Abstract on the topic: Infectious (transmissible) encephalopathy of minks. Mink encephalopathy Mink encephalopathy

Transmissible mink encephalopathy is a contagious disease characterized by a very long incubation period, symptoms of damage to the nervous system and pathological changes in the central nervous system. Since 1963, this disease has been considered widespread.

Clinical signs and pathological changes. The disease occurs in the form of epizootics; minks are susceptible, and in laboratory conditions, ferrets are susceptible. Incubation period lasts from 5 months to a year. Under natural conditions, adult animals are more often affected. Early symptoms The disease is considered to be a change in the appearance of minks. Their tail bends in a peculiar way, their fur becomes coarser, and their body weight decreases. While resting, minks twitch their hind legs sharply. Movements are slow, rear instability appears, and coordination of movements is gradually impaired. Some minks become aggressive, others become timid, fearful and inactive. As the disease progresses, short periods of drowsiness become longer and sleep becomes deeper.

The duration of the disease varies. In some minks, the prodromal period lasts from three to 4 weeks, after which the disease worsens and after 5-7 days the animals DIE. In other animals, clinical signs of the disease are not observed and anorexia is noted only 2-3 days before death. Sometimes minks with ataxia live more than 6 weeks.

There are no visible pathological changes, only sometimes moderate swelling of the brain is noted. Microscopic changes are constantly found only in the brain: an increase in glial elements, astrocytosis, vacuolization of neuroglia, infiltration, degeneration of neurons; some nerve cells contain eosinophilic granules. Changes are also found in the frontal cortex, olfactory bulbs, and corpus callosum (corpus stratum). Damage extends caudally, usually involving the thalamus, hypothalamus, pons, and medulla oblongata. In the white matter, cerebellum, spinal cord there are no defeats. In minks with progressive disease, ischemic cell necrosis is detected in these sections. Microscopic changes in mink transmissible encephalopathy resemble those in scrapie, but in sheep and goats their distribution is different, and vacuolation nerve cells less noticeable with scrapie.

CHARACTERISTICS OF THE PATIENT

The prion is similar to the pathogen called scrapie. The agents differ in that the causative agent of mink encephalopathy can infect hamsters, goats, striped skunks, raccoons, rhesus macaques, squirrels and blunt-tailed macaques, but does not infect Swiss mice. The scrapie agent is pathogenic in mice but less pathogenic in primates. In this aspect, the causative agent of mink encephalopathy is similar to the causative agents of human encephalopathy (kuru or CJD), which are also not pathogenic for mice and are not transmitted to primates.

Sustainability. The agent is resistant to high temperature n UV irradiation. Warming up in a boiling water bath for 15 minutes, exposure to a 0.3% formalin solution for 12 hours at 37°C does not inactivate it; a 10% formalin solution for 20 months reduced the infectious titer of the agent by more than 31%. When exposed to ether for 18 hours, the titer decreased slightly. The agent is destroyed by pronase. It was not possible to isolate the infectious nucleic acid fraction.

Experimental infection. It is successful with subcutaneous, intramuscular, intracerebral and intraperitoneal injection of 1 ml of brain homogenate in a dilution of 105-107, as well as by feeding minks with infected material. The duration of the incubation period depends on the method of infection and the number of passages of the agent on minks. With intramuscular inoculation, the incubation period is 2-3 months shorter than when feeding contaminated material or natural infection. In addition to minks, it is possible to infect hamsters, goats, striped skunks, raccoons, squirrels, and rhesus monkeys.

Cultivation. Perhaps only in minks for now.

EPISOOTOLOGICAL FEATURES Under natural conditions, the disease is transmitted through contact between sick and healthy animals.

DIAGNOSTICS

Diagnosis is based on disease symptoms and neurohistological changes similar to those observed in scrapie, but differing from scrapie in host type and location (CNS only).

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MINISTRY OF AGRICULTURE AND FOOD

THE REPUBLIC OF BELARUS

EE “VITEBSK ORDER “BADGE OF HONOR” STATE

ACADEMY OF VETERINARY MEDICINE”

COURSE WORK

on the topic: “Differential pathomorphological diagnosis of slow viral and prion diseases of animals”

VITEBSK - 2011

Introduction

1. Slow viral diseases of small cattle

1.1 Sheep pulmonary adenomatosis

1.2 Visna-madi sheep

2. Slow prion diseases of cattle and small ruminants

2.1 Scrape the sheep

2.2 Bovine spongiform encephalopathy

3. Slow viral and prion diseases of minks

3.1 Aleutian mink disease

3.2 Transmissible encephalopathy of minks

Introduction

Slow viral and prion diseases of ruminants and minks represent a serious veterinary and medical problem; they cause great economic damage, causing the death of a large (sometimes entire) animal population. The possibility of human infection with prion diseases from sick animals cannot be ruled out.

The classification of slow infections is based on the following criteria: long incubation period (months and years); long clinical course (several months), inevitably leading to death; disease of one animal species (ruminants, minks, humans); damage to an organ or organ system (lungs, central nervous system, immune system), i.e. pathology is determined at the organ and system levels.

Mostly adult animals are affected, which is associated with a long incubation period during which viruses and prions persist in the body. Etiological factors in slow infections there are viruses and prions. Thus, in sheep, viruses cause pulmonary adenomatosis, visnu-medi, prion - scrapie; at a large cattle the prion is the cause of spongiform encephalopathy; In minks, the virus causes Aleutian disease, and the prion causes transmissible encephalopathy.

Pathomorphological changes during slow infections are pathognomonic and serve as the basis for making a nosological diagnosis in sick animals. Thus, in sheep with adenomatosis, adenocarcinoma is detected in the lungs; in sheep with visna in the central nervous system - non-purulent lymphocytic encephalitis, with medi in the lungs - interstitial pneumonia; in Aleutian mink disease - plasmacytosis in bone marrow, spleen, lymph nodes, liver, kidneys; with scrapie in sheep, spongiform encephalopathy in cattle and transmissible encephalopathy in minks, a degenerative process is determined in the central nervous system - spongiform encephalopathy.

Slow infections are described according to the following scheme:

Definition of disease;

Etiology;

Pathogenesis;

Clinical and epidemiological features;

Pathomorphological changes (macro- and microscopic);

Pathological diagnosis;

The diagnosis is nosological;

The diagnosis is differential.

IN educational manual Tables of differential pathomorphological diagnosis of slow infections of animals are given.

Material equipment for the lesson: microscopes, museum and histological preparations, drawings, slides, tables (PAD).

1. Slow viral diseases of small cattle

1.1 Sheep pulmonary adenomatosis

Sheep adenomatosis is a slow viral disease characterized by the development of adenocarcinoma (glandular cancer) in the lungs.

Etiology. The causative agent of the disease is an RNA genomic virus of the family Retroviridae, genus Betaretrovirus. The virus has oncogenic properties and is pneumotropic.

