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Anthropogenic change is contributing to the rise in emerging infectious diseases, which are significantly correlated with socioeconomic, environmental and ecological factors 1 . Studies have shown that infectious disease risk is modified by changes to biodiversity 2-6 , climate change 7-11 , chemical pollution 12-14 , landscape transformations 15-20 and species introductions 21 . However, it remains unclear which global change drivers most increase disease and under what contexts. Here we amassed a dataset from the literature that contains 2,938 observations of infectious disease responses to global change drivers across 1,497 host-parasite combinations, including plant, animal and human hosts. We found that biodiversity loss, chemical pollution, climate change and introduced species are associated with increases in disease-related end points or harm, whereas urbanization is associated with decreases in disease end points. Natural biodiversity gradients, deforestation and forest fragmentation are comparatively unimportant or idiosyncratic as drivers of disease. Overall, these results are consistent across human and non-human diseases. Nevertheless, context-dependent effects of the global change drivers on disease were found to be common. The findings uncovered by this meta-analysis should help target disease management and surveillance efforts towards global change drivers that increase disease. Specifically, reducing greenhouse gas emissions, managing ecosystem health, and preventing biological invasions and biodiversity loss could help to reduce the burden of plant, animal and human diseases, especially when coupled with improvements to social and economic determinants of health., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

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.

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.

Environmental stressors, such as pollutants, can increase disease risk in wildlife. For example, the herbicide atrazine affects host defences (e.g. resistance and tolerance) of the amphibian chytrid fungus Batrachochytrium dendrobatidis (Bd), but the mechanisms for these associations are not entirely clear. Given that pollutants can alter the gut microbiota of hosts, which in turn can affect their health and immune systems, one potential mechanism by which pollutants could increase infection risk is by influencing host-associated microbiota. Here, we test whether early-life exposure to the estimated environmental concentration (EEC; 200 μg/L) of atrazine affects the gut bacterial composition of Cuban tree frog (Osteopilus septentrionalis) tadpoles and adults and whether any atrazine-induced change in community composition might affect host defences against Bd. We also determine whether early-life changes in the stress hormone corticosterone affect gut microbiota by experimentally inhibiting corticosterone synthesis with metyrapone. With the exception of changing the relative abundances of two bacterial genera in adulthood, atrazine did not affect gut bacterial diversity or community composition of tadpoles (in vivo or in vitro) or adults. Metyrapone did not significantly affect bacterial diversity of tadpoles, but significantly increased bacterial diversity of adults. Gut bacterial diversity during Bd exposure did not predict host tolerance or resistance to Bd intensity in tadpoles or adults. However, early-life bacterial diversity negatively predicted Bd intensity as adult frogs. Specifically, Bd intensity as adults was associated negatively with the relative abundance of phylum Fusobacteria in the guts of tadpoles. Our results suggest that the effect of atrazine on Bd infection risk is not mediated by host-associated microbiota because atrazine does not affect microbiota of tadpoles or adults. However, host-associated microbes seem important in host resistance to Bd because the early-life microbiota, during immune system development, predicted later-life infection risk with Bd. Overall, our study suggests that increasing gut bacterial diversity and relative abundances of Fusobacteria might have lasting positive effects on amphibian health., (© 2017 The Authors. Journal of Animal Ecology © 2017 British Ecological Society.)

For the past 20 years, research on biodiversity and ecosystem functioning (B-EF) has only implicitly considered the underlying role of environmental change. We illustrate that explicitly reintroducing environmental change drivers in B-EF research is needed to predict the functioning of ecosystems facing changes in biodiversity. Next we show how this reintroduction improves experimental control over community composition and structure, which helps to provide mechanistic insight on how multiple aspects of biodiversity relate to function and how biodiversity and function relate in food webs. We also highlight challenges for the proposed reintroduction and suggest analyses and experiments to better understand how random biodiversity changes, as studied by classic approaches in B-EF research, contribute to the shifts in function that follow environmental change., Competing Interests: The authors declare no conflict of interest., (Crown Copyright © 2016. Published by Elsevier Ltd. All rights reserved.)

