scholarly journals Expression of Multidrug Efflux Pump GenesacrAB-tolC,mdfA, andnorEinEscherichia coliClinical Isolates as a Function of Fluoroquinolone and Multidrug Resistance

2010 ◽  
Vol 55 (2) ◽  
pp. 921-924 ◽  
Author(s):  
Michelle C. Swick ◽  
Sonia K. Morgan-Linnell ◽  
Kimberly M. Carlson ◽  
Lynn Zechiedrich
Keyword(s):  
Escherichia Coli ◽  
Multidrug Resistance ◽  
Real Time ◽  
Quantitative Study ◽  
Real Time Pcr ◽  
Efflux Pump ◽  
Clinical Isolates ◽  
Strongly Correlated ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump

ABSTRACTIn a single quantitative study, we measuredacrA,acrB,tolC,mdfA, andnorEexpression inEscherichia coliclinical isolates by using real-time PCR.acrAandacrBoverexpression strongly correlated with fluoroquinolone and multidrug resistance;tolC,mdfA, andnorEexpression did not. The order of abundance of efflux pump transcripts in all fluoroquinolone-susceptible isolates wastolC(highest), thenacrAandacrB, and thenmdfAandnorE.Our findings suggestacrABoverexpression is an indicator of multidrug resistance.

scholarly journals oqxAB Encoding a Multidrug Efflux Pump in Human Clinical Isolates of Enterobacteriaceae

2009 ◽  
Vol 53 (8) ◽  
pp. 3582-3584 ◽  
Author(s):  
Hong Bin Kim ◽  
Minghua Wang ◽  
Chi Hye Park ◽  
Eui-Chong Kim ◽  
George A. Jacoby ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Klebsiella Pneumoniae ◽  
Efflux Pump ◽  
Clinical Isolates ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump

ABSTRACT The genes for multidrug efflux pump OqxAB, which is active on fluoroquinolones, were found in human clinical isolates on a plasmid in Escherichia coli and on the chromosome of Klebsiella pneumoniae. IS26-like sequences flanked the plasmid-mediated oqxAB genes, suggesting that they had been mobilized as part of a composite transposon.

scholarly journals Expression in Escherichia coli of a New Multidrug Efflux Pump, MexXY, from Pseudomonas aeruginosa

1999 ◽  
Vol 43 (2) ◽  
pp. 415-417 ◽  
Author(s):  
Tomoyuki Mine ◽  
Yuji Morita ◽  
Atsuko Kataoka ◽  
Tohru Mizushima ◽  
Tomofusa Tsuchiya
Keyword(s):  
Escherichia Coli ◽  
Pseudomonas Aeruginosa ◽  
Multidrug Resistance ◽  
Efflux Pump ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump ◽  
E Coli ◽  
Expression In Escherichia Coli ◽  
New Genes

ABSTRACT Two new genes (mexXY) similar to mexAB,mexCD, and mexEF and mediating multidrug resistance were cloned from the chromosome of Pseudomonas aeruginosa. Elevated ethidium extrusion was observed withEscherichia coli cells harboring the plasmid carryingmexXY. This MexXY system confers higher resistance to fluoroquinolones than the MexAB and MexCD systems, and E. coli TolC or P. aeruginosa OprM is necessary for the function of the MexXY system.

scholarly journals MarA-Like Regulator of Multidrug Resistance in Yersinia pestis

2006 ◽  
Vol 50 (9) ◽  
pp. 2971-2975 ◽  
Author(s):  
Rupa A. Udani ◽  
Stuart B. Levy
Keyword(s):  
Escherichia Coli ◽  
Multidrug Resistance ◽  
Yersinia Pestis ◽  
Efflux Pump ◽  
Multidrug Resistant ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump ◽  
E Coli ◽  
N Terminus ◽  
Resistant Mutants

ABSTRACT MarA47Yp from Yersinia pestis, showing 47% identity to Escherichia coli MarA in its N terminus, caused resistance to antibiotics and to organic solvents when expressed in both E. coli and Y. pestis. Resistance was linked to increased expression of the AcrAB multidrug efflux pump. In four of five spontaneous multidrug-resistant mutants of Y. pestis independently selected by growth on tetracycline, the marA47 Yp gene was overexpressed. The findings suggest that marA47 Yp is a marA ortholog in Y. pestis.

scholarly journals A Broad-Specificity Multidrug Efflux Pump Requiring a Pair of Homologous SMR-Type Proteins

2000 ◽  
Vol 182 (8) ◽  
pp. 2311-2313 ◽  
Author(s):  
Donald L. Jack ◽  
Michael L. Storms ◽  
Jason H. Tchieu ◽  
Ian T. Paulsen ◽  
Milton H. Saier
Keyword(s):  
Escherichia Coli ◽  
Efflux Pump ◽  
Multidrug Resistant ◽  
Drug Efflux ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump ◽  
Resistant Phenotype ◽  
Small Multidrug Resistance ◽  
Drug Efflux Pumps ◽  
Broad Specificity

