Agriculture Reference
In-Depth Information
2009; van Galen et al. 2010, 2011a). Sporadic cases have also been described
in the USA, New Zealand and Australia (Finno et al. 2006; van Galen et al.
2011a).
Horses of all races, as well as donkeys and zebra's, suffer from the
disease. However, no other species has been described to be affected. Most
cases are unexercised, young horses in normal body condition, but horses of
all ages can be affected. AM occurs in horses that spend significant time out
on pasture: most are full time pasturing and always more than 6H per day
(Votion et al. 2007, 2009; van Galen et al. 2011a).
Pastures on which the disease occurs are typically described as being
sparse, sloping and containing or being surrounded by trees, dead leaves and
wood and humid zones. Clinical cases have, however, also occurred on
pastures not resembling this description. Pastures can give rise to AM cases
for successive years (Votion et al. 2007, 2009; van Galen et al. 2011a).
AM has a strong seasonal appearance with the majority of cases declaring
in autumn and a limited amount of cases in spring and winter. Autumnal
outbreaks are often followed by a smaller one in spring (van Galen et al.
2011a). Although the condition is not contagious, cases often occur as
outbreaks probably because horses are submitted to the same environmental
and climatic factors that play a role in the aetiopathogenesis of AM. Cases
have been shown to occur during autumns that are warmer than usual (van
Galen et al. 2011a), and during periods with lack of solar radiation, low
temperature but without frost (Votion et al. 2007), stormy winds (Hosie et al.
1986; Harris and Whitwell 1990) and rain and thunderstorms (Finno et al.
2006).
1.2. Aetiopathogenesis
The metabolic defect occurring in AM affected horses is a multiple acyl-
CoA dehydrogenase deficiency (MADD), which blocks mitochondrial fatty
acid energy metabolism. Affected horses depend therefore largely on
carbohydrate metabolism for their energy supply (van Galen et al. 2008;
Westermann et al. 2008).
The aetiological agent of AM, however, is unknown up to now. Several
aetiological hypotheses have been refuted (Votion et al. 2004; Votion and
Serteyn 2008), whereas others such as a clostridial toxin, a phytotoxin or a
mycotoxin remain possible. Recently, an association between AM and
Clostridium sordelli
's lethal toxin has been demonstrated (Unger-Torroledo et
