development of normal pubescence during a new molt in former Samsons, indicate a complex mechanism for the development of this pathology. Apparently, hereditary predisposition to metabolic disorders plays an important role here.
The defect of pubescence in Arctic foxes (matting and abrasion of hair in the sacral area) largely depends on feeding conditions, keeping, rearing method and, to a lesser extent, on
hereditary characteristics of the animal. A similar defect is common in foxes - bruising and split hair in the sacral area, often manifested by heavy feeding.
Symptoms On different parts of the body (tail, rump, back, sides or abdomen), guard hairs are devoid of ends and do not cover downy hairs. If this is observed on the body, then the hairline takes on a so-called “cotton-like appearance.” When biting hair in the area of the sacrum and tail, the animals are monitored, waiting for the development of self-gnawing (automutilation).
Animals are often found with all their hairs bitten off - both coverts and downy hairs. Moreover, the cutting areas are beyond the reach of the animal’s teeth, which indicates not biting, but hair breaking. Hair falls out before shedding, and downy hair is also lost (the latter, in some cases, is depigmented). The causes of this pathology are hereditary factors (semi-lethal hairlessness). It is most often observed in puppies of individual litters and among brown minks, and during the suckling or early weaning period. Alopecia is often observed in mink and ferret puppies after illness with diarrhea. Diagnosis. They are placed taking into account changes in the hairline. At the same time, hereditary semi-lethal hairlessness of brown mink puppies is excluded.
Treatment. Not developed. The use of symptomatic agents is indicated: vitamins, aminopeptide, etc.
Prevention. During the period of formation and growth of winter hair (July - November), feeding recommendations are strictly adhered to, especially regarding protein rationing. At this time, both underfeeding and overfeeding of animals is unacceptable. The vitamin supply of diets must be reliable due to sources of vitamins (yeast, whole fish, etc.) and concentrates (fur-vit and individual vitamins). To prevent excessively rapid hair growth, the level of protein feed in the diet is slightly reduced and the level of grain is increased. Animals with hair defects are culled.
DISEASES OF THE CENTRAL NERVOUS SYSTEM
Self-gnawing (automutulation, auto-aggression) is a chronic disease manifested by periodic nervous excitation, during which the sick animal gnaws certain areas of its body. Automutilation (self-mutilation) occurs among fur-bearing animals in different zones, causing damage to farms due to the death of sick animals or deterioration in the quality of the skins. In addition, sick females often remain unmarried, and whelping ones are killed or killed.
their puppies.
blockage of the excretory ducts of the anal glands or disturbances in the feeding of animals. Proponents of stress etiology have shown on numerous materials that automutulation naturally develops in the majority of weaned puppies (for example, sables) 10-54 days after exposure to a stressor (loneliness), and without exposure to a virus or other microbiological
MINISTRY OF AGRICULTURE AND FOOD OF THE REPUBLIC OF BELARUS
VITEBSK STATE ACADEMY
VETERINARY MEDICINE
Department of Diseases of Small Animals and Birds
DISEASES OF FUR ANIMALS
DOGS AND CATS
(Training manual)
(Part III. Diseases of viral etiology)
Intended for students of the Faculty of Veterinary Medicine, students of the Faculty of Advanced Training and students of veterinary
technical school departments
V I T E B S K 1 9 9 8
The educational manual was compiled by:
V. S. PRUDNIKOV - Doctor of Veterinary Sciences, Professor
Y. G. ZELUTKOV - Candidate of Veterinary Sciences, Associate Professor
REVIEWERS:
E.A. SOLONEKO - Doctor of Veterinary Sciences, Professor
A.S. SHASHENKO - Doctor of Veterinary Sciences, Professor
PURPOSE OF THE EDUCATIONAL MANUAL:
To help FVM students, FPK students and technical school students in independent work on studying diseases of infectious etiology of small animals, dogs and cats in preparation for laboratory practical classes, colloquiums, tests and exams.
For the purpose of uniform requirements for the study of animal diseases, the department has adopted the following scheme for describing the disease:
1. Definition of disease
2. Etiology
3. Epizootological data
4. Pathogenesis
5. Clinical signs and course
6. Pathological changes
7. Diagnostics
8. Differential diagnosis
9. Treatment
10. Immunity and specific prevention
11. Prevention and control measures
The teaching aid was reviewed at a methodological meeting
Technical Commission of the Faculty of Veterinary Medicine
ABOUT THE CHAPTER
Bacteriosis. Mycoses.
Carnivore plague………………………………………………………..……….4
Parvovirus enteritis….……………………………………………………………..….12
Infectious hepatitis…..………………………………………………….….18
Rabies……...…………………………………………………………….….22
Aujeszky's disease……………………………………………………………..……………….…..28
Adenovirus. …………………………………………………………..………………..…..32
Alut mink disease..………………………………………………….……34
Self-chewing……. …………………………………………………….…….38
Mink encephalopathy………………………………………………………………………………39
Encephalomyelitis of fur-bearing animals………………………………………………………………..41
Viral hemorrhagic disease of rabbits…………………………………44
Myxomatosis of rabbits………………………….………………………….…….47
PLAGUE OF CARNIVORES(infectious bluetongue) (Febris catarrhalis infectiosa) is an acute viral disease characterized by fever, catarrh of the mucous membranes, pneumonia, skin exanthema and damage to the nervous system.
ETIOLOGY. The virus was first discovered by the French researcher Carré in 1905. The definitive viral nature of the plague was proven by Dunkin and Laidlaw in 1926 by experimentally infecting a ferret.
The causative agent of the disease is an RNA genomic virus of the family Paramixoviridae, 90-180 nm in size. The virus is epitheliotropic and neurotropic. Has immunosuppressive properties. It is immunologically related to the measles and rinderpest virus. The virus is quite stable, so in a dried state it retains biological activity for 3 months, in feces - up to 2 weeks, in the organs of dead animals - up to 6 months, in blood - up to 3 months, in mucus nasal cavity - up to 2 months. Inactivation at 100 o C occurs within 3 minutes, when exposed to sodium hydroxide - after 1 hour, under the influence of 1% formaldehyde - within 3 hours.
EPISOOTOLOGICAL DATA. Dogs, raccoons, wolves, foxes, minks, sables and other carnivores are susceptible to the canine distemper virus. Animals of all ages are affected, but puppies 2-5 months of age are most susceptible. Colostral immunity persists in puppies for 2-6 weeks after leaving their mothers, but more often for 1.5-2 months.
The source of the infectious agent is sick and recovered animals, as well as animals in incubation period. Virus carriage lasts 2-3 months in dogs and up to 6 months in fur-bearing animals.
The pathogen is released from the body with discharge from the nasal cavity and eyes, when coughing, sneezing, with saliva, with urine, with fecal matter. Infection occurs by sniffing, as well as through the respiratory tract and digestive tract.
Factors of transmission of the pathogen include infected care items, infected muzzles, bedding, clothing and footwear of service personnel. It should be noted that the reservoir of the virus is wild carnivores and outbred aborigines. A vertical method of transmission of the pathogen through the placenta from a sick female to offspring has been established. The virus can be carried by rodents, birds and insects.
The highest incidence is observed in autumn-winter-spring. With the onset of the rut, the risk of spreading the disease increases sharply.
Characterized by stationarity. The morbidity rate is 70-100%, the mortality rate in extensive epizootics is 25-75%.
The disease is promoted by helminthic infestation, vitamin deficiencies, related breeding, and cold, damp weather.
PATHOGENESIS. At the site of introduction, the virus causes hyperemia, swelling and ulceration of the tissue, then penetrates into the regional lymph nodes, and after 2-6 days into the blood, causing fever. The virus spreads throughout the body, is introduced into internal organs and in the central nervous system. Metabolism, blood circulation, breathing and digestion are disrupted. The virus, affecting the immunocompetent cells of animals in the early stages of the disease, reduces their resistance to secondary microflora. In pregnant females, the virus can penetrate the placental barrier and cause fetal death and abortion.
CLINICAL SIGNS AND COURSE. The incubation period is 2-3 weeks, but can be 2-4 days.
The course of the disease is hyperacute, acute, subacute, chronic, but can be atypical and abortive.
Depending on the symptoms, nervous, pulmonary, intestinal and skin forms of the disease are distinguished. The transition of one form of the disease to another or its manifestation in a mixed form is not excluded. The most dangerous form of plague is nervous, which is accompanied by the development of irreversible processes in the brain.
In case of hyperacute flow the illness lasts 2-3 days, the temperature rises sharply, the animals refuse food, coma and death occur.
In acute cases illness, the temperature rises to 39.5-41 o C and remains at this level for 10-15 days. The animal reluctantly responds to the owner’s call, refuses food, tries to hide in a dark place, and may vomit. The skin of the nasal planum is dry and there may be cracks.
1-2 days after the temperature rises, serous-mucous and then purulent discharge from the eyes appears, as a result of which the eyelids stick together and the eyes close. Rhinitis appears, while serous-purulent exudate is released from the nasal cavities, crusts form on the nasal mirror, the nostrils stick together, breathing becomes wheezing, first appears dry, and then moist cough. During hematological examination, the number of leukocytes increases to 34 thousand and higher per 1 mm 3.
With the development of catarrhal inflammation of the mucous membrane of the gastrointestinal tract, diarrhea appears. The feces are liquid, gray-yellow, and later brown. With hemorrhagic inflammation of the rectum, traces of blood are found in the feces.
In nervous form Plague in animals exhibits agitation, convulsive contraction of the masticatory muscles and limbs, there may be paresis and paralysis of the hind limbs, epileptic seizures, clonic and tetanic convulsions appear. In such cases, the prognosis is usually unfavorable. It should be noted that even if recovered, some dogs experience lifelong muscle twitching, loss of vision, hearing and smell. Sometimes relapses occur when, after improvement in the general condition, the disease worsens again. In this case, death is often observed.
The plague is characterized by an undulating course, when relapse occurs after 7-10 days.
Pulmonary form of the disease more often develops in animals in autumn or spring, which is facilitated by a decrease in resistance, increased contact, damp weather, the emergence of a susceptible contingent and is manifested by the development of catarrhal pneumonia.
Abortive course is characterized by 1-2-day suppression and is more often recorded in previously immunized dogs, when in the presence of nervous phenomena death can occur.
At the minks When infected with plague, the body temperature rises to 40 o C, they eat food poorly and are depressed. Then serous rhinitis and conjunctivitis develop, turning into purulent (in the latter case, the eyelids stick together, the nasal passages are clogged with clots of pus).
Body temperature decreases slightly after the first rise, but remains elevated throughout the entire period of illness.
Sick minks quickly lose body weight. A vesicular rash appears on the skin of the lips and nasal openings (in some it spreads to the entire body). In males, the paws and mainly the hind paws swell. Shortly before the death of the animal, diarrhea appears.
During this period, signs of damage to the nervous system often develop: coordination of movements is impaired, paralysis and paresis of the limbs are observed. The mortality rate of young minks reaches 70-90%, and for adults - 30-50%.
Clinical signs of plague in silver-black foxes, arctic foxes, raccoon dogs also begin with an increase in body temperature and the appearance of serous rhinitis. Animals refuse food and are inactive.
Catarrhal inflammation develops on the mucous membrane of the upper respiratory tract, and breathing is difficult. Catarrhal conjunctivitis and gastrointestinal dysfunction occur, and diarrhea appears.
The feces are initially dark in color and become greenish in color as the disease progresses. The presence of blood in them indicates hemorrhagic inflammation of the mucous membrane of the gastrointestinal tract.
Animals quickly lose weight, their hair loses its shine, and sometimes skin exanthema develops. Symptoms of damage to the nervous system appear at the end of the disease. In some animals, the optic nerve is affected and the pupil dilates. Mortality among adult silver-black foxes reaches 30%, puppies - up to 60-70%, among arctic foxes - up to 30-50 and 70-80%, respectively.
In dogs:
1. Catarrhal-purulent rhinitis, conjunctivitis, keratitis
2. Catarrhal-purulent bronchopneumonia (complication)
3. Serous-hemorrhagic lymphadenitis of bronchial, mesenteric and other nodes
4. Granular and fatty degeneration of the liver, kidneys and myocardium
5. Infectious skin rash (papules, vesicles, pustules, crusts)
6. Acute catarrhal cystitis with hemorrhages on the mucous membrane of the bladder
7. Catarrhal-ulcerative gastroenteritis
8. Edema and hyperemia of the brain
9. Hemorrhages on the rectal mucosa
10. Histo: in the epithelium of the bladder - cytoplasmic viral inclusion bodies, in the brain - non-purulent lymphocytic encephalitis
At the minks:
1. Swelling of paws, eyelid skin, nose, lips, ears
2. Purulent rhinitis and conjunctivitis
3. Catarrhal-ulcerative gastroenteritis
4. Hemorrhages on the rectal mucosa
6. Hemorrhagic or purulent inflammation of the renal pelvis
7. Catarrhal cystitis with hemorrhages on the mucous membrane of the bladder (it is empty)
8. Catarrhal bronchopneumonia with emphysematous areas
9. Hemorrhages on the endocardium and cardiac membrane, myocardial infarctions
10. Pustular or crustose rash on the skin of the extremities
11. The spleen is not changed
12. Wasting, stunted growth and development
:
1. Serous-purulent conjunctivitis and rhinitis
2. Catarrhal bronchopneumonia
3. Acute catarrhal enteritis and hemorrhages in the gastric mucosa
4. Dotted and streaky hemorrhages on the mucous membrane of the bladder
5. Hyperemia of cerebral vessels
6. Skin eczema
DIAGNOSTICS. The diagnosis is established on the basis of clinical and epizootological data and pathological changes, taking into account the results of histological examination for the presence of specific intracellular viral inclusion bodies in the epithelium of the bladder and non-purulent lymphocytic encephalitis in the brain. If necessary, a biological test is carried out on puppies and a virological study is carried out. The virus is cultivated on a culture of ferret kidney cells or chicken embryos, followed by identification using RIF, RN, RSK, RTGA, RGA and ELISA.
In order to study the epizootic situation, RN, RSK, PDP and RTGA are used.
DIFFERENTIAL DIAGNOSTICS. It is necessary to exclude rabies (aggressiveness, paralysis of the lower jaw, identification of Babes-Negri inclusions, positive bioassay on mice), Aujeszky's disease (itching in dogs, scratching in the head area, positive bioassay on rabbits with a characteristic clinical picture), infectious hepatitis (pain when pressing on the liver area, enlargement of the thymus gland), salmonellosis (occurs without conjunctivitis, bacteriological examination), pasteurellosis (microscopy (bipolarity), background examination).
TREATMENT. The difficulty of treatment lies in the fact that the disease, as a rule, most often occurs with complications. The success of treatment largely depends on the timeliness of the measures taken and the effectiveness of medications. Treatment should be comprehensive with the use of specific and symptomatic agents.
Polyvalent serum against plague, parvovirus infections and viral hepatitis of carnivores is somewhat less effective.
It must be remembered that specific drugs It is better to use at an early stage of the disease.
Positive results in the treatment of canine distemper are achieved by the use of leukocyte plasma prepared from the blood of dogs, which is administered intravenously at a dose of 0.3-0.4 ml per kg of animal weight. For subcutaneous and intramuscular injection, 1-2 ml of a 2-2.5% solution of novocaine should be added to the plasma.
In the absence of the above remedies, anti-measles gammaglobulin (1-3 ml intramuscularly for 2-3 days), normal horse serum (1st day - 1 ml, every other day - 2 ml, after 2 days - 3 ml), anti-anthrax serum (1st day - 1 ml, then until the 5th day the dose is increased daily by 1 ml, and from the 6th day the dose is reduced by 1 ml and brought to 1 ml).
To suppress secondary bacterial microflora, antibacterial drugs with a prolonged action are used: vetrim, bicillin, biseptol, ristomycin, kanamycin, lincomycin, spectolin, pentard, sulfetrim, linco-spectin, enroxil (5% solution), biosol, lincocin, geomycin V, vetrimoxin L.A., gallimycin 50, intramycin, spectam (for injection), baytril (2.5% solution for injection, tablets), amuril. After a course of antibiotic therapy, the use of probiotics is mandatory: lactobacterin, bifidum-bacterin, bactisubtil, enterobifidin, etc.
For pathologies of the gastrointestinal tract, the following are prescribed orally: furazolidone, phthalazole, biseptol, etc. For pulmonary complications, kefzol, cloforan, etc. are used.
To reduce the inhibitory effect of antibiotics and sulfonamides on the immunity of animals, they should be used (especially in the acute period of the disease) together with corticosteroid drugs that effectively relieve inflammation: prednisolone, dexamethasone.
Stimulation of tissue metabolism is carried out using B vitamins in combination with pantothenic acid, nicotinamide and ascorbic acid for 10 days.
Positive results in the treatment of canine distemper are achieved with intravenous administration once a day for 3-4 days of the following mixture of drugs: immunoglobulin, 40% solution of hexamine, 10% glucose solution, isotonic sodium chloride solution, 1% solution of diphenhydramine and 5% solution of ascorbic acid.
Borogluconate or calcium gluconate is used as an antitoxic agent once a day for 5-7 days in a row, subcutaneously or intravenously.
If paresis occurs, treatment should include galantamine in combination with dibazole. For persistent paralysis, the administration of strychnine has a good effect. Simultaneously with drug treatment, massage and electrical stimulation of the muscles in the area of the corresponding nerves and their roots can be performed. Good results in cases of paralysis can be obtained by irradiating the area of paralyzed nerves or their roots with a helium-neon laser. If the disease occurs with nervous attacks, tics, severe pain, massage and physiotherapy should be temporarily cancelled. Injecting medications should also be limited and should be administered intravenously.
In case of severe agitation, aminazine, pipolfen should be administered, and to restore normal central nervous system function it is recommended to use Cerebrolysin.
An integrated approach to the treatment of dogs with plague, including suprapleural novocaine blockade of the splanchnic nerves (intestinal and nervous forms) and stellate ganglia (pulmonary form) in combination with broad-spectrum antibacterial drugs, has high therapeutic effectiveness.
IMMUNITY AND SPECIFIC PREVENTION. In convalescent animals, immunity persists for a year.
The following vaccines are currently used to create active immunity.
Monovalent:
1. Dry culture virus vaccine from strain 668 KF
2. Dry culture vaccine against canine distemper from the EPM strain
3. Dry live culture vaccine against canine distemper "Vakchum"
4. Dry culture vaccine against canine distemper from the strain "VNIIVViM-88"
5. Dry live culture vaccine against canine distemper
Polyvalent (associated):
1. Associated vaccine against parvovirus enteritis, hepatitis and canine distemper
2. Tetravac vaccine against canine distemper, infectious hepatitis, adenovirus and parvovirus enteritis
3. Vaccine "Multican-4" against plague, adenoviral infections, parvovirus and coronavirus enteritis
4. Vaccine "Multican-6" against distemper, hepatitis, leptospirosis, parvovirus, coronavirus and rotavirus enteritis of dogs
5. Vaccine "Gexakanivac" against canine distemper, infectious hepatitis, adenovirosis, parvovirus enteritis and canine leptospirosis
6. Vaccine "Adenomun-7" against enteritis, hepatitis, plague, adenovirosis, parainfluenza and leptospirosis in dogs.
7. Associated vaccine against viral enteritis, botulism and canine distemper
PREVENTION AND CONTROL MEASURES. To prevent plague in carnivores, veterinary specialists are required to ensure a strict veterinary and sanitary regime
Prohibit visits to fur farms (kennels) by unauthorized persons, as well as establish control over the import of rodents and animals into the territory of farms (kennels);
Take measures to exclude the possibility of stray dogs and wild carnivores entering the territory of animal farms (kennels);
2 weeks before whelping, as well as before placing the animals, disinfect nests, houses, cages, feeders, drinkers and other equipment while simultaneously disinfecting protective clothing, and then carry out disinfection at least once a month;
Conduct a daily clinical examination of animals and, if sick, are detected, isolate them in a timely manner;
All fur-bearing animals newly received to farms must be quarantined for 30 days, and service dogs- 21 days and allow them into the general herd after quarantine only with the permission of a veterinary specialist;
When entering and entering the territory of farms (nurseries), install disinfection barriers and disinfection mats filled with a 2% sodium hydroxide solution;
Procurement of feed, as well as the purchase of animals for fur farms and nurseries, should only be carried out in farms that are free from carnivorous plague.
Citizens who own carnivorous animals are obliged to promptly notify local veterinary specialists about their acquisition of carnivorous animals, about the disease or death of their animals.
Carnivorous animals belonging to fur farms, dog nurseries, enterprises and organizations, as well as the population, are subjected to preventive immunization against plague.
All carnivorous animals subject to export from farms for breeding purposes are vaccinated against plague 15-30 days before export, regardless of previous vaccinations against this disease.
If carnivorous animals show signs that raise suspicion of plague, it is necessary to inform a veterinary specialist, deny access to the fur farm to unauthorized persons, stop the removal and movement of animals within the farm (except for the immediate isolation of patients) in order to avoid the spread of infection.
When diagnosing plague quarantine is imposed, under the terms of which PROHIBITED :
Import and export to an unfavorable point of carnivores susceptible to plague, as well as their removal and export outside the unfavorable point;
Weighing animals, tattooing, deworming, combing fur, which can lead to the spread of infection;
If the disease occurs during the rutting period, mating of clinically healthy animals is permitted 14 days after the animals are vaccinated against canine distemper.
In dysfunctional fur farms(dog kennels) carry out the following measures to eliminate the disease:
All sick and suspected carnivores with plague are immediately isolated and subjected to specific and symptomatic treatment, and the rest are immunized;
All service personnel are provided with additional protective clothing, rubberized aprons and rubber shoes;
Disinfect the overalls of service personnel daily;
After each case of isolation and isolation of a sick animal, cages, houses, the soil under the cages and portable boxes are disinfected. Routine disinfection is carried out every 5 days. In the isolation ward, disinfection is carried out daily, for which they use: 2% sodium hydroxide solution; 3% Lysol emulsion; clarified bleach solution containing 2% active chlorine;
Manure is placed in piles in a specially designated area for biothermal disinfection within 3 months after their closure;
The corpses of dead animals, as well as carcasses and skins of no value, are burned or dumped in the Beccari pit;
Skins from fallen or forcedly killed animals and animals suspected of having plague are allowed to be removed only in the isolation ward. Subsequently, they are dried at a temperature of 25-33 ° C for 3 days, followed by exposure at a temperature of 18-20 ° C for 10 days;
All carnivorous animals susceptible to plague are strictly registered and subjected to veterinary and sanitary examination at least 2 times a month, fur-bearing animals and dogs are vaccinated.
