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Research on the 'ecology of fear' posits that defensive prey responses to avoid predation can cause non-lethal effects across ecological scales. Parasites also elicit defensive responses in hosts with associated non-lethal effects, which raises the longstanding, yet unresolved question of how non-lethal effects of parasites compare with those of predators. We developed a framework for systematically answering this question for all types of predator-prey and host-parasite systems. Our framework reveals likely differences in non-lethal effects not only between predators and parasites, but also between different types of predators and parasites. Trait responses should be strongest towards predators, parasitoids and parasitic castrators, but more numerous and perhaps more frequent for parasites than for predators. In a case study of larval amphibians, whose trait responses to both predators and parasites have been relatively well studied, existing data indicate that individuals generally respond more strongly and proactively to short-term predation risks than to parasitism. Apart from studies using amphibians, there have been few direct comparisons of responses to predation and parasitism, and none have incorporated responses to micropredators, parasitoids or parasitic castrators, or examined their long-term consequences. Addressing these and other data gaps highlighted by our framework can advance the field towards understanding how non-lethal effects impact prey/host population dynamics and shape food webs that contain multiple predator and parasite species.

The first signs of sea star wasting disease (SSWD) epidemic occurred in just few months in 2013 along the entire North American Pacific coast. Disease dynamics did not manifest as the typical travelling wave of reaction-diffusion epidemiological model, suggesting that other environmental factors might have played some role. To help explore how external factors might trigger disease, we built a coupled oceanographic-epidemiological model and contrasted three hypotheses on the influence of temperature on disease transmission and pathogenicity. Models that linked mortality to sea surface temperature gave patterns more consistent with observed data on sea star wasting disease, which suggests that environmental stress could explain why some marine diseases seem to spread so fast and have region-wide impacts on host populations.

The first signs of sea star wasting disease (SSWD) epidemic occurred in just few months in 2013 along the entire North American Pacific coast. Disease dynamics did not manifest as the typical travelling wave of reaction-diffusion epidemiological model, suggesting that other environmental factors might have played some role. To help explore how external factors might trigger disease, we built a coupled oceanographic-epidemiological model and contrasted three hypotheses on the influence of temperature on disease transmission and pathogenicity. Models that linked mortality to sea surface temperature gave patterns more consistent with observed data on sea star wasting disease, which suggests that environmental stress could explain why some marine diseases seem to spread so fast and have region-wide impacts on host populations.