The effects of chlorate- and streptomycin-resistance mutations on nitrofurantoin resistance in Escherichia coli K-12

1984 ◽  
Vol 30 (12) ◽  
pp. 1448-1452
Author(s):  
Emmanuel E. Obaseiki-Ebor ◽  
Anthony S. Breeze
Keyword(s):  
Escherichia Coli ◽  
Reductase Activity ◽  
Resistance Mutation ◽  
Intermediate Level ◽  
Pleiotropic Effects ◽  
Resistance Mutations ◽  
Chlorate Resistance ◽  
Resistant Mutants ◽  
High Level ◽  
K 12

Chlorate-resistant mutants with none of the usual pleiotropic effects such as defective nitrate reductase activity were isolated from Escherichia coli K-12. These chlorate-resistant mutants (designated chlHW) did not yield strains with a high level of nitrofurantoin resistance following selection with nitrofurantoin. The chlorate-resistance mutation reduced the nitrofurantoin resistance of high-level mutants to an intermediate level. Further mutation to resistance to streptomycin and other aminoglycoside antibiotics suppressed the effect of chlHW on the level of nitrofurantoin resistance. Other chlorate-resistance genes examined did not have the same effect on nitrofurantoin resistance as chlHW. The gene was cotransducible (P1) with intermediate-level nitrofurantoin resistance and proC. It is suggested that the chlHW mutation may enhance the accumulation of nitrofurantoin inside the cell since it is known that a multiple aminoglycoside-resistance mutation with pleiotropic effects on the cell membrane can also confer high-level resistance to nitrofurantoin.

scholarly journals Increased Survival of Antibiotic-Resistant Escherichia coli inside Macrophages

2012 ◽  
Vol 57 (1) ◽  
pp. 189-195 ◽  
Author(s):  
Migla Miskinyte ◽  
Isabel Gordo
Keyword(s):  
Escherichia Coli ◽  
Antibiotic Resistance ◽  
Bacterial Infections ◽  
Resistance Mutation ◽  
Fitness Cost ◽  
Resistance Mutations ◽  
Content Type ◽  
E Coli ◽  
Fitness Effects ◽  
K 12

ABSTRACTMutations causing antibiotic resistance usually incur a fitness cost in the absence of antibiotics. The magnitude of such costs is known to vary with the environment. Little is known about the fitness effects of antibiotic resistance mutations when bacteria confront the host's immune system. Here, we study the fitness effects of mutations in therpoB,rpsL, andgyrAgenes, which confer resistance to rifampin, streptomycin, and nalidixic acid, respectively. These antibiotics are frequently used in the treatment of bacterial infections. We measured two important fitness traits—growth rate and survival ability—of 12Escherichia coliK-12 strains, each carrying a single resistance mutation, in the presence of macrophages. Strikingly, we found that 67% of the mutants survived better than the susceptible bacteria in the intracellular niche of the phagocytic cells. In particular, allE. colistreptomycin-resistant mutants exhibited an intracellular advantage. On the other hand, 42% of the mutants incurred a high fitness cost when the bacteria were allowed to divide outside of macrophages. This study shows that single nonsynonymous changes affecting fundamental processes in the cell can contribute to prolonged survival ofE. coliin the context of an infection.

scholarly journals Cell-Wall Lipopolysaccharides of Ampicillin-Resistant Mutants of Escherichia coli K-12

1976 ◽  
Vol 66 (2) ◽  
pp. 369-377 ◽  
Author(s):  
Peter PREHM ◽  
Stephan STIRM ◽  
Barbara JANN ◽  
Klaus JANN ◽  
Hans G. BOMAN
Keyword(s):  
Escherichia Coli ◽  
Cell Wall ◽  
Resistant Mutants ◽  
K 12

scholarly journals Polyamine-Mediated Resistance of Uropathogenic Escherichia coli to Nitrosative Stress

