Animal anatomy, histology, pathological anatomy

BIBLIOGRAPHY
1. Zharov A.V. Pathological anatomy of animals. – St. Petersburg; M.; Krasnodar: Lan, 2013. – 620 p. – Access mode: EBS “Lan” (http://e.lanbook.com), ISBN: 978-5-8114-1450-5 2. Zharov A.V. Forensic veterinary medicine. Textbook. – St. Petersburg; M.; Krasnodar: Lan, 2014. – 464 p.

LECTURE No. 10

PATHOMORPHOLOGY OF REMIERY AND INFECTIOUS ANEMIA IN HORSES.

Plan
1. Etiology, pathogenesis and pathological anatomy, diagnosis and comparative diagnosis of rabies.
2. Etiology, pathogenesis and pathological anatomy, diagnosis and comparative diagnosis of infectious anemia in horses.
Keywords: Aujeszky, botulism, piroplasmosis,infectious anemia,rabies, Babesha-Negri.
1. Rabies. (RABIES - fear of water) is a contagious disease. Clinically and anatomically, all species of animals and humans suffer from severe damage to the nervous system and encephalomyelitis, the formation of rabies nodules in the brain and Babes Negri bodies.
Etiology and pathogenesis The disease is caused by a virus that is transmitted through irritated tears, salivary fluid, pancreatic fluid, and in some cases through broken skin or recently damaged areas. All infected animals die. When the virus enters an injury, it spreads along nerve fibers, reaches the brain and spinal cord and multiplies there. The incubation period of the incubation period lasts 30–40 days, the disease lasts 5–7 days.
Pathanatomy: Specific changes are observed only in wild animals. Changes are not typical for other species. We see the following changes in the body of a dead dog: the body is very thin, the mucous membranes of the mouth are bluish-red, exudate in the corners of the eyes, a large amount of saliva around the mouth. wounds and erosions appear on the gums, tongue and oral mucosa. The most characteristic change is in the stomach. There are no foreign bodies in the stomach, no food is visible, the gastric mucosa is thickened and swollen, hemorrhages and wounds are observed on the surface of the folds, forming hard folds, stagnation of the remaining internal organs is characterized by hyperemia. In C.R.S, dried food is visible in the anterior parts of the stomach, and wrinkles and hemorrhages are sometimes observed in the gastric mucosa. Dogs have subcutaneous dehydration. Dystrophic changes are observed in parenchymal organs. With rabies in dogs, Babes Negri can be 95%, and in other animals - 75%. Babes Negri bodies may also not be detected in animals examined during the incubation period of the disease.
Diagnosis and comparative diagnosis of rabies is based on clinical signs, pathological changes, and histological examination. Rabies differs from the following diseases, false rabies (Aujeszky), neuroses, gastritis, stomatitis, proteinuria. In Aujeschi, the corpses of Babes-Negri are not formed, but the clinic is similar. Rabies differs from the above diseases in pathogenesis and the formation of rabies nodules.
