Chronic Exposure to an Environmentally Relevant Triclosan Concentration Induces Persistent Triclosan Resistance but Reversible Antibiotic Tolerance in Escherichia coli

2019 ◽  
Vol 53 (6) ◽  
pp. 3277-3286 ◽  
Author(s):  
Mingzhu Li ◽  
Yuning He ◽  
Jing Sun ◽  
Jing Li ◽  
Junhong Bai ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Chronic Exposure ◽  
Antibiotic Tolerance ◽  
Triclosan Resistance

scholarly journals Robustness analysis of culturing perturbations on Escherichia coli colony biofilm beta-lactam and aminoglycoside antibiotic tolerance

2010 ◽  
Vol 10 (1) ◽  
pp. 185 ◽  
Author(s):  
Trevor R Zuroff ◽  
Hans Bernstein ◽  
Jenna Lloyd-Randolfi ◽  
Lourdes Jimenez-Taracido ◽  
Philip S Stewart ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Robustness Analysis ◽  
Aminoglycoside Antibiotic ◽  
Antibiotic Tolerance ◽  
Beta Lactam

scholarly journals Role of Global Regulators and Nucleotide Metabolism in Antibiotic Tolerance in Escherichia coli

2008 ◽  
Vol 52 (8) ◽  
pp. 2718-2726 ◽  
Author(s):  
Sonja Hansen ◽  
Kim Lewis ◽  
Marin Vulić
Keyword(s):  
Escherichia Coli ◽  
Cell Formation ◽  
Nucleotide Metabolism ◽  
Flavin Mononucleotide ◽  
Formation Mechanisms ◽  
Antibiotic Tolerance ◽  
Persister Cells ◽  
Global Regulators ◽  
Persister Cell

ABSTRACT Bacterial populations produce a small number of persister cells that exhibit multidrug tolerance. Persister cells are largely responsible for the antibiotic recalcitrance of biofilm infections. The mechanism of persister cell formation largely remains unknown due to the challenges in identifying persister genes. We screened an ordered comprehensive library of 3,985 Escherichia coli knockout strains to identify mutants with altered antibiotic tolerance. Stationary-state cultures in 96-well plates were exposed to ofloxacin at a concentration which allows only tolerant persister cells to survive. The persister cell level of each culture was determined. A total of 150 mutants with decreased persistence were identified in the initial screen, and subsequent validation confirmed that neither the growth rate nor the ofloxacin MIC was affected for 10 of them. The genes affected in these strains were dnaJ and dnaK (chaperones), apaH (diadenosine tetraphosphatase), surA (peptidyl-prolyl cis-trans isomerase), fis and hns (global regulators), hnr (response regulator of RpoS), dksA (transcriptional regulator of rRNA transcription), ygfA (5-formyl-tetrahydrofolate cyclo-ligase), and yigB (flavin mononucleotide [FMN] phosphatase). The prominent presence of global regulators among these strains pointed to the likely redundancy of persister cell formation mechanisms: the elimination of a regulator controlling several redundant persister genes would be expected to produce a phenotype. This observation is consistent with previous findings for a possible role of redundant genes such as toxin/antitoxin modules in persister cell formation. ygfA and yigB were of special interest. The mammalian homolog of YgfA (methenyltetrahydrofolate synthetase) catalyzes the conversion of 5-formyl-tetrahydrofolate (THF) into the rapidly degraded 5,10-methenyl-THF, depleting the folate pool. The YigB protein is a phosphatase of FMN which would deplete the pool of this cofactor. Stochastic overexpression of these genes could lead to dormancy and, hence, tolerance by depleting the folate and FMN pools, respectively. Consistent with this scenario, the overexpression of both genes produced increased tolerance to ofloxacin.

scholarly journals Salmonella typhimurium intercepts Escherichia coli signaling to enhance antibiotic tolerance

