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The Role of Commensal Microflora of Animals in the Transmission of Extended Spectrum β-Lactamases (ESBLs)

Objective

<p>ESBL-producing E. coli and Salmonella isolated among pathogenic and commensal bacteria from the community, foods, health care and animal sources in The Netherlands, UK and Germany will be collected and characterised.</p>

<p>Isolates will be collected based on a standardized phenotypic selection protocol and a centralized strain collection built.</p>

The contribution of E. coli from animals to the dissemination of ESBLs to the community, food-borne pathogens and healthcare setting, all isolates will be characterized in four ways:
<ul><li>The genetic relatedness of a selection of E. coli harbouring ESBLs from animal and human sources will be determined by MLST, PFGE and phylogenetic grouping.</li>
<li>Resistance and virulence-associated genes in E. coli and Salmonella from all sources will be determined using microarrays.</li>
<li>The ESBL-expression and the precise ESBL-encoding genes will be defined by DNA sequencing.</li>
<li>Plasmid-mediated ESBLs will also be characterized by isolation, size determination and using a variety of molecular methods following conjugation and/or transformation experiments.</li></ul>

More information

<p>Background: The purpose of this study is to examine the zoonotic aspects of extended spectrum β-lactamase (ESBL)- positive commensal E. coli strains and their mobile genetic elements in food-producing animals, and animal products as a source for introduction of these enzymes into food-borne pathogens, commensals and pathogens in the community and health care settings. By studying the epidemiology and molecular biology of E.coli harbouring ESBLs it will promote our understanding about the contribution of commensals in these reservoirs to the disease burden of ESBL-producing E. coli causing serious infections in the human population. Understanding the genetic relatedness of ESBL strains in different niches is essential to understand the molecular epidemiology of these isolates and genes, and thereby contribute to lessening the impact on public health. </p>

Institution
Health Protection Agency
Start date
2009
End date
2011
Funding Source
Project number
B14017