Active efflux mediated by the AcrAB efflux pump is the primary mechanism of resistance to ciprofloxacin in Salmonella enterica serovar Typhimurium mutants, with increased resistance to multiple antibiotics.

The study identifies several genes involved in the physiological adaptation of E. coli to tetracycline, including marA, soxS, rob, micF, and acrAB, which contribute to the development of multidrug resistance through the upregulation of efflux pumps and downregulation of porins.

The study identified the overexpression of the AcrAB-TolC efflux pump in Salmonella enterica serovar Typhimurium variants, leading to reduced susceptibility to multiple antibiotics including ciprofloxacin, chloramphenicol, tetracycline, and ampicillin.

The study characterizes the AcrAB-TolC efflux system's role in ethidium bromide efflux in E. coli, demonstrating its impact on resistance mechanisms.

The study identifies three QRDR mutations in gyrA (D87G, G81C) and parE (E470K) that contribute to high-level fluoroquinolone resistance in Salmonella typhimurium. Overexpression of AcrAB/TolC efflux pump is also associated with resistance.

The study shows that efflux pump overexpression (acrAB) is an early step in quinolone resistance development in E. coli, followed by target site mutations in gyrA and parC. Deletion of acrAB delays the emergence of high-level resistance.

The study presents a computational model to predict efflux effects on antibiotics, focusing on the AcrA-AcrB-TolC efflux pump system and its impact on beta-lactam antibiotics.

The study shows that the transcriptional activators SoxS, RobA, and RamA regulate the expression of the AcrAB-TolC efflux pump in Enterobacter cloacae, contributing to multidrug resistance.

The study introduces the Ethidium Bromide-agar cartwheel method to assess efflux pump activity in MDR bacteria, highlighting the role of overexpressed efflux pumps like AcrAB and NorA in conferring resistance to antibiotics such as tetracycline, norfloxacin, and imipenem.

The study identifies the acrAB efflux operon as a key factor in the development of antibiotic resistance, leading to the loss of synergy in combination treatments. Deletion of the acrAB operon prevented the emergence of antagonism, maintaining synergy for longer periods.

The study identifies oqxAB and qnrS1 as key contributors to fluoroquinolone resistance in E. coli isolate HUE1, along with mutations in acrR and marR that lead to overexpression of efflux pumps.

The study identifies the amplification of a 316-kb sequence region containing the acrAB operon as a key mechanism for rapid antibiotic resistance evolution in E. coli under high antibiotic stress.

The paper discusses multidrug efflux pumps from various bacterial food pathogens including Enterobacteriaceae, Vibrio cholerae, and Staphylococcus aureus, highlighting their role in multidrug resistance.

The study identifies that PAβN primarily functions as an inhibitor of the AcrAB and AcrEF multidrug efflux pumps in Escherichia coli, distinguishing its effect from outer membrane destabilization.

The paper discusses the mechanisms of resistance in carbapenem-resistant Enterobacteriaceae (CRE), focusing on beta-lactamases such as KPC, NDM, and OXA-48, as well as regulatory genes and efflux pumps contributing to polymyxin and tigecycline resistance.

The study identified the presence of multidrug resistance genes such as AcrAB, mdtK, OmpK35, and OmpK36 in Klebsiella pneumoniae isolates. Additionally, virulence genes like fimH-1, mrkD, traT, entB, IucC, and irP-1 were detected, highlighting the complex nature of resistance and virulence in these isolates.

LASS strain exhibited increased resistance to linalool and several antibiotics, including tetracycline, chloramphenicol, and piperacillin, through mechanisms involving efflux pumps and membrane modifications.

The study identifies the AcrAB-TolC efflux pump as a key player in modulating the growth of neighboring bacteria under antibiotic pressure, demonstrating that cells with active efflux pumps can alter the local antibiotic concentration, thereby affecting the growth of nearby cells with impaired efflux capabilities.

Overexpression of the AcrAB efflux pump increases spontaneous mutation frequency in E. coli and Salmonella enterica serovar Typhimurium LT2, linking transient antibiotic resistance to higher mutation rates.

The study identified a high prevalence of multidrug-resistant Klebsiella pneumoniae isolates carrying various β-lactamase genes (bla KPC, bla TEM, bla SHV, bla OXA-1, and bla CTX-M-1) and efflux pump genes (AcrAB, tol C, mdt K) along with outer membrane porin genes (Omp K35 and Omp K36).