Quarantine is lifted 30 days after the last case of recovery or death of animals from canine distemper and the completion of final veterinary and sanitary measures.
The removal (withdrawal) of fur-bearing animals from the farm is permitted no earlier than 6 months, and dogs - 45 days after the quarantine is lifted.
PARVOVIRAL ENTERITIS(viral enteritis) (Parvovirus enteritis) is an acute contagious disease characterized by catarrhal-hemorrhagic inflammation of the mucous membrane of the gastrointestinal tract, necrotic damage to the mesenteric lymph nodes, spleen and myocardial damage.
ETIOLOGY. The causative agent of the disease is a DNA virus belonging to the Parvoviridae family. It has some antigenic affinity and identical immunological properties with the causative agent of enteritis in minks and panleukopenia in cats, but is not identical to them. Reproduction occurs in the nucleus of epithelial cells causing their death. In the body it causes the formation of virus-neutralizing, complement-fixing antibodies and antihemagglutinins. It has hemagglutinating activity against pig and monkey erythrocytes.
The virus retains its biological properties at a temperature of 20 0 C for 3 months, in dried feces for more than a year. It is resistant to chloroform, ether, alcohol, acidic environment (stored at pH=3). Boiling inactivates it instantly. In a 0.5% formaldehyde solution and a 4% chloramine solution it dies within 24 hours.
EPISOOTOLOGICAL DATA. Dogs (of all breeds), arctic foxes, silver foxes and cats are susceptible to the disease. Puppies 1-12 months of age are affected, but more often 3-5 months old.
The source of the infectious agent is sick animals and virus carriers, which persists for 4 months. The pathogen is released into the external environment with feces, vomit, saliva and urine. The virus can be transmitted directly by sniffing, as well as through care items and equipment, with special clothing, which is a factor in the transmission of the pathogen.
There is no strict seasonality when the disease occurs.
The reservoir of the pathogen is stray aboriginal dogs, which suffer from a mild form of the disease but retain the virus.
PATHOGENESIS. The main targets for parvovirus are lymphoid tissue, myocardium and intestinal epithelium. In newborn puppies obtained from non-immune mothers, the disease occurs with intense damage to the myocardium, and after weaning - to the gastrointestinal tract.
After the virus enters the animal’s body through the nutritional route, it multiplies locally in the lymphoid tissue. After 3-5 days, short-term viremia occurs with localization and reproduction of the virus in the cells of the crypts thin section intestines, thymus, spleen, and in newborn puppies myocardial cells are affected.
During the process of virus reproduction, lysis of the epithelial cells of the small intestine occurs, which entails the development of dysbiosis with disruption of the digestive process. Isolation of the virus in fecal matter begins already 3-4 days after infection. Bacterial intoxication develops intensively, which is accompanied by the body’s loss of sodium ions, leading to a large water deficit. Loss of water from the body has an extremely adverse effect on hemodynamics due to rapidly increasing blood thickening.
CLINICAL SIGNS AND COURSE. The incubation period is 2-10 days. The disease manifests itself in three forms: cardiac, intestinal and mixed, and occurs with lightning speed, acute and subacute.
Heart shape noted in puppies 1-8 weeks of age obtained from non-immune dams. Severe acute heart failure develops with shortness of breath, pulmonary edema, paroxysmal tachycardia, extrasystole and deformation of the ventricular complex (ECG). After 24-48 hours, blueness of the white membrane of the eyes is noted. In general good condition, the puppies refuse to fatten. After 48-96 hours, leukopenia is noted in the blood, when the number of leukocytes decreases from 2500 to 300 l/mm 3, neutrophilia, and then lymphocytosis. The death of animals occurs after 24, less often after 48 hours, with symptoms of sudden shortness of breath, vomiting and loud groans.
Intestinal form more common in puppies 3 months of age and older. Symptoms appear suddenly, where the most characteristic of them are: depression of general condition, lack of appetite and severe vomiting. Vomiting movements and urges are repeated every 30-40 minutes, while at the beginning the contents of the stomach are released, and then a watery-mucous liquid is released. Some animals develop signs of damage to the respiratory system after vomiting. Drinking liquid or force-fed food may be thrown out with vomit after some time. The elevated temperature lasts for a short time and in most cases there is no time to notice it, then it drops below normal. Profuse diarrhea begins 12-24 hours after the onset of vomiting. The feces first have a mushy consistency and a very fetid odor, then on the 2-5th day they become watery and dirty-reddish in color. Due to intense dehydration, retraction of the eyeball is noted, and in the presence of intoxication, a coma develops.
In some cases, conjunctivitis and pneumonia are observed in sick animals.
In mixed form. depending on the method of penetration of the pathogen into the body and the level of its natural resistance, pathology of the gastrointestinal tract or cardiovascular system may dominate.
in dogs:
1. Acute catarrhal-hemorrhagic gastroenteritis with the presence of bloody contents in the lumen of the small intestine
2. Acute catarrhal colitis with black-red contents in the lumen of the large intestine
3. Serous-hemorrhagic lymphadenitis of mesenteric nodes
4. Congestive hyperemia of the liver, kidneys and pancreas
5. Congestive hyperemia and pulmonary edema
6. Congestive hyperemia of the brain
7. Histo: necrosis of the villi of the small intestine, intranuclear eosinophilic inclusion bodies in the crypt epithelium
:
1. Acute catarrhal, catarrhal-hemorrhagic gastroenteritis with the presence of mucus and blood in the intestinal lumen
2. Serous lymphadenitis of mesenteric nodes
3. Granular dystrophy of the liver, kidneys, myocardium
4. Ascites. Hydrothorax
in cats:
1. Acute catarrhal, catarrhal-hemorrhagic enteritis
2. Serous-hemorrhagic lymphadenitis of mesenteric lymph nodes
3. Serous-catarrhal rhinitis, laryngitis, conjunctivitis
4. Ulceration of the edges of the tongue
5. Catarrhal bronchopneumonia
6. Acute pancreatitis
7. Septic spleen
8. Exicosis
9. Histo: intranuclear inclusions in intestinal epithelial cells
DIAGNOSTICS. The diagnosis is made comprehensively, taking into account clinical and epidemiological data, pathological changes and laboratory results. For this purpose, the following are sent to the laboratory during life: fecal samples at the time the first signs of the disease appear and paired blood serum samples, and in case of death of the animal - the affected area of the intestine with its contents, the spleen, thymus, and mesenteric lymph nodes. In the laboratory, the virus is isolated in cell culture, followed by identification. Serological methods include RGA, RTGA, RID, RSK, RN and enzyme immunoassay.
The diagnosis is considered established when the virus is isolated and identified; with an increase in antibody titer fourfold in paired samples of blood serum from sick animals.
DIFFERENTIAL DIAGNOSTICS. Parvovirus enteritis should be distinguished from plague, salmonellosis, and colibacillosis.
TREATMENT. It should be early, comprehensive, intensive and aimed, first of all, at eliminating vomiting, dehydration, acidosis and secondary infection.
Specific treatments are: polyvalent serum against plague, parvovirus infections and viral hepatitis of carnivores, which is administered subcutaneously, intramuscularly, and in severe cases - intravenously (with the addition of 0.5-1 ml of 1% diphenhydramine solution), in a dose of 5- 10 ml 1 time per day for the first two days. In approximately the same doses, hyperimmune serum of dogs specially immunized for this purpose or serum of convalescent animals can be used.
The most effective specific agents currently are: Avirokan (specific canine immunoglobulin against distemper, hepatitis, coronavirus enteritis and carnivore parvovirus); immunoglobulin against parvovirus enteritis and canine distemper; medicinal globulin against plague, enteritis and hepatitis of carnivores.
Therapy for enteritis involves the use of sulfonamides, antibiotics, heart medications, and novocaine blockade.
In order to suppress secondary microflora, the following are used: ampisur (intramuscular or subcutaneous 1 ml per 10 kg, 2 times a day for 3 days), vetrimoxin (1 ml per 10 kg, 2 times a day, again after 3 days), Spectam (intravenously, intramuscularly, subcutaneously at the rate of 10-15 ml per 50 kg, once a day, for 3 days), celbar (4.5% suspension, mixed with water and drunk once a day for 3 days), baytril (5% solution, for injection, subcutaneously, 1 ml per 20 kg of body weight, for 5 days), linco-spectin (for injection, 1st day 2 injections, then 1st for 2-4 days at a dose of 1 ml per 10 kg), intramycin (intramuscular or subcutaneous at the rate of 0.8 ml per 10 kg of body weight).
The following regimen has a fairly high therapeutic effect for enteritis: thylan -1 g per 5 ml of water, intramuscularly; camphor 20% oil solution - 2 ml subcutaneously; glucose 5% in saline solution - 100 ml subcutaneously. These drugs are administered once a day, and glucose is injected into 4 points.
To reduce spasms of smooth muscles, an intramuscular injection of a 2% solution of no-spa should be performed in a dose of 1-2 ml; in its absence, papaverine or cerucal can be used.
A necessary measure in the treatment of a sick animal is washing the intestines with enemas, which must be done immediately after the first signs of the disease appear. The procedure begins with the introduction of a 1% solution of sodium bicarbonate, then infusions of medicinal herbs (chamomile, oak bark, St. John's wort, etc.) are used. The enema should be a siphon, shallow, cleansing. The solution should be cool, which causes contraction of the intestinal muscles and vasoconstriction.
To increase the effectiveness of the sanitizing properties of solutions, antibiotics should be added to them: kanamycin, streptomycin (10 thousand units per 1 kg of weight), farmazin (1-4 ml).
To relieve and prevent vomiting, use: cerucal (intravenously or intramuscularly, 1-2 times a day, in a dose of 0.5-1 ml); golidor (intramuscularly at a dose of 0.02 ml/kg live weight); aminazine 2.5% solution (subcutaneously or intramuscularly, 1 time per day, in a dose of 1-2 ml); trisidil (triperidol, orally 2-3 times a day, 3-5 drops); haloperidol (haldol, 0.5% intramuscular solution, in a dose of 0.5-2 ml or 0.2% solution orally, 1-2 times a day, 3-6 drops).
Cardiotonic drugs are prescribed: sulfocamphocaine, cordiamine, camphor oil, caffeine, etc.
A large number of injections when providing medical care negatively affects the general condition of the animal. In this regard, it is recommended that the main symptomatic drugs be administered comprehensively in a general rehydration solution, by intravenous drip, taking into account their compatibility.
IMMUNITY AND SPECIFIC PREVENTION. After recovery from the disease, animals develop long-term, intense immunity, accompanied by virus carriage. For active prevention use:
1. A cultural vaccine against viral enteritis of minks, which is administered once in endangered farms, and twice in unfavorable farms, with an interval of 12-14 days, intramuscularly in the area of the inner thigh, in a dose of 1 ml, immunity occurs on the 14th day and does not persist less than 12 months
2. Dry culture vaccine against enteritis of carnivores
3. Virus vaccine "Multican-2" against parvovirus enteritis and adenoviral infections of dogs
4. Liquid inactivated virus vaccine against parvovirus enteritis and hepatitis of carnivores
5. Associated vaccine against parvovirus enteritis, hepatitis and canine distemper
6. Tetravac vaccine against canine distemper, infectious hepatitis, adenovirosis and parvovirus enteritis
7. Vaccine "Multican-4" against plague, adenoviral infections, parvovirus and coronavirus enteritis
8. Vaccine "Multican-6" against distemper, hepatitis, leptospirosis, parvovirus, coronavirus and rotavirus enteritis of dogs
9. Vaccine "Gexakanivac" against canine distemper, infectious hepatitis, adenovirosis, parvovirus enteritis and canine leptospirosis
10. Vaccine "Adenomun-7" against enteritis, hepatitis, plague, adenovirosis, parainfluenza and leptospirosis in dogs
11. Associated vaccine against viral enteritis, botulism and canine distemper.
It is recommended to carry out deworming 2 weeks before immunization, exclude the use of antibiotics and sulfonamides, and on the day of vaccination, thermometry and a thorough clinical examination should be carried out. After vaccination, puppies must be protected from hypothermia and the use of antibacterial drugs and sulfonamides must be limited.
PREVENTION AND CONTROL MEASURES. When a diagnosis is made, restrictions are imposed. A thorough clinical examination is carried out, all sick and suspected animals are isolated and treated. At the entrance to the farm territory, a disinfection barrier filled with a 2% solution of formaldehyde or sodium hydroxide is installed and kept in working condition. At the entrance to the sheds, disinfection mats are installed, moistened with one of the above solutions. Cages where sick animals were kept, portable boxes, drinking bowls, feeders, and equipment are subjected to wet disinfection with a 2% formaldehyde solution. Overalls and shoes are disinfected in a paraformalin chamber.
Manure, bedding and feed residues are removed daily and stored for biothermal disinfection. The soil under the cells is irrigated with a 2% hot solution of sodium hydroxide or a hot solution of formaldehyde.
PROHIBITED:
Moving animals within the farm, as well as weighing, grading, etc., which is associated with picking them up;
Deny access to the territory of the unfavorable farm to unauthorized persons;
The economic connection between prosperous and disadvantaged brigades, as well as with other animal farms, is terminated;
It is prohibited to remove animals from the farm, as well as to remove inventory, equipment and other items for caring for animals outside the epizootic focus;
They organize the scaring away of wild birds, the destruction of rodents and insects, and also take measures to prevent dogs, cats and other animals from entering the fur farm.
Every day, a clinical examination of animals, sick and animals suspected of disease is carried out, they are isolated in an isolation ward and veterinary and sanitary measures are carried out.
Sick and recovered animals, after the fur has matured, are subject to mandatory slaughter as virus carriers. Clinically healthy animals are vaccinated.
Organize daily disinfection of animal care items, as well as at least once a week of cages and houses with a 2% hot formaldehyde solution.
The removal of skins from dead animals is carried out in an isolated room, specially assigned by workers provided with special clothing.
Corpses, sawdust and fat are destroyed daily by burning. Skins obtained from dead animals are allowed to be exported after they have been disinfected.
Restrictions are lifted 30 days after the last case of death or recovery of animals from parvovirus enteritis and the implementation of veterinary and sanitary measures.
After the restrictions are lifted, it is prohibited for a year to transport animals outside the farm, as well as to remove them from a previously unfavorable farm.
INFECTIOUS HEPATITIS OF CARNIVORES(Hepatitis infectiosa) is an acute contagious viral disease characterized by fever, catarrh of the mucous membranes of the respiratory tract and intestines, damage to the liver, gall bladder and disorders of the central nervous system.
ETIOLOGY. The causative agent of the disease is a DNA-containing virus of the Adenoviridae family, type I. It has the shape of an icosahedron, with a diameter of 70-90 nm, is epithelial, neuro-, hepatotropic, and is capable of causing the synthesis of complement-fixing, precipitating and virus-neutralizing antibodies. It is cultivated in the kidney cells of puppies, arctic foxes and dogs, causing the formation of intranuclear inclusion bodies. It has a fairly high resistance to physical and chemical environmental factors. Thus, in the secretions of sick dogs (feces, urine, mucus), the virus can remain active for up to 1.5 years, at room temperature - up to 0.5-1 year. Boiling inactivates the pathogen in 1 minute. Formalin and alkalis in a 2-3% concentration inactivate the virus within 30 minutes. A 10% phenol solution does not inactivate the virus within 12 hours. It should be noted that a virus isolated from dogs can cause disease in arctic foxes, foxes, raccoons, and vice versa, a virus isolated from the pathological material of these fur-bearing animals causes disease in dogs with characteristic changes in the liver.
EPISOOTOLOGICAL DATA. Viral hepatitis affects foxes, arctic foxes, dogs and other canine animals of all ages, but young individuals aged 1.5-6 months are most susceptible to it. Most often, puppies become ill on the fifth day after weaning from their mothers.
The source of the infectious agent is sick animals, as well as virus carriers. Which release the virus into the external environment with urine, feces, nasal mucus, mother's milk, conjunctival secretions, as well as when coughing and sneezing. After recovery, animals remain virus carriers for several years.
Under natural conditions, infection occurs through the mucous membranes of the nasal and oral cavities, the gastrointestinal tract and genitals, as well as through damaged areas of the skin. Intrauterine infection is possible. Cases of the spread of the disease due to non-compliance with the rules of asepsis and antisepsis during surgical operations have been established. Stray animals serve as reservoirs for the pathogen.
The disease occurs in the form of extensive epizootics, with a clearly defined stationarity.
PATHOGENESIS. Once in the body, the virus multiplies in the lymph nodes and bone marrow, then appears in the blood and forms clusters in the form of intranuclear inclusions in the endothelial cells of capillaries and venules of all organs, especially the liver and spleen. Developing dystrophic changes in the liver, kidneys, and myocardium lead to metabolic disorders and intoxication of the body. After damage to the nerve centers of the brain and spinal cord, locomotor disorders appear. During the period of pronounced clinical signs, the virus is in the blood, in all secrets and excrements, later only in the kidneys and urine.
CLINICAL SIGNS AND COURSE. The incubation period, depending on the method of penetration of the pathogen into the body, lasts 2-5 days for the aerogenic method of infection and 2-14 days for the alimentary method. Depending on the resistance of the organism and the degree of virulence of the pathogen, acute, subacute and chronic course of the disease is distinguished.
In acute cases of dogs, arctic foxes and foxes. become inactive, have difficulty standing up, have an unsteady gait, and refuse to feed. Subsequently, vomiting with bile appears (the main symptom), unilateral or bilateral keratitis and tonsillitis develop. Anemia occurs in the mucous membranes of the eyes and mouth, and yellowness of the sclera. Urine becomes dark brown in color, which is a characteristic sign of hepatitis.
Temperature reaction deserves special attention in hepatitis. Starting from the 4th day, the temperature rises to 41-41.7 o C and is maintained at this level until the death of the animal, which rarely happens with viral diseases. Leukopenia is pronounced in the blood (2-3 thousand cm 3).
The duration of the disease in acute cases ranges from several days to 2-3 weeks. Animals die while in a deep comatose state. Sometimes before death, involuntary movements of the limbs and convulsions are recorded.
In puppies under the age of 1 month, a rise in body temperature to 41 o C is noted. They squeak and do not suckle their mother. They experience paresis of the hind limbs, unilateral or bilateral keratitis, and wheezing in the lungs.
In puppies 2-4 months old, on the third day of illness, a rise in body temperature to 41 o C, decreased appetite and thirst are recorded. They develop catarrhal inflammation of the mucous membranes and conjunctivitis. Serous discharge from the nose and eyes is observed, later (on the 8-9th day) unilateral or bilateral keratitis. In addition, a disorder of the gastrointestinal tract (diarrhea is replaced by constipation), paresis and paralysis of the hind limbs are established. On palpation in the area of the xiphoid process and the right iliac, severe pain is observed. The mucous membranes are pale with a yellow tint.
Subacute course The disease most often begins with symptoms of depression and the presence of remitting fever. The animals mostly lie upright, have poor standing, a wobbly gait and weakness of the hind limbs are noted. A characteristic symptom is anemia and yellowness of the mucous membranes of the eyes, mouth, paresis and paralysis of the hind limbs. In some animals, unilateral or bilateral keratitis is observed. During the period of fever, the body temperature of sick animals rises to 41 o C and higher. With an increase in body temperature, a disorder of the cardiovascular system is established. The number of heart contractions reaches 100-120 per minute, the pulse is arrhythmic and weak. These signs may periodically fade away and then reappear in a more pronounced form.
Urine takes on a dark brown color. Sometimes the depressed state is replaced by temporary excitement, the animals try to hide in the corner of the cage, when given food they become aggressive, and twitching of individual muscle groups is observed. Then the excitement gives way to pronounced depression. The subacute course of the disease lasts about a month and ends in death or becomes chronic.
Chronic course found mainly in permanently disadvantaged farms. Clinical signs are usually vague in animals under one year of age and older. There are periodic rises in temperature, progressive emaciation, discharge from the eyes and nose, systematic upset of the gastrointestinal tract, and sometimes jaundice.
Abortions are observed in pregnant animals in the second half of pregnancy. In males, the disease, which is most dangerous, is asymptomatic. Their reproductive sphere is affected, which facilitates the transmission of the pathogen during mating.
The following changes are observed in animals: the liver is enlarged by 1.5-2 times, its color varies from yellow to dark brown, with fibrinous deposits on the surface. The mucous membrane of the bladder is edematous, the spleen is enlarged.
In the subacute course: the subcutaneous tissue in the chest, groin, and abdomen has pronounced gelatinous infiltrates and hemorrhages. A yellowish-tinged liquid is found in the chest and abdominal cavities.
Pathological diagnosis:
in dogs:
1. Alternative hepatitis
2. Fibrinous perihepatitis
3. Cholecystitis
4. Catarrhal gastroenteritis with hemorrhages on the mucous membrane of the digestive tract
5. Enlargement and hyperemia of the spleen and, sometimes, heart attacks in it
6. Keratitis, tonsillitis
7. Ascites with accumulation of bloody fluid with fibrin in the abdominal cavity
8. Jaundice and hyperemia of the conjunctiva
9. Erosive stomatitis and hemorrhages on the gums
10. Histo: in the liver cells, intranuclear inclusion bodies of Rubart
In arctic foxes and black-brown foxes:
1. Alternative hepatitis
2. Jaundice and hyperemia of skeletal muscles
3.Hyperemia of lymph nodes
4. Enlarged spleen
5. Catarrhal-ulcerative gastroenteritis
6.Gelatinous swelling of the thymus
7. Ascites, hydrothorax with the presence of pale pink or red fluid
8.Anemia and exhaustion
DIAGNOSTICS. The diagnosis of infectious hepatitis is established on the basis of epidemiological data, clinical signs, pathological changes with mandatory laboratory tests. In this case, in order to detect antibodies, RID is used (a special kit is produced). To identify the antigen, RGA, RIF, RSC and cultivation in cell culture are used with subsequent identification.
DIFFERENTIAL DIAGNOSTICS. During the diagnostic process, it is necessary to exclude: leptospirosis, plague, encephalomyelitis, Aujeszky's disease.
TREATMENT. Among the specific treatment agents, it is recommended to use polyvalent serum against plague, parvovirus infections and viral hepatitis of carnivores; polyvalent immunoglobulin; serum from specially immunized donor dogs; serum of convalescent animals.
Efficiency therapeutic assistance is determined by the stage of the infectious process and it should be carried out comprehensively, using, first of all, drugs or substances that have a normalizing effect on liver detoxification: Essentiale Forte, Karsil, which are administered daily for 5 days.
To stimulate metabolic processes, multivitamins are prescribed: trivit, tetravit, etc.
In order to improve liver function, B vitamins (B 1, B 2, B 12), folic acid, sirepar, cytochrome C are used.
