African swine fever and classical swine fever: a review of the pathogenesis.

This paper describes major pathogenetic mechanisms of African and Classical Swine Fever virus infections. The interactions between both viruses and the monocyte-macrophage-system result in the release of mediator molecules, which are important for the further progression of the diseases. The causes of the thrombocytopenia and the mechanisms of the haemorrhages, which are characteristic in both infections, are described. Apoptotic cell death is regarded as the predominant cause of lymphopenia in both virus infections.

Two cases of feline visceral and cutaneous leishmaniosis in Spain.

This paper describes clinical signs and lesions in two cases of leishmaniosis--one visceral and one cutaneous in the cat (Felis catus domesticus). The diagnosis was achieved by a combination of serology, light and electron microscopic studies. The vague nature of the clinical signs observed in both cases was particularly striking, and clinical features were similar to many other diseases commonly found in cats. Therefore, the use of various investigations to detect leishmaniosis (serum chemistry, serology and histopathology) is highly recommended in cases where clinical signs do not respond to conventional treatment.

Ultrastructural changes related to the lymph node haemorrhages in acute African swine fever.

In order to determine the pathogenic mechanisms involved in lymph node haemorrhages in acute African swine fever (ASF), eight pigs were inoculated with ASF virus, strain Malawi'83. Lymph node haemorrhages were observed from three days post infection (dpi) onwards, coinciding with ASF virus replication in monocytes and macrophages adjacent to stimulated endothelial cells, phagocytic stimulation of capillary and small-vessel endothelial cells, increase in the number of fenestrations of endothelial cells, and endothelial cell loss, as well as clusters of blood cells and necrotic material beneath the endothelium. Vascular lumina were blocked by platelet plugs and fibrin microthrombi. These phenomena became more marked as the disease progressed. At five dpi, virus replication was also found in circulating neutrophils. At seven dpi, lesions were more intense and were accompanied by virus replication in sinus and capillary endothelial cells, and in other cell populations including pericytes, fibroblasts, smooth muscle fibres and reticular cells. The results obtained in this study suggest that lymph node haemorrhages are related to endothelial stimulation and the onset of disseminated intravascular coagulation. Virus replication in vessel wall cells occurs only in the final stages of the disease and plays a secondary role.

Development of microscopic lesions in splenic cords of pigs infected with African swine fever virus.

Acute forms of African swine fever are characterized by hemorrhagic lesions in the lymphoid organs. This paper reports the evolution of lesions in the splenic cords of pigs inoculated with African swine fever (ASF) virus (strain Malawi'83). Ultrastructural examination of the splenic cords of the infected pigs revealed numerous macrophages attached to the muscle cells harboring virus replication center and cytopathic effects at 3 dpi (days post-infection). From 5 dpi, the splenic cords contained a large number of erythrocytes associated with abundant fibrin deposits, mainly arranged around the muscle cells, from which macrophages had disappeared. It is likely that the ASF virus replication, and consequent cytopathic effects, observed in the fixed macrophages of splenic cords, may be responsible for the fibrin deposition.