This is the last of four articles about plants likely to poison horses in North America. Because most horses are selective grazers, they are poisoned less frequently than other livestock, but some plants are palatable or they may be reluctantly accepted when feed selection is limited.
The three previous articles covered hepatoxic, neurotoxic and myotoxic plants. This final installment covers nephrotoxic and miscellaneous toxic plants, with descriptions of poisoning and plant-induced disease, along with recommended treatment and management practices to avoid poisoning.
Hemolysis with hemoglobin-induced nephrosis:
Red maple is highly toxic for horses; about 1.5 gm leaf/kg BW or 1 kg of wilted leaves will kill a 450-g horse. The wilted and shed leaves are most toxic. Most poisoning occurs in the fall, after storms cause branches to fall into paddocks or when trimmings are fed to animals.
Although only red maple has been associated with poisoning in horses, red-maple hybrids should be considered toxic until proven otherwise.
Red maple leaves contain an unidentified toxin that causes oxidative hemolysis. The clinical signs of poisoning usually develop within 24 hours of exposure and include anorexia, depression, weakness and methemoglobinemia.
Fatally poisoned horses develop intravascular and extravascular hemolysis, icterus, anemia, hemoglobinuria, respiratory distress, Heinz body anemia, colic, laminitis, coma and death. Post-mortem findings include icterus, enlarged and swollen spleen, liver and kidneys and red urine.
Treatment is symptomatic and includes blood transfusions, fluid replacement and oxygen therapy. Because methemoglobinemia is limited, response to methylene blue is minimal. Other antioxidants such as ascorbic acid also may be helpful.
Allium spp. (onion): Onions contain an oxidant (N-propyl disulfide) similar to red maple in that it can cause acute hemolytic anemia. Because only large amounts of onion contain enough toxin, it rarely poisons horses.
Oaks contain toxic tannins, such as gallotannin. Not all tree parts contain enough tannins to be toxic, but animals have been poisoned from eating flowers, leaf buds or acorns.
Clinical signs begin as depression, acute colic, straining (constipation, frequent urination) followed by bloody diarrhea, hematuria, rapid heartbeat and rapid breathing. Because tannic and gallic acid cause severe renal tubular nephrosis (kidney disease), clinical signs include dehydration, azotemia, hyperphosphatemia, hypocalcemia and hypoproteinemia.
Treatment should include extensive fluid therapy to maintain kidney perfusion, electrolyte and acid-base balances (diuresis).
Oxalate-induced nephrosis and hypocalcemia:
Sarcobatus vermiculatus (black greasewood), western-range plant, 10 percent to 20 percent oxalates.
Halogeton glomeratus (halogeton), invading and expanding desert weed.
Rumex crispus (curly dock) and other dock species.
These plants all contain soluble oxalates that are metabolic toxins that also cause renal disease (nephrosis) and hypocalcemia. The oxalates are oral irritants, so most horses avoid eating them. Though poisoning in horses is infrequent and poorly described, clinical signs in sheep and cattle begin as depression, colic, weakness, irregular gait that can progress to lateral recumbency, coma and convulsions. Clinical chemistry changes begin as a hypocalcemia that progresses to azotemia and hypercreatinemia.
Treatment, though it may not be effective once clinical signs have developed, should include aggressive fluid therapy (diuresis).
Cestrum diurnum is found on disturbed soil in Florida, Texas, California, Mexico and Hawaii. Similar to Solanum malacoxylon (the cause of enzootic calcification in South America), jasmine contains a steroidal glycoside of 1,25-(OH)2 cholecalciferol (a vitamin D analog). This induces increased intestinal absorption of Ca with sustained secretion of calcitonin and decreased parathyroid activity. All these contribute to hypercalcemia and the deposition of calcium in many organs and tissues.
Clinical signs of poisoning include weight loss, lameness and a humped-up appearance with choppy gait. In the serum there is a moderate hypercalcemia with normal phosphorus levels. Altered calcium metabolism causes mineral deposition or dystrophic calcification of elastic tissues, including tendons, ligaments, major arteries, heart and kidney.
Although there is no proven treatment, most lesions slowly resolve after exposure is discontinued.
Gastrointestinal toxic plants
Mechanical damage — foxtail, bristlegrass, sandbur, cheatgrass.
These weedy grasses are poor-quality forages and their grass awns can become embedded in the mucous membranes of the gums and tongue, causing ulcers and abscesses. Affected horses salivate excessively and have difficulty eating normally. The more invasive species often displace good forage and contaminate forages.
The economic impact is high, because extensive care is required to extract the foreign plant material, drain and clean wounds and maintain appropriate antibiotic therapy. Larger plant awns and burrs also can cause gastrointestinal obstruction and colic. Avoiding contaminated hay and maintaining pastures to avoid exposure is recommended.
Ranunculaceae (buttercup family).
Buttercup contains the toxin ranunculin that is converted to protoanemonin, a mucosal irritant. Clinical signs of poisoning include blistered lips, stomatitis, gastroenteritis, increased salivation, abdominal pain and diarrhea. Most poisonings occur in sheep because buttercup is not very palatable to horses. Dried plants appear to be non-toxic.
Nightshade poisoning has been associated with several syndromes because these plants contain various toxins, such as steroidal glycoalkaloids that cause severe gastroenteritis and cholinesterase inhibitors that cause neurologic disease. The most common alkaloid is solanine, a potent mucosal irritant that causes stomatitis.