To reduce intoxication of the body, it is recommended to use glucose, hexamethylenetetramine, ascorbic acid, which are administered intravenously, once a day, for 3-4 days. For the same purpose, you can use rheopolyglucin, Ringer-Locke solution, and sorbitol.
For edema, diuretics are used: furosemide (0.02 g orally or 0.5-2 ml of a 1% solution intramuscularly once every 2 days), veroshpiron (0.025 g orally 1-2 times a day).
To suppress secondary microflora, a course of antibacterial drugs is prescribed.
Throughout the illness, if necessary, cardiotonic drugs are prescribed: cordiamine and sulfocamphocaine.
As desensitizing therapy (to reduce sensitivity to toxins), diphenhydramine (0.5-1 ml subcutaneously or intramuscularly 1-2 times a day), pipolfen (1 tablet 1-2 times a day) are used.
For clouding of the cornea, use Sofradex, a 0.5% solution of atropine. FiBS is injected daily intramuscularly for 2 weeks at a dose of 1 ml. In addition, it is recommended to use the powder as prescribed: iodoform - 5 g, calomel (or powdered sugar) - 5 g, which is applied to the cornea of the eye or conjunctiva of the lower eyelid 3-4 times a day until visible improvement.
IMMUNITY AND SPECIFIC PREVENTION. Animals that have recovered from the disease, regardless of the severity of the infectious process suffered, gain lifelong immunity.
In order to create active immunity, the following is used:
Inactivated aluminum hydroxide formol vaccine against hepatitis of carnivores;
Associated vaccine against parvovirus enteritis, hepatitis and canine distemper.
Other vaccines are also used (see canine plague).
The main polyvalent vaccines used for the specific prevention of viral hepatitis are indicated in the topic “Carnivore Plague”.
PREVENTION AND CONTROL MEASURES. When a diagnosis is made, the fur farm (kennel) is declared unfavorable and restrictions are introduced according to which PROHIBITED export, import, regrouping, grading, weighing of animals.
Carry out general veterinary and sanitary measures.
Animals that are sick or suspected of being infected are immediately isolated and treated, and after the skins have matured, they are killed.
The vacated cages and houses are subjected to thorough mechanical cleaning and disinfection with a blowtorch fire. The soil is treated with a 10-20% solution of bleach.
All clinically healthy animals are immunized.
Females and young animals in whose litter there were cases of infectious hepatitis, as well as animals that had close contact with patients, are culled.
The corpses of dead animals are destroyed.
They carry out deratization and disinfection of work clothes at least twice a week.
Restrictions are lifted 30 days after the last case of recovery or death of an animal from infectious hepatitis with mandatory final disinfection.
RABIES(Rabies) is an acute viral disease of warm-blooded animals, characterized by damage to the central nervous system, which is expressed by attacks of excitement and the development of paralysis.
ETIOLOGY. The causative agent of the disease is RNA-genomic, bullet-shaped, large virus with a diameter of 75-80 nm. It belongs to the family Rhabdoviridae, genus Lysavirus. The atypical structure of the street and fixed virus is identical. Virus fixe, obtained by Pasteur as a result of 133 passages through the body of rabbits, has the following properties:
1. The incubation period is 4-7 days
2. Characterized by uniformity of symptoms when rabbits are infected
3. Does not cause the formation of Babes Negri bodies
4. Causes a silent paralytic form in dogs and guinea pigs
5. Has a high speed of movement along nerve fibers
In the saliva secreted by sick animals, the virus persists for up to 24 hours, in a rotting corpse - 2-3 weeks, in soil - 2-3 months. Boiling destroys the virus instantly; at 60 0 C, inactivation occurs in 5-10 minutes. The virus is not resistant to disinfectants: 1-5% formalin solutions inactivate it in 5 minutes, 5% phenol solution in 5-10 minutes.
EPISOOTOLOGICAL DATA. All types of domestic and wild animals, as well as humans, are susceptible to rabies. Young animals are more sensitive than adults.
There are two epizootic types of rabies:
Forest natural (sylvanic), maintained and distributed by wild animals;
Urban (urban), observed among stray dogs, cats and other domestic animals, which is now almost eliminated.
The leading one is forest rabies.
Currently, rabies is considered a natural focal disease of wild animals, periodically introduced into the sphere of domestic animals.
The source of the infectious agent is sick animals, as well as virus carriers that secrete the pathogen 2-10 days before the appearance of clinical signs of the disease and within 31 days after recovery.
The main reservoir of the virus is foxes.
Transmission of the rabies virus occurs mainly through saliva through bites (in salivary glands The virus is found in 54-90% of dogs killed by rabies). Since shedding of the virus in saliva begins 2-10 days before the onset of symptoms of the disease, dogs and cats that have bitten people must be isolated and kept under observation for 10 days. If the animal does not get sick during this time, it means there was no virus in its saliva at the time of the bite. The most dangerous are deep, extensive lacerations, face-
all parts of the head and areas of the body rich in nerve fibers.
Infection is also possible when saliva gets on mucous membranes and damaged skin surfaces.
A fairly strict cyclicity in the rise of the epizootic has been noted, which depends on the number of wild animals, the activity of their migration, the presence of mouse-like rodents and their number. The frequency of outbreaks is 2-3, in some cases 3-4 years.
The seasonality of the disease is related to the biology of wild carnivores.
PATHOGENESIS. Having penetrated the body, the virus lingers for some time at the site of introduction, and then moves centripetally along the nerve fibers to the synapses of the spinal cord at a speed of 2-4 mm per hour and further into the brain, where it reproduces, causing non-purulent encephalitis. After this, the centrifugal action of the pathogen begins in the salivary glands, where it multiplies in the nerve ganglia. In them it can appear 2-8 days before the development of clinical signs of the disease. The virus can also be found in the cornea of the eye. After damaging nerve cells, the virus enters
ducts of the salivary glands and onto the surface of the oral mucosa, infecting saliva. Can be transported to the mammary gland and excreted in milk. In addition, it infects the lungs, kidneys and skeletal muscles.
CLINICAL SIGNS AND COURSE. The incubation period can vary from several days to a year, but most often it is 3-6 weeks. Its duration is largely determined by the proximity of the bite to the head, the size and depth of the wound, the amount of virus ingested and the individual resistance of the body.
The course of the disease is acute, lasting 3-11 days.
According to the nature of the manifestation of the disease, two forms are distinguished - violent and quiet (paralytic). In addition, atypical and abortive and recurrent (remitting) forms of the disease are possible.
The most well studied rabies is in dogs, in which the incubation period lasts 14-60 days.
In violent form Three stages of the development of the disease are clearly defined: prodromal (melancholic), stage of excitement (manic) and stage of paralysis (depressive).
The prodromal stage lasts 1.5-2 days and is characterized by a change in the dog’s behavior, which is expressed in the following: it becomes less attentive to the owner, does not immediately respond to calls, and has difficulty getting up; often becomes unusually affectionate, begins to lick the hands and face of the person (owner); her gaze is dull, indifferent, absent, her eyes are dull; as the disease progresses, she tries to hide in a dark corner, gasps for air (catches flies); a perverted appetite appears (swallows stones, pieces of wood, paper, own feces, etc.); sometimes itching appears at the site of the bite, which is accompanied by fierce scratching; by the end of the second day there is a disorder in the act of swallowing; the dog does not touch the food, does not drink water, barks hoarsely, and profusely drools.
The stage of excitement lasts 3-4 days and is characterized by: pronounced attacks of violence; the desire to break free and run away from home; rushes at other animals, aggression increases sharply, she attacks other dogs without barking and bites them mercilessly. A sick dog experiences extreme thirst, but cannot drink, as a result of convulsive contraction of the swallowing muscles and severe pain; at the sight of water, the dog becomes enraged and becomes very agitated.
The paralytic stage lasts 2-4 days and is characterized by the development of paralysis of the muscles of the hind limbs, torso, and tail. It can be returned to the owner. Such an animal is severely emaciated, the fur is disheveled, the eyes are deeply sunken, the lower jaw is drooping, the tongue hangs out, saliva flows profusely from the mouth. The gait becomes unsteady, and then the animal cannot rise at all. Death occurs on the 6-8-11th day from the onset of the disease.
In silent form in dogs, in the complete absence of aggressiveness, paralysis of the muscles of the lower jaw, pharynx, and hind limbs quickly develops, severe salivation and difficulty swallowing are noted. The dog behaves calmly, does not react to stimuli or to the owner’s call. Difficulty breathing and excessive salivation give uninformed people the impression that the dog has choked on something. Attempts to help may cause infection.
This form is more often observed when infected from foxes and the main signs of the disease are, in addition to those mentioned above, dilated pupils, a “meaningless” look, an unsteady gait and a perverted appetite.
Abortive form proceeds with mild symptoms and ends with recovery.
Atypical form accompanied by gastroenteritis, late paralysis, and lack of aggression.
Return form characterized by the fact that after apparent recovery, clinical signs of rabies develop again. This alternation usually happens 2-3 times with an interval of several days, less often 2-3 weeks.
In fur animals rabies manifests itself in violent form. Clinical signs and course of the disease are similar to those described in dogs.
In cats Rabies usually occurs in violent form. At the onset of the disease, anxiety, perverted appetite, severe salivation, and difficulty swallowing are noted. Caged cats lunge furiously at the stimulus. The silent form is extremely rare among them.
In wild animals the most characteristic signs are loss of fear of people and aggressiveness. There is no hydrophobia. From the point of view of the risk of infection, the silent form of rabies is of particular importance.
PATHOLOGANATOMICAL CHANGES. When autopsying the corpses of the fallen
animals find the following:
1. Presence of bite wounds and scratching at the bite sites
2. Empty stomach or foreign objects in it
3. Venous hyperemia, hemorrhages and erosions in the gastric mucosa
4. Blood thickening (anhydremia), dry mucous membranes, subcutaneous tissue and skin
5. General venous congestion: cyanosis of visible mucous membranes, acute venous hyperemia of the liver, lungs, spleen, brain
6. Catarrhal gastroenteritis with hemorrhages on the mucous membrane of the stomach and intestines (not always)
7. Exhaustion
8. Histo: non-purulent lymphocytic encephalitis in the brain stem (quadrigeminal, pons, prognosis) rabies nodules in the brain stem Babes-Negri bodies in the nerve cells of the ammon's horns
DIAGNOSTICS. A preliminary diagnosis is made taking into account the epizootic situation and characteristic symptoms. The final diagnosis is made based on the results of laboratory tests.
To do this, a fresh corpse and the animal's head or brain are sent to the laboratory. In the laboratory, a virological study is carried out (light and fluorescence (RIF) microscopy), a biological test is performed (carried out if a negative result of two previous studies is obtained by intracerebral injection of a suspension of brain tissue treated with antibiotics) and a serological test is carried out (RIF in agar gel).
Babes-Negri bodies are formed in the final stage of the disease, and therefore they are detected only in 65-85% of cases. Therefore, their absence is not a basis for a negative conclusion and a biotest is mandatory.
DIFFERENTIAL DIAGNOSTICS. Rabies must be distinguished from Aujeszky's disease (scratching is detected, there is no aggressiveness and paralysis of the lower jaw, no Babes-Negri bodies), from the plague (conjunctivitis, no aggressiveness and paralysis of the lower jaw, the presence of pneumonia and enteritis).
TREATMENT. They don't. Sick animals are killed. The corpses are burned or disposed of.
IMMUNITY AND SPECIFIC PREVENTION. For active immunization of animals against rabies, the following vaccines are used:
1. Dry inactivated rabies vaccine prepared using the Pasteur strain accumulated in the BHK-21 cell culture and subjected to inactivation with betapropiolactone. It is intended for preventive and compulsory vaccinations. During forced immunization, animals are injected with the vaccine intramuscularly in the morning and evening, 2 ml, 3 days in a row and after 16 days another injection. Immunity is formed on the 10-15th day and lasts up to one year.
2. Dry inactivated ethanol vaccine against animal rabies. During primary immunization, the vaccine is administered twice with an interval between injections of 21 days, in doses: dogs large breeds subcutaneously or intramuscularly in a dose of 3 ml; puppies 3 months of age, cats and adult dogs of decorative breeds - 1 ml. Immunity is formed by the 14th day after the second administration and lasts for 1-1.5 years.
3. Dry culture concentrated inactivated rabies vaccine (CCIAV). It is prepared on the basis of the cultural strain KP-85, adapted in the cell culture of Japanese quail embryos and inactivated with diethylene. Administered once, subcutaneously, to cats and dogs from 3 months of age at a dose of 1 ml. Immunity is formed by the 14-16th day and lasts for 12 months.
4. Dry rabies vaccine (DRV).
5. Dry rabies virus vaccine for oral immunization of wild carnivores.
In addition to the above vaccines, a recombinant rabies vaccine based on the smallpox virus has been developed and tested under production conditions.
PREVENTION AND CONTROL MEASURES. Preventive measures against rabies include regulating the keeping of dogs and cats and regulating the number of wild predatory animals; preventive vaccination of dogs, cats, etc.; timely diagnosis of sick people; identification and elimination of foci of disease; explaining to the population the essence of the disease and the rules for keeping animals.
All dogs, regardless of their identity, and, if necessary, cats, are vaccinated against rabies with an anti-rabies vaccine.
To prevent rabies, citizens OBLIGED:
Comply with the established rules for keeping dogs, cats, fur-bearing animals and predatory animals;
Deliver their dogs and cats to a veterinary institution for examination and preventive vaccinations;
Do not allow dogs and cats that have not been vaccinated against rabies into fur farms, dog kennels, hunting, etc.;
Take measures to prevent attacks by wild animals on dogs and cats in personal use;
About each case of a dog being bitten by wild predators, dogs, cats or suspected rabies IMMEDIATELY report to a veterinarian, and securely isolate animals suspected of having a disease or bitten by stray dogs (cats) and wild predators.
Dogs, cats and other animals that have bitten people or animals IMMEDIATELY are delivered by the owner to the nearest veterinary institution for examination and quarantine under the supervision of a specialist for 10 days, which are carefully examined at least 3 times a day.
The sale, purchase and transportation of dogs is permitted only if there is a veterinary certificate indicating that the animal has been vaccinated against rabies no more than 12 months and no less than 30 days before export.
If a diagnosis is made, the locality or part of it is declared unfavorable and restrictions are introduced.
Obviously sick dogs and cats, as well as animals suspected of disease, are subject to destruction. Corpses are burned, skinned PROHIBITED.
Animals suspected of being infected with rabies are forced to be vaccinated and left in an isolation facility for 60 days after vaccination.
Fur-bearing animals suspected of being infected with rabies, but not showing clinical signs of the disease, are allowed to be killed, regardless of vaccination, using skins after they have been thoroughly disinfected.
Places where there were animals sick or suspected of having rabies, care items, special clothing and other equipment contaminated with saliva and secretions of animals with rabies are disinfected.
Restrictions are canceled after 2 months from the date of the last case of animal rabies and the implementation of the measures provided for in the plan.
AUJESKY'S DISEASE(Morbus Aujeszcy) is an acute disease characterized by damage to the central nervous system, respiratory system and severe itching (except for minks and sables).
ETIOLOGY. The disease is caused by a DNA virus from the Herpesviridae family. The size of mature virions is 180-190 nm, it can be detected in the blood, brain and spinal cord, lymph nodes and internal organs. Among laboratory animals, high sensitivity to the Aujeszky's disease virus has been established in rabbits, which are widely used for bioassays.
The virus retains biological activity in the corpses of rodents for up to 175 days, in winter indoors, in water and manure - for 60 days, in summer - up to 3 weeks. Biothermal disinfection of manure inactivates the virus within 8-15 days, at 100 ° C inactivation occurs in 2 minutes, a hot 3% solution of sodium hydroxide, 1% formaldehyde solution, 20% slurry of freshly slaked lime inactivates the virus in 5-20 minutes. The virus is resistant to creolin and phenol.
EPISOOTOLOGICAL DATA. Dogs of all ages, regardless of breed, are susceptible to Aujeszky's disease, and minks, sables, arctic foxes, foxes, cats and rodents are also affected. Young animals are most susceptible. In puppies 1-2 months of age, the mortality rate is 55-67%.
The source of the infectious agent is sick animals and virus carriers. Starting from the 6th day after infection, the virus is able to be released with conjunctival secretions, with discharge from the nose, mouth, as well as with urine, semen, milk and feces.
Factors of transmission of the pathogen include slaughterhouse waste and offal obtained from sick or recovered pigs, infected feed, equipment, bedding, and rodent corpses. The possibility of spread of the virus by hematophyte mites has been proven.
Rats and mice, which are the main natural reservoir of the virus, play a major role in the spread of the pathogen.
Infection of animals occurs through nutritional and aerogenic routes. Young puppies are infected with colostrum; in addition, the possibility of virus penetration through the placenta has been proven.
There is no strictly defined seasonality, but most often the disease is recorded in the autumn-winter period, which is associated with intensive migration of rodents. The disease is characterized by stationarity.
PATHOGENESIS. The virus, having entered the body, penetrates the bloodstream and, during the process of viremia, spreads throughout the body, accumulating in parenchymal organs, muscles and skin. During this period, swelling occurs and hemorrhages appear. Then the virus overcomes the blood-brain barrier and affects the central nervous system, localizing in the medulla oblongata, ammon's horns, causing paralysis. In most animal species (except pigs, sables and minks), severe itching appears, which is caused by an increased amount of histamine and acetylcholine in the skin.
CLINICAL SIGNS AND COURSE. The incubation period for dogs, minks, ferrets and sables lasts 1-6 days, for foxes, arctic foxes and raccoons - 6-12 days.
In dogs in the initial period of the disease, decreased appetite and severe itching throughout the skin are noted. They rub and bite their lips until they bleed, make playful movements, become restless, become timid, and sometimes have squints and unequal pupil widths. The itching and scratching do not stop until the animal dies; the dog can gnaw the skin and muscles to the bone.
The animal often experiences severe agitation, aggressiveness towards dogs (it does not show aggression towards people), perverted appetite, serous conjunctivitis, body temperature rises by 0.5-1 o C. At the end of the disease, as a result of paralysis of the pharynx and larynx, increased salivation and the dog stops barking. Death occurs within 2-3 days from the moment signs of the disease appear.
In foxes and arctic foxes salivation and vomiting, increased excitability, narrowness of the palpebral fissure and pupil are recorded. Sick animals use their paws to scratch the skin in the neck, lips, and cheeks. Attacks of scratching are repeated after 1-2 minutes. The animals become very restless, roll over from side to side, and when scratching, tear not only the skin, but also the muscles. Paresis and paralysis of the limbs subsequently develop. Animals die in a state of severe comatose depression 1-8 hours after the appearance of the first clinical signs.
In some cases, symptoms of damage to the respiratory tract are more pronounced: breathing becomes shallow, difficult, abdominal type. Sick animals groan and cough hoarsely. At the end of the disease, a foamy, bloody fluid is released from the nostrils and mouth. Scratching with this form of the disease is rare. Animal death occurs within 2-24 hours.
At the minks a comatose state, an oblique palpebral fissure, profuse salivation, and sometimes vomiting and diarrhea are recorded. Excitement may occur from time to time, with minks bumping into walls, falling, crawling, making circular movements and rubbing their faces with their paws, but there is no itching or scratching. Later paresis and paralysis of the hind limbs appear. Body temperature with pronounced clinical signs is within normal limits.
In cats Itching is rare. They are very excited, saliva flows from their mouths, and they experience paralysis of the pharynx.
PATHOLOGANATOMICAL CHANGES. When autopsying the corpses of dead animals, the following changes are found:
in dogs:
1. Scratching and baldness on the skin in the head, limbs and tail
2. Hyperemia and hemorrhagic infiltration of subcutaneous tissue in the lips and muzzle
3. Serous tracheitis and hemorrhages on the tracheal mucosa
4. Serous-catarrhal gastritis with hemorrhages on the gastric mucosa, sometimes with the presence of foreign objects in it
5. Serous-hemorrhagic lymphadenitis of nodes regional to the site of scratching
6. Congestive hyperemia and granular degeneration of the liver and kidneys and hemorrhages in them
7. Congestive hyperemia and pulmonary edema or catarrhal bronchopneumonia
8. Hemorrhages under the epicardium and on the endocardium
9. Foci of necrosis in the liver and spleen (in puppies)
10. Hydropericardium with accumulation of fluid mixed with fibrin in the cardiac membrane
11. Histo: non-purulent lymphocytic encephalitis, serous meningitis, degeneration and vacuolization of neurons
at the minks:
1. Cyanosis of visible mucous membranes
2. Acute catarrhal gastroenteritis with the presence of ulcers in the stomach
3. Slight enlargement of the spleen
4. Congestive hyperemia and dystrophy of the liver and kidneys with hemorrhages in the kidneys
5. Congestive hyperemia and pulmonary edema or serous-hemorrhagic pneumonia
6. Accumulation of pink foam around the mouth
in arctic foxes and black-brown foxes:
1. Serous swelling and tissue damage in the area of scratching
2. Serous-hemorrhagic lymphadenitis regional to the site of scratching of nodes
3. Congestive hyperemia of internal organs
4. Accumulation of pink foamy fluid around the nostrils and mouth
5. Poorly clotted, dark red blood
DIAGNOSTICS. The diagnosis is made on the basis of epizootic data, clinical signs, pathological changes and the results of a bioassay (on rabbits, guinea pigs, kittens, fur-bearing animals). To perform a bioassay, prepare a suspension in saline solution (1:5) from pieces of lung, brain, liver and spleen. It is administered, after pre-treatment with antibiotics, intramuscularly or subcutaneously in a dose of 1-2 ml. After 2-5 days, severe itching appears at the injection site, accompanied by scratching. Infected animals die 2-5, less often 12-24 hours after the appearance of clinical signs of the disease. If rabbits die without specified symptoms, then carry out the second passage using pathological material from rabbits. The death of rabbits without signs of itching and scratching indicates the circulation of the vaccine strain of the virus.
In addition, it is possible to isolate the virus in a chicken fibroblast cell culture with subsequent identification of the virus in the RN.
For retrospective diagnosis, RNGA, RIF, RID, RSK are used.
The diagnosis is considered established when the virus is detected and identified in the pathological material; when specific antibodies are detected in a titer of 1:8 or higher in the blood serum of sick animals in the RNGA or RN; with positive results of the bioassay.
DIFFERENTIAL DIAGNOSTICS. During the diagnostic process, it is necessary to exclude rabies, encephalomyelitis, plague (nervous form) and botulism (in minks).
TREATMENT. As specific agents in the early stages of the disease, globulin is used against Aujeszky's disease of farm animals and fur-bearing animals, as well as hyperimmune serum obtained by hyperimmunization of horses.
