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 12:Pathomorphology of smallpox in mammals and birds.
Plan
1. Etiology and pathogenesis and pathomorphology of smallpox, differential
2. Etiology and pathogenesis of mammals and birds and pathomorphology, diagnosis and differential diagnosis of the disease.
1. Mammal Pox(Variola) is an acute contagious disease characterized by a papulopustular rash (exanthema) on the skin and mucous membranes. Small (goats, sheep) and cattle, pigs, horses, buffaloes, camels, rabbits, birds, as well as humans are susceptible. Etiology. Animal pox of various species is caused by a group of independent DNA-containing poxviruses (from the Latin ros, ross - pustule, ulcer) of the family Poxviridae, which are epitheliotropic. Having a common morphological similarity and the presence of a double-stranded linear DNA molecule, they differ in biological properties. Cowpox and vaccinia viruses have a wide range of pathogenicity. They can cause enzootics in animals of different species.
Pathogenesis.The main source of infection is sick animals. Smallpox viruses are transmitted to a healthy person aerogenously, nutritionally through contact, or mechanically through arthropods. By multiplying in epithelial cells of the skin and mucous membranes of the cutaneous type, the virus causes proliferation of the epithelium, and then hydropic degeneration (vacuolization of the cytoplasm, intracellular edema, karyolysis and plasmolysis) and focal inflammation at the sites of its penetration. From the primary focus, viruses penetrate regional lymph nodes, blood and internal organs, causing viremia. Then from the blood they again penetrate the skin and mucous membranes, causing the development of secondary changes characteristic of smallpox. With the development of smallpox exanthema, viruses are not detected in the blood, and the body temperature normalizes. Smallpox exanthema develops in several stages. The first stage is the appearance of roseola in the form of small focal redness due to inflammatory hyperemia of the papillary dermis. The second stage is the formation of a papule or a dense nodule that rises above the surface of the skin, surrounded by a red belt, resulting from the proliferation and swelling of epithelial cells and the development of acute serous inflammation with infiltration of leukocytes, lymphocytes and monocytes. The third stage is the formation of vesicles (bubbles), the cavities of which are filled with serous exudate, as well as dead cells of hematogenous and epithelial origin. In mammals, unlike birds, at the edges of the vesicles, the proliferation of epithelial cells in combination with serous inflammation is more intense, and in the middle part of the pockmarks, retraction of the vault occurs in the form of an umbilical-shaped depression (umbilicus phenomenon). The fourth stage is the formation of a pustule, when the number of polymorphonuclear leukocytes in the contents of the vesicles increases, undergoing dystrophic and necrotic changes with the formation of purulent bodies. With the development of purulent-necrotic inflammation, vesicular pox turns into a pustule. This process usually involves not only viruses, but also pyogenic bacteria. The fifth stage is further destruction of the epidermis and partially affected dermis, the pustule opens, pus in the form of a flowing viscous mass pours onto the surface of the skin, dries out and turns into a crust (scab). The sixth stage is healing under the scab with the formation of a scar by secondary intention. In such places there is no pigmentation, the sebaceous and sweat glands are not restored,
hair, and the resulting scar tissue, as it hardens, gives the surface of the skin a wrinkled, or pockmarked, appearance (pockmarked face). The development of smallpox in the classic (benign) form has only been described
in humans, as well as in cattle, horses, monkeys, camels, including the possible development of an abortive (stone) form. In other animals, the smallpox process has its own characteristics associated with a more severe manifestation of the disease. In animals highly sensitive to the smallpox virus (sheep, goats, rabbits, pigs, rodents), the infectious process acquires a generalized, malignant course with the formation of immune complexes that damage microcirculatory vessels, cellular and tissue elements with fatal
