Review of monensin toxicosis in horses

Results of experimental studiesindicate that horses are much more sensitive to monensin toxicity than cattle. Single dose studies by gavage with mycelial monensin resulted in an estimated LD₅₀ of 1.38 mg/kg of body weight. Subacute feeding studies indicate that horses will tolerate the highest use level for cattle of 33 ppm without any evidence of toxicity. Evidence of intoxication was apparent with the highest use level for chickens of 121 ppm.In pasture supplement studies, horses ate supplement containing high levels of nonensin upon initial exposure which resulted in toxicity and/or death. Following initial exposure to sublethal levels, consumption of monensin containing supplements was negligible.The clinical signs of toxicity includedpartial to complete anorexia, colicky pain, sweating and tachycardia, uneasiness, polyuria, progressive ataxia, recumbency with frequent attempts to rise and thrashing of the limbs followed by death. Examination at necropsy of animals that die soon after initial exposure to monensin may show no significant lesions, otherwise hemorrhage and pale areas in the heart with transudation into body cavities may be seen. Evidence of degenerative cardiomyopathy and congestive heart failure may be observed on histopathologic examination. Increased activities of muscle origin enzymes may also be found.The results of controlled studiesand evidence from field reports indicated that the greatest risk of intoxication was upon initial exposure to feed or supplement containing monensin. Feed mistakes and mixing errors were the two most common causes of monensin toxicity in field cases.     

Suspected monensin toxicosis in feedlot cattle

Suspected monensin toxicosis was seen in feedlot cattle aged 6 to 9 months. Twenty cattle died following inclusion of monensin in the feed at 400g/tonne, which was 13 times the recommended level. The deaths occurred over 2 weeks. Clinical signs were inappetance, respiratory distress and sudden death. Post-mortem features were those of right-sided heart failure and included dependent subcutaneous oedema, ascites, hydrothorax, and periancinar hepatocyte congestion and necrosis. However, in contrast to previous reports no myocardial necrosis was found, but focal skeletal muscle necrosis was observed. Additional findings were marked pulmonary oedema accompanied by fibrin and erythrocyte exudation into alveoli and interlobular lymphatics. From these findings it appears that monensin, as well as affecting both cardiac and skeletal muscle, has a primary effect on lung vasculature.     

Salinomycin toxicosis in horses

CASE DESCRIPTION: A 4-month-old American Paint filly was evaluated because of sudden onset of ataxia that progressed to recumbency. Five additional horses from the same and neighboring premises developed signs of poor performance, generalized weakness, ataxia, and recumbency; 2 of those horses were also evaluated. A new batch of a commercial feed supplement had been introduced to the horses' diet on each farm within the preceding 3 days. CLINICAL FINDINGS: Other than recumbency, findings of physical and neurologic examinations of the foal were unremarkable. The other 2 horses had generalized weakness and mild ataxia, and 1 horse also had persistent tachycardia. The foal had mild leukocytosis with neutrophilia, hyperglycemia, and mildly high serum creatine kinase activity. Results of cervical radiography, CSF analysis, and assessments of heavy metals and selenium concentrations in blood and vitamin E concentration in serum were within reference limits. Feed analysis revealed high concentrations of the ionophore antimicrobial salinomycin. TREATMENT AND OUTCOME: The 5 affected horses survived, but the foal was euthanized. At necropsy, a major histopathologic finding was severe vacuolation within neurons of the dorsal root ganglia, which was compatible with ionophore toxicosis. The surviving horses developed muscle atrophy, persistent weakness, and ataxia. CLINICAL RELEVANCE: In horses, ionophore toxicosis should be considered as a differential diagnosis for acute weakness, ataxia, recumbency, or sudden death. Furthermore, ionophore toxicosis should be considered as a cause of poor performance, weakness, muscle wasting, and cardiac arrhythmias in horses. Surviving horses may have impaired athletic performance.     

Acute monensin toxicosis in broiler breeder chickens

Peracute onset of disease was reported in a 42-wk-old broiler breeder flock that was presented by error with feed containing monensin at approximately seven times the approved level for broiler chickens. Morbidity and mortality were extremely high, and the affected chickens displayed feed refusal, decreased water consumption, and severe paralysis that ranged from abnormal gait to a complete inability to move. During the first 10 days postingestion of the suspect feed, mortality in hens reached 13.7% and 70.9% in the roosters. Hen day production decreased from 67% to 3% in the same period of time. A total of 638 g/ton of monensin was detected in suspect feed samples by one laboratory and 740 g/ton in a second laboratory. Twenty-one days after removal of the suspect feed, the mortality rate returned to normal levels in both hens and roosters, albeit feed consumption and egg production remained extremely low, which prompted the company involved to eliminate the flock.     

