Cassone L.This article is intended to highlight toxicosis-associated pathology in horses that might be observed by a clinician in the living animal and at gross necropsy. When the clinician is aware of these pathologic changes (particularly when coupled with a suggestive environmental or herd history), then collaboration with a diagnostic laboratory can begin to help identify specific toxicants. Proper sampling and communication with the diagnostic laboratory will vastly improve the likelihood of a specific diagnosis; postmortem sampling and specimen submission are reviewed in the last section of this a...
Bischoff K.Plants in the maple genus, Acer, and pistachio genus, Pistacia, have been reported to cause acute hemolysis in horses. The cause of hemolysis seems to be metabolism of gallic acids to the potent oxidant pyrogallol by enteric bacteria of the horse. Diagnosis is often tentative and circumstantial. Treatment is symptomatic and supportive and can include detoxification, fluid and electrolyte therapy, supplemental oxygen, and pain control. Corticosteroid and antioxidant therapies do not improve prognosis. Prognosis is guarded to poor but horses that survive 6 days postexposure are expected to reco...
Pollio D, Michau TM, Weaver E, Kuebelbeck KL.This case report describes ivermectin-induced blindness in a dog and a foal with normal ophthalmic fundic examinations and attenuated electroretinography (ERG). Subsequent recovery in ERG was noted following intravenous lipid emulsion (ILE) therapy. A dog and a foal were evaluated for ivermectin-induced blindness. Clinical signs included dull mentation, absent pupillary light reflexes (PLRs), and absent menace on presentation. The animals had normal fundoscopic examinations; however, in both cases ERG was consistent with neurosensory retinal dysfunction. Following ILE therapy for ivermectin to...
Bautista AC, Tahara J, Mete A, Gaskill CL, Bryant UK, Puschner B.Two separate incidents of monensin exposure in horses resulting in toxicosis provided insight into the diagnostic value and interpretive criteria of various biological samples. In case 1, 25 horses broke into a shed and ingested feed that was supplemented with 800 g/ton (880 µg/g) of monensin. Within 48 hr, 1 horse had died, 2 developed cardiac arrhythmias, lethargy, and recumbency, and another was euthanized due to severe deterioration. Minimal histologic lesions were noted in the horse that died peracutely, while another showed characteristic lesions of acute cardiomyocyte degeneration and ...
Rosychuk RA.Noninflammatory, nonpruritic alopecias are uncommonly encountered in the horse. Alopecia areata, an apparently autoimmune hair follicle bulbitis produces focal, multifocal to widespread hair loss. The skin is otherwise normal. Diseases that can mimic the widespread hair loss associated with alopecia areata include telogen and anagen effluvium, seasonal alopecias, follicular dysplasias (including color dilution alopecia), various nutritional deficiencies and chemical toxicosis, and diseases that result in defective hair shafts (eg, trichorrhexis nodosa and piedra). These problems are differenti...
Cerqueira VD, Riet-Correa G, Barbosa JD, Duarte MD, Oliveira CM, de Oliveira CA, Tokarnia C, Lee ST, Riet-Correa F.In the Amazon region of northern Brazil, Panicum maximum cultivars Mombaça, Tanzânia, and Massai cause severe colic and death in horses and mules. The disease occurs in the rainy season, when sprouting pastures are grazed by equidae. In the 8 separate disease outbreaks studied, a total of 52 out of 153 equidae were affected, including 19 that died (10 mules and 9 horses). Clinical signs were colic and abdominal dilatation, with a clinical manifestation period of 12 hr to 4 days. Serum activities of gamma-glutamyl transferase and aspartate aminotransferase were within reference intervals; how...
Schultz CL, Lodge-Ivey SL, Bush LP, Craig AM, Strickland JR.To determine the amount of ergovaline and lysergic acid retained or excreted by geldings fed endophyte-infected seed containing known concentrations of these alkaloids, and the effects of exposure time on clinical expression of toxicosis. Methods: Mature geldings (n=10) received diets containing either endophyte-free (E-) or endophyte-infected (E+) tall fescue seed during three experimental phases. The first phase (Days -14 to -1) was an adaptation phase, to allow all horses to adapt to a diet containing E- tall fescue seed. The second (Days 0 to 3) was the initial exposure phase to E+ tall fe...