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 cross-continental, 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.

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 meta-analysis 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.

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. 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. 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. 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. 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., (© 2013 The Authors. Journal of Animal Ecology © 2013 British Ecological Society.)

Although studies on biodiversity and ecosystem function are often framed within the context of anthropogenic change, a central question that remains is how important are direct vs. indirect (via changes in biodiversity) effects of anthropogenic stressors on ecosystem functions in multitrophic-level communities. Here, we quantify the effects of the fungicide chlorothalonil on 34 species-, 2 community- and 11 ecosystem-level responses in a multitrophic-level system. At ecologically relevant concentrations, chlorothalonil increased mortality of amphibians, gastropods, zooplankton, algae and a macrophyte (reducing taxonomic richness), reduced decomposition and water clarity and elevated dissolved oxygen and net primary productivity. These ecosystem effects were indirect and predictable based on changes in taxonomic richness. A path analysis suggests that chlorothalonil-induced reductions in biodiversity and top-down and bottom-up effects facilitated algal blooms that shifted ecosystem functions. This work emphasises the need to re-evaluate the safety of chlorothalonil and to further link anthropogenic-induced changes in biodiversity to altered ecosystem functions., (© 2012 Blackwell Publishing Ltd/CNRS.)

Invertebrates provide the majority of ecosystem services; thus, it is important that they be inventoried, monitored, and protected. Nevertheless, inventories, monitoring, and management generally focus on vertebrates and flowering plants. Consequently, there are few guidelines or case studies for invertebrates. We present a procedure for developing a monitoring program for species-rich invertebrates that entails (1) characterizing the community; (2) identifying surrogates for biodiversity; and (3) establishing efficient methods to monitor surrogates and any ecologically important or sensitive taxa. We used these procedures, biodiversity-based statistical advances, and a survey of arthropods to develop a monitoring plan for the forests of Shenandoah National Park, Virginia (U.S.A.). Our case study revealed that mixed hardwood and hemlock forests had significantly different compositions of arthropods in their soil and understory strata. Of the 10 orders tested Coleoptera and Hymenoptera were the only two to pass most of the five surrogate tests, and their combination improved predictions of overall arthropod diversity. Because arthropods represent the majority of macroscopic species in most ecosystems, the ability of this assemblage to predict overall arthropod diversity makes it a powerful surrogate. Of the 11 collecting methods used, the beat-sheet method was the most efficient for monitoring this surrogate assemblage. To complement this coarse-filter approach to monitoring at-risk, invasive, or other important taxa (fine filter), we used ordination analyses to match 66 taxa with the methods that most effectively sampled them. Our methods serve as a model for developing an invertebrate monitoring plan and should facilitate linking such monitoring with ecosystem functions and management.

Losses in biodiversity can alter disease risk through changes in host species composition. Host species vary in pathogen susceptibility and competence, yet how changes in diversity alter host–pathogen dynamics remains unclear in many systems, particularly with respect to generalist pathogens. Amphibians are experiencing worldwide population declines linked to generalist pathogens, such as ranavirus, and thus represent an ideal group to investigate how host species composition affects disease risk. We conducted experiments in which amphibian larvae of three native species (Pacific tree frogs, Pseudacris regilla; Cascades frogs, Rana cascadae; and Western toads, Anaxyrus boreas) were exposed to ranavirus individually (in the laboratory) or as assemblages (in outdoor mesocosms). In a laboratory experiment, we observed low survival and high viral loads in P. regilla compared to the other species, suggesting that this species was highly susceptible to the pathogen. In the mesocosm experiment, we observed 41% A. boreas mortality when alone and 98% mortality when maintained with P. regilla and R. cascadae. Our results suggest that the presence of highly susceptible species can alter disease dynamics across multiple species, potentially increasing infection risk and mortality in co‐occurring species. [ABSTRACT FROM AUTHOR]

