The study identifies that alterations in the C-terminal region of the OprD porin, particularly loop L7, are responsible for the unusual meropenem hypersusceptibility in imipenem-resistant Pseudomonas aeruginosa clinical isolates.

The study identifies oprD as a gene encoding the outer membrane porin protein D, which plays a role in the uptake of beta-lactam antibiotics in Pseudomonas aeruginosa. Sialylation of OprD reduces its interaction with beta-lactam antibiotics, contributing to antibiotic resistance.

The study identified ampC derepression and oprD loss as the primary mutation-driven resistance mechanisms in ceftazidime-nonsusceptible Pseudomonas aeruginosa isolates from U.S. hospitals.

A novel Pseudomonas aeruginosa strain with an oprD mutation was linked to an imipenem-resistant nosocomial respiratory infection outbreak in an ICU. The 4-bp insertion in the oprD gene led to a frameshift, causing a nonfunctional OprD porin and imipenem resistance.

The study identified several AMR genes and mutations in Pseudomonas aeruginosa, including beta-lactamases (blaVIM-2, blaOXA-2, blaPSE-1), aminoglycoside-modifying enzymes (aac(6')-Ib, aacA7), and efflux pumps (mexAB-oprM, mexXY-oprM). Mutations in gyrA (T83I) and parC (S87L) were associated with fluoroquinolone resistance.

The study compares label-free SRM-based mass spectrometry with RT-qPCR for quantifying antibiotic resistance mechanisms in Pseudomonas aeruginosa, focusing on efflux pumps, AmpC beta-lactamase, and OprD porin. SRM showed superior accuracy in classifying efflux pump overexpression and predicting resistance.

The study identifies the blaSPM-1 gene as a key factor in carbapenem resistance in Pseudomonas aeruginosa ST277 isolates, along with other resistance genes in genomic islands.

Inactivating mutations and decreased expression of the OprD gene contribute to carbapenem resistance in Pseudomonas aeruginosa isolates.

Carbapenem resistance in Pseudomonas aeruginosa isolates from burn patients in Tehran, Iran, is primarily mediated by blaVIM and blaIMP carbapenemase genes, oprD mutations, and AmpC overproduction.

The study identified various AMR genes and mutations in extensively drug-resistant Pseudomonas aeruginosa isolates from Spain, including beta-lactamases, aminoglycoside-modifying enzymes, and mutations in genes such as ampC, oprD, gyrA, parC, mexZ, and glpT, which contribute to resistance against multiple antibiotics.

The study identifies IS Ppu 21 insertion in the oprD gene as a novel mechanism of carbapenem resistance in Pseudomonas aeruginosa isolates from burn patients in Tehran, Iran.

The study identified several beta-lactamase genes (blaTem, blaOXA, blaCTX-M-15, blaVim, blaGes, blaVeb, blaDIM, AmpC) and efflux pump genes (MexA, MexB, OprM, MexC, MexD, OprJ, MexX, MexY, OprN, nfxB, MexR, OprD) in Pseudomonas aeruginosa clinical isolates, highlighting their roles in mediating resistance to various antibiotics.

The study identifies multiple AMR genes and mutations in Pseudomonas aeruginosa CL232, including bla PDC-34, bla OXA-488, and various efflux pumps, which contribute to resistance against ceftazidime, fosfomycin, and other antibiotics. It also shows that the combination of ceftazidime-avibactam and fosfomycin is effective against multidrug-resistant P. aeruginosa.

The study identifies mutations in ampR, ampD, and oprD genes in Pseudomonas aeruginosa isolates causing prosthetic valve endocarditis, which are associated with variable resistance profiles to ceftazidime, piperacillin-tazobactam, and carbapenems.

The study identifies multiple genes and mutations associated with antibiotic resistance in Pseudomonas aeruginosa through experimental evolution and whole-genome sequencing, highlighting the clinical relevance of these findings.

The study identified several genes and mutations associated with imipenem resistance in Gram-negative bacteria, including rpoD, amiC, nlpD, wecA, slt, and oprD, through mutagenesis and functional validation experiments.

VAMPr identifies AMR genes and variants through association and prediction models, confirming known resistance mechanisms like blaKPC and oprD, and detecting novel variants.

The study identifies known and novel antimicrobial resistance genes using a machine learning approach on pan-genomes of Staphylococcus aureus, Pseudomonas aeruginosa, and Escherichia coli. Key findings include the detection of resistance genes such as gyrA, parC, ermC, lmrS, aac(6')-aph(2"), dfrG, tetK, and various beta-lactamases.

The study identified various AMR genes and mutations in Pseudomonas spp. isolated from raw milk, highlighting the prevalence of multidrug-resistant strains and the presence of resistance determinants such as beta-lactamases, aminoglycoside-modifying enzymes, and efflux pumps.

The study identified multiple AMR genes including IMP, VIM, OPR, SIM, SPM, GIM, NDM, VEB, PER, KPC, OXA, intI, intII, intIII, SHV, TEM, and CTXM in extensively drug-resistant Pseudomonas aeruginosa isolates. These genes conferred resistance to various antibiotics, particularly carbapenems and beta-lactams.

