This is the third in a series of articles on toxic plants that are likely to poison horses in North America. This installment covers myotoxic plants, those that damage muscle and the cardiovascular system.
Horses find many of these plants unpalatable, but, when feed selection is restricted or when toxic plants are included in prepared feeds, many horses eat them and become poisoned. Some are very palatable ornamentals; animals are poisoned whenever they are allowed access to the plants or to plant clippings.
Following are some common myotoxic plants, for which we outline the clinical signs, lesions and sequelae of poisoning and present current recommendations for treatment and prognosis for poisoned animals.
Haplopappus spp. (rayless goldenrod, jimmy weed, burrow weed — Photo 1b)
White snakeroot poisoning, or "milk sickness," is an important historical disease that in the 1800s probably caused half of the deaths in early settlers in Illinois, Indiana, Kentucky, North Carolina, Ohio and Tennessee. Entire settlements were abandoned due to the unexplained epidemic deaths of stock and people. Although various causes, including infectious bacteria, were proposed, it took nearly a century to positively identify Eupatorium rugosum as the cause.
Though animal-husbandry improvements, feeding practices and quality-assurance programs for dairy products have eliminated human exposure, poisoning in livestock continues to be a problem throughout the Midwest and East.
Though less widely distributed, rayless goldenrod contains similar toxins and consistently causes problems in the Southwest.
Both white snakeroot and rayless goldenrod are toxic year round and probably are toxic in stored feeds. Most poisoning occurs in summer and late fall when other forages are exhausted.
The toxin, trematol, has a long excretion time, allowing it to accumulate until a toxic dose is obtained. Trematol is highly lipid-soluble and is transferred in the milk. Poisoning in nursing neonates and people that drink the contaminated milk is commonly reported even with no signs of toxicity in lactating cows. Doses of 1 percent or higher body weight of the plant are toxic if ingested over one to three weeks.
Clinical signs of poisoning include incoordination, muscle tremors, elevated heart rate, muscle weakness, congestive heart failure, jugular pulse, tachycardia, cardiac arrhythmias, profuse sweating, pitting edema and quidding.
As these plants directly damage muscle, especially heart muscle, poisoned animals often are cardiac cripples with decreased work capacity. More information is needed to determine long-term effects and costs of sublethal poisoning.
Clinical blood changes are those indicative of muscle damage (increased activities of many serum enzymes that leak into the blood from damaged muscle — CK, AST and LDH).
Most animals have increased myoglobin in the blood and urine. Post-mortem findings include patchy necrosis of heart and skeletal muscle, liver necrosis and myoglobin-induced kidney disease.
Cardiac glycoside-containing plants
As cardiac glycoside-containing plants are relatively common, this list is incomplete. The preceding are examples of those likely to poison horses in North America. Most are ornamentals that are used in residential landscaping and as hedges. They rarely are eaten fresh; however, livestock, including horses, generally will eat the clippings or prunings. Others can escape cultivation and may invade fields and pastures. They remain toxic when they are included in hay and prepared feeds.
Most contain mixtures of toxins, including cardiac glycosides that are similar to digoxin. Toxicity varies according to the glycoside, with highly toxic oleandrin, andromedotoxin or grayanotoxin causing poisoning at doses as low as 0.2 percent of body weight. All these glycosides alter membrane sodium/potassium channels and calcium homeostasis, with toxicity generally resulting in A-V block and ventricular fibrillation.
Initial signs of poisoning that occur hours after ingestion include GI upset, salivation, anorexia, frequent defecation, diarrhea, colic, depression, weakness, incoordination, stupor, leg paralysis, weak heart rate, recumbence, coma and death.
With high doses, animals may quickly die without developing the classic microscopic lesions. Lower doses, when the initial myocardial necrosis is non-fatal, nearly always produce microscopic heart lesions (myocardial necrosis, fibrosis and regeneration). Heart damage may lead to congestive heart failure (stocking up, ventral edema, jugular pulse, etc.). Little is known of possible sequelae of poisoning but sub-lethally poisoned animals are likely to have impaired endurance and performance.