Adverse effects of anthropogenic changes on biodiversity might be mediated by their impacts on the stress response of organisms. To test this hypothesis, we crossed exposure to metyrapone, a synthesis inhibitor of the stress hormone corticosterone, with exposure to the herbicide atrazine and the fungal pathogen Batrachochytrium dendrobatidis (Bd) to assess whether the effects of these stressors on tadpoles and post-metamorphic frogs were mediated by corticosterone. Metyrapone countered atrazine- and Bd-induced corticosterone elevations. However, atrazine- and Bd-induced reductions in body size were not mediated by corticosterone because they persisted despite metyrapone exposure. Atrazine lowered Bd abundance without metyrapone but increased Bd abundance with metyrapone for tadpoles and frogs. In contrast, atrazine reduced tolerance of Bd infections because frogs exposed to atrazine as tadpoles had reduced growth with Bd compared to solvent controls; this effect was not countered by metyrapone. Our results suggest that the adverse effects of atrazine and Bd on amphibian growth, development, and tolerance of infection are not mediated primarily by corticosterone. A possible mechanism for these effects is energy lost from atrazine detoxification, defense against Bd, or repair from damage caused by atrazine and Bd. Additional studies are needed to evaluate how often the effects of anthropogenic stressors are mediated by stress hormones. [ABSTRACT FROM AUTHOR]

ABSTRACT Chemical contamination has impaired ecosystems, reducing biodiversity and the provisioning of functions and services. This has spurred a movement to restore contaminated ecosystems and develop and implement national and international regulations that require it. Nevertheless, ecological restoration remains a young and rapidly growing discipline and its intersection with toxicology is even more nascent and underdeveloped. Consequently, we provide guidance to scientists and practitioners on when, where, and how to restore contaminated ecosystems. Although restoration has many benefits, it also can be expensive, and in many cases systems can recover without human intervention. Hence, the first question we address is: 'When should we restore contaminated ecosystems?' Second, we provide suggestions on what to restore-biodiversity, functions, services, all 3, or something else-and where to restore given expected changes to habitats driven by global climate change. Finally, we provide guidance on how to restore contaminated ecosystems. To do this, we analyze critical aspects of the literature dealing with the ecology of restoring contaminated ecosystems. Additionally, we review approaches for translating the science of restoration to on-the-ground actions, which includes discussions of market incentives and the finances of restoration, stakeholder outreach and governance models for ecosystem restoration, and working with contractors to implement restoration plans. By explicitly considering the mechanisms and strategies that maximize the success of the restoration of contaminated sites, we hope that our synthesis serves to increase and improve collaborations between restoration ecologists and ecotoxicologists and set a roadmap for the restoration of contaminated ecosystems. Integr Environ Assess Manag 2016;12:273-283. © 2015 The Authors. Integrated Environmental Assessment and Management published by Wiley Periodicals, Inc. on behalf of SETAC [ABSTRACT FROM AUTHOR]

Conflicts of interest, situations where personal or organizational considerations have compromised or biased professional judgment and objectivity, can weaken scientific credibility, pose threats to biodiversity and ecosystem services, and are often precursors to corruption. Here, we review historical and international examples of conflicts of interest and their impacts on global biodiversity. We present a contemporary example of a conflict of interest that might have implications for the U.S. Environmental Protection Agency's re-evaluation of the safety of the herbicide atrazine. To help scientists, natural resource managers, policy makers, and judicial officials identify and thwart conflicts of interest, we review strategies used by individuals and organizations with conflicts of interest to evade environmental and public health decisions, discuss the role of the scientific and governmental review processes in maintaining scientific integrity, and offer recommendations to reduce bias and facilitate sound and swift decision making for enhanced environmental health. [ABSTRACT FROM AUTHOR]