Metal toxicosis in horses.

The ubiquity and stability of metals in the environment make them unique as a pollutant or an essential dietary component. Metals are neither created nor destroyed by chemical processes but are redistributed in the environment. In combination with other elements, metal compounds and alloys are essential materials of the contemporary world. Inappropriate use or distribution in the environment leads to adverse health effects on all biologic systems, including horses. Gastrointestinal upset is a common feature of acute toxicosis with metals in general. Among the metals discussed, arsenic and inorganic mercury have a propensity to do severe damage to the gut. Deposition of cadmium on forage is the source most likely to intoxicate horses. This subchronic to chronic problem in horses is manifest as disease of the musculoskeletal system and kidneys. Iron-containing hematinics are widely used in racetrack horses and occasionally result in hepatopathy when excessive doses are administered. Lead continues to be recognized as the most significant environmental metal pollutant. Poisoning is encountered routinely in humans and animals. Of the animal species of veterinary concern, lead-poisoned horses are not a frequent encounter. Lead-intoxicated horses show signs of peripheral neuropathy (laryngeal hemiplegia), intermittent colic, and mild anemia. Acute mercury poisoning sometimes occurs from the common use of mercury-containing blistering agents, with most clinical findings related to acute renal failure. Chronic excessive intake of zinc by horses is uncommon but devastating in rapidly growing foals. The mechanism of chronic zinc toxicosis is coupled to the induced copper deficiency. The condition is a disease of cartilage in the articular and growth physes.     

Atypical myoglobinuria: an acute myopathy in grazing horses

Four out of 12 horses grazing a field in Berkshire, England, suffered a prostrating illness and died within 12 to 72 h. Serum biochemical abnormalities, including markedly elevated muscle enzymes, were demonstrated and at post mortem widespread myodegeneration was found in both skeletal muscle and myocardium. Urine analysis revealed myoglobinuria, and renal changes were seen histologically. Although similar pathologically, the clinical syndrome and circumstances of the outbreak were not typical of equine exertional rhabdomyolysis (EER). The outbreak bore a striking resemblance to other reported sporadic outbreaks of an atypical myoglobinuria occurring in grazing horses. A number of potential aetiological and contributory factors (including herbicide toxicity) were considered, but the aetiology remains unresolved.     

Black walnut toxicosis in ten horses

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.     

Acute monensin toxicosis in sheep: light and electron microscopic changes

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.     

Pathologic changes associated with experimental lasalocid and monensin toxicosis in cattle

The acute toxicity of lasalocid and monensin was studied in 36 Holstein steers. The cattle were given (orally) a single dosage of lasalocid (1, 10, 50, or 100 mg/kg of body weight) or monensin (25 mg/kg of body weight) or rice hulls. Animals were observed once a day until they died or were euthanatized at 32 days after the dose was given. All cattle were necropsied. Heart, kidney, adrenal gland, liver, spleen, pancreas, lungs, brain, sciatic nerve, skeletal muscle, small intestine, large intestine, and rumen tissue sections, stained with hematoxylin and eosin, were studied microscopically. Lasalocid was lethal at dosages of 50 and 100 mg/kg, and monensin was lethal at the dosage given (25 mg/kg). Cattle dying of lasalocid and monensin toxicoses had gross and microscopic lesions consistent with cardiomyopathy. Dilated heart or petechial and ecchymotic hemorrhages were observed with both drugs. Microscopically, multifocal areas of myocyte necrosis were observed. Those cattle that died within 3 days of dosing with either drug had a marked degranulation of pancreatic acinar cells. Changes were not observed in any other tissues.     

Survey of ocular abnormalities in draft horses

Objective

To determine the prevalence of ocular disease in draft horses in the United States.

Animals

Draft horses of various breeds and ages.

Procedure

Nondilated ophthalmic examination was performed using slit lamp biomicroscopy and indirect ophthalmoscopy. Intraocular pressures were measured when possible.

