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Predicting how climate change will affect disease risk is complicated by the fact that changing environmental conditions can affect disease through direct and indirect effects. Species with fast-paced life-history strategies often amplify disease, and changing climate can modify life-history composition of communities thereby altering disease risk. However, individuals within a species can also respond to changing conditions with intraspecific trait variation. To test the effect of temperature, as well as inter- and intraspecifc trait variation on community disease risk, we measured foliar disease and specific leaf area (SLA; a proxy for life-history strategy) on greater than 2500 host (plant) individuals in 199 communities across a 1101-m elevational gradient in southeastern Switzerland. There was no direct effect of increasing temperature on disease. Instead, increasing temperature favoured species with higher SLA, fast-paced life-history strategies. This effect was balanced by intraspecific variation in SLA: on average, host individuals expressed lower SLA with increasing temperature, and this effect was stronger among species adapted to warmer temperatures and lower latitudes. These results demonstrate how impacts of changing temperature on disease may depend on how temperature combines and interacts with host community structure while indicating that evolutionary constraints can determine how these effects are manifested under global change.This article is part of the theme issue ‘Infectious disease ecology and evolution in a changing world’.

Anthropogenic change is contributing to the rise in emerging infectious diseases, but it remains unclear which global change drivers most increase disease and under what contexts. We amassed a dataset from the literature that includes 1,832 observations of infectious disease responses to global change drivers across 1,202 host-parasite combinations. We found that biodiversity loss, climate change, and introduced species were associated with increases in disease-related endpoints or harm (i.e., enemy release for introduced species), whereas urbanization was associated with decreases in disease endpoints. Natural biodiversity gradients, deforestation, forest fragmentation, and most classes of chemical contaminants had non-significant effects on these endpoints. Overall, these results were consistent across human and non-human diseases. Context-dependent effects of the global change drivers on disease were common and are discussed. These findings will help better target disease management and surveillance efforts towards global change drivers that increase disease.One-Sentence SummaryHere we quantify which global change drivers increase infectious diseases the most to better target global disease management and surveillance efforts.

Plant species can show considerable morphological and functional variation along environmental gradients. This intraspecific trait variation (ITV) can have important consequences for community assembly, biotic interactions, ecosystem functions and responses to global change. However, directly measuring ITV across many species and wide geographic areas is often infeasible. Thus, a method to predict spatial variation in a species’ functional traits could be valuable. We measured specific leaf area (SLA), height and leaf area (LA) of grasses across California, covering 59 species at 230 sampling locations. We asked how these traits change along climate gradients within each species and used machine learning to predict local trait values for any species at any location based on phylogenetic position, local climate and that species’ mean traits. We then examined how much these local predictions alter patterns of assemblage-level trait variation across the state. Most species exhibited higher SLA and grew taller at higher temperatures and produced larger leaves in drier conditions. The random forests predicted spatial variation in functional traits very accurately, with correlations up to 0.97. Because trait records were spatially biased towards warmer areas, and these areas tend to have higher SLA individuals within each species, species means of SLA were upwardly biased. As a result, using species means over-estimates SLA in the cooler regions of the state. Our results also suggest that height may be substantially under-predicted in the warmest areas. Synthesis. Using only species mean traits to characterize the functional composition of communities risks introducing substantial error into trait-based estimates of ecosystem properties including decomposition rates or NPP. The high performance of random forests in predicting local trait values provides a way forward for estimating high-resolution patterns of ITV without a massive data collection effort.

Parasites can affect and be affected by the host's microbiome, with consequences for host susceptibility, parasite transmission, and host and parasite fitness. Yet, two aspects of the relationship between parasite infection and host microbiota remain little understood: the nature of the relationship under field conditions, and how the relationship varies among parasites. To overcome these limitations, we performed a field survey of the within-leaf fungal community in a tall fescue population. We investigated how diversity and composition of the fungal microbiome associate with natural infection by fungal parasites with different feeding strategies. A parasite's feeding strategy affects both parasite requirements of the host environment and parasite impacts on the host environment. We hypothesized that parasites that more strongly modify niches available within a host will be associated with greater changes in microbiome diversity and composition. Parasites with a feeding strategy that creates necrotic tissue to extract resources (necrotrophs) may not only have different niche requirements, but also act as particularly strong niche modifiers. Barcoded amplicon sequencing of the fungal ITS region revealed that leaf segments symptomatic of necrotrophs had lower fungal diversity and distinct composition compared to segments that were asymptomatic or symptomatic of other parasites. There were no clear differences in fungal diversity or composition between leaf segments that were asymptomatic and segments symptomatic of other parasite feeding strategies. Our results motivate future experimental work to test how the relationship between the microbiome and parasite infection is impacted by parasite feeding strategy and highlight the potential importance of parasite traits.