The study identified several AMR genes and mutations in Pseudomonas spp. isolated from chicken meat in Norway, including beta-lactamases, efflux pumps, and genes involved in resistance to aminoglycosides, fluoroquinolones, and colistin.

The study identifies blaCTX-M2, blaPER, and blaTEM as the primary ESBL genes in MDR P. aeruginosa isolates from burn patients in Algeria, highlighting the spread of these resistance genes in the region.

The study identifies mutations in oprD, wbpM, and mexAB-OprM that contribute to carbapenem and β-lactam resistance in Pseudomonas aeruginosa during an acute infection. Additionally, plasmid-borne resistance genes such as bla-Oxa10, aacA4, and sul1 were found to play a role in antibiotic resistance.

The study identified multiple carbapenemase genes (blaIMP, blaNDM-1, blaVIM, blaGES-5, blaKPC-2) and chromosomal mutations (ampD, ampR, dacB, mexZ, armZ, nalD, oprD, gyrA, parC) associated with carbapenem resistance in Pseudomonas aeruginosa isolates from Singapore.

The study identified several AMR genes and mutations in Pseudomonas aeruginosa isolates from the Philippines, including bla VIM-2, bla VIM-6, bla NDM-1, bla IMP-26, aac(6')-Ib, aac(6')-Ib4, aac(6')-IIa, aac(6')-31, ant(2")-Ia, aadA1, acc(6')-Ib, qnrVC, gyrA, parC, oprD, nalC, and nalD. These genes and mutations were associated with resistance to carbapenems, aminoglycosides, and fluoroquinolones.

Compound 62520 inhibits ompA expression and biofilm formation in carbapenem-resistant Acinetobacter baumannii strains, demonstrating therapeutic potential against these pathogens.

The paper discusses various mechanisms of β-lactam resistance in Pseudomonas aeruginosa, including target-site modifications, reduced uptake, efflux pumps, and β-lactamase production. It highlights the role of ampC, PIB-1, and poxB in resistance, along with mutations in ftsI.

The study identified bla AmpC, bla PER-1, and oprD as key genes contributing to resistance in non-MBL-producing XDRPA strains, highlighting the importance of these mechanisms in CZA and IPM resistance.

The study identified several beta-lactamase genes, including bla OXA-50, bla OXA-10, bla OXA-488, bla GES-5, bla IMP-1, bla IMP-10, bla NDM-1, bla VIM-2, bla VIM-6, and bla VIM-11, as well as inactivating mutations in the porin gene oprD, which contribute to carbapenem resistance in Pseudomonas aeruginosa isolates from Pakistan.

Imipenem resistance in P. aeruginosa evolved through loss of function mutations in the oprD gene, which encodes the outer membrane porin. These mutations were observed in isolates from 4 μg/ml and 8 μg/ml imipenem concentrations, and the presence of S. maltophilia increased the rate of resistance evolution in 4 μg/ml imipenem concentrations.

The study identifies mutations in oprD and mexR that contribute to meropenem resistance in Pseudomonas aeruginosa, demonstrating the role of within-host evolution and antibiotic selection in shaping resistance dynamics.

The study identifies 14 dominant and ubiquitous antibiotic resistance genes (ARGs) in global soils, including the beta-lactamase gene fox5 and multidrug resistance genes oprJ, oprD, and acrA-05. These genes are prevalent in various biomes and are associated with multidrug resistance mechanisms.

The study identified blaIMP-45 as a major determinant of meropenem resistance in P. aeruginosa, and mutations in oprD, mexR, nalD, and armR were associated with meropenem resistance.

The study identified blaKPC-2 as a gene conferring resistance to ceftazidime and imipenem, and oprD mutations as a mechanism of imipenem resistance in Pseudomonas aeruginosa. Overexpression of ampC was also linked to resistance mechanisms.

The study identified bla PDC, bla OXA-50, bla OXA-50-like, bla KPC-2, and bla OXA-486 as key resistance genes in imipenem-nonsusceptible Pseudomonas aeruginosa isolates. Additionally, mutations in PBP3 (F533L) and disruptions in oprD were associated with resistance. The ST463 lineage was highlighted as a multidrug-resistant and hypervirulent strain.

The study identifies a novel deletion in ampD and ampE associated with cefepime resistance and a porin mutation in oprD linked to carbapenem resistance in Pseudomonas aeruginosa during treatment.

The study identified ampC, oprD, mexA, and mexB as key genes involved in the resistance of Pseudomonas aeruginosa to ceftazidime and meropenem through proteomic analysis and qRT-PCR validation.

The paper discusses the relationship between antibiotic resistance and bacterial fitness/virulence in Pseudomonas aeruginosa, focusing on horizontally-acquired and mutation-driven resistance mechanisms. It highlights that certain β-lactamases and the mcr-1 gene can confer resistance without significant fitness costs, while others may lead to virulence attenuation.

