ORIGINAL ABSTRACT

The rise of antimicrobial resistance (AMR) constitutes a serious threat to global health. Environmental bacterial communities are a key reservoir of AMR genes (ARGs) that can spread to clinical pathogens. Biocides, which include broad-spectrum herbicides, can co-select for ARGs, posing a potential driver for AMR spread. Glyphosate, the world's most widely used herbicide with known bactericidal properties, targets the shikimate pathway and may thus exert selective pressure favoring resistant bacteria, potentially elevating clinical AMR risk from a One Health perspective. We assessed glyphosate resistance in multidrug-resistant (MDR) species isolated from nosocomial infections. Furthermore, we investigated the relationship between glyphosate-resistant environmental species and clinically relevant MDR pathogens using whole-genome sequencing of environmental and clinical strains. Multidrug-resistant species from hospital-acquired infections exhibited high levels of glyphosate resistance. We established a link between glyphosate-resistant environmental species and typically MDR species common in nosocomial settings. Genomic analysis revealed that glyphosate resistance is partially independent of mutations in the target enzyme (5-enolpyruvylshikimate-3-phosphate synthase), suggesting the contribution of alternative mechanisms, such as efflux pumps. Our findings indicate that glyphosate exposure could favor the prevalence of bacteria associated with nosocomial infections and the rise of MDR clinical strains. This suggests that intensive glyphosate use may accelerate the dissemination of AMR. Consequently, the AMR dimension should be incorporated into the environmental risk assessment of biocidal products that are not used as antimicrobial agents.