Invertebrate herbivores are important and diverse, and their abundance and impacts are expected to undergo unprecedented shifts under climate change. Yet, past studies of invertebrate herbivory have documented a wide variety of responses to changing temperature, making it challenging to predict the direction and magnitude of these shifts. One explanation for these idiosyncratic responses is that changing environmental conditions may drive concurrent changes in plant communities and herbivore traits. Thus, the impacts of changing temperature on herbivory might depend on how temperature combines and interacts with characteristics of plant communities and the herbivores that occupy them. Here, we test this hypothesis by surveying invertebrate herbivory in 220, 0.5 meter-diameter herbaceous plant communities along a 1101-meter elevational gradient. Our results suggest that increasing temperature can drive community-level herbivory via at least three overlapping mechanisms: increasing temperature directly reduced herbivory, indirectly affected herbivory by reducing phylogenetic diversity of the plant community, and indirectly affected herbivory by altering the effects of functional and phylogenetic diversity on herbivory. Consequently, increasing functional diversity of plant communities had a negative effect on herbivory, but only in colder environments while a positive effect of increasing phylogenetic diversity was observed in warmer environments. Moreover, accounting for differences among herbivore feeding guilds considerably improved model fit, because different herbivore feeding guilds varied in their response to temperature and plant community composition. Together, these results highlight the importance of considering both plant and herbivore community context in order to predict how climate change will alter invertebrate herbivory.

Plant community succession is structured by initial richness, plant consumer pressure and soil resource supply. These drivers influence species' trait trade‐offs that underlie temporal changes in plant community diversity. Importantly, how these drivers interact with each other and through time and whether they act on different facets of plant community diversity by promoting different plant trade‐off strategies remains poorly understood. We experimentally manipulated initial plant richness, consumer pressure via pesticide spraying and soil resource supply via fertilization across 4 years of old field succession. We then allowed natural colonization and extinction to occur and examined how the three drivers influenced succession. Specifically, we examined changes in temporal dynamics by conducting yearly taxonomic cover surveys and measuring light penetration to the ground. In the third year, we measured vegetative height and specific leaf area (SLA), and investigated seed mass using a trait database. Higher initial richness, lower consumer pressure and increased soil resource supply all decreased colonizing species richness and light availability and variably altered species evenness. These effects generally acted additively rather than interactively in driving community diversity during succession. However, soil resource supply suppressed consumer pressure effects on species richness and light availability, while consumer pressure and soil resource supply modified initial richness effects on light availability. Treatments acted on different trait identities, revealing different mechanisms underlying taxonomic responses. Initial richness effects on seed mass of colonizing species were modified by soil resource supply. Decreased consumer pressure increased intraspecific community height and decreased interspecific SLA. Increased soil resource supply increased community height, SLA and seed mass. Synthesis. Our results suggest species' resource strategies underlie plant diversity responses to consumer pressure and soil resource supply. Resource addition promoted resource‐acquisitive species; consumer pressure disadvantaged resource‐conservative species. Meanwhile, initial richness altered subsequent community composition primarily through persistence of early residents. We show that community responses to drivers of succession depend on underlying trait trade‐offs of resident species, and these trade‐offs influence community diversity across succession.

Lay Summary: Competition often occurs among diverse parasites within a single host, but control efforts could change its strength. We examined how the interplay between competition and control could shape the evolution of parasite traits like drug resistance and disease severity.

Disease may modulate variation in host community structure by modifying the interplay of deterministic and stochastic processes. For instance, deterministic processes like ecological selection can benefit species less impacted by disease. When disease consistently selects for certain host species, this can reduce variation in host community composition. On the other hand, when host communities are less impacted by disease and selection is weaker, stochastic processes (e.g., drift, dispersal) may play a bigger role in host community structure, which can increase variation in structure among communities. While effects of disease on host community structure have been quantified in field experiments, few have addressed the role of disease in modulating variation in structure among host communities. To address this, we conducted a field experiment spanning three years, using a tractable system: foliar fungal pathogens in an old-field grassland community dominated by the grass Lolium arundinaceum, tall fescue. We reduced foliar fungal disease burden in replicate host communities (experimental plots in intact vegetation) in three fungicide regimens that varied in the duration of fungicide exposure and included a fungicide-free control. We measured host diversity, biomass, and variation in community structure among replicate communities. Disease reduction generally decreased plant richness and increased aboveground biomass relative to communities experiencing ambient levels of disease. Despite changes in structure of the plant communities over the experiment’s three years, the effects of disease reduction on plant richness and biomass were consistent across years. However, disease reduction did not reduce variation in host community structure, providing little evidence for ecological selection by competition or other deterministic processes. Instead, disease reduction tended to amplify variation in host community structure among replicate communities (i.e., within fungicide treatment groups), suggesting that disease diminished the degree to which host communities were structured by stochastic processes. These results of experimental disease reduction both highlight the potential importance of stochastic processes in plant communities and reveal the potential for disease to regulate variation in host community structure.