Pathogenesis. Infection occurs through the respiratory route. The virus causes tumor metaplasia of the squamous epithelium of the alveoli and prismatic epithelium bronchioles, resulting in the development of malignant tumor- adenocarcinoma (glandular cancer). The tumor metastasizes to regional lymph nodes, pleura, peritoneum, mesentery, liver and other organs.

Clinical and epidemiological features. Adult sheep 2 to 4 years of age are affected. Young animals and goats rarely get sick. The incubation period varies from 4 to 9 months and can last up to 3 years. The duration of clinically pronounced disease is 2-8 months. The outcome is fatal. viral disease livestock encephalopathy mink

Sick animals exhibit respiratory syndrome: depression, increased frequency and abdominal type breathing, shortness of breath, worsening with a 20-minute run, wheezing when breathing, wet, prolonged, coughing, mucopurulent discharge from the nasal cavities. Exhaustion with preserved appetite.

Pathomorphological changes. The corpses of emaciated animals, catarrhal-purulent exudate is released from the nasal openings.

Pathognomonic pathomorphological changes are found in the lungs - the posterior and middle lobes. Tumor nodes are visible in them different sizes- from miliary (the size of a millet grain) to a chicken egg (5 cm) and more. The nodes, merging, form large tumor infiltrates, covering entire lobes (lobar tumor lesions). Tumor nodes of dense consistency, gray-white, yellow-white or pale pink, resemble fish or boiled meat, are located under the pleura and deep in the lungs, sharply demarcated from the surrounding tissue. There may be hyperemia, edema and emphysema around them. The weight of the affected lungs increases to 2.5-3 kg, while the norm is 300-500 g. The cut surface is smooth or granular, moist, slightly shiny, gray-white. When pressed, a pale yellow viscous liquid is released. The tumor may contain foci of necrosis and abscesses.

Histological examination reveals cancerous nests of different sizes in tumor nodes. In them, the epithelium is cubic and prismatic, multiplies intensively, forming papillary growths protruding into the cavity of the cancer nest. Cellular atypia is noted: 2-3-nucleated cancer cells, symplasts cancer cells, their cubic and prismatic shape, mitoses of cancer cells are often detected.

In the surrounding lung tissue catarrhal-purulent, fibrinous inflammation, abscesses and necrosis are noted; the same processes can occur in a tumor.

As a result of tumor metastases, the bronchial and mediastinal lymph nodes are increased in volume and weight by 3-5 times. Tumor metastases are also observed in the pleura (parietal), peritoneum, mesentery, mesenteric lymph nodes, liver, spleen, kidneys, myocardium.

Pathological diagnosis

1. Adenocarcinoma (glandular cancer) of the lungs.

2. Tumor metastases in the parietal pleura, peritoneum, mesentery, bronchial, mediastinal and mesenteric lymph nodes, liver, spleen, kidneys.

3. Wasting (cancer cachexia): lack of fat in the fat depot, skeletal muscle atrophy.

4. Histo: in the lungs - adenocarcinoma (glandular cancer).

The diagnosis (nosological) is made taking into account clinical and epidemiological data, the results of autopsies of sheep corpses and histological examination of the lungs. Pathomorphological changes in the lungs, determined by macroscopic and histological examination, are pathognomonic for sheep adenomatosis.

Differentiate adenomatosis from visna-medi; catarrhal, catarrhal-purulent and fibrinous pneumonia bacterial or viral etiology; dictyocaulosis.

When sheep hang, there are no pathomorphological changes in the lungs. in the brain, histological examination shows non-purulent lymphocytic meningoencephalitis in the brain stem (quadrigeminal, pons, medulla oblongata) and cerebellum: lymphocytic perivasculitis, glial nodules and large cellular infiltrates, focal necrosis of the medulla, demyelination of the pulp nerve fibers.

Madi is characterized by interstitial pneumonia: thickening of the alveolar walls due to lymphocytes, histiocytes, fibroblasts, lymphocytic perivasculitis and peribronchitis, focal pneumosclerosis.

Catarrhal, catarrhal-purulent and fibrinous pneumonia do not have morphological similarity with lung adenocarcinoma in sheep adenomatosis.

With dictyocaulosis, there are helminths in the bronchi, and catarrhal-purulent inflammation in the lung tissue.

1.2 Visna-madi sheep

Sheep Visna-Medi is a slow viral disease characterized by the development of non-suppurative lymphocytic meningoencephalomyelitis (Visna) or interstitial pneumonia (Madi). Inflammation of the central nervous system and lungs is possible at the same time.

Etiology. The causative agent of the disease is an RNA genomic virus of the family Retroviridae, genus Lentivirus.

Pathogenesis. The virus is neuro- and pneumotropic. Infection occurs through the respiratory route, and in lambs through the nutritional route through the milk of a sick ewe. Virus reproduction occurs in cells immune system(lymphocytes), then it concentrates in the central nervous system and lungs, where pathognomonic pathomorphological changes develop in the form of non-purulent lymphocytic encephalitis in visna or interstitial pneumonia in medi.

Clinical and epidemiological features. The incubation period is several months and years. Clinical stage The illness lasts several months and ends in death. Sheep 3-4 years of age and older are more often affected.

With visna, a nervous syndrome is observed: impaired coordination of movements, twitching of the head and lips, curvature of the neck, paresis and paralysis of the limbs.

With medi, a respiratory syndrome is determined: difficulty, rapid breathing, shortness of breath, dry cough.

Pathomorphological changes. Visna - in dead animals, exhaustion is noted (lack of fat in the fat depot, atrophy of skeletal muscles, liver, kidneys, spleen), brain hyperemia, choroid plexuses lateral ventricles.

Histologically, pathognomonic changes characteristic of non-purulent lymphocytic demyelinating meningoencephalomyelitis in the brainstem (quadrigemole, pons, medulla oblongata) and cerebellum are detected in the brain. In the white and gray matter of the brain there are lymphocytic perivasculitis, focal or diffuse proliferations of lymphocytes, microglia and astrocytes, demyelination of pulpal nerve fibers, disintegration of axial cylinders (in the brain and spinal cord), focal necrosis of the medulla.

Pathological diagnosis of visna

1. Wasting: lack of fat in the adipose depot, skeletal muscle atrophy, especially severe in the muscles hind limbs.

2. Hyperemia of the brain and choroid plexuses of the lateral ventricles.

3. Histo: non-purulent lymphocytic demyelinating meningoencephalomyelitis.

In case of sheep fever, pathognomonic pathomorphological changes are detected in the lungs - interstitial pneumonia. In addition, the corpses of emaciated animals. The lungs are not collapsed, gray-yellow or gray-white in color (white lungs), 2-4 times heavier in weight than normal, compacted, rubber-like consistency. On the cut - dryish, uniform in color (gray color). The interlobular interstitial tissue is thickened, the pattern of the lobules is well defined. Localization in the posterior lobes, lobar coverage.

