International Journal of Plant & Soil Science

The disease triangle, in which disease arises from the intersection of a susceptible host, a virulent pathogen and a conducive environment, has organised plant pathology for more than half a century. Its environmental apex was conceived as a relatively stable backdrop, yet heatwaves, compound drought and heat episodes, extreme humidity and short-duration flooding now perturb that apex on timescales shorter than a single crop cycle. This review critically evaluates whether the accumulated mechanistic, ecological and agronomic evidence justifies a structural revision of the framework, and what such a revision would mean for crop protection. Literature was identified through open scholarly indexes and institutional sources, appraised for design adequacy and translational relevance, and synthesised thematically rather than catalogued. Three conclusions are defensible. Moderately elevated temperature suppresses salicylic-acid-dependent immunity through identifiable molecular nodes, and this suppression has been partially reversed by genetic manipulation, which establishes mechanism rather than mere correlation. Water status functions as an actively contested resource rather than a passive variable, since bacterial effectors manipulate host abscisic acid signalling to hydrate the leaf apoplast. Drought and warming reshape root and leaf microbiota in partially conserved directions, although the inference that such reshaping causes disease remains supported mainly by association, by artificial community reconstitution and by a small number of host-genetic experiments. Confidence is weakest where it matters most for agriculture: almost all mechanistic work uses a narrow set of model pathosystems under constant-temperature growth conditions, field validation under realistic fluctuating extremes is scarce, and microbiome interventions have rarely been tested for efficacy under the stress conditions that justify them. The evidence supports treating the microbiota as a modifier that operates within each apex rather than as a self-contained fourth apex, and supports prioritising thermoresilient resistance, stress-validated biological products and extremes-aware forecasting. Claims that climate extremes uniformly intensify plant disease are not supported; the direction of change is pathosystem-specific and frequently non-monotonic.