The highly contagious disease tuberculosis (TB) is caused by the bacterium Mycobacterium tuberculosis (Mtb), which has been evolving drug resistance at an alarming rate due to the harsh, long drug treatments. Like all human pathogens, iron is essential for Mtbâs survival and virulence. Consequently, Mtb iron transport is an emerging drug target. However, the development of anti-TB drugs aimed at these metabolic pathways have been restricted by the dearth of information on Mtb iron acquisition. Mtb has multiple strategies utilized to acquire ferric iron and heme-iron. Mtb iron uptake is a complex process requiring biosynthesis and subsequent export of Mtb siderophores, followed by ferric iron scavenging and ferric-siderophore import into Mtb. Additionally, Mtb uptakes heme and has a Mtb-specific mechanism of heme degradation that yields iron and novel heme-degradation products. Here we present several aspects of these pathways to close the knowledge gaps of iron acquisition in mycobacteria.
