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43 results for “white-nose syndrome”

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dryad32/100

Body mass and hibernation microclimate may predict bat susceptibility to white-nose syndrome

<p>In multi-host disease systems, differences in mortality between species may reflect variation in host physiology, morphology, and behavior. In systems where the pathogen can persist in the environment, microclimate conditions, and the adaptation of the host to these conditions, may also impact mortality. White-nose syndrome is an emerging disease of hibernating bats caused by an environmentally persistent fungus, Pseudogymnoascus destructans. We assessed the effects of body mass, torpid metabolic rate, evaporative water loss, and hibernaculum temperature and water vapor deficit on predicted overwinter survival of bats infected by P. destructans. We used a hibernation energetics model in an individual-based model framework to predict the probability of survival of nine bat species at eight sampling sites across North America. The model predicts time until fat exhaustion as a function of species-specific host characteristics, hibernaculum microclimate, and fungal growth. We fit a linear model to determine relationships with each variable and predicted survival and semi-partial correlation coefficients to determine the major drivers in variation in bat survival. We found host body mass and hibernaculum water vapor deficit explained over half of the variation in survival with white-nose syndrome across species. As previous work on the interplay between host and pathogen physiology and the environment has focused on species with narrow microclimate preferences, our view on this relationship is limited. Our results highlight some key predictors of interspecific survival among western bat species and provide a framework to assess impacts of white-nose syndrome as the fungus continues to spread into western North America.</p>

opencc-zeroNov 2021View details →
dryad32/100

Data from: Host and pathogen ecology drive the seasonal dynamics of a fungal disease, white-nose syndrome

Seasonal patterns in pathogen transmission can influence the impact of disease on populations and the speed of spatial spread. Increases in host contact rates or births drive seasonal epidemics in some systems, but other factors may occasionally override these influences. White-nose syndrome, caused by the emerging fungal pathogen Pseudogymnoascus destructans, is spreading across North America and threatens several bat species with extinction. We examined patterns and drivers of seasonal transmission of P. destructans by measuring infection prevalence and pathogen loads in six bat species at 30 sites across the eastern United States. Bats became transiently infected in autumn, and transmission spiked in early winter when bats began hibernating. Nearly all bats in six species became infected by late winter when infection intensity peaked. In summer, despite high contact rates and a birth pulse, most bats cleared infections and prevalence dropped to zero. These data suggest the dominant driver of seasonal transmission dynamics was a change in host physiology, specifically hibernation. Our study is the first, to the best of our knowledge, to describe the seasonality of transmission in this emerging wildlife disease. The timing of infection and fungal growth resulted in maximal population impacts, but only moderate rates of spatial spread.

opencc-zeroDec 2013View details →
dryad32/100

Long-term changes in occurrence, relative abundance, and reproductive fitness of bat species in relation to arrival of White-nose Syndrome in West Virginia, USA

<p>White-nose syndrome (WNS) is a disease caused by the fungus Pseudogymnoascus destructans which has resulted in the deaths of millions of bats across eastern North America. To date, hibernacula counts have been the predominant means of tracking the spread and impact of this disease on bat populations. However, an understanding of the impacts of WNS on demographic parameters outside the winter season is critical to conservation and recovery of bat populations impacted by this disease. We used long-term monitoring data to examine WNS-related impacts to summer populations in West Virginia, where WNS has been documented since 2009. Using capture data from 290 mist-net sites surveyed from 2003–2019 on the Monongahela National Forest, we estimated temporal patterns in presence and relative abundance for each bat species. For species that exhibited a population-level response to WNS, we investigated post-WNS changes in adult female reproductive state and body mass. Myotis lucifugus (little brown bat), M. septentrionalis (northern long-eared bat), and Perimyotis subflavus (tri-colored bat) all showed significant decreases in presence and relative abundance during and following the introduction of WNS, while Eptesicus fuscus (big brown bat) and Lasiurus borealis (eastern red bat) responded positively during the WNS invasion. Probability of being reproductively active was not significantly different for any species, though a shift to earlier reproduction was estimated for E. fuscus and M. septentrionalis. For some species, body mass appeared to be influenced by the WNS invasion, but the response differed by species and reproductive state. Results suggest that continued long-term monitoring studies, additional research into impacts of this disease on the fitness of WNS survivors, and a focus on providing optimal non-wintering habitat may be valuable strategies for assessing and promoting recovery of WNS-affected bat populations.</p>

opencc-zeroJul 2022View details →
dryad32/100

Data from: Genetic structure of little brown bats (Myotis lucifugus) corresponds with spread of white-nose syndrome among hibernacula

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publicJan 2014View details →
dryad32/100

Data from: Energy conserving thermoregulatory patterns and lower disease severity in a bat resistant to the impacts of white-nose syndrome

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publicJun 2018View details →
dryad32/100

Data from: Conservation implications of ameliorating survival of little brown bats with White-Nose Syndrome

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publicMay 2015View details →
dryad32/100

Data from: Immune responses in hibernating little brown myotis (Myotis lucifugus) with white-nose syndrome

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publicJan 2017View details →
dryad32/100

Data from: Efficacy of visual surveys for white-nose syndrome at bat hibernacula

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publicJul 2016View details →
dryad32/100

Data from: Sex and hibernaculum temperature predict survivorship in white-nose syndrome affected little brown myotis (Myotis lucifugus)

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publicDec 2014View details →
dryad32/100

Data from: Prelude to a panzootic: gene flow and immunogenetic variation in northern little brown myotis vulnerable to bat white-nose syndrome

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publicJul 2018View details →
dryad32/100

