Ecology of antimicrobial resistance: humans, animals, food and environment

Antimicrobial resistance is a major health problem. After decades of research, numerous difficulties in tackling resistance have emerged, from the paucity of new antimicrobials to the inefficient contingency plans to reduce the use of antimicrobials; consequently, resistance to these drugs is out of control. Today we know that bacteria from the environment are often at the very origin of the acquired resistance determinants found in hospitals worldwide. Here we define the genetic components that flow from the environment to pathogenic bacteria and thereby confer a quantum increase in resistance levels, as resistance units (RU). Environmental bacteria as well as microbiomes from humans, animals, and food represent an infinite reservoir of RU, which are based on genes that have had, or not, a resistance function in their original bacterial hosts. This brief review presents our current knowledge of antimicrobial resistance and its consequences, with special focus on the importance of an ecologic perspective of antimicrobial resistance. This discipline encompasses the study of the relationships of entities and events in the framework of curing and preventing disease, a definition that takes into account both microbial ecology and antimicrobial resistance. Understanding the flux of RU throughout the diverse ecosystems is crucial to assess, prevent and eventually predict emerging scaffolds before they colonize health institutions. Collaborative horizontal research scenarios should be envisaged and involve all actors working with humans, animals, food and the environment.

Garvicin A, a novel class IId bacteriocin from Lactococcus garvieae that inhibits septum formation in L. garvieae strains

Lactococcus garvieae 21881, isolated in a human clinical case, produces a novel class IId bacteriocin, garvicin A (GarA), which is specifically active against other L. garvieae strains, including fish- and bovine-pathogenic isolates. Purification from active supernatants, sequence analyses, and plasmid-curing experiments identified pGL5, one of the five plasmids found in L. garvieae [M. Aguado-Urda et al., PLoS One 7(6):e40119, 2012], as the coding plasmid for the structural gene of GarA (lgnA), its putative immunity protein (lgnI), and the ABC transporter and its accessory protein (lgnC and lgnD). Interestingly, pGL5-cured strains were still resistant to GarA. Other putative bacteriocins encoded by the remaining plasmids were not detected during purification, pointing to GarA as the main inhibitor secreted by L. garvieae 21881. Mode-of-action studies revealed a potent bactericidal activity of GarA. Moreover, transmission microscopy showed that GarA seems to act by inhibiting septum formation in L. garvieae cells. This potent and species-specific inhibition by GarA holds promise for applications in the prevention or treatment of infections caused by pathogenic strains of L. garvieae in both veterinary and clinical settings.