Delayed monensin sodium toxicity in horses

Muylle, E.; Vandenhende, C.; Oyaert, W.; Thoonen, H.; Vlaeminck, Karel

doi:10.1111/j.2042-3306.1981.tb04129.x

Cited by 44 publications

(39 citation statements)

References 5 publications

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“…18,19 Typically, pathologic evidence of skeletal and cardiac myopathy along with a clinical history of possible or known exposure to monensin is used to confirm toxicosis. 8,13,16,17,20 However, several studies have shown individual variations in the severity of cardiac and skeletal muscle pathology, with some horses having no detectable histological changes 1,2,14 as shown in the current report. In those cases, diagnosis was made based on clinical signs of tachycardia, ataxia, depression, anorexia, and/or profuse sweating in conjunction with detection of high concentrations in the feed and/or stomach content.…”

Section: Research-article2014mentioning

confidence: 70%

“…9 Several cases of monensin toxicosis in horses have been reported in the veterinary literature. 1,2,7,13,14 In all these cases, a diagnosis of monensin poisoning was based on finding high levels of monensin in the feed in association with appropriate clinical or histologic evidence of myopathy. To the authors' knowledge, a fatal monensin poisoning in horses has not been confirmed based on detection of monensin in tissues or blood.…”

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confidence: 99%

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Diagnostic value of tissue monensin concentrations in horses following toxicosis

et al. 2014

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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 necrosis. Stomach content, heart, liver, urine, and serum revealed various detectable concentrations of monensin in clinically affected and unaffected horses with known exposure. In case 2, a pastured horse had access to a mineral mix containing 1,600 g/ton (1,760 µg/g) of monensin. Within 48 hr, the horse became symptomatic and was euthanized because of severe respiratory distress. Histologic cardiac lesions were minimal but detectable amounts of monensin were found in blood, heart, liver, and stomach contents. In both cases, monensin toxicosis was confirmed with toxicological analysis. These cases demonstrate an overall lack of correlation of monensin concentrations in various biological samples with clinical outcome. However, serum, urine, blood, liver, heart, and stomach content can be tested to confirm exposure. More importantly, the consistently higher concentrations found in heart tissue suggest this is the most useful diagnostic specimen for postmortem confirmation of toxicosis in horses especially in cases in which associated feed cannot be tested for monensin or in cases with no histologic lesions.

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Section: Research-article2014mentioning

confidence: 70%

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confidence: 99%

Diagnostic value of tissue monensin concentrations in horses following toxicosis

et al. 2014

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“…Fatal arrhythmias were previously reported as a cause of death in horses poisoned by monensin. 11,24 The 2 horses with cardiac disease (increased heart rates and cTnI values), but without physical signs of heart failure, had a gradual decline in heart rate and cTnI over time. In these horses, 17 (horse no.…”

Section: Discussionmentioning

confidence: 99%

Clinical Findings and Serum Cardiac Troponin I Concentrations in Horses after Intragastric Administration of Sodium Monensin

et al. 2009

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Abstract. Six adult horses were administered sodium monensin, 1.0-1.5 mg/kg, via gastric gavage. Anorexia and/or diarrhea occurred within 24 hr after monensin administration in all 6 horses. Cardiac disease and dysfunction were evaluated by both elevations in heart rate, echocardiography, and an increase in serum concentrations of cardiac troponin I (cTnI), occurred in 4 horses. The development and severity of cardiac disease was likely affected by the monensin dose, vehicle (water or corn oil) mixed with monensin, and/or whether the monensin was administered to fed or fasted horses. Initial increases in cTnI concentrations occurred between 24 and 72 hr after monensin administration. The 2 horses with the highest cTnI concentrations died or were euthanized within 5 days after monensin administration and had severe cardiac disease. One horse had increased cTnI concentrations from day 2 to day 16, but no apparent change in ventricular contractile function was evident on echocardiography. The fourth diseased horse did not return to cTnI reference intervals until day 27 after monensin administration, and the ventricular function was still abnormal just before euthanasia 9 months later. Cardiac troponin I measurements could be useful in managing farm outbreaks of accidental monensin feeding by the early identification of horses with cardiac disease.

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“…Since they have good oral absorption (24,191), these products are quite toxic for mammalians and birds. Several accidents have been reported with overdoses of ionophores in mammalians, mostly involving acute intoxications, although reports of chronic intoxications have also appeared (156,162,170). Horses and rabbits seem to be particularly susceptible to ionophore intoxications (22).…”

Section: Vol 16 2003 Antimicrobial Growth Promoters In Animals 181mentioning

confidence: 99%

Antimicrobial Growth Promoters Used in Animal Feed: Effects of Less Well Known Antibiotics on Gram-Positive Bacteria

2003

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There are not many data available on antibiotics used solely in animals and almost exclusively for growth promotion. These products include bambermycin, avilamycin, efrotomycin, and the ionophore antibiotics (monensin, salinomycin, narasin, and lasalocid). Information is also scarce for bacitracin used only marginally in human and veterinary medicine and for streptogramin antibiotics. The mechanisms of action of and resistance mechanisms against these antibiotics are described. Special emphasis is given to the prevalence of resistance among gram-positive bacteria isolated from animals and humans. Since no susceptibility breakpoints are available for most of the antibiotics discussed, an alternative approach to the interpretation of MICs is presented. Also, some pharmacokinetic data and information on the influence of these products on the intestinal flora are presented

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Delayed monensin sodium toxicity in horses

Cited by 44 publications

References 5 publications

Diagnostic value of tissue monensin concentrations in horses following toxicosis

Diagnostic value of tissue monensin concentrations in horses following toxicosis

Clinical Findings and Serum Cardiac Troponin I Concentrations in Horses after Intragastric Administration of Sodium Monensin

Antimicrobial Growth Promoters Used in Animal Feed: Effects of Less Well Known Antibiotics on Gram-Positive Bacteria

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