Trees provide shelter, shade and wind breaks for large animals but may also be a contributing cause of illness. Typically, animals with adequate nutrition will not browse foliage or ingest leaves or seeds, but drought, storms resulting in fallen branches, curiosity or boredom may result in their consumption.
The top five trees poisonous to large animals are the red maple, oak, box elder, chokecherry and black walnut. Careful attention must be paid to animals pastured close to these trees, and every effort must be made to prevent access. Pastures should be examined, especially after storms, and fallen limbs, branches and leaves should be removed. The black walnut tree itself is not toxic, but shavings made from it are and should not be used as horse bedding.
1. Red maple (Acer rubrum)
Red maple trees are commonly found in the northern and eastern parts of the United States. Dry or wilted leaves from these trees are poisonous for up to four weeks after falling from the tree. Horses ingesting 1 to 3 lb of dry or wilted leaves/450 kg of body weight may show clinical signs within a day.1,2 Common signs include anorexia, pale mucous membranes, red to brown urine, an increased respiratory rate and recumbency. Hemoglobin, the cause of the discolored urine, is toxic to the kidneys and can cause acute renal damage with little or no urine production.
The toxin in red maples is unknown but is suspected to be a gallotannin present within the wilted and dried leaves that is metabolized to pyrogallol by intestinal bacteria.3 This toxin, once absorbed, causes reactive oxidation of red blood cells (RBCs), RBC lysis, methemoglobinemia and the formation of Heinz bodies. The decrease in the number (acute hemolytic anemia) and oxygen-carrying capacity (methemoglobinemia) of circulating RBCs causes a severe lack of oxygen delivery and poor perfusion. Horses can die from the secondary effects of poor perfusion as well as acute renal failure.
Diagnosis is based on a combination of ingestion history, clinical signs and laboratory analysis. There is not a specific test for the toxin itself, but renal and liver enzyme activities are often elevated, and Heinz body formation is present on a blood smear. Hemolytic anemia is evident, with a decrease in packed cell volume (PCV) in the face of a normal total plasma protein concentration.
Activated charcoal and mineral oil administered by nasogastric tube should be used for decontamination in an acute exposure. More often, however, horses are not treated until after signs have developed. It is vitally important that these horses not be stressed and that treatment is administered in a calm manner. The judicious use of intravenous fluids will promote excretion of toxins and help decrease the onset of kidney damage. If the PCV is low or falling rapidly, administer blood products before fluids. Furosemide may be helpful in horses with decreased urine output. Vitamin C may be used to stabilize RBCs, and oxygen therapy may be needed in cases of severe respiratory distress.
Twice-a-year danger: Green buds in the spring and green or sprouted acorns in the fall are the toxic culprits from the oak tree. Drying or freezing does not decrease their poisonous potential. (Photo courtesy of Dr. Lynn Hovda.)
2. Oak (Quercus species)
Oak trees, well distributed throughout the eastern half of the United States, are poisonous to all large animal species. Oak poisoning occurs most often in cows and calves and less so in sheep and horses. Goats have tannin-binding proteins in their saliva that allow them to tolerate higher amounts than cows and sheep. Tasty green buds in the spring and green or sprouted acorns in the fall are sources of the toxin; the tree’s toxicity does not decrease with drying or freezing. Poisoning is associated with the ingestion of large amounts of buds or young leaves and acorns over a two- to three-day period.
The signs observed depend on the particular species and amount ingested. In ruminants, early signs include anorexia, dullness, rumen atony and constipation. Feces are often hard and covered with mucus but may be black and fluid-filled if hemorrhagic enteritis has developed. Later signs are associated with kidney and liver damage and include dehydration, icterus, hematuria and polyuria. Death may occur three to seven days after ingestion. In horses, the toxins primarily affect the gastrointestinal (GI) tract, causing anorexia, colic, bloody diarrhea and, less commonly, kidney damage.
An oak leaf. (Photo courtesy of Dr. Lynn Hovda.)
The toxins are tannins that bind and precipitate proteins. In the rumen, gallotannins are hydrolyzed and release phenolic acids (gallic acid, pyrogallol, resorcinol) that, once absorbed, bind and precipitate proteins in the GI mucosa and kidneys and, less often, the liver.
The diagnosis is based on history of exposure and ingestion, clinical signs and laboratory analysis. Renal indices (creatinine and blood urea nitrogen concentrations) and liver enzyme activities are elevated, and PCV may be decreased or increased depending on hydration status. Often, acorn pieces and parts are found in the rumen or GI tract at postmortem.
Early and aggressive treatment in ruminants is imperative and may include a rumenotomy to remove mass amounts of acorns, supportive care, GI protectants, and intravenous fluids to treat dehydration and increase urine output and perfusion. Activated charcoal and mineral oil may be useful in an acute ingestion. Horses should receive GI protectants and intravenous fluids as needed. The addition of 10 to 15 percent calcium hydroxide to grain has been used as a preventative in many parts of the country to aid precipitation of tannins and reduce mortality in cattle grazing on pastures with oak trees.
Box elder exposure is often fatal in horses. (Photo courtesy of Dr. Lynn Hovda.)