Histologically, chronic interstitial pneumonia is determined: lymphocytic perivasculitis and peribronchitis, thickened alveolar walls due to lymphocytes, histiocytes, plasmacytes, fibroblasts. The same is true in the interlobular interstitial connective tissue. On late stages diseases, foci of pneumosclerosis are identified. Bronchial and mediastinal lymph nodes are enlarged 3-5 times, in a state of hyperplastic inflammation.

Pathological diagnosis of medi

1. Chronic lobar interstitial pneumonia.

2. Hyperplastic inflammation of the bronchial and mediastinal lymph nodes.

3. Exhaustion: lack of fat in the fat depot, atrophy of skeletal muscles, liver, kidneys.

4. Histo: chronic interstitial (productive) pneumonia: lymphocytic perivasculitis and peribronchitis, thickening of the walls of the alveoli and interlobular interstitial tissue due to lymphocytes, histiocytes, fibroblasts, focal pneumosclerosis.

The diagnosis (nosological) of visna-madi is made taking into account clinical and epidemiological data, the results of autopsies of sheep, histological examination of the lungs and brain. In these organs, pathognomonic pathomorphological changes are revealed: in the lungs - interstitial pneumonia, in the stem part and cerebellum of the brain - non-purulent lymphocytic demyelinating meningoencephalitis.

They differentiate medi from pulmonary adenomatosis, various types pneumonia, dictyocaulosis; visny - from sheep scrapie, coenurosis, listeriosis, rabies. Pulmonary adenomatosis differs from medi in that with it adenocarcinoma (glandular cancer) is noted in the lungs, and with medi - interstitial pneumonia. Pneumonia, by the nature of inflammation, refers to exudative inflammation in the lungs, while in case of medi it is productive inflammation. With dictyocaulosis, helminths and exudative pneumonia (catarrhal-purulent) are detected in the bronchi; with medi, interstitial pneumonia (productive).

Sheep scrapie differs from visna in that in the brain with it spongiform encephalopathy (dystrophic process) is observed, and with visna - non-purulent lymphocytic encephalitis.

Sheep coenurosis is characterized by the fact that coenurus blisters and atrophy of the medulla around the blisters are detected in the brain.

With listeriosis, unlike visna, in the brain (stem part) purulent encephalitis and the formation of micro- and macroabscesses of the brain of non-purulent lymphocytic encephalitis are detected: lymphocytic perivasculitis, rabies nodules, Babes-Negri bodies in the neurons of the ammonian horns and cerebellum.

2. Slow prion diseases of cattle and small ruminants

2.1 Scrape the sheep

Sheep scrapie is a slow infectious disease of prion etiology, characterized by nervous syndrome as a result of the development of spongiform encephalopathy in the central nervous system.

Etiology. The causative agent of the disease is an infectious prion (a specific protein that does not contain nucleic acids).

Pathogenesis. Infection occurs through the nutritional route. The pathogen spreads throughout the body hematogenously. It accumulates first in macrophages of the spleen, lymph nodes, thymus and other organs, then enters the central nervous system, where it causes encephalopathy (vacuolar degeneration of neurons and medulla), clinically manifested by nervous syndrome.

Clinical and epidemiological features. Animals 2-5 years of age and older are most often affected. The incubation period is long, several months and even years. Clinically pronounced disease lasts for several months (from 2 to 5 months) with a nervous syndrome. Ends fatal. There is no immune response or inflammation in the central nervous system.

Nervous syndrome: observed in sick animals increased sensitivity and severe itching of the skin, causing them to constantly itch various items(fence), excitement, anxiety, tremor (shaking) of the head, lips, ears, then depression, drowsiness, lack of coordination of movement - stumbling gait, marking time, fidgeting. Scratching and biting of the skin, scabs, and hemorrhages in the skin are observed. The animals are exhausted.

Pathomorphological changes. The corpses of emaciated animals, in the skin of the head and limbs - scratches and bites, scabs at the site of scratching, hyperemia and swelling of the brain. Histological examination of the gray matter of the stem part of the brain (quadrigemole, optic thalamus, pons and medulla oblongata), cerebellum, cervical part of the spinal cord reveals pathognomonic pathomorphological changes characteristic of spongiform encephalopathy: vacuolar degeneration of neurons, their cytolysis and pyknosis (wrinkling), vacuolization and swelling of astrocytes. Single large or multiple small vacuoles are found in neurons. The gray matter swells and may become soft. The number of vacuolated neurons in a histosection can be from 3 to 200.

Pathological diagnosis:

1. Scratching and biting the skin, scabs in their place, in the head, tail, buttocks, and limbs.

3. Wasting: lack of fat in the fat depot, atrophy of skeletal muscles, liver, kidneys and other organs.

4. Histo: spongiform encephalopathy: vacuolization of neurons and swelling of astrocytes in the stem and cerebellum of the brain, cervical spinal cord.

The diagnosis (nosological) is made taking into account clinical and epidemiological data, the results of autopsies and histological examination of the brain, electron microscopy.

They differentiate sheep scrapie from listeriosis, rabies, Aujeszky's disease, coenurosis, and scabies.

In case of listeriosis, histological examination of the brainstem and cervical part of the spinal cord reveals purulent encephalomyelitis with melting of the brain matter and the formation of macro- and microabscesses.

In case of rabies, overflow of the forestomach with dry food masses, general venous hyperemia, and dryness are noted. subcutaneous tissue and serous membranes. Histological examination in the stem part of the brain reveals morphological signs of non-purulent lymphocytic encephalitis: lymphocytic perivasculitis, rabies nodules, Babes-Negri bodies in the neurons of the ammonian horns and cerebellum.

Aujeszky's disease is accompanied by scratching of the skin and lacerations in the head and extremities, serous-hemorrhagic edema of the subcutaneous cell in the area of ​​scratching the skin and wounds. Histological examination in all parts of the brain reveals non-purulent lymphocytic encephalitis: lymphocytic perivasculitis, glial nodules, dystrophy and necrosis of neurons.

Coenurosis is characterized by the presence of coenurus blisters in the hemispheres, brain stem, cerebellum, atrophy of the medulla around the coenurus blisters, and atrophy of the bones of the skull.

Scabies (psorptosis) is an invasive disease caused by scabies mites, characterized by skin itching and dermatitis. During life, scrapings and biopsies from affected areas of the skin are examined in order to detect mites and their eggs.

2.2 Bovine spongiform encephalopathy

Bovine spongiform encephalopathy is a slow infectious disease of prion etiology, occurring with a nervous syndrome as a result of the development of spongiform encephalomyelopathy in the central nervous system.

Etiology. The causative agent of the disease is an infectious prion (a specific protein that does not contain nucleic acids).

