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1. Wildfire alters the disturbance impacts of an emerging forest disease via changes to host occurrence and demographic structure

   https://doi.org/10.1111/1365-2745.13495  

   Simler‐Williamson, Allison B. ; Metz, Margaret R. ; Frangioso, Kerri M. ; Rizzo, David M. ; Thrall, ed., Peter ( September 2020 , Journal of Ecology)

   Anthropogenic activities have altered historical disturbance regimes, and understanding the mechanisms by which these shifting perturbations interact is essential to predicting where they may erode ecosystem resilience. Emerging infectious plant diseases, caused by human translocation of nonnative pathogens, can generate ecologically damaging forms of novel biotic disturbance. Further, abiotic disturbances, such as wildfire, may influence the severity and extent of disease‐related perturbations via their effects on the occurrence of hosts, pathogens and microclimates; however, these interactions have rarely been examined.

   The disease ‘sudden oak death’ (SOD), associated with the introduced pathogenPhytophthora ramorum, causes acute, landscape‐scale tree mortality in California's fire‐prone coastal forests. Here, we examined interactions between wildfire and the biotic disturbance impacts of this emerging infectious disease. Leveraging long‐term datasets that describe wildfire occurrence andP. ramorumdynamics across the Big Sur region, we modelled the influence of recent and historical fires on epidemiological parameters, including pathogen presence, infestation intensity, reinvasion, and host mortality.

   Past wildfire altered disease dynamics and reduced SOD‐related mortality, indicating a negative interaction between these abiotic and biotic disturbances. Frequently burned forests were less likely to be invaded byP. ramorum, had lower incidence of host infection, and exhibited decreased disease‐related biotic disturbance, which was associated with reduced occurrence and density of epidemiologically significant hosts. Following a recent wildfire, survival of mature bay laurel, a key sporulating host, was the primary driver ofP. ramoruminfestation and reinvasion, but younger, rapidly regenerating host vegetation capable of sporulation did not measurably influence disease dynamics. Notably, the effect ofP. ramoruminfection on host mortality was reduced in recently burned areas, indicating that the loss of tall, mature host canopies may temporarily dampen pathogen transmission and ‘release’ susceptible species from significant inoculum pressure.

   Synthesis. Cumulatively, our findings indicate that fire history has contributed to heterogeneous patterns of biotic disturbance and disease‐related decline across this landscape, via changes to the both the occurrence of available hosts and the demography of epidemiologically important host populations. These results highlight that human‐altered abiotic disturbances may play a foundational role in structuring infectious disease dynamics, contributing to future outbreak emergence and driving biotic disturbance regimes.

    

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2. The Magnitude of Regional‐Scale Tree Mortality Caused by the Invasive Pathogen Phytophthora ramorum

   https://doi.org/10.1029/2020EF001500  

   Cobb, Richard C. ; Haas, Sarah E. ; Kruskamp, Nicholas ; Dillon, Whalen W. ; Swiecki, Tedmund J. ; Rizzo, David M. ; Frankel, Susan J. ; Meentemeyer, Ross K. ( July 2020 , Earth's Future)

   Forest pathogens are important drivers of tree mortality across the globe, but it is exceptionally challenging to gather and build unbiased quantitative models of their impacts. Here we harness the rare data set matching the spatial scale of pathogen invasion, host, and disease heterogeneity to estimate infection and mortality for the four most susceptible host species ofPhytophthora ramorum, an invasive pathogen that drives the most important biological cause of tree mortality in a broad geographic region of coastal California and southwest Oregon. As of 2012, the most current field survey year, we estimate 17.5 (±4.6, 95% CI [confidence interval]) million tanoak (Notholithocarpus densiflorus) stems were pathogen killed with an additional 71 (±21.5) million infected. We estimated 9.0 million (±2.2) coast live oak (Quercus agrifolia) and 1.7 million (±0.5) California black oak (Quercus kelloggii) stems are disease impacted (mortality and infection combined). Lastly, our estimates suggest infection in 95.2 million (±8.6) California bay laurel (Umbellularia californica), which does not suffer mortality from infection and represents a critical source of continued spread. Prevalent infection as of 2012 suggests the cumulative number of disease‐killed stems likely increased from 20.8 to 42.8 million between 2012 and 2019 for all species. While these impacts are substantial, most host populations occur in a yet to be invaded region of northern California indicating that the disease will intensify in the coming decades.

