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Abstract
[...]the aim of this study was to determine the effect of colistin use in hospitalized patients on emergence of colistin-resistant (CoR) E. coli (EC) and K. pneumoniae (KP) colonization and infection. Sample size calculation and data analysis An overall colonization and infection rate of colistin-resistant Gram-negative bacteria in a cohort of critically-ill patients in intensive care units was 27% [3]. [...]it was estimated that at least 30% of subjects who received colistin would develop colonization with CoR EC or CoR KP during the study period. In addition to the use of colistin, transmission of CoR EC or CoR KP from other hospitalized patients with colonization or infection with these colistin-resistant bacteria and/or from the hospital environment during hospitalization could also be potential causes of CoR EC or CoR KP colonization. Since the present study did not have a concurrent cohort of hospitalized patients who did not receive colistin, the effect and magnitude of these other potential causes of CoR EC or CoR KP colonization (in addition to colistin exposure) could not be quantified. Again, similar to data from our previous study, the MICs of colistin in CoR EC isolates with the mcr-1 gene were lower than the colistin MICs in CoR KP isolates with the mcr-1 gene [28]. Since the mcr-1 gene was detected in only some isolates of CoR EC and in only a small portion of CoR KP isolates, CoR EC and CoR KP without the mcr-1 gene isolated from subjects in our study could be resistant to colistin via other types of plasmid-mediated mcr genes (including mcr-2, mcr-3, mcr-4, mcr-5), or other resistance mechanisms, or combined mechanisms of resistance [29–33].
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