distrofia muscular nutricional em ovinos na paraíba nutritional muscular dystrophy in sheep in paraíba
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ID: 259547
2005
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Abstract
Descreve-se um surto de distrofia muscular nutricional em ovinos no semi-árido Nordestino. Foram afetados animais de 3-4 meses de idade, da raça Dorper, pesando 30-40 kg. Os animais eram alimentados, à vontade, com leite, ração balanceada, capim Tifton e sal mineral. Dos 70 animais Dorper, 6 adoeceram e morreram em um período de 48 horas. Apresentaram temperatura, entre 40 e 41ºC, incoordenação com posterior paralisia e decúbito, depressão, prostração e diminuição dos reflexos pupilar e de ameaça, flacidez da língua e mandíbula, salivação, edema submandibular, dispnéia e aumento da freqüência cardíaca. A morte ocorreu após curso clínico de 6- 12 horas. Na necropsia de 3 animais, os músculos esqueléticos estavam de coloração pálida, o fígado estava aumentado de volume e de coloração amarelada, os gânglios parotídeos, submandibulares, retrofaríngeos, prescapulares e mediastínicos estavam aumentados de volume e avermelhados e os pulmões apresentavam áreas vermelhas. Na histologia havia necrose segmentar de todos os músculos examinados e congestão dos gânglios linfáticos e pulmão. Posteriormente mais três animais adoeceram, sendo tratado com oxitetraciclina e complexo vitamínico A,D e E. Desses 3 animais, 2 morreram e um sobreviveu. Na mesma fazenda havia e não adoeceram 20 ovinos da raça Santa Inês, da mesma idade que os animais afetados, que recebiam a mesma alimentação exceto o leite, e 900 ovinos de outras idades. A superalimentação em animais com rápido crescimento e o estresse causado pela restrição de água durantes 2 dias, para aumentar o consumo de leite, parecem ter sido fatores predisponentes para a ocorrência da doença. É possível, também, que algum dos minerais suplementados tenha antagonizado o Se presente na alimentação.
An outbreak of nutritional muscular dystrophy is reported in the semiarid region of northeastern Brazil affecting 3-4 months old Dorper sheep. The animals, weighing 30-40 kg, were fed ad libitum with milk, concentrated ration, Tifton hay, and a mineral mixture. Six out of 70 lambs were affected and died in the first 48 hours after the onset of the outbreak. Clinical signs were fever of 40-41ºC, incoordination followed by paralysis and recumbence, depression, prostration with decreased pupillary and corneal reflexes, decreased tonus of the tongue and maxilla, salivation, submaxillar edema, and increased cardiac and respiratory rates. Death occurred after a clinical manifestation period of 6-12 hours. At necropsy of three animals, skeletal muscles were pale, the liver was yellowish and enlarged, the parotid, submaxillary, retropharyngeal, prescapular and mediastinal lymph nodes were enlarged with red surface, and red areas were observed on the lung surface. On histology, segmental muscular necrosis was observed in all skeletal muscles examined. The liver had centrilobular fatty degeneration, and congestion was observed in the lung and lymph nodes. From 48-96 hours after the begin of the outbreak, another 3 animals were affected. They were treated with Vitamin A, E and D complex; two of them died and one survived. On the same farm, a flock of 20 Santa Inês sheep of the same age as the affected animals, fed with the same food, but no milk, and another 900 sheep of different ages were not affected. The over nutrition of sheep with fast growing rates, and the stress caused by two days of water restriction to improve milk consumption had been predisposing factors for the occurrence of the disease. It is also possible that some of the minerals supplemented interfered with selenium availability.
An outbreak of nutritional muscular dystrophy is reported in the semiarid region of northeastern Brazil affecting 3-4 months old Dorper sheep. The animals, weighing 30-40 kg, were fed ad libitum with milk, concentrated ration, Tifton hay, and a mineral mixture. Six out of 70 lambs were affected and died in the first 48 hours after the onset of the outbreak. Clinical signs were fever of 40-41ºC, incoordination followed by paralysis and recumbence, depression, prostration with decreased pupillary and corneal reflexes, decreased tonus of the tongue and maxilla, salivation, submaxillar edema, and increased cardiac and respiratory rates. Death occurred after a clinical manifestation period of 6-12 hours. At necropsy of three animals, skeletal muscles were pale, the liver was yellowish and enlarged, the parotid, submaxillary, retropharyngeal, prescapular and mediastinal lymph nodes were enlarged with red surface, and red areas were observed on the lung surface. On histology, segmental muscular necrosis was observed in all skeletal muscles examined. The liver had centrilobular fatty degeneration, and congestion was observed in the lung and lymph nodes. From 48-96 hours after the begin of the outbreak, another 3 animals were affected. They were treated with Vitamin A, E and D complex; two of them died and one survived. On the same farm, a flock of 20 Santa Inês sheep of the same age as the affected animals, fed with the same food, but no milk, and another 900 sheep of different ages were not affected. The over nutrition of sheep with fast growing rates, and the stress caused by two days of water restriction to improve milk consumption had been predisposing factors for the occurrence of the disease. It is also possible that some of the minerals supplemented interfered with selenium availability.
| Reference Key |
amorim2005pesquisadistrofia
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|---|---|
| Authors | ;Sara Lucena Amorim;Alex Cicinato P. de Oliveira;Franklin Riet-Correa;Sara Vilar Dantas Simões;Rosane M. T. Medeiros;Inácio José Clementino |
| Journal | AIP Conference Proceedings |
| Year | 2005 |
| DOI |
10.1590/S0100-736X2005000200010
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| URL | |
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