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. 2025 Feb 15;53(4):1469–1481. doi: 10.1007/s15010-025-02474-3

Table 3.

Comparison of common antimicrobial resistance mechanisms in KPC-Kp resistant to CAZ–AVI and/or IMI–REL

Strains Mutationa Increased expression of blaKPCb Efflux pump inhibitor testsc
KPC OmpK35 OmpK36 PBP2 PBP3
Only CAZ–AVI-resistant (n = 16)

D179Y (n = 3;729, CR059, CR063)

A172V (n = 1;ZSS072)

n = 10 (CR059, CR063, ZSS072, ZSS048, 617, 430, 794, A398, A206, 795) n = 2 (794,795)
CAZ–AVI- and IMI–REL-resistant (n = 5)

Q296*(n = 1;A125)

K196E(n = 1;ZSS129)

S125fs(n = 1;A301)

Lack(n = 1;744)

D343N(n = 1;ZSS129) n = 4 (CR067, ZSS129, A125, A301) n = 2 (ZSS129,744)
Only IMI–REL-resistant (n = 1) Lack(n = 1;478) n = 0 n = 0

a”–” indicates that no mutations were detected in KPC or PBP2/3 and no additional mutations were detected in OmpK35/36, except for a common mutation (a premature stop codon at amino acid position 63 in OmpK35, 134 to 135 GD insertion in OmpK36)

bIndependent two-sample t-tests were conducted to determine the differences in blaKPC expression between resistant and sensitive strains, and p < 0.05 considered to be statistically significant

cMICs of CAZ–AVI and IMI–REL in combination with CCCP at a concentration of 10 mg/L were determined. A four-fold decrease in the MIC after the addition of CCCP was considered significant