Temperature-driven within-host pathogen dynamics reshapes epidemic invasion in vector-borne plant diseases
Climate-driven disease forecasts typically assess whether environmental conditions favor pathogen growth, yet epidemic spread also depends on how temperature shapes pathogen dynamics within infected hosts. This is particularly important for vector-borne plant diseases, where vectors acquire infection from hosts whose pathogen load, infectivity, and recovery are temperature-dependent. We develop a mechanistic framework in turn determine transitions governed by pathogen accumulation and decay. Parameterized for Pierce's disease of grapevine (Xylella fastidiosa), we analyze invasion under constant, seasonal, stochastic, and empirical temperature regimes. Temperature influences invasion through its effects on pathogen growth, which, in turn, determines progression and recovery rates within hosts. Temperatures maximizing pathogen growth do not necessarily maximize epidemic spread: rapid growth accelerates disease progression and shortens transmission opportunities, whereas intermediate growth rates can prolong infectiousness. Cool temperatures suppress invasion by slowing pathogen accumulation and promoting recovery.
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