Sycamore tree seeds, which can poison horses, pose risks to other herbivores – study

Seed pods from a sycamore tree on the ground in a pasture. Ingestion of these seeds can prove toxic to horses.

Sycamore trees, the seeds of which can cause atypical myopathy in horses, carry a potential poisoning risk in several other grazing species, researchers warn.

Equine atypical myopathy is a muscular disease caused by eating the seeds or seedlings of some steel treespecies. 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.

It has been recognized in horses for more than 60 years but its cause, the toxin hypoglycin A, was not identified until 2013.

In Britain, the most common source of the toxin is now known to be the Sycamore tree (Acer pseudoplatanus), a member of the maple family. Today, it has a worldwide distribution. It has become naturalized in most of Europe and in other countries and continents, such as North and South America, New Zealand, Australia and India.

The Box Elder (acer negundo) is the most common tree to cause the disease in North America. Both trees produce helicopter-shaped fruit that helps to distribute seeds over several hundred meters.

Benoît Renaud and his fellow researchers, writing in the journal toxinssaid hypoglyxin A is known to be responsible for poisoning in various species, including humans, equids, Père David’s deer and two-humped camels.

They hypothesized that any herbivore grazing with A. pseudoplatanus in their vicinity may be at risk for hypoglycin A poisoning.

In their study, they surveyed hypoglycin A exposure from sycamore maples in species not yet described as being at risk. Animals in zoological parks were the major focus, as they have a high probability of exposure if sycamore maples are in or near their enclosures.

Serum samples were selected from biobanks at zoological parks. The studied species were herbivorous mammals which are either foregut fermenters or hindgut fermenters. The tested species were cattle, gnu, blackbucks, sheep, goats, Timor deer, alpacas, camels, lamas and vicuna, all of which are foregut fermenters; and elephants, donkeys and zebras, all of which are hindgut fermenters.

To meet the study criteria, the samples had to be from grazing animals with sycamore maples nearby. Also, they had to have been sampled during the highest risk periods of seed dispersal. Most of the animals were healthy in appearance at the time, with no obvious clinical signs.

The study team tested for the presence of hypoglycin A and a related toxic metabolite, methylenecyclopropylacetyl-carnitine. They also looked for changes in the acylcarnitine profile in animals positive for hypoglycin A. The acylcarnitine profile can provide evidence of problems with fatty acid oxidation and organic acid metabolism.

Animals fell into three categories: negative for both hypoglycin A and methylenecyclopropylacetyl-carnitine; positive for hypoglycin A and negative for methylenecyclopropylacetyl-carnitine; and positive for methylenecyclopropylacetyl-carnitine.

Of the 75 blood samples from 70 animals, two gnus (Connochaetes taurinus taurinus) were assessed as being diseased at the time of sample collection. The authors said they represent the first identified instances of hypoglycin A poisoning in Bovidae.

The gnus, which were exposed to sycamore maples in their enclosure, presented severe clinical signs at the time their blood samples were taken. The testing showed both hypoglycin A and methylenecyclopropylacetyl-carnitine in their blood. They also had marked changes to their acylcarnitine profile.

Evidence of some degree of exposure was found in sheep, goats, alpacas, a camel, elephants, and the one vicuna tested, but none was classified as diseased.

The authors said the freedom from exposure in the tested donkeys and zebras suggests that the toxic material was not available in sufficient quantities in their enclosures when they were sampled.

“This study underlines the existence of yet undescribed subclinical hypoglycin A poisoning in species other than equids,” the study team said.

Apparently healthy animals that tested positive for the toxin showed increases in their serum acylcarnitines profile.

They said the poisoning of the gnus seemed to follow a similar pathophysiological pathway to the one described in atypical myopathy with equids.

“Like equids, some foregut fermenters (Père David’s deer, gnus) are now proven susceptible to this poisoning,” they said. “This raises the question of the difference of sensitivity between species under a similar toxic pressure. Equids are, besides foregut fermenters, the species most subjected to A. pseudoplatanus poisoning.”

They noted that hypoglycin A is soluble. Once ingested, its absorption takes place in the small intestine. The presence of a fermentation compartment proximal to the small intestine might be protective, they said. “Indeed, the toxic molecule may be transformed by the rumen microbiota even more when the rumen retention time is long.”

In equids, which have a fermenting compartment, the caecum, beyond the hypoglycin A absorption area (the small intestine), most of the ingested toxin is available for absorption.

Serum hypoglycin A has been detected in mixed feeders (goats, sheep), they noted. In mixed feeders, the toxin’s absorption could be explained by short rumen retention time and large salivary production coupled with a highly functional ventral groove.

Following initial chewing, the soluble amino acids, including hypoglycin A, bypass ruminal fermentation which leads to the toxin being absorbed within the proximal small intestine.

“Hypoglycin A ruminal transformation (and possibly degradation or metabolization) may explain why it was not observed in serum of cattle.”

It has to be noted, they added, that hypoglycin A has been detected in cow’s milk in one study. “In those cows, some hypoglycin A must have gotten through the rumen, which leads to the hypothesis that, under a high toxic pressure, even these grazers might be at risk of hypoglycin A poisoning.”

The authors said zoos should take measures to reduce the exposure of herbivores to the seeds and seedlings of the sycamore maple. This also applies to acer negundo and Acer palmatum species, which are also commonly found as ornamental trees in zoological parks.

In conclusion, the authors said the gut structure of some herbivores may provide some protection from hypoglycin A, as the toxin may be transformed in the rumen. “Indeed, the degree of protection against A. pseudoplatanus may be directly linked to the rumen retention time of soluble molecules.”

The global increase of the serum acylcarnitines profile in apparently healthy animals exposed to hypoglycin A suggests a gradual fatty acid metabolism alteration, and thus the existence of subclinical cases, they said.

The study team came from a range of institutions in Belgium, Germany and France.

Renaud, B.; Kruse, C.-J.; Francois, A.-C.; Grund, L.; Bunert, C.; Brisson, L.; Boemer, F.; Gault, G.; Ghislain, B.; Petitjean, T.; Gustin, P.; Votion, D.-M. Acer pseudoplatanus: A Potential Risk of Poisoning for Several Herbivore Species. Toxins 2022, 14, 512.

The study, published under a Creative Commons Licensecan be read here.

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