Focal infectious processes may produce a systemic syndrome whose description has been recently standardized by the definitions of sepsis, severe sepsis and septic shock. This classification should only be used as an adjunct to the microbiological and clinical diagnosis of a given infection. The incidence of sepsis and septic shock has been increasing over recent decades, but the ratio of gram-negative to gram-positive causative organisms has remained largely similar (most often between 1:1 and 3:2). Recent advances in understanding of the pathophysiology of sepsis and septic shock have made it possible to delineate more clearly the role of bacterial products such as lipopolysaccharide, exotoxins or cell wall fragments. These products are able either to directly trigger inflammatory pathways, or to stimulate target cells (such as monocytic cells, PMN or endothelial cells) to produce pro-inflammatory cytokines. Management of the infectious process itself with antibiotics, and with surgery if needed, is the cornerstone of the therapy of sepsis and septic shock. More recent approaches aim at inhibiting the bioactivity of bacterial or pro-inflammatory mediators. Up to now, however, none of these approaches has led to therapeutic modalities that can be applied routinely to patients.