Hemostasis and Infectious Agents

Many infectious agents can affect hemostasis, either by affecting bone marrow production of platelets, affecting platelet function, inducing vasculitis or initiating DIC.
  • Rickettsial disease: RMSF induces a coagulopathy mainly due to endothelial cell injury from invasion of endothelial cells (see Vasculitis for more information). Ehrlichia canis and platys can produce thrombocytopenia (partly by immune-mediated mechanisms) and decreased platelet function.

  • Viral diseases: Disseminated intravascular coagulation is a complication of feline infectious peritonitis virus and feline panleukopenia virus infections. Feline leukemia virus can produce thrombocytopenia or thrombocytosis. In one study, cats with feline immunodeficiency virus had thrombocytopenia, prolonged APTTs (which was shortened by dilution with pooled cat plasma) and high fibrinogen concentrations. The reasons for the prolonged APTTs were not found.

  • Parasites: Dogs with severe heartworm infection can develop DIC, which can be mimicked by experimental injection of heartworm extract. There is also platelet hyperaggregability in canine heartworm disease, rationalizing the use of aspirin as one of the components of treatment for this disorder.

  • Bacteria: Acute endothelial injury results in DIC in animals with leptospirosis. Sepsis is also a good initiator of DIC.

  • Snake bites: Many snake venoms contain enzymes which can activate coagulation factors, initiate DIC or break down fibrinogen. In fact, the snake venom from Bothrops atrox (Reptilase) is incorporated into serum FDP collection tubes to cause clotting of intact fibrinogen.