Epidemiological modeling of invasion in heterogeneous landscapes: spread of sudden oak death in California (1990-2030)

The spread of emerging infectious diseases (EIDs) in natural environments poses substantial risks to biodiversity and ecosystem function. As EIDs and their impacts grow, landscape- to regional-scale models of disease dynamics are increasingly needed for quantitative prediction of epidemic outcomes a...

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Published inEcosphere (Washington, D.C) Vol. 2; no. 2; pp. art17 - 24
Main Authors Meentemeyer, Ross K, Cunniffe, Nik J, Cook, Alex R, Filipe, Joao A. N, Hunter, Richard D, Rizzo, David M, Gilligan, Christopher A
Format Journal Article
LanguageEnglish
Published Washington Ecological Society of America 01.02.2011
John Wiley & Sons, Inc
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Abstract The spread of emerging infectious diseases (EIDs) in natural environments poses substantial risks to biodiversity and ecosystem function. As EIDs and their impacts grow, landscape- to regional-scale models of disease dynamics are increasingly needed for quantitative prediction of epidemic outcomes and design of practicable strategies for control. Here we use spatio-temporal, stochastic epidemiological modeling in combination with realistic geographical modeling to predict the spread of the sudden oak death pathogen ( Phytophthora ramorum ) through heterogeneous host populations in wildland forests, subject to fluctuating weather conditions. The model considers three stochastic processes: (1) the production of inoculum at a given site; (2) the chance that inoculum is dispersed within and among sites; and (3) the probability of infection following transmission to susceptible host vegetation. We parameterized the model using Markov chain Monte Carlo (MCMC) estimation from snapshots of local- and regional-scale data on disease spread, taking account of landscape heterogeneity and the principal scales of spread. Our application of the model to Californian landscapes over a 40-year period (1990-2030), since the approximate time of pathogen introduction, revealed key parameters driving the spatial spread of disease and the magnitude of stochastic variability in epidemic outcomes. Results show that most disease spread occurs via local dispersal (<250 m) but infrequent long-distance dispersal events can substantially accelerate epidemic spread in regions with high host availability and suitable weather conditions. In the absence of extensive control, we predict a ten-fold increase in disease spread between 2010 and 2030 with most infection concentrated along the north coast between San Francisco and Oregon. Long-range dispersal of inoculum to susceptible host communities in the Sierra Nevada foothills and coastal southern California leads to little secondary infection due to lower host availability and less suitable weather conditions. However, a shift to wetter and milder conditions in future years would double the amount of disease spread in California through 2030. This research illustrates how stochastic epidemiological models can be applied to realistic geographies and used to increase predictive understanding of disease dynamics in large, heterogeneous regions.
AbstractList The spread of emerging infectious diseases (EIDs) in natural environments poses substantial risks to biodiversity and ecosystem function. As EIDs and their impacts grow, landscape- to regional-scale models of disease dynamics are increasingly needed for quantitative prediction of epidemic outcomes and design of practicable strategies for control. Here we use spatio-temporal, stochastic epidemiological modeling in combination with realistic geographical modeling to predict the spread of the sudden oak death pathogen ( Phytophthora ramorum ) through heterogeneous host populations in wildland forests, subject to fluctuating weather conditions. The model considers three stochastic processes: (1) the production of inoculum at a given site; (2) the chance that inoculum is dispersed within and among sites; and (3) the probability of infection following transmission to susceptible host vegetation. We parameterized the model using Markov chain Monte Carlo (MCMC) estimation from snapshots of local- and regional-scale data on disease spread, taking account of landscape heterogeneity and the principal scales of spread. Our application of the model to Californian landscapes over a 40-year period (1990-2030), since the approximate time of pathogen introduction, revealed key parameters driving the spatial spread of disease and the magnitude of stochastic variability in epidemic outcomes. Results show that most disease spread occurs via local dispersal (<250 m) but infrequent long-distance dispersal events can substantially accelerate epidemic spread in regions with high host availability and suitable weather conditions. In the absence of extensive control, we predict a ten-fold increase in disease spread between 2010 and 2030 with most infection concentrated along the north coast between San Francisco and Oregon. Long-range dispersal of inoculum to susceptible host communities in the Sierra Nevada foothills and coastal southern California leads to little secondary infection due to lower host availability and less suitable weather conditions. However, a shift to wetter and milder conditions in future years would double the amount of disease spread in California through 2030. This research illustrates how stochastic epidemiological models can be applied to realistic geographies and used to increase predictive understanding of disease dynamics in large, heterogeneous regions.
