Mink encephalopathy. Infectious encephalopathy of minks. Slow prion diseases in cattle and small cattle

Veterinary Dictionary

Mink encephalopathy

ENZOOTIC OSTEODYSTROPHY, disease of page - x. animals, characterized by a violation of phosphorus-calcium metabolism and structural changes in the skeleton. The cause of the disease in the zone South. Ural - deficiency in soil, water and feed of cobalt, manganese with an excess of strontium, boron, magnesium and nickel in them; in the Far East biogeochemical provinces - calcium deficiency with an excess of phosphorus salts; all in. and southeast. zones - a lack of phosphorus with a relatively small content of cobalt and copper.
E.'s symptoms about. similar to the signs of osteodystrophy that occurs with phosphorus-calcium and D-vitamin deficiency. But E. o., unlike osteodystrophy, manifests itself from year to year in the same x-wah, covering a large number of animals. Sick preim. productive and working livestock brought from other regions or countries.
E. o. (without treatment) in most cases ends in death from sepsis (pressure sores) and other complications (bronchopneumonia; traumatic reticulin, pericarditis). Basic diagnosis. on symptoms, pathologist. changes, X-ray photometry, blood tests, liver, bones, as well as feed (for the content of phosphorus, calcium and trace elements in them).
Prevention and treatment. Balance diets for mineral composition. Improve the forage composition of meadows and pastures. In biogeochemistry. provinces with a low content of cobalt, manganese and an excess of salts of strontium, barium and magnesium, animals are fed with salts of cobalt and manganese (respectively, 10 and 30 mg per 100 kg of body weight).
Sick animals are prescribed cobalt chloride up to 30 mg, manganese chloride up to 45 mg (per 100 kg of body weight). Animals are fed with these salts 2-3 times a year (Sept.-Oct., Jan.-Feb., Apr.-May) for 30-60 days. Also used symptomatically. treatment.

Source: Encyclopedic Agricultural Dictionary.

PESTICIDES (from lat. pestis - plague, infection and caedo - I kill), chemical. means that have a detrimental effect on organisms harmful to humans, animals and cultivated plants. P. usually means pesticides used in villages. and forest x-ve to control pests and pathogens of plants, weeds, as well as carriers of dangerous diseases

CONTRAPERTURE (from Latin contra - opposite and apertura - opening), counter-hole, additional surgical incision to ensure drainage (evacuation) of wound secretion or other fluid (blood, lymph). K. is made in the lowest part of the cavity filled with liquid. In order for K. not to close, gauze turundas, rubber, rubber are introduced into it.

REMOVAL OF TEETH, surgical surgery to remove a diseased or abnormally growing tooth. W. h. performed on recumbent animals after novocaine blockade of the maxillary, infraorbital or mandibular alveolar nerves. For horses, in addition, shallow chloral hydrate anesthesia is used, for carnivores - neuroleptic. means. In small animals

Made by Alena Ivanyuk

Infectious (transmissible) mink encephalopathy(Infectiosa encephalopathiae lutreolarum) is a little-studied disease characterized by a long incubation period, a slow course, damage to the central nervous system with an almost always fatal outcome. The disease is common in countries with artificial breeding of fur animals. Causes significant economic damage.

The causative agent of the disease- RNA genomic virus belonging to the family Retroviridae, subfamily Lentivirinae (slow retroviruses). Virions are spherical, 47 x 100 nm in size, covered with a lipid membrane. The virus is isolated from almost all organs of a sick animal, is found in the highest concentration in the brain, and is not found in the blood. Cultivated in glial cells of the brain.

The virus is extremely stable in the external environment. It is stored for years in faeces, urine and other pathological material. Not destroyed by ultraviolet irradiation, boiling for 15 minutes. Sensitive to phenol and formaldehyde.