The study identifies several genes and mutations associated with carbapenem resistance in Acinetobacter baumannii, including efflux pump components (AdeB, AdeC, AdeS), penicillin-binding proteins (PBP1a), and outer membrane porins (OprB, OprD, CarO). Mutations in these genes are linked to altered carbapenem susceptibility.

The study identified several AMR genes in P. aeruginosa isolates, including aac(3)-II, aac(3)-III, blaOXA-48, blaSPM, blaIMP, blaNDM, blaPER, blaVIM, and oprD, which confer resistance to various antibiotics. These genes were detected using PCR and are associated with resistance mechanisms such as enzymatic modification and reduced antibiotic uptake.

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 presents an updated Pseudomonas aeruginosa AMR database and evaluates the performance of various AMR prediction tools, highlighting the importance of chromosomal variants in improving AMR detection accuracy.

Cefepime-taniborbactam showed potent in vitro activity against Enterobacterales and P. aeruginosa, particularly effective against isolates with carbapenemase genes such as blaIMP, blaNDM, and blaVIM, as well as those with mutations in ftsI, ompK35, and ompK36.

The study identifies several carbapenem resistance mechanisms in Pseudomonas aeruginosa, including carbapenemase genes (blaIMP, blaVIM, blaNDM, blaKPC), mutations in the outer membrane porins oprD and opdP, and overexpression of multidrug efflux pumps.

The study developed a Recombinase-Aided Amplification (RAA) assay for the rapid detection of imipenem-resistant (IRPA) and rifampin-resistant (RRPA) Pseudomonas aeruginosa. The RAA assay successfully detected the oprD and arr genes, which are associated with resistance to imipenem and rifampin, respectively. Mutations in the oprD gene were identified as the primary cause of imipenem resistance in P. aeruginosa.

The study presents a hybridisation-based capture system for the enrichment of genes related to P. aeruginosa antimicrobial resistance, allowing the direct sequencing of clinical samples. The panel successfully identified key resistance mutations, including ampC-T96I, oprD-Q142X, mexZ-G195D, gyrA-T83I, gyrA-D87N, parC-S87W, ampR-G154R, and others, demonstrating its effectiveness in detecting resistance mechanisms in various clinical scenarios.

The study identifies mutations in the oprD gene that lead to reduced OprD expression and carbapenem resistance in Pseudomonas aeruginosa. The role of OprD and OpdP porins in carbapenem permeability is highlighted.

The study characterizes various carbapenemase genes such as blaIMP-13, blaIMP-94, blaNDM-1, blaNDM-5, blaNDM-7, blaNDM-23, blaVIM-1, blaVIM-2, blaVIM-20, blaKPC-2, blaKPC-3, blaGES-1, blaGES-5, blaGES-7, blaGES-20, blaPER-1, blaVEB-1, blaCTX-M-15, blaCTX-M-9, blaSHV-12, blaFOX-4, blaCMY-2, blaDHA-1, blaOXA-2, blaOXA-10, blaOXA-14, blaOXA-15, and blaOXA-48 in Pseudomonas aeruginosa using MALDI-TOF MS hydrolysis assays.

The study identified the upregulation of the MexAB-OprM efflux pump, downregulation of the OprD porin, production of metallo-beta-lactamases (MBLs), and overexpression of bla AmpC as the primary resistance mechanisms in carbapenem-resistant Pseudomonas aeruginosa (CRPA) isolates. Colistin and amikacin remained effective against these isolates.

The study identifies oprD mutations and structural disruptions as the primary mechanisms of carbapenem resistance in CROPA strains, with wild-type oprD restoration reversing resistance.

The study identified several genes and mutations associated with resistance to ceftazidime-avibactam (CZA) and meropenem (MEM) in Pseudomonas aeruginosa, including dacB, ftsI, oprD, mexB, mexR, and ampC. Mutations in these genes were linked to resistance mechanisms, and CRISPR-Cas9 experiments confirmed the role of certain mutations in altering resistance levels.

The study identifies various AMR genes and mutations in Pseudomonas paraeruginosa, including carbapenemases like blaVIM-2, blaVIM-6, blaVIM-28, and blaKPC-2, as well as efflux pump genes (mexAB-oprM, mexCD-oprJ, etc.), and mutations in oprD, mexS, mexR, mexZ, lasR, mvfR, and vqsM that contribute to antibiotic resistance.

The study identified bla OXA-48 as a carbapenem resistance gene in Providencia stuartii and a premature stop codon in oprD contributing to carbapenem resistance in Pseudomonas aeruginosa. Additionally, a premature stop codon in the cirA-like gene was linked to cefiderocol resistance in P. stuartii.

The study identifies minimal gene signatures for high-accuracy prediction of antibiotic resistance in Pseudomonas aeruginosa, highlighting the role of efflux pumps, metabolic adaptations, and porin alterations in resistance mechanisms.

The study identified mutations in the oprD gene as the primary cause of carbapenem resistance in Pseudomonas aeruginosa isolates from farm animals in Shandong, China. Additionally, the bla OXA−10 gene was detected in several CRPA isolates, contributing to resistance against penicillins and cephalosporins.

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.