Vitamin E deficiency can be seen in horses that eat low-quality grass, that have very little or no access to normal grazing pasture and that are not given vitamin E supplements. Oxidative damage is mainly noted in the muscle fibres, which actively contract, and this is because of loss of anti-oxidant activity. Affected foals are most likely born to mares with selenium deficiency.
Foals present with generalized weakness which may be observable at birth or appears immediately afterwards. Foals may present in decubitus but are generally alert and reactive.
The foals often continue to suck if they are artificially fed but weakness of the tongue muscles and pharyngeal muscles makes suction difficult.
Adult horses often present with temporal and masseter muscle involvement too (indicated as maxillary myositis or masseter myositis), with swelling and difficult mastication. Involvement of pharyngeal muscles leads to dysphagia which may point to botulism.
Careful examination of these animals often reveals generalized weakness, with stiff gait and short stride. Seriously affected horses may have an acute presentation with decubitus which mimics neurological signs.
Serum CK and AST levels are moderately or reasonably raised, or extremely high in seriously-affected foals or horses.
Electromyogram shows spontaneous abnormal activity (acute positive waves, fibrillation, myotonic bursts)
Horse muscles with myopathy have pale areas, of different sizes (which is where the commonly-used term white muscle disease comes from).
The muscles which are most seriously affected are the more active ones ( e.g. cervical muscles, proximal limb muscles, tongue and masticatory muscles).
Macroscopic appearance depends on extent and stage of necrosis. In the early stages, yellow and white striations can be observed, whereas later, chalk-white striations are often observed. Horses that have difficulty swallowing can develop aspiration pneumonia in the cranio-ventral areas of the lungs.
In foals with serious acute myopathy, after death or euthanasia, the lesions that can be identified are massive muscle necrosis and mineralization, with very little macrophage infiltration (monophasic). In sub-acute cases, the lesions are polyphasic, with active necrosis, macrophage infiltration, and regeneration. If the myocardium is involved, then necrosis of cardiomyocytes is seen with mineralization.
Degeneration and necrosis of fibres with macrophage activation (arrows).
A diagnosis of nutritional myopathy is based on a typical clinical history, raised serum CK and AST levels, deficiency of selenium or vitamin E concentrations in blood, and on typical macroscopic and histopathologic lesions. If the horse lives for a long time, myofibre regeneration can mean the muscle returns to normal. Disorders in foals can be prevented by supplementing mares’ feed with selenium during gestation.
Adult horses can be given a sufficient concentration of vitamin E and selenium in their diet.
Treatment once clinical signs have started to show is much less effective than prevention.
There are various poisonous plants which are known to cause muscle necrosis in horses and these include Cassia Occidentalis (coffee senna) and Thermopsis spp. In horses, myopathies like these are due to the presence of the plant on grazing land or in hay. The necrosis is often polyphasic.