Oldest and most feared disease

Abstract

Mycobacterium leprae the organism that causes leprosy is the only bacterial pathogen known to invade peripheral nerves causing axonal degeneration increased fibrosis and demyelinization. The mode of entry of the bacteria is not known but it is hypothesized that it enters via the persons circulation by breaking the blood-nerve barrier. However the effects of M. leprae invasion on the physiology and metabolism of Schwann cell are poorly understood. It is noted that the infection might increase the expression of inflammatory cytokines disturbing the homeostasis of the nerve cell. This theory is substantiated by the fact that corticosteroids are able to greatly improve existing neuronal pathology. Furthermore one such cytokine--tumor necrosis factor alpha (TNFalpha)--has been implicated in the development of nerve injury in leprosy. Researchers believe that TNFalpha is important in the induction of demyelination and toxic effects in neural cells. It was also noted that TNFalpha promotes neurodegeneration by inhibiting survival signals. Therefore the unbalanced concentration of TNFalpha might promote neuropathy by direct cytotoxic effect on Schwann cells and axons and by acting as an inflammatory mediator.