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We consider the spread of an infectious disease in a heterogeneous environment modeled as a network of patches. We focus on the invasibility of the disease, as quantified by the corresponding value...

We study a two-species competition model in a patchy advective environment, where the species are subject to both directional drift and undirectional random dispersal between patches and there are losses of individuals in the downstream end (e.g., due to the flow into a lake or ocean). The two competing species are assumed to have the same growth rates but different advection and random dispersal rates. We focus our studies on the properties of an associated eigenvalue problem which characterizes the extinction/persistence dynamics of the underlying patch population model. We also derive conditions on the advection and random dispersal rates under which a mutating species can or cannot invade the resident species., Comment: 45 pages, 8 figures

A cholera model has been formulated to incorporate the interaction of bacteria and phage. It is shown that there may exist three equilibria: one disease free and two endemic equilibria. Threshold parameters have been derived to characterize stability of these equilibria. Sensitivity analysis and disease control strategies have been employed to characterize the impact of bacteria-phage interaction on cholera dynamics.

The dynamics of an SIS epidemic patch model with asymmetric connectivity matrix is analyzed. It is shown that the basic reproduction number $R_0$ is strictly decreasing with respect to the dispersal rate of the infected individuals, and the model has a unique endemic equilibrium if $R_0>1$. The asymptotic profiles of the endemic equilibrium for small dispersal rates are characterized. In particular, it is shown that the endemic equilibrium converges to a limiting disease-free equilibrium as the dispersal rate of susceptible individuals tends to zero, and the limiting disease-free equilibrium has a positive number of susceptible individuals on each low-risk patch. Moreover a sufficient and necessary condition is found to guarantee that the limiting disease-free equilibrium has no positive number of susceptible individuals on each high-risk patch. Our results extend earlier results for symmetric connectivity matrix, and we also partially solve an open problem by Allen et al. (SIAM J. Appl. Math., 67: 1283-1309, 2007)., 41 pages; 4 figures

A general framework for threshold parameters in population dynamics is developed using the concept of target reproduction numbers. This framework identifies reproduction numbers and other threshold parameters in the literature in terms of their roles in population control. The framework is applied to the analysis of single and multiple control strategies in ecology and epidemiology, and this provides new biological insights.

Syphilis is caused by the bacterium Treponema pallidum subspecies pallidum, and is a sexually transmitted disease with multiple stages. A model of transmission of syphilis in an MSM population (there has recently been a resurgence of syphilis in such populations) that includes infection stages and treatment is formulated as a system of ordinary differential equations. The control reproduction number is calculated, and it is proved that if this threshold parameter is below one, syphilis dies out; otherwise, if it is greater than one, it is shown that there exists a unique endemic equilibrium and that for certain special cases, this equilibrium is globally asymptotically stable. Using data from the literature on MSM populations, numerical methods are used to determine the variation and robustness of the control reproduction number with respect to the model parameters, and to determine adequate treatment rates for syphilis eradication. By assuming a closed population and no return to susceptibility, an epidemic model is obtained. Final outbreak sizes are numerically determined for various parameter values, and its variation and robustness to parameter value changes is also investigated. Results quantify the importance of early treatment for syphilis control.

A mathematical model is formulated for the transmission and spread of cholera in a heterogeneous host population that consists of several patches of homogeneous host populations sharing a common water source. The basic reproduction number ℛ0 is derived and shown to determine whether or not cholera dies out. Explicit formulas are derived for target/type reproduction numbers that measure the control strategies required to eradicate cholera from all patches.

Several relations involving closed walks and closed cycles in a weighted digraph are established. These relations are used to derive new expressions for target reproduction numbers for controlling the spectral radius of nonnegative matrices. The results are illustrated by an application to infectious disease control.

The ability of disease to invade a community network that is connected by environmental pathogen movement is examined. Each community is modeled by a susceptible–infectious–recovered (SIR) framework that includes an environmental pathogen reservoir, and the communities are connected by pathogen movement on a strongly connected, weighted, directed graph. Disease invasibility is determined by the basic reproduction number $$\mathcal{{R}}_0$$ for the domain. The domain $$\mathcal{{R}}_0$$ is computed through a Laurent series expansion, with perturbation parameter corresponding to the ratio of the pathogen decay rate to the rate of water movement. When movement is fast relative to decay, $$\mathcal{{R}}_0$$ is determined by the product of two weighted averages of the community characteristics. The weights in these averages correspond to the network structure through the rooted spanning trees of the weighted, directed graph. Clustering of disease “hot spots” influences disease invasibility. In particular, clustering hot spots together according to a generalization of the group inverse of the Laplacian matrix facilitates disease invasion.

A new model for the dynamics of cholera is formulated that incorporates both the infection age of infectious individuals and biological age of pathogen in the environment. The basic reproduction number is defined and proved to be a sharp threshold determining whether or not cholera dies out. Final size relations for cholera outbreaks are derived for simplified models when input and death are neglected.

A mathematical model for cholera is formulated that incorporates hyperinfectivity and temporary immunity using distributed delays. The basic reproduction number \(\mathcal{R}_{0}\) is defined and proved to give a sharp threshold that determines whether or not the disease dies out. The case of constant temporary immunity is further considered with two different infectivity kernels. Numerical simulations are carried out to show that when \(\mathcal{R}_{0}>1\), the unique endemic equilibrium can lose its stability and oscillations occur. Using cholera data from the literature, the quantitative effects of hyperinfectivity and temporary immunity on oscillations are investigated numerically.

