ABSTRACT
Hemostatic abnormalities accompanied by endothelial changes are among the earliest manifestations of invasive bacterial infections. The process begins with the proliferation of the bacteria in the nidus of infection, typically the tissue site where the organisms have penetrated the host mucosal membranes. Bacteria may invade the bloodstream directly or may proliferate locally and release various substances into the circulation. Gram-positive bacteria, such as streptococci and staphylococci, produce proteins that interact directly with components of the coagulation and fibrinolytic systems. Bacterium-bound plasminogen may also be activated by host-derived plasminogen activator. S fimbriae, which are surface proteins produced by Escherichia coli strains causing neonatal sepsis and meningitis, bind both plasminogen and tissue-type plasminogen activator (t-PA) in a lysine-dependent manner and enhance the rate of plasmin formation. The early increase in t-PA activity is associated with plasminogen activation as indicated by concomitant appearance of plasmin-a2-antiplasmin complexes in plasma.
