The prompt identification, localization and characterization of focal sites of infection in the patients with fever is a critical step in clinical management, particularly, when localizing symptoms are not present. Although the classic signs of inflammation are suitable to localize injury at superficial sites or in the extremities, inflammation of internal structures, such as in the brain, chest and abdomen, can be difficult to localize without additional diagnostic procedures. Tissue injury, regardless of cause or anatomical site, results in a complex series of physiologic changes that we recognize as the inflammatory response. The inflammatory response is characterized by a series of biochemical events in the insulted cells and surrounding structures that results in the three major pathophysiological components: increased tissue perfusion, increased vascular permeability, and leukocytic exudation. Exploitation of the early attributes of the inflammatory process are not sufficient for the routine detection of inflammation. Currently, reagents for targeting infection represent cellular or protein components involved in the inflammatory process. Such approaches have met with some success as these agents comprise integral parts of the complex phenomena known as inflammation. This same fact also limits their utility. Improved agents for targeting infection will likely be based on small molecules whose diffusion into the lesion is not hindered by molecular size constraints and which bind to molecular targets at the site of infection/inflammation. In general, the lower molecular weight should also lead to enhanced blood clearance, avoiding elevated blood pool activity which contributes to background. New agents should also obviate the need to handle blood, as this represents potential hazards to both patient and the medical personnel alike.