Clode AB, Davis JL, Salmon J, Michau TM, Gilger BC.To determine penetration of topically and orally administered voriconazole into ocular tissues and evaluate concentrations of the drug in blood and signs of toxicosis after topical application in horses. Methods: 11 healthy adult horses. Methods: Each eye in 6 horses was treated with a single concentration (0.5%, 1.0%, or 3.0%) of a topically administered voriconazole solution every 4 hours for 7 doses. Anterior chamber paracentesis was performed and plasma samples were collected after application of the final dose. Voriconazole concentrations in aqueous humor (AH) and plasma were measured via...
Dey S, Dwivedi SK.A cross sectional study recorded the Lead (Pb) concentrations in blood from 288 horses in urban areas. Mean blood Pb concentration was estimated as 0.47 +/- 0.02 and 0.55 +/- 0.02 ppm in horses for industrial and highway-adjacent localities respectively. Mean blood Pb in horses from rural areas was 0.38 +/- 0.03 ppm. The mean Pb in forage samples from these horses was 36.96 +/- 6.23, 52.08 +/- 9.86 and 11.72 +/- 1.34 ppm in industrial, highway-adjacent and rural localities respectively. No overt signs of Pb toxicosis were seen in these animals
Osweiler GD.Horses consume feed grains and forages that can produce a range of mycotoxins resulting from mold invasion. Toxicosis of horses often occurs from fumonisins or aflatoxin in grains, from the tremorgenic mycotoxins in dallis grass, or from slaframine in red clover. Fumonisin toxicosis often is severe and fatal, and aflatoxin can be acute or chronic and debilitating. Other mycotoxins reported in horses may cause moderate to mild signs that regress when the contaminated feedstuff is removed. Overall, horses appear to have a relatively low prevalence of reported mycotoxicoses among domestic animals...
Henninger RW, Horst J.Magnesium sulfate, a saline laxative, is often used for treatment of intestinal impactions in horses. Clinical signs of hypermagnesemia are an uncommon complication following oral administration of magnesium sulfate. Overdose of magnesium sulfate in combination with renal insufficiency, hypocalcemia, or compromise of intestinal integrity may predispose horses to magnesium toxicosis. Establishment of diuresis with fluids and IV administration of calcium may provide successful treatment of magnesium toxicosis in horses.
Vivrette S, Cowgill LD, Pascoe J, Suter C, Becker T.Acute renal failure in a 4-day-old foal secondary to oxytetracycline toxicosis was treated by hemodialysis. Oxytetracycline had been administrered as treatment for forelimb flexor tendon contracture. Conservtive treatment with fluids, furosemide, and dopamine partially alleviated serum electrolyte concentration imbalances, but was ineffective in promoting diuresis or decreasing azotemia. Three hemodialysis treatments over 4 days were administered, after which the clinical appearance of the foal improved, and biochemical and electrolyte values returned to within reference ranges. The nephrotoxi...
Thu00e9on AP, Pascoe JR, Carlson GP, Krag DN.Twenty horses with 30 lesions were studied to evaluate the effects of intratumoral chemotherapy with cisplatin in sesame oil on equine sarcoids (n = 19), squamous cell carcinomas (n = 7), and squamous cell papillomas (n = 4). Treatment consisted of 4 sessions of intratumoral cisplatin chemotherapy at 2-week intervals. A controlled-release formulation of cisplatin in sesame oil was used to limit drug egress from the injection site. Mean dosage per session was 0.97 (+/- 0.17, SEM) mg of cisplatin/cm3 of tumor tissue treated for tumor volumes ranging from 10 to 20 cm3. Dosage tended to be slightl...
Muir WW, Reed SM, McGuirk SM.Intravenous administration of quinidine gluconate converted atrial fibrillation (AF) to sinus rhythm in 9 of 12 horses. Twelve horses that were diagnosed by ECG to have AF were administered up to 11 mg of quinidine gluconate/kg of body weight in 1.0- to 1.5-mg/kg bolus injections every 10 to 15 minutes. The total dose of quinidine administered IV ranged from 1.8 to 5.8 g. Increased ventricular rate, apprehension, and mild depression were observed during treatment. Other signs of toxicosis were not observed. One horse was successfully treated with IV administered quinidine gluconate on 3 occasi...
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.
