Tuberculosis pathophysiology and anti-VEGF intervention

The pathophysiological understanding of tuberculosis is growing, and with this growth comes the possibility of applying established pharmaceuticals in new ways. These new ways interlude with the many mechanisms by which the intracellular pathogen, Mycobacterium tuberculosis, thrives in its human host. This article will discuss those mechanisms in the context of the pathophysiological processes associated with tuberculosis. Tuberculosis is a disease that results in systemic lesions arising from bacterial-immune interactions. The pathophysiology of this disease proceeds as aerosolization, phagocytosis, phagolysosome blockage and replication, T- helper response, granuloma formation, clinical manifestations, and concluding with active disease and transmission. Herein are the brief details of each of these processes. The conclusion of this article will be current tuberculosis treatments and future promising pharmacological directions. Particularly using the anti-vascular endothelial growth factor treatments currently used in cancer therapy, which are rationally presented with support from case studies. The purpose of this article is thus to present the pathophysiology of tuberculosis to convince the reader of the logical theory behind why anti-VEGF intervention should be used in tuberculosis treatment.