The pathogenesis of African horsesickness
Abstract
The pathogenesis of African horsesickness (AHS) has not been well characterized in North American horses. These studies were undertaken to further characterize the pathogenesis and manifestations of disease through the use of clinical pathology, histopathology, electron microscopy and through evaluation of endothelial cell (EC) cultures infected with virus isolates of differing virulence. Infection of horses with virulence variants of African horsesickness virus (AHSV) resulted in three distinct disease forms: the acute, subacute and febrile forms of disease. Thrombocytopenia, increased fibrin degradation products, and prolongation of prothrombin time, activated partial thromboplastin time and thrombin clotting time indicated that the pathogenesis in acute and fatal subacute cases of AHS involved activation of coagulation and fibrinolysis, and clotting factor consumption. In vitro, virulence variants of AHSV differed in their ability to infect and injure cultured EC. The results of these studies indicate: (1) the primary determinant of the form of disease in naive horses is the virus inoculum, (2) infection and injury to EC (in vivo) results in disseminated intravascular coagulation, (3) AHSV isolates differ in their ability to injure EC in vitro, (4) virulence is related to an isolate's ability to infect and ultimately injure EC, and (5) the relative degree of EC injury and viral protein synthesis can be used to differentiate between virulent and avirulent isolates.
Degree
Ph.D.
Advisors
Thacker, Purdue University.
Subject Area
Veterinary services|Animal diseases|Microbiology
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