In addition, immunomodulators are used and symptomatic, pathogenetic and antibacterial therapy is carried out.
IMMUNITY AND SPECIFIC PREVENTION. In order to create active immunity, the following is used:
1. Inactivated vaccine against Aujeszky's disease of pigs, sheep and fur-bearing animals, which is administered once intramuscularly in a dose of 1 ml in disadvantaged and endangered farms.
2. Liquid cultural inactivated vaccine UNIEV against Aujeszky's disease of pigs, sheep and fur-bearing animals. Minks, foxes and arctic foxes are vaccinated twice from 60 days of age intramuscularly or subcutaneously with an interval of 7-8 days at a dose of 1 and 2 ml.
3. Inactivated concentrated emulsified vaccine against Aujeszky's disease (BAK vaccine). Minks, foxes and arctic foxes are vaccinated from the age of 60 days once intramuscularly at a dose of 0.5 ml.
PREVENTION AND CONTROL MEASURES. Prevention of the disease consists in preventing pork by-products from being fed to animals without heat treatment.
Considering that the main reservoir and source of spread of the virus are rodents, it is necessary to systematically destroy them, and in the event of a mass death of rodents, their corpses are sent to a veterinary laboratory.
Categorically PROHIBITED feeding uncooked meat and offal obtained from forcedly killed animals, as well as waste from slaughterhouses, canteens and kitchens.
When a diagnosis is made, the farm is declared unfavorable and quarantine is imposed, under the terms of which:
A thorough clinical examination is carried out, sick and suspected animals are isolated and treated;
Immediately exclude meat feed and offal from the diet;
Clinically healthy animals are vaccinated;
Thorough ongoing disinfection is carried out (in the isolation ward - daily, in other rooms - every 5 days);
Carry out deratization and catching of stray dogs and cats;
Manure and litter are removed daily for biothermal disinfection;
Skins from animals that were forced to be killed or died from disease are subjected to disinfection (disinfected for 40 hours at a temperature of 30-35 o C, and then for 10 days at a temperature of 18-20 o C;
Animal corpses are burned or disposed of;
Summer skins that are of no value are destroyed along with the corpses.
PROHIBITED:
Regrouping within the farm and indoors;
Export of skins without prior disinfection;
Weighing and grading of animals.
Quarantine from an unfavorable farm is lifted 15 days after the cessation of the disease, removal of sick animals, sanitary repairs of the premises and a full range of veterinary, sanitary and special measures.
ADENOVIROSIS IN DOGS(Adenovirosis cani) is an acute disease of young carnivores, characterized by fever, damage to the respiratory, digestive, conjunctival and lymphoid tissues.
ETIOLOGY. The causative agent of the disease is an RNA-containing virus from the Adenoviridae family, with a diameter of 70-90 nm.
Adenoviruses are not pathogenic for laboratory animals and chicken embryos. There is an antigenic relationship with the carnivore hepatitis virus. Under the influence of a 5% solution of phenol it is inactivated after 10 minutes, under the influence of a 1% solution of chloramine, and a 3% solution of hydrogen peroxide - after 15-30 minutes.
EPISOOTOLOGICAL DATA. The disease is common among carnivores of all breeds and ages, but young animals aged from 2 weeks to 4 months are most susceptible. Cats are especially sensitive.
The source of the infectious agent is sick animals, which release the pathogen into the external environment when coughing, sneezing, with nasal discharge and feces. Infection occurs by airborne droplets and alimentary routes and through the conjunctiva of the eyes, with direct contact. Depending on the method of penetration, the location of the pathogenetic process is determined.
Transmission factors include infected feed residues, water, bedding, air, care items, equipment, etc.
In adult animals, adenovirosis occurs latently, accompanied by prolonged virus carriage. In young animals, the disease manifests itself in sporadic enzootic outbreaks.
There have been cases of complications of adenovirosis by bacterial microflora.
There is no strict seasonality, but stationarity is characteristic.
Mortality among or in the form of young animals can be 10-15%.
PATHOGENESIS. Initially, the inflammatory process is localized in the upper respiratory tract and conjunctiva. The virus then enters the blood and lower parts of the lungs, causing pneumonia. Subsequently, when the process generalizes as a result of viremia, the virus penetrates the epithelium of the small intestines, causing their lysis during its reproduction.
CLINICAL SIGNS AND COURSE. The incubation period is 5-6 days. The disease usually begins with persistent and prolonged fever, increasing coughing and sneezing due to the localization of the primary process in the upper respiratory tract. Then serous discharge from the nose and eyes appears, signs of pharyngitis, bronchitis, conjunctivitis. Some animals develop swelling in the neck area, accompanied by small hemorrhages on the skin. In puppies, gastrointestinal disorder in the form of diarrhea mixed with blood is recorded. The duration of the disease is from 2-4 days to 2 weeks.
PATHOLOGANATOMICAL CHANGES. During autopsy of dead dogs, the following is recorded:
1. Serous conjunctivitis and rhinitis
2. Acute catarrhal pharyngitis and bronchitis
3. Focal catarrhal bronchopneumonia with predominant damage to the middle and caudal lobes
4. Fibrinous-purulent perihepatitis and tonsillitis
5. Serous-hyperplastic lymphadenitis of bronchial, submandibular and portal nodes
6. Catarrhal gastroenteritis (in puppies)
7. Histo: inclusion bodies in epithelial cells of the respiratory tract
DIAGNOSTICS. The diagnosis is established taking into account clinical and epidemiological data, autopsy results with mandatory laboratory tests. To do this, nasopharyngeal secretions, swabs with mucus from the nasal cavity and pharynx, and samples of blood serum and feces are sent to the laboratory. After death, the corpses of small animals are sent whole or in pieces nasal septum, trachea, lungs, a segment of the small intestine with contents and regional lymph nodes.
Laboratory studies include detection of adenoviral antigen in RIF and RSC, isolation of the virus in cell culture with subsequent identification in RID, RSC and RTNGA. If necessary, determine the type of isolated adenoviruses in RN and RTNGA. Serological diagnosis is based on the detection of antibody titers during the study of paired sera in the RNGA.
DIFFERENTIAL DIAGNOSTICS. Adenovirosis must be differentiated from infectious hepatitis, plague, parvovirus enteritis, chlamydia, streptococcosis, escherichiosis, pasteurellosis, infectious rhinotracheitis and parainfluenza, which is based on the results of laboratory tests.
TREATMENT. Therapeutic immunoglobulin and hyperimmune serum are used as specific agents. In addition, the use of drugs for pathogenetic, symptomatic and immunostimulating therapy is provided. The treatment is described in detail in previous topics.
IMMUNITY AND SPECIFIC PREVENTION. After recovery from the disease, natural active immunity is formed, which lasts for 3 years.
In order to create active immunity in animals, the following vaccines are used:
Vaccine against adenoviral infections and canine parvovirus enteritis
2. Vaccine "Tetravac" against canine distemper, infectious hepatitis, adenovirus and parvovirus enteritis.
3. Vaccines "Multican-4", "Multican-6", "Gexakanivac" and "Adenomun-7".
PREVENTION AND CONTROL MEASURES. The well-being of animal farms and nurseries is based on strict adherence to veterinary and sanitary rules for the acquisition, maintenance and operation of animals.
All imported replacement young stock must undergo serological control for the presence of specific antibodies in the blood serum. When seropositive animals are identified, they are treated with hyperimmune serum followed by immunization.
If sick animals are found, they are immediately isolated and treated. Clinically healthy people are vaccinated.
Manure is disinfected using the biothermal method. For disinfection, use a 2-3% hot solution of sodium hydroxide, a 2% solution of formaldehyde, a clarified solution of bleach containing 3% active chlorine, and a 20% suspension of freshly slaked lime.
A fur farm is considered safe if there are no sick animals, total immunization is carried out and final veterinary and sanitary measures are carried out.
ALEUT MINK DISEASE(PLASMOCYTOSIS) (Morbus aleutica lutreolarum, plasmazytose) is a contagious, slow-onset disease characterized by systemic proliferation of plasma cells in the liver, kidneys and other organs and tissues (plasmocytosis), as well as hemorrhages from the nasal and oral cavities, arthritis and progressive emaciation.
ETIOLOGY. The causative agent of the disease is a DNA virus belonging to the Parvoviridae family. It is simply organized, has the shape of an icosahedron, with a diameter of 20-25 nm, and is characterized by pantropy. Resistant to ether, freon, phenol, acids, alkalis, acetone.
EPISOOTOLOGICAL DATA. Under natural conditions, only minks get sick, regardless of gender and age. The virus can persist in the body of foxes, arctic foxes, sables, ferrets, dogs, cats without causing visible abnormalities.
The source of the infectious agent are sick minks and virus carriers, in whose bodies the virus is contained in all organs and tissues and is released into the external environment with saliva, feces and urine.
Transmission factors include infected care items, food, clothing, water, and unneutralized mink carcasses. Mechanical carriers are flies, blood-sucking insects and birds.
The pathogen can be transmitted both vertically and horizontally. Infection occurs through nutritional and airborne routes, with bites - through damaged mucous membranes and skin, as well as in utero and during mating.
The highest incidence and mortality of minks is observed in the period from May to June and in the fall (September) with the onset of cold weather.
The disease is characterized by pronounced stationarity. In a fresh outbreak, where a progressive form is observed, mortality can reach 70-80%, and in a stationary outbreak, an asymptomatic (inaparasite) infection is observed.
PATHOGENESIS. In the body of minks, parvovirus stimulates the B-lymphocyte system and their intensive proliferation, as a result of which plasma cells and lymphocytes infiltrate lymph nodes, bone marrow, spleen, liver, kidneys and other organs.
Plasmocytes begin to synthesize a large number of immunoglobulins, which, in the presence of complement, interact with the virus to form immune complexes (virus + immunoglobulin + complement), in which the virus retains its infectious activity. Fixing on the walls of arteries, capillaries of the glomeruli of the kidneys, on the surface of red blood cells, immune complexes cause the development of inflammatory processes (glomerulonephritis, hyperarthritis, hepatitis). During phagocytosis of immune complexes by macrophages, the virus is released and reactivated. Insufficiency of T-lymphocytes and deficiency of suppressor cells contributes to the development of severe anemia due to the breakdown of red blood cells.
CLINICAL SIGNS AND COURSE. The incubation period lasts from 3-4 weeks to 7-9 months. The course of the disease is acute, chronic and latent.
Acute course without characteristic symptoms of the disease is observed in minks with the Aleutian coloring genome and in sapphire minks at the age of 3-5 weeks, which did not receive specific antibodies from their mothers (that is, the females were healthy and were not carriers). Such puppies show signs of pneumonia and die within a few hours from asphyxia. Mortality is 50-80%.
Chronic course accompanied by diarrhea. In this case, the stool has a black, tarry color (associated with bleeding in the intestines). Animals feel thirsty, which is a sign of chronic kidney inflammation. Subsequently, minks experience bleeding from the nasal and oral cavities, the formation of small ulcers on the mucous membrane of the lips, mouth and hard palate, and bleeding gums. At the same time, the water in the drinking bowls becomes pink. As a result of constant blood loss, animals become anemic; visible mucous membranes and paw pads become pale pink, sometimes with a jaundiced tint.
In some minks, coordination of movements is impaired, paresis and paralysis of the limbs are noted. Death occurs from renal failure or as a result of the accumulation of opportunistic infections: salmonellosis, colibacillosis, pseudomonosis, etc.
Mortality reaches 20-30%.
With latent flow There is an annual decrease in the fertility of females, abortions, celibacy (emptiness) or loss of reproductive qualities (a characteristic sign of the Aleutian disease) appear.
PATHOLOGANATOMICAL CHANGES.
1. Exhaustion
2. Bleeding ulcers on the gums, hard and soft palate
3. Granular dystrophy of the kidneys, nephroso-nephritis, with the presence of gray-white lesions and hemorrhages in them
4. Kidney atrophy (in the form of mulberries)
5. Liver dystrophy, often with a nutmeg pattern
6. Enlargement of the spleen by 2-5 times with the presence of gray-white lesions in it
7. Histo: pronounced plasmacytosis in the liver, kidneys, spleen, lymph nodes and bone marrow
DIAGNOSTICS. Comprehensive: taking into account the epizootological situation, clinical signs, pathological autopsy data, histopathological examination of internal organs, with the obligatory conduct of a serological test of blood serum RIEOF (immunoelectro-osmophoresis reaction) and IAT (iodine agglutinating test), enzyme immunoassay(ELISA).
In autumn, an undiagnosable stage of the disease is recorded in 15-20% of infected minks, and in the post-weaning period (July-August) up to 65%.
The diagnosis is considered established: if plasmacytocyte proliferations are detected in the histological specimens characteristic of this disease in the kidneys, liver, spleen, and lymph nodes; an increase in the gammaglobulin fraction in blood serum from 15 to 50%; upon receipt of positive results in YAT tests, RIEOF and ELISA.
DIFFERENTIAL DIAGNOSTICS. Aleutian disease of minks must be distinguished from toxic liver dystrophy, which usually affects a significant part of the mink population, regardless of their color, accompanied by a large mortality of animals.
In toxic dystrophy, the spleen and lymph nodes are not enlarged, the kidneys are a uniform gray-yellow color, the liver is bright yellow or clayey in color.
Pseudomonas is characterized by a sudden appearance, high contagiousness, profuse bleeding from the nose and mouth and rapid death of the animal. An autopsy reveals hemorrhagic pneumonia and pulmonary edema.
TREATMENT. There are no specific treatments. Symptomatic treatment is carried out using antibiotics and sulfonamides. In addition, vitamin therapy is carried out (vitamin B 12 in combination with folic acid); glucose, protein hydrolysates, electrolyte solutions, and immunosuppressants are administered, which allow the minks to be preserved until the slaughter period.
Immunity does not develop in minks that have recovered from the disease. No effective means of active prevention have been developed.
PREVENTION AND CONTROL MEASURES. In prosperous farms, minks that have just died, were forcedly killed, and are suspected of being infected, as well as those intended for breeding sale, are examined (October). In addition, in such farms, every year in May-June, blood samples of females without offspring (suspected of the disease) are examined at RIEOF.
Once a diagnosis is made, the animal farm is declared unfavorable and restrictions are introduced.
In order to identify sero-positive minks, blood samples of all breeding minks are examined 3 times a year: in the fall (September and October), when the main herd is completed; in winter (January-February) and in the spring-summer period (March-April) after the rut and in May-June - before weaning the puppies. In the fall, seropositive minks are isolated and killed after the hair has matured. In January-February, those who react positively are killed. Seropositive minks identified in the third round are isolated (lactating minks are kept together with their offspring until the hair coat matures, ensuring the prevention of further spread of the pathogen outside the epizootic focus.
In May-June (after whelping), females that were empty (with empty nesters) and unsuccessfully whelped, as well as puppies that had a large loss of life, are examined; Males that did not participate in the rut are also subject to study.
In December, a random study of blood samples from minks of those teams in which in the fall the level of positive reactions was higher than the average for the farm is carried out. If seropositive minks are detected, an extraordinary test is ordered in the shed where the reacting animals were located. Seropositive animals are isolated and killed after hair maturation.
Current disinfection is carried out with a 4% hot formaldehyde solution or a 2% glutaraldehyde solution. Working clothes and care items are sanitized in a steam-formalin chamber or in an autoclave at least once a week and after work associated with mass mink catching.
The farm is considered safe and restrictions are lifted after receiving a three-fold negative result from routine blood serum tests of the main and replacement mink stock according to the Russian Institute of Economics and Physics.
SELF-GREATNING- a chronic disease characterized by periodic agitation, gnawing on various areas of the skin, muscles, ligaments, bones and tail.
ETIOLOGY. Currently, the viral etiology of the disease has been proven, but the biological, morphological and cultural properties of the virus have not been fully studied.
EPISOOTOLOGICAL DATA. Under natural conditions, self-gnawing is observed in foxes, arctic foxes, minks, and sables. Young animals aged 30-45 days are most susceptible to the disease. In adult animals, the disease is recorded less frequently.
The source of the infectious agent is sick females. Puppies born from such females are retarded in growth and development and subsequently show a pronounced clinical picture of self-gnawing.
The disease is registered at any time of the year, but more often in spring and especially in autumn. Contagiousness is weakly expressed. The routes of natural infection are not clear.
The PATHOGENESIS of the disease has not been studied.
CLINICAL SIGNS AND COURSE. The incubation period ranges from 20-45 days or more. The disease is characterized by a sudden, acute and chronic course.
In acute cases the sick animal begins to circle in one place, emitting a characteristic squeak, and grabs the tip of the tail with its teeth without violating the integrity of the tissues. After some time, these phenomena disappear and then repeat again. Sometimes sick animals bite the hair from the tip of their tail and expose it.
Animals are often markedly agitated; they make circular movements, gnaw at various parts of their body, begin to gnaw at the tail from the tip, then gnaw at the paws and abdominal wall. If the disease progresses, the animal bites off the tissue around the root of the tail, exposing the rectum and opening the abdominal cavity, which leads to the development of peritonitis, sepsis and, ultimately, death.
In case of chronic course attacks of self-gnawing are repeated at various intervals (5-30 days or more). During the period between attacks, no deviations from the norm are observed.
PATHOLOGANATOMICAL CHANGES. Gnawing sites are found on the corpse. Upon opening they find:
1. Injuries (gnawing) in the tail area
2. Dystrophy of the liver and kidneys
3. Hyperplasia of the spleen
DIAGNOSTICS. The diagnosis is made based on the characteristic clinical signs of the disease.
TREATMENT. No specific treatment has been developed. Local treatment of wounds is used by lubricating them with a paste consisting of 10 parts streptocide and 1 part novocaine with the addition of water.
It is recommended that sick animals be administered intramuscularly with a 5% solution of calcium chloride and a 10% solution of calcium gluconate in a dose of 1.5-2 ml, as well as B vitamins; subcutaneously 0.1% solution of potassium permanganate in a dose of 1.5-2 ml for 3 days in a row; 1-2% solution of novocaine intramuscularly in a dose of 0.5 ml for 3 days in a row.
Sick animals can recover on their own if they are kept on the ground, in a pen.
PREVENTION AND CONTROL MEASURES. All sick animals are isolated and treated, and in the fall they are killed for their fur. If one or more puppies in a litter are sick, the entire litter is discarded.
Cages, houses, and equipment are thoroughly disinfected.
In order to prevent disease, animals must be provided with a balanced and nutritious diet.
MINK ENCEPHALOPATHY. (Transmissible encephalopathy mink) (Encephalopathy lutreolarum) is a slow-onset disease characterized by a long incubation period, progressive dysfunction of the central nervous system and dystrophic changes in the brain.
ETIOLOGY. The causative agent of mink encephalopathy has not been isolated. However, it has been found that its physical and chemical properties are similar to the pathogen of sheep scrapie. Its dimensions are less than 50 nm.
Resistant to ultraviolet rays and boiling for 15 minutes. The infectious activity of the pathogen persists for 20 months of storage in a 10% formaldehyde solution.
Morbidity ranges from 10-30% to 90-100%, mortality 100%.
EPISOOTOLOGICAL DATA. Under natural conditions, only minks get sick. Adult animals aged one year and older are affected.
The routes of transmission of the pathogen have not been precisely established, but it is believed that when sick and healthy animals are kept together, it is either not transmitted or is transmitted extremely rarely.
Cannibalism contributes to the spread of the disease.
The occurrence of epizootics is observed after feeding minks meat contaminated with the scrapie pathogen from sheep.
Hamsters, ferrets, striped skunks, raccoons, squirrels and monkeys are susceptible to experimental infection.
PATHOGENESIS. Not studied enough. The pathogen accumulates mainly in the tissues of the lymphoid and central nervous systems, which leads to the absence of classical cellular and humoral immunity to the introduction of the infectious agent.
CLINICAL SIGNS AND COURSE. The duration of the incubation period under natural conditions is 8-12 months. For experimental infection - 5-6 months.
The disease develops slowly and imperceptibly and ends in death. At the onset of the disease, subtle deviations from normal behavior animals: sometimes the instinct to maintain cleanliness disappears, the nest remains dirty, the food in the feeder is trampled. Minks have some difficulty swallowing. Often the animals become more excitable and run around the cage aimlessly. Females neglect to care for their puppies and this sign is often detected earlier than others. The tail, as a rule, is located over the back; there are animals with severely mutilated tails. Symptoms of impaired motor coordination soon develop,
the gait becomes stiff, and the gait is uncertain, shaky, jerky, sharp movements of the hind limbs are observed, sometimes convulsions, animals bite their tail, moving in a circle. Then the movement disorders progress, and soon the animal completely loses the ability to move. In the final stage of the disease, animals sit in the corner of the cage, clinging to the mesh wire with their teeth, and can remain in this position for a long time. During this period they are on the floor sleepy state, but can easily be awakened. Mild tremor is often observed. Vision, hearing, and tactile sensitivity are usually not impaired, and the non-alpha reflex is preserved. The disease lasts 3-6 weeks and ends in death. Males, as a rule, die before females. Various unfavorable conditions accelerate the death of animals.
An asymptomatic course of the disease is possible, in which periodic refusals of food and progressive emaciation are noted.
PATHOLOGANATOMICAL CHANGES. When autopsying the corpses of dead animals, the following is observed:
1. Exicosis and exhaustion
2. Shrinkage of the spleen
Anemia and cerebral edema
4. Histo: in the brain, vacuoles and astrocytosis in neuroglia, vacuolization of neurons in the gray matter of the cerebral cortex is especially characteristic
DIAGNOSTICS. The diagnosis of encephalopathy is established on the basis of clinical signs, epidemiological data, and the results of histological examination of the brain.
For histological examination, pieces of ammon's horns and cerebral cortex in the area of the lateral ventricle are selected. The material is fixed in a 10% solution of neutral formalin.
DIFFERENTIAL DIAGNOSTICS. When making a diagnosis, mink encephalopathy must be differentiated from self-gnawing, which affects puppies from 30-45 days of age and adult animals, while encephalopathy manifests itself only in adult animals. When self-gnawing, minks often also exhibit injuries that are absent in encephalopathy.
TREATMENT. Not developed.
IMMUNITY AND SPECIFIC PREVENTION. Sick minks do not develop an immune response. Specific prevention measures have not been developed.
PREVENTION AND CONTROL MEASURES. The main preventive measure is
This includes veterinary and sanitary control of meat fed to minks, as well as strict control over the supply of minks from unconditionally safe farms.
If encephalopathy is suspected, a clinical examination of animals is carried out daily; patients and those suspected of the disease are transferred to an isolation ward until the slaughter period. After their release, the cells are treated with a 5% solution of sulfur-carbolic mixture or with a blowtorch fire.
