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ABSTRACT Dispersal can affect individual‐level fitness and population‐level ecological and evolutionary processes. Factors that affect dispersal could therefore have important eco‐evolutionary implications. Here, we investigated the extent to which an inflammation and tissue repair response—peritoneal fibrosis—which is known to restrict movement, could influence dispersal by conducting a mark‐recapture experiment in a lake in Alaska with threespine stickleback (Gasterosteus aculatus). A subset of captured stickleback were injected with aluminium phosphate to experimentally induce fibrosis (‘treatment group’), and another subset were injected with saline or received no injection—both of which do not induce fibrosis (‘control group’). We released all fish at one introduction point and re‐sampled stickleback throughout the lake for 8 days. We recaptured 123 individuals (n = 47 fibrosis treatment;n = 76 control) and dissected them to determine fibrosis levels. Overall, fibrosis did not affect dispersal. Some compelling (but not statistically significant) trends suggest that early‐stage inflammation may affect dispersal, providing opportunities for future work. By showing that effects on dispersal are not important side effects of fibrosis, these findings improve our understanding of the ecological implications of immune responses. 

Emerging infectious diseases, biodiversity loss, and anthropogenic environmental change are interconnected crises with massive social and ecological costs. In this Review, we discuss how pathogens and parasites are responding to global change, and the implications for pandemic prevention and biodiversity conservation. Ecological and evolutionary principles help to explain why both pandemics and wildlife die-offs are becoming more common; why land-use change and biodiversity loss are often followed by an increase in zoonotic and vector-borne diseases; and why some species, such as bats, host so many emerging pathogens. To prevent the next pandemic, scientists should focus on monitoring and limiting the spread of a handful of high-risk viruses, especially at key interfaces such as farms and live-animal markets. But to address the much broader set of infectious disease risks associated with the Anthropocene, decision-makers will need to develop comprehensive strategies that include pathogen surveillance across species and ecosystems; conservation-based interventions to reduce human–animal contact and protect wildlife health; health system strengthening; and global improvements in epidemic preparedness and response. Scientists can contribute to these efforts by filling global gaps in disease data, and by expanding the evidence base for disease–driver relationships and ecological interventions. 

Habitat degradation can increase zoonotic disease risks by altering infection dynamics in wildlife and increasing wildlife–human interactions. Bats are an important taxonomic group to consider these effects, because they harbour many relevant zoonotic viruses and have species‐ and context‐dependent responses to degradation that could affect zoonotic virus dynamics. Yet our understanding of the associations between habitat degradation and bat virus prevalence and seroprevalence are limited to a small number of studies, which often differ in the bats or viruses sampled, the study region, and methodology. To develop a broad understanding of the associations between bat viruses and habitat degradation, we conducted an initial phylogenetic meta‐analysis that combines published prevalence and seroprevalence (‘(sero)prevalence') with remote‐sensing habitat degradation data. Our dataset includes 588 unique records of (sero)prevalence across 16 studies, 64 bat species, and five virus families. We quantified the overall strength and direction of the relationship between habitat degradation and bat virus outcomes and tested how this relationship is moderated by the time between habitat degradation and bat sampling and by ecological traits of bat hosts while controlling for phylogenetic non‐independence among bat species. We found no effect of degradation on prevalence overall, although a weak effect may exist when forest loss occurs the year prior to bat sampling. In contrast, we detected a negative but weak association between degradation and seroprevalence overall that was strengthened when forest loss occurred the year prior to bat sampling. No bat traits that we investigated interacted with habitat degradation to impact virus outcomes, suggesting observed trends are independent of these traits. Biases in our initial dataset highlight opportunities for future work; prevalence was highly zero‐inflated, and seroprevalence was dominated byDesmodus rotundusand rabies virus. These findings and subsequent analyses will improve our understanding of how global change affects host–pathogen dynamics.