Resultado da pesquisa (3)
Termo utilizado na pesquisa miopathy
#1 - Accidental monensin poisoning in sheep in Rio de Janeiro State, 29(9):743-746
Abstract in English:
ABSTRACT.- França T.N., Nogueira V.A., Yamasaki E.M., Caldas S.A., Tokarnia C.H. & Peixoto P.V. 2009. [Accidental monensin poisoning in sheep in Rio de Janeiro State.] Intoxicação acidental por monensina em ovinos no Estado do Rio de Janeiro. Pesquisa Veterinária Brasileira 29(9):743-746. Departamento de Epidemiologia e Saúde Pública, Instituto de Veterinária, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ 23890-000, Brazil. E-mail: ticianafranca@terra.com.br
An outbreak of monensin poisoning in sheep in the State of Rio de Janeiro is described. From 180 animals, eight died after they had been fed with ration containing the ionophore. The poisoning had a variable course and was clinically characterized by apathy, heart arrhythmia, myoglobinuria, incoordenation, incapacity of getting up, and sternal decubitus; one sheep aborted. The macroscopic lesions consisted of pale areas in the myocardium, hydroperitoneum, hydrothorax, and pulmonary edema. Histopathological examination revealed degenerative-necrotic alterations in heart and skeletal muscles. In the myocardium lesions were more severe and were characterized by multifocal necrosis with substitution of the myofibres by fibrous tissue and interstitial mononuclear infiltration. Proliferation of satellite cells and mononuclear inflammatory reaction in skeletal muscles were also verified. It seems that the exaggerated addition of sodic monensin, eventually associated with improper homogenization of monensin in the ration, was responsible for the excessive ingestion of monensin by some animals.
Abstract in Portuguese:
RESUMO.- França T.N., Nogueira V.A., Yamasaki E.M., Caldas S.A., Tokarnia C.H. & Peixoto P.V. 2009. [Accidental monensin poisoning in sheep in Rio de Janeiro State.] Intoxicação acidental por monensina em ovinos no Estado do Rio de Janeiro. Pesquisa Veterinária Brasileira 29(9):743-746. Departamento de Epidemiologia e Saúde Pública, Instituto de Veterinária, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ 23890-000, Brazil. E-mail: ticianafranca@terra.com.br
Descreve-se um surto de intoxicação por monensina em ovinos no Estado do Rio de Janeiro, no qual de 180 animais, oito morreram após serem alimentados com ração contendo o ionóforo. A enfermidade, de evolução variável, caracterizou-se clinicamente por apatia, arritmia cardíaca, mioglobinúria, incoordenação, incapacidade de se levantar, decúbito esternal; uma ovelha abortou. As lesões macroscópicas consistiram de áreas pálidas no miocárdio, hidroperitônio, hidrotórax e edema pulmonar. O exame histopatológico evidenciou alterações degenerativo-necróticas no coração e na musculatura esquelética. No miocárdio, as lesões eram mais marcadas e caracterizavam-se por necrose multifocal com substituição das miofibras por tecido conjuntivo fibroso e inflamação intersticial mononuclear. Adicionalmente, verificaram-se proliferação de células satélite e reação inflamatória mononuclear em músculos esqueléticos. Ao que tudo indica, a adição excessiva de monensina sódica, talvez associada à homogeneização inadequada da droga ao alimento, tenha determinado a ingestão de grande quantidade de monensina por parte dos animais.