The study shows that the AcrAB-TolC efflux pump system plays a role in carbapenem non-susceptibility in Escherichia coli, with AcrA overexpression strongly correlated with ertapenem resistance and AcrB overexpression observed under imipenem stress.

The study identified several genes involved in triclosan resistance, including fabI, acrAB, ompF, marR, soxS, rpoN, pcnB, infB, lon, rbsB, and trkHA. These genes were found to play roles in triclosan sensitivity through various mechanisms such as efflux pumps, porins, and stress response regulation.

The study identified several genes involved in fluoroquinolone susceptibility in Salmonella enterica serovar Typhi, including efflux pumps (acrA, acrB, tolC), regulatory genes (marA, phoP), and DNA repair genes (uvrD, xseA).

The study shows that SmpB and tmRNA regulate purine metabolism, influencing trimethoprim resistance in Aeromonas veronii. Overexpression of acrAB in Δ ssrA strain restored trimethoprim resistance.

Deletion of efflux pump genes such as acrAB and tolC significantly reduced the evolvability of tetracycline resistance in E. coli K-12 strains.

The study identifies gene amplifications in Escherichia coli, particularly of the acrAB, emrE, and rrlB genes, which contribute to erythromycin resistance under varying antibiotic dosages.

The study demonstrates the use of nanopore sequencing for rapid identification of pathogens, antibiotic resistance genes, and virulence genes from simulated blood samples and positive blood cultures. It identified 39 antibiotic resistance genes and 77 virulence genes in a Klebsiella pneumoniae strain, including blaKPC-2, blaSHV-12, blaTEM-1, blaCTX-M-65, rmtB, aadA, AAC(6')-IIb, baeR, mdtABC, acrAB, oqxAB, tet, H-NS, gyrA, and parC.

The paper discusses the role of various efflux pumps in multidrug resistance in Acinetobacter spp., highlighting their contribution to resistance against multiple antibiotics and the complexity of their regulation.

The study identifies several genes and mutations contributing to ciprofloxacin resistance in Salmonella, including parC T57S, gyrA mutations, and plasmid-mediated quinolone resistance genes like oqxAB, aac(6')-Ib-cr, and qnrS.

The paper reviews the genetic determinants of antibiotic resistance in Francisella, focusing on intrinsic resistance mechanisms and the roles of specific genes such as beta-lactamases, efflux pumps, and LPS modification genes.

The study identifies that the soxS gene regulates antimicrobial resistance in multidrug-resistant Klebsiella pneumoniae MGH78578, particularly affecting tetracycline resistance through the regulation of efflux pumps like acrAB-tolC and others.

The study identifies multiple beta-lactamase genes, including a novel CMY/ACT-type AmpC beta-lactamase and several metallo-beta-lactamases, as well as multidrug efflux pumps in Cedecea neteri, highlighting its resistance mechanisms against various antibiotics.

The paper reviews intrinsic and acquired colistin resistance mechanisms in bacteria, highlighting the role of genes such as pmrA, pmrB, phoP, phoQ, mgrB, arnBCADTEF, and mcr genes in conferring resistance. It discusses the importance of these genes in the context of colistin resistance and their implications for clinical treatment.

The study identifies AcrAB-TolC as a crucial efflux pump contributing to chlorhexidine and other biocide tolerance in Klebsiella pneumoniae. Mutations in ramR lead to increased expression of acrAB and decreased susceptibility to antibiotics and biocides.

The study highlights the role of RND efflux pump systems in mediating multidrug resistance (MDR) in Salmonella, particularly focusing on AcrAB, AcrEF, MdsAB, and MdtAB. Experimental data shows that overexpression of these efflux pumps leads to resistance against fluoroquinolones, chloramphenicol-florfenicol, and tetracyclines.

Complex antibiotic environments drive the evolution of latent novel traits in E. coli through the spread of pleiotropic mutations affecting multiple resistance mechanisms.

The paper discusses the role of mobile genetic elements, such as integrons, transposons, and plasmids, in the dissemination of antimicrobial resistance genes (ARGs) among bacterial pathogens. It highlights the importance of specific genes like blaTEM-1, blaKPC-3, blaCTX-M-15, blaNDM-1, and mcr-1 in conferring resistance to various antibiotics.