Epizootology of the disease. The disease is observed among adult animals aged one year. Affected minks excrete the virus in their feces and urine. Infection occurs through the digestive canal when feeding feed contaminated with the pathogen. It is assumed that the mink is not a natural host of the causative agent of infectious encephalopathy, and the virus enters its body with raw meat, offal, and when raw lamb heads are fed from animals infected with the scrapie virus. The disease occurs mainly in summer and autumn. It is characterized by a very slow enzootic, which, however, under the influence of unfavorable conditions, can quickly cover the entire unfavorable herd and cause mass death of minks.

The pathogenesis is not well understood. From the digestive canal, the virus enters the bloodstream, spreads throughout the body, overcomes the blood-brain barrier and penetrates the central nervous system, causing lesions characteristic of encephalopathy, such as neuronal vacuolization and astrocytosis. Penetration and reproduction of the virus in the central nervous system also leads to the development of characteristic clinical signs - epileptic seizures, convulsions, paralysis, and impaired coordination of movements. The pathological process is often complicated by the addition of secondary bacterial infections.

Clinical signs and course of the disease. The incubation period lasts 6 - 12 months or more. The most characteristic are clinical signs that are predetermined by damage to the central nervous system. Manifested in a steady increase in the excitation of the animal and progressive ataxia, which periodically change with spontaneous convulsions and drowsiness. Sick minks run around the cage, make circular movements and bite their tails. Females do not pay any attention to their puppies, forget the acquired skills, scatter feces all over the cage. Excitation is replaced by oppression, drowsiness, ataxia, epileptic seizures develop, the fur loses its luster, becomes disheveled. The duration of the disease is 2-7 weeks, then death occurs, recovery does not happen. Before death in burrows, excitation and epileptic seizures are often noted.

Pathological and histological changes. In the internal organs are not observed. Sometimes there is an exhaustion of the beast, swelling of the brain and its membranes. All pathohistological changes are detected in the brain, during the study of which vacuolar degeneration of nerve cells and gray intercellular medulla, proliferation of astrocytic glia in the region of the vestibular nuclei, pons varolii and midbrain are established (N. I. Arkhipov, 1984). In the affected neurons, single or numerous vacuoles of various sizes and shapes are observed, some neurons are completely lysed. Particularly characteristic are large vacuoles, which occupy almost the entire cell, and the protoplasm appears in the form of a narrow rim along the periphery of the cell. There is also vacuolization and softening of the gray medulla, which leads to its porous (spongy) appearance. There are no inflammatory reactions.

Diagnosis is based on the analysis of clinical and epizootological data and pathomorphological studies of the brain. The diagnosis is considered established with the characteristic slow course of the disease in adult minks with damage to the central nervous system and the detection of at least 10 vacuolated nerve cells (especially large ones) in at least one histological specimen in the absence of an inflammatory reaction.

Differential diagnosis. Provides for the need to exclude avitaminosis B and self-mutilation. It should be borne in mind that infectious encephalopathy fatally affects only adult animals, while beriberi B and self-mutilation are observed among young minks and are accompanied by low mortality. Both of these diseases are characterized by the absence of a viral etiological factor. At autopsy of puppies who died with vitamin deficiency B, hyperemia of the brain, liver damage, hemorrhages under the endocardium and epicardium, and dermatitis are revealed. Histological examination establishes fatty degeneration and necrosis of hepatocytes, granular and vacuolar degeneration of neurons, proliferation and degeneration of the vascular endothelium, degeneration of the simyarid epithelium. Self-explosion occurs under the influence of various stress factors, manifested by excitation, itching, gnawing and injury to various parts of the body, followed by infection and suppuration of tissues. Histological studies reveal vacuolization and necrosis of brain neurons and spongiosis of the spinal cord pathways.

Treatment. No specific therapy has been developed. Symptomatic treatment is carried out, vitamins of group B and vitamin C are used.

Immunity. Taking into account the absence of cases of recovery of diseased minks, it can be argued that immunity is not formed in infectious encephalopathy.