Rabies (Rabies) is an acute viral disease of animals and humans, characterized by transmission of the virus through a bite with saliva and signs of severe damage to the central nervous system. Pathogen: RNA containing virus, resistant to low temperatures, destroyed instantly when boiled. All warm-blooded animals are susceptible. The fox, jackal, and wolf are most sensitive to it. The susceptibility of cats and cattle is considered high, the susceptibility of dogs, sheep, goats, horses and primates is considered medium, and the susceptibility of birds is low. Young animals are more sensitive to the virus than adults. The sources of the pathogen are sick animals that secrete the virus in their saliva and transmit it through a bite. Saliva can become infectious within 8-10 days. before signs of illness appear. Infection is possible when saliva gets on mucous membranes or damaged skin. The experiment succeeds in transmitting the rabies virus through nutritional and aerogenic routes. Pathogenesis. The virus, which has entered the body of a susceptible animal, moves along the centripetal nerve trunks to the brain and spinal cord, where it multiplies and causes non-suppurative polioencephalitis. The virus enters the salivary glands along the centrifugal nerves, multiplies in the nerve ganglia and, after their destruction, appears in the saliva. The largest amount of virus is found in the horns of ammon, the medulla oblongata, the cerebellum, in the nuclei of the cranial nerves and in the lumbar part of the spinal cord. The virus first causes irritation of nerve cells, and then their destruction and paralytic phenomena. 105 Symptoms: in dogs - unbalanced behavior, impaired swallowing, drooling, aggressiveness. In cattle - more often paralysis, less often aggressiveness, drooling, and impaired swallowing. The picture is similar for sheep and camels. Horses and pigs often have a violent form. Pathological changes. At autopsy, the corpses are emaciated, there may be traces of bites, scratches on the skin, and in carnivores - injuries to the lips, damage to the teeth. Congestive hyperemia of internal organs is noted. The stomach is usually empty, but sometimes inedible objects are encountered, especially in carnivores. Often the mucous membrane of the stomach and small intestine is catarrhally inflamed, with hemorrhages. The brain and its membranes are edematous, with pinpoint hemorrhages. Histologically: diffuse non-purulent encephalitis. The cytoplasm of ganglion cells is characterized by the presence of Babes-Negri bodies. In rabies spread by wild predators, these bodies are found relatively rarely. In cattle, overflow of the proventriculus with feed masses due to their atony, dehydration, exhaustion, and minor hemorrhages in the mucous membrane of the abomasum and under the peritoneum are noted. The liver and kidneys are filled with blood. The mesenteric lymph nodes are swollen. In the brain there is hyperemia, swelling of the medulla and pia mater. Diagnostics. The laboratory conducts histological studies of the brain to detect Babes-Negri bodies, immunoluminescence microscopy, RP in agar gel, identification of the virus by neutralization reaction and bioassay on young white mice or rabbits. A fresh corpse (small animal) or head or brain is sent to the laboratory. Suspicion of rabies may arise from poisoning, colic and other diseases accompanied by pain and anxiety of the animal, as well as the presence of foreign bodies in the mouth or pharynx. Differential diagnosis. It is necessary to differentiate from Aujeszky's disease, listeriosis, malignant catarrhal fever, infectious encephalitis. For Aujeszky's disease: severe itching, especially in the head area and a more acute course, but there is no paralysis and no aggressiveness. In the nervous form of listeriosis there is no aggressiveness and paralysis of the lower jaw. In malignant catarrhal fever, agitation is rare. With infectious encephalitis, severe yellowness of the mucous membranes and lack of aggressiveness are noted. Veterinary and sanitary examination. If rabies is detected in animals, slaughter for meat is prohibited. If rabies is detected during slaughter and cutting of carcasses, then all slaughter products must be destroyed by burning. Slaughter animals that have been bitten by rabid animals, but do not have clinical signs of the disease, are allowed to be killed directly on the farm. The bite sites are cleaned and destroyed, and the VSE of slaughter products is carried out on a general basis. Animals vaccinated against rabies with rabies vaccine are allowed to be killed for meat 3 months after vaccination. Disinfection of the room where sick animals were located, as well as equipment, is carried out with a hot 10% solution of caustic soda or a 4% solution of formaldehyde. Wooden care items and leftover food are burned. The soil contaminated by the secretions of sick animals is dug up to a depth of 30 cm with dry lime and filled with a disinfectant solution. Laboratory workers must comply with established safety precautions when conducting research. Human rabies. People usually become infected when bitten or salivated by a rabid animal (mainly a dog, but also a wolf, cat, fox, etc.). The most dangerous bites are to the head, face, and hands. The incubation period is from 12 days. up to 1 year, on average 30-90 days. There are 3 periods of the disease: prodromal, period of excitement and paralysis. The disease lasts 3-7 days. Possibly an atypical course. Anti-rabies vaccinations are carried out when a person is suspected or overtly infected. 