Infectious diseases of humans, wildlife, and domesticated species are increasing worldwide, driving the need to understand the mechanisms that shape outbreaks. Simultaneously, human activities are drastically reducing biodiversity. These concurrent patterns have prompted repeated suggestions that biodiversity and disease are linked. For example, the dilution effect hypothesis posits that these patterns are causally related; diverse host communities inhibit the spread of parasites via several mechanisms, such as by regulating populations of susceptible hosts or interfering with parasite transmission. However, the generality of the dilution effect hypothesis remains controversial, especially for zoonotic diseases of humans. Here we provide broad evidence that host diversity inhibits parasite abundance using a metaanalysis of 202 effect sizes on 61 parasite species. The magnitude of these effects was independent of host density, study design, and type and specialization of parasites, indicating that dilution was robust across all ecological contexts examined. However, the magnitude of dilution was more closely related to the frequency, rather than density, of focal host species. Importantly, observational studies overwhelmingly documented dilution effects, and there was also significant evidence for dilution effects of zoonotic parasites of humans. Thus, dilution effects occur commonly in nature, and they may modulate human disease risk. A second analysis identified similar effects of diversity in plant-herbivore systems. Thus, although there can be exceptions, our results indicate that biodiversity generally decreases parasitism and herbivory. Consequently, anthropogenic declines in biodiversity could increase human and wildlife diseases and decrease crop and forest production.H uman activities are dramatically reducing biodiversity (1), and the frequency and severity of infectious disease outbreaks in human, wildlife, and domesticated species are increasing (2-5). These concurrent patterns have prompted suggestions that biodiversity and the spread of diseases may be causally linked. For example, the dilution effect hypothesis proposes that diverse host communities inhibit the abundance of parasites through several mechanisms, such as regulating populations of susceptible hosts or interfering with the transmission process (6-8). Thus, diverse communities may inhibit the proliferation of parasites, thereby promoting the stability of ecological communities and ecosystem services (e.g., nutrient cycling, carbon sequestration, and natural product production) (9).Understanding the generality of these dilution effects is crucial for projections of future disease outbreaks, which can threaten human health, species conservation, and ecosystem services (3, 9). If biodiversity generally inhibits parasites, then human-driven biodiversity loss could exacerbate disease risk for humans and wildlife. Biodiversity conservation might then limit the abundance of many parasites of wildlife and humans (10-12). However, if parasites a...

Parasites typically have broader thermal limits than hosts, so large performance gaps between pathogens and their cold- and warm-adapted hosts should occur at relatively warm and cold temperatures, respectively. We tested this thermal mismatch hypothesis by quantifying the temperature-dependent susceptibility of cold- and warm-adapted amphibian species to the fungal pathogen Batrachochytrium dendrobatidis (Bd) using laboratory experiments and field prevalence estimates from 15 410 individuals in 598 populations. In both the laboratory and field, we found that the greatest susceptibility of cold- and warm-adapted hosts occurred at relatively warm and cool temperatures, respectively, providing support for the thermal mismatch hypothesis. Our results suggest that as climate change shifts hosts away from their optimal temperatures, the probability of increased host susceptibility to infectious disease might increase, but the effect will depend on the host species and the direction of the climate shift. Our findings help explain the tremendous variation in species responses to Bd across climates and spatial, temporal and species-level variation in disease outbreaks associated with extreme weather events that are becoming more common with climate change.

Humans are altering the distribution of species by changing the climate and disrupting biotic interactions and dispersal. A fundamental hypothesis in spatial ecology suggests that these effects are scale dependent; biotic interactions should shape distributions at local scales, whereas climate should dominate at regional scales. If so, common single-scale analyses might misestimate the impacts of anthropogenic modifications on biodiversity and the environment. However, large-scale datasets necessary to test these hypotheses have not been available until recently. Here we conduct a crosscontinental, cross-scale (almost five orders of magnitude) analysis of the influence of biotic and abiotic processes and human population density on the distribution of three emerging pathogens: the amphibian chytrid fungus implicated in worldwide amphibian declines and West Nile virus and the bacterium that causes Lyme disease (Borrelia burgdorferi), which are responsible for ongoing human health crises. In all three systems, we show that biotic factors were significant predictors of pathogen distributions in multiple regression models only at local scales (∼10 2 -10 3 km 2 ), whereas climate and human population density always were significant only at relatively larger, regional scales (usually >10 4 km 2 ). Spatial autocorrelation analyses revealed that biotic factors were more variable at smaller scales, whereas climatic factors were more variable at larger scales, as is consistent with the prediction that factors should be important at the scales at which they vary the most. Finally, no single scale could detect the importance of all three categories of processes. These results highlight that common single-scale analyses can misrepresent the true impact of anthropogenic modifications on biodiversity and the environment.ecology | dilution effect | chytridiomycosis | West Nile virus | Lyme disease

Summary1. The dilution effect, the hypothesis that biodiversity reduces disease risk, has received support in many systems. However, few dilution effect studies have linked mechanistic experiments to field patterns to establish both causality and ecological relevance. 2. We conducted a series of laboratory experiments and tested the dilution effect hypothesis in an amphibian-Batrachochytrium dendrobatidis (Bd) system and tested for consistency between our laboratory experiments and field patterns of amphibian species richness, host identity and Bd prevalence. 3. In our laboratory experiments, we show that tadpoles can filter feed Bd zoospores and that the degree of suspension feeding was positively associated with their dilution potential. The obligate suspension feeder, Gastrophryne carolinensis, generally diluted the risk of chytridiomycosis for tadpoles of Bufo terrestris and Hyla cinerea, whereas tadpoles of B. terrestris (an obligate benthos feeder) generally amplified infections for the other species. In addition, G. carolinensis reduced Bd abundance on H. cinerea more so in the presence than absence of B. terrestris and B. terrestris amplified Bd abundance on H. cinerea more so in the absence than presence of G. carolinensis. Also, when ignoring species identity, species richness was a significant negative predictor of Bd abundance. 4. In our analysis of field data, the presence of Bufo spp. and Gastrophryne spp. were significant positive and negative predictors of Bd prevalence, respectively, even after controlling for climate, vegetation, anthropogenic factors (human footprint), species richness and sampling effort. These patterns of dilution and amplification supported our laboratory findings, demonstrating that the results are likely ecologically relevant. 5. The results from our laboratory and field data support the dilution effect hypothesis and also suggest that dilution and amplification are predictable based on host traits. Our study is among the first to link manipulative experiments, in which a potential dilution mechanism is supported, with analyses of field data on species richness, host identity, spatial autocorrelation and disease prevalence.

Disease outbreaks among wildlife have surged in recent decades alongside climate change, although it remains unclear how climate change alters disease dynamics across different geographic regions. We amassed a global, spatiotemporal dataset describing parasite prevalence across 7346 wildlife populations and 2021 host-parasite combinations, compiling local weather and climate records at each location. We found that hosts from cool and warm climates experienced increased disease risk at abnormally warm and cool temperatures, respectively, as predicted by the thermal mismatch hypothesis. This effect was greatest in ectothermic hosts and similar in terrestrial and freshwater systems. Projections based on climate change models indicate that ectothermic wildlife hosts from temperate and tropical zones may experience sharp increases and moderate reductions in disease risk, respectively, though the magnitude of these changes depends on parasite identity.