Staphylococcus aureus small colony variants use heme and staphyloferrin B for iron acquisition
Abstract
Iron is an essential nutrient for the bacterium Staphylococcus aureus. Wild-type S. aureus utilizes various iron acquisition systems to support growth in iron deplete conditions. S. aureus small colony variants (SCVs) are associated with chronic infections, yet the mechanisms by which these variants acquire iron are unknown. Mutation of hemB, involved in heme biosynthesis, generated a stable SCV that was auxotrophic for hemin and formed small colonies on solid media. To support growth under iron deplete conditions, my data revealed that S. aureus hemB synthesizes the siderophore staphyloferrin B, but not staphyloferrin A, although both siderophores could be utilized by the hemB mutant if provided exogenously. Additionally, I demonstrated that the hemB mutant, in comparison to wild-type S. aureus, was defective for xenosiderophore utilization, including the clinically approved drug Desferal. This study yields important insight into the mechanisms by which S. aureus SCVs acquire iron to cause persistent infection.