2006 ◽  
Vol 188 (3) ◽  
pp. 928-933 ◽  
Author(s):  
Jean M. Bower ◽  
Matthew A. Mulvey
Keyword(s):  
Escherichia Coli ◽  
Nitrosative Stress ◽  
Resistance Mutation ◽  
Reactive Nitrogen ◽  
E Coli ◽  
Exogenous Addition ◽  
Reactive Nitrogen Intermediates ◽  
Transposon Mutants ◽  
Increased Sensitivity ◽  
K 12

ABSTRACT During the course of a urinary tract infection, substantial levels of nitric oxide and reactive nitrogen intermediates are generated. We have found that many uropathogenic strains of Escherichia coli display far greater resistance to nitrosative stress than the K-12 reference strain MG1655. By selecting and screening for uropathogenic E. coli transposon mutants that are unable to grow in the presence of acidified nitrite, the cadC gene product was identified as a key facilitator of nitrosative stress resistance. Mutation of cadC, or its transcriptional targets cadA and cadB, results in loss of significant production of the polyamine cadaverine and increased sensitivity to acidified nitrite. Exogenous addition of cadaverine or other polyamines rescues growth of cad mutants under nitrosative stress. In wild-type cells, the concentration of cadaverine produced per cell is substantially increased by exposure to acidified nitrite. The mechanism behind polyamine-mediated rescue from nitrosative stress is unclear, but it is not attributable solely to chemical quenching of reactive nitrogen species or reduction in mutation frequency.

scholarly journals Mutations that increase expression of the EmrAB-TolC efflux pump confer increased resistance to nitroxoline in Escherichia coli

2019 ◽  
Author(s):  
Fabiola Puértolas-Balint ◽  
Omar Warsi ◽  
Marius Linkevicius ◽  
Po-Cheng Tang ◽  
Dan I Andersson
Keyword(s):  
Escherichia Coli ◽  
Target Genes ◽  
Efflux Pump ◽  
Resistance Mechanisms ◽  
Cross Resistance ◽  
Resistance Mutations ◽  
Double Knockout ◽  
Low Level ◽  
Resistant Mutants ◽  
Level Resistance

Abstract Objectives To determine the mechanism of resistance to the antibiotic nitroxoline in Escherichia coli. Methods Spontaneous nitroxoline-resistant mutants were selected at different concentrations of nitroxoline. WGS and strain reconstruction were used to define the genetic basis for the resistance. The mechanistic basis of resistance was determined by quantitative PCR (qPCR) and by overexpression of target genes. Fitness costs of the resistance mutations and cross-resistance to other antibiotics were also determined. Results Mutations in the transcriptional repressor emrR conferred low-level resistance to nitroxoline [nitroxoline MIC (MICNOX) = 16 mg/L] by increasing the expression of the emrA and emrB genes of the EmrAB-TolC efflux pump. These resistant mutants showed no fitness reduction and displayed cross-resistance to nalidixic acid. Second-step mutants with higher-level resistance (MICNOX = 32–64 mg/L) had mutations in the emrR gene, together with either a 50 kb amplification, a mutation in the gene marA, or an IS upstream of the lon gene. The latter mutations resulted in higher-level nitroxoline resistance due to increased expression of the tolC gene, which was confirmed by overexpressing tolC from an inducible plasmid in a low-level resistance mutant. Furthermore, the emrR mutations conferred a small increase in resistance to nitrofurantoin only when combined with an nfsAB double-knockout mutation. However, nitrofurantoin-resistant nfsAB mutants showed no cross-resistance to nitroxoline. Conclusions Mutations in different genes causing increased expression of the EmrAB-TolC pump lead to an increased resistance to nitroxoline. The structurally similar antibiotics nitroxoline and nitrofurantoin appear to have different modes of action and resistance mechanisms.

scholarly journals A Combination of sbmA and tolC Mutations in Escherichia coli K-12 Tn10-Carrying Strains Results in Hypersusceptibility to Tetracycline

