Understanding changes in the gut bacteria of horses may help in developing therapeutic or preventive strategies for those at risk for atypical myopathy, according to researchers.
Equine atypical myopathy is a muscular disease caused by eating the seeds or seedlings of some Acer tree species.
The hypoglycin A and methylenecyclopropylglycine contained in the plant material can cause a non-exercise-induced breakdown of muscle, affecting mainly postural and respiratory muscles, and the heart.
The clinical picture is characterized by the sudden onset of stiffness, muscular weakness, a fast heart rate and the darkening of urine as a result of the presence of myoglobin. The disease progresses in many cases to recumbency, respiratory difficulties and death.
Outbreaks have occurred in Europe since the mid-1990s, with more than 2500 cases reported in the last 10 years, mostly from central European countries.
The disease typically affects horses kept on pasture during spring/autumn, with the sycamore maple (Acer pseudoplatanus) the most likely culprit among Acer species.
Despite the discovery of its cause, there is still no cure, and treatment for the symptoms is often unsuccessful.
Horses and ponies of any age and breed can be affected, and the reported mortality rate ranges from 43% to 97%.
Christina Wimmer-Scherr and her colleagues at the University of Liege in Belgium said there was a general consensus that intestinal absorption of hypoglycin A and methylenecyclopropylglycine and their subsequent transformation to toxic metabolites are needed to develop atypical myopathy.
Researchers have noticed one interesting aspect of the syndrome.
“Interestingly, and for a reason still unknown, not all horses pastured in the same contaminated environment develop clinical signs of the disease,” the study team noted in the journal Animals.
Previous studies have shown that hypoglycin A can be detected in the blood of clinically healthy horses pastured in at-risk fields.
Although the incidence of clinical disease has been linked to specific factors such as age, body condition, feeding and pasture management, the exact reason protecting certain horses from developing clinical signs remains largely unknown.
Wimmer-Scherr and her fellow researchers noted that the role of intestinal bacteria (the microbiota) in this selective impairment is still poorly understood.
They set out to describe and compare the fecal microbiota of horses suffering from atypical myopathy and healthy co-grazers. They also looked into potential differences in fecal microbiota regarding the outcome for diseased animals.
The research involved 59 horses with atypical myopathy (29 survivors and 30 non-survivors) referred to three Belgian equine hospitals, and 26 clinically healthy co-grazers simultaneously sharing contaminated pastures during spring and autumn outbreak periods.
Fresh fecal samples (either taken from the rectum or collected within 30 minutes of defecation) were obtained from all horses for analysis to determine the bacterial families present.
The researchers found fecal microbial diversity and evenness were significantly higher in disease-affected horses as compared with their non-affected co-grazers.
The relative abundance of families Ruminococcaceae, Christensenellaceae and Akkermansiaceae were higher, whereas those of the Lachnospiraceae, Bacteroidales and Clostridiales, were lower in horses with atypical myopathy, especially in those with a poor prognosis.
While significant shifts were observed, it is still unclear whether they result from the disease or might be involved in the onset of disease, the researchers said.
“Prospective studies following exposure to the toxin and its consequences on fecal microbiota in horses grazing in at-risk pastures could help to answer that question.
“Either way, the findings of this study constitute a first step in understanding the possible role of intestinal microbiota.
“We concluded that fecal microbiota of horses suffering from atypical myopathy is different from their co-grazers and changes are more severe in horses that do not survive the disease,” the researchers said.
“Understanding those changes may help in developing therapeutic and/or preventive strategies for horses at risk for atypical myopathy.”
Discussing their findings, the researchers noted that most bacterial shifts observed in this study between horses suffering from atypical myopathy and healthy co-grazers were significantly more pronounced in non-survivors than in survivors.
“This gradual increase/decrease in certain bacterial populations in the feces of horses with atypical myopathy associated with severity of the disease could suggest a dysbiosis (gut bacterial imbalance) that worsens as the disease progresses.
“The significance of this finding is unclear, and the nature of this correlation remains to be determined, but may be related to the amount of toxin ingested, which could be higher in non-survivors.
“Because the study was conducted in naturally occurring cases of atypical myopathy, the exact amount of hypoglycin A and methylenecyclopropylglycine ingested by each horse remains undetermined, and this factor might have influenced morbidity and mortality.”
Considering the potential of some bacteria to metabolize amino acids, another hypothesis could be that intestinal microbiota might contribute to the conversion of the ingested agents into toxic metabolites.
The study team comprised Wimmer-Scherr, Bernard Taminiau, Benoît Renaud, Dominique Votion, Hélène Amory, Georges Daube and Carla Cesarini, with the University of Liege; Gunther van Loon, with Ghent University in Belgium; and Katrien Palmers, with De Morette Equine Clinic in Asse, Belgium.
Wimmer-Scherr, C.; Taminiau, B.; Renaud, B.; van Loon, G.; Palmers, K.; Votion, D.; Amory, H.; Daube, G.; Cesarini, C. Comparison of Fecal Microbiota of Horses Suffering from Atypical Myopathy and Healthy Co-Grazers. Animals 2021, 11, 506. https://doi.org/10.3390/ani11020506