Pathogenesis. Infection occurs through the nutritional route. The prion is first localized in macrophages of the tonsils, intestinal mucosa, lymph nodes (submandibular, retropharyngeal and mesenteric), spleen, from which it enters the spinal cord, then into the brain, causing a degenerative process in them (encephalopathy and myelopathy) in the form of vacuolization and neuronal necrosis and glial cells. Immunity does not develop with this disease.

Clinical and epidemiological features. The incubation period lasts from 2.5 to 8 years. The duration of clinically significant disease is from 1 to 5 or more months. Clinical symptoms appear only in adult animals (from 3 to 11 years). The outcome is fatal.

In sick animals, a nervous syndrome is detected: fearfulness, inadequate response to noise, touching the body (fright, falling); sometimes aggressiveness; grinding of teeth; muscle tremors in the lower neck, shoulder area, and sometimes the entire torso; increased pain sensitivity.

Ataxia: unsteady gait, weakness of the hind limbs, stumbling, entangling limbs, falling, movements similar to a horse trotting, swaying of the body, lowering of the pelvis. When jogging, all clinical symptoms clearly manifest themselves.

Pathomorphological changes. When opening corpses or carcasses of killed animals, emaciation is noted, characterized by the absence of fat in the fat depot, atrophy of skeletal muscles, liver, kidneys, spleen and other organs. Serous edema of the medulla is noted in the brain.

Histologically in the brainstem (quadrigeminal, pons, medulla oblongata) and cervical region spinal cord, pathognomonic pathomorphological changes characteristic of encephalo- and myelopathy (dystrophic process) are revealed. There is no inflammatory reaction. The gray matter of the brain and spinal cord is predominantly affected.

The most striking pathomorphological changes are detected in neurons of the brain and spinal cord; small or large vacuoles are visible in them, the cytoplasm has the appearance of a narrow belt, the nucleus is pyknotic and shifted to the periphery of the cell, which is why the vacuolated neuron with one large vacuole has a signet ring shape. Some neurons are in a state of swelling and cytolysis or shrinkage (cytopyknosis). Swelling and vacuolization of the pulpal nerve fibers located in the gray matter are also noted. Astrocytic glia in a state of edema, lysis or hypertrophy.

1. Wasting: lack of fat in the fat depot, atrophy of skeletal muscles, liver, kidneys, spleen and other organs.

2. Serous cerebral edema.

3. Histo: in the central nervous system - spongiform encephalopathy: in the stem part of the brain and cervical part of the spinal cord - vacuolar degeneration of neurons, edema, vacuolization and lysis of astrocytes, vacuolization and edema of pulpal nerve fibers.

The diagnosis (nosological) is made taking into account clinical and epizootological data, the results of autopsy of corpses or carcasses of killed animals, histological examination of the brain (stem part) and spinal (cervical part) of the cord.

Differentiate from listeriosis, Aujeszky's disease, rabies, and malignant catarrhal fever.

With listeriosis, hyperemia and swelling of the soft tissue are macroscopically noted. meninges and brain substances, weakly expressed hemorrhagic diathesis. Histological examination in the stem part of the brain (quadrigeminal, pons, medulla oblongata) and cervical part of the spinal cord reveals purulent encephalomyelitis with melting of the brain matter and the formation of macro- and microabscesses.

Aujeszky's disease is accompanied by scratching of the skin and lacerations in the head and limbs, serous-hemorrhagic swelling of the subcutaneous tissue in the area of ​​scratching the skin and wounds. Histopathological examination reveals non-purulent lymphocytic encephalitis (lymphocytic perivasculitis, glial nodules, dystrophy and necrosis of neurons) in all parts of the brain.

In case of rabies, overflow of the forestomach with dry food masses, general venous hyperemia, dryness of the subcutaneous tissue and serous membranes are noted. Histological examination in the stem part of the brain (quadrigemole, pons, medulla oblongata) reveals morphological signs of non-purulent lymphocytic encephalitis: lymphocytic perivasculitis, rabies nodules (glial nodules in place of necrotic and phagocytosed neurons), as well as Babes-Negri bodies in the neurons of the ammon's horns and cerebellum.

Malignant catarrhal fever is characterized by catarrhal-purulent conjunctivitis, keratitis, necrosis of the epidermis of the nasal mirror, necrosis of the mucous membrane of the oral cavity, tongue, purulent-fibrinous rhinitis, laryngitis, tracheitis, histo: non-purulent lymphocytic encephalitis in all parts of the brain (lymphocytic perivasculitis, glial nodules , degeneration and necrosis of neurons).

3. Slow viral and prion diseases of minks

3.1 Aleutian mink disease

Aleutian disease (viral plasmacytosis) of mink is a slow viral disease characterized by generalized plasmacytosis and hypergammaglobulinemia.

Etiology. The causative agent of the disease is a DNA genomic virus of the Parvoviridae family, genus Parvovirus.

Pathogenesis. The virus is immunotropic. Infection occurs through the nutritional and respiratory routes, through blood from bites and in utero. The virus causes differentiation (transformation) of B-lymphocytes into plasma cells that synthesize immunoglobulins, causing a generalized plasmacytic reaction (plasmocytosis) and hypergammaglobulinemia with the formation of immune complexes (virus-antibody), which, settling in tissues, cause cell damage, resulting in the appearance of autoantigens and autoantibodies and autoimmune pathological processes develop.

Clinical and epidemiological features. The incubation period is long and the disease develops slowly. In sick minks, depression, lethargy, thirst, bleeding from the nose and mouth, erosive and ulcerative bleeding rhinitis and stomatitis, and a tarry appearance of feces are noted. The content of gammaglobulins in the blood increases 3-5 times. Sick animals quickly lose weight, their eyes become sunken, and their fur becomes dull.

Pathomorphological changes. Corpses of emaciated animals with signs of exicosis. In the mucous membranes of the nasal and oral cavity, there are erosions and bleeding ulcers on the gums, hard and soft palate, stomach and intestines. Bleeding from the nose and mouth. Feces are tarry.

The spleen is enlarged 2-5 times or more in size (splenomegaly), the consistency is dense, the pulp on the cut is dark red-brown, the pattern of lymphoid nodules is enhanced. In some cases, the spleen is atrophied.

Lymph nodes (the entire system) are enlarged in size, gray-white or light brown in color (hyperplastic inflammation). The liver is enlarged in size, full-blooded, brown-red in color, with a pronounced pattern nutmeg, bile ducts cystically dilated, gallbladder empty. The kidneys are enlarged 1.5-2 times, their surface is slightly granular, gray-brown in color, in the cortex there are multiple pinpoint and spotty hemorrhages and multiple white miliary lesions; Often the buds are wrinkled, atrophied, the color is gray-yellow, the surface is lumpy.

