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

Artikel i vetenskaplig tidskrift
Författare Nahid Karami
Anna Martner
Virve Enne
Svante Swerkersson
Ingegerd Adlerberth
Agnes E Wold
Publicerad i Journal of Antimicrobial Chemotherapy
Volym 60
Nummer/häfte 5
Sidor 1142-1145
ISSN 0305-7453
Publiceringsår 2007
Publicerad vid Institutionen för biomedicin, avdelningen för infektionssjukdomar
Institutionen för kliniska vetenskaper
Sidor 1142-1145
Språk en
Länkar dx.doi.org/10.1093/jac/dkm327
Ämnesord Amoxicillin, therapeutic use, Ampicillin, pharmacology, Anti-Bacterial Agents, pharmacology, Drug Resistance, Bacterial, genetics, Escherichia coli, drug effects, enzymology, genetics, Escherichia coli Proteins, genetics, Feces, microbiology, Gastrointestinal Tract, microbiology, Gene Transfer, Horizontal, Humans, Infant, Newborn, Urinary Tract Infections, drug therapy, beta-Lactamases, genetics
Ämneskategorier Klinisk bakteriologi

Sammanfattning

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. beta-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 bla(TEM-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 bla(TEM-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.

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