Agriculture Reference
In-Depth Information
al. 2010), but further proof should be provided before assuming that this is the
cause, or the solely cause, of AM. It has also been noted that cases very
frequently occur in the presence of
Acer pseudopalatanus
(maple tree) (Votion
et al. 2007; van der Kolk et al. 2010; van Galen et al. 2011a). Even though this
common European tree has no proven toxic potential, it might contain yet
undiscovered phytotoxins. Moreover, this tree is often covered with tar spot
(
i.e.
Rhytisma acerinum
) (van der Kolk et al. 2010). As any tree it contributes
to organic waste on the ground and as such might favour mould formation and
mycotoxin production.
The development of AM is probably multifactorial with several
endogenous and exogenous factors leading to MADD. On one side, certain
factors cause and aggravate MADD and thus an imbalance in energy
metabolism: the aetiological agent, risk factors, and other predisposing and/or
triggering factors such as stress (
e.g.
inclement weather, exercise and
transport), nutritional deficiencies and possible environmental substrates.
Contact time, dosage and pathogenicity of the aetiological agent probably
influence the severity of disease. On the other side, other factors may limit the
development or reduce the impact of the MADD: physiological compensatory
mechanisms, protective factors and a possible development of immunity. In
subclinical affected horses (Delguste et al. 2002; Votion et al. 2007), the
energetic balance is probably more or less maintained. But if the horse's
metabolism gets out of balance because it is too severely affected by the
aetiological agent or is further disturbed by other interfering factors, severe
disease follows and death can occur.
1.3. Clinical Description
AM is distinguished by the acute and unpredictable nature of its
appearance. Most affected horses die within 72 hours after presenting the first
clinical signs (Votion et al. 2007; van Galen et al. 2011a). The disease has a
high fatality rate, which was at first estimated at 85-100% (Puyalto-Moussu et
al. 2004; Votion et al. 2004), but it has recently been demonstrated to be 74%
(van Galen et al. 2011a).
The presented clinical signs are due to the acute and severe destruction of
postural, respiratory and cardiac muscles. More than 50% of affected horses
suffers from depression, weakness, stiffness, recumbence, trembling, sweating,
myoglobinuria, congestive mucous membranes, tachycardia, and normo-
thermia, and horses can develop respiratory, cardiac, renal and digestive
