Analysis of mgrB gene mutations in colistin-resistant Klebsiella pneumoniae in Tehran, Iran

Abstract

BackgroundThe emergence of multiple drug resistance (MDR) Klebsiella pneumoniae (KP) is a public health concern. Colistin is used as a last-resort treatment option for MDR-KP. The emergence of colistin-resistant isolates is a major public health challenge. The aim of this study was to explore genes and the responsible mechanisms of colistin resistance in MDR-KP isolates in Tehran, Iran. Methods94 KP isolates suspected to be colistin-resistant (by disc diffusion) from urine, sputum, blood collected between 2018 and 2019 were studied. Isolates were tested for antibiotic resistance determinants and their colistin minimum inhibitory concentration (MIC). The presence of β-lactamase and quinolone genes, plasmid-encoded resistance genes, mcr-1 and mcr-2 genes, and nucleotide sequences of mgrB were determined by polymerase chain reaction (PCR). Results20 of 94 isolates were colistin resistance KP (Col-R KP) (21%) with MIC ranged from 4 to 128 μg/ml. Coproduction of β-lactamases, and quinolones was in 18 (90%) Col R KP isolates. Four (20%) isolates had mutations in mgrB. mgrB was inactivated by nonsense mutations at codons 21 and insertion of IS 903B elements (IS5); and elongation of mgrB. 16 (80%) ColR KP isolates harbored wild type of mgrB. There is not any mcr-1, mcr-2 encoding genes on plasmids among all the isolates. ConclusionWe detected a high frequency of both qnr and ESBL resistance genes among colistin-resistant K. pneumoniae. Also, colistin resistance mainly occur with lipopolysaccharide (LPS) modification by different mechanisms. Spread of resistance against colistin resulting in treatment failure the colistin-included therapy regimen which is used as a last line of defense against infection due to MDR Gram-negative pathogens. The control of usage of colistin in hospital is necessary to prevent the spread of resistance among isolates.