Clinical pathology and hemostatic abnormalities in experimental African horsesickness.

This research investigates the clinical pathology and abnormalities related to blood clotting in North American horses infected with different virulence variants of African horsesickness virus. It reveals distinct clinicopathological and hemostatic abnormalities related to each of these forms of the disease and suggests a role for intravascular coagulation in its progress.

Research Methodology

• The researchers infected naive North American horses with large amounts of cell culture infectious doses (CCID50) of virulence variants of African horsesickness virus (AHSV). These included AHSV/4SP, AHSV/9PI, and AHSV/4PI.
• The resulting diseases reproduced three classical forms of African horsesickness: acute (pulmonary), subacute (cardiac), and febrile, respectively.

Findings and Observations

• Each form of African horsesickness was associated with distinct clinicopathological and hemostatic abnormalities, which are disruptions in the system that prevents bleeding.
• The researchers noted hemostatic abnormalities, including increased concentration of fibrin degradation products and prolongation of prothrombin, activated partial thromboplastin, and thrombin clotting times.
• An indication of the activation of clotting and fibrinolysis was seen in acute and subacute cases, implying that clotting factor consumption occurs during these stages of African horsesickness.
• Hematological anomalies were observed such as decreased white cell and platelet counts, increased red cell counts and hemoglobin concentration, as well as an elevated hematocrit. The observed leukopenia had characteristics such as lymphopenia, neutropenia, and a left shift.
• Increased levels of specific enzymes and breakdown products, like creatine kinase and lactate dehydrogenase, along with lower levels of certain proteins, were found in some, but not all, horses.
• Metabolic acidosis was present in horses with the acute form of the disease and was indicated by decreased total bicarbonate and increased lactate and anion gap.
• Mild decreases in platelets and white blood cells were occasionally associated with the febrile form of the disease.

Conclusion

• Collectively, these results suggest a role for intravascular coagulation in the pathogenesis of African horsesickness.