Poisoning in horses refers to the ingestion, inhalation, or absorption of toxic substances that can adversely affect their health. These substances may include plants, chemicals, medications, or environmental toxins. Poisoning can lead to a range of clinical signs, from mild gastrointestinal upset to severe neurological or systemic effects, depending on the toxin involved. Common toxic substances for horses include certain plants like oleander and yew, heavy metals such as lead and arsenic, and specific pesticides or herbicides. This page compiles peer-reviewed research studies and scholarly articles that investigate the causes, effects, diagnosis, and management of poisoning in horses.
Schryver HF.Horses are subject to poisoning from many sources. This article considers poisonings from minerals and vitamins of nutritional significance and from minerals as environmental contaminants.
Kamphues J, Meyer H.Following feeding of a new delivery of hay (bought in Southern Germany) 3 horses out of a unit of 17 developed colic within a few days one horse died. Post-mortem there was an intensive accumulation of serous or serous-haemorrhagic fluid in the thorax and abdomen. The hay was heavily contaminated by autumn crocus (colchicum autumnale)--about 1.48% of total mass. Other feedstuffs were of good quality and following removal of the affected hay no further cases of colic occurred. The pathological findings also indicated a colchicine intoxication.
Milne EM, Pogson DM, Doxey DL.Poisoning with Senecio jacobaea (ragwort) is a common cause of chronic liver disease in horses in Britain. The major clinical signs are the result of hepatic failure but gastric impaction has recently been associated with the disease. The present paper describes three cases of secondary gastric impaction associated with ragwort poisoning. In each case the impaction was the cause of death or necessitated euthanasia.
Beier RC, Norman JO.White snakeroot (Eupatorium rugosum Houtt) has been known to cause trembles in animals and milk sickness in humans since the American Revolution. It still continues to poison animals. Horses and goats are particularly sensitive to white snakeroot poisoning. Resurgence of livestock production on small farm units, and utilization of fresh raw milk may result in milk sickness; if the animals have white snakeroot exposure. The goat is the only animal with good toxicity threshold data. In other animals and humans the toxicity thresholds of white snakeroot are not known, and that until responsible t...
Edwards WC, Edwards RM, Ogden L, Whaley M.Cantharidin content of male and female Epicauta occidentalis and E conferta was determined. Aspects of the life cycle of blister beetles, taxonomy, pheromonal and adaptive functions of cantharidin relative to the medico-legal aspects of cantharidin poisoning, prevention and control in horses are discussed.
Uhlinger C.Black walnut toxicosis was diagnosed in 10 horses at one stable. The time from exposure to shavings to development of clinical signs was 8 to 12 hours. Most common clinical signs were moderate to severe laminitis (Obel grade 2 or 3), pitting edema of the distal portion of the limbs, and rapid respiratory rate. Two horses had clinical signs of colic and 2 other horses had anorexia and lethargy. All 10 horses recovered without complications.
Nicholson SS.Grasses that are essential components of livestock grazing programs sometimes are the source of tremorgenic toxicants to the animals consuming them. Morbidity can be high but mortality need not be if management closely observes the cattle daily and removes them at first sign of trouble. Specific treatment generally is not available nor needed. Survivors recover completely within a few days or weeks, except in chronic phalaris poisoning, where sheep and cattle may die after prolonged illness--or at least not make an economical recovery. Certain poisonous plants are responsible for tremorgenic s...
Nation PN.Trifolium hybridum (alsike clover) has been implicated as the cause of two diseases of the horse. One of these is photosensitivity, of which alsike clover is only one of a number of presumed causal agents. The other is a fatal syndrome which is known as "alsike clover poisoning" and which is manifest by progressive loss of condition, signs of hepatic failure, and varying degrees of neurological impairment. The underlying lesion of alsike clover poisoning is fibrosis and proliferation of the biliary tree. The experimental evidence implicating alsike clover as the cause of this syndrome comes en...
