Despite the enormous progress in prevention and treatment, tuberculosis disease remains a leading cause of death worldwide and one of the major sources of concern is the drug resistant strain, MDR-TB (multidrug resistant tuberculosis) and XDR-TB (extensively drug resistant tuberculosis). In this work, we extend the standard SEIRS epidemiology model of tuberculosis to include MDR-TB. For that, we considered compartments of susceptible, exposed, infected, resistant to a first line of treatment and recovered humans and we modeled the natural growth, the interactions between these populations and the effects of treatments. We calculate the basic reproduction number, 0  , using the next generation method. The DFE and the EE are established and their stability analysis done to show that they are locally and globally asymptotically stable. Numerical analysis for the model with and without delay is done and demonstrated that in the case of patients with both active tuberculosis and MDR tuberculosis, both strains will still persist due to lack of permanent immunity to tuberculosis while the recovered can still lose their immunity to become susceptible again.

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In this study, we develop an SIS model for two types of mosquitoes, a traditional one and one that is resistant to IRS and ITNs. The resistant mosquito develops behavioral adaptation to control measures put in place to reduce their biting rate. They also bite early before dusk and later after dark when people are outside the houses and nets. We determine the effect of the two types of mosquitoes on malaria transmission in Kenya. The basic reproduction number 0  is established as a sharp threshold that determines whether the disease dies out or persists in the population. Precisely, if 0  ≤ 1, the disease-free equilibrium is globally asymptotically stable and the disease always dies out and if 0  > 1, there exists a unique endemic equilibrium which is globally stable and the disease persists. The contribution of the two types of mosquitoes to the basic reproduction number and to the level of the endemic equilibrium is analyzed.

Malaria prevalence in sub-Saharan Africa remains high. Kenya for example, records about 3.5 million new cases and 11 thousand deaths each year.1 Most of these cases and deaths are among children under five. The main control method in malaria endemic regions has been through the use of insecticide-treated nets (ITNs). Although this approach has been fairly successful, the gains are threatened by mosquito-resistance to pyrethroids (insecticides on nets), physical and chemical degradation of ITNs that reduce their efficacy, inconsistent and improper use by humans, etc. We present a model to investigate the effects of ITN use and mosquito-resistance and adaptation to pyrethroids used to treat bed nets on malaria prevalence and control in malaria endemic regions. The model captures the development and loss of resistance to insecticides, the effects of ITN use on malaria control in a setting where proper and consistent use is not guaranteed, as well as differentiated biting of human hosts by resistant and sensitive mosquitoes. Important thresholds, including the basic reproduction number [Formula: see text], and two parameter groupings that are important for disease control and for establishing the existence of endemic equilibria to the model are calculated. Furthermore, a global sensitivity analysis is carried out to identify important parameters such as insecticide treated bed-net coverage, ITN, the maximum biting rate of resistant mosquitoes, etc., that drive the system and that can be targeted for disease control. Threshold levels of ITN coverage and ITN efficacy required for containing the disease are identified and shown to depend on the type of insecticide-resistance. For example, when mosquito-resistance to insecticides is not permanent and is acquired only through recruitment and the efficacy of ITNs is [Formula: see text], about [Formula: see text] net coverage is required to contain malaria. However, for the same ITN efficacy, i.e., [Formula: see text], approximately [Formula: see text] net coverage is required to contain the disease when resistance to insecticides is permanent and is acquired through recruitment and mutation in mosquitoes. The model exhibits a backward bifurcation, which implies that simply reducing [Formula: see text] slightly below unity might not be enough to contain the disease. We conclude that appropriate measures to reduce or eliminate mosquito-resistance to insecticides, ensure that more people in endemic areas own and use ITNs properly, and that the efficacy of these nets remain high most of the time, as well as educating populations in malaria endemic areas on how to keep mosquito densities low and minimize mosquito bites are important for containing malaria.

We consider a rift valley fever model with treatment in human and livestock populations and trapping in the vector (mosquito) population. The basic reproduction number 0  is established and used to determine whether the disease dies out or is established in the three populations. When 0 1  ≤ , the disease-free equilibrium is shown to be globally asymptotically stable and the disease does not spread and when 0 1  > , a unique endemic equilibrium exists which is globally stable and the disease will spread. The mathematical model is analyzed analytically and numerically to obtain insight of the impact of intervention in reducing the burden of rift valley fever disease's spread or epidemic and also to determine factors influencing the outcome of the epidemic. Sensitivity analysis for key parameters is also done.