International audience; Host individuals are often coinfected with diverse parasite assemblages, resulting in complex interactions among parasites within hosts. Within hosts, priority effects occur when the infection sequence alters the outcome of interactions among parasites. Yet, the role of host immunity in this process remains poorly understood. We hypothesized that the host response to the first infection could generate priority effects among parasites, altering the assembly of later-arriving strains during epidemics. We tested this by infecting sentinel host genotypes ofPlantago lanceolatawith strains of the fungal parasitePodosphaera plantaginisand measuring susceptibility to subsequent infection during experimental and natural epidemics. In these experiments, prior infection by one strain often increased susceptibility to other strains, and these facilitative priority effects altered the structure of parasite assemblages, but this effect depended on host genotype, host population and parasite genotype. Thus, host genotype, spatial structure and priority effects among strains all independently altered parasite assembly. Using a fine-scale survey and sampling of infections on wild hosts in several populations, we then identified a signal of facilitative priority effects, which altered parasite assembly during natural epidemics. Together, these results provide evidence that within-host priority effects of early-arriving strains can drive parasite assembly, with implications for how strain diversity is spatially and temporally distributed during epidemics.By combining an analysis of common garden and field experiments, together with a survey of wild hosts, the authors show that prior infection by a plant fungal parasite increases susceptibility to infection by other strains and that this priming effect influences the assembly of the parasite community.

Successful colonization and growth of trees within herbaceous communities may result from different interactions with the herbaceous community. First, colonizing trees compete against larger, established herbs, while subsequent growth occurs among similarly sized or smaller herbs. This shift from colonization to growth may lead three drivers of community dynamics-nutrients, consumers, and herbaceous diversity-to differentially affect tree colonization and, later, tree performance. Initially, these drivers should favor larger, established herbs, reducing tree colonization. Later, when established trees can better compete with herbs, these drivers should benefit trees and increase their performance. In a 4-year study in a southeastern US old field, we added nutrients to, excluded aboveground consumers from, and manipulated initial richness of, the herbaceous community, and then allowed trees to naturally colonize these communities (from intact seedbanks or as seed rain) and grow. Nutrients and consumers had opposing effects on tree colonization and performance: adding nutrients and excluding consumers reduced tree colonization rate, but later increased the size of established trees (height, basal diameter). Adding nutrients and excluding consumers also restricted tree colonization to earlier years of study, which partially explained the effect of nutrient addition on plant size. Together, this shows differing impacts of nutrients and consumers: factors that initially limited tree colonization also resulted in larger established trees. This suggests that succession of grasslands that are either eutrophied or have diminished consumer pressure may experience lags and pulses in woody encroachment, leading to an extended period of herbaceous dominance followed by accelerated woody growth.

Diverse host communities commonly inhibit the spread of parasites at small scales. However, the generality of this effect remains controversial. Here, we present the analysis of 205 biodiversity–disease relationships on 67 parasite species to test whether biodiversity–disease relationships are generally nonlinear, moderated by spatial scale, and sensitive to underrepresentation in the literature. Our analysis of the published literature reveals that biodiversity–disease relationships are generally hump-shaped (i.e., nonlinear) and biodiversity generally inhibits disease at local scales, but this effect weakens as spatial scale increases. Spatial scale is, however, related to study design and parasite type, highlighting the need for additional multiscale research. Few studies are unrepresentative of communities at low diversity, but missing data at low diversity from field studies could result in underreporting of amplification effects. Experiments appear to underrepresent high-diversity communities, which could result in underreporting of dilution effects. Despite context dependence, biodiversity loss at local scales appears to increase disease, suggesting that at local scales, biodiversity loss could negatively impact human and wildlife populations., Understanding the relationship between biodiversity and infectious disease is important for predicting the effects of biodiversity loss. Here, the authors analyze 205 published biodiversity–disease relationships and show that these tend to be nonlinear and might depend on spatial scale.

