Abstract

This review will focus on patients with genetic defects predisposing to infections with poorly pathogenic mycobacteria [Bacillus Calmette-Guerin and environmental Non-Tuberculous Mycobacteria (NTM)] as well as Salmonella species. Mycobacteria and Salmonella are facultative intracellular pathogens capable of surviving and multiplying within mononuclear phagocytes. Host defense against these pathogens depends on the action of cell-mediated immunity (CMI), effected by interactions between T cells and macrophages. The principal effector mechanism responsible immunity against these pathogens is the activation of infected macrophages by type 1 cytokines, particularly interferon-γ (IFN-γ) and Tumor necrosis factor alpha (TNF-α)[1].