During histological examination, pathognomonic pathomorphological changes are found in the bone marrow, spleen, lymph nodes, liver, kidneys in the form of generalized plasmacytosis. Extensive plasma cell infiltrates varying degrees maturity are localized: in the bone marrow everywhere, displacing hematopoietic tissue; in the spleen - around lymphoid nodules and in the red pulp; in the lymph nodes - medullary cords, cortex and lymphatic sinuses; in the liver - in the interlobular connective tissue around triads and sinusoidal capillaries; in the kidneys - around the vascular glomeruli and tubules.

In addition to the plasmacytic reaction, chronic cystic cholangitis, mucoid and fibrinoid swelling are found in the liver blood vessels microvasculature; in the kidneys - sclerosis and hyalinosis of the vascular glomeruli, granular and fatty degeneration of the convoluted tubule epithelium.

Pathological diagnosis.

1. Erosive-ulcerative bleeding rhinitis, stomatitis, gastroenteritis. Tarry feces.

2. Venous hyperemia, granular degeneration and nutmeg pattern in the liver.

3. Grainy and fatty degeneration kidneys, glomerular sclerosis.

4. Splenomegaly (2-5 times increase).

5. Exhaustion, general anemia, exicosis.

6. Histo: pathognomonic pathomorphological changes in the form of generalized plasmacytosis in the bone marrow, spleen, lymph nodes, liver, kidneys.

The diagnosis (nosological) is made taking into account clinical and epizootological data, the results of autopsy of mink corpses, histological examination of bone marrow, spleen, lymph nodes, liver, kidneys to identify pathognomonic plasmacytosis in them. In addition, the amount of gammaglobulins in the blood is determined intravitally, an immunoelectrophoresis reaction and an iodine agglutination test are used.

Differentiate from toxic liver dystrophy, nutritional dystrophy, pseudomonosis.

Toxic liver dystrophy - with it there is no generalized plasmacytosis in the organs.

With nutritional dystrophy, there is no generalized plasmacytosis in organs.

Pseudomonas is characterized by hemorrhagic pneumonia, which is associated with heavy bleeding from the nose and mouth. The disease is acute.

3.2 Transmissible encephalopathy of minks

Transmissible mink encephalopathy is a slow infectious disease of prion etiology, characterized by nervous syndrome and spongiform encephalopathy.

Etiology. The causative agent of the disease is an infectious prion.

Pathogenesis. Infection occurs through the nutritional route. From digestive tract The prion spreads hematogenously throughout the body, then penetrates the blood-brain barrier into the brain, causing a degenerative process in it - spongiform encephalopathy, accompanied by a nervous syndrome during life.

Clinical and epidemiological features. The incubation period is long, 7-9 months; adult minks are more often affected. There is no immune response or inflammatory reaction in the central nervous system.

The disease occurs with a nervous syndrome and ends in death. Sick minks are agitated, run around the cage, make circular movements and bite their tails. Excitement is replaced by depression, drowsiness, ataxia (paresis of the limbs, unsteady gait). May be observed epileptic seizures, self-chewing. The fur loses its shine and is disheveled.

Pathomorphological changes. Corpses of emaciated minks, in the brain - hyperemia and edema. There are no visible pathomorphological changes in other organs.

During histological examination, pathognomonic pathomorphological changes are found in the brainstem. These changes are characteristic of spongiform encephalopathy. In the stem part of the brain - the quadrigeminal region, the pons, medulla oblongata a dystrophic process is noted: vacuolar degeneration of neurons and gray intercellular matter, proliferation of astrocytes. In neurons, single large or multiple small vacuoles are detected. Some neurons undergo cytolysis and cytopyknosis (shrinkage), pericellular edema. There are no inflammatory changes.

Pathological diagnosis.

1. Exhaustion, lacerations tail

2. Hyperemia and cerebral edema.

3. Histo: spongiform encephalopathy in the brainstem (vacuolization of neurons and gray medulla, proliferation of astrocytes).

The diagnosis (nosological) is made taking into account clinical and epizootological data, the results of autopsies of mink corpses and histological examination of the brain, which determines spongiform encephalopathy. If at least 10 vacuolated neurons are detected in one histological specimen, especially with large vacuoles, in the absence of an inflammatory reaction, a final diagnosis of this disease is made.

Differentiate from vitamin B1 deficiency and self-gnawing.

With vitamin B1 deficiency, hyperemia, edema and hemorrhages are observed macroscopically in the brain; histologically - encephalopathy: hemorrhages, focal necrosis of the brain matter; in the liver - granular and fatty degeneration, necrosis of hepatocytes. Mortality - 20%.

Self-chewing is more common in puppies. In the brain, vacuolization, chromatolysis, pyknosis and lysis of neurons, swelling of the spinal cord pathways and white matter brain.

Table 1. Differential pathomorphological diagnosis of slow viral and prion diseases of large and small livestock.

Table 2. Differential pathomorphological diagnosis of slow viral and prion diseases of minks

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Infectious diseases, predominantly affecting the human central nervous system. General characteristics of slow infections. Factors causing the development of the disease. Subacute sclerosing panencephalitis. Diseases caused by prions.

presentation, added 11/27/2013


Slow viral infections, factors determining their development. Diseases caused by the measles virus. Subacute sclerosing panencephalitis. Characteristics of the rubella virus. Forms of prion protein. The process of accumulation of infectious prion molecules.

report, added 06/17/2012


Mechanism of transmission of pathogens of infectious diseases. Localization of the pathogen in the human body. Scheme of infectious diseases accompanied by skin lesions. Differential diagnosis exanthem and enanthem. Classification of infectious diseases.

abstract, added 10/01/2014


Malignant proliferation of cells of the hematopoietic organs with disruption of their maturation as the main cause of leukemia in cattle. Enzootic and sporadic forms of leukemia in cattle. Methods of prevention and control of the disease.

presentation, added 05/18/2016


B-lymphotropic RNA virus as the main causative agent of leukemia in cattle. Clinical manifestation of the disease. Pathomorphological changes in cattle with leukemia. Diagnosis of the disease, methods of its treatment and problems of prevention.

presentation, added 09/21/2016


Methods of ichthyopathological studies. Pathoanatomical dissection of fish. Rules for taking and sending pathological material for histological examination. Pathomorphological diagnosis of fish viruses and bacterioses. Cellular and humoral protective factors.

course work, added 05/25/2012


Study of traditional medical practitioners in the life of Russian peasants in the Russian North. Studying the causes of morbidity among peasants and the formation traditional views on the causes of diseases. Description traditional methods treatment of diseases.

Mink encephalopathy ENCEPHALOPATHY OF NOCKS(Infektiose enzephalopathie), an infectious disease characterized by a long incubation period and progressive dysfunction of the central nervous system. Common in the USA, Canada, Great Britain, East Germany, USSR and other countries. Mortality up to 100%.