Prevention and control measures. Means of specific prevention of this disease is not proposed. Minks suspected of infectious encephalopathy are transferred to an isolation ward, where they are kept until the slaughter period. The premises and cages where the infected animals were located, inventory and care items for them, are disinfected with a 5% solution of a sulfur-carbolic mixture, a 20% bleach solution, and, if possible, they are burned with a blowtorch. Females with encephalopathy observed in their broods are culled from breeding herds.

Mink encephalopathy (transmissible mink encephalopathy) is a pri-on disease characterized by progressive damage to the central nervous system, degenerative changes in the brain and death of animals.

Historical information, distribution, degree of danger and damage. The disease was first discovered in 1947, and then, after a long break, again in 1961 in a number of farms in the USA and Canada. Registered in North America and Europe (Finland, Germany, Russia), where it causes significant damage to fur farms.

The causative agent of the disease. A prion related to the sheep scrapie prion.

Epizootology. Sick adult mink older than 1 year. The source of the infectious agent is sick minks, the main transmission factor is contaminated feed. Animals become infected by eating infected meat (mink and sheep), offal, carcasses and corpses, during cannibalism. Morbidity 10 ... 100%, mortality 100%.

Pathogenesis. In general, it is similar to the pathogenesis of other prion diseases.

course and clinical about e pr about phenomenon. The incubation period lasts 8 ... 12 months. The course is slow and progressive. The duration of the disease from the onset of manifestation to the death of minks is 3-6 weeks.

At first, behavior changes: the so-called instinct of cleanliness disappears (the nest becomes dirty with droppings), then arousal increases, turning into aggressiveness. Minks overreact to sounds and touches, rush to objects; females stop caring for puppies, unsteady gait, ataxia of the hind limbs progress; then excitation is replaced by oppression - drowsiness, stupor develop; violation of coordination of movements, slight trembling turns into convulsions, epileptic seizures. Then comes complete immobility - the animals sit, clutching the mesh with their teeth, at the end of the disease blindness develops, the hind limbs are tucked in. Animal fur becomes dull, dirty, disheveled; note self-nibbling. Animals die in a coma.

Pat about log about anat about mimic signs. They observe mainly exhaustion, as a rule, there are no other signs of the disease. Anemia and cerebral edema, spleen atrophy, liver dystrophy are sometimes noticeable. Histologically, dystrophy of brain cells, non-purulent meningoencephalitis, spongy vacuolization of gray matter neurons of the brain (similar to other prion infections) are detected.

Diagn about tics and differential diagnostics. The diagnosis is established in a complex manner, taking into account epizootological signs, the clinical manifestation of the disease and the results of laboratory (histological) studies.

470 vany. In a laboratory study, vacuolization is noted most often in the cortex, ammon horn (hippocampus) and in the region of the lateral ventricles of the brain.

In differential diagnosis, rabies, Aujeszky's disease, botulism, self-gnawing should be excluded.

Immunity. Not formed.

specific prophylaxis. Missing.

Treatment. Not developed.

Prevention and control measures. Measures for the prevention and elimination of the disease include preventing the introduction of the pathogen into the farm with diseased minks; veterinary and sanitary control of incoming feed; prohibition of feeding raw lamb offal; timely diagnosis; isolation, slaughter of patients and disposal of carcasses and thorough disinfection in a hard mode.

Control questions and tasks for the section "Prion infections". 1. What is the main reason for the spread of spongiform encephalopathy in an unfavorable herd? 2. Describe the main changes in the brain of animals with prion infections. 3. What explains the lack of immunity in prion infections? 4. What are the basic principles for the rehabilitation of dysfunctional farms with bovine spongiform encephalopathy in cattle and scrapie sheep? 7. ANIMAL DISEASES CAUSED BY FUNGI

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MINISTRY OF AGRICULTURE AND FOOD

THE REPUBLIC OF BELARUS

UO “VITEBSK ORDER “Badge of Honour” STATE

ACADEMY OF VETERINARY MEDICINE”

COURSE WORK

on the topic: "Differential pathomorphological diagnosis of slow viral and prion animal diseases"

