Platelet activation, homotypic and heterotypic binding to other platelets and leukocytes, and sequestration of platelets and myeloid leukocytes within thrombi are common complications of septic syndromes in humans. Pathogens, pathogen-derived factors, or agonists present in the septic milieu (A) induce platelet activation and aggregation, signaling to areas of injured or inflamed endothelium, and (B) orchestrating deposition of fibrin, platelets, and myeloid leukocytes within micro- and macrovascular thrombi (modified from Rondina et al.⁸ ). In the figure, platelets are indicated as blue, irregularly- or spherically-shaped cells.