Equine Health Update EHU Vol 20 Issue 02 - Page 49

African Horse Sickness | EQUINE additional clinical signs 2 . Although these four clinically recognized forms of the disease are often perceived to represent distinct manifestations of AHSV infection, it is more likely that they simply represent points on a continuum of virulence of the same disease, and the ultimate outcome of infection will depend upon the susceptibility of the animal. This is based on the observation that different strains of AHS virus display selective tropism to specific organs depending upon the form of the disease, with accumulation of AHSV antigen found in cardio-pulmonary tissues of horses with peracute disease; and in the spleen and lymphoid tissue of horses with the febrile form 11-14 . After infection, initial viral replication occurs in the regional lymph nodes, followed by a primary viraemia and subsequent infection of endothelial cells in target organs, including the lungs and myocardium 10,11,15 . Endothelial cell damage causes an increase in vascular permeability, leading to extravasation of fluid, and death in most cases of AHS is attributed to pulmonary oedema, presumably due to pulmonary alveolar flooding and subsequent asphyxia. Pulmonary oedema can occur extremely rapidly in some cases however, and is often precipitated by exercise 2 . This clinical observation, together with inconsistent structural evidence of pulmonary vascular injury that can be directly attributed to the virus 10,15-17 , suggests that the pulmonary oedema seen in horses with AHS is not solely due to the effect of the virus on vascular permeability, and that other mechanisms of pulmonary oedema must also be present. Following investigation into the role of pulmonary intravascular macrophages in the pathogenesis of AHS, Carrasco et al. (1999) concluded that changes in pulmonary microvasculature and the subsequent oedema are not solely due to the effect of the virus on endothelial cells, but are also due to pulmonary intravascular macrophage activation and the subsequent release of inflammatory mediators. Furthermore, the authors recognized that additional mechanisms of pulmonary oedema are likely to exist, and encouraged further investigation into the myocardial changes seen in AHS and their role in the pathogenesis of pulmonary oedema 18 . This was based on the observation that viral replication also occurs in myocardial vessels, and histological evidence of haemorrhage and necrosis of the myocardium in cases of AHS suggests that cardiogenic pulmonary oedema may play a role in the pathogenesis of this disease 12 . Hypothesis and Objectives Our hypothesis was that myocardial dysfunction plays a major role in the pathogenesis of AHS and that the clinical signs seen in horses with AHS can be attributed (in part) to per acute left sided heart failure (pulmonary oedema with per acute left sided heart failure – pulmonary form) and subacute/chronic right sided heart failure (subcutaneous oedema, supraorbital fossa swelling, chemosis, etc – cardiac and mixed form). The aim of this study was therefore to evaluate myocardial function in horses with AHS and use this information to provide a framework for therapeutic intervention in clinical cases using cardiac specific drugs. Methods Three adult horses were infected with AHSV serotypes 3,5,9 as part of an Onderstepoort Biological Products (OBP) vaccination trial. The study protocol was approved by the OBP animal ethics committee and the Department of Agriculture Forestry and Fisheries (DAFF). A full cardiac examination was performed prior to infection and at a predetermined clinical end- point. The clinical end-point was defined as a horse that becomes recumbent; with a weak pulse of >60 beats per minute and a rapid, shallow respiration rate of >60 breaths per minute. The cardiac examination included determination of cardiac troponin I (cTnI), electrocardiography, and echocardiography. Tissue Doppler imaging [TDI] was used to measure radial systolic velocity and strain. All horses were euthanized • Volume 20 Issue 2 | July 2018 • 49