
The study examined KPC-14-producing K. pneumoniae, revealing that ceftazidime-avibactam resistance stems from increased ceftazidime hydrolysis and reduced avibactam binding. In contrast, imipenem-relebactam restored susceptibility, as the KPC-14 enzyme showed weakened carbapenemase activity. The ΔG242-T243 deletion alters loop 237–243, expanding ceftazidime activity but compromising carbapenem resistance, highlighting distinct resistance mechanisms from Ω-loop mutations.
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