Treatment is limited and generally related to minimizing absorption or enhancing transient through the gastrointestinal tract (activated charcoal and cathartics). Immunologic antidotes used in small animals are very expensive and have not been recommended for use in horses. Care should be taken to avoid exposing horses to these plants and their clippings.
Yew is an introduced ornamental that most commonly poisons animals when clippings are thrown into paddocks. Yew toxicity is attributed to taxine alkaloids but they also contain traces of cyanogenic glycosides, lignins, flavonoids and volatile oils. The taxines and taxols alter myocardial calcium and electrolyte balance, resulting in cardiac arrest (negative ionotroph).
All portions of the plant, green or dry, are toxic. Doses as low as 0.1 percent to 0.5 percent of body weight are toxic (just over 100 mg could be toxic for a 450-kg horse).
Clinical signs are related to toxin disruption of cardiac function. They include colic, sweating, incoordination, shallow and difficult breathing, muscle tremors, recumbence, diarrhea, bloody diarrhea and death from cardiac arrest. Most poisonings result in sudden death, with minimal gross or microscopic lesions. Some animals may have non-specific lesions of myocardial hemorrhage, pulmonary congestion and edema. Diagnosis most often is made by documenting exposure and identifying plant parts in gastrointestinal contents.
As most cases are fatal, prevention of ingestion of trimmed shrubs is paramount. If possible, treatments should include evacuation of the GI tract and minimization of absorption with activated charcoal and cathartics. As poisoned animals are likely to have compromised cardiovascular function, precautions are needed to avoid stress and minimize animal exertion.
Avocado leaves, fruit, bark and seeds contain persin and an unidentified cardiac toxin. Persin produces a non-infectious mastitis and agalactia. Signs of poisoning in lactating mares are mastitis with occasional gastritis and colic. Other signs related to cardiotoxin-induced heart failure include dsypnea, coughing and increased respiratory and heart rates. Other less-common changes include cardiac arrhythmias, edema of the neck and ventral abdomen, cyanosis, anorexia, general weakness and recumbency. Post-mortem findings include microscopic lesions in the heart, with generalized edema and congestion of many organs.
As damage may be fatal and many of the cardiac changes are irreversible, preventing a horse's access to avocado groves is essential.
Death camas contains a steroidal alkaloid called zygacine. Vasoactive zygacine causes arteriole dilation and venous constriction. This floods vascular beds (hypotensive effect), resulting in reduced venous return and, if severe, cardiovascular collapse or shock.
Though poisoning in horses is rare, the signs of poisoning are likely to be similar to those seen in sheep, including depression, staggering, profuse salivation, papillary constriction, decreased respiration and heart rates, weakness, dsypnea, prostration and death. Post-mortem lesions are those of hypotensive shock. As most animals are found dead, few treatments have been reported.
Ergot and fescue
The ergot alkaloids have been linked to abortion (in late gestation), prolonged gestation (mares carrying foals 20 to 27 days longer than normal), dystocia (prolonged gestation results from fetal-dam size disparity), thickened placenta, increased foal deaths, retained placenta with secondary endometritis, laminitis and septicemia, agalactia with profound drop in prolactin, increased mare mortality and, because mares don't have normal udder development, vulvar swelling and other signs of partutrition.
Maintaining endophyte-free pastures and ensuring grains are free from contaminating sclerotium are essential for pregnant mares. Various treatments, including domperidone, have been used with limited success. It probably is best to avoid exposure of susceptible pregnant mares in late gestation to endophyte-infected pastures or contaminated screenings or hay.
Little is known about poisoned animals that recover. However, they are likely to be cardiac cripples or impaired animals that do no perform up to their genetic potential.
For some plants, nursing foals are often most susceptible to poisoning and may be poisoned with no evidence of maternal toxicity. As these plants are readily eaten, identifying potential toxic plants and avoiding exposure is essential.
Dr. Stegelmeier is a researcher at the United States Department of Agriculture's Poisonous Plant Research Laboratory in Ogden, Utah.