The corpses of dead animals, as well as carcasses and skins of no value, are burned or dumped in the Beccari pit.
Manure is disinfected biothermally.
ENCEPHALOMYELITIS OF FUR ANIMALS(Encephalomyelitis bestiarum natarum) is an acute viral disease of fur-bearing animals, characterized by damage to the central nervous system.
ETIOLOGY. The causative agent of the disease is a DNA virus of the Adenoviridae family, has the shape of an icosahedron, 55-96 nm in size.
The virus persists in secretions from sick animals for up to several months, and in the organs of sick animals for up to 4-6 months. At a temperature of 60 o C it collapses in 3-5 minutes, at 100 o C - instantly. Formalin, alkalis, Lysol, phenol, used in normal concentrations, inactivate the virus after 30 minutes. The virus is resistant to antibiotics.
EPISOOTOLOGICAL DATA. Under natural conditions, silver-black foxes, arctic foxes and sables are susceptible to encephalomyelitis, mainly at the age of 8-10 months.
The absence of B vitamins in the diet sharply reduces the animals’ resistance to infection.
The source of the infectious agent is sick animals, as well as virus-carrying females, which can secrete the virus for a number of years. In sick animals, the virus persists for a long time in the epithelium of the upper respiratory tract and is released through nasal discharge.
The disease is transmitted through contact, as well as during mating of animals, through infected equipment, feed, and service personnel.
Typically, the infection begins in various areas of the farm in June, spreads slowly and reaches a maximum after about 3 weeks and lasts until December, i.e. until the animals are slaughtered.
Having appeared on the farm, encephalomyelitis usually becomes a stationary disease.
There is no seasonality.
Mortality among dogs ranges from 10-20% to 36% or more.
PATHOGENESIS. During experimental infection, the virus is detected in the central nervous system on the 4th day, and clinical signs of the disease appear on the 5th day. During this period, it is contained in the liver, spleen, lymph nodes, blood and epithelium of the upper respiratory tract. The virus causes dystrophic changes in the central nervous system, which causes the symptom complex of the disease.
CLINICAL SIGNS AND COURSE. The incubation period for natural infection ranges from 4 days to 3 months; for experimental infection it lasts up to 30 days.
Clinical signs of the disease are varied.
Lightning course of the disease characterized by a sudden onset of convulsions (often epileptic) and the death of animals.
In acute cases duration of illness is up to 3 days. The main clinical symptoms include nervous disorders. They may manifest themselves inappropriately, without warning signs, or develop in a known sequence before the onset of epileptic seizures (convulsions). Sometimes the disease begins with some loss of appetite and gastrointestinal upset in the form of diarrhea.
The disease may also manifest itself as drowsiness, decreased mobility, and then progresses rapidly. The animal stands with its head bowed and eyes half-closed, sometimes resting its head on the ground. As the disease progresses, it lies in a sleepy state for a long time (sublethargy). The saliva on the lips forms foam. This state turns into lethargy and ends with the death of the animal.
In other cases, the animal suddenly begins to stagger, increased excitability is noted, and when the skin is touched with a stick, the animal shudders and angrily gnaws at it. Individual muscle groups contract convulsively, the pupils dilate, the animal falls, has convulsive convulsions (epileptic seizure) with the release of foamy saliva. During a seizure, the pulse increases sharply and breathing is difficult. Seizures can be repeated at various intervals, several times a day, lasting 3-5 minutes, after which the phenomena of excitation are replaced by general depression. An unsteady gait is noted, the animal moves slowly, bumps into various objects. Body temperature is within normal limits or slightly increases. Sometimes there is a pronounced itching of the skin, similar to that of Aujeszky's disease. The animal first lightly scratches the itchy area, and then can chew on its abdominal wall, tail and other parts of the body. Sometimes keratitis appears with the formation of a cataract. Diarrhea and circular (manege) movements lasting for hours are often observed. Paresis and then paralysis of the limbs may develop.
Acute course with damage to the central nervous system usually ends in the death of animals and predominates at the beginning of the disease outbreak. Respiratory tract involvement is rare. At the end of the outbreak, the disease progresses subacutely and chronically. In this case, appetite is disturbed, gastrointestinal distress is observed, weight loss progresses, and conjunctivitis is sometimes observed. The course of the disease in these cases lasts 15-30 days and up to several months. At the same time, abortions and unsuccessful whelping are observed in females. In these cases, the young die in the first days of life.
A significant portion of recovered animals remain virus carriers for a long time. The disease in them takes on a hidden latent form with periodic relapses.
PATHOLOGANATOMICAL CHANGES. When autopsying the corpses of livestock animals, the following is found:
At the minks:
1. Hemorrhagic diathesis
2. Congestive liver hyperemia
3. The spleen is not changed
4. Edema and hyperemia of the brain
5. Hemorrhages in the medulla oblongata and spinal cord
6. Catarrhal gastroenteritis
In arctic foxes and foxes:
1. Hemorrhagic diathesis
2. Swelling of the thymus and hemorrhages in it
3. Severe hyperemia of the meninges
4. Catarrhal, erosive and ulcerative gastritis
5. Congestive liver hyperemia
Histological examination reveals three types of changes in the central nervous system: necrobiotic (micronecrosis, demyelination), vascular-inflammatory (perivasculitis) and proliferative (focal proliferation of mesoglia, histiocytosis of macroglia).
DIAGNOSTICS. When making a diagnosis, epidemiological data, clinical signs, and pathological changes are taken into account. A background investigation is carried out to exclude bacterial infections.
They perform a bioassay by infecting foxes and young dog puppies (4-8 weeks of age) with brain emulsion.
For diagnosis, recently they began to use the precipitation reaction in agar gel and the method of fluorescent antibodies, which make it possible to make a diagnosis within 1-3 days.
DIFFERENTIAL DIAGNOSTICS. It is necessary to exclude plague, leptospirosis, toxoplasmosis, rabies, Aujeszky's disease and poisoning.
TREATMENT. Not developed. In the subacute course of the disease, hyperimmune serum is used in a dose of 10-15 ml per head.
IMMUNITY AND SPECIFIC PREVENTION. Animals that have recovered from the disease acquire strong immunity.
For active immunization, I.A. Buzinov’s tissue formol vaccine was tested, which protects 70-80% of immunized animals from the disease.
PREVENTION AND CONTROL MEASURES. If a disease occurs, the farm is declared unfavorable and restrictions are imposed on it.
The herd is being rehabilitated from virus-carrying animals. From the breeding herd, females whose puppies died or had cases of illness along with young animals, as well as females who aborted and became bachelors, are culled.
Sick and suspected animals are isolated.
Cages and houses are disinfected with a blowtorch fire, a 10-15% solution of freshly slaked lime, and a 2% solution of caustic soda. The soil under the cells is covered with bleach.
Manure is disinfected biothermally.
The farm is declared free from encephalomyelitis in the absence of new cases of animal disease, removal of virus-carrying animals, and completion of final veterinary and sanitary measures.
VIRAL HEMORRHAGIC DISEASE OF RABBITS (VHD)(“necrotizing hepatitis”, “hemorrhagic pneumonia” of rabbits) is an acute, highly contagious disease characterized by hemorrhagic diathesis in all organs, especially in the lungs and liver.
ETIOLOGY. The causative agent of the disease is an RNA virus of the Caliciviridae family. The virion size is 28-33 nm, icosahedral in shape, highly virulent. The virus is capable of causing the formation in the animal’s body of virus-neutralizing, complement-binding, antihemagglutinating and other antibodies, which can be detected 4-5 days after vaccination of rabbits. The virus is resistant to ether, chloroform, and is inactivated by a 0.1% formaldehyde solution within 24 hours.
EPISOOTOLOGICAL DATA. Only rabbits are sensitive to the pathogen, regardless of breed and sex, among which the most sensitive are adults weighing 3.0-3.5 kg. In dysfunctional farms, young rabbits up to 1.5 months of age are usually resistant to the disease, but when they reach an age over 2 months, they can get sick and die.
The source of the infectious agent is sick and recovered rabbits, as well as those in the incubation period and the convalescence stage. The virus is released into the external environment through discharge from the nose and mouth.
Infection occurs mainly through the respiratory route when sick and healthy animals are kept together.
Contributing factors for the spread of the pathogen are:
Import of infected animals that are in the incubation period, the stage of convalescence or virus carriage;
Contact of healthy rabbits with infected animals at exhibitions, fairs, markets, during mating;
Use without disinfection of infected vehicles for transporting rabbits, raw materials or feed;
Concentrated feeds infected at procurement points with an infectious agent when receiving infected rabbit skins;
Plant feed contaminated by sick rabbits;
Enterprises for processing rabbit skins, fur farms, slaughterhouses that do not disinfect production waste;
Enterprises for the production of meat and bone meal, production of feed from food waste, secondary raw materials.
There is no pronounced seasonality in this disease; it is characterized by stationarity.
The incidence reaches 70-80% with 90-100% mortality.
PATHOGENESIS. Not studied enough.
CLINICAL SIGNS AND COURSE. In rabbits, the incubation period lasts 48-72 hours, sometimes up to 120 hours, and the disease hardly manifests itself clinically.
In case of hyperacute flow Usually, apparently healthy rabbits make several convulsive movements of their limbs and die. Body temperature is within normal limits, appetite is preserved.
In acute cases illness, 2-4 days after infection, rabbits show signs of depression, nervous system disorders, agitation, throwing their heads back, respiratory distress, animals moan and squeak. Shortly before death, yellow-red discharge appears from the nasal openings. The duration of the disease is 1-2 days.
PATHOLOGANATOMICAL CHANGES. When autopsying the corpses of the fallen
animals show the following changes:
1. Hemorrhagic diathesis
2. Acute catarrhal rhinitis, laryngitis, tracheitis with foamy bloody fluid in the lumen of the trachea, larynx
3. Catarrhal-hemorrhagic pneumonia and hemorrhages in the lungs
4. Enlarged spleen (it is dark cherry in color with a characteristic purple tint)
5. Serous-hemorrhagic lymphadenitis
Congestive hyperemia, granular and fatty degeneration of the liver
7. Congestive hyperemia, granular dystrophy of the kidneys and hemorrhages in them
8. Catarrhal-hemorrhagic gastroenteritis with hemorrhages on the serous membranes
DIAGNOSTICS. The diagnosis of VGB is made on the basis of clinical and epidemiological data, pathological changes and laboratory test results, for which the affected internal organs are sent to the laboratory.
A positive diagnosis for VGBV is made on the basis of serological reactions of RGA, RDSC, RZGA and ELISA.
DIFFERENTIAL DIAGNOSTICS. VGBK must be differentiated from pasteurellosis, salmonellosis, colibacillosis, myxomatosis, eimeriosis, poisoning, etc.
TREATMENT. During the period of development of the first clinical signs of the disease, a specific anti-VGBV serum is used, which is administered once, subcutaneously in a volume of 0.5 ml.
IMMUNITY AND SPECIFIC PREVENTION. It has been established that passive immunity in rabbits up to 30 days of age, obtained from immunized rabbits, provides them with 100% protection, and at 50-60 days of age, immunity to the disease is 70-80%.
After the animal recovers from the disease, lifelong immunity remains.
To create active immunity, use:
1. Inactivated tissue aluminum hydroxide formol vaccine, which is administered to 45-day-old rabbits intramuscularly or subcutaneously in a volume of 0.5 ml. Immunity occurs on the 3rd day and lasts for at least 12 months.
2. Dry associated vaccine against myxomatosis and VGBV.
3. Inactivated associated vaccine against pasteurellosis VGBV.
PREVENTION AND CONTROL MEASURES. In order to prevent VGBV, it is necessary to strictly observe veterinary and sanitary rules for the acceptance, transportation and processing of rabbits and rabbit raw materials; carry out routine preventive vaccinations in a timely manner; joint storage of rabbit skins and feed is not allowed; are subject to mandatory cleaning and disinfection vehicles after transporting rabbits and rabbit raw materials.
When diagnosing VGBK the farm (economy) is declared unfavorable and restrictions are established on which PROHIBITED:
Import and export of rabbits, products of their slaughter, skins, fluff;
Regrouping of the rabbits;
Organization of exhibitions, fairs and other events related to the accumulation of rabbits;
Trade in rabbits, products of their slaughter, skins;
Exchange of animals between rabbit breeders;
Operation of breeding stations for rabbits;
Feeding rabbits without disinfection of waste from markets, public catering facilities, and pioneer camps;
Conducting meetings and meetings of rabbit breeders.
At a disadvantaged point they carry out:
Accurate accounting of the entire rabbit population;
Thorough clinical examination of the entire livestock to identify sick animals;
Slaughter of sick and suspected animals using a bloodless method;
Disposal of corpses;
Thorough mechanical cleaning and disinfection of premises where the above animals were kept;
Forced immunization of the remaining conditionally healthy livestock;
Rabbit skins collected at a disadvantaged point are sent to a processing plant for disinfection, bypassing bases and warehouses.
In the absence of a vaccine, the chief veterinarian of the district makes a proposal to the executive committee to slaughter all rabbits in the disadvantaged area. Sick and young rabbits under 2 months of age are killed using a bloodless method and disposed of along with the skin.
Adult rabbits are killed for meat directly at the disadvantaged point, preventing the spread of the disease.
Carcasses of rabbits killed for meat are boiled, heads, paws, internal organs and blood are destroyed by burning or buried to a depth of 1.5-2 m with preliminary treatment with disinfectants.
Manure, bedding, leftover feed, and low-value equipment are burned or treated with a disinfectant solution and buried to a depth of 1.5-2 m.
When carrying out routine disinfection, a 5% solution of chloramine, a 2% solution of formaldehyde, a clarified solution of bleach containing 5% active chlorine, and a 1% solution of glutaraldehyde are used. Disinfectant solutions are used 2-3 times with an exposure of at least 3 hours.
Restrictions are lifted 15 days after the last case of disease or destruction of sick rabbits, vaccination and final veterinary and sanitary measures.
The import of rabbits into a former disadvantaged area and a threatened zone is allowed after restrictions are lifted, but not earlier than 15 days after vaccination with an inactivated tissue vaccine.
RABBIT MYXOMATOSIS(Myxomatosis cuniculorum) is an acute, highly contagious disease of rabbits, characterized by inflammation of the mucous membranes, edematous and gelatinous infiltration of the subcutaneous tissue in the head, external genitalia, anus and other parts of the body, as well as high mortality.
ETIOLOGY. The causative agent of the disease is a DNA virus of the Poxviridae family. Its morphological properties do not differ from the vaccinia virus. The virus has a brick-shaped shape, size 390x260 nm, and includes five antigens.
In immunological and antigenic terms, it is related to the causative agent of fibromatosis in rabbits, due to which rabbits that have recovered from fibromatosis acquire immunity to myxomatosis.
The virus grows well on tissue cultures of rabbits, white rats, guinea pigs, hamsters, humans, and on the chorioallantoic membrane of chicken embryos (pockmarks are formed).
The virus is sensitive to ether, formalin and alkalis. Warming up at a temperature of 55 o C kills it in 25 minutes. At 8-10 o C the virus persists for 3 months, in corpses - 7 days, in the ground in winter - up to 10 weeks, in skins dried at 15-20 o C - up to 10 months. When frozen, it lasts for more than two years.
EPISOOTOLOGICAL DATA. The most susceptible to the disease are domestic and wild rabbits, regardless of breed, sex and age, in which the disease manifests itself in the form of a generalized infection.
The source of the infectious agent in individual farms, rabbit farms and laboratories are sick and recovered rabbits that secrete the virus with discharge from the nose and eyes.
In patients, the virus is found in the blood, skin, subcutaneous edema and parenchymal organs.
The main reservoir of the pathogen in nature is wild rabbits, as well as hares. Myxomatosis virus spreads among them through mechanical transmission by arthropods, causing benign localized fibroma. In the same way, it can be transmitted to domestic rabbits, but they have a generalized form with high mortality.
Mechanical carriers of the virus over long distances (up to 500-1000 km within 1-2 weeks) can be people associated with the trade in animals and skins, vehicles, predatory mammals, and birds.
Epizootics of myxomatosis occur at any time of the year, but the disease is most severe in damp and cool summers. Under such conditions, the virus can remain viable for a long time.
Recovered rabbits remain carriers of a latent virus for a long time, which can be reactivated by various forms of stress and cause new outbreaks of the disease.
PATHOGENESIS. With skin infection, the virus enters the regional lymph node through the lymphatic vessels after about 48 hours, and after 72 hours into the bloodstream and then localizes in the liver and spleen. After intensive reproduction, secondary viremia develops in the liver parenchyma and spleen, as a result of which lesions appear in the skin and mucous membranes. The virus is detected: in the skin and testes on the 4th day, in the conjunctiva and in the area of the external genitalia - after 5 days. With a complicated course of the disease, acute catarrh of the respiratory system occurs.
CLINICAL SIGNS AND COURSE. The incubation period lasts 2-28 days. The course of the disease is acute, the incidence is 95-100%. Myxomatosis can occur in two forms: classical, characterized by the appearance of gelatinous edema on the body, and nodular (nodular), in which limited tumors appear.
Classic shape has a malignant course, as a rule, with 100% mortality, and nodular is accompanied by a more benign course, although the mortality rate is also high (70-90%).
The first signs of myxomatosis are characterized by hyperemia of the skin in the form of spots or the appearance of tubercles in the eyelid area and on the ears. In sick animals, acute serous-purulent conjunctivitis and swelling of the eyelids occur; first mucous and then purulent discharges are released from both eyes, causing the eyelids to stick together (bilateral blepharoconjunctivitis develops). In the area of the head, anus, genitals, back and other parts of the body, swelling of the skin and underlying tissues measuring 3-4 cm, as well as nodules on the skin, appear. Orchitis is observed in males. The front of the head, especially in the area of the eyes and ears, swells, the skin in these places gathers into roller-like folds, as a result of which the rabbit's head resembles the head of a lion ("lion-like appearance"). By the 9-11th day of illness, the process reaches its maximum development. Rhinitis, pneumonia occur, animals sniffle, shortness of breath and cyanosis of the mucous membranes appear. Multiple tumors (the size of a bean or larger) appear on the head and chest, limbs, and on the sides of the body, which, merging with each other, give the rabbit an ugly shape. On the 10-14th day of illness, foci of necrosis form at the site of nodular growths, which, upon recovery, gradually heal within 3-4 weeks.
Patients initially retain their appetite, but as the disease progresses, depression, refusal to feed, and drowsiness appear. Body temperature rises to 41.5 o C, and later becomes normal. Breathing and swallowing are difficult. With the nodular form, the temperature is often within the physiological norm.
Typically, in adult animals the disease lasts 10-14 days, and in young animals up to one week. If the disease appears for the first time, only a few individuals recover.
With a protracted course of the disease, myxomatosis in rabbits manifests itself mainly in a nodular form. At the same time, only isolated myxoma nodes are found on the skin of patients, which subsequently shrink and gradually resolve.
PATHOLOGANATOMICAL CHANGES. During autopsy of rabbits that died from myxomatosis, the following is found:
1. Focal tumor-like formations and gelatinous infiltrates in the subcutaneous tissue of the trunk, neck, head, limbs and genital area
2. Serous-hemorrhagic splenitis and lymphadenitis
3. Edema and focal catarrhal bronchopneumonia
4. Purulent blepharoconjunctivitis
5. Cyanosis of visible mucous membranes
DIAGNOSTICS. The diagnosis is made on the basis of characteristic clinical signs, pathological changes, epidemiological data and laboratory test results. Pieces of parenchymal organs or the entire corpse and affected areas of skin are sent to the veterinary laboratory in a 10-15% formaldehyde solution (for histological examination) and in a thermos with ice. At the same time, measures are taken to prevent the spread of the infectious agent.
Histological examination of nodules and edematous areas reveals tissue hyperemia, hemorrhages, dilation of lymphatic vessels, an increase in the number of fibroblasts, the formation of myxoma (mucosal) cells, and cytoplasmic acidophilic inclusions. Adipose tissue is not detected in areas of proliferation of healthy cells. The vascular endothelium is exfoliated, as a result of which their permeability is increased. Muscles are in a state of atrophy, myolysis, intermuscular tissue is infiltrated with cellular elements. In the myocardium, lungs and testes, specific infiltrates consisting of myxoma (mucosal) cells are often visible.
If the histological examination results are negative and there are no characteristic clinical signs of the disease, a biological test is performed. In this case, healthy rabbits infected with pathological material die on the 3-6th day with characteristic clinical signs of myxomatosis.
Recently, serological research methods have also been used - immunofluorescence, RSC, RDP, RN and ELISA.
DIFFERENTIAL DIAGNOSTICS. This disease must be differentiated from staphylococcosis (“wandering pyaemia”) and smallpox.
Abscesses in staphylococcosis as opposed to myxomatous lesions
TREATMENT. Not developed.
IMMUNITY AND SPECIFIC PREVENTION. Rabbits that have recovered from the disease acquire long-term immunity. Rabbits born from females who have recovered from the disease develop colostral immunity lasting up to five weeks.
For active immunization, a dry live culture vaccine from the B-82 strain is used against myxomatosis. It is recommended for preventive immunization of clinically healthy rabbits in farms and settlements that are free, threatened, and unaffected by myxomatosis.
In safe and threatened farms, adult rabbits are immunized once. Immunity occurs in 9-1 days and lasts 9 months. Young animals are vaccinated from 1.5 months of age and revaccinated after 3 months.
In disadvantaged farms and settlements, clinically healthy rabbits and baby rabbits are vaccinated from the age of 28 days, and after 3 months the young animals are revaccinated. Rabbits are vaccinated at any time during pregnancy.
Vaccinated animals during the incubation period may develop cases of clinical disease. Such animals are killed and burned with their skins.
It is strictly prohibited to vaccinate clinically sick rabbits; emaciated animals and rabbits with elevated body temperature are also not vaccinated. Vaccinations are recommended in the spring before the appearance of the main carriers of the disease - mosquitoes.
The vaccine is administered intradermally using a two-needle injector, which is immersed in the diluted vaccine, and then the rabbit's ear is pierced with it. inside at the level of the upper third in the area of the hairless area; can be administered intramuscularly in a dose of 1 ml in the area of the inner thigh.
In the absence of a monovalent vaccine, an associated dry vaccine against myxomatosis and viral hemorrhagic disease of rabbits is used, which is administered to 45-day-old rabbits once in safe and endangered areas. In unfavorable cases, they are revaccinated after 3 months, intramuscularly or subcutaneously at a dose of 0.5 ml, intradermally 0.2 ml.
PREVENTION AND CONTROL MEASURES. To prevent myxomatosis in rabbits, farm veterinary specialists must strictly implement the measures provided for in the “Basic Veterinary and Sanitary Rules for Rabbit Farms.”