3. Box elder (Acer negundo)
Box elder trees are widespread throughout North America and found in and surrounding many pastures. The seeds pose a serious and often fatal threat to horses. The toxic dose is not yet well-defined, but ingestion of as few as 165 seeds could cause toxicosis.4 It is important to note that further investigation needs to be undertaken as the variation in the amount of toxin per seed, seed maturity and environmental conditions can dramatically affect the total amount of toxin ingested.
Ingestion of box elder seeds, which contain the toxin hypoglycin A, has been associated with the onset of seasonal pasture myopathy, a syndrome affecting horses in the fall. The toxin has also been isolated from seeds of the European sycamore maple tree (Acer pseudoplatanus). This tree is found in northern European pastures where horses have died of atypical myopathy, a syndrome similar to seasonal pasture myopathy.
In affected horses, significant necrosis of the respiratory and postural muscles occurs. Horses are weak and reluctant to move and may exhibit fine muscle tremors. Recumbent horses may not be able to stand without assistance. Urine is often dark brown to red. The respiratory rate is rapid, and breathing is difficult by 48 hours after ingestion. Death occurs at 72 hours in 75 percent of affected horses. Those horses not as severely affected show signs of stiffness, lethargy, ataxia and muscle weakness within three days of ingestion.
Common risk factors for poisoning not only include the presence of box elder trees within or near pastures, but also overgrazed and sparse pastures, little supplemental feeding of hay or grain and prolonged turnout time. There is no treatment; horses should not be grazed on pastures with box elder trees.
4. Chokecherry (Prunus virginiana)
Chokecherry trees, along with other Prunus species (wild cherry, apricots, peaches and cherry laurel), are often found adjacent to pastures as windbreaks or ornamental trees or shrubs. Members of this group pose a deadly hazard to all ruminants, horses and swine. The toxins, cyanide glycosides, are found in the leaves and seeds of the plants but not in the fresh fruit. Ruminants are more sensitive because of the rapid break down and absorption of cyanide by the rumen.
The most common clinical sign is sudden death within minutes to a few hours after ingestion. Most often animals are just found dead in the field, but tremors and twitching progressing to prolonged seizures and death have been observed. The antidote, an intravenous combination of sodium nitrite and sodium thiosulfate, is rarely used because of the rapid onset of intoxication.
These trees should not be planted in or near pastures, and any existing trees or shrubs should be removed. Trimmings should not be fed or disposed of in a pasture where animals have access to them.
5. Black walnut (Juglans nigra)
Black walnut trees are commonly found in the eastern half of the United States, and the wood can be prized for woodworking potential. However, shavings made from black walnut wood and used as bedding for horses are considered poisonous. The toxin within the black walnut shavings is unknown but was originally thought to be juglone. Experimental attempts to recreate the effects through topical or oral ingestion of juglone have been unsuccessful. Bedding contaminated with 20 percent or more of black walnut shavings has been shown to cause clinical signs. Aged or old wood shavings are both toxic, but shavings exposed to air for more than a month are less harmful.
Stocking up and early signs of laminitis (shifting legs, warm hoof walls, digital pulses) appear within 24 hours of exposure to bedding. They are generally reversible if the horse is removed from the bedding at this point. Neck and shoulder sweating, colic, fever and painful laminitis (egg shell stance, hot feet, pounding digital pulses, reluctance to move, recumbency) occur after continued exposure. Fatalities are uncommon but can be seen with laminitis complications such as coffin bone rotation in some horses.
Treatment includes removing the horses from the contaminated bedding and providing supportive care including pain management and farrier intervention if needed. Bedding should be purchased from a reputable dealer knowledgeable in horse husbandry.
1. Martinson K, Hovda LR, Murphy M. Plants poisonous or harmful to horses in the North Central United States. St. Paul, Minnesota: University of Minnesota Press, 2008.
2. Alward A, Corriher CA, Barton MH, et al. Red maple (Acer rubrum) leaf toxicosis in horses: a retrospective study of 32 cases. J Vet Intern Med 2006;20(5):1197-1201.
3. Agrawal K, Ebel JG, Altier C, et al. Identification of protoxins and a microbial basis for red maple (Acer rubrum) toxicosis in equines. J Vet Diag Invest 2012:25(1):112-119.
4. Valberg SJ, Sponseller BT, Hegeman AD, et al. Seasonal pasture myopathy/atypical myopathy in North America associated with ingestion of hypoglycin A within seeds of the box elder tree. Equine Vet J 2013;45(4):419-426.
> Burrows GE, Tyrl RJ. Toxic plants of North America. Ames, Iowa: Iowa State University Press, 2001;8-10, 162-163, 726-727, 1043-1049.
> Nicholson SS. Southeastern plants toxic to ruminants. Vet Clin North Am Food Anim Pract 2011;27(2):447-458.
Melissa Franssen is a 2016 DVM candidate at the University of Minnesota College of Veterinary Medicine. Lynn R. Hovda, RPH, DVM, MS, DACVIM, is the Director of Veterinary Services at Pet Poison Helpline, Bloomington, Minnesota.
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