outcome. Hemorrhagic (black) or confluent smallpox often occurs, which is complicated by purulent-putrefactive dermatitis, septicopyemia with a fatal outcome. Pathomorphological changes. Smallpox in cattle, caused by the vaccinia virus, occurs in a benign form with the sequential development of roseola, vesicles, papules, pustules in the skin of the udder with their predominant formation on the nipples (Fig. 20.18). In cows, the smallpox virus affects the deep layers of the dermis with necrosis when pustules form, and in the presence of hemorrhages
the pockmarks take on a bluish-black color. Healing occurs under the scab with the formation of connective tissue scars. Possible complication
mastitis. In bulls, smallpox exanthema affects the skin of the scrotum. In calves, it is observed on the skin of the face, head, neck, back, thighs, mucous
the lining of the gums and tongue. Histologically in cows with smallpox at the papule stage
Cytoplasmic basophilic or eosinophilic Guarnieri inclusion bodies are found in the epithelium. Electron microscopy reveals vacuolization of karyoplasm and accumulation of virions (Paschen bodies) in the cytoplasm of epithelial cells. In sheep, smallpox is severe as a generalized infection with the formation of pockmarks not only in the skin, but also on the mucous membranes of the respiratory, digestive and other organs. Unlike animals of other species, 90% of sheep affected by smallpox develop clearly defined, raised, dense papules measuring 0.5–1 cm, which are first red and then gray. As they merge and become necrosis, they are separated by a thin film, exposing the weeping surface of the dermis with necrosis down to the subcutaneous layer. Necrotic tissues dry out, become denser, acquire a brown-brown color, and partially or completely peel off from the skin. With the development of gangrene in the skin and lungs, the process is complicated by sepsis. In 80% of sick sheep, dense white smallpox nodules with a red rim are found in the lungs, as well as in the liver, kidneys, mucous membranes of the nasal cavity, trachea, rumen, abomasum, and intestines. When they are rejected, ulcers form, especially in the digestive tract. Regional lymph nodes and the spleen of the affected organs are swollen and gray-red in color. Histological changes. Along with the changes, as in animals of other species, “sheep pox cells” characteristic of the disease are found, first described by Borel in 1903. They are altered macrophages or epithelial cells with a vacuolated nucleus and the presence of a swollen cytoplasm of homogeneous oxyphilic or basophilic inclusions of round shape. In goats, smallpox occurs like in sheep, but is less severe. In horses, smallpox is caused by cowpox and vaccinia viruses. It occurs with the formation of pockmarks in the skin of the butt area, shoulders, thighs, near the labia, as well as in the mucous membranes of the genital organs, nasal cavity, eyes, oral cavity with the development of papulopustular
stomatitis. The smallpox process of the integumentary tissues is accompanied by inflammation of the regional lymph nodes. In camels, smallpox occurs with the development of exanthema near the lips and oral mucosa, less often in the form of a generalized infection. In pigs, smallpox is caused by pigpox, cowpox and vaccinia viruses. Smallpox exanthema covers the skin of the abdomen, back, ears, head, and thighs. The pockmarks are up to 1–2.5 cm in size and often merge. The vesicle stage is very short, papules quickly turn into pustules. In rabbits, pockmarks are found in the gums, lips, tongue, palate, ears, abdomen, back, labia, scrotum, as well as in the testes, lungs and liver. Pockmarks often become necrotic. In addition, catarrhal-ulcerative keratoconjunctivitis, complicated by corneal opacification or purulent panophthalmitis, is often detected. Diagnosis is made on the basis of clinical-epidemiological, epidemiological and pathoanatomical data, results of laboratory studies (virological, serological, histological and electron microscopic), as well as bioassays on rabbits and identification of viruses in cell cultures. The detection of specific inclusion bodies in pockmark epithelial cells is of diagnostic significance. Differential diagnosis. It is necessary to exclude foot and mouth disease (typically the formation of aphthae), vesicular disease of pigs, exanthema of non-contagious etiology, in which there is no fever and the bioassay is negative. Exanthema in other diseases occurs without staged development.

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