PLA2G2D and subacute bacterial endocarditis: sPLA2s act through hydrolysis of phospholipids with release of inflammatory mediators as well as through a cytotoxic pore-forming mechanism.10, 12 Organ-specific injury from these toxins occurs via binding of the sPLA2 to proteins on the surface of target cells.12 13 Through these mechanisms, sPLA2s contribute to all major categories of SBE pathology: cytotoxicity, coagulopathy, haemolysis, nephrotoxicity, cardiovascular instability and neurotoxicity.8