الفهرس 
The role of pmrcab and mcr-1 genes in colistin- resistant acinetobacter baumannii
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Abstract
The progressively increasing antimicrobial resistant Acinetobacter baumannii (A. baumannii) infections have enforced the use of colistin as the last-resort therapy, resulting in the evolution of colistin resistance. We aimed to study the polymyxin resistance (pmr) CAB expression and mutations in A. baumannii clinical isolates as well as the presence of the plasmid-encoded mobile colistin resistance-1 (mcr-1). Colistin MICs of a total of 100 A. baumannii isolates were measured using broth microdilution method. The relative expression of pmrA, pmrB and pmrC genes was measured using quantitative reverse transcription PCR (qRT-PCR) followed by Sanger sequencing in 4 colistin-resistant and 4 colistin-susceptible isolates. Finally, detection of the mcr-1 gene was done using conventional PCR. Colistin resistance rate among the studied isolates was 49%. The expression levels of pmrA and pmrB were statistically significantly higher in colistin-resistant compared to colistin-susceptible isolates, while the pmrC expression had no statistically significant change. There was a weak positive correlation between colistin MICs and the expression levels of each of pmrA and pmrB genes. pmrC I138N mutation was observed in two colistin resistant isolates with high pmrC expression. Only one isolate (1%) was positive for the presence of mcr-1. It was concluded that the increased expression of pmrA and pmrB and mutations in pmrC may cause colistin resistance in A. baumannii. However, increased pmrC expression is not necessarily associated with colistin resistance. The current study is the first to report the plasmid-mediated mcr-1 in A. baumannii in Egypt which should raise attention due to its high tendency of spreading colistin resistance in clinical settings