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In general, the burn wound or lungs are the most likely sites for an infection in the severely burned patient that subsequently develops MODS [ 1 ]. The release of endotoxins and/or exotoxins from an infective process initiates a cascade of inflammatory mediators that leads to organ damage and ultimately organ failure. Targeting the different cascade systems involved in the pathogenesis of burn-induced MODS is often not a feasible option [ 8 ]. Prevention of sepsis from burn wound infection is the most promising approach, as illustrated by the following examples: