The most common type of fulminant purpura is associated with infectious disease, usually bacterial sepsis, with meningococcal sepsis, streptococcal sepsis, carbon dioxide phagocytic sepsis (from dog bites), staphylococcal sepsis and urogenital sepsis being the most common causes; rickettsial disease and malaria may also present as fulminant purpura. Patients without a spleen are prone to pneumococcal or meningococcal sepsis and are also favoured for fulminant purpura. However, sometimes it is a viral infection (chickenpox); active replication of HHV-6 with acquired protein S deficiency can also present as fulminant purpura.
Fulminant purpura may occur in newborns with a pure protein C or protein S gene deletion; temporary protein C and protein S defects can occur in some patients after infection and fulminant purpura may also occur.
Acquired fulminant purpura has been reported to occur after ingestion of alcohol, acetaminophen, diclofenac or propylthiouracil.
In other diseases such as fibrinolytic syndrome, fulminant purpura may occur as part of this syndrome; malignant anticardiolipin antibody syndrome should be considered if fulminant purpura occurs early in SLE; and fulminant purpura has been reported as a characteristic manifestation of Churg-Strauss syndrome and other ANCA-positive vasculitis.