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. – Access mode: EBS “Lan” (http://e.lanbook.com), ISBN: 978-5-8114-1581-6 3. Latypov D.G., Zalyalov I.N. Autopsy and pathological diagnosis of animal diseases. – St. Petersburg; M.; Krasnodar: Lan, 2015. – 384 p.

Topic 11:PATHOMORPHOLOGY OF MALIGNANT CATARHAL FEVER AND FOOTH AND MOUTH MOUTH.

Plan
1. Etiology, pathogenesis and pathological anatomy, diagnosis and comparative diagnosis of malignant catarrhal fever.
2. Etiology, pathogenesis and pathological anatomy, diagnosis and comparative diagnosis of foot and mouth disease.
3. Z.K.G - an acute infectious disease of cattle, explained by fibrino-necrotic inflammation of the digestive and respiratory tract, as well as the development of keratoconjunctivitis and encephalitis.
Keywords:keratoconjunctivitis, catarrhal stomatitis, fibrin,ulcerative keratitis, purulent rhinitis, catarrhal-purulent pneumonia, pustular rash, conjunctivitis.
Etiology and pathogenesis. The disease is caused by a virus. The virus enters the body through aerogenic and elementary routes and penetrates epithelial cells (epitheliotrope). In addition, it enters nerve cells (neutrotrope) and multiplies, forming lesions that spread into blood vessels, damaging the vessel walls and developing necrotic inflammation. The virus also affects the mucous membranes of the eyes. Cattle aged 4-6 years are very susceptible to the disease. The infection spreads through sick cattle, as well as ticks, including virus carriers. The incubation period lasts from several weeks to 4 months. The disease can be acute (4-12 days) or semi-acute (14-20 days). In rare cases, a very sharp course occurs (12-20 hours), which ends in death. Clinical signs include keratoconjunctivitis, the appearance of ulcers and necrosis on the lips and nose, and increased body temperature.
Pathanatomy. It varies depending on the virulence of the virus, the body’s resistance and the course of the disease. With fulminant progression of the disease, serous keratoconjunctivitis and rhinitis develop, and catarrhal stomatitis appears. The cornea is cloudy in color. In acute illness, the virus enters the body alimentarily. We see the following changes: catarrhal purulent conjunctivitis, eyeball, purulent fluid flows from the eye and lip. Fibrinous deposits appear on the mucous membranes of the gums and mouth; by dividing them, we see that wounds are formed.
Fibrinous-necrotic inflammation and hemorrhage appear in the gastrointestinal tract. When the virus enters the body through the air, yellow fibrinous coatings appear on the nose and wings of the nose, blood clots appear in the larynx, edema and congestion in the lungs, necrotizing inflammation of fibrin and ulceration of the meninges.
Diagnostics and comparative diagnosis. The disease is diagnosed based on clinical signs, virological studies, the number of sick cattle and pathological changes.
Z.K.G differs from the following diseases: conjunctivitis, stomatitis, smallpox, meningitis, encephalitis, mycotoxicosis. Z.K.G differs from the above diseases in the causative agent and changes in the eyes, gastrointestinal tract.To Ch.P. dogs, arctic foxes, foxes, ferrets, minks, sables, martens, etc. are susceptible. Young animals aged 2 months and older are more often affected. up to 1 year. Dogs are the most resilient, ferrets less so. Among dogs, boxers, chow-chows, and foxes are stable, and to a lesser extent, poodles, shepherds, and setters. The source of the pathogen is sick animals. The disease is highly contagious, occurs more often in the form of epizootics and less often in the form of sporadic cases, and is observed at any time of the year. Transmission factors are various objects infected with the secretions of patients. Infection occurs through aerogenic and nutritional routes, through the genitals. Immunity. Animals that have recovered from the disease develop a stable and intense immunity, which begins to form from the first week and after 2-3 weeks reaches its greatest intensity. Puppies that receive milk from immune mothers are immune to infection for 1-2 weeks. after jigging. Course and symptoms. The incubation period lasts from 3 to 90 days. Clinically, dogs, arctic foxes, and foxes are most characterized by fever, catarrhal or catarrhal conjunctivitis, ulcerative keratitis and purulent rhinitis, catarrhal-purulent pneumonia, gastroenteritis, as well as various forms of nervous disorder (convulsions, excitement, and then depression, paresis, paralysis). Minks have 98 dermatitis (pustular rash), swelling of the limbs, conjunctivitis and nervous disorders. Pathological changes. Catarrhal-purulent conjunctivitis and rhinitis, bronchitis and focal fibrinous pleurisy, often catarrhal-purulent pneumonia with foci of hemorrhage are found, on the mucous membrane of the gastrointestinal tract hemorrhages, erosions and ulcers, intussusception. The lymph nodes of the mesentery are enlarged, there are hemorrhages on the myocardium, the brain and spinal cord are edematous and hyperemic. The diagnosis is made on the basis of epizootic and clinical