The role of global climate change in the decline of biodiversity and the emergence of infectious diseases remains controversial, and the effect of climatic variability, in particular, has largely been ignored. For instance, it was recently revealed that the proposed link between climate change and widespread amphibian declines, putatively caused by the chytrid fungus Batrachochytrium dendrobatidis (Bd), was tenuous because it was based on a temporally confounded correlation. Here we providetemporally unconfounded evidence that global El Niño climatic events drive widespread amphibian losses in genus Atelopus via increased regional temperature variability, which can reduce amphibian defenses against pathogens. Of 26 climate variables tested, only factors associated with temperature variability could account for the spatiotemporal patterns of declines thought to be associated with Bd Climatic predictors of declines became significant only after controlling for a pattern consistent with epidemic spread (by temporally detrending the data). This presumed spread accounted for 59% of the temporal variation in amphibian losses, whereas El Niño accounted for 59% of the remaining variation. Hence, we could account for 83% of the variation in declines with these two variables alone. Given that global climate change seems to increase temperature variability, extreme climatic events, and the strength of Central Pacific El Niño episodes, climate change might exacerbate worldwide enigmatic declines of amphibians, presumably by increasing susceptibility to disease. These results suggest that changes to temperature variability associated with climate change might be as significant to biodiversity losses and disease emergence as changes to mean temperature. [ABSTRACT FROM AUTHOR]

Abstract: Widespread declines of foundation species, such as many corals, kelps, and overstory trees, are of grave concern because, by definition, these species create and maintain habitat that supports other species. Nevertheless, past responses to their declines, many of which were caused by invasive species, have been late and ineffective, underscoring the need to predict changes in biodiversity and ecosystem function associated with species invasions and foundation species losses. One predictive, but under-used, approach is to compare the species and functions associated with the afflicted foundation species to its projected replacement communities. The taxa associated with the foundation species and subsequent successional stages would be expected to decline and increase, respectively. We used this approach to generate hypotheses for how arthropod diversity might change in response to extensive losses of eastern hemlock trees caused by the invasive, hemlock woolly adelgid (insect: Hemiptera, Adelgidae). Our all-strata survey of the arthropods in an eastern hemlock forest and its expected replacement climax community in the mid-Atlantic region of the United States, mixed hardwood forest, suggests that eastern hemlock losses might initiate increases in arthropod abundance, alpha diversity, and 23 arthropod taxa, might produce no change in evenness or composition of arthropod functional groups, but might trigger decreases in beta diversity and seven hemlock indicator taxa. These predictions are consistent with observed trends in arthropod responses to hemlock losses in other studies, and thus might be useful for targeting early monitoring, management, and conservation efforts. This research is exploratory, however, and tests of these predictions across larger spatial scales will be necessary to determine the generality of the findings. [Copyright &y& Elsevier]

Community ecotoxicology is defined as the study of the effects of contaminants on patterns of species abundance, diversity, community composition, and species interactions. Recent discoveries that species diversity is positively associated with ecosystem stability, recovery, and services have made a community-level perspective on ecotoxicology more important than ever. Community ecotoxicology must explicitly consider both present and impending global change and shift from a purely descriptive to a more predictive science. Greater consideration of the ecological factors and threshold responses that determine community resistance and resilience should improve our ability to predict how and when communities will respond to, and recover from, xenobiotics. A better understanding of pollution-induced community tolerance, and of the costs of this tolerance, should facilitate identifying contaminantimpacted communities, thus forecasting the ecological consequences of contaminant exposure and determining the restoration effectiveness. Given the vast complexity of community ecotoxicology, simplifying assumptions, such as the possibility that the approximately 100,000 registered chemicals could be reduced to a more manageable number of contaminant classes with similar modes of action, must be identified and validated. In addition to providing a framework for predicting contaminant fate and effects, food-web ecology can help to identify communities that are sensitive to contaminants, contaminants that are particularly insidious to communities, and species that are crucial for transmitting adverse effects across trophic levels. Integration of basic ecological principles into the design and implementation of ecotoxicological research is essential for predicting contaminant effects within the context of rapidly changing, global environmental conditions. [ABSTRACT FROM AUTHOR]