Results

One hundred sixty-five draft horses were examined. Age range: 10 days to 33 years (mean 10.8 years, median 10 years); 87 geldings (52.7%), 71 mares (43.0%), 7 stallions (4.2%); 64 Percherons (38.8%), 51 Belgians (30.9%), 29 Clydesdales (17.6%), 15 Shires (9%), and 6 other draft breed (3.6%). Intraocular pressure: mean 24.7 mmHg OD, range 13-37 mmHg; mean 25.0 mmHg OS, range 11-37 mmHg. Vision-threatening disease was present in 9 horses (5.5%): complete cataracts 1, post-traumatic optic nerve atrophy 1, uveitis and secondary glaucoma 1, retinal detachment 1, large chorioretinal scar 3, phthisis bulbi 2. Non-vision-threatening ocular disease was present in 56 horses (33.9%) involving one or more ocular structures: eyelid trauma/notch defect 14 (8.5%), SCC-type adnexal lesions 12 (7.3%), corneal scars 16 (9.7%), keratitis 6 (3.6%), corpora nigra cyst 15 (9.1%), incipient/punctate cataract 50 (30.3%), vitreous degeneration 10 (6.1%), asteroid hyalosis 1, “bullethole” chorioretinal scars 3, RPE coloboma 1. Linear keratopathy was present in 28 horses (17%) with 2/28 having concurrent vision threatening ocular disease.

Conclusions

Ocular abnormalities, in particular minor cataracts, were relatively common in this population, but not typically vision-threatening. Additionally, this survey demonstrated a greater prevalence of linear keratopathy in draft horses compared with reports in other breeds; however, it does not appear to be associated with concurrent ocular disease.     

Effect of pretreatment with selenium-vitamin E on monensin toxicosis in cattle

Ten female beef calves weighing approximately 180 kg each were allotted to 2 groups of 5 each before they were given (orally) monensin (50 mg/kg of body weight). In group A, the calves were given (IM) a commercial selenium-vitamin E (Se-E) preparation (0.25 mg of Se and 17 IU of alpha-tocopherol/kg of body weight) at 72 and 24 hours before monensin was given. The calves in group B were injected at the 2 times with isotonic saline solution. Clinical signs of monensin toxicosis, including lethargy and recumbency, appeared on day 2 in the calves given the Se-E pretreatment, compared with the onset on day 1 in the saline solution-pretreated calves. All calves in the 2 groups died, but mean survival time was longer in group A (4.4 vs 2.2 days). Lesions of monensin toxicosis were myocardial necrosis, skeletal myonecrosis, pulmonary congestion, and rumenitis. The frequency and severity of the lesions were similar for both groups of calves. The results of the present study indicate that Se-E pretreatment modifies the development of monensin toxicosis in cattle.     

Slaframine toxicosis in Brazilian horses causing excessive salivation

Ingestion of food contaminated with slaframine, an alkaloid produced by Rhizoctonia leguminicola, causes a mycotoxicosis, characterised by excessive salivation. Twenty‐eight horses demonstrated this clinical sign after the consumption of alfalfa hay which on inspection showed dark patches on many of the stems. The presence of slaframine (1.5 ppm) in this hay was confirmed by gas chromatography and mass spectroscopy. This is the first equine slaframine toxicosis case reported in Brazil.     

Polysaccharide storage myopathy in Cob Normand draft horses

Gluteus medius muscle was sampled from 53 Cob Normand horses for histologic evaluation. Twenty horses (38%) exhibited amylase-resistant material in myocytes consistent with polysaccharide storage myopathy. Diameter of affected type II fibers was increased (67.7 +/- 21.4 microm) compared with normal ones (57.3 +/- 19.7 microm). Two groups were distinguished by quantitative study. The first group (n = 14; 26%) was characterized by a low percentage of fibers (m = 0.98%) containing aggregates occurring singly or in perifascicular clusters without myopathic changes. The second group (n = 6; 11%) was characterized by a high percentage (m = 18.1%) of fibers containing aggregates scattered in biopsy with chronic myopathic changes. Re-biopsy of 4 horses showed an increase with time in the number of aggregate-containing fibers for horses of the first group only. In 1 necropsied horse, aggregates were observed in a wide range of muscles including smooth muscles. Ultrastructurally, granular material was found interspersed among arrays of filamentous material.