scholarly journals Differential regulation of the mcb and emr operons of Escherichia coli: role of mcb in multidrug resistance.

1996 ◽  
Vol 40 (4) ◽  
pp. 1050-1052 ◽  
Author(s):  
O Lomovskaya ◽  
F Kawai ◽  
A Matin
Keyword(s):  
Escherichia Coli ◽  
Multidrug Resistance ◽  
Differential Regulation ◽  
Negative Regulator ◽  
Toxic Compounds ◽  
Microcin B17

The mcb operon (which is responsible for microcin B17 production) and the emr operon (which encodes a multidrug resistance pump) share a common negative regulator, EmrR. Nevertheless, compounds that induce the emr operon repress the mcb operon. The pump dedicated to microcin B17 extrusion can also protect the calls against sparfloxacin and other toxic compounds.

scholarly journals Pathologic and microbiologic aspects of pet psittacine infected by Escherichia coli and Salmonella Typhimurium

2017 ◽  
Vol 37 (4) ◽  
pp. 379-384
Author(s):  
Raul A.S. Siqueira ◽  
William C. Maciel ◽  
Ruben H. Vasconcelos ◽  
Windleyanne G.A. Bezerra ◽  
Elisângela S. Lopes ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Multidrug Resistance ◽  
Salmonella Typhimurium ◽  
Antimicrobial Susceptibility ◽  
Inflammatory Infiltrate ◽  
State University ◽  
Antimicrobial Susceptibility Test ◽  
Salmonella Spp ◽  
E Coli

ABSTRACT: The role of Escherichia coli in healthy microbiota of psittacine is controversial, and the presence of Salmonella sp. indicates possible disease. Therefore, this study aimed to identify the presence of E. coli and Salmonella spp. in a psittacine pet that died in Fortaleza, Brazil, correlating pathogenicity aspects of the isolates through the evaluation of lesions and antimicrobial susceptibility. Psittacine pets sent to the Laboratory of Ornithological Studies, State University of Ceará, that died in 2014 and 2015 were necropsied. Fragments of liver, kidneys, intestine, lung, heart, spleen and brain were collected for microbiological and histopathological analyses. Scores were attributed to lesions and isolated strains submitted to antimicrobial susceptibility test. From the seventy necropsied birds, nineteen were positive for E. coli and one for Salmonella Typhimurium. Congestive lesions and lymphoplasmocitic inflammatory infiltrate were observed varying from light to moderate and were the main findings. In the analyzed strains, multidrug resistance against different groups of antibiotics was observed. In conclusion, according to the results, E. coli strains and the Salmonella Typhimurium isolate produced significant lesions in the psittacine pets, and multidrug resistance may hinder treatments with antibiotics used in avian pet medicine.

scholarly journals Hha Controls Escherichia coli O157:H7 Biofilm Formation by Differential Regulation of Global Transcriptional Regulators FlhDC and CsgD

2013 ◽  
Vol 79 (7) ◽  
pp. 2384-2396 ◽  
Author(s):  
Vijay K. Sharma ◽  
Bradley L. Bearson
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Type Strain ◽  
Molecular Mechanisms ◽  
Wild Type Strain ◽  
Differential Regulation ◽  
Negative Regulator ◽  
Wild Type ◽  
Content Type ◽  
Global Regulators

ABSTRACTAlthough molecular mechanisms promoting adherence of enterohemorrhagicEscherichia coli(EHEC) O157:H7 on epithelial cells are well characterized, regulatory mechanisms controlling biofilm formation are not fully understood. In this study, we demonstrate that biofilm formation in EHEC O157:H7 strain 86-24 is highly repressed compared to that in an isogenichhamutant. Thehhamutant produced large quantities of biofilm compared to the wild-type strain at 30°C and 37°C. Complementation of thehhamutant reduced the level of biofilm formation to that of the wild-type strain, indicating that Hha is a negative regulator of biofilm production. While swimming motility and expression of the flagellar genefliCwere significantly reduced, the expression ofcsgA(encoding curlin of curli fimbriae) and the ability to bind Congo red were significantly enhanced. The expression of bothfliCandcsgAand the phenotypes of motility and curli production affected by these two genes, respectively, were restored to wild-type levels in the complementedhhamutant. ThecsgAdeletion abolished biofilm formation in thehhamutant and wild-type strain, andcsgAcomplementation restored biofilm formation to these strains, indicating the importance ofcsgAand curli in biofilm formation. The regulatory effects of Hha on flagellar and curli gene expression appear to occur via the induction and repression of FlhDC and CsgD, as demonstrated by reducedflhDand increasedcsgDtranscription in thehhamutant, respectively. In gel shift assays Hha interacted withflhDCandcsgDpromoters. In conclusion, Hha regulates biofilm formation in EHEC O157:H7 by differential regulation of FlhDC and CsgD, the global regulators of motility and curli production, respectively.

