4.7 Article

Transfer of antimicrobial resistance plasmids from Klebsiella pneumoniae to Escherichia coli in the mouse intestine

期刊

JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
卷 62, 期 5, 页码 1086-1093

出版社

OXFORD UNIV PRESS
DOI: 10.1093/jac/dkn323

关键词

MGH78578; horizontal gene transfer; streptomycin-treated mice; gastrointestinal tract; indigenous flora; selective pressure

资金

  1. European Commission [CT-2003-506214]

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Objectives and methods: Klebsiella pneumoniae is a nosocomial pathogen and is considered the most common Gram-negative bacterium that exhibits multiple antimicrobial resistances. In this study, the transfer of antimicrobial resistance genes from the clinical multiresistant K. pneumoniae MGH75875 isolate was assessed in vitro and in vivo in an intestinal colonization animal model. The ability to colonize and transfer was tested under different antimicrobial treatments. The frequency of the horizontal gene transfer was also examined in vitro. Results: The clinical isolate of K. pneumoniae colonized the intestine of mice at levels up to 10(9) cfu/g faeces in antimicrobial-treated mice. In mice without antimicrobial treatment, the strain quickly decreased to below the detection limit due to competitive exclusion by the indigenous mouse flora. Onset of antimicrobial treatment gave immediate rise to detectable levels of the strain in the faeces of up to 10(9) cfu/g faeces. The experiment clearly shows that the treatment selects resistant strains and gives advantages to colonize the gastrointestinal tract. Furthermore, high transfer frequency of different plasmids was observed during colonization of the mouse intestine. The bla(SHV) and bla(TEM) genotypes were transferred to both an indigenous recipient in the in vivo setting and to an MG1655 Escherichia coli recipient strain in vitro. Conclusions: K. pneumoniae is an excellent colonizer of the intestine and is extremely promiscuous with respect to the transferability of its numerous plasmids. Antimicrobial treatment enhances the selection of resistant strains and results in an increase in the resistance gene pool, which ultimately raises the risk of spreading resistance genes.

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