Turk MA, Thomas DE.To study the role of cytochrome P-450-dependent mixed function oxidase reactions in equine 3-methylindole (3MI) toxicosis, ponies were given 20 mg of phenobarbital/kg of body weight at 72, 60, 48, 36, and 24 hours before 100 mg of oral 3MI/kg to induce cytochrome P-450 or no treatment (controls). Maximal 3MI plasma concentration was decreased and clearance was faster in phenobarbital-treated ponies. Plasma 3MI was still detectable 12 and 36 hours after dosing in phenobarbital-treated and control ponies, respectively. Phenobarbital treatment induced a distribution phase with transition from a 1...
Lyons ET, Drudge JH, Tolliver SC.Antiparasitic activity of a micronized formulation of the benzothiazole compound, tioxidazole, at the dose rate of 11 mg/kg, was evaluated by the critical test method. Drug was given by stomach to 3 horses and on feed to 3 horses. Excellent removal activity was found for Strongylus vulgaris (100%) in 5 naturally infected horses, S edentatus (91% to 100%) in 5 horses, small strongyles (88% to 99%) in 6 horses, immature Oxyuris equi (100%) in 5 horses, and Parascaris equorum (100%) in 5 horses (a 6th horse had 10 small specimens present at necropsy). There was no measurable activity against bots...
Scott EA, Byars TD, Lamar AM.The hematologic and clinical effects of anticoagulation with warfarin were documented in 4 horses. All of the animals had thrombophlebitis (external jugular vein). Measures of coagulation were monitored, with a prothrombin time of 1.5 to 2.5 x base-line value being used as the effective range of anticoagulation. Recanalization was achieved in 2 of 4 cases. Hemorrhage, both subcutaneous and through a surgical incision, was a complication. Vitamin K1, an antidote to warfarin toxicosis, was administered intravenously to reverse anticoagulation and to control hemorrhage.
Steffey EP, Zinkl J, Howland D.The potential toxicity to horses of 7.33 +/- 0.87 SD minimal alveolar concentration hours of isoflurane anesthesia was evaluated by sequential determination of blood cell counts, electrolyte concentrations, and certain blood chemical values. Minimal or no serious toxicosis was observed for up to 7 days after anesthesia was terminated.
Clode AB, Davis JL, Salmon J, Michau TM, Gilger BC.To determine penetration of topically and orally administered voriconazole into ocular tissues and evaluate concentrations of the drug in blood and signs of toxicosis after topical application in horses. Methods: 11 healthy adult horses. Methods: Each eye in 6 horses was treated with a single concentration (0.5%, 1.0%, or 3.0%) of a topically administered voriconazole solution every 4 hours for 7 doses. Anterior chamber paracentesis was performed and plasma samples were collected after application of the final dose. Voriconazole concentrations in aqueous humor (AH) and plasma were measured via...
Thu00e9on AP, Pascoe JR, Carlson GP, Krag DN.Twenty horses with 30 lesions were studied to evaluate the effects of intratumoral chemotherapy with cisplatin in sesame oil on equine sarcoids (n = 19), squamous cell carcinomas (n = 7), and squamous cell papillomas (n = 4). Treatment consisted of 4 sessions of intratumoral cisplatin chemotherapy at 2-week intervals. A controlled-release formulation of cisplatin in sesame oil was used to limit drug egress from the injection site. Mean dosage per session was 0.97 (+/- 0.17, SEM) mg of cisplatin/cm3 of tumor tissue treated for tumor volumes ranging from 10 to 20 cm3. Dosage tended to be slightl...
Vivrette S, Cowgill LD, Pascoe J, Suter C, Becker T.Acute renal failure in a 4-day-old foal secondary to oxytetracycline toxicosis was treated by hemodialysis. Oxytetracycline had been administrered as treatment for forelimb flexor tendon contracture. Conservtive treatment with fluids, furosemide, and dopamine partially alleviated serum electrolyte concentration imbalances, but was ineffective in promoting diuresis or decreasing azotemia. Three hemodialysis treatments over 4 days were administered, after which the clinical appearance of the foal improved, and biochemical and electrolyte values returned to within reference ranges. The nephrotoxi...
