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Colistin resistance occurs via either the chromosomal mutations or transfer of plasmid-mediated mobilized colistin resistance (mcr-1) and mcr-2 genes. The objective of this study was characterization of plasmid-mediated colistin-resistant Klebsiella oxytoca clinical isolates.A total of five colistin-resistant K. oxytoca isolates were obtained from patients with antibiotic-associated haemorrhagic colitis. The resistance pattern and phenotypic tests, and the virulence genes were investigated by the phenotypic method and the PCR.Four mcr-1 and one mcr-2-positive K. oxytoca isolates were detected. The ceftazidime and cefotaxime minimum inhibitory concentrations was more than 128 μg/ml and imipenem minimum inhibitory concentrations were 4 μg/ml for four isolates and 1 μg/ml for one isolate. The extended-spectrum beta-lactamases including blaCTX-M1, blaSHV and blaTEM1 and Citrobacter-like (CIT) (encoding AmpC) genes were detected among all the isolates, and blaIMP (100%, n = 5) and blaOXA-48 (80%, n = 4) carbapenemase genes were also detected, but none amplified blaKPC-2, blaVIM or blaNDM1 and the fosA3 (fosfomycin-resistant) genes. The virulence encoding genes including npsB (100%, n = 5), fimA (4/5, 80%), matB (100%, n = 5), mrkA (80%, n = 4) and pilQ (100%, n = 5) were detected among them. There was no significant difference regarding the presence of any of adhesion genes between colistin-resistant and susceptible isolates (P > 0.05). In this study, carbapenem and colistin-resistant K. oxytoca with a high rate of adhesions and toxin-encoding genes were detected from hospitalized patients with antibiotic-associated hemorrhagic colitis (AAHC)A high rate of carbapenem resistance and emergence of colistin resistance which have been located on mobile genetic elements is a concern. Detection, surveillance and control of multidrug-resistant Enterobacteriacea spread are essential to eradicate due infections.