Bifurcation analysis of a phage-bacteria interaction model with prophage induction.

A predator-prey model is used to investigate the interactions between phages and bacteria by considering the lytic and lysogenic life cycles of phages and the prophage induction. We provide answers to the following conflictual research questions: (1) what are conditions under which the presence of phages can purify a bacterial infected environment? (2) Can the presence of phages triggers virulent bacterial outbreaks? We derive the basic offspring number $\mathcal N_0$ that serves as a threshold and the bifurcation parameter to study the dynamics and bifurcation of the system. The model exhibits three equilibria: an unstable environment-free equilibrium, a globally asymptotically stable (GAS) phage-free equilibrium (PFE) whenever $\mathcal N_0<1$, and a locally asymptotically stable environment-persistent equilibrium (EPE) when $\mathcal N_0>1$. The Lyapunov-LaSalle techniques are used to prove the GAS of the PFE and estimate the EPE basin of attraction. Through the center manifold approximation, topological types of the PFE are precised. Existence of transcritical and Hopf bifurcations are established. Precisely, when $\mathcal N_0>1$, the EPE loses its stability and periodic solutions arise. Furthermore, increasing $\mathcal N_0$ can purify an environment where bacteriophages are introduced. Purposely, we prove that for large values of $\mathcal N_0$, the overall bacterial population asymptotically approaches zero, while the phage population sustains. Ecologically, our results show that for small values of $\mathcal N_0$, the existence of periodic solutions could explain the occurrence of repetitive bacteria-borne disease outbreaks, while large value of $\mathcal N_0$ clears bacteria from the environment. Numerical simulations support our theoretical results.

A simple mathematical model for Ebola in Africa.

We deal with the following question: Can the consumption of contaminated bush meat, the funeral practices and the environmental contamination explain the recurrence and persistence of Ebola virus disease outbreaks in Africa? We develop an SIR-type model which, incorporates both the direct and indirect transmissions in such a manner that there is a provision of Ebola viruses. We prove that the full model has one (endemic) equilibrium which is locally asymptotically stable whereas, it is globally asymptotically stable in the absence of the Ebola virus shedding in the environment. For the sub-model without the provision of Ebola viruses, the disease dies out or stabilizes globally at an endemic equilibrium. At the endemic level, the number of infectious is larger for the full model than for the sub-model without provision of Ebola viruses. We design a nonstandard finite difference scheme, which preserves the dynamics of the model. Numerical simulations are provided.

Mathematical analysis of a model for AVL-HIV co-endemicity.

A model for the transmission dynamics of Anthroponotic Visceral Leishmaniasis (AVL) and human immunodeficiency virus (HIV) in a population is developed and used to assess the impact of the spread of each disease on the overall transmission dynamics. As for other vector-borne disease models, the AVL component of the model undergoes backward bifurcation when the associated reproduction number of the AVL-only sub-model (denoted by RL) is less than unity. Uncertainty and sensitivity analyzes of the model, using data relevant to the dynamics of the two diseases in Ethiopia, show that the top three parameters that drive the AVL infection (with respect to the associated response function, RL) are the average number of times a sandfly bites humans per unit time (σV), carrying capacity of vectors (KV) and transmission probability from infected humans to susceptible sandflies (ß2). The distribution of RL is RL∈[0.06,3.94] with a mean of RL=1.08. Furthermore, the top three parameters that affect HIV dynamics (with respect to the response function RH) are the transmission rate of HIV (ßH), HIV-induced death rate (δH), and the modification parameter for the increase in infectiousness of AIDS individuals in comparison to HIV infected without clinical symptoms of AIDS (ωH). The distribution of RH is RH∈[0.88,2.79] with a mean of RH=1.46. The dominant parameters that affect the dynamics of the full VL-HIV model (with respect to the associated reproduction number, RLH, as the response function) are the transmission rate of HIV (ßH), the average number of times a sandfly bites humans per unit time (σV), and HIV-induced death rate (δH) (the distribution of RLH is RLH∈[0.88,3.94] with a mean of RLH=1.64). Numerical simulations of the model show that the two diseases co-exist (with AVL dominating, but not driving HIV to extinction) whenever the reproduction number of each disease exceeds unity. It is shown that AVL can invade a population at HIV-endemic state if a certain threshold quantity, known as invasion reproduction number, exceeds unity.

Dynamics of Mycobacterium and bovine tuberculosis in a human-buffalo population.

A new model for the transmission dynamics of Mycobacterium tuberculosis and bovine tuberculosis in a community, consisting of humans and African buffalos, is presented. The buffalo-only component of the model exhibits the phenomenon of backward bifurcation, which arises due to the reinfection of exposed and recovered buffalos, when the associated reproduction number is less than unity. This model has a unique endemic equilibrium, which is globally asymptotically stable for a special case, when the reproduction number exceeds unity. Uncertainty and sensitivity analyses, using data relevant to the dynamics of the two diseases in the Kruger National Park, show that the distribution of the associated reproduction number is less than unity (hence, the diseases would not persist in the community). Crucial parameters that influence the dynamics of the two diseases are also identified. Both the buffalo-only and the buffalo-human model exhibit the same qualitative dynamics with respect to the local and global asymptotic stability of their respective disease-free equilibrium, as well as with respect to the backward bifurcation phenomenon. Numerical simulations of the buffalo-human model show that the cumulative number of Mycobacterium tuberculosis cases in humans (buffalos) decreases with increasing number of bovine tuberculosis infections in humans (buffalo).

On nonstandard finite difference schemes in biosciences.

We design, analyze and implement nonstandard finite difference (NSFD) schemes for some differential models in biosciences. The NSFD schemes are reliable in three directions. They are topologically dynamically consistent for onedimensional models. They can replicate the global asymptotic stability of the disease-free equilibrium of the MSEIR model in epidemiology whenever the basic reproduction number is less than 1. They preserve the positivity and boundedness property of solutions of advection-reaction and reaction-diffusion equations.