Below is a review the main hypotheses from recent years.
1. The viral hypothesis
No evidence has been found today to suggest a viral origin.
2. The hypothesis of a nutritional origin
The hypothesis of an outbreak of atypical myopathy linked to a nutritional problem (lack of vitamin E and selenium) was examined because of some clinical similarities. This hypothesis is unlikely as a primary cause but it cannot be excluded that a specific metabolic disorder can result from the synergistic action of a toxin and a nutritional deficiency.
3. The hypothesis of the presence of a toxin
Antibiotic ionophores poisoning due to accidental ingestion of other animals species food is a potential cause of acute myopathy offering many similarities with atypical myopathy. The confirmed cases study in Belgium has ruled out this potential cause. However, the hypothesis of poisoning by ingestion of ionophores due to Streptomyces spp. (A soil bacterium) in the environment cannot be ruled out. The hypothesis is supported by similarities between clinical signs, biochemical changes, as well as necropsies and histological observations of atypical myopathy and ionophores poisoning.
The ionophore antibiotics (monensin, salinomycin, lasalocid, the nasarine, maduramycin and diclazuril, as well as nicarbazin metabolites such as halofuginone, robenidine and dinitrocarbanilide) were looked for in samples of plants selected out of meadows where ant at the time cases of atypical myopathy occurred and in gastrointestinal contents, feces and muscle samples of confirmed cases. The analysis did not show evidence of the ionophore antibiotics presence.
4. The Clostridium sordellii hypothesis
Bacillus sporogenes oedematous, isolated in 1922 by Sordelli when studying a case of gangrene, has been known as Bacillus Sordelli then Clostridium sordellii since 1927. The bacterium was first identified in 1956 by Brookes and collaborator in a suddenly dead sheep in Devon. Autopsies performed on many unexpectedly dead sheep in 1982, revealed the presence of Clostridium sordellii associated with other pathogens.
The nature of muscular changes observed and the usual presence of Clostridium sordellii in the environments led to consider the hypothesis of its role as a causal factor of atypical myopathy.
Latest works published in 2010 in “Veterinary Microbiology” favor the idea of Clostridium sordellii as a factor responsible for the pathology (Lethal toxin of Sordello Clostidium is associated with equine atypical myopathy fatal. Unger-Torroledoet al., 2010).
Considering the presence of Clostridium sordellii in the material collected in the intestine of horses with atypical myopathy and comparative studies of changes in muscles of horses dead from the disease with those obtained by inoculating the toxin in mice, University of Berne researchers focused on search of the toxin into the horses muscles.
An analysis of muscle tissues of horses having died of atypical myopathy has shown the presence of the toxin, but does not demonstrate with certainty a cause-effect relationship between the presence of the toxin and an onset of the disease.
All the various hypotheses studied up to now consider as essential the role of specific environmental conditions for the organisation ( development ) of the pathogen system. Data collection based on the “epidemiological” questionnaires for owners as well as the ones dedicated to veterinarians is essential in this context, in order to gather as many information as possible.