Pathomorphological Changes in Intestinal Yersiniosis in Cats

Abstract

Mammalian yersinioses arouse the interest of researchers in different countries of the world. The majority of publications of the past years concerned mainly productive animals, the spread of the pathogen in environmental objects (soil, water, plant and animal products). In recent years, reports began to appear about the isolation of pathogens, yersiniosis from non-productive animals and the course of diseases caused by them. Bacteriologists and epidemiologists are increasingly interested in the presence of these pathogens in the body of so-called companion animals, which are often directly in close contact with the host. In addition, the possibility of contamination of housing with pathogens by an animal keeper and the possibility of human infection from a carrier of bacteria have been proven. The purpose of the research was to find out the main vectors of the pathogenesis of spontaneous intestinal yersiniosis in cats by studying changes in the architecture of parenchymal organs. Materials for research were the internal organs of cats that died as a result of spontaneous intestinal yersiniosis, the diagnosis of which was established on the basis of the clinical picture and determination of diagnostic titers of antibodies to standard yersiniosis antigens. It has been established that the disease in cats is mostly asymptomatic, and due to the affinity of many causative agents of yersiniosis in animals and humans, it acquires both epizootological and epidemiological character. The most essential pathomorphological changes in the organs of cats with intestinal yersiniosis were revealed; in the organs of the gastrointestinal tract (congestion, uneven damage to intestinal villi, sometimes crypts of the submucosal layer and vessel walls, active cell proliferation in areas of desquamation); in the liver - mainly protein dystrophies, local areas of necrobiosis and cytolysis of hepatocytes; stagnant hyperemia and the development of hemorrhagic diathesis, signs of vascular fragility and diapedesis bleeding were detected in the kidneys, and in the case of chronicity of the process - a response to vascular endothelium damage in the form of migration of mononuclear cells to the future focus of inflammation; in the spleen and lymph nodes, delymphotization of the white pulp was observed, in other cases, an increase in the number of secondary lymph nodes with the formation of large reactive centers was detected in the spleen.