data, pathological changes and histological studies (detection of intraplasmic inclusion bodies in the epithelial cells of the mucous membrane of the bladder, stomach, conjunctiva and liver). In homogenates of the liver and spleen, a specific antigen is detected in the RDP and RSC. Differentiated from infectious encephalomyelitis, infectious canine hepatitis, rabies, Aueszky's disease, Aleutian mink disease, mink viral enteritis. Malignant bluetongue (fever) is caused by a DNA virus belonging to the herpes virus family. Cattle and buffaloes, and sometimes other artiodactyls, are affected. The source of infection is sick animals, as well as virus carriers: sheep, goats, in which the disease does not manifest itself clinically. Clinically, the disease is manifested by increased body temperature, especially at the base of the horns, mucopurulent discharge from the nose, clouding and ulceration of the cornea, and nervous phenomena. Pathoanatomical changes: First, there is swelling of the eyelids, redness of the conjunctiva, then clouding of the cornea, peeling of its epithelial cover, impregnation with exudate, formation of erosions, ulcers, perforation followed by panophthalmitis. In the oral and nasal cavities, redness is first observed, then necrosis of the epithelium, impregnation with exudate, deposition of fibrin films, the removal of which forms erosions. The same changes are observed in the larynx. The frontal and maxillary sinuses contain purulent-ichorous exudate. In the genitourinary organs there are inflammatory processes and hemorrhages. The symptoms of edema are pronounced in the lungs and foci of inflammation are often found. In the gastrointestinal tract, hyperemia, necrosis and diphtheritic inflammation of individual areas in the book, abomasum and intestines are observed. A rash in the form of papules and vesicles appears on the skin of the udder. In the brain there is hyperemia, accumulation of cloudy reddish fluid in the ventricles. Histological examination reveals hemorrhages, accumulations of lymphoid cells and glial cells around the vessels (non-purulent encephalitis). In the chronic course of the disease (2 weeks or more), severe emaciation of the animal and blindness occur. When diagnosing, epizootological data are taken into account (the disease manifests itself, as a rule, sporadically in cattle aged 1 to 4 years), and clinical signs. Important are the characteristic pathomorphological changes in the eyes and mucous membranes of the oral and nasal cavities, keratitis, 99 lobar inflammation of the mucous membranes of the head area and the results of a histological examination of the medulla oblongata (non-purulent encephalitis), in which, more often than in other parts, the presence of couplings around the vessels is detected. It is necessary to differentiate infectious rhinotracheitis, which is characterized by high contagiousness and predominant damage to the respiratory and genital organs. Questions for self-control 1. Pathomorphological signs of classical swine fever. 2. Pathological signs of African swine fever. 3. Pathomorphological signs of rinderpest. 4. Pathomorphological signs of malignant catarrhal fever. When diagnosing, epizootological data are taken into account (the disease manifests itself, as a rule, sporadically in cattle aged 1 to 4 years), and clinical signs. Important are the characteristic pathomorphological changes in the eyes and mucous membranes of the oral and nasal cavities, keratitis, 99 lobar inflammation of the mucous membranes of the head area and the results of a histological examination of the medulla oblongata (non-purulent encephalitis), in which, more often than in other parts, the presence of couplings around the vessels is detected. It is necessary to differentiate infectious rhinotracheitis, which is characterized by high contagiousness and predominant damage to the respiratory and genital organs. Questions for self-control 1. Pathomorphological signs of classical swine fever. 2. Pathological signs of African swine fever. 3. Pathomorphological signs of rinderpest. 4. Pathomorphological signs of malignant catarrhal fever. When diagnosing, epizootological data are taken into account (the disease manifests itself, as a rule, sporadically in cattle aged 1 to 4 years), and clinical signs. Important are the characteristic pathomorphological changes in the eyes and mucous membranes of the oral and nasal cavities, keratitis, 99 lobar inflammation of the mucous membranes of the head area and the results of a histological examination of the medulla oblongata (non-purulent encephalitis), in which, more often than in other parts, the presence of couplings around the vessels is detected. It is necessary to differentiate infectious rhinotracheitis, which is characterized by high contagiousness and predominant damage to the respiratory and genital organs. Questions for self-control 1. Pathomorphological signs of classical swine fever. 2. Pathological signs of African swine fever. 3. Pathomorphological signs of rinderpest. 4. Pathomorphological signs of malignant catarrhal fever.