Solanine concentrations can be high, especially in berries, and doses as small as 0.1 percent to 0.3 percent BW of silverleaf nightshade berries are toxic.
Signs of poisoning include anorexia, salivation, abdominal pain, diarrhea, dilation of pupils, dullness, depression, weakness, progressive paralysis, prostration and rarely death. Treatment generally is symptomatic and most animals quickly recover when exposure is discontinued.
Ricinus communis (castor bean)
Castor bean is an ornamental or weed found mostly in southern states. Poisoning usually occurs when animals are fed concentrates that are contaminated with castor-bean seeds. The toxin, ricin, inhibits protein synthesis (ribosome function) and also may be antigenic, causing anaphylaxis in sensitive animals. The seeds or beans are highly toxic, especially to horses; 0.1 mg/kg BW of well-chewed or ground seeds can be lethal.
Most animals develop clinical signs of poisoning 12 to 48 hours after ingestion. Signs include dull appearance, depression, anorexia, thirst, weakness, colic, trembling, sweating, incoordination, difficult breathing, progressive CNS depression, fever, bloody diarrhea, convulsions and death. Treatment is palliative to reduce absorption, including activated charcoal, cathartics and supportive care. Poisoning often is fatal; many animals die without early intervention.
Bindweed is an invasive, noxious weed that invades many pastures and paddocks. Horses grazing extensively on bindweed may develop diarrhea, colic, gastrointestinal ulceration and intestinal thickening and fibrosis. The resinoid convolvulin and several tropane alkaloids have been proposed as potential toxins. Little information is available on the required dose or duration of exposure that will produce toxicity. Because poisoning appears to be irreversible, care should be taken to control its spread, minimize its availability to horses and insure that other forages are available.
Juglans nigra (black walnut).
J. cinerea (butternut).
J. regia (English walnut).
Walnut shavings (>20 percent) used for bedding consistently causes laminitis in horses. Some also develop digestive problems. Signs of laminitis develop in just over eight hours of exposure (depression, anorexia, stocking up, colic). Most animals recover if exposure is discontinued.
Additional precautions to minimize absorption and minimize the effects of laminitis include washing legs, cooling fluids, hoof wraps and pads and possibly anti-inflammatory agents.
Hoary alyssum is found in many northern states and Canada. It commonly grows in disturbed areas and can invade pastures and hay fields. Most poisoning occurs in prepared and dried hay, within hours after exposure. Horses develop fever, distal limb edema (stocking up), colic, bloody diarrhea, laminitis, abortion, dystocia, anorexia, dehydration and death. Post-mortem changes are those of laminitis.
Treatment includes removing exposure, treating for laminitis and monitoring pregnant mares for abortion.
Brassica spp (white mustard, yellow mustard, wild mustard, charlock, black mustard, indian mustard); Erysemum cheiranthoide (wormseed mustard); Raphanus raphanastrum (wild radish); Thlaspi arvense (fanweed, field pennycrest); Barbarea vulgari (yellow rocket, wintercrest).
These weeds rarely are eaten unless they are included in hay. Several toxins have been proposed and various syndromes have been associated with Brassica ingestion. However, the only proven toxicity is related to toxic isothicyanates and subsequent thyroid disturbances. As a result, possible clinical signs are variable, but most are related to digestive-tract irritation that causes repeated mild colic. Most animals recover if they are removed from the source.
Fagopyrin: Fagopyrum saggitatum (buckwheat).
Furocoumarins and psoralens
Ammii majus (Bishopsweed), Cymopterus watsonii (spring parsley) Lomatium spp., Thamnosma texana and T. montana (Dutchman's breeches)
When mature, these plants are rarely eaten, but young plants are more palatable and when eaten cause toxicity. Because they contain a primary photodynamic toxin (hypericum, fagopyrin, furocoumarins or psoralens), they induce photosensitization or sunburn. This is seen clinically as skin redness (erythema), edema, blisters, crusting, sloughing and secondary bacterial dermatitis.
The eyes especially are sensitive. Animals develop severe keratitis and conjunctivitis that is seen as tearing and photophobia. Animals will recover if the source is removed and they are allowed time to clear the toxin. Treatment should include protection from sun and standard wound care for burned areas.
Hairy vetch, an introduced European plant, grows across North America. It becomes a problem when animals are poisoned in late spring and midsummer.
The toxin has not been identified and the development of disease is poorly understood.
Poisoning generally affects black animals (horses and cows) by introducing a multi-systemic granulomatous disease (most likely an allergic or hypersensitivity disease).
Toxic plants are a significant health concern for horses. Most poisoning occurs when hay and prepared feeds are contaminated. Caution should be exercised in buying hay to ensure that it is safe and of good quality.
Because most weed infestations are patchy, the best way to do this is to inspect the hay field before it is harvested. Hay should also be closely inspected prior to feeding it.
Less commonly, horses can be poisoned when they are pastured with toxic plants with limited alternative forages. Most of these poisonings can be prevented by monitoring pasture and grazing animals.
Because many poisonings can cause permanent damage, avoiding exposure is best. Knowledge of which plants are toxic and when horses are likely to be poisoned also will help reduce these losses and ensure animal health and safety.
Dr. Stegelmeier is a researcher at the U.S. Department of Agriculture's Poisonous Plant Research Laboratory in Ogden, Utah.