Doonan GR, Brown CM, Mullaney TP, Brooks DB, Ulmanis EG, Slanker MR.Several hundred Michigan horses were accidentally exposed to varying levels of monensin. Severity of effects was proportional to the level of feed contamination; sudden death resulted on at least two premises. Acute signs of cardiovascular impairment occurred on one premises having received feed containing over 200 grams of monensin per tonne. Gross and histological postmortem lesions consisted of acute myocardial necrosis. Although only circumstantially confirmed, investigations led to the suspicion that the source of poisoning was a ration formulation error in a feedmill in southwestern Onta...
Mullaney TP, Brown CM.Newborn Shetland foals died of acute hepatic failure following oral administration of approximately 16 mg/kg body weight ferrous fumarate. Lesions in these foals were indistinguishable from lesions in foals given an oral digestive inoculant containing ferrous fumarate and were also similar to the syndrome characterised as 'toxic hepatopathy' in foals in the United States in 1983. We conclude that foals are susceptible to toxicity from low doses of iron compounds in the first few days of life. Vitamin E and selenium deficiency may contribute to this susceptibility.
Rollinson J, Taylor FG, Chesney J.Six cases of accidental salinomycin poisoning in horses are described. The horses were fed a contaminated ration and presented clinical signs which were extremely varied in nature and severity. However, the range of signs, including anorexia, colic, weakness and ataxia bore similarities to those described in horses poisoned with the related ionophore monensin. Other similarities became apparent in serum biochemical profiles of the clinical cases. Although ionophore toxicity is rarely reported in horses they appear to be particularly susceptible, and it should therefore be considered as a diffe...
van den Dikkenberg MI, Holtkamp BM.Seven cases of poisoning in horses are reported. This was caused by ingestion of branches of the alder buckthorn (Frangula alnus (mill.) syn. Rhamnus frangula L.), which had been thrown on the pasture. The biological characteristics and the toxic action of the plant are discussed more fully.
Lessard P, Wilson WD, Olander HJ, Rogers QR, Mendel VE.Twenty horses of various ages had inadvertently ingested alfalfa hay contaminated with Senecio vulgaris. Among them, 4 died of liver disease. Blood was collected from affected horses at monthly intervals for 7 months and at the 9th and 14th months. The following serum enzymes and chemical items were assayed: aspartate aminotransferase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transferase, sorbitol dehydrogenase, total bilirubin, BUN, glucose, cholesterol, inorganic phosphate, calcium, total protein, and albumin. Amino acid profiles, conjugated bile acids, sulfobromophthalein...
Tennant B, Dill SG, Glickman LT, Mirro EJ, King JM, Polak DM, Smith MC, Kradel DC.From June 1975 through June 1979, acute hemolytic anemia developed in 11 horses from 7 New York farms. Of the 7 horses that died, 6 had methemoglobinemia. In the 4 horses that recovered, methemoglobinemia was not observed. but Heinz body formation was seen in 3 of the 4. On 2 of the premises involved, frank methemoglobinemia was observed concurrently with Heinz body formation, suggesting a relationship between the pathogenesis of methemoglobinemia and Heinz body formation in the hemolytic process. In addition to the 11 cases described, 22 clinically similar cases were reported to us during the...
Wilson SJ, Taylor J, Gibson J, McKenzie R.A dense population of Pimelea trichostachya plants (Family Thymelaeaceae) in pasture poisoned a horse herd in southern inland Queensland in October-November 2005. Plant density was 2 to 45 g wet weight/m(2) (mean 16 g/m(2)) from 5 to 69 plants/m(2) (mean 38 plants/m(2)) representing 3 to 20% (mean 9%) of the volume of pasture on offer. Ten of 35 mares, fillies and geldings were affected. Clinical signs were loss of body weight, profound lethargy, serous nasal discharge, severe watery diarrhoea and subcutaneous oedema of the intermandibular space, chest and ventral midline. Pathological finding...
Hall JO.Poisoning cases in horses associated with dietary exposures can encompass a wide variety of etiologies that can be caused by natural or man-made components. Feed mixing errors and ingestion of feed formulated for other species are the most common means by which poisonings from man-made materials occur. Ionophore feed additives and antibacterial agents are especially toxogenic to horses. Effects of ionophores in horses include clinical, clinicopathologic, and pathologic changes associated with cardiac, muscular, and neurologic tissues involvement. The acute effects of ionophores, however, can r...