2. FMD. An acute infectious disease is characterized by the formation of specific blisters on the skin and mucous membranes, which affect all domestic and wild even ungulates.
Etiology and pathogenesis. The virus that causes the disease has three different properties. 1) epitheliotrope, 2) myotrope, 3) pantrope,
1) epiteliotrop allows the virus to enter the skin and mucous membrane of epithelial cells and primary changes, after which the virus enters the blood and subsequent changes. Initially, epithelial cells develop hydropic dystrophy and serous inflammation, rupture of one of the cells, and specific aphthae are formed.
2) the virus with miotron properties in the heart muscle develops protein and fatty degeneration, yellowish spots in the heart muscle resemble tiger skin, death occurs precisely because of paralysis of the heart muscle.
Characteristics of changes in foot and mouth disease Foot and mouth disease (Aphtae epizooticae) is a highly contagious, acute viral disease of domestic and wild artiodactyl animals, characterized by fever and aphthous lesions of the mucous membrane of the oral cavity, skin of the udder and limbs. The causative agent is an RNA virus. Sustainability. The best disinfectants are solutions of formaldehyde (2%) and sodium hydroxide (1-2%), which have a detrimental effect on the foot-and-mouth disease virus with an exposure of 10-30 minutes. Epizootological data. Cattle and pigs are most susceptible to foot and mouth disease; sheep and goats, as well as wild even-toed ungulates, are less sensitive. Cases of foot-and-mouth disease occurring in natural conditions in elk, deer, saigas, roe deer, buffalo, antelope and wild pigs, as well as infection of wild ungulates in zoos, have been described. Other animal species get foot and mouth disease quite rarely. Sporadic illnesses have been reported in hedgehogs, dogs, cats, rabbits and rats. People (especially children) can also get foot and mouth disease. The source of the causative agent of foot-and-mouth disease is sick animals, including those in the incubation period of the disease, as well as virus carriers (more than 400 days). Infection of animals occurs mainly through the mucous membranes of the oral cavity, through damaged skin of the udder and (more often) limbs, and also aerogenously when kept together. Foot and mouth disease, as a rule, manifests itself in the form of an epizootic, sometimes a panzootic. Course and symptoms. The most typical signs of the disease are expressed in adult cattle. In other susceptible animals, especially lambs and piglets, they may be less typical. There are possible benign and malignant manifestations of foot and mouth disease. The incubation period for a benign process lasts from 36 hours to 7 days, very rarely - up to 21 days. The first sign of the disease is an increase in the animal’s body temperature to 41 °C or higher. Patients experience a state of prostration, increased heart rate, redness of the mucous membrane of the oral cavity and conjunctiva, impaired chewing of cud and decreased milk secretion, dry nasal mucosa, and swelling of the crown of the hooves. The animals have their heads down and often moan. Then profuse salivation begins, which is accompanied by grinding of teeth. Animals chew food very carefully; swallowing is painful. They become thirsty and lame. Swelling is noticeable on the skin of the crown of the hooves and the interhoof gap, and increased sensitivity is noted. After 3 days of illness, body temperature decreases and exanthema appears. 102 When examining the oral cavity, significant lesions are found. Aphthae have a round or oblong shape, their walls are stretched as a result of the accumulation of lymph, and easily burst when pressed with a finger. Very painful aphthae are located mainly on the back of the tongue and often reach the size of a child's fist. Aphthous lymph is initially colorless, but then, due to the development of bacteria, it acquires a gray-white color. Sometimes aphthae are so flat that their presence can only be determined by palpation. Smaller aphthae are found on the inside of the lips and cheeks, on the gums, the toothless edge of the upper jaw and on the roof of the mouth. Large aphthae, the size of a walnut, occur on the nasal planum. Occasionally, the conjunctiva is affected, as well as the skin at the base of the horns and other parts of the body. Papules the size of a pea first form on the crown of the hooves and in the interhoof cleft, and then blisters reaching the size of a pigeon egg. The animals limp, stand with their backs arched and their legs tucked under their stomachs. With mechanical impact, the aphthae burst within 1-3 days and in their place erosions of various sizes, irregular shapes and torn edges are visible. Lesions of the nasopharynx and trachea make swallowing and breathing difficult. Tachycardia and arrhythmia develop. Sometimes paresis, ataxia, paralysis, and muscle tremors occur. The foot and mouth disease virus can cause abortions and the birth of still or weak fetuses in pregnant animals. Under good conditions, the prognosis is usually favorable. The mortality rate in cattle is 0.2-0.5%. Recovery usually occurs 3-4 weeks after infection. With