Scientists have long predicted large-scale responses of infectious diseases to climate change, giving rise to a polarizing debate, especially concerning human pathogens for which socioeconomic drivers and control measures can limit the detection of climate-mediated changes. Climate change has already increased the occurrence of diseases in some natural and agricultural ecosystems, but in many cases, outcomes depend on the form of climate change and details of the host-pathogen system. Here, we describe how climate change will affect terrestrial ecosystems and their capacity to reduce infectious diseases. Rhizosphere and bulk soil was collected from grassland, forest and agricultural ecosystems at the Hawkesbury and EUC-FACE climate change field and greenhouse experiments in Western Sydney (Australia). Real-time PCR approaches targeting toxins-encoding genes revealed that elevated CO₂ and rainfall patterns intensified the effect of warming by significantly increasing the virulence of soil-borne human pathogens associated with grassland and forest rhizosphere and bulk soils. As opposed to simply increasing the biomass of soil-borne pathogens at ambient CO₂ under changes in rainfall patterns and temperature, elevated atmospheric CO₂ strongly selected for virulent human pathogens and effected shifts in pathogens composition. 16S rRNA, 18S rRNA and ITS region sequencing with the Illumina Miseq platform revealed the dominance of several opportunistic and true human pathogens in the rhizosphere microbiome, including E.coli 0157:H7, Enterobacteriacae, Chlamydia, Staphylococcus, Salmonella and Clostridium species. The potential mechanisms involved in the interplay between human pathogens in the rhizosphere microbiome are presented in a bioclimatic model of relative microbial abundance that specifically incorporates interactions between biological units.