Journal of Veterinary Diagnostic Investigation Vol. 18 Issue 5, 494-496
Copyright © 2006 by the American Association of Veterinary Laboratory Diagnosticians
Monensin toxicosis in water buffaloes (Bubalus bubalis)
Daniela Bernadete Rozza,
Ingrid Vervuert,
Josef Kamphues,
Cláudio Estêvão Farias da Cruz and
David Driemeier1
Correspondence: 1Corresponding Author: David Driemeier, Departamento de Patologia Clínica Veterinária Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Avenida Bento Gonçalves, n ° 9090, 91540-000 Porto Alegre RS, Brazil
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Abstract
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The consumption of monensin-containing feed resulted in deaths of water buffaloes from a feedlot in which cattle and buffaloes were kept together. The monensin formulation was recommended only for use in cattle. Anorexia, muscular weakness, dyspnea, and recumbency were the major clinical findings. The most significant gross lesions were focal pale areas in semitendinosus and semimembranosus muscles, in which segmental necrosis of myofibers was seen microscopically. To compare susceptibilities of species to monensin, 3 bovine calves and 3 buffalo calves were orally dosed. At 5, 7.5, and 10 mg/kg of monensin, only the buffaloes became ill and died. Clinical signs initiated 18–20 h postdosing and were comparable to those from field cases. Gross changes consisted of ascites, hydrothorax, hydropericardium, hepatomegaly, and focal pale areas in the myocardium and to a lesser degree in semitendinosus and semimembranosus muscles. Histopathologicalchanges also resembled those from the field cases, but were especially pronounced in the myocardial cells. The hypothesis that buffaloes could have a lower tolerance to monensin than cattle has been supported by experimental cases.
Key Words: Buffaloes • degenerative myopathy • monensin tolerance • monensin toxicity
The ionophore monensin has been widely used as a feed additive to improve performance in livestock production systems. Unfortunately, accidental monensin intoxication has been reported in cattle,4,5,11 sheep,7 horses,9 and a number of other animal species.6 Accidental intoxication usually results from monensin overdosage, misuse, and mixing errors in feed preparation.8
The toxic concentration of monensin is variable and dependent upon the animal species and type of diet involved. Adverse effects have been reported at about 3 mg/kg in horses, 12 mg/kg in sheep, and above 20 mg/kg in cattle.6,10 Clinical signs depend on the amount of toxic substance consumed and may include anorexia, dyspnea, diarrhea, tremors, ataxia, muscular weakness, locomotion disorders, tachycardia, myoglobinuria, and death.4,8,10
Pale foci or streaks in the myocardium and skeletal muscles are the most common gross lesions. Necrosis in skeletal and cardiac muscles are the main histopathological changes, which may include tumefaction, hyaline or floccular necrosis, lysis of myofibrils, and regenerative processes or fibrosis.6,8 This communication reports an episode of monensin poisoning in water buffaloes and describes the experimental findings observed in monensin-dosed buffaloes.
In a southern Brazilian farm, a feedlot composed of 125 mixed-breed beef cattle calves and 160 water buffalo calves was kept on pastures of Brachiaria sp. and Paspallum sp. and supplemented with a diet that included corn silage, dendê bran, mineral mix, and sodium monensina (at 200 g per 1.5 ton of feed mix). The quantitative analysis by gas chromatography and mass spectroscopyb revealed 90.7 mg of sodium monensina/kg of the total mix. Within 1 week of feeding, in which the daily group consumption was 300 kg of the mix, 40 buffaloes became ill and 10 of them died, but none of the cattle showed adverse clinical signs. The major clinical findings were anorexia, muscular weakness, apathy, ataxia, dyspnea, and recumbency. The main gross necropsy findings observed in 3 buffaloes were focal pale areas irregularly scattered in semitendinosus (Fig. 1) and semimembranosus muscles. One buffalo had hydrothorax, lung edema, ascites, and pale areas in the myocardium. The microscopic changes included segmental necrosis of skeletal muscle fibers associated with regenerative changes. In areas of hyaline and floccular necroses (Fig. 2), necrotic myocytes showed enhanced eosinophilia and loss of cross striations and were often fragmented. In the myocardial fibers there was necrosis and infiltration with macrophages. No significant change was detected in other tissues.