18.5. Characteristics of changes in B. Aujeszkyi (Morbus Aujeszkyi, Pseudorabies) Aujeszky's disease (synonyms: false rabies, pseudorabies, infectious bulbar palsy) is an acute viral disease of all types of agricultural, domestic and wild animals; characterized by damage to the central nervous system, severe itching and deep scratching (in various animal species, except pigs). In dogs, the disease usually ends in death. Pathogen. The disease is caused by a DNA virus of the herpes virus family. The pathogen is not resistant to high temperatures and dies within 15 minutes at 70°C. Susceptible are pigs, large and small livestock, horses, dogs, cats, chickens, ducks, rabbits, guinea pigs, white rats, mice, arctic foxes, minks, sables and other animals. However, pigs, which are the main reservoir host of the disease pathogen, are most susceptible to the disease. At the same time, in adult pigs the disease is usually benign, but in newborns the mortality rate reaches 70-100%. A person is little susceptible to the disease. The source of the infectious agent is sick, recovered pigs and virus carriers capable of releasing the virus into the external environment for up to 10-12 months, as well as rodents. Infection occurs nutritionally, aerogenously. The incubation period is 1-9, sometimes 15 days. B. Aueschi is characterized by a lack of seasonality and a tendency towards stationarity, due to long-term virus carriage. Symptoms In dogs and cats, the disease usually occurs in an acute form and ends in the death of the animal. Initially, a sharp decrease in appetite, and later a complete refusal to feed (anorexia), anxiety, fearfulness and profuse drooling. Then the animals experience increased excitability and characteristic severe itching in the head area, as well as in certain areas of the body and limbs. Itching (modified pain sensation) in animals can be localized or generalized. In approximately 50% of sick animals, the itching is so unbearable that they become uncontrollable and scratch or chew the itchy areas very hard, down to the subcutaneous tissue. Itching, deep painful scratching and developing encephalomyelitis cause behavior that is reminiscent of rabies in some symptoms: animals constantly whine, howl or bark, roll on their backs, chew various foreign objects, sometimes rush at other animals, but unlike rabies, they are rarely aggressive. In addition, sick animals drink water greedily. 107 There may sometimes be little or no itching. The height of the disease lasts 1-2 days, and the initial stage of excitement quickly turns into deep depression, caused by severe mental and physical exhaustion of the animal (asthenic depression) and severe organic damage to the brain (symptomatic depression). Animals develop paralysis of the pharynx, larynx, clonic convulsions, etc. Death occurs within 48 hours after the initial clinical signs of the disease. B. Aueschi in pigs manifests itself depending on age. In infected sows, reproduction is impaired (death and resorption of fetuses, abortions, birth of still and non-viable piglets). Piglets are born sick or become ill, becoming infected through colostrum and mother's milk, and almost all die in the first days after birth. Piglets up to 3 months of age become ill with signs of nervous system disorders. Older pigs show signs of respiratory disease and develop pneumonia. Pathological changes. During an external examination of the corpses of dogs and cats, deep scratches are found in the head, torso and limbs. When opening the brain, hyperemia and swelling of the meninges and pinpoint hemorrhages are detected. Histological studies of the brain and spinal cord show non-purulent meningoencephalitis. Diagnosis. The disease is diagnosed on the basis of epidemiological, clinical and pathological data, as well as the results of laboratory tests. For laboratory diagnostics, the methods of IF, RDP, RN, RSK, bioassay, etc. are used. In differential diagnosis, rabies, canine distemper, generalized demodicosis, toxoplasmosis, and skin allergic reactions are excluded. Questions for self-control 1. Pathomorphological signs of bird pox. 2. Pathological signs of swine pox. 3. Pathomorphological signs of foot and mouth disease. 4. Pathomorphological signs of infectious anemia. 5. Pathomorphological signs of equine infectious encephalomyelitis. 6. Pathomorphological signs of rabies. 7. Pathomorphological signs of Aujeszky’s disease.
2. Infectious anemia (INAN) (Anemia influenctiosa eguorum) is an acute infectious disease characterized by a sharp decrease in the number of red blood cells in the blood with subcutaneous tissue and yellowing of the mucous membranes in only one ungulate animal (horse, donkey, mule) with the disease, the disease is characterized by purulent septic changes.
Etiology and pathogenesis: the disease is caused by a virus that enters the body through airborne droplets. The disease occurs in an acute, semi-acute and chronic course. In addition, a distinction is also made between very sharp and latent (hidden) currents. There are two different ideas about the pathogenesis of the disease. The first is that the virus penetrates red blood cells, multiplies and hemolysis occurs, so the number of red blood cells in the blood decreases. The second concept is that the virus damages the organs that produce red blood cells, leading to a decrease in the number of red blood cells in the blood and an increase in the production of bilirubin from hemoglobin.
