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 •
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