prev next front |1 |2 |3 |4 |5 |6 |7 |8 |9 |10 |11 |12 |13 |14 |15 |16 |17 |18 |19 |20 |21 |review
Death may occur in CME as a consequence of hemorrhage and/or secondary infections. Immunological mechanisms are involved with Coombs' and autoagglutination tests in infected animals, and the demonstration of antiplatelet antibodies (APA) in dogs experimentally infected with E. canis. Both platelet bindable and platelet-bound APA have been demonstrated in the blood of infected dogs and this likely related to thrombocytopenia and thrombocytopathia.

Involvement of the spleen in the pathogenesis of CME is prominent. The typical lymphoplasmacytic splenitis with the resultant liberation of splenic inflammatory mediators and other splenic substances has been thought to play a key role in the pathogenesis of this disease.