Summary
Hog cholera is an excellent model to study virus related haemorrhagic diatheses of man, since coagulation parameters and morphology of swine platelets are quite similar to those of man. 15 pigs were infected with hog cholera virus. The volume distribution curves of platelets, immediately stabilized with glutaraldehyde after sampling, indicates a right shift of their peaks after infection, which is due to increase in number of megathrombocytes and aggregates. Electron microscopy shows from the first day p.i. an increase in number of giant platelets, and thrombocytes with multiple dense granules including “bull’s eyes”, more mitochondria, endoplasmic reticulum and Golgi apparatus. These findings indicate an accelerated thrombocytopoiesis, in which more immature platelets appear in the blood stream. The other changes (dilatation of surface connecting system, increase of dense tubular system and microtubuli, formation of aggregates) are obviously due to a release-reaction, following adsorption and phagocytosis of the virus by the platelets. The studies reveal that in the beginning of acute hog cholera platelets already are directly damaged by the virus. Since thrombocytopoiesis cannot match the severe and progredient destruction of platelets, from the second day p.i. marked thrombocytopenia develops. Together with virus-induced endothelial lesions and disseminated intravascular coagulation, as described by us, it causes the haemorrhagic diathesis, typical for terminal stages of acute hog cholera.
