COLD INHIBITION OF BIOACTIVITY OF PROBIOTIC MYCOBACTERIA AND AEROCOCCI IN THE MICROBIOME

The organism of farm animals is constantly under the influence of various factors of the external environment, and one of the negative factors of violation of the technology of keeping and creation of unsatisfactory conditions of existence with deterioration of well-being is cold injury. Mostly it manifests itself as a permanent effect of positive temperatures well below the physiological norm or periodic fluctuations of an uncomfortable temperature. Such a stress factor of low intensity, but permanent over a long period of time, causes negative pathophysiological changes in the macroorganism with the development of immune-depression, metabolic syndrome, perversions of the qualitative composition of the microbiome and, as a result, disruption of native physiological processes of stimulation of cellular mechanisms of nonspecific innate immunity, induced by immune-biological mechanisms of the functioning of neutrophil granulocytes. The negative effect of low-intensity permanent cold stress was studied on a model object - murchakаs, which were kept for two weeks at a temperature of 4-6 °C under conditions of light and movement restriction. Before the start of the experiment, initial microbiological studies of the microbiome of the large intestine were conducted using generally accepted methods. Resident indigenous probiotic prokaryotes - M. vaccae & A. viridans, which possessed typical species characteristics, were isolated. Pathogenic variants of enterobacteria were not isolated, isolated cultures of E. coli were apathogenic and belonged to the usual normal flora. A two-week cold injury resulted in the disappearance of the indigenous probiotic microbiota M. vaccae & A. viridans, which are indicator prokaryotes of the physiological well-being of the macroorganism, from the microbiome. At the same time, the number of potentially pathogenic enteral microorganisms, coccal and rod-shaped, increased. This was correlated with a decrease in the phagocytic activity of native neutrophil granulocytes and their preformed filamentous spatial nucleoprotective mesh structures, which inhibit the de-fragmentary function in relation to genetically non-syngenic objects.