Data from: Host and pathogen ecology drive the seasonal dynamics of a fungal disease, white-nose syndrome

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publicNov 2014View details →
dryad32/100

Data from: Multi-scale model of regional population decline in little brown bats due to white-nose syndrome

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publicJul 2019View details →
dryad32/100

Long-term changes in occurrence, relative abundance, and reproductive fitness of bat species in relation to arrival of White-nose Syndrome in West Virginia, USA

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publicAug 2021View details →
dryad32/100

Body mass and hibernation microclimate may predict bat susceptibility to white-nose syndrome

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publicNov 2021View details →
dryad28/100

MHC variation is similar in little brown bats before and after white-nose syndrome outbreak

<p>White-nose syndrome (WNS), caused by the fungal pathogen <i>Pseudogymnoascus destructans</i><i> </i>(Pd), has driven alarming declines in North American hibernating bats, such as little brown bat (<i>Myotis lucifugus</i>). During hibernation, infected little brown bats are able to initiate anti-Pd immune responses, indicating pathogen-mediated selection on the major histocompatibility complex (MHC) genes. However, such immune responses may not be protective as they interrupt torpor, elevate energy costs, and potentially lead to higher mortality rates. To assess whether WNS drives selection on MHC genes, we compared the MHC <i>DRB</i> gene in little brown bats pre- (Wisconsin) and post- (Michigan, New York, Vermont, and Pennsylvania) WNS (detection spanning 2014-2015). We genotyped 131 individuals and found 45 nucleotide alleles (27 amino acid alleles) indicating a maximum of 3 loci (1-5 alleles per individual). We observed high allelic admixture and a lack of genetic differentiation both among sampling sites and between pre- and post-WNS populations, indicating no signal of selection on MHC genes. However, post-WNS populations exhibited decreased allelic richness, reflecting effects from bottleneck and drift following rapid population declines. We propose that mechanisms other than adaptive immunity are more likely driving current persistence of little brown bats in affected regions.</p>

opencc-zeroAug 2021View details →
dryad28/100

Data from: Profiling the immunome of little brown myotis provides a yardstick for measuring the genetic response to white-nose syndrome

White-nose syndrome (WNS) has devastated populations of hibernating bats in eastern North America, leading to emergency conservation listings for several species including the previously ubiquitous little brown myotis (Myotis lucifugus). However, some bat populations near the epicenter of the white-nose syndrome panzootic appear to be stabilizing after initial precipitous declines, which could reflect a selective immunogenetic sweep. To investigate the hypothesis that WNS exerts significant selection on the immunome of affected bat populations, we developed a novel, high-throughput sequence capture assay targeting 138 adaptive, intrinsic, and innate immunity genes of putative adaptive significance, as well as their respective regulatory regions (~370-kbp of genomic sequence/individual). We used the assay to explore baseline immunogenetic variation in M. lucifugus and to investigate whether particular immune genes/variants are associated with WNS susceptibility. We also used our assay to detect 1,038 putatively neutral single-nucleotide polymorphisms and characterize contemporary population structure, providing context for the identification of local immunogenetic adaptation. Sequence capture provided a cost-effective, 'all-in-one' assay to test for neutral genetic and immunogenetic structure and revealed fine-scale, baseline immunogenetic differentiation between sampling sites &lt; 600 kilometers apart. We identified functional immunogenetic variants in M. lucifugus associated with WNS susceptibility. This study lays the foundations for future investigations of range-wide immunogenetic adaptation to white-nose syndrome in M. lucifugus, and provides a blueprint for studies of evolutionary rescue in other host-pathogen systems.

opencc-zeroDec 2016View details →
dryad28/100

Incorporating evaporative water loss into bioenergetic models of hibernation to test for relative influence of host and pathogen traits on white-nose syndrome

<p class="Paragraph">Hibernation consists of extended durations of torpor interrupted by periodic arousals. The 'dehydration hypothesis' proposes that hibernating mammals arouse to replenish water lost through evaporation during torpor. Arousals are energetically expensive, and increased arousal frequency can alter survival throughout hibernation. Yet we lack a means to assess the effect of evaporative water loss (EWL), determined by animal physiology and hibernation microclimate, on torpor bout duration and subsequent survival. White-nose syndrome (WNS), a devastating disease impacting hibernating bats, causes increased frequency of arousals during hibernation and EWL has been hypothesized to contribute to this increased arousal frequency. WNS is caused by a fungus, which grows well in humid hibernaculum environments and damages wing tissue important for water conservation. Here, we integrated the effect of EWL on torpor expression in a hibernation energetics model, including the effects of fungal infection, to determine the link between EWL and survival. We collected field data for <i>Myotis lucifugus, </i>a species that experiences high mortality from WNS, to gather parameters for the model. In saturating conditions, we predicted healthy bats experience minimal mortality. Infected bats, however, suffer high fungal growth in highly saturated environments, leading to exhaustion of fat stores before spring. Our results suggest that host adaptation to humid environments leads to increased arousal frequency from infection, which drives mortality across hibernaculum conditions. Our modified hibernation model provides a tool to assess the interplay between host physiology, hibernaculum microclimate, and diseases such as WNS on winter survival.</p>

opencc-zeroOct 2019View details →
dryad28/100

Incorporating evaporative water loss into bioenergetic models of hibernation to test for relative influence of host and pathogen traits on white-nose syndrome

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publicOct 2019View details →
dryad28/100

Data from: Profiling the immunome of little brown myotis provides a yardstick for measuring the genetic response to white-nose syndrome

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publicJun 2017View details →
dryad28/100

MHC variation is similar in little brown bats before and after white-nose syndrome outbreak

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publicJan 2021View details →

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