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JAC Advance Access originally published online on September 3, 2007
Journal of Antimicrobial Chemotherapy 2007 60(5):1142-1145; doi:10.1093/jac/dkm327
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Transfer of an ampicillin resistance gene between two Escherichia coli strains in the bowel microbiota of an infant treated with antibiotics

Nahid Karami1,*, Anna Martner1, Virve I. Enne2, Svante Swerkersson3, Ingegerd Adlerberth1 and Agnes E. Wold1

1 Department of Clinical Bacteriology, Göteborg University, Sweden 2 Department of Cellular and Molecular Medicine, University of Bristol, UK 3 Department of Paediatrics, Göteborg University, Sweden

Received 5 April 2007; returned 18 July 2007; accepted 31 July 2007


* Correspondence address. Department of Clinical Bacteriology, Guldhedsgatan 10A, SE-413 46 Göteborg, Sweden. Tel: +46-31-3424729; Fax: +46-31-3424975; E-mail: nahid.karami{at}microbio.gu.se

Objectives: To investigate the presumed acquisition of ampicillin resistance by an Escherichia coli strain residing in the gut of an infant.

Methods: E. coli strains were quantified in faecal samples obtained at regular intervals from an infant followed from birth to 12 months of age and their resistance profiles were determined. ß-Lactamases were identified by isoelectric focusing and genes by PCR followed by DNA sequencing. Plasmids were characterized by restriction fragment analysis and Southern-blot hybridization, and tested for conjugative transfer.

Results: The infant carried two E. coli strains, termed 29A and 29B, simultaneously in the microbiota during the first month of life. All isolates of 29A were resistant to ampicillin, whereas strain 29B, which was initially ampicillin susceptible, acquired resistance following treatment of the infant with ampicillin/amoxicillin because of urinary tract infection. Acquisition of resistance by strain 29B was associated with acquisition of a blaTEM-1b-encoding plasmid, pNK29, which was also present in strain 29A. Transfer of plasmid pNK29 could be replicated by conjugation from strain 29A to strain 29B in vitro. Strain 29A also adapted to ampicillin treatment by mutation of the blaTEM-1b promoter gene to yield a higher level of resistance.

Conclusions: This is an unequivocal demonstration of gene transfer between two strains co-residing in the human gut, as the donor, recipient and transconjugant strains were isolated. The results suggest the dynamic adaptation by commensal bacteria in response to antibiotic treatment may occur readily.

Keywords: blaTEM-1b gene , plasmid , pNK29


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