Modulation of haemostasis by Staphylococcus aureus and Pseudomonas species infections. Severe bacterial infections can modulate haemostasis via multiple mechanisms. Long-chain polyphosphates (≥500 phosphate units) produced by bacteria promote FXIIa-mediated activation of blood coagulation. Polyphosphates also incorporate into fibrin clots and render the clots resistant to fibrinolysis. Staphylococcus aureus secretes coagulase and von Willebrand binding protein which activate prothrombin to thrombin in a non-enzymatic manner. Staphylococcus aureus also secretes fibronectin-binding protein A and clumping factor A which activate platelets. With respect to NETosis, Staphylococcus aureus secretes pore-forming toxins (such as Panton–Valentine leucocidin) which induces a unique and rapid (5–60 min) form of NETosis that occurs in an oxidant-independent mechanism. Elastase, a major virulence factor in Pseudomonas species, activates FXII in the coagulation cascade. Pseudomonas species also secrete protease IV which inhibits fibrinolysis via the degradation of plasminogen and fibrinogen. The result of severe infections of Staphylococcus aureus and Pseudomonas species is immunothrombosis, whose dysregulation may lead to vascular occlusion and thromboinflammation. Created with Biorender.com. vWbp, von Willebrand binding protein; FnbpA, fibronectin-binding protein A; ClfA, clumping factor A; NETs, neutrophil extracellular traps.