Abstract

It is difficult to differentiate the disease by clinical signs; therefore, the main criteria for diagnosing hemophilic polyserositis should be considered pathological changes characteristic of the disease. Piglets are aged 30–60 days are most often affected. On average, pigs can die five hours after the manifestation of clinical signs. The autopsy results have revealed severe polyserositis, fibrinous layering around the lungs and heart, swelling of the liver with fibrinous deposition, and intestinal epithelium overloaded with fibrin pellicle. The autopsy of the dead piglets has shown the changes, characterized by massive overlays of fibrin pellicles and threads on the surface of the costal and pulmonary pleura, diaphragm, peritoneum, omentum, the serous membrane of the intestine, as well as the liver capsule. In the thoracic and abdominal cavities and pericardium, a significant accumulation of straw-yellow exudate with abundant fibrin threads has been revealed. Rib and lung pleura were covered with fibrinous overlays of gray-white and gray-yellow color. When the overlays were removed, swelling, dullness, matting, and sometimes bluishness of the pleura with a grayish tint were found. In several cases, fibrinous layering was of considerable thickness, which caused the fusion of serous sheets. Macroscopically, the bronchial and mediastinal lymph nodes were enlarged, juicy, grayish, or grayish-red in color; sometimes, dotted hemorrhages were observed in them. A cloudy, reddish liquid was flowing from the surface of their cut. At the pathological examination, the lungs were enlarged in volume, dense in consistency, and dark red. Interstitial pneumonia was observed, and in some cases, fibrinous inflammation of the pleura and foci of atelectasis alternated with small emphysema areas. The liver was enlarged and flabby; the lobular structure was weakly expressed. The cut surface was dull, gray-red, and sometimes red-brown. The vessels of the small intestine were injected. That is, fibrinous polysterositis, arthritis, and meningoencephalitis are characteristic of the pathology. Therefore, from the pathomorphological changes, it can be assumed that the dissemination of the causative agent of hemophilic polyserositis occurs in a short time. In the acute stage of the disease and fatal cases, the pathogen is often found in the joints, serous membranes, spleen, liver, lungs, pericardium, and brain. The localization of the pathogen is specific – it is the serous membranes. The penetration of the causative agent into the brain can indirectly judge the relatively high invasive properties of the microorganism.

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