The basic reproduction number ℛ(0) for a compartmental disease model is often calculated by the next generation matrix (NGM) approach. When the interactions within and between disease compartments are interpreted differently, the NGM approach may lead to different ℛ(0) expressions. This is demonstrated by considering a susceptible-infectious-recovered-susceptible model with free-living pathogen (FLP) growing in the environment. Although the environment could play different roles in the disease transmission process, leading to different ℛ(0) expressions, there is a unique type reproduction number when control strategies are applied to the host population. All ℛ(0) expressions agree on the threshold value 1 and preserve their order of magnitude. However, using data for salmonellosis and cholera, it is shown that the estimated ℛ(0) values are substantially different. This study highlights the utility and limitations of reproduction numbers to accurately quantify the effects of control strategies for infections with FLPs growing in the environment.

We propose a general class of multistage epidemiological models that allow possible deterioration and amelioration between any two infected stages. The models can describe disease progression through multiple latent or infectious stages as in the case of HIV and tuberculosis. Amelioration is incorporated into the models to account for the effects of antiretroviral or antibiotic treatment. The models also incorporate general nonlinear incidences and general nonlinear forms of population transfer among stages. Under biologically motivated assumptions, we derive the basic reproduction number $R_0$ and show that the global dynamics are completely determined by $R_0$: if $R_0\leq 1$, the disease-free equilibrium is globally asymptotically stable, and the disease dies out; if $R_0>1$, then the disease persists in all stages and a unique endemic equilibrium is globally asymptotically stable.

A general compartmental model for cholera is formulated that incorporates two pathways of transmission, namely direct and indirect via contaminated water. Non-linear incidence, multiple stages of infection and multiple states of the pathogen are included, thus the model includes and extends cholera models in the literature. The model is analyzed by determining a basic reproduction number R0 and proving, by using Lyapunov functions and a graph-theoretic result based on Kirchhoff's Matrix Tree Theorem, that it determines a sharp threshold. If R0≤1, then cholera dies out; whereas if R0>1, then the disease tends to a unique endemic equilibrium. When input and death are neglected, the model is used to determine a final size equation or inequality, and simulations illustrate how assumptions on cholera transmission affect the final size of an epidemic.

The global-stability problem of equilibria is investigated for coupled systems of differential equations on networks. Using results from graph theory, we develop a systematic approach that allows one to construct global Lyapunov functions for large-scale coupled systems from building blocks of individual vertex systems. The approach is applied to several classes of coupled systems in engineering, ecology and epidemiology, and is shown to improve existing results.

We investigate a class of multi-group epidemic models with distributed delays. We establish that the global dynamics are completely determined by the basic reproduction number R 0 . More specifically, we prove that, if R 0 ⩽ 1 , then the disease-free equilibrium is globally asymptotically stable; if R 0 > 1 , then there exists a unique endemic equilibrium and it is globally asymptotically stable. Our proof of global stability of the endemic equilibrium utilizes a graph-theoretical approach to the method of Lyapunov functionals.

A class of global Lyapunov functions is revisited and used to resolve a long-standing open problem on the uniqueness and global stability of the endemic equilibrium of a class of multi-group models in mathematical epidemiology. We show how the group structure of the models, as manifested in the derivatives of the Lyapunov function, can be completely described using graph theory.

In this paper, n-impulsive harvest problems of general simple population are discussed by models with Dirac function. The optimal impulsive harvest policies to protect the renewable resource better are obtained under conditions of fixed quantity per impulsive harvest. Then, a concept of the sequence for Ϝ-optimal harvest moments for general simple population is presented which is beneficial to protect resource better and sustainable development. Finally, we apply the conclusions to some special models.

Compartmental models for infectious disease transmission among heterogeneous host populations are surveyed. Mathematical methodologies for analyzing heterogeneous disease models are reviewed. Specifically, three methods are provided to establish the global stability of the endemic equilibrium for a multigroup SIS model. The survey is concluded with several open problems.

In this paper, we established the exploitation of impulsive harvesting single autonomous population model by Logistic equation. By some special methods, we analysis the impulsive harvesting population equation and obtain existence, the explicit expression and global attractiveness of impulsive periodic solutions for constant yield harvest and proportional harvest. Then, we choose the maximum sustainable yield as management objective, and investigate the optimal impulsive harvesting policies respectively. The optimal harvest effort that maximizes the sustainable yield per unit time, the corresponding optimal population levels are determined. At last, we point out that the continuous harvesting policy is superior to the impulsive harvesting policy, however, the latter is more beneficial in realistic operation.

Bovine Babesiosis in cattle is caused by the transmission of protozoa of Babesia spp. by ticks as vectors. Juvenile cattle ( $$

A mathematical model for cholera is formulated that incorporates direct and indirect transmission, patch structure, and both water and human movement. The basic reproduction number R0 is defined and shown to give a sharp threshold that determines whether or not the disease dies out. Kirchhoff’s Matrix Tree Theorem from graph theory is used to investigate the dependence of R0 on the connectivity and movement of water, and to prove the global stability of the endemic equilibrium when R0 > 1. The type/target reproduction numbers are derived to measure the control strategies that are required to eradicate cholera from all patches.

In this paper, we consider an autonomous model with impulsive harvest. We investigate the impulsive harvest policies for constant effort harvest and proportional harvest. For different harvest effort function, it is shown that there exists an unique impulsive periodic solution which is semi-stable or globally asymptotically stable. For the latter, the optimal harvest effort that maximizes the sustainable yield per unit time is determined.

In this paper, we consider the ODE system corresponding to a diffusive-convective model for the dynamics of a population living in a polluted environment. Sufficient criteria on persistence and extinction of the population are derived.