The spread of emerging infectious diseases (EIDs) in natural environments poses substantial risks to biodiversity and ecosystem function. As EIDs and their impacts grow, landscape‐ to regional‐scale models of disease dynamics are increasingly needed for quantitative prediction of epidemic outcomes and design of practicable strategies for control. Here we use spatio‐temporal, stochastic epidemiological modeling in combination with realistic geographical modeling to predict the spread of the sudden oak death pathogen (Phytophthora ramorum) through heterogeneous host populations in wildland forests, subject to fluctuating weather conditions. The model considers three stochastic processes: (1) the production of inoculum at a given site; (2) the chance that inoculum is dispersed within and among sites; and (3) the probability of infection following transmission to susceptible host vegetation. We parameterized the model using Markov chain Monte Carlo (MCMC) estimation from snapshots of local‐ and regional‐scale data on disease spread, taking account of landscape heterogeneity and the principal scales of spread. Our application of the model to Californian landscapes over a 40‐year period (1990–2030), since the approximate time of pathogen introduction, revealed key parameters driving the spatial spread of disease and the magnitude of stochastic variability in epidemic outcomes. Results show that most disease spread occurs via local dispersal (<250 m) but infrequent long‐distance dispersal events can substantially accelerate epidemic spread in regions with high host availability and suitable weather conditions. In the absence of extensive control, we predict a ten‐fold increase in disease spread between 2010 and 2030 with most infection concentrated along the north coast between San Francisco and Oregon. Long‐range dispersal of inoculum to susceptible host communities in the Sierra Nevada foothills and coastal southern California leads to little secondary infection due to lower host availability and less suitable weather conditions. However, a shift to wetter and milder conditions in future years would double the amount of disease spread in California through 2030. This research illustrates how stochastic epidemiological models can be applied to realistic geographies and used to increase predictive understanding of disease dynamics in large, heterogeneous regions.
Author Hunter, Richard D
Gilligan, Christopher A
Cunniffe, Nik J
Filipe, Joao A. N
Rizzo, David M
Meentemeyer, Ross K
Cook, Alex R
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  organization: Department of Geography and Earth Sciences, University of North Carolina, Charlotte, 9201 University City Boulevard, Charlotte, North Carolina 28223 USA
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  givenname: Nik J
  surname: Cunniffe
  fullname: Cunniffe, Nik J
  organization: Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge, CB2 3EA United Kingdom
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  givenname: Alex R
  surname: Cook
  fullname: Cook, Alex R
  organization: Department of Statistics and Applied Probability, National University of Singapore, Singapore 117546
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  fullname: Filipe, Joao A. N
  organization: Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge, CB2 3EA United Kingdom
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  organization: Department of Plant Pathology, University of California, Shields Avenue, Davis, California 95616 USA
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  givenname: Christopher A
  surname: Gilligan
  fullname: Gilligan, Christopher A
  organization: Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge, CB2 3EA United Kingdom
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i2150-8925-2-2-art17-Meentemeyer2
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i2150-8925-2-2-art17-Meentemeyer1
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Snippet The spread of emerging infectious diseases (EIDs) in natural environments poses substantial risks to biodiversity and ecosystem function. As EIDs and their...
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SubjectTerms Agricultural production
Biodiversity
computational biology
Disease
Disease spread
Dispersal
Ecosystems
emerging infectious disease
Environmental conditions
Environmental impact
Epidemics
Epidemiology
GIS
Heterogeneity
Hypotheses
Infections
Infectious diseases
Landscape
landscape epidemiology
Markov chain Monte Carlo
Markov chains
Pathogens
Phytophthora ramorum
Scale models
spatial heterogeneity
species distribution model
Weather
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Title Epidemiological modeling of invasion in heterogeneous landscapes: spread of sudden oak death in California (1990-2030)
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