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Under global change, plant invasions may alter tick-borne disease (TBD) transmission. The direction and magnitude of changes in TBD risk resulting from invasions remain poorly understood because research has often been species-specific or insufficient to quantify mechanisms. In this overview, we describe how invasive plant functional traits can mediate microclimates, how tick survival and abundance vary under altered environmental conditions created by invasive plants, and how invasive plants can impact blood meal host activity and pathogen prevalence. These findings are synthesized within a One Health framework that considers climate, landscape, and disturbance to ultimately predict TBD risk. Finally, we discuss range expansion of ticks and pathogens, spatial and temporal research scales, and modeling approaches for predicting TBD risk amidst global change. We highlight how plant invasions and climate change can impact ticks, hosts, and pathogens, and we identify research needs to improve models of TBDs in a changing world. 

Abstract Non‐native plants are typically released from specialist enemies but continue to be attacked by generalists, albeit at lower intensities. This reduced herbivory may lead to less investment in constitutive defences and greater investment in induced defences, potentially reducing defence costs. We compared herbivory on 27 non‐native and 59 native species in the field and conducted bioassays and chemical analyses on 12 pairs of non‐native and native congeners. Non‐natives suffered less damage and had weaker constitutive defences, but stronger induced defences than natives. For non‐natives, the strength of constitutive defences was correlated with the intensity of herbivory experienced, whereas induced defences showed the reverse. Investment in induced defences correlated positively with growth, suggesting a novel mechanism for the evolution of increased competitive ability. To our knowledge, these are the first linkages reported among trade‐offs in plant defences related to the intensity of herbivory, allocation to constitutive versus induced defences, and growth. 

Abstract The densities of highly competent plant hosts (i.e. those that are susceptible to and successfully transmit a pathogen) may shape pathogen community composition and disease severity, altering disease risk and impacts. Life history and evolutionary history can influence host competence; longer lived species tend to be better defended than shorter lived species and pathogens adapt to infect species with which they have longer evolutionary histories. It is unclear, however, how the densities of species that differ in competence due to life and evolutionary histories affect plant pathogen community composition and disease severity.We examined foliar fungal pathogens of two host groups in a California grassland: native perennial and non‐native annual grasses. We first characterized pathogen community composition and disease severity of the two host groups to approximate differences in competence. We then used observational and manipulated gradients of native perennial and non‐native annual grass densities to assess the effects of each host group on pathogen community composition and disease severity in 1‐m²plots.Native perennial and non‐native annual grasses hosted distinct pathogen communities but shared generalist pathogens. Native perennial grasses experienced 26% higher disease severity than non‐native annuals. Only the observational gradient of native perennial grass density affected disease severity; there were no other significant relationships between host group density and either disease severity or pathogen community composition.Synthesis. The life and evolutionary histories of grasses likely influence their competence for different pathogen species, exemplified by distinct pathogen communities and differences in disease severity. However, there was limited evidence that the density of either host group affected pathogen community composition or disease severity. Therefore, competence for different pathogens likely shapes pathogen community composition and disease severity but may not interact with host density to alter disease risk and impacts at small scales.