Climate change is expected to have complex effects on infectious diseases, causing some to increase, others to decrease, and many to shift their distributions. There have been several important ...advances in understanding the role of climate and climate change on wildlife and human infectious disease dynamics over the past several years. This essay examines 3 major areas of advancement, which include improvements to mechanistic disease models, investigations into the importance of climate variability to disease dynamics, and understanding the consequences of thermal mismatches between host and parasites. Applying the new information derived from these advances to climate-disease models and addressing the pressing knowledge gaps that we identify should improve the capacity to predict how climate change will affect disease risk for both wildlife and humans.
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Recent epidemics of Zika, dengue, and chikungunya have heightened the need to understand the seasonal and geographic range of transmission by Aedes aegypti and Ae. albopictus mosquitoes. We use ...mechanistic transmission models to derive predictions for how the probability and magnitude of transmission for Zika, chikungunya, and dengue change with mean temperature, and we show that these predictions are well matched by human case data. Across all three viruses, models and human case data both show that transmission occurs between 18-34°C with maximal transmission occurring in a range from 26-29°C. Controlling for population size and two socioeconomic factors, temperature-dependent transmission based on our mechanistic model is an important predictor of human transmission occurrence and incidence. Risk maps indicate that tropical and subtropical regions are suitable for extended seasonal or year-round transmission, but transmission in temperate areas is limited to at most three months per year even if vectors are present. Such brief transmission windows limit the likelihood of major epidemics following disease introduction in temperate zones.
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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.
Thermal biology of mosquito‐borne disease Mordecai, Erin A.; Caldwell, Jamie M.; Grossman, Marissa K. ...
Ecology letters,
October 2019, Volume:
22, Issue:
10
Journal Article
Peer reviewed
Open access
Mosquito‐borne diseases cause a major burden of disease worldwide. The vital rates of these ectothermic vectors and parasites respond strongly and nonlinearly to temperature and therefore to climate ...change. Here, we review how trait‐based approaches can synthesise and mechanistically predict the temperature dependence of transmission across vectors, pathogens, and environments. We present 11 pathogens transmitted by 15 different mosquito species – including globally important diseases like malaria, dengue, and Zika – synthesised from previously published studies. Transmission varied strongly and unimodally with temperature, peaking at 23–29ºC and declining to zero below 9–23ºC and above 32–38ºC. Different traits restricted transmission at low versus high temperatures, and temperature effects on transmission varied by both mosquito and parasite species. Temperate pathogens exhibit broader thermal ranges and cooler thermal minima and optima than tropical pathogens. Among tropical pathogens, malaria and Ross River virus had lower thermal optima (25–26ºC) while dengue and Zika viruses had the highest (29ºC) thermal optima. We expect warming to increase transmission below thermal optima but decrease transmission above optima. Key directions for future work include linking mechanistic models to field transmission, combining temperature effects with control measures, incorporating trait variation and temperature variation, and investigating climate adaptation and migration.
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Predicting ecological effects of contaminants remains challenging because of the sheer number of chemicals and their ambiguous role in biodiversity-ecosystem function relationships. We evaluate ...responses of experimental pond ecosystems to standardized concentrations of 12 pesticides, nested in four pesticide classes and two pesticide types. We show consistent effects of herbicides and insecticides on ecosystem function, and slightly less consistent effects on community composition. Effects of pesticides on ecosystem function are mediated by alterations in the abundance and community composition of functional groups. Through bottom-up effects, herbicides reduce respiration and primary productivity by decreasing the abundance of phytoplankton. The effects of insecticides on respiration and primary productivity of phytoplankton are driven by top-down effects on zooplankton composition and abundance, but not richness. By demonstrating consistent effects of pesticides on communities and ecosystem functions and linking pesticide-induced changes in functional groups of organisms to ecosystem functions, the study suggests that ecological risk assessment of registered chemicals could be simplified to synthetic chemical classes or types and groups of organisms with similar functions and chemical toxicities.
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.
Changes in the early-life microbiota of hosts might affect infectious disease risk throughout life, if such disruptions during formative times alter immune system development. Here, we test whether ...an early-life disruption of host-associated microbiota affects later-life resistance to infections by manipulating the microbiota of tadpoles and challenging them with parasitic gut worms as adults. We find that tadpole bacterial diversity is negatively correlated with parasite establishment in adult frogs: adult frogs that had reduced bacterial diversity as tadpoles have three times more worms than adults without their microbiota manipulated as tadpoles. In contrast, adult bacterial diversity during parasite exposure is not correlated with parasite establishment in adult frogs. Thus, in this experimental setup, an early-life disruption of the microbiota has lasting reductions on host resistance to infections, which is possibly mediated by its effects on immune system development. Our results support the idea that preventing early-life disruption of host-associated microbiota might confer protection against diseases later in life.Early-life microbiota alterations can affect infection susceptibility later in life, in animal models. Here, Knutie et al. show that manipulating the microbiota of tadpoles leads to increased susceptibility to parasitic infection in adult frogs, in the absence of substantial changes in the adults' microbiota.
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 plantâherbivore 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 hypothesis suggests that diverse ecological communities limit disease spread via several mechanisms. Therefore, biodiversity losses could worsen epidemics that harm humans and wildlife. However, there is contentious debate over whether the hypothesis applies broadly, especially for parasites that infect humans. We address this fundamental question with a formal meta-analysis of >200 assessments relating biodiversity to disease in >60 hostâparasite systems. We find overwhelming evidence of dilution, which is independent of host density, study design, and type and specialization of parasites. A second analysis identified similar effects of diversity in plantâherbivore systems. Thus, biodiversity generally decreases parasitism and herbivory. Consequently, human-induced declines in biodiversity could increase human and wildlife diseases and decrease crop and forest production.
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