VITEBSK - 2011

Introduction

1. Slow viral diseases of small ruminants

1.1 Adenomatosis of the lungs of sheep

1.2 Wisna-medy sheep

2. Slow prion diseases in cattle and small cattle

2.1 Scrape the sheep

2.2 Bovine spongiform encephalopathy

3. Slow viral and prion diseases in minks

3.1 Aleutian mink disease

3.2 Transmissible mink encephalopathy

Introduction

Slow viral and prion diseases of ruminants and minks are a serious veterinary and medical problem, they cause great economic damage, causing the death of a large (sometimes all) animal population. The possibility of human infection with prion diseases from sick animals is not excluded.

The classification of slow infections is based on the following criteria: a long incubation period (months and years); long clinical course (several months), inevitably leading to death; disease of one species of animals (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 get sick, which is associated with a long incubation period during which viruses and prions persist in the body. Etiological factors in slow infections are viruses and prions. So, in sheep, viruses cause adenomatosis of the lungs, visnu-medi, prion - scrapie; in cattle, the prion is the cause of spongiform encephalopathy; in minks, the virus causes Aleutian disease, and the prion causes transmissible encephalopathy.

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

The description of slow infections is carried out according to the following scheme:

definition of illness;

Etiology;

Pathogenesis;

Clinical and epizootological features;

Pathological changes (macro- and microscopic);

Pathological anatomical diagnosis;

nosological diagnosis;

The diagnosis is differential.

The teaching aid provides tables of differential pathomorphological diagnosis of slow infections in animals.

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

1. Slow viral diseases of small ruminants

1.1 Adenomatosis of the lungs of sheep

Adenomatosis of sheep 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 Retroviridae family, Betaretrovirus genus. The virus has oncogenic properties, pneumotropic.

Pathogenesis. Infection occurs by the respiratory route. The virus causes tumor metaplasia of the squamous epithelium of the alveoli and the prismatic epithelium of the bronchioles, as a result of which a malignant tumor develops in the lungs - adenocarcinoma (glandular cancer). The tumor metastasizes to regional lymph nodes, pleura, peritoneum, mesentery, liver and other organs.

Clinical and epizootological features. Sick adult sheep 2 - 4 years of age. Young animals and goats rarely get sick. The incubation period varies from 4 to 9 months, it can last up to 3 years. The duration of a clinically pronounced disease is 2-8 months. The outcome is lethal. viral disease livestock encephalopathy mink

In sick animals, a respiratory syndrome is noted: depression, increased frequency and abdominal type of breathing, shortness of breath, which increases with a 20-minute run, wheezing during breathing, a wet, prolonged, severe cough, mucopurulent discharge from the nasal cavities. Emaciation with retained appetite.

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

Pathognomonic pathomorphological changes are found in the lungs - posterior and middle lobes. Tumor nodes of different sizes are visible in them - from miliary (with 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 a dense consistency, gray-white, yellow-white or pale pink, reminiscent of fish or boiled meat, are located under the pleura and in the depths of the lungs, sharply delimited from the surrounding tissue. Around them there may be hyperemia, edema and emphysema. The mass of the affected lungs increases to 2.5-3 kg at a rate of 300-500 g. The incision 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 of the tumor nodes reveals different sizes of cancerous nests. In them, the epithelium is cubic and prismatic, intensively multiplies, forming papillary outgrowths protruding into the cavity of the cancer nest. Cellular atypism is noted: 2-3-nuclear cancer cells, symplasts of cancer cells, their cubic and prismatic form, 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 be in the tumor.

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

Pathological anatomical 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 (cancerous 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 epizootological data, the results of the autopsy of the corpses of sheep and histological examination in the lungs. Pathological 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 of bacterial or viral etiology; dictyocaulosis.

When hanging sheep in the lungs, there are no pathomorphological changes. in the brain during a histological examination, non-purulent lymphocytic meningoencephalitis is noted in the brainstem (quadremium, pons, medulla oblongata) and cerebellum: lymphocytic perivasculitis, glial nodules and large cell infiltrates, focal necrosis of the medulla, demyelination of the pulpy 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 similarities with lung adenocarcinoma in sheep adenomatosis.