scholarly journals The role of potentiating mutations in the evolution of pandemic Escherichia coli clones

2021 ◽  
Author(s):  
Elizabeth A. Cummins ◽  
Ann E. Snaith ◽  
Alan McNally ◽  
Rebecca J. Hall
Keyword(s):  
Escherichia Coli ◽  
Multidrug Resistance ◽  
Multidrug Resistant ◽  
Vast Array ◽  
Sequence Of Events ◽  
Resistance Plasmids ◽  
Evolutionary Trajectories ◽  
Global Threat ◽  
Evolutionary Emergence

AbstractThe Escherichia coli species exhibits a vast array of variable lifestyles, including environmental, commensal, and pathogenic organisms. Many of these E. coli contribute significantly to the global threat of antimicrobial resistance (AMR). Multidrug-resistant (MDR) clones of E. coli have arisen multiple times over varying timescales. The repeated emergence of successful pandemic clones, including the notorious ST131 lineage, highlights a desperate need to further study the evolutionary processes underlying their emergence and success. Here, we review the evolutionary emergence of E. coli ST131 pandemic clones and draw parallels between their evolutionary trajectories and those of other lineages. From colonization and expansion to the acquisition of multidrug resistance plasmids, potentiating mutations are present at each stage, leading to a proposed sequence of events that may result in the formation of an antimicrobial-resistant pandemic clone.

scholarly journals Role of Histone-Like Protein H-NS in Multidrug Resistance of Escherichia coli

2004 ◽  
Vol 186 (5) ◽  
pp. 1423-1429 ◽  
Author(s):  
Kunihiko Nishino ◽  
Akihito Yamaguchi
Keyword(s):  
Escherichia Coli ◽  
Drug Resistance ◽  
Multidrug Resistance ◽  
Enteric Bacteria ◽  
Resistance Pattern ◽  
Pcr Analysis ◽  
Reverse Transcription Pcr ◽  
Double Deletion ◽  
Outer Membrane Channel

ABSTRACT The histone-like protein H-NS is a major component of the bacterial nucleoid and plays a crucial role in global gene regulation of enteric bacteria. It is known that the expression of a variety of genes is repressed by H-NS, and mutations in hns result in various phenotypes, but the role of H-NS in the drug resistance of Escherichia coli has not been known. Here we present data showing that H-NS contributes to multidrug resistance by regulating the expression of multidrug exporter genes. Deletion of the hns gene from the ΔacrAB mutant increased levels of resistance against antibiotics, antiseptics, dyes, and detergents. Decreased accumulation of ethidium bromide and rhodamine 6G in the hns mutant compared to that in the parental strain was observed, suggesting the increased expression of some drug exporter(s) in this mutant. The increased drug resistance and decreased drug accumulation caused by the hns deletion were completely suppressed by deletion of the multifunctional outer membrane channel gene tolC. At least eight drug exporter systems require TolC for their functions. Among these, increased expression of acrEF, mdtEF, and emrKY was observed in the Δhns strain by quantitative real-time reverse transcription-PCR analysis. The Δhns-mediated multidrug resistance pattern is quite similar to that caused by overproduction of the AcrEF exporter. Deletion of the acrEF gene greatly suppressed the level of Δhns-mediated multidrug resistance. However, this strain still retained resistance to some compounds. The remainder of the multidrug resistance pattern was similar to that conferred by overproduction of the MdtEF exporter. Double deletion of the mdtEF and acrEF genes completely suppressed Δhns-mediated multidrug resistance, indicating that Δhns-mediated multidrug resistance is due to derepression of the acrEF and mdtEF drug exporter genes.

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