ABSTRACT The Bacillus subtilis genome encodes seven homologues of the small multidrug resistance (SMR) family of drug efflux pumps. Six of these homologues are paired in three distinct operons, and coexpression in Escherichia coli of one such operon,ykkCD, but not expression of either ykkC orykkD alone, gives rise to a broad specificity, multidrug-resistant phenotype including resistance to cationic, anionic, and neutral drugs.

scholarly journals Influence of Transcriptional Activator RamA on Expression of Multidrug Efflux Pump AcrAB and Tigecycline Susceptibility in Klebsiella pneumoniae

2005 ◽  
Vol 49 (3) ◽  
pp. 1017-1022 ◽  
Author(s):  
Alexey Ruzin ◽  
Melissa A. Visalli ◽  
David Keeney ◽  
Patricia A. Bradford
Keyword(s):  
Multidrug Resistance ◽  
Klebsiella Pneumoniae ◽  
Antibacterial Agent ◽  
Northern Blot Analysis ◽  
Efflux Pump ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump ◽  
Transposon Insertion ◽  
Constitutive Overexpression ◽  
Parental Phenotype

ABSTRACT Tigecycline is an expanded broad-spectrum antibacterial agent that is active against many clinically relevant species of bacterial pathogens, including Klebsiella pneumoniae. The majority of K. pneumoniae isolates are fully susceptible to tigecycline; however, a few strains that have decreased susceptibility have been isolated. One isolate, G340 (for which the tigecycline MIC is 4 μg/ml and which displays a multidrug resistance [MDR] phenotype), was selected for analysis of the mechanism for this decreased susceptibility by use of transposon mutagenesis with IS903φkan. A tigecycline-susceptible mutant of G340, GC7535, was obtained (tigecycline MIC, 0.25 μg/ml). Analysis of the transposon insertion mapped it to ramA, a gene that was previously identified to be involved in MDR in K. pneumoniae. For GC7535, the disruption of ramA led to a 16-fold decrease in the MIC of tigecycline and also a suppression of MDR. Trans-complementation with plasmid-borne ramA restored the original parental phenotype of decreased susceptibility to tigecycline. Northern blot analysis revealed a constitutive overexpression of ramA that correlated with an increased expression of the AcrAB transporter in G340 compared to that in tigecycline-susceptible strains. Laboratory mutants of K. pneumoniae with decreased susceptibility to tigecycline could be selected at a frequency of approximately 4 × 10−8. These results suggest that ramA is associated with decreased tigecycline susceptibility in K. pneumoniae due to its role in the expression of the AcrAB multidrug efflux pump.

scholarly journals Genetic Characterization of Highly Fluoroquinolone-Resistant Clinical Escherichia coli Strains from China: Role ofacrR Mutations

2001 ◽  
Vol 45 (5) ◽  
pp. 1515-1521 ◽  
Author(s):  
Hui Wang ◽  
Joann L. Dzink-Fox ◽  
Minjun Chen ◽  
Stuart B. Levy
Keyword(s):  
Escherichia Coli ◽  
Blot Analysis ◽  
Genetic Basis ◽  
Efflux Pump ◽  
Pcr Amplification ◽  
Fluoroquinolone Resistance ◽  
Multidrug Efflux ◽  
Multidrug Efflux Pump ◽  
E Coli ◽  
High Level

ABSTRACT The genetic basis for fluoroquinolone resistance was examined in 30 high-level fluoroquinolone-resistant Escherichia coliclinical isolates from Beijing, China. Each strain also demonstrated resistance to a variety of other antibiotics. PCR sequence analysis of the quinolone resistance-determining region of the topoisomerase genes (gyrA/B, parC) revealed three to five mutations known to be associated with fluoroquinolone resistance. Western blot analysis failed to demonstrate overexpression of MarA, and Northern blot analysis did not detect overexpression of soxS RNA in any of the clinical strains. The AcrA protein of the AcrAB multidrug efflux pump was overexpressed in 19 of 30 strains of E. colitested, and all 19 strains were tolerant to organic solvents. PCR amplification of the complete acrR (regulator/repressor) gene of eight isolates revealed amino acid changes in four isolates, a 9-bp deletion in another, and a 22-bp duplication in a sixth strain. Complementation with a plasmid-borne wild-type acrR gene reduced the level of AcrA in the mutants and partially restored antibiotic susceptibility 1.5- to 6-fold. This study shows that mutations in acrR are an additional genetic basis for fluoroquinolone resistance.

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