Topic:Poisoning
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.
Tremorgenic syndromes in livestock. 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...
Alsike clover poisoning: A review. 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...
Monensin poisoning in horses – an international incident. 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...
Iron toxicity in neonatal foals. 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.
Salinomycin poisoning in horses. 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...
[Alder buckthorn poisoning in horses]. 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.
Clinicopathologic study of horses surviving pyrrolizidine alkaloid (Senecio vulgaris) toxicosis. 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...
Haemolytic crisis associated with ragwort poisoning and rail chewing in two thoroughbred fillies. Events leading to the deaths of two fillies at pasture are described. Pasture hay containing the flowering stages of Senecio jacobea (ragwort) had been fed three to four months earlier. Paddocks were subdivided with posts and rails treated with copper chrome arsenate. Six horses on the property chewed rails spasmodically. Both fillies presented with haemoglobinurea. Values in liver of 83 mg Cu kg and kidney 35 mg Cu kg wet weight and serum 1.4 mg Cu/l together with histophathology of seneciosis support a sequence of ragwort poisoning followed by copper accumulation in liver and kidney terminat...
[An undesirable drug interaction in horses? Complications which can occur during the administration of coumarin derivatives and phenylbutazone]. A study of the literature was done because of questions asked in a court of justice concerning possible poisoning in a jumper, resulting from administration of both phenylbutazone and a coumarin derivative within a particular period. In view of the mechanisms of action and the pharmacokinetic characteristics of the agents, these forms of combined treatment are also highly inadvisable in horses.
Reserpine toxicosis in a horse. A single injection of reserpine in an adult horse was believed to induce toxicosis for several days. Clinical signs included erratic, colic-like behavior followed by depression, bradycardia, miosis, ptosis, and paraphimosis. Diarrhea was not observed and may have been due to the effect of xylazine given with the reserpine. The horse was supported with IV fluids and intensive nursing care. Gradual improvement was noted 72 hours after the horse received the drug. Qualitative analysis via high-performance liquid chromatography was positive for reserpine. Methamphetamine is the recommended antidot...
Bilateral laryngeal paralysis in the horse. Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especial...
Experimental cantharidiasis in the horse. Crystalline cantharidin in an alfalfa cake or in aqueous suspension was given to 8 horses at a dosage level of 450 to 489 micrograms/kg of body weight (group 1) and 2 horses at a dosage level of 720 micrograms/kg (group 2) via nasogastric tube. Both group 2 horses and 1 group 1 horse died. Horses were evaluated at 6-hour intervals for 36 hours and then again at postcantharidin hours 48. Data evaluation consisted of a comparison of the nonsurvival and survival data to one another and their respective base-line values at each sampling period, irrespective of the route of administration and dosag...
Suspected tremetol poisoning in horses. Of 10 horses in a heavily overgrazed pasture, 4 died within 1 week. Clinical signs included muscle tremors, ataxia, reluctance to walk, heavy sweating, and myoglobinuria. Serum creatine kinase, aspartate transaminase, and alkaline phosphatase activities were high. Histopathologic findings were nonspecific. On the basis of clinical signs, clinicopathologic findings, nonspecific histopathologic findings, the condition of the pasture, the identification of numerous white snakeroot plants from which trematone was extracted, and evidence that these plants had been heavily browsed, it was believed t...