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

1.2 Wisna-medy sheep

Visna-mady sheep is a slow viral disease characterized by the development of non-purulent lymphocytic meningoencephalomyelitis (visna) or interstitial pneumonia (mady). Perhaps simultaneously inflammation of the central nervous system and lungs.

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

Pathogenesis. The virus is neuro- and pneumotropic. Infection occurs by the respiratory route, and in lambs - by the alimentary route through the milk of a sick ewe. The reproduction of the virus is carried out in the cells of the 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 epizootological features. The incubation period is several months and years. The clinical stage of the disease lasts several months and ends fatally. Sheep 3-4 years of age and older get sick more often.

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

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

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

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

Pathological anatomical diagnosis of visna

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

2. Hyperemia of the brain and vascular plexuses of the lateral cerebral ventricles.

3. Histo: non-purulent lymphocytic demyelinating meningoencephalomyelitis.

When Madi sheep 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 section - 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 walls of the alveoli due to lymphocytes, histiocytes, plasmocytes, fibroblasts. The same is in the interlobular interstitial connective tissue. In the later stages of the disease, foci of pneumosclerosis are detected. Bronchial and mediastinal lymph nodes are enlarged 3-5 times, in a state of hyperplastic inflammation.

Pathological anatomical diagnosis

1. Chronic lobar interstitial pneumonia.

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

3. Depletion: 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-mady is made taking into account clinical and epizootological data, the results of the autopsy of the corpses of sheep, histological examination of the lungs and brain. In these organs, pathognomonic pathomorphological changes are revealed: in the lungs - interstitial pneumonia, in the brain stem and cerebellum - non-purulent lymphocytic demyelinating meningoencephalitis.

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

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

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

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

2. Slow prion diseases in cattle and small cattle

2.1 Scrape the sheep

Scrapie of sheep is a slow infectious disease of prion etiology, characterized by a 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 in an alimentary way. The causative agent spreads throughout the body hematogenously. It accumulates first in the 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), which is clinically manifested by a nervous syndrome.

Clinical and epizootological features. More often animals 2-5 years of age and older get sick. The incubation period is long, several months and even years. Clinically expressed illness proceeds within several months (from 2 to 5 months) with a nervous syndrome. Ends in death. There is no immune response and inflammation in the CNS.

Nervous syndrome: in sick animals, there is increased sensitivity and severe itching of the skin, which is why they constantly itch on various objects (fence), agitation, anxiety, tremor (trembling) of the head, lips, ears, then depression, drowsiness, impaired coordination of movement - stumbling gait, stomping on the spot, whirling. There are scratches and bites of the skin, scabs, hemorrhages in the skin. Animals are exhausted.

pathological changes. Corpses of emaciated animals, in the skin of the head, limbs - scratching and bites, scabs at the site of scratching, hyperemia and swelling of the brain. Histological examination in the gray matter of the brainstem (quadrigemina, optic tubercle, 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 pycnosis (wrinkling), vacuolization and edema of astrocytes. Neurons contain single large or multiple small vacuoles. The gray matter swells and may soften. The number of vacuolated neurons in a histosection can be from 3 to 200.

Pathological anatomical diagnosis:

1. Scratches and bites of the skin, scabs in their place, in the head, tail, buttocks, limbs.

3. Depletion: 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 brain stem and cerebellum, cervical part of the spinal cord.

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

Differentiate scrapie sheep from listeriosis, rabies, Aujeszky's disease, coenurosis, scabies.

With listeriosis, histological examination in the brain stem and cervical part of the spinal cord reveals purulent encephalomyelitis with melting of the medulla and the formation of macro- and microabscesses.

