Tuberculosis (TB), a serious public health infection that mainly affects the lungs, is caused by bacteria (Mycobacterium tuberculosis, TB). This research is designed and analyzed using a compartmental modelling approach to study the transmission dynamics of TB with different stages of infection. Qualitative analysis of the proposed model reveals that the model exhibits two equilibrium points: the disease-free equilibrium point (DFE) and the endemic equilibrium (EE). The basic reproduction number (R0 ) is determined using the next generation matrix technique, and stability analysis is carried out to show whether the disease can persist or die out in population. Further analysis of the model shows that the EE is globally asymptotically stable (GAS) when R0 > 1. With the aid of the forward sensitivity index method, we determine the most sensitive parameters of the model to control the spread of TB infection effectively. Our analysis shows that treatment (medication) and campaign awareness coupled with other key control measures, could help maintain the spread of MTB infection in human geographical boundaries.
Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), is the leading bacterial cause of infectious disease mortality. The current WHOapproved treatment for TB involves a three- or four-drug regimen comprising isoniazid, rifampin, pyrazinamide, and/or ethambutol for a minimum of 6 months. While these first-line agents remain useful in treating susceptible Mycobacterium tuberculosis strains, the emergence of multidrug resistant tuberculosis demands the development of new drugs [1]. Iron acquisition is an essential process for M. tuberculosis as well as almost all other microorganisms. However, this essential micronutrient is highly sequestered in a mammalian host. In response to iron starvation, Mtb produces small-molecule iron chelators, a pair of related peptidic siderophores known as mycobactin and carboxymycobactins that vary by the appended lipid residue termed siderophores [4, 5, 7, 8]. Because mycobactins are critical for growth and virulence of M. tuberculosis, they have emerged as attractive targets for the development of anti-TB agents [4]. Biosynthesis of mycobactin is initiated by the aryl acid adenylation enzyme MbtA which activates salicylic acid forming an acyladenylate intermediate (Sal- AMP). MbtA is also responsible for loading the acyladenylate intermediate onto the thiolation domain of MbtB-SH – the enzyme taking part in the next step of biosynthesis process [10]. Given the documented importance of many siderophores for virulence and lack of human aryl acid adenylation enzymes homologues, several analogues possessing stable linkers as bioisosteres of the labile acyl phosphate function have been synthesized as the potent enzyme inhibitors [13]. The initial lead compound 5’-O-[N- (salicyl)sulfamoyl]adenosine (Sal-AMS) has emerged as a promising inhibitor of MbtA and was shown to possess promising whole-cell activity toward M. tuberculosis.