Schultz CL, Lodge-Ivey SL, Bush LP, Craig AM, Strickland JR.To determine the amount of ergovaline and lysergic acid retained or excreted by geldings fed endophyte-infected seed containing known concentrations of these alkaloids, and the effects of exposure time on clinical expression of toxicosis. Methods: Mature geldings (n=10) received diets containing either endophyte-free (E-) or endophyte-infected (E+) tall fescue seed during three experimental phases. The first phase (Days -14 to -1) was an adaptation phase, to allow all horses to adapt to a diet containing E- tall fescue seed. The second (Days 0 to 3) was the initial exposure phase to E+ tall fe...
Steffey EP, Zinkl J, Howland D.The potential toxicity to horses of 7.33 +/- 0.87 SD minimal alveolar concentration hours of isoflurane anesthesia was evaluated by sequential determination of blood cell counts, electrolyte concentrations, and certain blood chemical values. Minimal or no serious toxicosis was observed for up to 7 days after anesthesia was terminated.
Muir WW, Reed SM, McGuirk SM.Intravenous administration of quinidine gluconate converted atrial fibrillation (AF) to sinus rhythm in 9 of 12 horses. Twelve horses that were diagnosed by ECG to have AF were administered up to 11 mg of quinidine gluconate/kg of body weight in 1.0- to 1.5-mg/kg bolus injections every 10 to 15 minutes. The total dose of quinidine administered IV ranged from 1.8 to 5.8 g. Increased ventricular rate, apprehension, and mild depression were observed during treatment. Other signs of toxicosis were not observed. One horse was successfully treated with IV administered quinidine gluconate on 3 occasi...
Scott EA, Byars TD, Lamar AM.The hematologic and clinical effects of anticoagulation with warfarin were documented in 4 horses. All of the animals had thrombophlebitis (external jugular vein). Measures of coagulation were monitored, with a prothrombin time of 1.5 to 2.5 x base-line value being used as the effective range of anticoagulation. Recanalization was achieved in 2 of 4 cases. Hemorrhage, both subcutaneous and through a surgical incision, was a complication. Vitamin K1, an antidote to warfarin toxicosis, was administered intravenously to reverse anticoagulation and to control hemorrhage.
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.
Bautista AC, Tahara J, Mete A, Gaskill CL, Bryant UK, Puschner B.Two separate incidents of monensin exposure in horses resulting in toxicosis provided insight into the diagnostic value and interpretive criteria of various biological samples. In case 1, 25 horses broke into a shed and ingested feed that was supplemented with 800 g/ton (880 µg/g) of monensin. Within 48 hr, 1 horse had died, 2 developed cardiac arrhythmias, lethargy, and recumbency, and another was euthanized due to severe deterioration. Minimal histologic lesions were noted in the horse that died peracutely, while another showed characteristic lesions of acute cardiomyocyte degeneration and ...
Rosychuk RA.Noninflammatory, nonpruritic alopecias are uncommonly encountered in the horse. Alopecia areata, an apparently autoimmune hair follicle bulbitis produces focal, multifocal to widespread hair loss. The skin is otherwise normal. Diseases that can mimic the widespread hair loss associated with alopecia areata include telogen and anagen effluvium, seasonal alopecias, follicular dysplasias (including color dilution alopecia), various nutritional deficiencies and chemical toxicosis, and diseases that result in defective hair shafts (eg, trichorrhexis nodosa and piedra). These problems are differenti...
Henninger RW, Horst J.Magnesium sulfate, a saline laxative, is often used for treatment of intestinal impactions in horses. Clinical signs of hypermagnesemia are an uncommon complication following oral administration of magnesium sulfate. Overdose of magnesium sulfate in combination with renal insufficiency, hypocalcemia, or compromise of intestinal integrity may predispose horses to magnesium toxicosis. Establishment of diuresis with fluids and IV administration of calcium may provide successful treatment of magnesium toxicosis in horses.
Pollio D, Michau TM, Weaver E, Kuebelbeck KL.This case report describes ivermectin-induced blindness in a dog and a foal with normal ophthalmic fundic examinations and attenuated electroretinography (ERG). Subsequent recovery in ERG was noted following intravenous lipid emulsion (ILE) therapy. A dog and a foal were evaluated for ivermectin-induced blindness. Clinical signs included dull mentation, absent pupillary light reflexes (PLRs), and absent menace on presentation. The animals had normal fundoscopic examinations; however, in both cases ERG was consistent with neurosensory retinal dysfunction. Following ILE therapy for ivermectin to...
