Climate change is an escalating global crisis that profoundly accelerates the development and dissemination of antimicrobial resistance (AMR), posing a severe threat to planetary health. This review elucidates the complex mechanisms through which climate change amplifies AMR across bacterial, fungal, and protozoal pathogens. We demonstrate that rising temperatures promote horizontal gene transfer, stress-induced mutagenesis, and efflux pump expression, with a 10 °C increase correlating with a 4%–17% rise in bacterial resistance. Concurrently, increased UV-B radiation enhances plasmid conjugation by 2–10-fold and facilitates the uptake of fragmented extracellular DNA, driving resistance evolution. The analysis extends to the emergence of antifungal and antiprotozoal resistance, where climate stressors co-select for resistance mechanisms, as seen in azole-resistant Aspergillus fumigatus and the simultaneous multi-continent emergence of multidrug-resistant Candida auris. Furthermore, ecological drivers, including extreme weather events that elevate antibiotic residues in floodwaters by up to 30 times, migratory birds that carry multidrug-resistant bacteria (with 38% MDR E. coli prevalence in some species), and intensified agricultural practices using over 200 fungicide compounds, create global hotspots for resistance exchange. Alarmingly, the rapid thawing of polar regions is mobilizing ancient resistomes, with metagenomic surveys revealing up to 944 distinct antibiotic resistance genes in glacial ice. These synergistic processes underscore the urgent need for a unified “One Health” approach that integrates climate-resilient policies, stringent antimicrobial stewardship, enhanced environmental surveillance, and innovative interventions to curb the global spread of AMR in an era of rapid environmental change.
Nahiduzzaman et al. (2026) studied this question.