Pathogenesis of tuberculosis caused by Mycobacterium bovis

Mycobacterium bovis, the etiologic agent of bovine tuberculosis, is a slow-growing nonphotochromogenic acid-fast bacillus. In human monocyte-derived dendritic cells and macrophages, the M. tuberculosis and M. leprae microorganisms transfer into phagolysosomes prior to translocation into the cytoplasm early in infection. Pathogenicity of mycobacteria is a multifactorial phenomenon requiring the participation and cumulative effects of several virulence factors, including complex lipids and proteins in both the cell wall and the cytoplasm of tubercle bacilli. Innate immunity is the first response to mycobacterial infections and is a preparatory step for adaptive immunity. Secretion of interleukin (IL)-12, IL-18, and tumor necrosis factor alpha by antigen-presenting cells (APCs) triggers the proinflammatory response with the activation of effector cells including NK that are cytotoxic, and gamma-delta T cells that are involved in granuloma formation.