No Arabic abstract
We present and analyze a model aiming at recovering as dynamical outcomes of tree-grass interactions the wide range of vegetation physiognomies observable in the savanna biome along rainfall gradients at regional/continental scales. The model is based on two ordinary differential equations (ODE), for woody and grass biomass. It is parameterized from literature and retains mathematical tractability, since we restricted it to the main processes, notably tree-grass asym-metric interactions (either facilitative or competitive) and the grass-fire feedback. We used a fully qualitative analysis to derive all possible long term dynamics and express them in a bifur-cation diagram in relation to mean annual rainfall and fire frequency. We delineated domains of monostability (forest, grassland, savanna), of bistability (e.g. forest-grassland or forest-savanna) and even tristability. Notably, we highlighted regions in which two savanna equilibria may be jointly stable (possibly in addition to forest or grassland). We verified that common knowledge about decreasing woody biomass with increasing fire frequency is recovered for all levels of rainfall, contrary to previous attempts using analogous ODE frameworks. Thus, this framework appears able to render more realistic and diversified outcomes than often thought of. Our model can help figure out the ongoing dynamics of savanna vegetation in large territories for which local data are sparse or absent. To explore the bifurcation diagram with different combinations of the model parameters, we have developed a user-friendly R-Shiny application freely available at : https://gitlab.com/cirad-apps/tree-grass.
Observed bimodal tree cover distributions at particular environmental conditions and theoretical models indicate that some areas in the tropics can be in either of the alternative stable vegetation states forest or savanna. However, when including spatial interaction in nonspatial differential equation models of a bistable quantity, only the state with the lowest potential energy remains stable. Our recent reaction-diffusion model of Amazonian tree cover confirmed this and was able to reproduce the observed spatial distribution of forest versus savanna satisfactorily when forced by heterogeneous environmental and anthropogenic variables, even though bistability was underestimated. These conclusions were solely based on simulation results. Here, we perform an analytical and numerical analysis of the model. We derive the Maxwell point (MP) of the homogeneous reaction-diffusion equation without savanna trees as a function of rainfall and human impact and show that the front between forest and nonforest settles at this point as long as savanna tree cover near the front remains sufficiently low. For parameters resulting in higher savanna tree cover near the front, we also find irregular forest-savanna cycles and woodland-savanna bistability, which can both explain the remaining observed bimodality.
Fires and rainfall are major mechanisms that regulate woody and grassy biomasses in savanna ecosystems. Conditions of long-lasting coexistence of trees and grasses have been mainly studied using continuous-time modelling of tree-grass competition. In these frameworks, fire is a time-continuous forcing while the relationship between woody plant size and fire-sensitivity is not systematically considered. In this paper, we propose a new mathematical framework to model tree-grass interaction that takes into account both the discrete nature of fire occurrence and size-dependent fire sensitivity (via two classes of woody plants). We carry out a qualitative analysis that highlights ecological thresholds and bifurcations parameters that shape the dynamics of the savanna-like systems within the main ecological zones. Moreover, through a qualitative analysis, we show that the impulsive modelling of fire occurrences leads to more diverse behaviors and a more realistic array of solutions than the analogous time-continuous fire models. Numerical simulations are provided to illustrate the theoretical results and to support a discussion about the bifurcation parameters and future developments.
An outbreak of respiratory disease caused by a novel coronavirus is ongoing from December 2019. As of July 22, 2020, it has caused an epidemic outbreak with more than 15 million confirmed infections and above 6 hundred thousand reported deaths worldwide. During this period of an epidemic when human-to-human transmission is established and reported cases of coronavirus disease 2019 (COVID-19) are rising worldwide, investigation of control strategies and forecasting are necessary for health care planning. In this study, we propose and analyze a compartmental epidemic model of COVID-19 to predict and control the outbreak. The basic reproduction number and control reproduction number are calculated analytically. A detailed stability analysis of the model is performed to observe the dynamics of the system. We calibrated the proposed model to fit daily data from the United Kingdom (UK) where the situation is still alarming. Our findings suggest that independent self-sustaining human-to-human spread ($R_0>1$, $R_c>1$) is already present. Short-term predictions show that the decreasing trend of new COVID-19 cases is well captured by the model. Further, we found that effective management of quarantined individuals is more effective than management of isolated individuals to reduce the disease burden. Thus, if limited resources are available, then investing on the quarantined individuals will be more fruitful in terms of reduction of cases.
Understanding how to effectively control an epidemic spreading on a network is a problem of paramount importance for the scientific community. The ongoing COVID-19 pandemic has highlighted the need for policies that mitigate the spread, without relying on pharmaceutical interventions, that is, without the medical assurance of the recovery process. These policies typically entail lockdowns and mobility restrictions, having thus nonnegligible socio-economic consequences for the population. In this paper, we focus on the problem of finding the optimum policies that flatten the epidemic curve while limiting the negative consequences for the society, and formulate it as a nonlinear control problem over a finite prediction horizon. We utilize the model predictive control theory to design a strategy to effectively control the disease, balancing safety and normalcy. An explicit formalization of the control scheme is provided for the susceptible--infected--susceptible epidemic model over a network. Its performance and flexibility are demonstrated by means of numerical simulations.
The spread of an epidemic process is considered in the context of a spatial SIR stochastic model that includes a parameter $0le ple 1$ that assigns weights $p$ and $1- p$ to global and local infective contacts respectively. The model was previously studied by other authors in different contexts. In this work we characterized the behavior of the system around the threshold for epidemic spreading. We first used a deterministic approximation of the stochastic model and checked the existence of a threshold value of $p$ for exponential epidemic spread. An analytical expression, which defines a function of the quotient $alpha$ between the transmission and recovery rates, is obtained to approximate this threshold. We then performed different analyses based on intensive stochastic simulations and found that this expression is also a good estimate for a similar threshold value of $p$ obtained in the stochastic model. The dynamics of the average number of infected individuals and the average size of outbreaks show a behavior across the threshold that is well described by the deterministic approximation. The distributions of the outbreak sizes at the threshold present common features for all the cases considered corresponding to different values of $alpha>1$. These features are otherwise already known to hold for the standard stochastic SIR model at its threshold, $alpha=1$: (i) the probability of having an outbreak of size $n$ goes asymptotically as $n^{-3/2}$ for an infinite system, (ii) the maximal size of an outbreak scales as $N^{2/3}$ for a finite system of size $N$.