PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Polioencephalomalacia (PEM) is the morphological characterization for softening of brain gray matter, and excess sulfur intake is one of its main causes. This study describes an outbreak of this disease in 1-to-3-month-old calves in a farm located in Santa Catarina state, Brazil. The herd consisted of 27 Jersey male calves whose diet was composed of initial feed, ground whole corn, and mineral salt. From this herd, 10 animals became ill, showing signs of apathy, anorexia and blindness, evolving to generalized weakness and death. Necropsy was performed in three of these animals, which showed flattening of the cerebral convolutions in addition to softened, yellowish areas in the cerebral cortex. Histopathological examination revealed deep laminar necrosis associated with perineuronal and perivascular edema, as well as neurons with wrinkled, eosinophilic, or vacuolated cytoplasm. The following sulfur doses were observed: 8,010mg/kg in corn, 6,385mg/kg in initial feed, 1,060mg/kg in mineral salt and 2.3mg/L in water, reaching dose values ​​far above the accepted, totaling a daily intake of approximately 6,533.5mg sulfur/animal/day. As differential diagnosis, lead was dosed in the kidneys and liver of the three calves, with negative results. Also, the calf that sickened last was treated with 20mg/kg thiamin and 0.2mg/kg dexamethasone (IM; QID) for three days and eventually recovered. According to anatomopathological findings, excess sulfur intake and therapeutic diagnosis, sulfur poisoning was suggested as the cause of PEM in these 1-to‑3-month-old calves. Occurrence of PEM is rare in calves at such a young age.

• Polioencephalomalacia calves excess sulfur intake sulfur neurological diseases thiamin ruminants cattle pathology

Abstract in Portuguese:

A polioencefalomalacia (PEM) é a caracterização morfológica para o amolecimento da substância cinzenta encefálica, e uma de suas principais etiologias é a ingestão excessiva de enxofre. Este trabalho descreve um surto desta enfermidade em bezerros de um a três meses de idade em uma propriedade de Santa Catarina. O lote era composto por 27 bezerros machos da raça Jersey, com alimentação composta por ração inicial, milho inteiro triturado e sal mineral. Deste lote, 10 animais adoeceram, apresentando sinais de apatia, anorexia e cegueira, com evolução para fraqueza generalizada. Nove bezerros morreram e três foram submetidos a necropsia, que demonstraram achatamento das circunvoluções cerebrais além de áreas de amolecimento e coloração amarelada no córtex cerebral. Realizou-se exame histopatológico que evidenciou necrose laminar profunda associada a edema perineuronal e perivascular, além de neurônios com citoplasma enrugado, eosinofílico ou vacuolizado. A dosagem de enxofre resultou em 8010mg/Kg no milho, 6385mg/Kg na ração, 1060mg/Kg no sal mineral e 2,3mg/L na água, atingindo valores muito acima do tolerado, totalizando a ingestão diária de cerca de 6533,5mg de enxofre/animal/dia. Como diagnóstico diferencial realizou-se dosagem de chumbo de amostras de rim e fígado dos três bezerros com resultado negativo. Ainda, o último bovino a adoecer foi tratado com 20mg/Kg de tiamina e 0,2mg/Kg de dexametasona IM, QID, durante três dias e recuperou-se. De acordo com os achados anatomopatológicos e o excesso de enxofre na dieta, sugere-se que a intoxicação por enxofre seja a causa de PEM nestes bezerros de um a três meses de idade, sendo essa enfermidade rara em bovinos tão jovens.

• Polioencefalomalacia bezerros enxofre doenças neurológicas tiamina ruminantes bovinos patologia

Abstract in English:

ABSTRACT.- Delfiol D.J.Z., Cagnini D.Q., Cunha P.H.J., Crosignani N., Wouters A.T.B., Wouters F., Driemeier D. & Borges A.S. 2013. [Clinical and laboratory aspects of sheep supplemented with high levels of sulfur in diet to induce polioencephalomalacia.] Aspectos clínicos e laboratoriais em ovinos submetidos a dietas com níveis elevados de enxofre com objetivo de indução de polioencefalomalácia. Pesquisa Veterinária Brasileira 33(4):435-442. Departamento de Clínica Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Estadual Paulista, Botucatu, SP 18618970, Brazil. E-mail: asborges@fmvz.unesp.br Polioencephalomalacia (PEM) is a neuropathologic condition of ruminants that can be induced by a variety of factors including excessive sulfur intake. This study aimed to investigate the relationship between diets rich in sulfur, high levels of ruminal hydrogen sulfide and the occurrence of polioencephalomalacia in sheep. Eighteen sheep were divided into three groups (G1, G2, and G3) and supplemented with 0.2%, 0.9% and 1.2% sulfur in the diet respectively. Clinical evaluation (i.e. heart rate, respiratory rate, rectal temperature and rumen motility) and laboratory exams (i.e. ruminal hydrogen sulfide concentration, venous gas analysis, ruminal pH, serum and liver copper concentration, computed axial tomography, necropsy, and histopathological examination) were performed. Rectal temperature, venous gas and ruminal pH were within normal limits. Tachycardia and tachypnea were observed in sheep of the three groups. Rumen motility was decreased in animals of group G2 and G3 when compared with G1. The higher the sulfur intake, the lower was the serum and liver levels of copper. Increased ruminal hydrogen sulfide concentration was detected in G2 and G3 sheep. None of the animals had clinical signs of PEM. Computed axial tomography, macroscopic and histopathological examination of the central nervous system showed no evidence of PEM. It is suggested that other factors are associated with excessive sulfur consumption for a PEM outbreak to occur in sheep.