With rabies, overflow of the proventriculus with dry feed masses, general venous hyperemia, dryness of the subcutaneous tissue and serous membranes are noted. Histological examination in the brain stem revealed morphological signs of non-purulent lymphocytic encephalitis: lymphocytic perivasculitis, rabies nodules, Babesh-Negri bodies in the neurons of the ammon horns and cerebellum.

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

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

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

2.2 Bovine spongiform encephalopathy

Bovine spongiform encephalopathy is a slow infectious disease of prion etiology that occurs 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 in an alimentary way. The prion is first localized in macrophages of the tonsils, intestinal mucosa, lymph nodes (submandibular, pharyngeal and mesenteric), spleen, from which it enters the spinal cord, then the brain, causing a dystrophic process in them (encephalopathy and myelopathy) in the form of vacuolization and necrosis of neurons and glial cells. Immunity in this disease is not formed.

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

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

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

pathological changes. When opening the corpses or carcasses of slaughtered 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 (quadrigemina, pons, medulla oblongata) and the cervical spinal cord, pathognomonic pathomorphological changes characteristic of encephalo- and myelopathy (dystrophic process) are detected. There is no inflammatory response. The gray matter of the brain and spinal cord is predominantly affected.

The most striking pathomorphological changes are detected in the neurons of the brain and spinal cord, small or large vacuoles are visible in them, the cytoplasm looks like a narrow belt, the nucleus is pycnotic and shifted to the cell periphery, which is why a vacuolized neuron with one large vacuole has a cricoid shape. Some neurons are in a state of swelling and cytolysis or wrinkling (cytopyknosis). There is also swelling and vacuolization of the pulpy nerve fibers located in the gray matter. Astrocyte glia in a state of edema, lysis or hypertrophy.

1. Depletion: 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 CNS - spongiform encephalopathy: in the stem part of the head and cervical part of the spinal cord - vacuolar degeneration of neurons, edema, vacuolization and lysis of astrocytes, vacuolization and edema of the pulpy nerve fibers.

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

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

With listeriosis, hyperemia and edema of the pia mater and brain substance, mild hemorrhagic diathesis are noted macroscopically. Histological examination in the stem part of the brain (quadrigemina, pons, medulla oblongata) and the cervical part of the spinal cord reveals purulent encephalomyelitis with melting of the medulla 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 edema of the subcutaneous tissue in the area of scratched skin and wounds. During histoexamination, non-purulent lymphocytic encephalitis (lymphocytic perivasculitis, glial nodules, dystrophy and necrosis of neurons) is noted in all parts of the brain.

With rabies, overflow of the proventriculus with dry feed masses, general venous hyperemia, dryness of the subcutaneous tissue, and serous membranes are noted. Histological examination of the brainstem (quadrigemina, pons, medulla oblongata) reveals morphological signs of non-purulent lymphocytic encephalitis: lymphocytic perivasculitis, rabies nodules (glial nodules in the place of necrotic and phagocytosed neurons), as well as Babesh-Negri bodies in the neurons of ammon 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 dystrophy and necrosis of neurons).

3. Slow viral and prion diseases in minks

3.1 Aleutian mink disease

Aleutian disease (viral plasmacytosis) of minks 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, Parvovirus genus.

Pathogenesis. The virus is immunotropic. Infection occurs through the alimentary and respiratory route, through the blood during 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 develop autoimmune pathological processes.

Clinical and epizootological features. The incubation period is long, the disease develops slowly. In sick minks, oppression, lethargy, thirst, bleeding from the nose and mouth, erosive and ulcerative bleeding rhinitis and stomatitis, tarry appearance of feces are noted. In the blood, the content of gamma globulins increases by 3-5 times. Sick animals quickly lose weight, eyes sink, fur becomes dull.

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

The spleen is enlarged in size by 2-5 times or more (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 (entire system) are enlarged, gray-white or light brown in color (hyperplastic inflammation). The liver is enlarged, full-blooded, brown-red in color, a nutmeg pattern is expressed, the bile ducts are cystically dilated, the gallbladder is empty. The kidneys are enlarged 1.5-2 times, their surface is slightly granular, gray-brown in color, in the cortical substance there are multiple dotted and spotty hemorrhages and multiple white miliary foci; often the kidneys are wrinkled, atrophied, the color is gray-yellow, the surface is bumpy.

