Abstract
BackgroundUnderstanding the survival of resistance plasmids in the absence of selective pressure for the antibiotic resistance genes they carry is important for assessing the value of interventions to combat resistant bacteria. Here, several poorly explored questions regarding the fitness impact of IncP1 and IncN broad host range plasmids on their bacterial hosts are examined; namely, whether related plasmids have similar fitness impacts, whether this varies according to host genetic background, and what effect antimicrobial resistance gene silencing has on fitness.ResultsFor the IncP1 group pairwise in vitro growth competition demonstrated that the fitness cost of plasmid RP1 depends on the host strain. For the IncN group, plasmids R46 and N3 whose sequence is presented for the first time conferred remarkably different fitness costs despite sharing closely related backbone structures, implicating the accessory genes in fitness. Silencing of antimicrobial resistance genes was found to be beneficial for host fitness with RP1 but not for IncN plasmid pVE46.ConclusionsThese findings suggest that the fitness impact of a given plasmid on its host cannot be inferred from results obtained with other host-plasmid combinations, even if these are closely related.
Highlights
Understanding the survival of resistance plasmids in the absence of selective pressure for the antibiotic resistance genes they carry is important for assessing the value of interventions to combat resistant bacteria
Broad-host range plasmids, such as those belonging to the IncN and IncP1 groups are important to the dissemination of antibiotic resistance due to their ability to replicate in a variety clinically relevant bacterial species and environments [1,2]
The small sulphonamide and streptomycin resistance plasmid p9123 confers a 4% per generation fitness benefit in E. coli [22], and a benefit has been demonstrated for some apramycin resistance plasmids isolated from bovine E. coli [23]
Summary
Understanding the survival of resistance plasmids in the absence of selective pressure for the antibiotic resistance genes they carry is important for assessing the value of interventions to combat resistant bacteria. Broad-host range plasmids, such as those belonging to the IncN and IncP1 groups are important to the dissemination of antibiotic resistance due to their ability to replicate in a variety clinically relevant bacterial species and environments [1,2]. Both IncN and IncP1 group plasmids have been shown to encode clinically important resistance determinants such as blaCTX-M, blaIMP, blaNDM, blaVIM and qnr [3,4,5,6,7,8], whilst IncN plasmids have been strongly implicated in the recent spread of blaKPC encoded carbapenemases [9]. The genetic factors, be they plasmid or host-encoded, that influence fitness are poorly understood, and it is not known whether related plasmids influence fitness in similar ways
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