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Preventive antibiotic treatment of calves: emergence of dysbiosis causing propagation of obese state-associated and mobile multidrug resistance-carrying bacteria
Authors:Dorota A. Dobrzanska  Matthew T. F. Lamaudière  Jessica Rollason  Lauren Acton  Michael Duncan  Sharon Compton  John Simms  Gareth D. Weedall  Igor Y. Morozov
Affiliation:1. School of Life Sciences, Coventry University, Coventry, UK;2. Centre for Sport, Exercise and Life Sciences, Coventry University, Coventry, UK;3. Moreton Morrell College Farm, The Warwickshire College, Warwickshire, CV35 9BL UK;4. School of Natural Sciences and Psychology, Liverpool John Moores University, Liverpool, UK
Abstract:In agriculture, antibiotics are used for the treatment and prevention of livestock disease. Antibiotics perturb the bacterial gut composition but the extent of these changes and potential consequences for animal and human health is still debated. Six calves were housed in a controlled environment. Three animals received an injection of the antibiotic florfenicol (Nuflor), and three received no treatment. Faecal samples were collected at 0, 3 and 7 days, and bacterial communities were profiled to assess the impact of a therapy on the gut microbiota. Phylogenetic analysis (16S-rDNA) established that at day 7, antibiotic-treated microbiota showed a 10-fold increase in facultative anaerobic Escherichia spp, a signature of imbalanced microbiota, dysbiosis. The antibiotic resistome showed a high background of antibiotic resistance genes, which did not significantly change in response to florfenicol. However, the maintenance of Escherichia coli plasmid-encoded quinolone, oqxB and propagation of mcr-2, and colistin resistance genes were observed and confirmed by Sanger sequencing. The microbiota of treated animals was enriched with energy harvesting bacteria, common to obese microbial communities. We propose that antibiotic treatment of healthy animals leads to unbalanced, disease- and obese-related microbiota that promotes growth of E. coli carrying resistance genes on mobile elements, potentially increasing the risk of transmission of antibiotic resistant bacteria to humans.
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