#2 - Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul
Abstract in English:
ABSTRACT.- Carvalho N.M., Alonso L.A., Cunha T.G., Ravedutti J., Barros C.S.L. & Lemos R.A.A. 2006. [Poisoning of cattle by Tetrapterys multiglandulosa in Mato Grosso do Sul, Brazil.] Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul. Pesquisa Veterinária Brasileira 26(3):139-146. Departamento de Medicina Veterinária, Universidade Federal de Mato Grosso do Sul, Avenida Senador Filinto Müller 2443, Caixa Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br
Two outbreaks of poisoning by Tetrapterys multiglandulosa in cattle and the experimental reproduction of the toxicosis in sheep are described. Both outbreaks occurred on the same farm in the municipality of Bataiporã, state of Mato Grosso do Sul, Brazil. The first outbreak occurred in July-October 2004 and involved a cattle population at risk of 290 pregnant cows, which were introduced into a 60 hectare pasture with a legal reservation area heavily infested by T. multiglandulosa. Of these, 230 cows (79.3%) aborted, had stillbirths or delivered weak calves that died few days after birth. Seven cows died, and one cow and a 10-day-old calf were necropsied. The second outbreak occurred in September-October 2005, 40 days after 285 2-year-old heifers were introduced into the same pasture infested by T. multiglandulosa and where the first outbreak had occurred in the previous year. Nine heifers got sick and died, and three of then were necropsied. Clinical signs of affected cattle, including a 10-day-old calf, were marked lethargy, loss of weight with distension of the abdomen (ascites), subcutaneous dependant edema, distended and pulsating jugular veins, dyspnea and cardiac arrhythmia. Necropsy findings included a round and dilated heart with whitish and firm areas in the myocardium, and changes related to cardiac failure such as cavitary edema, nutmeg liver, pulmonary edema, a large blood clot in the left ventricle. Histopathological changes included necrosis and fibrosis in the myocardium, chronic passive hepatic centrolobular congestion, pulmonary edema, and spongy degeneration in the white matter of the brain. Experimental sheep died 29 (Sheep 1) and 35 (Sheep 2) days after being fed average daily doses of T. multiglandulosa corresponding to 14g/kg (Sheep 1) and 7,5 g/kg (Sheep 2) per day. Clinical signs were observed from the 7th day (Sheep1) and the 4th day (Sheep 2) of the experiment and included tachycardia, arrhythmia, lethargy and head pressing. Necropsy and histopathologic findings in both experimental sheep were very similar to those observed in affected cattle of the two spontaneous outbreaks.
Abstract in Portuguese:
ABSTRACT.- Carvalho N.M., Alonso L.A., Cunha T.G., Ravedutti J., Barros C.S.L. & Lemos R.A.A. 2006. [Poisoning of cattle by Tetrapterys multiglandulosa in Mato Grosso do Sul, Brazil.] Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul. Pesquisa Veterinária Brasileira 26(3):139-146. Departamento de Medicina Veterinária, Universidade Federal de Mato Grosso do Sul, Avenida Senador Filinto Müller 2443, Caixa Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br
Two outbreaks of poisoning by Tetrapterys multiglandulosa in cattle and the experimental reproduction of the toxicosis in sheep are described. Both outbreaks occurred on the same farm in the municipality of Bataiporã, state of Mato Grosso do Sul, Brazil. The first outbreak occurred in July-October 2004 and involved a cattle population at risk of 290 pregnant cows, which were introduced into a 60 hectare pasture with a legal reservation area heavily infested by T. multiglandulosa. Of these, 230 cows (79.3%) aborted, had stillbirths or delivered weak calves that died few days after birth. Seven cows died, and one cow and a 10-day-old calf were necropsied. The second outbreak occurred in September-October 2005, 40 days after 285 2-year-old heifers were introduced into the same pasture infested by T. multiglandulosa and where the first outbreak had occurred in the previous year. Nine heifers got sick and died, and three of then were necropsied. Clinical signs of affected cattle, including a 10-day-old calf, were marked lethargy, loss of weight with distension of the abdomen (ascites), subcutaneous dependant edema, distended and pulsating jugular veins, dyspnea and cardiac arrhythmia. Necropsy findings included a round and dilated heart with whitish and firm areas in the myocardium, and changes related to cardiac failure such as cavitary edema, nutmeg liver, pulmonary edema, a large blood clot in the left ventricle. Histopathological changes included necrosis and fibrosis in the myocardium, chronic passive hepatic centrolobular congestion, pulmonary edema, and spongy degeneration in the white matter of the brain. Experimental sheep died 29 (Sheep 1) and 35 (Sheep 2) days after being fed average daily doses of T. multiglandulosa corresponding to 14g/kg (Sheep 1) and 7,5 g/kg (Sheep 2) per day. Clinical signs were observed from the 7th day (Sheep1) and the 4th day (Sheep 2) of the experiment and included tachycardia, arrhythmia, lethargy and head pressing. Necropsy and histopathologic findings in both experimental sheep were very similar to those observed in affected cattle of the two spontaneous outbreaks.
