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  1. Abstract

    Resistance and tolerance are unique host defence strategies that can limit the impacts of a pathogen on a host. However, for most wildlife–pathogen systems, there are still fundamental uncertainties regarding (a) how changes in resistance and tolerance can affect disease outcomes and (b) the mechanisms underlying resistance and tolerance in host populations.

    Here, we first compared observed patterns of resistance and tolerance and their effects on disease outcomes among salamander species that are susceptible to infection and mortality from the emerging fungal pathogenBatrachochytrium salamandrivorans(Bsal). We then tested whether two putative mechanisms that contribute to host resistance and tolerance, skin sloughing and skin lesion reduction, predicted reducedBsalgrowth rate or increased host survival during infection, respectively.

    We performed multi‐doseBsalchallenge experiments on four species of Salamandridae found throughout North America. We combined the laboratory experiments with dynamic models and sensitivity analysis to examine how changes in load‐dependent resistance and tolerance functions affectedBsal‐induced mortality risk. Finally, we used our disease model to test whether skin sloughing and lesion reduction predicted variability in infection outcomes not described byBsalinfection intensity.

    We found that resistance and tolerance differed significantly among salamander species, with the most susceptible species being both less resistance and less tolerant ofBsalinfection. Our dynamic model showed that the relative influence of resistance versus tolerance on host survival was species‐dependent—increasing resistance was only more influential than increasing tolerance for the least tolerant species where changes in pathogen load had a threshold‐like effect on host survival. Testing two candidate mechanisms of resistance and tolerance, skin sloughing and lesion reduction, respectively, we found limited support that either of these processes were strong mechanisms of host defence.

    Our study contributes to a broader understanding of resistance and tolerance in host–pathogen systems by showing that differences in host tolerance can significantly affect whether changes in resistance or tolerance have larger effects on disease outcomes, highlighting the need for species and even population‐specific management approaches that target host defence strategies.

    A freePlain Language Summarycan be found within the Supporting Information of this article.

     
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  2. Abstract

    Host behaviour is known to influence disease dynamics. Additionally, hosts often change their behaviours in response to pathogen detection to resist and avoid disease. The capacity of wildlife populations to respond to pathogens using behavioural plasticity is critical for reducing the impacts of disease outbreaks. However, there is limited information regarding the ability of ectothermic vertebrates to resist diseases via behavioural plasticity.

    Here, we experimentally examine the effect of host behaviour on ranaviral infections, which affect at least 175 species of ectothermic vertebrates. We placed metamorphic (temporal block 1) or adult (block 2) southern toads (Anaxyrus terrestris) in thermal gradients, tested their temperature preferences before and after oral inoculation by measuring individual‐level body temperature over time, and measured ranaviral loads of viral‐exposed individuals.

    We found significant individual‐level variation in temperature preference and evidence for behavioural fever in both metamorphic and adultA. terrestrisduring the first 2 days after exposure. Additionally, we found that individual‐level change in temperature preference was negatively correlated with ranaviral load and a better predictor of load than average temperature preference or maximum temperature reached by an individual. In other words, an increase in baseline temperature preference was more important than simply reaching an absolute temperature.

    These results suggest that behavioural fever is an effective mechanism for resisting ranaviral infections.

    A freePlain Language Summarycan be found within the Supporting Information of this article.

     
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