2007 ◽  
Vol 190 (4) ◽  
pp. 1491-1494 ◽  
Author(s):  
Ricardo E. de Cristóbal ◽  
Paula A. Vincent ◽  
Raúl A. Salomón
Keyword(s):  
Escherichia Coli ◽  
Double Mutant ◽  
Phenotypic Expression ◽  
Tetracycline Resistance ◽  
Additive Effect ◽  
Complete Suppression ◽  
High Level ◽  
K 12 ◽  
Level Resistance

ABSTRACT Previously, we demonstrated that Escherichia coli tolC mutations reduce the high-level resistance to tetracycline afforded by the transposon Tn10-encoded TetA pump from resistance at 200 μg/ml to resistance at 40 μg/ml. In this study, we found that the addition of an sbmA mutation to a tolC::Tn10 mutant exacerbates this phenotype: the double mutant did not form colonies, even in the presence of tetracycline at a concentration as low as 5 μg/ml. Inactivation of sbmA alone partially inhibited high-level tetracycline resistance, from resistance at 200 μg/ml to resistance at 120 μg/ml. There thus appears to be an additive effect of the mutations, resulting in almost complete suppression of the phenotypic expression of Tn10 tetracycline resistance.

scholarly journals Isolation and characterization of norfloxacin-resistant mutants of Escherichia coli K-12.

1986 ◽  
Vol 30 (2) ◽  
pp. 248-253 ◽  
Author(s):  
K Hirai ◽  
H Aoyama ◽  
S Suzue ◽  
T Irikura ◽  
S Iyobe ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Isolation And Characterization ◽  
Resistant Mutants ◽  
K 12

scholarly journals Molecular Correlates of High-Level Antifolate Resistance in Rwandan Children with Plasmodium falciparum Malaria

2009 ◽  
Vol 54 (1) ◽  
pp. 477-483 ◽  
Author(s):  
Corine Karema ◽  
Mallika Imwong ◽  
Caterina I. Fanello ◽  
Kasia Stepniewska ◽  
Aline Uwimana ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Resistance Mutation ◽  
Plasmodium Falciparum Malaria ◽  
Drug Susceptibility ◽  
Resistance Mutations ◽  
Genes Encoding ◽  
High Level ◽  
Cure Rates ◽  
Antifolate Drugs ◽  
Antifolate Resistance

ABSTRACT Antifolate drugs have an important role in the treatment of malaria. Polymorphisms in the genes encoding the dihydrofolate reductase and dihydropteroate synthetase enzymes cause resistance to the antifol and sulfa drugs, respectively. Rwanda has the highest levels of antimalarial drug resistance in Africa. We correlated the efficacy of chlorproguanil-dapsone plus artesunate (CPG-DDS+A) and amodiaquine plus sulfadoxine-pyrimethamine (AQ+SP) in children with uncomplicated malaria caused by Plasmodium falciparum parasites with p fdhfr and p fdhps mutations, which are known to confer reduced drug susceptibility, in two areas of Rwanda. In the eastern province, where the cure rates were low, over 75% of isolates had three or more p fdhfr mutations and two or three p fdhps mutations and 11% had the p fdhfr 164-Leu polymorphism. In the western province, where the cure rates were significantly higher (P < 0.001), the prevalence of multiple resistance mutations was lower and the p fdhfr I164L polymorphism was not found. The risk of treatment failure following the administration of AQ+SP more than doubled for each additional p fdhfr resistance mutation (odds ratio [OR] = 2.4; 95% confidence interval [CI] = 1.01 to 5.55; P = 0.048) and each p fdhps mutation (OR = 2.1; 95% CI = 1.21 to 3.54; P = 0.008). The risk of failure following CPG-DDS+A treatment was 2.2 times higher (95% CI = 1.34 to 3.7) for each additional p fdhfr mutation, whereas there was no association with mutations in the p fdhps gene (P = 0.13). The p fdhfr 164-Leu polymorphism is prevalent in eastern Rwanda. Antimalarial treatments with currently available antifol-sulfa combinations are no longer effective in Rwanda because of high-level resistance.

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