Canopy-level interactions have been largely ignored in epidemiological models and their applications in defining disease risks under climate change, although these interactions are important for disease management. This paper uses anthracnose of Stylosanthes scabra as a case study and reviews research on dynamics of the pathogen (Colletotrichum gloeosporioides) at the canopy level and pathogen evolution under changing climate. It argues that linking of pathogen dynamics, crop growth and climate models is essential in predicting disease risks under climate change. A plant functional-structural model was used to couple S. scabra growth and architecture with disease under ambient and elevated CO 2 . A level of induced resistance in plants with enlarged canopy determined anthracnose severity at elevated CO 2 . Moisture-related microclimatic variables determined infection at ambient but not at elevated CO 2 . At high CO 2 increased disease level from raised pathogen fecundity in enlarged canopy accelerated pathogen evolution after 25 sequential infection cycles. Modelling of pathogen dynamics under climate change currently suffers from a paucity of quantitative data, mismatch of scales in coupling climate and disease models, and model uncertainties. Further experimental research on interactions of biotic and abiotic factors on plant diseases under climate change and validation of models are essential prior to their use in climate-change prediction. Understanding and anticipating trends in host-pathogen evolution under climate change will improve the durability of resistance and lay the foundation for increased crop adaptation through pre-emptive plant breeding.

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This study examines the relative importance of canopy size and induced resistance to Colletotrichum gloeosporioides at 350- and 700-ppm atmospheric CO(2) concentrations on susceptible Stylosanthes scabra 'Fitzroy' from two studies in a controlled environment facility (CEF) and in the field. Plants were grown at the two CO(2) concentrations in a repeated experiment in the CEF and inoculated at 6, 9, or 12 weeks of age. Although the physiological maturity of plants was at a similar stage for all three ages, the number of lesions per plant increased with increasing plant age at both CO(2) concentrations. At 350 ppm, the increase was associated with canopy size and increasing infection efficiency of the pathogen, but at 700 ppm, it was associated only with canopy size, because infection efficiency did not change with increasing age. A level of resistance was induced in plants at 700 ppm CO(2). In a second study, plants were raised for 12 to 14 weeks at the two CO(2) concentrations in the CEF and exposed to C. gloeosporioides inoculum in replicated field plots under ambient CO(2) over three successive years. Fitzroy developed a dense and enlarged canopy, with 28 to 46% more nodes, leaf area, and aboveground biomass at high CO(2) than at low CO(2). Up to twice as many lesions per plant were produced in the high CO(2) plants, because the enlarged canopy trapped many more pathogen spores. The transient induced resistance in high CO(2) plants failed to operate when exposed to pathogen inoculum under ambient CO(2) in the field. These results highlight the need to consider both canopy size and host resistance in assessing the influence of elevated CO(2) on plant disease.

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