Dey S, Dwivedi SK.A cross sectional study recorded the Lead (Pb) concentrations in blood from 288 horses in urban areas. Mean blood Pb concentration was estimated as 0.47 +/- 0.02 and 0.55 +/- 0.02 ppm in horses for industrial and highway-adjacent localities respectively. Mean blood Pb in horses from rural areas was 0.38 +/- 0.03 ppm. The mean Pb in forage samples from these horses was 36.96 +/- 6.23, 52.08 +/- 9.86 and 11.72 +/- 1.34 ppm in industrial, highway-adjacent and rural localities respectively. No overt signs of Pb toxicosis were seen in these animals
Cerqueira VD, Riet-Correa G, Barbosa JD, Duarte MD, Oliveira CM, de Oliveira CA, Tokarnia C, Lee ST, Riet-Correa F.In the Amazon region of northern Brazil, Panicum maximum cultivars Mombaça, Tanzânia, and Massai cause severe colic and death in horses and mules. The disease occurs in the rainy season, when sprouting pastures are grazed by equidae. In the 8 separate disease outbreaks studied, a total of 52 out of 153 equidae were affected, including 19 that died (10 mules and 9 horses). Clinical signs were colic and abdominal dilatation, with a clinical manifestation period of 12 hr to 4 days. Serum activities of gamma-glutamyl transferase and aspartate aminotransferase were within reference intervals; how...
Osweiler GD.Horses consume feed grains and forages that can produce a range of mycotoxins resulting from mold invasion. Toxicosis of horses often occurs from fumonisins or aflatoxin in grains, from the tremorgenic mycotoxins in dallis grass, or from slaframine in red clover. Fumonisin toxicosis often is severe and fatal, and aflatoxin can be acute or chronic and debilitating. Other mycotoxins reported in horses may cause moderate to mild signs that regress when the contaminated feedstuff is removed. Overall, horses appear to have a relatively low prevalence of reported mycotoxicoses among domestic animals...
Turk MA, Thomas DE.To study the role of cytochrome P-450-dependent mixed function oxidase reactions in equine 3-methylindole (3MI) toxicosis, ponies were given 20 mg of phenobarbital/kg of body weight at 72, 60, 48, 36, and 24 hours before 100 mg of oral 3MI/kg to induce cytochrome P-450 or no treatment (controls). Maximal 3MI plasma concentration was decreased and clearance was faster in phenobarbital-treated ponies. Plasma 3MI was still detectable 12 and 36 hours after dosing in phenobarbital-treated and control ponies, respectively. Phenobarbital treatment induced a distribution phase with transition from a 1...
Lyons ET, Drudge JH, Tolliver SC.Antiparasitic activity of a micronized formulation of the benzothiazole compound, tioxidazole, at the dose rate of 11 mg/kg, was evaluated by the critical test method. Drug was given by stomach to 3 horses and on feed to 3 horses. Excellent removal activity was found for Strongylus vulgaris (100%) in 5 naturally infected horses, S edentatus (91% to 100%) in 5 horses, small strongyles (88% to 99%) in 6 horses, immature Oxyuris equi (100%) in 5 horses, and Parascaris equorum (100%) in 5 horses (a 6th horse had 10 small specimens present at necropsy). There was no measurable activity against bots...
Bischoff K.Plants in the maple genus, Acer, and pistachio genus, Pistacia, have been reported to cause acute hemolysis in horses. The cause of hemolysis seems to be metabolism of gallic acids to the potent oxidant pyrogallol by enteric bacteria of the horse. Diagnosis is often tentative and circumstantial. Treatment is symptomatic and supportive and can include detoxification, fluid and electrolyte therapy, supplemental oxygen, and pain control. Corticosteroid and antioxidant therapies do not improve prognosis. Prognosis is guarded to poor but horses that survive 6 days postexposure are expected to reco...
Cassone L.This article is intended to highlight toxicosis-associated pathology in horses that might be observed by a clinician in the living animal and at gross necropsy. When the clinician is aware of these pathologic changes (particularly when coupled with a suggestive environmental or herd history), then collaboration with a diagnostic laboratory can begin to help identify specific toxicants. Proper sampling and communication with the diagnostic laboratory will vastly improve the likelihood of a specific diagnosis; postmortem sampling and specimen submission are reviewed in the last section of this a...
English
French