Predicting disease risk in an era of unprecedented biodiversity and climate change is more challenging than ever, largely because when and where hosts are at greatest risk of becoming infected depends on complex relationships between hosts, parasites, and the environment. Theory predicts that host species characterized by fast-paced life-history strategies are more susceptible to infection and contribute more to transmission than their slow-paced counterparts. Hence, disease risk should increase as host community structure becomes increasingly dominated by fast-paced hosts. Theory also suggests that environmental gradients can alter disease risk, both directly, due to abiotic constraints on parasite replication and growth, and indirectly, by changing host community structure. What is more poorly understood, however, is whether environmental gradients can also alter the effect of host community structure on disease risk. We addressed these questions using a detailed survey of host communities and infection severity along a 1100m elevational gradient in southeastern Switzerland. Consistent with prior studies, increasing elevation directly reduced infection severity, which we attribute to abiotic constraints, and indirectly reduced infection severity via changes in host richness, which we attribute to encounter reduction. Communities dominated by fast pace-of-life hosts also experienced more disease. Finally, although elevation did not directly influence host community pace-of-life, the relationship between pace-of-life and disease was sensitive to elevation: increasing elevation weakened the relationship between host community pace-of-life and infection severity. This result provides the first field evidence, to our knowledge, that an environmental gradient can alter the effect of host community structure on infection severity.

For succession to proceed from herbaceous to woody dominance, trees must colonize herbaceous communities and grow. Success across these two phases of succession might result from different interactions with the herbaceous community. First, colonizing trees must compete against larger, established herbs, while subsequent growth occurs among similarly sized or smaller herbs. This shift from colonization to growth may cause three drivers of secondary succession— nutrients, consumers, and herbaceous diversity—to differentially affect tree colonization and growth. Initially, these drivers should favor larger, established herbs, reducing colonization. Later, when established trees can better compete with herbs, these drivers should benefit trees and increase their growth. In a four-year study, we added nutrients to, excluded aboveground consumers from, and manipulated initial richness of, the herbaceous community, then allowed trees to naturally colonize these communities (from intact seedbanks or as seed-rain) and grow. Nutrients and consumers had opposing effects on tree colonization and growth: adding nutrients and excluding consumers reduced tree colonization, but later increased established tree growth (height, basal diameter). Together, this shows stage-specific impacts of nutrients and consumers that may improve predictions of the rate and trajectory of succession: factors that initially limited tree colonization later helped established trees to grow.

Parasites can affect and be affected by the host’s microbiome, with consequences for host susceptibility, parasite transmission, and host and parasite fitness. Yet, there are two aspects of the relationship between parasite infection and the host microbiome that remain little understood: the nature of the relationship under field conditions, and how the relationship varies among parasite species. To overcome these limitations, we assayed the within-leaf fungal community in a grass population to investigate how diversity and composition of the fungal microbiome are associated with natural infection by fungal parasites with different feeding strategies. We hypothesized that parasites that more strongly modify niches available within a host will thereby alter the microbial taxa that can colonize the community and be associated with greater changes in microbiome diversity and composition. A parasite that creates necrotic tissue to extract resources (necrotrophs) may act as a particularly strong niche modifier whereas one that does not (biotrophs) may not. Barcoded amplicon sequencing of the fungal ITS region revealed that the microbiome of leaf segments that were symptomatic of necrotrophs had lower fungal diversity and distinct composition compared to segments that were asymptomatic or symptomatic of other parasites. There were no clear differences in fungal diversity or composition between leaf segments that were asymptomatic and segments that were symptomatic of other parasite feeding strategies. This supports the hypothesis that within-host niches link infection by parasites to the host’s microbiome. Together, these results highlight the importance of parasite traits in determining parasite impacts on the host’s microbiome.

The disease ecology community has struggled to come to consensus on whether biodiversity reduces or increases infectious disease risk, a question that directly affects policy decisions for biodiversity conservation and public health. Here, we summarize the primary points of contention regarding biodiversity–disease relationships and suggest that vector-borne, generalist wildlife and zoonotic pathogens are the types of parasites most likely to be affected by changes to biodiversity. One synthesis on this topic revealed a positive correlation between biodiversity and human disease burden across countries, but as biodiversity changed over time within these countries, this correlation became weaker and more variable. Another synthesis—a meta-analysis of generally smaller-scale experimental and field studies—revealed a negative correlation between biodiversity and infectious diseases (a dilution effect) in various host taxa. These results raise the question of whether biodiversity–disease relationships are more negative at smaller spatial scales. If so, biodiversity conservation at the appropriate scales might prevent wildlife and zoonotic diseases from increasing in prevalence or becoming problematic (general proactive approaches). Further, protecting natural areas from human incursion should reduce zoonotic disease spillover. By contrast, for some infectious diseases, managing particular species or habitats and targeted biomedical approaches (targeted reactive approaches) might outperform biodiversity conservation as a tool for disease control. Importantly, biodiversity conservation and management need to be considered alongside other disease management options. These suggested guiding principles should provide common ground that can enhance scientific and policy clarity for those interested in simultaneously improving wildlife and human health., There has been intense debate as to whether biodiversity increases or reduces the risk of infectious disease. This Review is the result of researchers from both sides of the debate attempting to reach a consensus.