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Epidemic clonal groups of Escherichia coli as a cause of antimicrobial-resistant urinary tract infections in Canada, 2002 to 2004.

https://arctichealth.org/en/permalink/ahliterature151298
Source
Antimicrob Agents Chemother. 2009 Jul;53(7):2733-9
Publication Type
Article
Date
Jul-2009
Author
James R Johnson
Megan Menard
Brian Johnston
Michael A Kuskowski
Kim Nichol
George G Zhanel
Author Affiliation
Infectious Diseases (111F), Minneapolis VA Medical Center, 1 Veterans Drive, Minneapolis, MN 55417, USA. johns007@umn.edu
Source
Antimicrob Agents Chemother. 2009 Jul;53(7):2733-9
Date
Jul-2009
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Anti-Infective Agents - pharmacology - therapeutic use
Canada - epidemiology
Child
Child, Preschool
Drug Resistance, Multiple, Bacterial
Escherichia coli - drug effects - genetics - physiology
Escherichia coli Infections - drug therapy - epidemiology - microbiology
Female
Humans
Infant
Male
Middle Aged
Urinary Tract Infections - drug therapy - epidemiology - microbiology
Young Adult
Abstract
The extent to which clonal spread contributes to emerging antimicrobial resistance in Escherichia coli is incompletely defined. To address this question within a recent, nationally representative strain collection, three established drug-resistant E. coli clonal groups (i.e., clonal group A, E. coli O15:K52:H1, and sequence type 131 [ST131]) were sought among 199 E. coli urine isolates recovered from across Canada from 2002 to 2004, with stratification by resistance to trimethoprim-sulfamethoxazole (TS) and fluoroquinolones (FQs). The isolates' clonal backgrounds, virulence genotypes, and macrorestriction profiles were assessed. The three clonal groups were found to account for 37.2% of isolates overall, but accounted for 0% of TS-susceptible (TS-S) and FQ-susceptible (FQ-S) isolates, 20% of TS-resistant (TS-R) and FQ-S isolates, 60% of TS-S and FQ-R isolates, and 68% of TS-R and FQ-R isolates (P
Notes
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PubMed ID
19398649 View in PubMed
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Introduction of quinolone resistant Escherichia coli to Swedish broiler population by imported breeding animals.

https://arctichealth.org/en/permalink/ahliterature279811
Source
Vet Microbiol. 2016 Oct 15;194:74-78
Publication Type
Article
Date
Oct-15-2016
Author
Stefan Börjesson
Thomas Guillard
Annica Landén
Björn Bengtsson
Oskar Nilsson
Source
Vet Microbiol. 2016 Oct 15;194:74-78
Date
Oct-15-2016
Language
English
Publication Type
Article
Keywords
Animals
Anti-Bacterial Agents - pharmacology
Breeding
Chickens
DNA Gyrase - genetics
Drug Resistance, Bacterial - genetics
Environmental Microbiology
Escherichia coli - drug effects - genetics - physiology
Housing, Animal
Minisatellite Repeats - genetics
Mutation
Quinolones - pharmacology
Sweden
Transportation
Abstract
During recent years a rapid increase of quinolone resistant Escherichia coli have been noted in the Swedish broiler population, despite the lack of a known selective pressure. The current study wanted to investigate if imported breeding birds could be a source for the quinolone resistant E. coli. The occurrence of quinolone resistant E. coli was investigated, using selective cultivation with nalidixic acid, in grand-parent birds on arrival to Sweden and their progeny. In addition, sampling in hatcheries and empty cleaned poultry houses was performed. Clonality of isolates was investigated using a 10-loci multiple-locus variable number tandem repeat analysis (MLVA). To identify the genetic basis for the resistance isolates were also analysed for occurrence of plasmid-mediated quinolone resistance (PMQR) determinants and characterization of chromosomal mutations. E. coli resistant to nalidixic acid occurred in grandparent birds imported to Sweden for breeding purposes. Four predominant MLVA types were identified in isolates from grandparent birds, parent birds and broilers. However, resistant E. coli with identical MLVA patterns were also present in hatcheries and poultry houses suggesting that the environment plays a role in the occurrence. Nalidixic acid resistance was due to a mutation in the gyrA gene and no PMQR could be identified. The occurrence of identical clones in all levels of the production pyramid points to that quinolone resistant E. coli can be introduced through imported breeding birds and spread by vertical transmission to all levels of the broiler production pyramid.
PubMed ID
26608722 View in PubMed
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[Mineral salt-dependent inhibition of light emission from the luminescent microorganism Escherichia coli Z9051]

https://arctichealth.org/en/permalink/ahliterature46101
Source
Biofizika. 2001 Mar-Apr;46(2):251-5
Publication Type
Article
Author
A N Boiandin
L Iu Popova
Author Affiliation
Institute of Biophysics, Siberian Branch, Russian Academy of Sciences, Krasnoyarsk, Akademgorodok, 660036 Russia.
Source
Biofizika. 2001 Mar-Apr;46(2):251-5
Language
Russian
Publication Type
Article
Keywords
Chlorides - pharmacology
Culture Media
Depression, Chemical
English Abstract
Escherichia coli - drug effects - genetics - physiology
Luminescence
Magnesium - pharmacology
Photobacterium - genetics
Salts
Sodium - pharmacology
Sulfates - pharmacology
Abstract
The influence of some mineral salts on the recombinant strain Escherichia coli Z9051 was investigated. It was shown that the composition (NaCl, Na2SO4, MgCl2 and MgSO4) and concentration (5 and 10%) of the salts substantially affect the expression of genes for the luminescence system of light-emitting bacteria cloned in the plasmid under the control of the lac-promoter. In some cases, the luminescence level of the microorganism in the presence of salts was similar to the luminescence level under catabolite repression by glucose, the more strong influence of the salts exceeding the effect of catabolite repression. The possibility of adaptation of the genetically modified microorganism to the salinity factor is discussed.
PubMed ID
11357338 View in PubMed
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