Histological examination reveals pathognomonic pathomorphological changes in the bone marrow, spleen, lymph nodes, liver, kidneys in the form of generalized plasmacytosis. Extensive infiltrates from plasma cells of varying degrees of maturity are localized: in the bone marrow everywhere, displacing the hematopoietic tissue; in the spleen - around the lymphoid nodules and in the red pulp; in the lymph nodes - cerebral cords, cortical substance and lymphatic sinuses; in the liver - in the interlobular connective tissue around the triads and sinusoidal capillaries; in the kidneys - around the vascular glomeruli and tubules.

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

pathological diagnosis.

1. Erosive and ulcerative bleeding rhinitis, stomatitis, gastroenteritis. Tar-like feces.

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

3. Granular and fatty degeneration of the kidneys, sclerosis of the vascular glomeruli.

4. Splenomegaly (2-5 times increase).

5. Exhaustion, general anemia, exsicosis.

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 the autopsy of mink corpses, histological examination of the bone marrow, spleen, lymph nodes, liver, kidneys to identify pathognomonic plasmacytosis in them. In addition, the amount of gamma globulins in the blood is determined in vivo, the immunoelectrophoresis reaction and the iodine agglutination test are used.

Differentiate from toxic liver dystrophy, alimentary dystrophy, pseudomonosis.

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

With alimentary dystrophy, there is no generalized plasmacytosis in the organs.

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

3.2 Transmissible mink encephalopathy

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 in an alimentary way. From the digestive tract, the prion spreads hematogenously throughout the body, then penetrates through the blood-brain barrier into the brain, causing a dystrophic process in it - spongiform encephalopathy, accompanied by a nervous syndrome during life.

Clinical and epizootological features. The incubation period is long, 7-9 months, adult minks are more likely to get sick. There is no immune response and inflammatory response in the CNS.

The disease proceeds with a nervous syndrome and ends fatally. Sick minks are excited, run around the cage, make circular movements and bite their tails. Excitation is replaced by depression, drowsiness, ataxia (paresis of the limbs, unsteady gait). There may be epileptic seizures, self-gnawing. Fur loses its luster, disheveled.

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

Histological examination reveals pathognomonic pathomorphological changes in the brain stem. These changes are characteristic of spongiform encephalopathy. In the stem part of the brain - the quadrigemina, the pons varolii, the medulla oblongata, a dystrophic process is noted: vacuolar degeneration of neurons and gray intercellular substance, proliferation of astrocytes. Single large or multiple small vacuoles are detected in neurons. Some neurons undergo cytolysis and cytopyknosis (wrinkling), pericellular edema. There are no inflammatory changes.

pathological diagnosis.

1. Exhaustion, lacerations of the tail.

2. Hyperemia and cerebral edema.

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

The diagnosis (nosological) is made based on clinical and epizootological data, the results of the autopsy of mink corpses and histological examination of the brain, in which spongiform encephalopathy is determined. If at least 10 vacuolated neurons, especially with large vacuoles, are found in one histological preparation, in the absence of an inflammatory reaction, the final diagnosis of this disease is made.

Differentiate from avitaminosis B 1 and self-gnawing.

With avitaminosis B 1, hyperemia, edema and hemorrhages are noted macroscopically in the brain; histologically - encephalopathy: hemorrhages, focal necrosis of the medulla; in the liver - granular and fatty degeneration, hepatocyte necrosis. Lethality-20%.

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

Table 1. Differential pathomorphological diagnosis of slow viral and prion diseases in cattle and small ruminants.

