Indeed, both IncN and IncP1 group plasmids have been GSK126 solubility dmso shown to encode clinically important resistance

determinants such as bla CTX-M, bla IMP, bla NDM, bla VIM and qnr [3–8], whilst IncN plasmids have also been strongly implicated in the recent spread of bla KPC encoded carbapenemases [9]. Antimicrobial resistance can sometimes be accompanied by a reduction in biological CH5424802 datasheet fitness in the absence of antibiotic selection. Hence, less fit resistant bacteria may be outcompeted and displaced by fitter, susceptible bacteria in the absence of antibiotic use, leading to the suggestion that it may be possible to reduce the prevalence of antibiotic resistance by temporarily restricting prescribing. In practice, however, such approaches have enjoyed mixed success [10–14]. A fitness cost of antibiotic resistance has often been demonstrated in the case of chromosomal mutations conferring resistance, for example in the case of fusA mutations Selleckchem Ispinesib conferring resistance to fusidic acid [15] and gyrA mutations conferring resistance to fluoroquinolones [16]. However,

compensatory mutations can arise at secondary sites that reduce or eliminate this cost [17]. In the case of acquired antibiotic resistance genes encoded on mobile genetic elements such as plasmids and transposons, the existence of a fitness cost is less clear. While early studies Niclosamide which often investigated cloning plasmids and/or laboratory strains demonstrated a cost to plasmid carriage [18–21], some more recent data using naturally-occurring plasmids and/or wild-type bacteria have failed to demonstrate significant costs and have sometimes shown a benefit. For example, the small sulphonamide and streptomycin resistance plasmid p9123 confers a 4% per generation fitness benefit in E. coli [22], and a benefit has

also been demonstrated for some apramycin resistance plasmids isolated from bovine E. coli [23]. A number of antibiotic resistance encoding plasmids and transposons conferred only a low fitness cost or were cost-neutral in the wild-type E. coli strain 345-2RifC in vitro and in the pig gut [24], whilst the resistance plasmid R751 and variants of it enhanced fitness under some growth conditions in E. coli [25]. It is likely that the fitness cost a particular plasmid exerts on its host is variable depending on the plasmid as well as on the host itself. However, few studies have examined the fitness cost of a single plasmid on different strains of bacteria. 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.