Nik Cunniffe

Dr. Nik Cunniffe


Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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21 May 2021 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
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JRJean Beagle Ristaino
Jean Beagle Ristaino
PAPamela K. Anderson
Pamela K. Anderson
DBDaniel Bebber
Daniel Bebber
KBKate A. Brauman
Kate A. Brauman
NCNik Cunniffe
Nik Cunniffe
Qingshan WeiQingshan Wei
Qingshan Wei
Plant disease outbreaks are increasing and threaten food security for the vulnerable in many areas of the world. Now a global human pandemic is threatening the health of millions on our planet. A stable, nutritious food supply will be needed to lift people out of poverty and improve health outcomes. Plant diseases, both endemic and recently emerging, are spreading and exacerbated by climate change, transmission with global food trade networks, pathogen spillover, and evolution of new pathogen lineages. In order to tackle these grand challenges, a new set of tools that include disease surveillance and improved detection technologies including pathogen sensors and predictive modeling and data analytics are needed to prevent future outbreaks. Herein, we describe an integrated research agenda that could help mitigate future plant disease pandemics.

2 May 2016 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Open access
PDF file
NCNik Cunniffe
Nik Cunniffe
RCRichard C. Cobb
Richard C. Cobb
RMRoss Meentemeyer
Ross Meentemeyer
DRDavid M. Rizzo
David M. Rizzo
CGChristopher A. Gilligan
Christopher A. Gilligan
Sudden oak death, caused by Phytophthora ramorum, has killed millions of oak and tanoak in California since its first detection in 1995. Despite some localized small-scale management, there has been no large-scale attempt to slow the spread of the pathogen in California. Here we use a stochastic spatially explicit model parameterized using data on the spread of P. ramorum to investigate whether and how the epidemic can be controlled. We find that slowing the spread of P. ramorum is now not possible, and has been impossible for a number of years. However, despite extensive cryptic (i.e., presymptomatic) infection and frequent long-range transmission, effective exclusion of the pathogen from large parts of the state could, in principle, have been possible were it to have been started by 2002. This is the approximate date by which sufficient knowledge of P. ramorum epidemiology had accumulated for large-scale management to be realistic. The necessary expenditure would have been very large, but could have been greatly reduced by optimizing the radius within which infected sites are treated and careful selection of sites to treat. In particular, we find that a dynamic strategy treating sites on the epidemic wave front leads to optimal performance. We also find that “front loading” the budget, that is, treating very heavily at the start of the management program, would greatly improve control. Our work introduces a framework for quantifying the likelihood of success and risks of failure of management that can be applied to invading pests and pathogens threatening forests worldwide.

1 March 2015 in Epidemics
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Journal Article
Open access
NCNik Cunniffe
Nik Cunniffe
BKBritt Koskella
Britt Koskella
CMC. Jessica E. Metcalf
C. Jessica E. Metcalf
SPStephen Parnell
Stephen Parnell
TGTim R. Gottwald
Tim R. Gottwald
CGChristopher A. Gilligan
Christopher A. Gilligan
The underlying structure of epidemiological models, and the questions that models can be used to address, do not necessarily depend on the host organism in question. This means that certain preoccupations of plant disease modellers are similar to those of modellers of diseases in human, livestock and wild animal populations. However, a number of aspects of plant epidemiology are very distinctive, and this leads to specific challenges in modelling plant diseases, which in turn sets a certain agenda for modellers. Here we outline a selection of 13 challenges, specific to plant disease epidemiology, that we feel are important targets for future work.