Name of the disease				Other organs

Adenomatosis of the lungs of sheep (virosis)		Adenocarcinoma. Metastases in regional lymph nodes, pleura, peritoneum, mesentery, liver, kidneys, spleen.		exhaustion
Wisna-medi sheep (viroz)	Wisna. Histo: non-purulent demyelinating lymphocytic meningoencephalitis in the brainstem (lymphocytic perivasculitis, glial nodules)	Madi: chronic interstitial pneumonia, pneumosclerosis		exhaustion
Scrape sheep (prion disease)			Skin scratches and lacerations	exhaustion
Bovine spongiform encephalopathy (prion disease)	Histo: spongiform encephalopathy in the brain stem (vacuolization of neurons and glial cells)			exhaustion
Sheep listeriosis (bacteriosis)	Histo: purulent encephalomyelitis in the stem part of the brain and cervical part of the spinal cord
Aujeszky's disease of sheep (virosis)			Skin scratches and lacerations
Sheep rabies (virosis)	Histo: non-purulent lymphocytic encephalitis in the brainstem: lymphocytic perivasculitis, rabies nodules, Babes-Negri bodies in the neurons of the ammon horns and cerebellum		Combing the skin at the site of the bite	Overfilling of the proventriculus with dry feed masses; general venous hyperemia; dryness of the subcutaneous tissue and serous membranes
MCG in cattle (virosis)	Histo: non-purulent lymphocytic encephalitis in all parts of the brain (lymphocytic perivasculitis and glial nodules)		Catarrhal-purulent conjunctivitis, keratitis, purulent-fibrinous rhinitis, laryngitis, tracheitis, necrotic stomatitis

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

№ №	Name of the disease		Bone marrow, spleen, lymph nodes, liver, kidneys, blood	Digestive tract, respiratory tract	Other organs
	Aleutian mink disease (virosis)		Macro: granular and fatty degeneration of the liver and kidneys; splenomegaly; hyperplastic (systemic) lymphadenitis. Histo: generalized plasmacytic infiltration (diffuse plasmacytosis) in the bone marrow, spleen, lymph nodes, liver, kidneys.	Erosive and ulcerative rhinitis, stomatitis, gastroenteritis, bleeding ulcers in the nasal and oral cavity, stomach and intestines (bleeding from the nasal and oral cavities); tarry feces.	Wasting, general anemia, exsicosis
	Transmissible mink encephalopathy (prion disease)	Macro: hyperemia and cerebral edema. Histo: spongiform encephalopathy in the brainstem (vacuolization of neurons and gray matter, proliferation of astrocytes)			Exhaustion, tail lacerations
	Avitaminosis B 1	Macro: hyperemia, edema and hemorrhages in the brain. Histo: encephalopathy - hemorrhages and focal necrosis in the medulla.	Granular dystrophy of the liver, kidneys, myocardium	Chronic atrophic catarrhal gastroenteritis, erosive enteritis	Wasting, general anemia

Mink encephalopathy. Infectious encephalopathy of minks. Slow prion diseases in cattle and small cattle

Mink encephalopathy

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Introduction

1. Slow viral diseases of small ruminants

1.1 Adenomatosis of the lungs of sheep

1.2 Wisna-medy sheep

2. Slow prion diseases in cattle and small cattle

2.1 Scrape the sheep

2.2 Bovine spongiform encephalopathy

3. Slow viral and prion diseases in minks

3.1 Aleutian mink disease

3.2 Transmissible mink encephalopathy

Introduction

Slow viral and prion diseases of ruminants and minks are a serious veterinary and medical problem, they cause great economic damage, causing the death of a large (sometimes all) animal population. The possibility of human infection with prion diseases from sick animals is not excluded.

The description of slow infections is carried out according to the following scheme:

definition of illness;

Etiology;

Pathogenesis;

Clinical and epizootological features;

Pathological changes (macro- and microscopic);

Pathological anatomical diagnosis;

nosological diagnosis;

The diagnosis is differential.

Pathological anatomical diagnosis of visna

Pathological anatomical diagnosis

Table 1. Differential pathomorphological diagnosis of slow viral and prion diseases in cattle and small ruminants.

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

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