It is believed that the causative agent E. n. is related to the pathogen, but unlike it, it acquires virulence for mice only after the first passage on animals of certain lines. Only adult minks (over 1 year old) get sick, more often in summer and autumn, then the disease subsides on its own. Minks are apparently infected by eating meat products obtained from the slaughter of sheep infected with scrapie virus. Immunity has not been studied. The incubation period is from 6 months to 1 year or more, the course of the disease is 26 weeks. Sick animals show excitement, aggressiveness, then depression, drowsiness, and fear. Pathomorphological changes in the central nervous system are characterized by a dystrophic process. The diagnosis is established on the basis of epidemiological data and clinical signs, taking into account the results of pathomorphological studies.

Treatment, prevention and control measures insufficiently developed. Sick animals are isolated. Carcasses of killed animals should not be allowed to feed minks; corpses must be removed from cages in a timely manner. It is advisable not to feed minks raw lamb by-products harvested in areas where sheep are vulnerable to scrapie.

Literature: Danilov E.P., Encephalopathy, in the book: Diseases of fur-bearing animals, ed. S. Ya. Lyubashenko, 2nd ed., M., 1973, p. 6467.

Veterinary encyclopedic Dictionary. - M.: "Soviet Encyclopedia". Chief Editor V.P. Shishkov. 1981 .

See what “Mink Encephalopathy” is in other dictionaries:

Slugin, Vladimir Stepanovich- Vladimir Stepanovich Slugin (1933 (1933) 2007) Honored veterinarian RSFSR, Doctor of Veterinary Sciences, Professor. Contents 1 Biography 2 Patents 3 ... Wikipedia

Prions- ICD 10 A81 ICD 9 046046 This term has other meanings, see Prions (meanings). Not to be confused with hypothetical elementary particles preons Prions (from the English p ... Wikipedia

Prion

Prion disease- Protein that forms β amyloids, a precursor of prions. Not to be confused with hypothetical elementary particles, prions. Prions (from the English proteinaceous infectious particles, protein infectious particles) are a special class. infectious agents, pure protein,... ... Wikipedia

Prion infection- Protein that forms β amyloids, a precursor of prions. Not to be confused with hypothetical elementary particles, prions. Prions (from the English proteinaceous infectious particles, proteinaceous infectious particles) are a special class of infectious agents, purely proteinaceous, ... ... Wikipedia

Encephalopathy (transmissible encephalopathy) is the least studied infection from the group of slow ones; affects minks, is characterized by a long incubation period, progressive dysfunction of the central nervous system and degenerative changes in the brain.
Spreading. The disease is registered only in the USA and Canada. Described by Hartsough, Burger in 1965. The first outbreaks of the disease were observed in 1947 in the state of Wisconsin, in 1961, 1963. in this state and the state of Idaho, as well as in Canada, in the province of Ontario.
Etiology. The causative agent of mink encephalopathy is prion. It has been established that according to physical and chemical properties it is similar to the scrapie pathogen. Its dimensions, as determined by filtration, are less than 50 nm. Resistant to ultraviolet radiation, boiling for 15 minutes, destroyed by the enzyme pronase, reduces infectious activity after treatment with ether for 18 hours at a temperature of 4°C. The infectious activity of the pathogen persists for 20 months of storage in a 10% formaldehyde solution. Attempts to isolate infectious nucleic acid from the brain tissue of sick animals using phenol extraction were unsuccessful.
Epizootology. 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.
Under the same housing and feeding conditions, as well as when the offspring were kept together with a sick female, cases of disease in young animals were not recorded in any of the described outbreaks. However, the fact of illness and death of the offspring was established 8-9 months after the death of the female. At the same time, young animals were observed to eat internal organs and carcasses of the corpse. Experiments have established the same sensitivity of newborn and adult minks to intracerebral infection. Apparently, selective encephalopathy in minks older than one year is explained not by different age-related sensitivity of animals, but by the characteristics of infectious process with slow infections, in particular the length of the incubation period, as well as the peculiarities of the biology of minks. There were also no differences in the sensitivity of minks depending on the breed or color of the animal’s fur.
The occurrence of an epizootic was observed after feeding minks meat believed to be contaminated with the scrapie pathogen. The minks were kept on a regular diet, which included raw meat, sometimes from forcedly killed livestock, offal, liver, and fish.
In 1961, in Wisconsin (USA), an outbreak affected animals on five farms that received feed from one factory. In 1963, the disease was observed on two more farms that also received feed from a common source.
The issues of the origin of the causative agent of encephalopathy, which have important epizootological significance, deserve closer attention and discussion.
Hartsough and Burger believe that minks play a minor role in the epizootology of the disease. The main host is apparently other animal species, which have not yet been definitively established.
The similarity of clinical and anatomical signs of scrapie in sheep and encephalopathy in minks, as well as the same properties of the causative agents of these infections, determine the legitimacy of raising the question of whether the disease in minks is the result of feeding them meat and offal of sheep infected with scrapie. Although direct evidence of the use of such products has not been obtained, such a possibility, as observations have shown, cannot be completely excluded. The results of experimental infection of minks indicate their sensitivity to the pathogen scrapie. Intracerebral infection of minks with a suspension of brain or spleen tissue from sheep infected with scrapie caused a typical picture of encephalopathy.
Goats, hamsters, albino ferrets, striped skunks, raccoons, rhesus monkeys, squirrel and short-tailed monkeys are susceptible to experimental infection.
20-28 months after intracerebral inoculation of goats with a suspension of the brain of sick minks, clinical signs of the disease (gait disturbance, eyelid ptosis, blindness) and histological changes in the brain characteristic of encephalopathy were observed in goats. Rhesus monkeys after subcutaneous, intramuscular, intravenous and oral infection remained clinically healthy for 33 months (observation period). However, histological examination of the brain revealed a polyencephalopathy similar to that observed in mink encephalopathy. It was also found in hamsters degenerative changes in the brain, characteristic of encephalopathy.
Minks became ill after inoculation with a suspension of hamster brains.
In infected white mice (Swiss strain), cats, and calves, no clinical signs of the disease or histological changes in the brain were observed, while the administration of a suspension of the brain of these animals to minks caused the latter to become ill. The question is being debated: does the pathogen replicate in this case or does it persist in the brain? Due to the fact that after the introduction of material obtained from animals that have not shown clinical signs, the picture of the disease in minks develops after a long incubation period (200-250 days), a conclusion is made about a low titer of the pathogen in the administered material and, therefore, about its possible persistence without replication.
Thus, the data discussed, in our opinion, do not establish a clear understanding of the connections between scrapie and mink encephalopathy, but only indicate the clinical and anatomical similarity of these diseases. It is not yet possible to draw definitive conclusions.
The disease can cause significant economic losses. The incidence ranges from 10-30 to 90-100%. Mortality is always 100%.
Pathogenesis has not been studied enough. It is similar to that of scrapie. The pathogen accumulates mainly in the cells and tissues of the lymphatic and central nervous systems, causing dystrophic and necrotic processes in them. Just like with scrapie, there is a lack of the body’s classic cellular and humoral response to the introduction of an infectious agent.
Symptoms The duration of the incubation period under natural conditions has not been established; it is considered to be from 8 to 12 months. During experimental infection by subcutaneous administration material, the incubation period lasts 5-6 months and 8 months when feeding tissues and organs from affected animals.
The disease develops slowly and imperceptibly, and always ends in death. At first, subtle deviations from normal animal behavior are observed. The instinct to maintain cleanliness disappears: the nest becomes dirty, droppings are not collected as usual in one place, but are scattered throughout the cage, food in the feeder is usually 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, like a squirrel, and animals with severely mutilated tails are often found. Soon symptoms of impaired motor coordination develop, the gait becomes stiff, and the gait is uncertain, shaky, jerky movements are observed. sudden movements hind limbs, sometimes cramps. Animals bite their tails, moving in a circle, and a gait disturbance is clearly visible. Then the movement disorders progress, and soon the animals almost completely lose the ability to move. However flaccid paralysis are never observed. 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 long time. During this period, they are half asleep, but can be easily awakened. Mild tremor is often observed. Vision, hearing, and tactile sensitivity are usually not impaired, the corneal reflex is preserved.
The disease lasts from 3 to 6 weeks and ends in the death of animals. Males, as a rule, die somewhat earlier than females.
Various unfavorable conditions, such as sudden temperature fluctuations, accelerate death. Dead animals are usually found in a characteristic position: in the corner of the cage with teeth tightly clenched on the mesh wire.
An asymptomatic course is possible, in which periodic refusals of food and progressive weight loss are noted.
Pathological changes. When examining the corpse, tissue dehydration and a sharp decrease in fat deposits are striking; the corpse is emaciated. In the brain - anemia and edema. There are no macro- or microscopic lesions of skeletal muscles, bones, or internal organs.
Histological changes. When examining brain sections, significant dystrophic changes are revealed. The most characteristic is diffuse vacuolization of the gray matter, leading to the formation of sponge-like areas in the brain tissue. Dystrophic changes in nerve cells, characterized by chromatolysis, sclerosis, pyknosis, are found in the cortex and brain stem and cerebellum. In neurons of the midbrain, pons and cerebellar peduncles, vacuolation of the cytoplasm is observed. Vacuoles vary in size, can be large or small, one or several in each neuron. They can be empty or contain eosinophilic inclusions. Typically, vacuoles are found in the cells of one or two gray matter nuclei and are absent in others.
IN initial stage lesions of brain tissue in neurons - small vacuoles, later they enlarge, merge and push the nucleus to the periphery of the cell. Vacuoles are also found in the intercellular substance of the brain. Located around the neuron, they are often deeply pressed into outer membrane cells.
In the cerebellum, pyknosis of Purkinje cells is noted. Severe astrocytosis and vacuolization of neuroglia are a consistent finding.
The diagnosis of transmissible encephalopathy is established on the basis of clinical (slow progressive increase in symptoms of damage to the central nervous system), epizootic data (high morbidity, 100% mortality, damage to animals over a year old), the results of histological examination.
Pieces of Ammon's horn and bark are selected for research. cerebral hemispheres in the area of ​​the lateral ventricle, fixed in a 10% solution of neutral formalin. Sections are stained with hematoxylin-eosin. Characteristic vacuolization of neurons in the gray matter of the cerebral cortex, hypertrophy and proliferation of astroglial cells are detected. Signs of inflammation are not detected. The period of histological examination is up to 7 days.
Differential diagnosis. When making a diagnosis, it is necessary to differentiate mink encephalopathy from self-gnawing, which affects puppies from 30 to 45 days of age and adult animals, while encephalopathy manifests itself only in adults. When self-gnawing in minks, clinical and pathological examinations reveal injuries that are absent in encephalopathy.
Immunity. As with other spongy encephalopathies, sick minks do not develop an immune response. Serological tests failed to detect specific antibodies.
Prevention and control measures. Specific prevention measures have not been developed. The main preventive measure is veterinary and sanitary control of meat fed to minks.