unsatisfactory living and feeding conditions, as well as with untimely provision of medical care, significant complications arise. The malignant course of foot and mouth disease is characterized by a predominance of cardiac and circulatory disorders. Death in the malignant course of foot and mouth disease occurs suddenly on the 7-14th day of illness, and the mortality rate can be 70-100%. The malignant course of foot and mouth disease is usually observed in calves. High body temperature, severe depression and weakness, sometimes gastroenteritis, tachycardia and cardiac paralysis are noted. They die within 12-30 hours due to myocarditis. In sheep, foot and mouth disease is somewhat milder than in cattle. The most constant is high body temperature. Aphthae that appear in the oral cavity in the form of flat, rapidly passing bubbles the size of a millet grain usually go unnoticed. Aphthae in the upper part of the hoof pulp, on the corolla and in the interhoof cleft usually form on the 5th day of illness. In such cases, lameness develops. When foot and mouth disease appears during the lambing period, there is a massive death rate of newborn lambs from damage to the heart muscle and central nervous system. Due to the relatively low sensitivity of adult sheep to the foot-and-mouth disease virus, the disease of animals in the flock lasts a long time. Foot and mouth disease in pigs occurs with the formation of aphthae on the “piglet”, udder and on the crown of the hooves. Animals lie down a lot and move by crawling, relying on their wrist joints. With the development of the exudative process and injury to the diseased limbs, the horny shoe detaches and falls off. In a dysfunctional herd, all suckling piglets usually die from foot and mouth disease. Pathological changes. An exanthematous process and the presence of aphthae in the oral cavity, on the udder and limbs are characteristic. Sometimes aphthae and erosions occur on the mucous membrane of the scar and book. In the cardiac sac there is an accumulation of transudate, in the myocardium there are gray-yellow or whitish spots (tiger heart). In 103 piglets, diffuse dystrophic petrification of the heart muscle sometimes develops; in cattle, focal lesions and scars from previous myocarditis develop. In the generalized form of foot and mouth disease, local inflammatory changes are found mainly in the thigh muscles, swelling of the abomasum, emphysema, changes in the pancreas, brain and spinal cord. Diagnosis. It is assigned based on an analysis of epizootic data, clinical signs and laboratory results. Differential diagnosis. Vesicular stomatitis occurs like foot and mouth disease, affecting the extremities. However, not only cattle, but horses and donkeys are affected. The bioassay can be performed on adult mice that are sensitive to the vesicular stomatitis virus, or on suckling mice (sensitive to the foot-and-mouth disease virus). FMD differs from other diseases that occur with signs of exanthema, stomatitis and dermatitis in the following indicators. Thus, simple vesicular stomatitis, which occurs as a result of eating spoiled feed, occurs without fever and lesions on the extremities; it is not contagious. Porcine vesicular disease does not affect other animal species. Smallpox lesions in cows are usually limited to localization on the udder. Viral diarrhea, malignant catarrhal fever and rinderpest do not cause changes in the area of ​​​​the corolla and interhoof cleft. Immunity. The immunity of animals to subsequent infection with the same virus lasts from 1 to 10 years.
3) When the pantropic nature of the virus intensifies, parenchymal organs and their cells are affected
The incubation period can be 1-7 days, sometimes 20 days or more. This depends on the virulence of the virus, the age of the animal and environmental factors.
Aphthae are found in the mouth, especially on the tongue, the skin between the hooves and the udder. When the aphtha ruptures, erosions form and body temperature normalizes.
Death in a dangerous form occurs within 7-14 days.
In calves, the myotropic form is common. The temperature rises, appetite disappears, teeth grind, heart function is severely impaired, and the animal dies within 12-14 hours.
Pathanatomy. Foot and mouth aphthae consist of a thin membrane, a cavity and serous fluid. Aphthae form on the skin between the hooves and the skin of the mammary glands, which can be the size of a needle, the size of a pea, a walnut or even an egg. Aphthae form on the mucous membrane of the oral cavity, in the gums and in the vagina, anus, and large mucous membrane of the abdomen. Aphthae formed in the mammary gland lead to the development of mastitis, aphthae formed between the hooves lead to the development of dermatitis, and aphthae formed in the mucous membranes lead to the development of sepsis. Diagnostics and comparative diagnosis: The diagnosis is made on the basis of virological studies, epizootic data and pathological anatomical changes. Foot and mouth disease differs from the following diseases: smallpox, dermatitis, stomatitis, mastitis, necrobacteriosis, plague, Z, K, G. Foot and mouth disease differs from the above diseases in pathogenesis and the formation of specific aphthae.