Evolution of Antibiotic Resistance from Environmental Microbiota to Pathogens and Back

The study on antibiotic resistance has manly focused on bacterial pathogens and their behavior in clinical settings. However, we need to take into consideration that with the exception of some few determinants as mosaic PBPs acquired by some Gram positive bacteria from commensals, the large majority of antibiotic resistance genes that bacterial pathogens have acquired through horizontal gene transfer have originated in environmental microorganisms. This shows that the environment is the source of resistance and thus the study of antibiotic resistance in non-clinical settings has relevance for understanding in full the process of acquisition and dissemination of antibiotic resistance among clinically-relevant microorganisms. On the other hand, the use along the last decades of antibiotics, not just for human heath but for other purposes as animal farming has produced an enrichment in the populations of bacterial pathogens containing antibiotic resistance genes, which are released into the environment in waste disposals. These resistance determinants can be considered as biological, auto-replicative pollutants and their presence in natural ecosystems and animals, including migratory birds, shows that these environments are reservoirs of resistance and might be vectors for its transmission. Recent works indicate that the variability of resistance determinants present in natural ecosystems is much higher than that observed in the population of bacterial pathogens, which indicates the existence of bottlenecks in the transfer of resistance from the environment to the clinic. In this presentation we will discuss the ecological role that resistance determinants may have in their original environmental hosts, the selective forces triggering the transfer of resistance from environmental microbiota to bacterial pathogens and the mechanisms that allow persistence of resistance genes in pristine, non-contaminated ecosystems, in the absence of selective pressure by antibiotics.