All farms must operate on the principle of closed enterprises. Veterinary specialists must carry out special veterinary measures on farms, as provided for in the plans, aimed at preventing the disease of rabbits with myxomatosis.
If a disease with signs of myxomatosis is detected in rabbits, the veterinarian of the farm must immediately notify the chief veterinarian of the area and, before his arrival, take measures to stop the sale of rabbits and their slaughter products, as well as prohibit the entry of any type of transport into the territory of the farm and the exit of service personnel outside the premises. farms without appropriate veterinary treatment.
When a diagnosis of myxomatosis is made, the farm (settlement) is declared unsafe and quarantine is imposed.
Under quarantine conditions PROHIBITED:
Import and export from disadvantaged areas of rabbits, their slaughter products, skins, fluff, equipment and feed;
Regrouping of animals within the farm;
Access of people, with the exception of service personnel, to the territory of farms where rabbits are kept;
Holding exhibitions, as well as trade in rabbits, their slaughter products, skins, down and their procurement in disadvantaged areas and threatened areas.
In a troubled area, security and quarantine posts are set up with round-the-clock duty; at the entrance to the farm territory, disinfection barriers are installed, which are filled with a 3-5% sodium hydroxide solution; take measures to prevent domestic and wild animals from entering the farm. Disinfestation is carried out daily in the premises of rabbits, as well as in the surrounding area.
All rabbits in a disadvantaged area are divided into two groups:
Sick and suspected of illness;
Animals suspected of being infected.
Animals of the first group are killed on the spot and burned along with their skins. Manure, bedding, feed residues, containers and low-value equipment are also burned.
Rabbits of the second group are killed for meat directly in a disadvantaged area on a specially equipped site. After boiling for 1.5 hours, the meat is used for food, the internal organs are burned or disposed of.
To disinfect rabbit hutches, cages, and equipment, use a 3% solution of sodium hydroxide, a 3% solution of commercial formaldehyde, a clarified solution of bleach containing 2% active chlorine, etc.
At the unfavorable point, all remaining clinically healthy rabbits are vaccinated against myxomatosis, and a set of veterinary and sanitary measures are carried out aimed at preventing the spread of the myxomatosis pathogen.
Quarantine from a point unfavorable for myxomatosis is removed 15 days after the last case of the disease and the destruction of sick rabbits there, vaccination and final veterinary and sanitary measures.
After the quarantine is lifted, the following temporary restrictions remain:
The importation of rabbits into a former disadvantaged area is prohibited for 2 months;
To the endangered zone - within 1 month after the quarantine is lifted.
Home > LectureLECTURE « Diseases of fur-bearing animals"
Lecture outline:
1. Diseases of the digestive system
1.1.Gastritis
1.2.Gastroenterocolitis
1.3.Peptic ulcer
1.4.Hepatitis
1.5.Hepatosis
3. Diseases of the urinary system
3.1.Jade
3.2.Glomerulonephritis
3.3.Nephrosis
3.4.Urocystitis (inflammation of the bladder)
3.5. Urolithiasis
3.6. Hematuria
4. Metabolic disorders
Of the non-contagious diseases of fur-bearing animals bred in captivity, diseases associated with metabolic disorders occupy a special place, and among young animals - diseases of the digestive and respiratory organs. 1.Diseases of the digestive system
1.1.Gastritis
Inflammation of the gastric mucosa with disruption of the structure, secretory, motor and endocrine functions.
Gastritis can be acute or chronic.
The disease can occur with increased acidity ( hyperacid gastritis), a decrease (hypoacid gastritis) or with the absence of hydrochloric acid in the gastric juice (anacidic gastritis), with a normal content of hydrochloric acid against the background of a decrease in the formation of pepsin (normacid gastritis). There are cases when gastric juice lacks both hydrochloric acid and pepsin (Achilia).
Etiology.
Acute gastritis can occur as a result of fast and greedy eating of food, diseases of the teeth and oral mucosa. Inflammation of the stomach can occur when feeding hot, cold (ice cream) or spoiled food (sour, moldy, rotten, containing toxic substances). Overfeeding an animal is also a common cause of gastritis. Sometimes acute gastritis is a consequence of the transition of the inflammatory process from the intestines, esophagus, liver or pancreas.
Chronic gastritis occurs as a result of the action of exogenous and endogenous factors on the stomach.
Exogenous factors: violation of the feeding regime, feeding too hot, cold, mechanically and chemically irritating food; long-term use of medications that irritate the stomach (reserpine, non-steroidal anti-inflammatory drugs, glucocorticoids, antibiotics,
sulfonamides, etc.); campylobacter, worms, neuropsychic stress, untreated acute gastritis, food allergy.
Endogenous factors: inflammatory diseases abdominal organs, chronic infections, diseases endocrine system(adrenal insufficiency, diabetes mellitus, thyroid disease, hyperparathyroidism, pancreatitis), metabolic disorders (hypovitaminosis, microelementosis), iron deficiency, diseases leading to tissue hypoxia (cardiovascular and respiratory failure, emphysema, chronic bronchitis) , autointoxication and release of toxic substances from the gastric mucosa (acidosis in diabetes mellitus, renal failure), genetic factor.
Pathogenesis.
Gastritis causes reflex disorders of the stomach and associated organs - intestines, liver, pancreas.
The composition and amount of gastric juice, its acidity depend on the prevalence of the pathological process in the stomach and the state of excitability of its glands. Spasm of the pylorus and cardiac sphincter, tension or relaxation of the stomach walls excite the vomiting center, belching and vomiting occur. Violation of the secretory-motor activity of the stomach is accompanied by a disorder in the evacuation of contents from the stomach into the intestines, putrefactive decay of food with the formation of toxic substances that increase irritation of the stomach wall.
Symptoms
In acute gastritis, depression is observed. The temperature can increase by 0.5-2°C, then decrease. Appetite disappears. After eating or drinking water, vomiting occurs; the vomit consists of food particles mixed with saliva and gastric mucus, sometimes with bile and blood. An unpleasant sour odor emanates from the mouth. A whitish or grayish coating appears on the back of the tongue. When palpating the abdomen and the area where the stomach is located, tension in the abdominal wall and pain are determined. Defecation is frequent, stool is liquid. In rare cases, constipation occurs, which later gives way to diarrhea.
With chronic gastritis, the animal is emaciated and has a decreased or variable appetite. With gastritis with normal or increased secretion, dogs develop a tendency to constipation, and with secretory insufficiency, diarrhea, rumbling and bloating are observed. The coat and hair acquire a matte tint, lose their shine, the skin is dry, low-elastic, and has a lot of dandruff. Visible mucous membranes become pale, often with an icteric tint.
In acute gastritis, the gastric mucosa is diffusely swollen in places, edematous, loose, with small and large folds. Redness, pinpoint and spotty hemorrhages, erosions or branched injection of blood vessels are noticeable. Inflamed areas of the stomach wall are sometimes covered with thick, viscous, slightly cloudy mucus or mucopurulent infiltrate, which contains epithelial cells and lymphocytes.
In chronic gastritis, hypertrophy of the glands and proliferation of connective tissue are recorded. The mucous membrane is thickened in places, unevenly tuberous, and warty.
Diagnosis
with gastritis can be diagnosed based on characteristic clinical symptoms, results of analysis of gastric contents (quantity of gastric contents, total acidity and hydrochloric acid content), scatological studies, data from radiography of the stomach using radiopaque substances (signs of hyper- or hyposecretion, restructuring of the relief of the mucous membrane with thickening of the folds ) and biopsy of the mucous membrane.
Treatment
begin with identifying and eliminating the causes that caused gastritis. In case of acute gastritis, the animal must be kept on a starvation diet for 1-2 days, without limiting it to water. During this time, the stomach is washed with a solution of sodium chloride, a solution of lactic acid or a solution of potassium permanganate (faint pink color). These drugs, as well as solutions of furatsilin and furazolidone, are also used when giving enemas.
For the same purpose, decoctions and infusions of medicinal plants are used - marshmallow, calendula, flax, plantain, chamomile, chicory, etc.
If the content of hydrochloric acid in the gastric juice is low, natural or artificial gastric juice, plantain juice or plantaglucide are used 20-30 minutes before feeding the dog. At the same time, vitamin preparations are prescribed: ascorbic acid, pyridoxine, thiamin, cyanocobalamin, nicotinic acid, and multivitamin preparations.
An increased content of hydrochloric acid (hyperacid gastritis) is eliminated by prescribing artificial Carlsbad salt. Anticholinergic drugs are indicated - becarbonate, bellalgin, bellasthesin, bellataminal, besalol or stomach tablets with belladonna extract. Suspensions of gastal are also used, and ven almagel is effective.
After a starvation diet, mucous decoctions of flax or rice seeds, liquid mucous porridges of rice and rolled oats are fed. Feeding is carried out in small portions 4-6 times a day.
On days 5-7 after symptoms of gastritis, fermented milk products are included in the diet: kefir, yogurt, acidophilus, bifidoc, bifilife, cottage cheese, and sometimes milk. For constipation, in addition to Carlsbad salt, sodium or magnesium sulfate, castor or vaseline oil are used.
To improve digestion, enzyme preparations are prescribed.
For hypoacid and anacid gastritis, use abomin, mezim forte pancreatin, pepsin (pepsidil), festal (digestal).
Panzinorm forte can be used for all forms of gastritis.
For frequent vomiting, you can use Cerucal (Raglan), Zofran.
The treatment regimen for a sick animal whose gastritis is caused by the action of pathogenic microflora includes antibiotics - chloramphenicol, baytril, enroxil and others, sulfonamides - enteroseptol, etazol, sulgin, phtha-zol, septrim. Imodium has a good effect.
Prevention
consists of adequate and regular feeding and proper maintenance. You cannot change your diet suddenly. Regular exercise is necessary. Teeth anomalies and other disorders in the oral cavity are promptly eliminated.
1.2.Gastroenterocolitis
Mainly acute polyetiological inflammation of the gastrointestinal tract, accompanied by digestive disorders and intoxication of the body.
By origin, they distinguish between primary and secondary, and by distribution - focal and diffuse gastroenterocolitis.
According to the nature of inflammation, they are divided into serous, catarrhal, hemorrhagic, purulent and fibrinous.
The most severe inflammation occurs when all layers of the wall of the stomach and intestines are involved in the pathological process.
Etiology.
The reasons are very varied.
The main ones are nutritional factors: irregular feeding, feeding of rough, spicy, irritating, poor-quality food, monotonous (mainly carbohydrate or protein) feeding. Ingestion of heavy metal salts, irritating drugs that damage the stomach and intestines (salicylates, glucocorticoids, resorcinol, anthelmintics, pyrethroids, cytostatics, antibiotics, etc.) with food. Food allergies may also be the cause.
Pathogenesis
Under the influence of etiological factors, an inflammatory and dystrophic process develops in the stomach, small and large intestine. Cavity and membrane (parietal) digestion is disrupted. Intestinal enzymatic deficiency (enzymopathy) increases, which accelerates the processes of lipid peroxidation. At the same time, dysbacteriosis develops. The functions of the endocrine and gastrointestinal systems are upset. The motor functions of the stomach and intestines are impaired. As a result, many food components, without being absorbed, follow in transit through the gastrointestinal tract.
Intoxication increases in the body, dehydration occurs due to diarrhea, and the functions and functioning of many organs and tissues are disrupted.
Symptoms
Sick animals experience depression, decreased or lack of appetite. Body temperature is at the upper limit of normal or elevated. With gastroenteritis resulting from poisoning or debilitating diarrhea, it is usually below normal. Thirst is moderate or absent. Diarrhea appears and intensifies.
Primary acute inflammation develops quickly. Diffuse fibrinous, hemorrhagic and purulent gastroenteritis and gastroenterocolitis are severe. Body temperature may increase by 1-2°C. Pain syndrome-colic occurs and intensifies. Appetite disappears. Vomiting appears and becomes more frequent.
Stomach motility and intestinal peristalsis are enhanced at the onset of the disease, but with increased intoxication and dehydration of the body, they weaken or disappear. Frequent bowel movements, liquid stools big amount mucus and undigested food particles, sometimes there is steatorrhea (fat in the feces). Depending on the nature of the inflammation, clots of fibrin, thick films or compacted clots of mucus, blood, sometimes pus, and gas bubbles can be found in the fecal matter. On palpation, the abdominal wall is tense and painful. At the same time, animals show anxiety and sometimes aggressiveness.
The animal becomes dehydrated. The eyes are sunken. The skin loses its elasticity, the hair becomes dull and dry. The animal is losing weight. The paws, ears, nose and tip of the tail become cold. Visible mucous membranes are pale, bluish, sometimes with a jaundiced tint. Signs of cardiovascular failure are increasing. Heart rhythm is disturbed. The pulse is arrhythmic and weak.
Pathomorphological changes.
The mesenteric vessels are injected, the lymph nodes are swollen and hyperemic. With serous inflammation, there is swelling and hyperemia of the mucous membrane, often with hemorrhages. Acute catarrhal gastroenteritis is accompanied by uneven hyperemia of the mucous membrane, swelling and loosening, loss of shine, and folding.
In most cases, a lot of mucus is found in the stomach and intestines in the form of strands, thick films or large compacted clots. The contents are usually liquid, cloudy, with a lot of mucus, sometimes mixed with blood.
Diagnosis
are placed taking into account the clinical symptoms of the disease and medical history data. During a scatological examination, undigested food particles, an increase in the amount of organic acids, blood pigments, mucus, etc. are detected.
consists of excluding bacterial and viral infections, as well as invasions. For this purpose, bacteriological, virological and scatological studies are carried out.
Treatment.
Initially, a fasting regime is prescribed for up to 12-48 hours with free access to water or rehydration solutions. Chicken or beef broth of the second cooking is prescribed and fed to it for several days. It is advisable to add decoctions or infusions from medicinal plants: marshmallow root, string, sage leaves, oak bark, chamomile, chaga, St. John's wort, blueberries, bird cherry fruits, flaxseed, etc. - have various medicinal properties - enveloping, astringent, mucous and anti-inflammatory.
In severe cases of gastroenteritis, accompanied by severe dehydration of the body, parenteral intravenous and subcutaneous injections are effective. For this purpose, saline solutions are used subcutaneously by jet, and intravenously by drip using droppers.
Often used: 0.9% sodium chloride solution, Ringer's or Ringer-Locke solutions with the addition or separately of 5-40% glucose solutions. Ascorbic acid or vikasol can be added to these solutions. Intravenously, along with isotonic ones, hypertonic (5-10%) solutions of sodium and calcium chloride, calcium gluconate can be used. Hemodez and hemodez “N” are injected by drip, polyglucin and reopoliglucin. The following also have good healing properties: hydrolysine, which is administered intravenously; polyamine intravenous drip; casein hydrolysate; polyfer intravenous drip, etc.
To improve digestion, natural or artificial gastric juice is prescribed orally before or after feeding; pepsin or abomin, trypsin and pancreatin; mezim forte; Pepsidil orally. Particularly effective are Festal (Digestal), Liv-52 (Hepaliv), Panzinorm Forte, Essentiale Forte.
For toxic gastroenteritis and gastroenterocolitis, solutions of saline laxatives - sodium sulfate, magnesium sulfate - are first used once; phenolphthalein; bisacodyl; artificial Karlovy Vary, as well as oils - castor, vaseline, sunflower, soybean and others. You can use laxatives of plant origin - aloe juice, joster fruits, rhubarb root, sedexin, senna leaf, steel-nickel tincture, laxative preparations.
At pain syndrome prescribe painkillers and sedatives - belladonna (belladonna) preparations: belladonna tincture, dry belladonna extract; complex tablets containing belladonna extract, papaverine hydrochloride, as well as tablets of becarbonate, bellalgin, belastesin, besalol, etc. For the same purpose, sick dogs are given almagel or almagel A, gastrofarm, gastrotsepin, calmagin, anestezin, but silo or 0.5% solution of novocaine, etc. Alcohol has good sedative and analgesic properties.
The treatment regimen includes adsorbents: aluminum oxide hydrate, activated carbon, talc, white clay; astringents - preparations of tannin, bismuth, oak bark, St. John's wort, alder fruit, chamomile flowers, string, blueberries and bird cherry fruits, sage leaves and others, as well as enveloping - decoctions of flax seeds, eggs, phospholugel and other gel-containing preparations. To suppress pathogenic microflora in the cavity of the stomach and intestines, various antimicrobial drugs are used: imodium; chloramphenicol; baytril (enrofloxacin); Tsifran, as well as other antibiotics from the groups of cephalosporins, tetracyclines and aminoglycosides, which are given orally or injected.
You can prescribe sulfonamide drugs - biseptol, norsulfazole, sulgin, sulfadimezin, sulfadimethoxine, sulfalene, sulfatene, phthalazole, etazol, etc. In some cases, nitrofuran derivatives are prescribed - furagin, furadonin, furazolidone or furatsilin.
For gastroenteritis and gastroenterocolitis, which are a consequence of infectious diseases, it is necessary to use immunomodulatory drugs: gamma and immunoglobulins, thymalin and thymogen, interferon and cycloferon, comedon and decaris, anandin and dibazol, lactoglobulin and others.
To prevent and relieve a possible allergic reaction to medicinal substances, it is prescribed antihistamines: solutions of gluconate and calcium chloride, diphenhydramine orally or parenterally, tavegil, suprastin, pipolfen, diazolin, fenkarol, trexil.
Physiotherapy and mechanotherapy consist of prescribing massage of the abdominal wall and abdomen, stroking and rubbing the abdomen, placing heating pads with warm water under the abdomen and groin area, and wrapping the animal. Electric lamps with infrared rays are used for heating.
Prevention
gastrointestinal diseases can be general and specific. The basis of general prevention is biologically complete feeding of fur-bearing animals, taking into account the physiological state, providing them with active exercise and maintaining good health. sanitary condition and microclimate in places where animals are kept.
The change in diet should be gradual.
Prevention of secondary gastroenteritis and gastroenterocolitis consists of timely treatment of primary diseases.
1.3.Peptic ulcer
This is a chronic relapsing disease in which an ulcer forms in the stomach as a result of disruption of nervous and hormonal mechanisms and gastric digestion disorders. Sometimes it can also occur in the duodenum.
Etiology.
Long-term feeding of food service waste with admixture large quantity salt, mustard, pepper and other irritating substances.
Violations of the feeding regime (long breaks, skipping regular feedings, etc.), feeding frozen fish, meat, hot food to hungry animals, and exposure to stress predispose to the disease. A hereditary predisposition cannot be ruled out. IN last years There is evidence that this disease can be caused by the bacterium Helicobacter pylori. Often occurs as a continuation of gastritis.
Pathogenesis.
In the mechanism of development of peptic ulcers in carnivores, disruption of the mucous barrier is important. Areas of the gastric mucosa, where mucus does not provide protection, are subject to self-digestion under the influence of pepsin and hydrochloric acid, as well as the influence of the bacterium Helicobacter pylori, and disorders in certain areas of the mucous hemomicrocirculation.
Symptoms
The course of the disease, with rare exceptions, is chronic. Against the background of signs of chronic gastritis (deterioration or perversion of appetite, frequent regurgitation), when an ulcer develops in animals, their general condition worsens, weakness and depression appear, and emaciation rapidly progresses.
A characteristic sign is the appearance of vomiting several hours after eating food and the presence of bile and blood in the vomit. Palpation of the stomach area (in the left hypochondrium) determines pain.
Intestinal peristalsis is weakened, constipation is common, and stool is dark in color.
Pathomorphological changes.
Simple ulcers of various shapes and sizes, often with a slight tissue deficiency, heal quickly, leaving traces in the form of scars or polyps. Sometimes deep ulcers with a large tissue defect causing adhesive peritonitis are recorded; in case of perforation of the stomach wall, septic (perforated) peritonitis occurs. Blood is often found in the stomach.
Diagnosis
confirmed by examining gastric juice (increased acidity, presence of blood) and X-ray examination with a contrast mass (slow evacuation of the contrast mass from the stomach into the duodenum). The reaction to the presence of blood pigments in feces during periods of exacerbation is positive.
Treatment.
Eliminate the causes of the disease. A diet is prescribed that consists of liquid or semi-liquid food with vitamins, especially vitamins U and C, milk soups, meat broths, tender liquid porridges, jelly with the addition of a small amount of vegetable oil, egg whites and milk.
Among the medicines, primarily enveloping and adsorbing ones are prescribed (mainly bismuth preparations) - Almagel A, Venter, white clay, flax seed, de-nol, gastrozol.
The use of astringents is indicated - oak bark, burnet, cinquefoil, chamomile flowers, string, blueberry and bird cherry fruits, chaga, as well as vicalin, bismuth nitrate basic, gastrocepin and gastrofarm. Medicinal substances from the groups of antispasmodics, sedatives, tranquilizers and analgesics are also used in treatment.
The use of antimicrobial drugs - chloramphenicol, trichopolum, erythromycin, etc. - is effective.
1.4.Hepatitis
Inflammation of the liver of a diffuse nature, accompanied by hyperemia, cellular infiltration, dystrophy, necrosis and lysis of hepatocytes, and severe liver failure.
Etiology.
Hepatitis of infectious origin includes viral hepatitis, canine distemper, parvovirus enteritis, leptospirosis, listeriosis, colibacillosis, salmonellosis, panleukopenia, feline infectious anemia, etc.
Chronic hepatitis is often a consequence of acute hepatitis.
Pathogenesis.
Harmful substances enter the liver mainly through the intestinal portal vein and cause damage to liver cells with the release of biologically active substances (serotonin, histamine, heparin, etc.), which cause exudative and proliferative changes in the organ. Lipid and pigment metabolism changes, parenchymal jaundice develops. The depositing, barrier and neutralizing functions of the liver are inhibited.
Symptoms
General symptoms include: depression, decreased or loss of appetite, thirst, vomiting, increased body temperature to 40-42°C, enlarged liver, tenderness on palpation. Parenchymal jaundice syndrome manifests itself: dyspeptic disorders, skin itching, scratching, intense yellow discoloration of the mucous membranes and non-pigmented areas of the skin, increased bilirubin levels in the blood.
There is a liver failure syndrome, manifested by a violation of the most important functions of the body - indigestion, intoxication, depression, loss of fatness, exhaustion.
The albumin content in the blood decreases and the amount of alpha- and beta-globulins increases, the concentration of ammonia, cholesterol, transaminase activity increases, and the activity of cholinesterase decreases. Urine is dark in color. Pathomorphological changes.
In acute inflammation, the liver is enlarged, the capsule is tense, the edges are rounded, the consistency is flabby, red-yellow, the pattern of the lobular structure is smoothed, dropsy or fatty degeneration. The beam structure is disturbed, the blood vessels are hyperemic, the stroma is edematous with the presence of cellular infiltrates around the vessels and in the lesions.