Bovine spongiform encephalopathy (BSE) is a slowly developing infectious prion vector-borne disease of adult cattle, characterized by a long incubation period of up to 2.5-8 years and manifested by damage to the central nervous system with 100% mortality.

Historical reference.

Spongiform encephalopathy was first reported in 1985–1986 in the UK under the name “mad cow disease”. Although there was previously evidence that a disease of this kind existed even earlier in 1965, when about 200 thousand cows aged 3 to 5 years fell ill.

Almost almost simultaneously this disease installed in Ireland.

Over the next 10 years, BSE spread to other countries - France, Portugal, Switzerland, Germany, the Netherlands, Italy, Denmark, Slovakia, Finland, etc. As a result of the importation of infected livestock, cases of BSE occurred in Canada, Israel, Oman, Japan, Australia.

To date, it has been established that BSE appeared as a result of exposure of cattle to scrapie (scrapie), a similar agent (the causative agent of scrapie in sheep), found in meat and bone meal, which was included in the diet of cattle.

The disease has not been registered in Russia.

Economic damage. BSE caused enormous economic damage to European countries, due to the fact that about 4 million heads of cattle were destroyed. The UK alone suffered economic losses amounting to £7 billion. As a result of BSE, devastation occurred large number farmers, the market for meat products has shrunk. The disease brought additional social tension, due to the fact that about 200 people died from it in the world and about 70 thousand people could get Creutzfeldt-Jakob disease for this reason.

Etiology. To date, the prion concept of BSE has been accepted in the world. Prion literally means “protein infectious particle.” It has very small dimensions (mm 28-30 KD) and high resistance to physical and chemical factors. In brain tissue and spleen, PrP 27-32 KD proteins polymerize to form specific scrapie-associated fibrils (SAF fibrils).

The pathogen itself is represented only by a protein without nucleic acid and therefore can withstand boiling, repeated freezing and thawing, and does not die at a temperature of 115 ° C for 30 minutes, at 90 ° C for 1 hour. Autoclaving (18 minutes at 134-138 ° C or with the same mode 6 cycles of 3 minutes). The pathogen can withstand the action of 12% formaldehyde and pH from 2 to 10.5 for several months. In a 20% formaldehyde solution, infectivity is not lost for 18 hours at 37°C.

As disinfectant use an 8% solution of sodium hydroxide, with exposure to the pathogen for 1 hour at a temperature of + 20°C. 2% sodium hypochlorite is relatively effective when exposed for 2 hours at a temperature of +20°C.

Epizootological data. Under natural conditions, cattle are susceptible to BSE, especially at 4 years of age, as well as artiodactyls of six species (South African antelope, kudu, and nyala, oryx, Arabian oryx, etc.) and felines of 4 species. Sheep, pigs, minks, rats, mice, hamsters and monkeys can be infected experimentally. Dairy cattle are more susceptible to the disease. BSE mainly affects cows, less often breeding bulls. When consuming slaughter products from patients with BSE, people may develop Creutzfeldt-Jakob disease. In this case, the brain and spinal cord of killed animals are especially dangerous to consume. Meat and milk from sick animals are, in principle, not dangerous, due to the fact that they contain prions in small quantities.