The study identified several antimicrobial resistance genes in Salmonella Typhimurium 69M, including aac(6')-Ib-cr, acrAB, acrEF, mdtABC, and macA, which are associated with resistance to various antibiotics. Additionally, mutations in rfbP were found to affect the O-antigen synthesis and may influence bacterial virulence.

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.

The study identified 26 chromosomal resistance genes in Salmonella Gallinarum strains, primarily encoding efflux pumps, and point mutations in gyrase genes (gyrA and gyrB) associated with quinolone resistance. The gyrB mutation S464T was frequently found in Colombian strains.

The study characterizes the role of RND multidrug efflux pumps in drug resistance and physiological functions in Salmonella enterica, Escherichia coli, and Pseudomonas aeruginosa. Key findings include the identification of multiple RND efflux pumps and their contributions to multidrug resistance, biofilm formation, and cellular processes.

The study identifies mutations in gyrB and upregulation of efflux pumps (acrAB, adeIJK, mdtK) as key mechanisms of resistance to GP6 in E. coli and A. baumannii.

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 review discusses the mechanisms of antibiotic resistance in pathotypes of E. coli, focusing on the role of beta-lactamases, carbapenemases, and other resistance genes. It highlights the importance of understanding these mechanisms to combat the growing problem of antibiotic resistance.

The paper reviews the molecular mechanisms of tigecycline resistance in Enterobacterales, highlighting the roles of efflux pumps, tet genes, and other resistance mechanisms. It identifies several tigecycline resistance genes, including tet(X), tet(X1), tet(X2), tet(X3), tet(X4), tet(M), tet(A), tet(B), tet(Y), and others, along with their associated resistance profiles.

The study identifies mutations in marR, acrR, envZ, and nlpD genes that contribute to ampicillin resistance in UPEC strains, leading to multidrug resistance through mechanisms such as increased efflux pump expression, decreased membrane permeability, and inhibited cell lysis.

The study identifies ramA and acrAB as key players in ciprofloxacin resistance in Salmonella Typhimurium, with ramA activating gatR to regulate galactitol metabolism.

The study identified 17 antimicrobial resistance genes in Cronobacter condimenti s37, including genes involved in resistance to multiple antibiotic classes such as beta-lactams, tetracyclines, macrolides, phenicols, quinolones, aminoglycosides, glycopeptides, peptide antibiotics, rifamycins, nitroimidazoles, phosphonic acid derivatives, diaminopyrimidine derivatives, and elphamycins.

The study identified several AMR genes and mutations in K. pneumoniae isolates from Ecuador, including bla KPC-3, bla OXA-9, aadA1, aac(6')-Ib-AKT, and mutations in ompK35, ompK36, ompK37, gyrA, parC, and acrR, contributing to resistance against beta-lactams, aminoglycosides, fluoroquinolones, and other antibiotics.

The study identified tetracycline resistance genes, including tetB, tetR, tetC, acrAB, and robA, in the IncI plasmid pRM18148 of Salmonella enterica serovar Infantis strains isolated from surface waters in California.

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 identified multiple AMR genes including acrAB, tolC, mdtK, ompK35, and ompK36 in Klebsiella pneumoniae isolates from North Iran, which were associated with resistance to various antibiotics.

The study identified several beta-lactamase genes (blaSHV-1, blaCTX-M_group_1, blaTEM-1, blaNDM-1, blaVEB-1, blaKPC) and efflux pump genes (AcrAB, tolC, mdtk) in K. pneumoniae isolates, along with virulence genes (wabG, uge, ureA, iucB).

The study identified several beta-lactamase genes (blaSHV-1, blaCTX-M_group_1, blaTEM-1, blaNDM-1, blaVEB-1, blaKPC) and efflux pump genes (AcrAB, tolC, mdtk) in K. pneumoniae isolates, along with virulence genes (wabG, uge, ureA, iucB).

The study identified the efflux pump genes acrAB and tolC in Klebsiella pneumoniae isolates from human and sheep respiratory infections, which contribute to multidrug resistance.

The study characterizes MBL-producing Enterobacterales strains, identifying NDM-1, NDM-5, and VIM-1 as the most prevalent metallo-beta-lactamases. It also identifies various aminoglycoside, quinolone, and sulfonamide resistance genes, highlighting the multidrug-resistant nature of these isolates.

The paper discusses various mechanisms of bacterial resistance, including intrinsic resistance, acquired resistance, and adaptive resistance, focusing on genetic mutations, efflux pumps, and enzymatic modifications.

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.