The aim of the work was to study the profile of antibiotic resistance of uropathogenic Escherichia coli strains isolated from patients with urinary tract infections in the urological inpatient facility of the clinical hospital in the Saratov city, depending on appurtenance to phylogenetic groups and subgroups, as well as O-serogroups.Materials and methods. We assessed sensitivity/resistance to 25 different antibacterial drugs in 102 strains of uropathogenic E. coli. The studies were carried out using the disk diffusion method. The production of extended spectrum beta-lactamases was evaluated by the double disk method. Carbapenemase output was determined using the CIM test. The PCR method was applied to determine appurtenance to phylogenetic groups and subgroups, O-serogroups, as well as the frequency of occurrence of the mcr‑1, mcr‑2, mcr‑3, mcr‑4, mcr‑5 genes encoding the proteins that mediate the development of resistance to colistin.Results and discussion. It has been established that all strains of uropathogenic E. coli are more or less resistant to antibacterial drugs. All studied 102 strains showed resistance to 23 antibacterial drugs from 8 functional groups. The resistance of uropathogenic E. coli had certain differences depending on belonging to phylogenetic groups and subgroups, O-serogroups. Strains of uropathogenic E. coli with high resistance (up to 100 %) belonged to the B23 phylogenetic group, the main representatives of which are cultures of the most common O-25 serogroup. The production of extended-spectrum beta-lactamases has been phenotypically confirmed for 69 (67.6 %) strains. No carbapenemaseproducing cultures were found in the study. The mcr‑1 and mcr‑2 genes encoding resistance to colistin have been identified in 3 uropathogenic E. coli strains (2.9 %).
The acquisition of new mobile genetic elements contributes to the genetic diversity of Vibrio cholerae strains. An important role in this process belongs to the genetic material obtained from phages. The aim of this work was to identify phage-induced PLE islands in strains of V. cholerae O1 serogroup and to determine the resistance of isolates with and without those mobile genetic elements to the lytic activity of the diagnostic cholera El Tor bacteriophage. Materials and methods. Whole genomes nucleotide sequences of toxigenic and non-toxigenic V. cholerae O1 strains presented in the NCBI GenBank were used for the work. Bioinformatic analysis was performed using the BLAST algorithm, MEGA X (or BioEdit v. 7.0.9.0). The test with phages was carried out according A. Gratia technique. Results and discussion. The analysis of 39 toxigenic strains imported to the territory of the Russian Federation and neighboring countries has revealed one strain of V. cholerae O1 of the classical biovar containing the PLE5 island, and 13 strains of V. cholerae O1 of the El Tor biovar containing the PLE4 island. PLE islands have not been found in non-toxigenic strains. It is shown that strains with PLE4 belong to V. cholerae O1 genovariants of the El Tor biovar and have the ctxB1 gene allele. Isolates with this mobile element caused sporadic cases of the disease in 1994–1999, as well as cholera outbreaks in the Russian Federation (in 1993–1994, in 1998 – Dagestan, and 1993 – Tatarstan) and Ukraine (1994–1995). It has been suggested that, perhaps, the presence of the PLE4 island makes a certain contribution to the resistance of V. cholerae O1 strains of the El Tor biovar to the diagnostic cholera El Tor phage (55.6 % of phage-resistant isolates were detected), but there are other mechanisms that have not yet been identified. Thus, the data on the presence of new mobile genetic elements in the genome of earlier imported toxigenic strains of V. cholerae O1, biovar El Tor have been obtained, which expands information about their genetic organization.
The review summarizes literature data on the Vibrio cholerae secretion system of the 6th type. This system is a contact-dependent macromolecular mechanism through which bacteria translocate toxic effector proteins into target cells. It is found in many Gram-negative bacteria, including Vibrio cholerae. V. cholerae infects phagocytic amoebae, nematodes, ciliates, bacteria belonging to different species, as well as unrelated strains of V. cholerae using this system. DNA released after lysis of competing bacteria can be taken up by Vibrio cholerae cells, which leads to the acquisition of new genetic material. The type VI secretion system is involved in the infectious process. The destruction of macrophages and microbiota contributes to the active reproduction of the pathogen and colonization of host epitheliocytes, and the production of effector proteins causes the development of diarrhea and intestinal inflammation. Cholera vibrio secretion system of the 6th type has a structure similar to other gram-negative bacteria. The genes encoding the proteins of this system are located in one large region of the second chromosome and in several additional clusters. It has been shown that toxigenic strains of V. cholerae contain an identical set of secretion system genes, while their composition is variable in non-toxigenic isolates. The regulation of secretion system protein expression differs in V. cholerae strains of different toxigenicity, depends on a number of environmental signals, and is associated with other cell regulatory networks. The paper provides experimental data on the analysis of the structure of the global regulatory gene, vasH, of the type VI secretion system in toxigenic and non-toxigenic V. cholerae O1, biovar El Tor strains isolated in the Russian Federation. Thus, the type VI secretion system is an important mechanism that facilitates the survival of V. cholerae in complex communities in vitro, protects against damaging factors of the macroorganism and increases virulence in vivo, and also provides evolutionary transformations of cholera vibrio. Further study of this system will allow a better understanding of the pathogen-host interaction processes, as well as the adaptation mechanisms of V. cholerae in the external environment.
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