Home range behaviour is a common pattern of space use, having fundamental consequences for ecological processes. However, a general mechanistic explanation is still lacking. Research is split into three separate areas of inquiry -movement models based on random walks, individual-based models based on optimal foraging theory, and a statistical modelling approach -which have developed without much productive contact. Here we review recent advances in modelling home range behaviour, focusing particularly on the problem of identifying mechanisms that lead to the emergence of stable home ranges from unbounded movement paths. We discuss the issue of spatiotemporal scale, which is rarely considered in modelling studies, as well as highlighting the need to consider more closely the dynamical nature of home ranges. Recent methodological and theoretical advances may soon lead to a unified approach, however, conceptually unifying our understanding of linkages among home range behaviour and ecological or evolutionary processes.
Influenza epidemics vary in intensity from year to year, driven by climatic conditions and by viral antigenic evolution. However, important spatial variation remains unexplained. Here we show predictable differences in influenza incidence among cities, driven by population size and structure. Weekly incidence data from 603 cities in the United States reveal that epidemics in smaller cities are focused on shorter periods of the influenza season, whereas in larger cities, incidence is more diffuse. Base transmission potential estimated from city-level incidence data is positively correlated with population size and with spatiotemporal organization in population density, indicating a milder response to climate forcing in metropolises. This suggests that urban centers incubate critical chains of transmission outside of peak climatic conditions, altering the spatiotemporal geometry of herd immunity.
The unprecedented scale of the Ebola outbreak in Western Africa (2014)(2015) has prompted an explosion of efforts to understand the transmission dynamics of the virus and to analyze the performance of possible containment strategies. Models have focused primarily on the reproductive numbers of the disease that represent the average number of secondary infections produced by a random infectious individual. However, these population-level estimates may conflate important systematic variation in the number of cases generated by infected individuals, particularly found in spatially localized transmission and superspreading events. Although superspreading features prominently in first-hand narratives of Ebola transmission, its dynamics have not been systematically characterized, hindering refinements of future epidemic predictions and explorations of targeted interventions. We used Bayesian model inference to integrate individual-level spatial information with other epidemiological data of community-based (undetected within clinical-care systems) cases and to explicitly infer distribution of the cases generated by each infected individual. Our results show that superspreaders play a key role in sustaining onward transmission of the epidemic, and they are responsible for a significant proportion (∼61%) of the infections. Our results also suggest age as a key demographic predictor for superspreading. We also show that community-based cases may have progressed more rapidly than those notified within clinical-care systems, and most transmission events occurred in a relatively short distance (with median value of 2.51 km). Our results stress the importance of characterizing superspreading of Ebola, enhance our current understanding of its spatiotemporal dynamics, and highlight the potential importance of targeted control measures.Ebola | superspreading | offspring distribution | Bayesian inference T he outbreak size of the 2014 Ebola virus (EBOV) epidemic in Western Africa was unprecedented, and control measures failed to contain the epidemic at its early rapidly growing stage (1, 2). Mathematical models played a key role in inferring the transmission dynamics of EBOV (3). Modeling work succeeded in inferring, in particular, the basic reproductive number R0 (and the time-varying reproductive number, Rt ), which represents the average number of secondary cases that may be generated by a given infectious case (e.g., refs. 4-6). Although these parameters encapsulate knowledge about the average transmission potential of the epidemic at the population level, they fail to reflect individual variation in transmission, which may be more informative for devising targeted control measures.An important phenomenon in disease transmission is so-called superspreading, in which certain individuals (i.e., superspreaders) disproportionately infect a large number of secondary cases relative to an "average" infectious individual (whose infectivity may be well-represented by Rt ). Mathematically, the distribution of secondary cases is given ...
Animal movement paths are often thought of as a confluence of behavioral processes and landscape patterns. Yet it has proven difficult to develop frameworks for analyzing animal movement that can test these interactions. Here we describe a novel method for fitting movement models to data that can incorporate diverse aspects of landscapes and behavior. Using data from five elk (Cervus canadensis) reintroduced to central Ontario, we employed artificial neural networks to estimate movement probability kernels as functions of three landscape-behavioral processes. These consisted of measures of the animals' response to the physical spatial structure of the landscape, the spatial variability in resources, and memory of previously visited locations. The results support the view that animal movement results from interactions among elements of landscape structure and behavior, motivating context-dependent movement probabilities, rather than from successive realizations of static distributions, as some traditional models of movement and resource selection assume. Flexible, nonlinear models may thus prove useful in understanding the mechanisms controlling animal movement patterns.
The epidemic dynamics of infectious diseases vary among cities, but it is unclear how this is caused by patterns of infectious contact among individuals. Here, we ask whether systematic differences in human mobility patterns are sufficient to cause inter-city variation in epidemic dynamics for infectious diseases spread by casual contact between hosts. We analyse census data on the mobility patterns of every full-time worker in 48 Canadian cities, finding a power-law relationship between population size and the level of organization in mobility patterns, where in larger cities, a greater fraction of workers travel to work in a few focal locations. Similarly sized cities also vary in the level of organization in their mobility patterns, equivalent on average to the variation expected from a 2.64-fold change in population size. Systematic variation in mobility patterns is sufficient to cause significant differences among cities in infectious disease dynamics—even among cities of the same size—according to an individual-based model of airborne pathogen transmission parametrized with the mobility data. This suggests that differences among cities in host contact patterns are sufficient to drive differences in infectious disease dynamics and provides a framework for testing the effects of host mobility patterns in city-level disease data.
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