Extracellular vesicles (EVs) are derived from the membrane of cells upon activation or injury. Most of the circulating EVs in blood are derived from platelets. Just like their parent cell, platelet derived EVs are attributed an important role in hemostasis and exhibit immunomodulatory effects by transfer of bioactive cargo to target cells. Platelet activation and release of circulating platelet derived EVs increase in several pathological inflammatory diseases, such as sepsis. We have previously described an IgG and fibrinogen dependent immune complex mediated platelet activation in response to pathogen derived M1 protein from Streptococcus pyogenes. In this study, we isolated EVs from activated platelets using acoustic trapping and applied quantitative mass spectrometry-based proteomics to characterize the differences in the protein cargo of EVs isolated from resting platelets, physiologically stimulated (Thrombin) platelets, and immune complex (Streptococcal M1 protein) stimulated platelets. We determined that M1 protein mediated platelet activation and generated platelet derived EVs that contain the M1 protein. The isolated EVs derived from all three conditions contained a protein cargo of platelet membrane proteins, granule proteins and cytoskeletal proteins, in combination with coagulation factors and immune mediators. The EVs isolated from M1 protein stimulated platelets also contained increased levels of complement proteins and IgG3. The isolated EVs derived from all three conditions exhibited proinflammatory effects on addition to blood, including platelet-neutrophil complex formation, neutrophil activation, and cytokine release. Collectively, our findings reveal novel aspects of pathogen mediated platelet activation that may contribute to the coagulation and immune dysfunction during invasive streptococcal infection.