Abstract
We identified four blaKPC-3 mutations in ceftazidime-avibactam-resistant clinical Klebsiella pneumoniae isolates, corresponding to D179Y, T243M, D179Y/T243M, and EL165-166 KPC-3 variants. Using site-directed mutagenesis and transforming vectors into Escherichia coli, we conclusively demonstrated that mutant blaKPC-3 encoded enzymes that functioned as extended-spectrum β-lactamases; mutations directly conferred higher MICs of ceftazidime-avibactam and decreased the MICs of carbapenems and other β-lactams. Impact was strongest for the D179Y mutant, highlighting the importance of the KPC Ω-loop.
Keywords:
KPC; ceftazidime-avibactam; drug resistance mechanisms; site-directed mutagenesis.
Copyright © 2017 American Society for Microbiology.
MeSH terms
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Anti-Bacterial Agents / pharmacology
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Azabicyclo Compounds / pharmacology*
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Bacterial Proteins / genetics*
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Carbapenem-Resistant Enterobacteriaceae / drug effects
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Carbapenem-Resistant Enterobacteriaceae / genetics
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Carbapenems / pharmacology
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Ceftazidime / pharmacology*
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Drug Combinations
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Drug Resistance, Multiple, Bacterial / genetics*
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Escherichia coli / drug effects
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Escherichia coli / genetics
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Humans
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Klebsiella pneumoniae / drug effects
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Klebsiella pneumoniae / genetics*
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Microbial Sensitivity Tests
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Mutagenesis, Site-Directed
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beta-Lactamase Inhibitors / pharmacology*
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beta-Lactamases / genetics*
Substances
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Anti-Bacterial Agents
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Azabicyclo Compounds
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Bacterial Proteins
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Carbapenems
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Drug Combinations
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avibactam, ceftazidime drug combination
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beta-Lactamase Inhibitors
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Ceftazidime
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beta-Lactamases
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beta-lactamase KPC-3, Klebsiella pneumoniae