A promising avenue to the control of tuberculosis is limiting iron acquisition by the pathogen. Mycobacterium tuberculosis produces non-ribosomal peptide mycobactins during periods of iron limitation. Full virulence has been shown to require production of these siderophores. Like its deadlier cousin M. tuberculosis, Mycobacterium paratuberculosis is known to survive assault from the immune system by living within macrophage lysosomes. We have shown that mycobactin J, produced by mycobacterium paratuberculosis, localized to lipid droplets upon metal binding within macrophages. We have also shown that mycobactin J causes large disruptions to cellular metabolism, including decreased protein production and changes in several major metabolic pathways. This lecture will describe our current efforts to understand the roles of siderophores in pathogenesis and host response.