Update on the cause of equine atypical myopathy.

The researchers provided an updated overview of the cause of equine atypical myopathy, a disease first identified in 1939 that causes recumbency and weakness in horses, often leading to death within 72 hours. The authors discuss how understanding of the condition’s pathophysiology has been guided toward a toxic origin linked to environmental factors.

Historical Background and Initial Identification

• Equine atypical myopathy first known in 1939 impacting grazing horses.
• The condition called acute myopathy or atypical myoglobinuria due to the clinical presentations initially seen.
• Cases presented sporadically in different countries, including the US, Canada, and Australia, but there it was known as a seasonal pasture disease.
• The first substantial outbreak to raise global awareness occurred in Germany in 1995.
• Since 2000, outbreaks and affected animals in central Europe have markedly increased, initiating the launch of epidemiological investigations for understanding disease mechanism and prevention.

Atypical Myopathy Alert Group (AMAG)

• The Atypical Myopathy Alert Group (AMAG) was created by the University of Liege in Belgium for surveillance purposes.
• In 2006, this group extended its domestic record tracking to include all European cases.
• The group consists of international equine veterinarians, national epidemiological networks, and university collaborators.
• The goal of AMAG is to disseminate information about disease outbreaks and foster collaborative research.

Search for the Disease Cause

• Environmental toxins were initially suspected to be the disease-causing agents, due to the common features of affected pastures.
• Epidemiological studies and histopathological examination of the muscle tissues of impacted animals guided the understanding of the disease’s pathophysiology towards a toxic origin.
• Further investigation into toxins that could potentially lead to mitochondrial dysfunction in horses were pursued, but results remained inconsistent.
• Insight from similar human conditions with shared clinical and histopathological attributes with atypical myopathy led to additional research.

Link to Mitochondrial Disorders

• Morphopathological examination of atypical myopathy cases showed intracellular lipid accumulation in slow oxidative type muscle fibres, prevalent in postural and respiratory muscles – indicating an acute and degenerative process.
• The biochemical changes suggested an impairment of the fatty acid oxidative metabolism, especially β oxidation.
• The disease showed similarities to human disorders like multiple Acyl-CoA dehydrogenase deficiency (MADD), suggesting a potential lead to the pathogenesis of equine atypical myopathy.