#3 - Nutritional miopathy in cattle in Rio Grande do Sul, Brazil
Abstract in English:
The occurrence of nutritional miopathy (white muscle disease) in calves in, Rio Grande de Sul, Brazil, is described. ln one property in São Gabriel county, 40 out of 140 yearling Hereford calves, which were held in a rye grass pasture, died within 1-3 days after presenting clinical signs consisting of stiffness of the limb muscles and impaired locomotion. ln some cases the animals died without showing any clinical signs. Necropsy performed in one animal revealed lesions in the skeletal muscles and, to a lesser degree, in the myocardium consisting of extensive areas of white or cream discoloration. These areas had either a patchy or linear distribution. The most affected muscles included the heavy muscle groups of the thigh and shoulders, as well as the loin muscles, diaphragm and tongue. Microscopic lesions involving the skeletal and cardiac miofibers were mainly degenerative in character consisting of swelling, hialinosis, discoid degeneration and segmental hypercontraction. Fiber calcification was prominent. Myolisis associated with macrophage active phagocytosis of degenerated fibers and neutrophil infiltrates were also observed. After treatment with vitamin E and selenium there was no occurrence of new cases and mildly affected animals recovered. ln another property, a small farm in Santa Maria county, an isolated case of miopathy affecting na 18-day old female BrownSwiss calf was observed. The animal died of a peracute disease with no premonitory signs. Muscular lesions, similar to the ones encountered in the above described outbreak, were seen at necropsy; however, in this case the lesions were more marked in the myocardium. Microscopic lesions were also similar but those of the myorcardium included marked proliferative changes associated with macrophages and other mononuclear cell infiltrates.
Abstract in Portuguese:
É descrita a ocorrência de miopatia nutricional (doença dos músculos brancos) em bovinos no Rio Grande do Sul. Numa propriedade do município de São Gabriel, de 140 bezerros de aproximadamente um ano de idade que eram mantidos em uma pastagem de azevém, 40 animais morreram. A evolução da doença foi de 1 a 3 dias e os sinais clínicos incluiram rigidez dos músculos dos membros e dificuldade de locomoção. Na necropsia realizada em um dos animais havia lesões nos músculos esqueléticos e, em menor grau, no miocárdio consistindo de áreas de cor branca ou creme. Essas áreas tinham uma distribuição em manchas grandes ou em forma linear. Os músculos mais afetados eram os grandes grupos musculares da coxa e paleta, bem como os músculos lombares, o diafragma e a língua. As lesões microscópicas eram principalmente degenerativas e restritas aos músculos esqueléticos e ao miocárdio, incluindo tumefação, hialinose, degeneração discóide e hipercontração segmentar das fibras musculares. Havia acentuada calcificação de fibras. Também se observava miólise associada à fagocitose de restos degenerados de fibras e infiltrado neutrofílico. Após tratamento com vitamina E e selênio não houve aparecimento de novos casos e alguns animais afetados levemente recuperaram-se. Um caso isolado de miopatia foi observado em uma bezerra da raça pardo-suiça no município de Santa Maria numa pequena propriedade de exploração leiteira. O animal morreu subitamente sem apresentar sinais clínicos prévios. Na necropsia foram vistas lesões musculares semelhantes às observadas nos animais do surto acima descrito, porém mais pronunciadas no coração. As lesões microscópicas também eram semelhantes, mas as do miocárdio incluiam marcadas alterações proliferativas acompanhadas por infiltrado de macrófagos e outras células mononucleares.