2013 ◽  
Vol 110 (35) ◽  
pp. 14420-14425 ◽  
Author(s):  
N. M. Vega ◽  
K. R. Allison ◽  
A. N. Samuels ◽  
M. S. Klempner ◽  
J. J. Collins
Keyword(s):  
Escherichia Coli ◽  
Salmonella Typhimurium ◽  
Antibiotic Tolerance

scholarly journals Aminoglycosides induce a bacterial senescent state that increases antibiotic tolerance in treatment-naïve cells

2021 ◽  
Author(s):  
Christian T. Meyer ◽  
Giancarlo N. Bruni ◽  
Ben Dodd ◽  
Joel M. Kralj
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Bacterial Species ◽  
Genetic Resistance ◽  
Membrane Integrity ◽  
Antibiotic Tolerance ◽  
Paracrine Signaling ◽  
E Coli ◽  
Evolutionary Innovation ◽  
Treatment Naïve

Bacterial evolution of antibiotic resistance is facilitated by non-genetic resistance that increases drug tolerance, buying time for evolutionary innovation. Escherichia coli treated with aminoglycosides permanently lose the ability to divide within four hours, yet we discovered a majority of cells maintain membrane integrity and metabolic activity greater than two days post treatment — a bacterial senescent-like state. These cells, which we term zombies, exhibit dynamic gene expression and metabolomic profiles, even after irreversible exit from the cell cycle. Our data reveal zombies upregulate the phage shock protein pathway to maintain membrane integrity. Remarkably, though unable to form new colonies, zombies increase the antibiotic tolerance of treatment-naïve cells, implying chemical communication. Chemical supplementation and genetic knockouts show that zombies communicate with treatment-naïve cells by secreting indole. In summary, our study revealed a bacterial senescent-like state, induced by aminoglycosides, that decreases the antibiotic susceptibility of multiple bacterial species. Thus, E. coli zombies utilize paracrine signaling to promote non-genetic antibiotic tolerance.

scholarly journals Overexpression of target enzyme gene fabI and efflux pump decrease triclosan susceptibility in Escherichia coli

2020 ◽  
Author(s):  
Weiliang Zeng ◽  
Wenya Xu ◽  
Ye Xu ◽  
Wenli Liao ◽  
Yajie Zhao ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Efflux Pump ◽  
Close Association ◽  
Opportunistic Pathogen ◽  
Cross Resistance ◽  
Dilution Method ◽  
Agar Dilution Method ◽  
E Coli ◽  
Resistant Strains ◽  
Triclosan Resistance

Abstract Background: Escherichia coli isolates, the most opportunistic pathogen in the gut, are responsible for the most acquired infections. Triclosan is an effective disinfectant for inhibits microorganisms, but its widespread use causes its residue in urine, resulting in long-term exposure of E. coli in the intestine to triclosan environment and increasing triclosan resistance. We aim to provide the mechanism of action of E. coli isolates against triclosan and the molecular epidemiological analysis of triclosan-resistant strains.Results: Five triclosan-resistant isolates were screened out from 200 E. coli isolates by agar dilution method by to further study, interestingly, multidrug-resistant and cross-resistance phenotypes were observed in triclosan-resistant strains, but not in susceptible strains, and all except one exhibited an inhibition of efflux pump activity by efflux pump inhibition testing. Furthermore, compared with susceptible E. coli strain ATCC 25922, except fabI, increased expression were also found in efflux pump encoding genes ydcV, ydcU, ydcS, ydcT, cysP, yihV, acrB, acrD and mdfA in studied strains which had different PFGE patterns and STs types.Conclusions: These findings indicated that triclosan resistance in E. coli were mainly involved by overexpression of fabI gene, and there was a close association between overexpression of efflux pump with reducing susceptibility to triclosan. Besides, we described cross-resistance between triclosan and antibiotics may be related to the exposure time of triclosan.

Starvation Elicits PspA-Dependent Phenotypic Antibiotic Tolerance in Escherichia Coli

2018 ◽  
Author(s):  
Miaomiao Wang ◽  
Edward Wai Chi Chan ◽  
Marcus Ho-yin Wong ◽  
Sheng Chen
Keyword(s):  
Escherichia Coli ◽  
Antibiotic Tolerance
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