Pathanatomy. In the acute form of the disease, yellowing of the subcutaneous tissue, mucous membranes and even serous membranes, and pinpoint red blood are observed. the cuts are also visible. Dystrophy and necrosis occur in parenchymal organs. As a result, the fullness of the spleen increases sharply by 5-6 times. Catarrhal inflammation is observed on the duodenal mucosa and excessive bleeding in the submucosal layer. In chronic disease, jaundice persists and the following characteristic changes develop. Hepatitis is an inflammation of the liver, splenitis is an inflammation of the spleen, nephritis is an inflammation of the kidneys, and a large amount of bleeding occurs in the epicardium.
Diagnostics and comparative diagnosis. The disease is diagnosed based on clinical signs, hematological studies and pathological changes. Infectious anemia differs from the following diseases: splenitis, hepatitis, nephritis, nutritional anemia, acute poisoning, endocarditis, epicarditis, in addition to pyroplasmidosis, nuttalliosis and bacterial sepsis. Infectious anemia differs from the diseases listed above in its pathogenesis and is characterized by specific pathological changes.Infectious anemia and equine infectious encephalomyelitis Infectious anemia was discovered in 1843. Causal agent: RNA virus. It is inactivated in 20 minutes by 2% solutions of caustic soda and formaldehyde, and by 3% solution of creolin or carbolic acid in 30 minutes. Epizootology. Susceptible: horses, ponies, donkeys, mules. Source of infectious agent: sick animals. The virus is mechanically transmitted by blood-sucking insects (horseflies, flies, mosquitoes). Incubation period: from 2-5 to 93 days, on average 10-20 days. Symptoms: in acute cases - fever, weakness and emaciation, cardiac dysfunction, swelling in the abdomen, limbs, hemorrhages, especially in the 3rd eyelid and frenulum of the tongue, anemia. In subacute and chronic cases, fever is noted. Pathological changes. Sepsis, mucous membranes are jaundiced, the lymph nodes are enlarged, the spleen is enlarged 2-3 times, flabby, lumpy, the liver is enlarged in acute cases, and nutmeg on the section. Diagnostics. Parenchymal organs, lymph nodes, and heart are sent to the laboratory. Conduct RDP. Blood is tested at intervals of 30 days until a double negative result is obtained for the group. Differential diagnosis. Distinguished from nuttaliosis, piroplasmosis, leptospirosis, influenza and rhinopneumonia. Infectious equine encephalomyelitis (Meningoencephalomyelitis enzootica equorum). 104 Pathogen: when boiled it is inactivated in a few seconds, under the influence of conventional disinfectants - after 10 minutes. Susceptible: horses from 2 to 12 years old. Routes of transmission: transmissible, alimentary and aerogenic. Incubation period: 2-6 weeks. Symptoms: characterized by striving forward, depression and violence. As the disease progresses, the horse lies in a lateral position and swims, convulsions, sweating, stiffness of the neck muscles with abduction of the head to the back, loss of strength, coma. The duration of the disease is 1-3, less often 5-6 days. Pathological changes. Yellowness of the mucous membranes, subcutaneous tissue, fascia, aponeurosis. In the subcutaneous tissue of the head, limbs, and dewlap, lemon-colored serous-hemorrhagic gelatinous infiltrates are found. Small hemorrhages are found on the mucous membranes, serous membranes, pleura, peritoneum, and spleen; the lungs are swollen with signs of bronchopneumonia. The liver is flabby, enlarged, yellowish or olive in color, or, on the contrary, decreases in volume, with sharp edges. The spleen is not enlarged, the kidneys show signs of fatty or granular degeneration. Diagnostics. Parenchymal organs are sent to the laboratory. Virus identification, RN, RZGA, RSC, immunofluorescence, ESR (deceleration) are carried out. Differential diagnosis. Distinguished from rabies, Aujeszky's disease, botulism, piroplasmosis, Born's disease. In Borna disease, acidophilic intranuclear bodies are found in dead horses.