Antimicrobial resistance is a natural phenomenon: bacteria produce antimicrobial substances as part of their repertoire to compete in the struggle for colonisation, space and nutrients. Resistance therefore existed long before the introduction of antimicrobial drugs: the effect of using antimicrobials has been to accelerate AMR through classical selective pressure. That this has happened in both veterinary and human populations of bacteria is not disputed; the evidence for interconnection of AMR in these two populations is, however, inconclusive and is the subject of continuing political and scientific debate with contradictory evidence produced by both sides [8–10]. It does appear that antimicrobial use in animals increases AMR in animal bacteria and that treating people with antimicrobials increases AMR in human bacteria. However, current scientific evidence does not allow definitive assessment of whether reducing antimicrobial use in animals has reduced AMR in medical pathogens. The extent to which AMR in populations of animal bacteria threatens public health therefore remains uncertain. The evidence for resistance in animal bacteria acting as genetic reservoirs of resistance for transfer to bacteria of public health importance is also inconclusive. Even for zoonotic bacteria such as Salmonella typhimurium DT104, the links between animal and human bacterial populations have become less clear with the application of sophisticated molecular typing bacterial methods and population genetics adding new complexity to the AMR debate [11].