1 February 2011 in Ecosphere
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Journal Article
Open access
RMRoss Meentemeyer
Ross Meentemeyer
NCNik Cunniffe
Nik Cunniffe
ACAlex Richard Cook
Alex Richard Cook
JFJoao A. N. Filipe
Joao A. N. Filipe
RHRichard D. Hunter
Richard D. Hunter
CGChristopher A. Gilligan
Christopher A. Gilligan

1 July 2013 in Annals of the American Association of Geographers
Verified
Journal Article
Closed access
RMRoss Meentemeyer
Ross Meentemeyer
WTWenwu Tang
Wenwu Tang
MDMonica Dorning
Monica Dorning
JVJohn B. Vogler
John B. Vogler
NCNik Cunniffe
Nik Cunniffe
DSDouglas A. Shoemaker
Douglas A. Shoemaker
We present a multilevel modeling framework for simulating the emergence of landscape spatial structure in urbanizing regions using a combination of field-based and object-based representations of land change. The FUTure Urban-Regional Environment Simulation (FUTURES) produces regional projections of landscape patterns using coupled submodels that integrate nonstationary drivers of land change: per capita demand, site suitability, and the spatial structure of conversion events. Patches of land change events are simulated as discrete spatial objects using a stochastic region-growing algorithm that aggregates cell-level transitions based on empirical estimation of parameters that control the size, shape, and dispersion of patch growth. At each time step, newly constructed patches reciprocally influence further growth, which agglomerates over time to produce patterns of urban form and landscape fragmentation. Multilevel structure in each submodel allows drivers of land change to vary in space (e.g., by jurisdiction), rather than assuming spatial stationarity across a heterogeneous region. We applied FUTURES to simulate land development dynamics in the rapidly expanding metropolitan region of Charlotte, North Carolina, between 1996 and 2030, and evaluated spatial variation in model outcomes along an urban–rural continuum, including assessments of cell- and patch-based correctness and error. Simulation experiments reveal that changes in per capita land consumption and parameters controlling the distribution of development affect the emergent spatial structure of forests and farmlands with unique and sometimes counterintuitive outcomes.

5 April 2016 in PLOS Computational Biology
Verified
Journal Article
Open access
PDF file
RTRobin N Thompson
Robin N Thompson
CGChristopher A Gilligan
Christopher A Gilligan
NCNik Cunniffe
Nik Cunniffe
We assess how presymptomatic infection affects predictability of infectious disease epidemics. We focus on whether or not a major outbreak (i.e. an epidemic that will go on to infect a large number of individuals) can be predicted reliably soon after initial cases of disease have appeared within a population. For emerging epidemics, significant time and effort is spent recording symptomatic cases. Scientific attention has often focused on improving statistical methodologies to estimate disease transmission parameters from these data. Here we show that, even if symptomatic cases are recorded perfectly, and disease spread parameters are estimated exactly, it is impossible to estimate the probability of a major outbreak without ambiguity. Our results therefore provide an upper bound on the accuracy of forecasts of major outbreaks that are constructed using data on symptomatic cases alone. Accurate prediction of whether or not an epidemic will occur requires records of symptomatic individuals to be supplemented with data concerning the true infection status of apparently uninfected individuals. To forecast likely future behavior in the earliest stages of an emerging outbreak, it is therefore vital to develop and deploy accurate diagnostic tests that can determine whether asymptomatic individuals are actually uninfected, or instead are infected but just do not yet show detectable symptoms. Emerging epidemics pose a significant challenge to human health worldwide. Accurate real-time forecasts of whether or not initial reports will be followed by a major outbreak are necessary for efficient deployment of control. For all infectious diseases, there is a delay between infection and the appearance of symptoms, i.e. an initial period following first infection during which infected individuals remain presymptomatic. We use mathematical modeling to evaluate the effect of presymptomatic infection on predictions of major epidemics. Our results show rigorously, for the first time, that precise estimates of the current number of infected individuals—and consequently the chance of a major outbreak in future—cannot be inferred from data on symptomatic cases alone. This is the case even if the values of epidemiological parameters, such as the average infection and death or recovery rates of individuals in the population, can be estimated accurately. Accurate prediction is in fact impossible without additional data from which the number of currently infected but as yet presymptomatic individuals can be deduced.