McDonald GK.A six year old Percheron mare was presented with a history of spontaneous unilateral epistaxis of 24 hours duration. The blood one stage prothrombin and partial thromboplastin times were markedly prolonged. A diagnosis of moldy sweetclover poisoning was made on the basis of the history and clinical and laboratory findings. A single whole blood transfusion and four daily intravenous injections of vitamin K(3) proved to be a successful treatment.
Dollahite JW, Younger RL, Crookshank HR, Jones LP, Petersen HD.Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days...
Divers TJ, George LW, George JW.Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included...
Schryver HF.Horses are subject to poisoning from many sources. This article considers poisonings from minerals and vitamins of nutritional significance and from minerals as environmental contaminants.
Guglick MA, MacAllister CG, Chandra AM, Edwards WC, Qualls CW, Stephens DH.Mercury toxicosis by ingestion was diagnosed in a 3-year-old Quarter Horse mare with a history of anorexia and signs of abdominal discomfort. Ten and 9 days prior to admission, an inorganic mercuric blistering agent has been applied for topical treatment of dorsal metacarpal disease. At referral, signs of depression, dependent edema, pollakiuria, nonproductive cough, and oral ulceration were noticed. Laboratory data were consistent with renal dysfunction. Mercury content of blood and urine was high, confirming the diagnosis. The horse responded to intensive care, consisting primarily of IV flu...
Barr AC, Reagor JC.Horses poisoned by a plant may show a myriad of clinical signs. Awareness of the poisonous plants growing in a given area and those that are likely to appear in hay and their associated clinical signs can be instrumental in making diagnoses. More importantly, the information can be shared with clients to help prevent plant poisonings in horses.
Goehring LS, Sloet van Oldruitenborgh-Oosterbaan MM.A 2 day old foal was presented with central nervous depression (coma) after moxidectin overdose. Moxidectin belongs to the milbemycin anthelmintics which elicit their working mechanism through a GABA (gamma-aminobutyric acid)-stimulatory mode of action. The foal developed profound hypothermia, bradycardia and hypoventilation. Absence of urine voiding and mild abdominal distension suggested a ruptured bladder, which was confirmed by transabdominal ultrasound and clinical-pathologic parameters. Repeat auscultation of the ventral lung parts and the occurrence of gastric reflux were suggestive of ...
Gish A, Robveille C, Gicquel T, Allorge D, Gault G, Gaulier JM.Analytical detection of Oenanthe crocata toxins in biological samples is challenging because of their instability, the lack of commercially available standards and the exceptionally low detection of these molecules using mass spectrometry. This work aims to report the used analytical methods that allowed identification of the main plant toxins in biological samples from an equid (an Arabian horse) fatality related to hemlock water dropwort (Oenanthe crocata Linnaeus) intake. Using both LC-DAD and LC-HRMS methods allowed identification (i) of oenanthotoxin in roots found on the site, root fragm...
Keeler RF, Balls LD, Shupe JL, Crowe MW.Cows, ewes, and mares varied considerably in susceptibility to toxicoses from the oral administration of the piperidine alkaloid, coniine. Cows were most susceptible and ewes least. Only calves had teratogenic effects from maternal administration of coniine during gestation; lambs and foals were apparently resistant. Results suggest that the marked differences between cattle and sheep are probably not due to variation in gut absorption or rumen metabolism.
O'Sullivan BM, Goodwin JA.On 6 properties in south-western Queensland an outbreak of nervous disease occurred horses due to ingestion of Swainsonia (Darling pea). Loss of condition, depression, hyperaesthesia and hyperexcitability were seen in affected horses. At autopsy of 2 horses generalised c ytoplasmic vacuolation was seen in the neurones of the central nervous system and in the liver, adrenal and thyroid. The clinical and pathological features were similar to those described in horses suffering from Swainsona poisoning in Australia and Astragalus and Oxytropis in North America.
