It is generally accepted that iron is the most important micronutrient used by bacteria. With members of the family Lactobacillae being the only exceptions so far (3), this metal is essential for cellular metabolism, since it is needed as a cofactor for a large number of enzymes (96). However, this element is not easily available to microorganisms in aerobic environments. While in anaerobic conditions Fe2+ is soluble at physiological pH and cells obtain iron without much difficulty from the external medium, the ion becomes quickly converted to Fe3+ upon exposure to oxygen and forms insoluble hydroxides at neutral pH, making the available metal very scarce (20). In order to acquire iron from the extracellular medium, virtually all aerobic bacteria produce and secrete low-molecular-weight compounds termed siderophores (sideros phoros, iron carriers). These compounds chelate Fe3+ with high affinity and specificity (68). Subsequently, the cell recovers the ferrisiderophore complexes through specific outer membrane receptors (30). Some of these high-affinity systems of iron uptake are important virulence factors in bacteria infecting animal ffuids and tissues because they can chelate the metal bound to host proteins (7, 36, 60, 71). Furthermore, because iron availability is generally growth limiting for bacteria thriving in an animal millieu, the lack of the metal is a major environmental signal to trigger expression of virulence determinants (60). However, an excess of iron is toxic because of its ability to catalyse Fenton reactions and formation of active species of oxygen. Iron uptake has to be, therefore, exquisitely regulated to maintain the intracellular concentration of the metal between desirable limits. Considering that excretion mechanisms for iron are not known in bacteria, microorganisms appear to control iron homeostasis, regulating its transport through the membrane (5, 21).