Cell geteromorphism in the conditions of persistence of sapronoses causative agents in various environments
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The paper discusses the issues of morphofunctional variability of causative agents of sapronoses under stressful environmental conditions. In the current century, sapronoses infections attract more and more attention. Under unfavorable habitat conditions, their pathogens use a strategy for the formation of resting (stable) states: viable but non-cultured cell forms and the persistence of bacteria, which are characterized by reduced metabolism, changes in the morphology and physiology of microorganisms, and termination of their replication. With the formation of resistant forms of bacteria, the possibility of survival of sapronoses causative agents in the interepidemic period, the formation of their antibiotic resistance, which plays an important role in the chronicity of infections, is associated. The literature widely discusses the mechanisms and conditions for the formation of resistant states of pathogenic bacteria, their pathogenetic significance in infectious pathology, whereas the ultrastructural organization and morphological variability of resistant cellular forms, as well as their differentiation, causing the heterogeneity of the pathogens population, are not yet well covered. The emergence of molecular cell biology methods and the discovery of genetic modules of toxin-antitoxin systems revealed a single mechanism for regulating the formation of resistant cellular forms of bacteria. This served as the basis for the development of fundamentally new technologies for the study of the mechanisms for the conservation of the pathogenic potential of resistant cellular forms of pathogens of natural focal sapronosis in interepidemic periods. Based on the analysis of current data, as well as their own experience, the authors assess the role of morphofunctional changes in resistant cellular forms of bacteria and their significance in the adaptation strategies of causative agents of sapronoses (on the example ofKeywords:
Cellular metabolism
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Intracellular parasite
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The occurrence of horizontal gene transfer between bacteria within digestive vacuoles and faecal pellets of the protozoan Tetrahymena pyriformis was investigated. More than 90% of the egested faecal pellets of T. pyriformis, added as predator to a suspension of Escherichia coli, contained viable bacteria. In a mixed population, containing donor (plasmid RP4) and recipient E. coli cells, the presence of T. pyriformis increased conjugational gene transfer by three orders of magnitude. Since the protozoa formed an average of 12–13 digestive vacuoles per cell, each protozoan had statistically egested one or more transconjugants. Thus, we show for the first time that digestive vacuoles of free-living protozoa appear to be an important ecological micro-niche, where gene transfer by conjugation (or retromobilisation) will be favoured. So far, digestive vacuoles have been ignored in genetic and ecological studies. This micro-biotope provides a selective pressure which might enhance the acquisition of virulence genes in cases of mutual interactions between genetically modified micro-organisms and wild-type pathogens. This finding is important for biosafety considerations.
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Axenically grown pathogenic and non-pathogenic isolates of Entamoeba histolytica have been shown to adhere to mammalian epithelial cells and bacteria by virtue of carbohydrate-binding proteins present on their cell surfaces. The interaction of amoeba isolates of low pathogenicity with a variety of gram-negative bacteria, mainly Escherichia coli strains which are readily ingested by the amoebae after relatively short periods, significantly increased the ability of the trophozoites to: (a) destroy and ingest intestinal epithelial cells; (b) secrete a cytopathic substance which morphologically affects a variety of tissue-cultured cells; and (c) cause hepatic abscesses in hamsters. Addition of carbohydrates that inhibit the lectin-mediated attachment of bacteria to amoebae prevented the enhancement of virulence. Interaction of the amoebae with bacteria that were heat-inactivated, glutaraldehyde-fixed or disrupted by sonication, as well as with bacteria precoated with antibodies or concanavalin A, did not lead to an increase in virulence. Moreover, short prior treatments of the bacteria with inhibitors of protein synthesis, but not with cell-wall synthesis inhibitors, also prevented the stimulation. The results indicate that interactions of amoebae with certain bacteria may be responsible for the increase in amoebic virulence.
Pathogenic bacteria
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