Colistin resistance in clinical isolates of <i>Salmonella enterica</i> from Izmir, Turkiye: association with <i>pmrA</i>/<i>pmrB</i> mutations and variations in adhesion and invasion capabilities

Background Salmonella enterica may contribute to the spread of colistin resistance and play a significant role in transferring mcr genes to other clinically important bacterial pathogens. Colistin resistance in Salmonella enterica arises from mcr genes and/or modifications of lipopolysaccharides caused by mutations in the pmrA/pmrB encoding two-component system. In this study, we evaluated the adhesion and invasion capabilities of colistin-susceptible and -resistant Salmonella enterica, as well as the relationship between colistin resistance and pmrA/pmrB mutations.Methods and resultsNinety-one clinical isolates from 2016 to 2019 were analyzed for colistin susceptibility testing, serotyping, PCR analysis of 16S rRNA, plasmid-mediated mcr genes, and mutations in pmrA and pmrB. Adhesion, invasion, and macrophage survival assays were conducted, considering serotype and colistin susceptibility. The majority of isolates were from pediatric emergency cases (n = 59, 64.84%) and stool samples (n = 83, 91.21%). Among the isolates, 95.60% (n = 87) were resistant to colistin (MIC >= 4 mu g/mL), while 4.40% (n = 4) were susceptible. No mcr genes were detected, and the most prevalent serotype was S. Enteritidis (n = 57,62.64%), followed by S. Typhimurium (n = 20, 21.98%) and non-typable isolates of S. enterica (n = 14, 15.38%). Mutations in pmrA were identified in 79 isolates, resulting in amino acid substitutions in PmrA. Similarly, mutations in pmrB were noted in 80 isolates, leading to substitutions in PmrB. Adhesion and invasion assays revealed variability across Caco-2 and HT-29 cell lines, while no intracellular survival was observed in RAW 264.7 macrophages.ConclusionTo our knowledge, this is the first study from Izmir to present findings suggesting that nucleotide mutations in pmrA and pmrB may contribute to colistin resistance and that adherence and invasion abilities differ according to serotype and colistin susceptibility.