The study identifies several extended-spectrum beta-lactamase (ESBL) genes, including blaCTX-M-2, blaCTX-M-10, blaSHV-12, and blaSHV-28, along with the loss of the outer membrane protein OmpK36, as mechanisms contributing to ertapenem resistance in Klebsiella pneumoniae isolates.

The paper discusses the mechanisms of carbapenem and polymyxin resistance in Enterobacteriaceae, highlighting the role of beta-lactamases such as blaKPC, blaNDM, and blaOXA-48, as well as mcr-1, mcr-2, mcr-3, mcr-5, and mcr-9 genes. It also identifies mutations in envZ, ompR, pmrAB, and phoPQ that contribute to resistance.

The study identifies several β-lactam resistance genes, including bla TEM-1, bla SHV-1, bla CTX-M-15, bla NDM-1, bla VIM-1, and bla OXA-48, as well as porin alterations in E. coli and K. pneumoniae isolates. These genes and mutations contribute to β-lactam resistance through enzymatic degradation and reduced membrane permeability.

The study introduces Kleborate, a tool for analyzing genomes of Klebsiella pneumoniae and its related species complex, focusing on AMR and virulence determinants. Key findings include the identification of SHV beta-lactamase, OmpK35 and OmpK36 porins, and MgrB/PmrB regulators as critical factors in carbapenem and colistin resistance.

The study identifies bla KPC-3, bla KPC-2, bla OXA-232, and mutations in ompK35, ompK36, and ompK37 as significant contributors to carbapenem resistance in Klebsiella pneumoniae isolates.

Relebactam restored imipenem susceptibility in K. pneumoniae isolates with bla KPC and AmpC but not in those with MBLs. Impaired porin expression and efflux pump activity contributed to imipenem resistance.

The study identifies increased blaKPC copy number and truncation of OmpK35 and OmpK36 porins as mechanisms of resistance to Imipenem/Relebactam and Meropenem/Vaborbactam in a KPC-producing Klebsiella pneumoniae clinical isolate.

The study identifies multiple AMR genes and mutations in carbapenemase-producing Klebsiella pneumoniae isolates, including bla NDM-1, bla OXA-48, and various aminoglycoside-modifying enzymes, as well as mutations in mgrB, gyrA, parC, and porin genes associated with colistin and fluoroquinolone resistance.

The study identifies mutations in ompK36 and blaKPC as key mechanisms of resistance to imipenem-relebactam in KPC-producing Klebsiella pneumoniae, highlighting the potential for cross-resistance to other β-lactam/β-lactamase inhibitor combinations.

The study identified bla KPC, bla OXA-48, bla NDM-1, and bla IMP as the primary genes responsible for ceftazidime/avibactam resistance in carbapenem-resistant Klebsiella pneumoniae isolates from cancer patients. Additionally, the absence of ompK35 and ompK36 was associated with resistance.

The study identifies various carbapenemase genes (blaKPC, blaNDM, blaOXA-48) and the CTX-M-15 beta-lactamase, as well as mutations in gyrA and ompK36 contributing to resistance in Enterobacterales isolates from Central Texas.

This review discusses proteomic approaches for diagnosing antibiotic resistance in ESKAPE pathogens, highlighting the importance of proteomic techniques in understanding resistance mechanisms and improving diagnostic accuracy.

The study identifies several AMR genes and mutations in Klebsiella pneumoniae that contribute to resistance against carbapenems, ceftazidime/avibactam, tigecycline, and colistin. Key findings include the acquisition of blaKPC and blaNDM harboring plasmids, specific mutations in blaKPC, porin deficiencies (ompK35 and ompK36), overexpression of efflux pumps (acrAB, oqxAB), and mutations in rpsJ, ramR, tetA, mgrB, and pmrB.

TolC is required for antimicrobial resistance, capsule production, and virulence in K. pneumoniae. Mutations in tolC lead to increased susceptibility to multiple antibiotics and impair capsule production and biofilm formation.

The study characterizes various AMR genes and mutations in Enterobacterales and Pseudomonas aeruginosa, including bla CTX-M-15, bla OXA-1, bla OXA-181, bla OXA-48, bla NDM-1, bla KPC-3, bla VIM-2, ampC, cmrA, mexAB-OprM, mexXY-OprM, oprD, ompK35, ompK36, and ftsI, which confer resistance to cefepime and carbapenems.

The study identifies a large deletion in the ompK36 gene in Klebsiella pneumoniae ST395, leading to carbapenem resistance during persistent bloodstream infection.

The study identifies multiple AMR genes and mutations in K. pneumoniae isolates from Armenia, highlighting the presence of XDR and MDR strains with resistance to various antibiotics, including carbapenems, aminoglycosides, and quinolones.

The study identifies blaNDM-1 as a gene conferring resistance to cefepime and meropenem, and highlights the role of ompK35 and ompK36 porin deletions in reducing susceptibility to these antibiotics in Klebsiella pneumoniae.

The study identified various carbapenemase genes (blaKPC-2, blaKPC-3, blaOXA-181, blaOXA-232, blaOXA-48, blaNDM-1, blaNDM-4, blaNDM-7, blaIMP-1) and extended-spectrum beta-lactamase genes (ampC, ctx-M-15, shv-9) in carbapenem-resistant Klebsiella pneumoniae isolates. Additionally, mutations in porin genes ompK35 and ompK36 were found to contribute to carbapenem resistance in isolates lacking carbapenemases.

The study identified multiple carbapenemase genes, including bla NDM-5, bla NDM-1, and bla OXA-232, as well as extended-spectrum beta-lactamases like bla CTX-M-15. Mutations in porin genes ompK36 and ompK37, and regulatory genes acrR and ramR, were associated with reduced susceptibility to carbapenems, cephalosporins, fluoroquinolones, and tigecycline.

The paper reviews molecular resistance mechanisms to newly approved antibiotics in WHO priority pathogens, identifying various beta-lactamases, efflux pumps, and target site modifications that confer resistance.