With chronic inflammation, the liver is initially enlarged, then decreases in volume, its consistency is dense, the color is gray-brown, the cut surface is dry. Fibrous connective tissue grows in the stroma, and the parenchyma undergoes atrophy.
Diagnosis.
Anamnesis data, results of clinical and laboratory studies are taken into account. In this case, it is necessary to exclude liver cirrhosis, hepatosis, and cholecystitis.
In all cases, the etiological factor is taken into account. Liver cirrhosis occurs chronically, without fever. Acute hepatitis differs from hepatosis in etiology, severity, and temperature reaction.
Treatment.
Eliminate the cause.
Dietary feeding is prescribed. At the same time, the age and breed characteristics of the animal are taken into account.
Fatty foods and salt are excluded from the diet. At the beginning of treatment, fasting for 24 hours with free access to water or rehydration solutions is useful. It is advisable to add decoctions and infusions of herbs to the water - marshmallow root, string, sage leaves, oregano, cinquefoil, yarrow, chamomile, licorice, St. John's wort, blueberry fruit, bird cherry, etc. All of these plants have various therapeutic effects on the liver and organs digestion. In addition to water, in the first days of treatment it is useful to prescribe lean meat and fish broths.
On the 2-4th day of treatment, rice, oatmeal or semolina porridge and rice broth are introduced into the diet in small frequent portions. A small amount of boiled chicken or ground beef is added to the porridge. If after such feeding the animal does not experience digestive disorders in the form of vomiting and diarrhea, then the dose of food is gradually increased.
On the 3-5th day of treatment, fresh warm, small amounts of low-fat lactic acid products are added to the specified diet: kefir, simply kvass, milk, cottage cheese, milk mixture, acidophilus or acidophilus milk, skim milk.
On the 6-9th day, boiled finely chopped vegetables are introduced into the diet - carrots, cabbage, potatoes. Starting from the 10th day of successful treatment, animals are transferred to a normal diet.
To relieve intoxication of the body and improve the functioning of the liver, injections of antitoxic substances and liquids are useful - isotonic sodium chloride solution, 5-10% glucose solution or its mixture with 0.9% sodium chloride solution. Solutions of Ringer, Ringer-Locke, adesol, disol, trisol, chlosol, sanasol, etc. are also widely used.
To replenish protein and sugar in the body and in case of blood loss, plasma substitutes are effective - hemodez, gelatinol, polyglucin, rheopolyglucin, enterodes, polyamine, hydrolysin, casein hydrolysate, etc.
For pain, as well as to normalize body temperature, painkillers and sedatives are prescribed. These are belladonna (belladonna) preparations - becarbon, bellalgin, bellasthesin, besalol, etc. For the same purpose, animals are given almagel, gastrofarm, 1-2% solutions of novocaine, salicylates and drugs from the analgin group.
To improve metabolism in the liver, hepatoprotective drugs are used. These include: legal, liv-52, silybor, essentiale forte, sirepar intramuscularly or intravenously, as well as glucose and vitamins B1, B2, B6, B12, ascorbic and nicotinic acids, vitagepate, lipoic acid, retinol and tocopherol.
In case of toxic hepatitis with symptoms of gastroenteritis and intoxication, the stomach is washed with warm water or water with the addition of potassium permanganate or furacilin, enemas are given with disinfectants or with decoctions of medicinal herbs. As agents that disinfect the bile ducts and enhance the secretion of bile, hexamethylenetetramine is used orally or intravenously, and cholagol and decholin are also prescribed, corn silk, magnesia sulfate, allochol.
For hepatitis of infectious etiology, antibiotics and sulfonamides are prescribed.
In case of heavy metal poisoning, a 5% solution of unithiol is administered intramuscularly, and sodium thio-sulfate is administered intravenously.
Prevention.
They carry out general and special measures to prevent the occurrence of infectious and invasive diseases, and provide their timely treatment.
Prevent feeding spoiled feed to animals. Diets must be balanced in nutrients, vitamins and minerals. Unreasonable use of toxic drugs is avoided.
1.5.Hepatosis
characterized by dystrophic changes in the liver parenchyma in the absence of signs of inflammation. There may be fatty degeneration - fatty hepatosis, amyloid degeneration - liver amyloidosis and other types of degeneration.
Etiology.
Fatty hepatosis is registered as a primary, and more often as a secondary concomitant disease.
The causes of primary hepatosis are feeding poor-quality, spoiled feed containing toxins of pathogenic fungi, protein rotting products, and rancid fats. Liver dystrophy is caused by alkaloids of some plants, medications, nitrates, nitrites, pesticides and mineral fertilizers.
As a concomitant (secondary) disease, hepatosis develops in obesity, diabetes mellitus, cachexia and many other diseases, which are based on metabolic disorders and the functions of endocrine organs.
The disease can also be a consequence of infectious and invasive diseases of the gastrointestinal tract, kidneys, uterus, heart and other organs.
Pathogenesis
increased entry into the liver and accumulation of fatty acids and their precursors in hepatocytes, as well as increased synthesis of triglycerides in hepatocytes and a decrease in the rate of their removal from the liver.
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 leads to disruption of bile formation, bile excretion, protein-forming, carbohydrate-synthesizing, barrier and other functions liver, leads to digestive and metabolic disorders, and the accumulation of toxic metabolic products in the body.
Symptoms
The clinical manifestation is characterized by signs of general intoxication and jaundice. Animal oppression is noted. Body temperature rises by 0.5-1°C, but does not stay at this level for long. Appetite is absent or reduced. The liver is enlarged and painful. Hepatic coma often develops.
Animals may have anorexia, vomiting, diarrhea, general muscle weakness, sometimes seizures, and skin rashes.
In chronic hepatosis, the symptoms are mild: depression, general weakness, loss of appetite, dyspeptic symptoms; the liver is moderately enlarged, painful on palpation and percussion. The yellowness of the mucous membranes and skin is insignificant. Body temperature is normal.
In the blood in acute and chronic hepatosis, a decrease in glucose content, an increase in pyruvic acid, lactic acid, bilirubin, and cholesterol are noted. With toxic liver dystrophy, the activity of AST, ALT, and LDH increases.
Flow.
Acute fatty hepatosis is accompanied by severe liver failure and often leads to the death of the animal.
In chronic hepatosis, when the cause is eliminated and appropriate treatment is carried out, the disease ends in recovery.
Acute fatty hepatosis can turn into chronic, and then into cirrhosis of the liver.
Pathomorphological changes.
In acute fatty hepatosis, the liver is sharply enlarged, yellowish or lemon-yellow in color, brittle and flabby, the pattern on the cut is smoothed.
Chronic fatty hepatosis is characterized by an enlarged liver, its edges are rounded, the organ has a motley mosaic pattern (brown-red areas alternate with gray or yellow).
Diagnosis.
Based on the results of clinical, laboratory, pathological and morphological data, analysis of animal feeding, scatology, urine examination and ultrasound method.
Treatment.
Dietary foods are introduced into the diets of animals: lactic acid, rye bread, boiled and stewed vegetables, fruits, lean soups and cereals. Fish, bones, dry food, spices, fats, butter, and white bread are excluded from the diet.
As medications Lipotropic, vitamin and choleretic drugs are mainly used.
Lipotropic agents include choline chloride, methionine, lipoic acid, lipamide, lipostabil forte, etc.
Essentiale Forte contains a complex of B vitamins and phospholipids. It is prescribed as an antitoxic and hepatoprotector. Among the agents that enhance bile formation and excretion, magnesium sulfate and oxafenamide are used.
Prevention.
The use of poor quality feed is not allowed. Avoid foods containing high amounts of fat. The structure of the diet must correspond to the physiological characteristics and capabilities of a particular animal.
2.Diseases of the respiratory system
Frequent causes of respiratory diseases are poor living conditions, colds, decreased body resistance caused by improper feeding (lack of protein, vitamins, macro- and microelements, and other nutritional factors). Diseases of the respiratory system are classified according to anatomical principles. They are divided into two groups: diseases of the upper respiratory tract (rhinitis, laryngitis, bronchitis) and diseases of the lungs and pleura (pneumonia, pleurisy, emphysema).
2.1. Catarrhal bronchopneumonia.
Inflammation of the bronchi and lobes of the lungs, accompanied by the formation of catarrhal exudate and filling the lumen of the bronchi and alveoli with it.
It can occur in acute, subacute and chronic forms.
Etiology.
a disease of a polyetiological nature.
Hypothermia of the animal, drafts, humidity, microbial and viral air pollution in the room, drinking cold water, feeding frozen food, etc. are essential in its occurrence.
Inadequate feeding, lack of vitamins in the diet, especially A and C, and lack of ultraviolet radiation contribute. These factors lead to a decrease in the natural resistance of the body, against the background of which the association of nonspecific viruses and opportunistic respiratory microflora acquires etiological significance. Secondary bronchopneumonia occurs as a complication of some non-communicable diseases - bronchitis, pleurisy, pericarditis, heart defects, and infectious diseases - plague, parainfluenza, colibacillosis, adenovirus, etc.
Pathogenesis.
under the influence of etiological factors, microcirculation disturbance occurs in the lungs and inflammation develops.
Disturbances in the lungs lead to disruption of gas exchange in the body - hypoxia and hypoxemia, disruption of redox processes, and the occurrence of acidosis.
Toxic waste products of microflora, under-oxidized and acidic products of impaired metabolism lead to changes in the functions of the nervous, cardiovascular, endocrine, gastrointestinal and other systems of the body.
Symptoms
The disease is characterized by general depression, an increase in body temperature by 1-2°C, and remitting fever.
At the onset of the disease, symptoms of damage to the respiratory system are clearly visible: cough, increased intense breathing and shortness of breath, serous-catarrhal or catarrhal transparent or slightly cloudy discharge from the nasal openings, hard vesicular breathing, initially dry and then wet rales, established by percussion areas of dullness in the area of the anterior lobes of the lungs.
The subacute form is characterized by a longer course - 2-4 weeks. Periods of fever alternate with non-febrile periods. There is an improvement and deterioration in the condition of the animals. The cough is often paroxysmal, the nasal discharge is serous-mucopurulent. Patients lose weight and are stunted in growth and development.
The chronic form is characterized by emaciation of animals, the coat and hair are tousled, dull, and the elasticity of the skin decreases. The cough is prolonged, with attacks.
Pathomorphological changes.
In the initial stages of bronchopneumonia and during its acute course, multiple lobular lesions in the form of pneumonic foci are found in the apical and cardiac lobes. They are blue-red or pale red in color, dense to the touch, sink in water, and when cut, catarrhal exudate is released from the bronchi.
In chronic bronchopneumonia, depending on the duration of the process, the presence of extensive pneumonic foci formed as a result of the fusion of lobular lesions is characteristic; pleurisy and pericarditis are detected.
Diagnosis
comprehensively based on anamnesis, clinical signs and pathoanatomical changes.
Blood examination is characterized by neutrophilic leukocytosis with a shift to the left, lymphopenia, eosinopenia, monocytosis, increased ESR, decreased reserve alkalinity and catalase activity of the blood, a relative decrease in albumin and an increase in globulin fractions, a decrease in the saturation of hemoglobin in arterial blood with oxygen.
At x-ray examination in the initial stages of bronchopneumonia in the cranial and cardiac lobes of the lungs, homogeneous foci of shading of moderate density, blurring of the pulmonary field, veiling of the anterior border of the heart, and unclear contours of the bronchial tree are recorded.
In the chronic course, dense, well-contoured foci of shading are detected in the lungs; the contours of the ribs in the affected areas are not clearly visible.
Differential diagnosis consists of excluding infectious diseases - pasteurellosis, salmonellosis, plague, parainfluenza, rhinotracheitis, mycoplasmosis; non-communicable diseases - bronchitis, laryngitis, pleurisy, purulent pneumonia, pulmonary edema, etc. Treatment.
Eliminate the causes of the disease.
Dietary food is prescribed.
For severe painful coughs, antitussive drugs are prescribed: broncholitin, glauvent, libexin and falimint.
Analgesic, antipyretic and anti-inflammatory drugs: amidopyrine, analgin, antipyrine, acetylsalicylic acid, baralgin, spazgan, which are given orally or injected intravenously and intramuscularly, as well as pentalgin, pirkofen, citramon, sedalgin, asphen, benalgin, reopirin, indomethacin , sodium methyl salicylate, ortofen, paracetamol, pyramidant, salicylamide, etc.
Antimicrobial drugs are used: antibiotics, sulfonamides, derivatives of nitrofuran and quinoxaline. Antibiotics are used taking into account the sensitivity of the microflora to them.
Vitamin preparations are prescribed in the form of powders, tablets, capsules, dragees or solutions: ascorbic acid, retinol, B vitamins, a nicotinic acid, rutin, vikasol, cocarboxylase, tocopherol and calciferol.
In combination with antimicrobial agents, proteolytic enzymes and substances are used that expand the lumen of the bronchi and dilute the clots of mucus that accumulate there. These include trypsin, trypsinogen, pepsin, lysozyme, ribonuclease and deoxyribonuclease, which are especially effective against viral pneumonia.
To relieve spasms and expand the lumen of the bronchi and bronchioles, aminophylline solution, ephedrine solution, diprophylline, diprofen, papaverine, theobromine, theophedrine, theophylline, solutan, etc. are administered subcutaneously or intramuscularly.
It is recommended to prescribe calcium chloride or gluconate, suprastin, diphenhydramine, pipolfen, tavegil, fenkarol, etc. as antiallergic agents and reduce the permeability of vascular walls for the entire period of treatment.
In case of severe bronchopneumonia, the antihistamine effect can be stimulated by the administration of glucocorticoids: cortisone and hydrocortisone acetate, prednisolone, as well as deoxycorticosteroids - dex-methasone.
To increase the nonspecific resistance of the body, it is recommended to administer gamma globulins, beta globulins, immunoglobulins and nonspecific polyglobulins to sick animals. For the same purpose, other well-known immunomodulators can be used: interferon, thymogen, thymalin, comedon, anandin, cycloferon, taktivin, dibazol and others in therapeutic doses.
Among expectorants, in addition to medicinal plants that have these properties, mucosalvin, mucaltin, per-tussin, bromhexine, bronchicum, broncholitin, glyceram, ledin, solutan, breast elixir, lycorin, breast collection for dogs and cats, etc. are prescribed .
Aminopeptide, hydrolysine, solutions of glucose, hexamethylenetetramine, isotonic sodium chloride solution, Ringer's solutions and polyglucin, as well as lactosol, disol, trisol, etc. are used as stimulating and antitoxic therapy.
A good therapeutic effect is obtained with complex treatment of animals using novocaine solutions, including blockade of the lower cervical sympathetic nodes.
Prevention.
The breed and age of the animal, as well as the natural and climatic conditions in which it is located, should be taken into account.
At the heart of the system preventive measures there must be compliance with zoohygienic standards for keeping animals and proper feeding of animals. The complex of preventive measures to combat diseases of the respiratory system includes measures aimed at increasing the body’s natural resistance and immunological resistance.
3. Diseases of the urinary system
3.1.Jade
inflammation of the kidney parenchyma of an immunoallergic nature with predominant damage to the glomerular vessels (glomerulonephritis). Based on localization, they distinguish between diffuse and focal, and according to their course - acute and chronic.
Etiology.
Acute nephritis can occur more often after infectious diseases (panleukopenia of cats, plague, viral hepatitis and parvovirus enteritis of dogs, leptospirosis, colibacillosis, etc.), as well as due to poisoning, hypothermia, trauma and other reasons. The disease arises both from the direct effect of pathogens and their toxins on the kidney tissue, and from the resulting allergic reaction of the body.
Sensitizing reasons may be the nature of feeding, living conditions and many other factors.
In the development of nephritis, factors that disrupt the barrier function of the endothelium during normal blood circulation in the vascular apparatus of the kidneys are of great importance. This contributes to the retention and damage of the glomeruli of the kidneys by microbes and toxins. Such factors include nephrotoxins, metabolic products, medicinal and irritating substances: antibiotics, sulfonamides, tar, turpentine, some plants, as well as spoiled feed and mineral supplements.
Pathogenesis.
In the process of inflammation, the urinary and excretory functions of the kidneys are disrupted, and the synthesis of erythropoietins decreases.
Symptoms
At the onset of the disease, appetite decreases, depression and increased body temperature are observed. Dogs, cats and fur-bearing animals often adopt an unnatural posture.
Pressure on the kidney area and palpation in the lumbar region cause anxiety in animals. Swelling of the abdomen, intermaxillary space, thighs, eyelids, dyspeptic symptoms, and vomiting are noted. Visible mucous membranes are pale. Thirst often increases. Due to cardiac weakness, blood stagnation develops in the pulmonary circulation and venous pressure increases. Cyanosis of the mucous membranes occurs.
From the respiratory system, shortness of breath, congestive moist wheezing, and sometimes a slight cough are recorded. Due to the presence of fever and overflow of blood, the pulmonary circulation systems detect bronchitis and bronchopneumonia.
At the first signs of the disease, a frequent urge to urinate appears. Oliguria or anuria develops quickly. Urine is cloudy, from light red to brown, usually high density, contains many red blood cells, leukocytes, tubular epithelium, casts and salts. The pH of urine changes.
Acute nephritis is characterized by short-term excretion of large amounts of protein in the urine, then throughout the entire period of the disease the protein is excreted in small quantities.
The blood is thinned (contains a lot of water), blood density is reduced. In severe cases, the amount of residual nitrogen in the blood increases.
The number of red blood cells and hemoglobin drops. Leukogram with normal total number leukocyte count may deviate towards lymphocytosis or monocytosis.
Flow.
Acute nephritis, depending on the degree of kidney damage, can last 1-2 weeks and end in recovery or death of the animal with symptoms of uremia. If the disease drags on for a long time and turns into a chronic form of diffuse nephritis, then it can last for months and even years.
Pathomorphological changes.
In severe cases of nephritis, a slight enlargement of the kidneys is noted; altered glomeruli in the form of gray grains of sand or small red dots are visible on the cut surface. The capsule is easily removed. Diagnosis.
Diagnosed on the basis of data from a clinical examination of the animal and laboratory urine analysis. Most characteristic symptoms - sudden appearance proteinuria in combination with hypertension and edema. Acute nephritis occurs after an acute infectious disease. Signs of urinary syndrome of acute nephritis include oliguria, the presence of blood, protein, renal epithelium and cylinders.
If patients have initial dysuria, pollakiuria, macrohematuria or prolonged leukocyturia, it is necessary to exclude pyelitis, urocystitis, urolithiasis, etc.
Nephrosis usually occurs without hematuria, increased blood pressure and cardiac hypertrophy. Chronic nephritis differs from acute nephritis in the duration of its course, persistent symptoms of hypertension and often alternating stages of improvement and deterioration of the patient’s condition.
Treatment.
Eliminate the causes of the disease (primarily cold factors). Patients are placed in a warm, dry, well-ventilated room. During the first day of illness, a starvation diet is recommended, then a limited amount of easily digestible, salt-poor food is prescribed - low-fat lactic acid products, porridges from various cereals and vegetables, lean meat broths and vegetable soups, decoctions and infusions of medicinal herbs. Feeds should contain more carbohydrates, vitamins, and an increased dose of potassium and calcium ions, which have a diuretic, hypotensive effect and stimulate the contractile function of the myocardium.
In case of acute nephritis, a course of treatment with antibiotics of different groups is carried out.
In parallel with their use, cardiac preparations are indicated - caffeine, camphor, digitalis and restoratives - polyglucin and rheopolyglucin, calcium chloride and gluconate. To enhance diuresis, Temisal, Furosemide, Veroshpiron, Diacarb, Lespenefril and herbal products are used - Birch buds, lingonberry leaf, horsetail herb, diuretic mixture and kidney tea.
In cases of severe toxicosis and the development of edema, copious bleeding is indicated. This changes the amount of salt and water and leads to a significant restructuring of the body's reactivity. After bloodletting, it is necessary to administer 5-40% glucose solution intravenously in normal doses. Of the drugs acting on the nervous system, perirenal novocaine blockade is used.
As antimicrobial drugs, in addition to antibiotics, nitrofuran derivatives, nevigramon, nitroxoline, sulfonamide drugs and trichopolum are successfully used.
Among the antiallergic drugs prescribed are diphenhydramine, tavegil, suprastin, pi-polfen, fenkarol and others, as well as hormonal drugs: prednisone, prednisolone, hydrocortisone.
Prevention.
It is necessary to promptly eliminate the causes that caused acute nephritis. Avoid hypothermia and prevent irritating and toxic substances from entering the animal’s body with food or medications.
3.2.Glomerulonephritis
Acute, subacute or chronic immunoinflammatory disease with predominant damage to the glomerular apparatus of both kidneys.
Etiology.
Acute and subacute glomerulonephritis often occurs in infectious diseases.
An allergic reaction (sensitization) as a result of the action of an infectious pathogen and its toxins on the animal’s body plays a decisive role in the etiopathogenesis of glomerulonephritis.
Infectious agents can enter the glomerular apparatus of the kidneys in several ways - lymphogenous (through lymph), hematogenous (through blood), from neighboring tissues and from the genital organs.
A large group of nephrotoxins is known that easily penetrate and damage the glomeruli of the kidneys - heavy metals, zoocoumarin, ratindan, zinc phosphide, turpentine, mineral fertilizers and chemically active substances of some poisonous plants.
Sensitizing reasons can be the nature of feeding, living conditions (drafts, high humidity, cold floors), as well as operations, injuries, physical overload, swimming in reservoirs with cold water, etc.
The development of glomerulonephritis is promoted by improper administration of vaccines, serums, antibiotics, immunoglobulins, etc.
Pathogenesis.
Toxins of microbes and viruses, especially streptococcus, damaging the structure of the basement membrane of the glomerular capillaries, cause the appearance of specific autoantigens in the body, in response to which antibodies of classes 10 and I M (anti-renal antibodies) are formed.
Under the influence of a nonspecific resolving factor, most often cooling, a new exacerbation of the disease, a violent allergic reaction of the combination of antigen with antibody occurs, the formation of immune complexes with the subsequent addition of complement to them. Immune complexes are deposited on the basement membrane of the glomeruli of the kidney and damage them. There is a release of inflammatory mediators, damage to lysosomes and the release of lysosomal enzymes, activation of the coagulation system, disturbances in the microcirculation system, increased platelet aggregation, resulting in the development of immune inflammation glomeruli of the kidneys.
Symptoms and course.
According to the course, acute, subacute and, less commonly, chronic glomerulonephritis is distinguished, which lasts for months and years, periodically exacerbating, resembling the acute form.
