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Plasmid-mediated colistin resistance gene  mcr-1  generally confers low-level resistance. The purpose of this study was to investigate the impact of  mcr-1  on the development of high-level colistin resistance (HLCR) in  Klebsiella pneumoniae  and  Escherichia coli . In this study,  mcr-1 -negative  K. pneumoniae  and  E. coli  strains and their corresponding  mcr-1 -positive transformants were used to generate HLCR mutants  via  multiple passages in the presence of increasing concentrations of colistin. We found that for  K. pneumoniae , HLCR mutants with minimum inhibitory concentrations (MICs) of colistin from 64 to 1,024 mg/L were generated. Colistin MICs increased 256- to 4,096-fold for  mcr-1 -negative  K. pneumoniae  strains but only 16- to 256-fold for the  mcr-1 -harboring transformants. For  E. coli , colistin MICs increased 4- to 64-folds, but only 2- to 16-fold for their  mcr-1 -harboring transformants. Notably,  mcr-1  improved the survival rates of both  E. coli  and  K. pneumoniae  strains when challenged with relatively high concentrations of colistin. In HLCR  K. pneumoniae  mutants, amino acid alterations predominately occurred in  crrB , followed by  phoQ ,  crrA ,  pmrB ,  mgrB , and  phoP , while in  E. coli  mutants, genetic alterations were mostly occurred in  pmrB  and  phoQ . Additionally, growth rate analyses showed that the coexistence of  mcr-1  and chromosomal mutations imposed a fitness burden on HLCR mutants of  K. pneumoniae . In conclusion, HLCR was more likely to occur in  K. pneumoniae  strains than  E. coli  strains when exposed to colistin. The  mcr-1  gene could improve the survival rates of strains of both bacterial species but could not facilitate the evolution of high-level colistin resistance.

Impact of mcr-1 on the Development of High Level Colistin Resistance in Klebsiella pneumoniae and Escherichia coli