The source of the infectious agent is sick and incubating animals. Factors of transmission of the infectious agent are the products of slaughter of sheep infected with scrapie, and cattle infected with HE, including those in the incubation period of the disease.

The causative agent of the disease is transmitted from a sick animal to a healthy one through nutritional means, when eating contaminated food (meat and bone meal). Vertical transmission is possible (up to 10-20%), but it does not significantly affect the spread of the epizootic.

In Great Britain, the following reasons contributed to the spread of the disease:

• Increase in the number of sheep and increased volumes of processing (including heads) into meat and bone meal.
• Changes since the mid-70s of the 20th century in the country's recycling plants in the sterilization regimes for raw materials of animal origin (replacing heat treatment with drying with organic solvents).
• Increased milk production, which required earlier weaning of calves and their intensive fattening using meat and bone meal.

Ultimately, all this led to more mass application in the food chain of meat and bone meal, which turned out to be contaminated with prions.

Pathogenesis. The pathogenesis is not well understood. It is assumed that a pathogenic prion, having entered the body, usually replicates through the alimentary route in the spleen and other organs of the mononuclear phagocyte system (lymphoid organs), and then in the brain.

When an infectious prion protein enters healthy body animal, as a result of the connection of one molecule of the infectious prion protein PrPsrc with one molecule of the cellular (normal) prion protein PrPc, spatial changes occur in the latter molecule: two of the four helical structures in the cellular prion protein molecule are extended, etc. Under the influence of a prion, the favorite location of which is the brain, the animal develops encephalopathy, i.e. in the cerebellum, the stem part of the brain, cacuolization of neurons and gray medulla occurs, and astrocyte proliferation takes place. In this case, there is no inflammatory reaction. About a million infectious units per gram accumulate in the brain of a patient with BSE, while no infectious particles are found in muscle and milk. There is no pathogen in the bones (with the exception of the skull and vertebrae, which may contain remains of the brain) and skin of cattle with HSE. This is very important as they are used to make gelatin and collagen. Pathomorphological changes in the brain lead to the development of corresponding symptoms of the disease, accompanied by a nervous syndrome.

Course and symptoms of the disease. The incubation period ranges from 2.5 to 8 years, in some cases it can stretch up to 25-30 years. Animals over the age of 2 years are most often affected. The course of the disease is progressive, without remissions. The disease proceeds without an increase in the animal’s body temperature, with preserved appetite. Despite normal appetite, cows' milk production decreases. Clinical manifestations of the disease are observed in animals older than 2 years and are characterized by signs of damage to the central nervous system. With GE we detect three types of nervous phenomena.

The first type of nervous phenomena is accompanied by the development in animals of a feeling of fear, nervousness, especially when the animal enters a room, fear of doorways, aggressiveness (which is only a consequence nervous condition animal), grinding of teeth, restlessness, fearfulness, change of hierarchical place in the herd, desire to separate from the rest of the animals of the herd, excitability, trembling of individual parts of the body or the whole body, failure to recognize obstacles, kicking when handling them normally, ataxia of the hind limbs (the cow rises from gender like a horse), frequent movements of the ears, licking the nose, scratching the head with the foot, and about various objects. The above symptoms occur in 98% of sick animals.

The second type of nervous phenomena characterized by the presence in sick animals movement disorders: trotting movements, “raking with the front limbs”, “shaking” of the hind limbs - when the animal turns quickly, falling, raised tail.

With the third type of nervous phenomena Sensitivity disturbance occurs when in sick animals we notice hypersthesia with noise, touch and light.

The duration of the disease ranges from several weeks to 12 months or more. The disease always ends in the death of the animal.

Pathological changes. When autopsying dead animals, characteristic pathological changes are either absent or weakly expressed. We note signs of exhaustion; there may be cerebral edema. When conducting a histological examination, vacuolization of neurons is detected in the brain and spinal cord, a section of brain tissue has the appearance of a sponge (spongiosis) and some other changes characteristic of spongiform encephalopathy (hyperplasia and proliferation of astrocytes, the formation of amyloid plaques).

Diagnosis. The diagnosis of BSE is made comprehensively, taking into account:

• epidemiological data;
• characteristic clinical signs of the disease;
• pathohistological studies.

Lifetime laboratory diagnostics not developed. Due to the lack of an immune response in animals, antibodies for BSE are not produced, which is why serological diagnosis is not feasible.

The brains of dead or forcedly killed animals are sent to the laboratory.

Basic research methods:

• histopathological method (detection of spongy degeneration of neurons with the formation of vacuoles, mainly in the gray matter of the medulla oblongata and midbrain);
• detection of scrapie-like myofibrils with negative contrast (electron microscopy + histology);
• immunohistochemical methods (determination of prion protein by immunoblotting, method of fluorescent probes in immunoblotting);
• immunoenzyme method;
• bioassay on white mice when they are infected with brain homogenate;

Differential diagnosis.

BSE must first be differentiated from the following groups of diseases:

• diseases manifested by nervous phenomena (, Treatment.

  Treatment is ineffective because it begins when clinical signs appear, when irreversible pathomorphological changes have developed in the brain. The prognosis for the disease is unfavorable.

  Prevention.

  The basis of prevention for prosperous countries are:

  • preventing the import from disadvantaged areas or countries of breeding livestock, meat, canned food, offal and semi-finished products, meat and bone meal, sperm, embryos, technical fat, intestinal raw materials and other products and feed of animal origin from ruminants;
  • careful control over the purchase of breeding stock and biological tissues, especially from disadvantaged countries;
  • a ban on feeding ruminant animals meat and bone meal and bone meal from cattle and sheep;
  • a ban on the use of feed and feed additives of any unknown origin;
  • thorough diagnosis for any suspicious case and laboratory monitoring of brain samples from slaughter cattle, especially from animals over 3 years of age.

  Control measures.

  In disadvantaged countries, it is prohibited to add animal proteins to ruminant feed, biological tissues to animal diets, the use of bovine by-products in the biological and food industries, and so on. They diagnose BSE of sick animals and destroy the carcasses.

  Strict sterilization and disinfection methods are used.

  Pathological material, utensils, instruments, and workwear are disinfected using one of the following methods: autoclaving at excess pressure (134°C) for at least 20 minutes; keeping for 12 hours in one of the solutions - 4% sodium hydroxide, 2% sodium hypochlorite, 5% bleach; burning packaged disposable tools and utensils.

  The implementation of such strict measures in the UK made it possible at one time to sharply reduce the incidence and improve the health of a number of areas of the country from BSE.