Bacterial pathogens are rapidly gaining resistance to antimicrobial therapeutics undermining the ability of modern medicine to treat such infections [1,2]. The Centers for Disease Control and Prevention reported over 2 million people in the United States become infected with drug-resistant bacteria annually, causing at least 23,000 deaths [3]. In light of such reports, the need to identify and study novel targets for antimicrobial intervention using emerging analytical technologies is paramount for the future successful treatment of infectious diseases. One potential target for antimicrobial therapeutics involves transition metal homeostasis at the pathogen-host interface [4,5]. Metals are an essential component of biological function for all cells. It is estimated that 30-45% of all enzymes utilize a transition metal cofactor to enhance catalysis and reactivity [6,7]. Therefore, bacterial pathogens proliferating within a host must obtain metals to survive and grow, causing disease. In response, hosts seek to sequester these elements from pathogens, a process known as nutritional immunity [4,8]. With a more detailed understanding of host mechanisms of metal sequestration and bacterial mechanisms of metal scavenging, novel therapeutic targets can be discovered. S. aureus is a Gram-positive pathogen that commensally colonizes the anterior nares of an estimated 25% of the human population [9]. To cause disease, S. aureus breaches the initial site of infection and enters the bloodstream where it can cause infectious lesions on virtually any organ [10]. A hallmark of these purulent infectious foci, called abscesses, is the recruitment of host immune cells, including neutrophils and macrophages, which generate oxidative stress in an attempt to kill the pathogen [11,12]. Abscess formation has been studied extensively using histologically methods [10,13,14]; however, a molecular understanding of organ-specific heterogeneity of bacterial virulence factor expression and host response is not yet understood.