Мікроскопічні зміни в печінці свійських кролів за сальмонельозу

Abstract

Infectious diseases of rabbits cause significant damage to industrial rabbits and to the owners of these animals both productive and domestic in the private sector. Salmonellosis is one of such diseases. Death caused by salmonellosis can occur both in young and adult animals. The pathomorphology of salmonellosis of some productive and small domestic animals, in particular rabbits remains completely unexplored. Sometimes macroscopic changes are mentioned, which are revealed during the autopsy of corpses of animals died because of salmonellosis. Microscopic changes, in particular in rabbits are not described. Meanwhile, such changes are of diagnostic importance, especially for the differentiation of salmonellosis from other diseases of young animals. The purpose of the study is to elucidate the little-known aspects of the pathomorphology of liver salmonellosis in rabbits and to supplement the concept of structural changes in this disease. The objectives of the research were: to select material for microscopic examination of the liver of rabbits which died because of salmonellosis, to make histopreparations out of it, to investigate microscopic changes in the liver of rabbits in case of salmonellosis. The material was taken from the corpses of four rabbits dead after salmonellosis. From the liver of these animals the histological preparations examined under light microscope and followed by the production of microphotographs were made. The microscopic changes in the liver of the animals in the control group did not differ from those described in the literature. We found most of the changes in the liver of animals of the experimental group. It clearly indicated the presence of an infectious disease with an acute or subacute course. All these changes are characteristic for salmonellosis of animals. However, it should be noted that some of these changes were not described exactly in rabbits. We found the changes in hepatocytes which were characteristic for granular dystrophy and lipid decomposition. Such changes are a consequence of intoxication, which inevitably occurs in all gastrointestinal infections, including salmonellosis. Toxins making influence on the cell destroy the organelles, resulting in the accumulation of proteins and peptides in the cytoplasm in the form of granules (granular dystrophy) and fat droplets formed from the residues of the bilipid membranes of the organelles of the membrane structure (fat decomposition). Histiocytic infiltration, both intraparticle and interparticle is apparently a response to chronic organ toxin excretion by the pathogen. It is evidenced by the formation of granuloma, since this type of inflammation, such as granulomatous belongs to focal proliferative inflammation and can occur only with prolonged exposure to the pathogen. Up to now, liver granulomatosis in rabbits has not been described in the literature available to us. Hyperemia of the particle vessels is also a reaction to the effect of toxins released by the pathogen. Toxins act on the vascular wall, paralyzing the vasoconstrictive nerves, resulting in vasodilation and blood accumulation. Due to the enlarged pores of the vascular wall a liquid part of the blood can be filtered into the tissues, which explains the swelling of the interparticular connective tissue which we have discovered. Further studies should clarify the morphological features of the structure of other organs of rabbits suffered from salmonellosis in order to improve the pathomorphological diagnosis of this disease.