    

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3. Warming and pollutants interact to modulate octocoral immunity and shape disease outcomes

   https://doi.org/10.1002/eap.2024  

   Tracy, Allison M. ; Weil, Ernesto ; Harvell, C. Drew ( November 2019 , Ecological Applications)

   Warming environments can alter the outcome of host–parasite relationships with important consequences for biodiversity. Warming often increases disease risk, and interactions with other environmental factors can intensify impacts by modifying the underlying mechanisms, such as host immunity. In coastal ecosystems, metal pollution is a pervasive stressor that influences disease and immunity in many organisms. Despite the crisis facing coral reefs, which stems in part from warming‐associated disease outbreaks, the impacts of metal pollutants on scleractinian and octocoral disease are largely unknown. We investigated how warming oceans and copper pollution affect host immunity and disease risk for two diseases of the abundant Caribbean octocoral, the sea fan Gorgonia ventalina. Field surveys across a sediment copper concentration gradient in Puerto Rico, USA revealed that cellular immunity of sea fans increased by 12.6% at higher sediment copper concentrations, while recovery from multifocal purple spots disease (MFPS) tended to decrease.MFPSseverity in the field increased at warmer sites. In a controlled laboratory experiment, sea fans were inoculated with live cultures of a labyrinthulid parasite to test the interactive effects of temperature and copper on immune activation. As in the field, higher copper induced greater immunity, but the factorial design of the experiment revealed that copper and temperature interacted to modulate the immune response to the parasite: immune cell densities increased with elevated temperature at lower copper concentrations, but not with high copper concentrations. Tissue damage was also greater in treatments with higher copper and warmer temperatures. Field and lab evidence confirm that elevated copper hinders sea fan immune defenses against damaging parasites. Temperature and copper influenced host–pathogen interactions in octocorals by modulating immunity, disease severity, and disease recovery. This is the first evidence that metal pollution affects processes influencing disease in octocorals and highlights the importance of immune mechanisms in environmentally mediated disease outbreaks. Although coral conservation efforts must include a focus on global factors, such as rapid warming, reducing copper and other pollutants that compromise coral health on a local scale may help corals fight disease in a warming ocean.

    

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4. Individual and temporal variation in pathogen load predicts long‐term impacts of an emerging infectious disease

   https://doi.org/10.1002/ecy.2613  

   Wells, Konstans ; Hamede, Rodrigo K. ; Jones, Menna E. ; Hohenlohe, Paul A. ; Storfer, Andrew ; McCallum, Hamish I. ( February 2019 , Ecology)

   Emerging infectious diseases increasingly threaten wildlife populations. Most studies focus on managing short‐term epidemic properties, such as controlling early outbreaks. Predicting long‐term endemic characteristics with limited retrospective data is more challenging. We used individual‐based modeling informed by individual variation in pathogen load and transmissibility to predict long‐term impacts of a lethal, transmissible cancer on Tasmanian devil (Sarcophilus harrisii) populations. For this, we employed approximate Bayesian computation to identify model scenarios that best matched known epidemiological and demographic system properties derived from 10 yr of data after disease emergence, enabling us to forecast future system dynamics. We show that the dramatic devil population declines observed thus far are likely attributable to transient dynamics (initial dynamics after disease emergence). Only 21% of matching scenarios led to devil extinction within 100 yr following devil facial tumor disease (DFTD) introduction, whereasDFTDfaded out in 57% of simulations. In the remaining 22% of simulations, disease and host coexisted for at least 100 yr, usually with long‐period oscillations. Our findings show that pathogen extirpation or host–pathogen coexistence are much more likely than theDFTD‐induced devil extinction, with crucial management ramifications. Accounting for individual‐level disease progression and the long‐term outcome of devil–DFTDinteractions at the population‐level, our findings suggest that immediate management interventions are unlikely to be necessary to ensure the persistence of Tasmanian devil populations. This is because strong population declines of devils after disease emergence do not necessarily translate into long‐term population declines at equilibria. Our modeling approach is widely applicable to other host–pathogen systems to predict disease impact beyond transient dynamics.

    

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5. Do not feed the wildlife: associations between garbage use, aggression, and disease in banded mongooses ( Mungos mungo )

   https://doi.org/10.1002/ece3.2343  

   Flint, Bonnie Fairbanks ; Hawley, Dana M. ; Alexander, Kathleen A. ( July 2016 , Ecology and Evolution)

   Urbanization and other human modifications of the landscape may indirectly affect disease dynamics by altering host behavior in ways that influence pathogen transmission. Few opportunities arise to investigate behaviorally mediated effects of human habitat modification in natural host–pathogen systems, but we provide a potential example of this phenomenon in banded mongooses (Mungos mungo), a social mammal. Our banded mongoose study population in Botswana is endemically infected with a novelMycobacterium tuberculosiscomplex pathogen,M. mungi, that primarily invades the mongoose host through the nasal planum and breaks in the skin. In this system, several study troops have access to human garbage sites and other modified landscapes for foraging. Banded mongooses in our study site (N = 4 troops, ~130 individuals) had significantly higher within‐troop aggression levels when foraging in garbage compared to other foraging habitats. Second, monthly rates of aggression were a significant predictor of monthly number of injuries in troops. Finally, injured individuals had a 75% incidence of clinical tuberculosis (TB) compared to a 0% incidence in visibly uninjured mongooses during the study period. Our data suggest that mongoose troops that forage in garbage may be at greater risk of acquiringTBby incurring injuries that may allow for pathogen invasion. Our study suggests the need to consider the indirect effects of garbage on behavior and wildlife health when developing waste management approaches in human‐modified areas.

    

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