Coagulopathy in experimental sepsis with Streptococcus pneumoniae in rabbits: effect of drug therapy and splenectomy.

The cause of death in bacteremia due to Streptococcus pneumoniae remains unclear. The role of intravascular coagulation and splenectomy was investigated in rabbits with lethal pneumococcal bacteremia. The staphylococcal clumping titer in serum, a measure of fibrin degradation products, increased early and persisted until death. This titer correlated with the level of bacteremia. The partial thromboplastin time and platelet-rich plasma clotting time also increased as the disease worsened. However, the prothrombin time remained normal. 125I-labeled fibrinogen was cleared normally from the plasma of infected rabbits, whether intact or splenectomized. Similarly, the concentration of fibrogen in plasma remained normal, even though the level of fibrin degradation products increased, and no difference in these parameters was noted between intact and splenectomized rabbits. Fibrin deposition could not be detected in any of the organs studied. Neither the level of fibrin degradation products nor survival was affected by treatment with hydrocortisone, hexadimethrine, cytochrome c, carboxypeptidase B, epsilon-aminocaproic acid, or heparin. These data suggest that intravascular coagulation occurs in this experimental infection prior to the onset of shock but probably plays only a minor role in lethality.