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Figure 1 Pale areas in semitendinosus muscle of a Murrah buffalo from an episode of monensin poisoning.
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Figure 2 Water buffalo. Monensin poisoning. Semitendinosus muscle with hyaline and floccular necroses and invasion of hyaline fibers by macrophages. Hematoxylin and eosin staining, 40x.
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Because no evidence of disease was noticed in cattle from this feedlot, the susceptibility of these species to monensin was compared. Three 9-month-old Murrah buffaloes and three 12-month-old, mixed-breed, beef cattle were dosed with monensin. Adaptation to the housing system lasted 3 weeks before dosing. Animals were kept individually in indoor pens, where they received alfafa hay, concentrate (without monensin), and fresh drinking water. Single doses of 5, 7.5, and 10 mg/kg of body weight of sodium monensina were mixed in 100 ml of water and given orally. Dosages of monensin given to the animals and a summary of the results observed are presented in Table 1.
Except for the cattle that did not show any evidence of disease even for the subsequent 3 months, clinical signs appeared 18–20 hours after dosing. In the 3 buffaloes, the clinical picture was similar to that reported in the field cases, however diarrhea was additionally seen in the buffalo #3. Dyspnea was particularly evident in the first 48 hours after dosing, but further signs persisted until death. Dead buffaloes were necropsied and main gross lesions were ascites, hydrothorax, hydropericardium, enlarged hearts and livers, and focal pale areas in the myocardium. Lesions in skeletal muscles were less pronounced than those from field cases. The mucosal surfaces of the small intestines from the 3 buffaloes were reddened. Necrotic changes in the myocardium were more pronounced in the experimental cases.
The clinical and pathological features observed in the water buffaloes were characteristic of monensin poisoning6,8 and were similar to those described previously in cattle suffering from monensin poisoning.4,11–13 Although individual intake by the buffaloes in field cases was not determined, the concentration of monensin in the diet was suggestive of poisoning.8 The individual daily consumption range of 50–200 mg of monensin for growing cattle and the claim "only for use in cattle" were between the label directions of the sodium monensin formulation used in the feedlot. Senna occidentalis poisoning is reported to induce similar pathological changes in the muscles,3 however the plant was not found on the farm. Typical white and chalky gross lesions associated with high levels of calcification in degenerated myocytes are frequently found in nutritional muscular dystrophy caused by selenium and vitamin E deficiencies,6 but such changes were not observed in these buffaloes.
The possibility that buffaloes in field cases could have monopolized feed bunks and consumed larger quantities of the diet than cattle was not confirmed. This episode of adverse reaction in a number of buffaloes fed the medicated diet and its absence in cattle from the same feedlot suggested a higher susceptibility of the former. This hypothesis has been supported by this experimental study, in which buffaloes tolerated less monensin than cattle. Although variable according to several management factors, the toxic dose of monensin for cattle has been reported to be around 20 mg/kg,6,10 and these buffaloes became ill after receiving considerably lower doses. Buffaloes in field cases predominantly developed lesions in skeletal muscles, and those from the trial had cardiac lesions as the most pronounced changes. Positive effects of monensin supplementation on general performance have been reported in buffaloes1,2 and several other animal species; however this communication highlights the level of caution required for feeding monensin to buffaloes.
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Acknowledgments
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Financial support was provided by Conselho Nacional de Desenvolvimento Cientifico e Tecnológico (CNPq) and Coordenação de Aperfeiçoamento de Pessoal de Nivel Superior (CAPES), Brazil.
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Sources and manufacturers
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From the Department of Veterinary Pathology, College of Veterinary Medicine, Federal University of Rio Grande do Sul (UFRGS), Avenida Bento Gonçalves 9090, 91540-000 Porto Alegre, RS, Brazil (Rozza, Cruz, Driemeier), and Institut of Animal Nutrition, University of Veterinary Medicine Hannover, Foundation, Bischofsholer Damm 15, D-30173 Hannover, Germany (Vervuert, Kamphues). 
a. Rumensin 100 Premix, Elanco Saúde Animal, Eli Lilly do Brasil, São Paulo, Brazil.
b. Institut of Animal Nutrition, University of Veterinary Medicine, Hannover, Germany.
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