Clinical signs are very diverse, so they are usually combined into syndromes.
Acute glomerular inflammation syndrome: pain in the back and lower back on both sides of the animal’s abdomen; increase in body temperature to 40°C and above; oliguria (small amount of urine when urinating); reddish color of urine or the color of “meat slop”, sometimes with streaks of blood; proteinuria (protein in the urine), microhematuria (less commonly macrohematuria); the appearance of casts (hyaline, granular, erythrocytes), epithelial cells in the urine; decreased glomerular filtration rate; leukocytosis, increased ESR; increased levels of alpha and gamma globulins in the blood).
Cardiovascular syndrome manifests itself in the form of shortness of breath; arterial hypertension (sometimes ephemeral), possible development of acute left ventricular failure and the appearance of a picture of cardiac asthma and pulmonary edema; signs of bradycardia; changes in the fundus - narrowing of arterioles, sometimes swelling of the optic nerve nipple, pinpoint hemorrhages.
Edema syndrome: doughy swelling, mainly in the area of the muzzle, intermaxillary space, eyelids, appears more often in the morning; in severe cases, hydrothorax, hydropericardium, and ascites are possible.
Cerebral syndrome: soreness of the head, vomiting, weakness, decreased vision, increased muscle and nervous excitability, motor restlessness; sometimes hearing loss, loss of sleep. Complications arising from glomerulonephritis include: acute cardiovascular failure (left ventricular failure, cardiac pulmonary edema); eclampsia (loss of consciousness, clonic and tonic convulsions); bleeding in the brain; acute visual impairment (sometimes blindness due to spasm and swelling of the retina).
Similar to changes in nephritis. However, coagulated protein, red blood cells, fibrin fibers and proliferation of epithelial cells are found in the capsule.
Diagnosis.
Acute glomerulonephritis is detected on the basis of such clinical data as the appearance of edema along the entire body of the animal, especially after a sore throat or acute respiratory disease, or increased blood pressure. The diagnosis is helped by identifying protein, red blood cells and casts in the urine, increasing titers of ASL-0, ASH.
Forecast.
Most often, recovery occurs within a month to a year. A transition to the chronic form and back is possible, which depends on the individual characteristics of the animal, timeliness of diagnosis, therapy, exposure to infections, hypothermia and physical stress. Signs of transition to a chronic form: persistence of any extrarenal sign and proteinuria throughout the year.
Treatment.
First of all, it is necessary to normalize the maintenance and feeding of sick dogs and cats. They must be placed in a warm, dry, draft-free room; walking patients is often prohibited.
During the first two days of the disease, fasting is recommended, then a limited amount of easily digestible, salt-poor food is prescribed - lactic acid, porridge from various cereals, boiled and raw vegetables and fruits. Feed should contain more carbohydrates and an increased amount of potassium and calcium ions, which have a diuretic, hypotensive effect, and stimulate myocardial contractile function. The diet should include ascorbic acid, retinol, tocopherol and B vitamins.
If acute glomerulonephritis has developed against the background of a general infection or due to an exacerbation of a focal infection, it is necessary to use antibiotics - cephalosporins, aminoglycosides, etc. Among penicillins, it is better to prescribe ampicillin, ampiox, isipen or oxacillin. The following have a gentle therapeutic effect for this pathology: claforan, fortum, kefzol, cefamezin, etc. In parallel, nitrofurans, palin, 5-NOK or sulfonamides are prescribed.
In case of severe intoxication and the development of edema, bloodletting is indicated, which not only reduces the amount of salt and water, but also leads to a significant restructuring of the body's reactivity. After bloodletting, a 5-20% glucose solution is administered subcutaneously or intravenously.
In case of cardiovascular failure, in addition to glucose solutions, agents containing cardiac glycosides are used: adonis herb, digalen-neo, digitoxin, digoxin, korglykon, cordigit, strophanthin K.
To stimulate diuresis and relieve hypertension, the following are widely used: Temisal; veroshpiron; furosemide intramuscularly or intravenously, as well as decoctions and infusions of bearberry, juniper fruits, blue cornflower flowers, lingonberry leaves, etc.
Care should be taken to use solutions of magnesium sulfate. It is a salt-removing, blood pressure-lowering, vasodilator and diuretic.
Treatment regimens for glomerulonephritis: as anti-inflammatory, desensitizing and antiallergic, it is necessary to include glucocorticoids - cortisone acetate intramuscularly; hydrocortisone; prednisolone; hydrocortisone; prednisolone.
To ease attacks renal colic and the inflammatory process, cystone, indomethacin, baralgin, spazgan, no-shpu and other analgesics and antispasmodics are used.
If blood or red blood cells appear in the urine sediment, it is necessary to use specific hemostatic and blood-clotting drugs: aminocaproic acid; vikasol; dicinone, as well as a 10% solution of gluconate and calcium chloride intravenously.
Symptomatic therapy sometimes includes narcotic, anabolic drugs, adrenergic blockers, etc.
Prevention.
It is necessary to make a timely and correct diagnosis with a mandatory laboratory test of urine, identify and eliminate the cause of the disease. During treatment, hypothermia of animals and the entry of toxic and irritating substances into their bodies with food, water or medications are not allowed.
3.3.Nephrosis
This kidney damage is non-inflammatory and is characterized by dystrophic changes, mainly in the medulla tubules. According to the course, acute and chronic are distinguished.
Etiology.
The main reasons include: feed intoxication; disturbances of protein, fat, mineral and vitamin metabolism; poisoning with organochlorine compounds, arsenic, phosphorus, feed; complications in some infectious and non-infectious purulent-septic processes (endometritis, pyometra, urocystitis).
Nephrosis often develops as a complication after illness with nephritis and pyelonephritis.
Pathogenesis
nephrosis has not been studied enough. As a rule, its development is associated with a violation of the immunobiological state of the body, sensitization and autosensitization reactions.
Long-term intoxication causes disturbances in the regulation of metabolic processes in the hypothalamic region, the pituitary-adrenal system, while simultaneously changing the enzymatic-oxidative activity of renal cells, which further aggravates the disturbance of protein and lipid metabolism. However, the function of excretion of nitrogenous waste by the kidneys is preserved.
Symptoms
Depending on the degree of kidney damage in dogs, cats and fur-bearing animals, along with general symptoms (decreased appetite, emaciation, gastrointestinal disorders), progression of signs of renal failure is noted: swelling of the eyelids, limbs, intermaxillary space, weakening of cardiac function (frequent, small filling and small wave pulse), increased nervous excitability and the appearance of tonic-clonic convulsions.
With mild nephrosis, urine output decreases, urine is low density and contains protein; the sediment contains degenerated renal epithelial cells, single hyaline and granular casts, and a few erythrocytes and leukocytes. The number of red blood cells in the blood is reduced.
In severe cases of the disease, renal failure often develops with signs of uremia. Improvement in the condition of the sick animal is accompanied by polyuria. The urine is light, low density, and contains a small amount of protein.
Pathomorphological changes
depend on the type of nephrosis and the severity of the process. In mild cases of nephrosis, the kidneys are macroscopically unchanged or slightly increased in volume, in severe cases they are greatly enlarged. The buds are smooth, pale yellowish in color, the capsule is easily removed. In the later stages of nephrosis, the kidneys become smaller, become denser, and the capsule is difficult to remove.
With fatty degeneration, the consistency of the kidneys is softer and resembles the so-called large “white” kidney.
The section reveals yellowish inclusions in the swollen cortex of the kidneys due to the abundant accumulation of lipoids. The medulla is violet-pink in color with a brownish tint.
Diagnosis.
Diagnosed on the basis of medical history, symptoms of the disease and the results of urine and blood tests. Nephrosis is characterized by: persistent high proteinuria with increased cholesterol in the blood, lipoids in the urine, normal or low blood pressure.
Treatment.
It must be comprehensive and aimed at eliminating the main cause of the disease.
For acute poisoning, antitoxic therapy is used. Sick animals are given rest. To neutralize poisons, milk and lactic acid products, egg whites are prescribed, as well as washing the stomach and large intestine with disinfectants and antitoxic agents (solutions of potassium permanganate, sodium bicarbonate, furatsilin, etc.). When a poisonous principle is known, an antidote is used. The diet is limited in table salt and water, and given lean meat and offal.
If the disease occurs as a result of an infection, then treatment is prescribed using immunostimulants, serums, antibiotics, sulfonamides and nitrofurans, as well as 5-NOK, palin, nolitsin.
Potassium acetate, theophylline, Lasix, bearberry decoction, kidney tea and other drugs are used as diuretics.
Disorders of the stomach and intestines are eliminated by appropriate dietary feeding, the prescription of laxatives, enzymatic and antiseptic agents.
3.4.Urocystitis (Inflammation of the bladder)
Can be primary or secondary.
Etiology.
When the body's resistance is weakened, especially when the placenta is retained, endometritis, vaginitis or pyometritis, pathogenic microflora (streptococci, staphylococci, Escherichia coli, corynebacteria and fungi) easily penetrates the urethra and bladder, causing their inflammation. A common cause of inflammation of the mucous membrane of the bladder is injury to it by a catheter, urinary stones or sand, and helminths.
Urinary retention leads to stagnation and decomposition, causing primary cystitis. Hypothermia of animals, especially the groin and abdominal areas, always contributes to the development of urocystitis.
Rarely, primary cystitis occurs with careless and improper use of acute irritating and potent drugs.
Secondary urocystitis occurs due to the spread of inflammation from the genital organs, kidneys, ureters, and prostate gland. Pathogenic microorganisms (fungi, viruses, microbes) can be introduced into the bladder through hematogenous and lymphogenous routes.
Pathogenesis.
Inflammatory products, moving with the urine, cause corresponding changes in it: pus, bladder epithelium and red blood cells appear in the urine.
Due to extreme irritation from the mucous membrane of the bladder, more frequent contractions are reflexively observed, accompanied by increased urination. Absorbed inflammatory products cause shifts in the body's metabolic processes, body temperature rises, and the number of leukocytes, especially neutrophils, increases in the peripheral blood.
Symptoms
In mild cases of the disease, frequent urination (pollakiuria) is observed. As inflammation progresses, it is accompanied by pain. When urinating, an admixture of blood is found in the last portions of urine, often in the form of clots. Despite pollakiuria, the daily amount of urine excreted not only does not increase, but may even be reduced.
Subsequently, the urge to urinate becomes so frequent that it even becomes continuous, although urine is not released or is released in drops. As the pain intensifies, urinary colic occurs.
On palpation of the bladder, pain is detected. Sometimes it is overflowing with urine as a result of blockage of the urethra by inflammatory products.
Urine is dark yellow or reddish, with an ammonia-like, and with purulent inflammation, a cadaverous odor, contains protein, mucus, mucopurulent flakes, and an admixture of blood. The urine sediment contains many leukocytes, epithelial cells of the bladder, erythrocytes, and microorganisms. During alkaline fermentation, the urine contains crystals of phosphate-acid ammonium magnesium and ammonium urate.
With purulent-hemorrhagic and phlegmonous urocystitis, the general condition is disrupted and worsened, body temperature rises, the animal becomes weak and exhausted.
Catarrhal cystitis with timely treatment usually ends in recovery. Other forms of inflammation of the bladder progress with delayed treatment and are complicated by the formation of ulcers, necrosis of the mucous membrane, paracystitis, septicopyemia, inflammation of the renal pelvis and nephritis.
Pathomorphological changes.
In the acute course of the disease, the mucous membrane of the bladder is swollen, reddened, covered with mucus, purulent exudate, fibrin, or ulcerated. In chronic urocystitis, the mucous membrane is thickened due to the proliferation of fibrous connective tissue and may have polypous growths. Urine is cloudy, with flakes, and a pungent odor.
Diagnosis.
Pollakiuria, which does not change during the day, pain when urinating, urinary colic, the results of a bladder examination, and a urinalysis are sufficient to make a diagnosis.
Urocystitis must be differentiated from pyelitis, urethritis and urolithiasis.
Treatment.
The sick animal is provided with rest, warmth, and soft bedding. At normal body temperature, heat is indicated on the area of the abdomen, groin, and wrapping. The diet should consist of lean beef, broths, rice and oatmeal porridge, vegetables (carrots, cabbage, potatoes), fruits (apples, pears, grapes) and an increased amount of vitamins and multivitamins (Revit, Undevit, Gendevit, etc.), access to water is not limited.
Drug treatment is aimed at eliminating the etiological factor, suppressing pathogenic microflora, removing inflammatory products from the bladder cavity, relieving spasms and pain. In all cases of the disease, antimicrobial agents are widely used: antibiotics, sulfonamides, nitrofurans and quinoxaline derivatives. For mild forms of urocystitis, it is advisable to use hexamethylenetetramine, urosulfan, cystenal, sulfacyl, urobesal, biseptol, etc.
Of the nitrofuran derivatives, furagin, furadonin or furazolidone are prescribed.
For severe bacteriouria, a variety of antibiotics are prescribed: penicillin, cephalosporins, gentamicin sulfate, tetracyclines, chloramphenicol.
To accelerate the release of inflammatory products from the bladder, Temisal, ammonium chloride, hypothiazide, decoctions of horsetail, juniper berries, lingonberry leaves, bearberry, and other diuretics are used.
In severe cases of urocystitis and in the chronic course of the disease, the bladder can be washed with disinfectant solutions using a catheter. The most commonly used solutions are ethacridine lactate (0.1%), boric acid (3%), ichthyol (1%), resorcinol (3%), potassium permanganate (1:10,000), furacilin (0.1%) in the amount 20-100 ml.
In cases of illness that occurs with severe urinary colic and spasms, the use of solutions of novocaine, analgin, no-shpa, paracetamol, cystone, atropine sulfate, etc. is indicated.
Prevention.
Aimed at timely treatment vaginitis, endometritis, infectious diseases. It is necessary to protect animals from hypothermia.
3.5. Urolithiasis
The disease is accompanied by the formation and deposition of urinary stones, varying in chemical composition, or sand in the renal pelvis, bladder or urethra.
Etiology.
The causes of the formation of urinary stones can be infections, metabolic disorders (mainly salt), acid-base balance, the physicochemical state of protective colloids that maintain salts in a dissolved state, the activity of the parathyroid glands, a lack of retinol in the diet and calciferol, water hardness, feeding, etc.
Urate and phosphate stones are found in dogs, cats and fur-bearing animals. Phosphate stones and sand form quickly, especially in neutered cats. The disease is acute and leads to the death of the animal. It was also noted that these stones are formed more often in pregnant females and in early-age puppies, when metabolism is especially intense. Microorganisms (hemolytic streptococcus, proteus, staphylococci) play an important role in the formation of stones in carnivores.
Pathogenesis.
The progression of the disease depends on where the stones form and where they migrate along the urinary tract.
With the growth of kidney stones, atrophy of tubular structures in the cortical layer is noted, and in the medulla - the formation of small cysts.
Large stones that are in a relatively fixed position may not cause pain for a long time; Small stones, when displaced, often clog the ureters or urethra and cause difficulty in urinating. When the outlet of the renal pelvis is blocked, the latter is stretched by the urine accumulated in it, which causes severe anxiety to the animal. This condition continues until the stone reaches a position where it does not interfere with the flow of urine in the bladder.
The presence of urinary stones in the bladder causes inflammation of the mucous membrane, resulting in blood in the urine. In some cases, such blockage can result in bladder rupture and uremia.
Symptoms
Before blockage of the urinary tract occurs, the disease occurs without obvious clinical signs, but the results of laboratory tests of urine and blood indicate its occurrence. During the latent period of urolithiasis, symptoms can be identified that indicate not only its development, but also presumably the localization of the stone.
Patients' appetite decreases, depression and drowsiness may occur. When a stone forms in the renal pelvis, symptoms characteristic of pyelitis may appear. At times, hematuria is detected, especially after active movements of the animal.
The presence of stones in the bladder is manifested by a frequent urge to urinate and anxiety.
When the urinary tract is blocked, the disease manifests itself as urinary colic, impaired urination or anuria, and changes in the composition of urine. Attacks of severe anxiety suddenly appear. The animal moves around a lot, squeals, meows, moans, and takes a position for urination. The duration of attacks can reach several hours. Between attacks, the animal is sharply depressed, lies indifferently, gets up and moves with difficulty. During an attack of illness, the pulse and breathing rates increase, and body temperature rises sharply. Urination is frequent and painful. Urine is released with difficulty, in small portions and even drops. When the urethra is completely blocked, anuria appears. Palpation of the kidneys and bladder in the lumbar and abdominal areas is painful. The lower wall of the abdomen protrudes and is tense.
The urine is cloudy, mixed with urinary sand, which quickly precipitates. The color of the urine is dark, with a reddish tint caused by blood.
Pathomorphological changes depend on the location of the stones, their size, structure and the complications they cause.
Diagnosis.
The diagnosis is made taking into account the diet, characteristic clinical signs and the results of a urine test.
Treatment. First of all, treatment is aimed at eliminating stagnation of urine and restoring patency of the urinary tract.
Obstruction can occur due to spasm of smooth muscles when the mucous membrane is overirritated by passing stones or sand. In these cases, antispasmodics are used - atropine sulfate subcutaneously, no-shpu intramuscularly, papaverine hydrochloride subcutaneously, spasmolitin, spasmol-gon, spazgan, baralgin orally, in severe cases - intravenously, and other substances. In parallel with antispasmodics, sedatives (Rovatin, Rovatinex, Enatin, chloral hydrate, bromocamphor, magnesium sulfate solution, sodium bromide, etc.) and analgesics (amidopyrine, analgin, aspisol, aspirin, methyl salicylate, voltaren, paracetamol, sedalgin, etc.) are prescribed .).
Attacks of urinary colic can be stopped with the help of lumbar novocaine blockade and heat. Positive results are achieved when ammonium chloride is given orally; Avisan can also be used for 10-15 days.
To destroy and remove urinary stones and sand, urodane, urolite, knotweed herb in the form of an infusion (10.0:200.0) 2 tablespoons 3 times a day before feeding, madder extract orally 0 25-0.75 g 2-3 times a day in 1/2 glass of warm water, cystone is effective.
In combination with these substances, medications that disinfect the urinary system are also prescribed: bearberry decoction, trichopolum, biseptol, urosulfan, urobesal, hexamethylenetetramine, etc.
If there is a threat to the life of an animal with a blockage of the urethra, a catheter is inserted to the site of the obstruction, the stone is dislodged and urine is removed. Catheterization is recommended to be carried out no more than 2-3 times. In emergency cases, surgery is indicated - urethrostomy.
3.6.Hematuria
A complex of symptoms of various diseases characterized by blood in the urine. It is registered everywhere in fur farms; Arctic foxes, foxes, and minks are especially often affected.
Etiology.
The reasons for the appearance of blood in the urine are: acute feed intoxication, deficiency of vitamins A, E, hereditary muscular dystrophy, inflammation of the urinary tract and urolithiasis, glomerulonephritis, external irritants (sharp forceful catching, mating), tumors in the genitourinary system , and in newborn puppies of foxes and arctic foxes - hemorrhagic diathesis (red feet, hypovitaminosis C).
Pathogenesis.
Toxic substances, released through the urinary system, act on the receptor apparatus of the mucous membrane of the bladder, causing expansion of the capillaries of the mucous layer with the subsequent release of blood. Long-term blood loss leads to the development of severe chronic posthemorrhagic anemia with all the ensuing consequences.
Against the background of anemia, degenerative changes develop in the liver, kidneys and other organs.
As a result of constant blood loss, the reserves of calcium, phosphorus, chlorine, iron, copper and protein in the body are depleted, which leads to disruption of bone marrow hematopoiesis,
Symptoms
Urine is bright bloody in color and contains blood. In many cases it turns brown. Depending on the etiology, other signs may develop - loss of appetite, depression, diarrhea, abortion, anemia of visible areas of the mucous membranes and skin, frequent and painful urination, increased bladder volume (determined by palpation) and bloody-purulent discharge. In newborn puppies, swelling and cyanosis of the paws are noted.
Pathomorphological changes
characterized by pinpoint hemorrhages under the capsule and in the renal parenchyma. The bladder is distended, filled with red-yellow urine, which contains a yellow sediment.
Diagnosis.
The symptoms of the disease are characteristic, but it is necessary to establish the underlying cause of its occurrence. Thus, with vitamin E deficiency, a significant number of animals become ill. Urine is usually brown in color. When autopsying dead animals, the skeletal and cardiac muscles are pale, dystrophic, and the subcutaneous fat is yellow or anemic. The seasonality of the disease is weakly expressed. A high percentage of empty females, analysis of diets and feed indicate an overload of diets with fat or the use of oxidized fat with insufficient supply of vitamin E. With feed intoxication, along with bloody urine, other symptoms are found in most animals - loss of appetite and diarrhea, and the amount In patients with these signs, the increase does not gradually, but quickly.
Urocystitis and urolithiasis are characterized by strict seasonality (mainly July-August), mainly male mink puppies are affected, and the disease, despite some coverage of the population, still remains sporadic and subsides by autumn. Some irritants (forcible capture of an animal, mating) cause hemorrhages in the organs of the urinary system. If there is a delay in emptying the bladder, the urine becomes brown in color. This disease usually occurs only during the rutting period in isolated cases. Male foxes and arctic foxes are most often affected.
In the case of tumors, the incidence is single. Red feet are observed in puppies under 5 days of age. Hereditary muscular dystrophy is differentiated using pathohistological studies for the presence of different diameters of myofibrils in a cross section of skeletal muscles, degenerative processes and phagocytosis of myofibrils, basophilia of their sarcoplasm, etc.
Treatment and prevention.
The main cause of the disease is eliminated, most often vitamin E deficiency and feed poisoning.
4. Metabolic disorders
4.1. Lactation exhaustion in minks.
Lactation exhaustion (lactation anemia) is a disease of minks, which is characterized by progressive weakness and severe exhaustion, and loss of maternal qualities in females. Minks with multiple litters get sick; young, poorly nourished females get sick more often. The disease develops rapidly in the second half of the lactation period.
Etiology.
The cause of the disease is insufficient or inadequate feeding of females during pregnancy and lactation, as well as the lack or absence of table salt in the feed during lactation. Metabolic disorders, retarded growth and development at an early age contribute to the disease.
Pathogenesis.
The basis of the disease is dehydration of the body due to the loss of sodium chloride in milk, which leads to the removal of sodium from the body, disruption of metabolic processes, and the development of cachexia.
Symptoms
The first signs of the disease are observed in minks with 5-6 week old puppies. Sick minks lose their appetite, quickly weaken, have an unsteady gait, dull, matted hair, and may have a tsar. With severe exhaustion, a coma develops, followed by death.
Pathological changes.Lectures
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