• Polioencephalomalacia sulfur polioencefalomalacia

Abstract in Portuguese:

RESUMO.- Delfiol D.J.Z., Cagnini D.Q., Cunha P.H.J., Crosignani N., Wouters A.T.B., Wouters F., Driemeier D. & Borges A.S. 2013. [Clinical and laboratory aspects of sheep supplemented with high levels of sulfur in diet to induce polioencephalomalacia.] Aspectos clínicos e laboratoriais em ovinos submetidos a dietas com níveis elevados de enxofre com objetivo de indução de polioencefalomalácia. Pesquisa Veterinária Brasileira 33(4):435-442. Departamento de Clínica Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Estadual Paulista, Botucatu, SP 18618970, Brazil. E-mail: asborges@fmvz.unesp.br A polioencefalomalacia (PEM) é uma doença neurológica que acomete ruminantes e pode ser desencadeada por diversos fatores, dentre eles o consumo excessivo de enxofre. Este trabalho teve como objetivo verificar a relação entre dietas ricas em enxofre, altos níveis de gás sulfídrico ruminal e a ocorrência de polioencefalomalácia em ovinos. Foram utilizados 18 ovinos, divididos em três grupos (G1, G2 e G3) que receberam diferentes níveis de enxofre na dieta; 0,2%, 0,9% e 1,2%, respectivamente. Exames físicos (frequência cardíaca, frequência respiratória, temperatura retal e motricidade ruminal) e complementares (concentração de sulfeto de hidrogênio ruminal, hemogasometria venosa, pH do fluído ruminal, concentração de cobre sérico e hepático, tomografia computadorizada, necropsia e histopatologia) foram realizados. A temperatura retal, a hemogasometria venosa e o pH do fluido ruminal permaneceram dentro dos valores de referência para a espécie. A motricidade ruminal estava diminuída nos grupos G2 e G3 em comparação com o G1 (controle). Quanto maior a ingestão de enxofre, menores foram os níveis de cobre sérico e hepático. Valores elevados de sulfeto de hidrogênio ruminal foram detectados nos grupos G2 e G3. Nenhum animal apresentou sinais clínicos de PEM. Nos exames de tomografia computadorizada, necropsia e exame histopatológico do sistema nervoso central (SNC), não foram observadas alterações compatíveis com PEM. É provável que algum outro fator esteja associado ao excesso de enxofre na dieta para o desenvolvimento de PEM em ovinos.

Abstract in English:

ABSTRACT.- Cunha P.H.J., Badial P.R., Cagnini D.Q., Oliveira Filho J.P., Moraes L.F., Takahira R.K., Amorim R.L. & Borges A.S. 2011. [Experimental polioencephalomalacia in cattle induced by sulfur toxicosis.] Polioencefalomalacia experimental em bovinos induzida por toxicose por enxofre. Pesquisa Veterinária Brasileira 31(1):41-52. Departamento de Medicina Veterinária, Escola de Veterinária, Universidade Federal de Goiás, Rua 13 no.278, Apto 400, Plaza Residencial Sol de La Plaza, Setor Oeste, Goiânia, GO 74120-060, Brazil. E-mail: phcunhavet@yahoo.com.br The aims of this study were to evaluate the clinical signs, the ruminal hydrogen sulfide concentration and the histological lesions induced by sulfur toxicosis in cattle. Ten crossbred calves were fed an experimental diet, four without sodium sulfate (G1) and six with (G2). The calves were submitted to clinical (rectal temperature, cardiac and respiratory rate and ruminal motricity) and laboratorial (hemogram, fibrinogen, total plasma protein, ruminal fluid pH, ruminal hydrogen sulfide concentration, cerebrospinal fluid and histopathological) evaluations. Rectal temperature, cardiac rate, hemogram, fibrinogen, total plasma protein, ruminal fluid pH and cerebrospinal fluid values were within normal reference ranges in animals from both groups. Ruminal hypomotricity and increased respiratory rate and ruminal hydrogen sulfide concentration occurred in G2 animals. One out of six calves in G2 developed neurological signs and lesions of PEM. Two calves of each Group were euthanized. Microscopic lesions of PEM were observed in G2 animals. Histologically there were cortical neuronal necrosis and hemorrhagic lesions in basal nuclei, thalamus, midbrain, pons and medulla oblongata. The experimental model consisting of a diet with high carbohydrate and low in long fiber content with high sulfur concentrations (0.52%) resulted in clinical and histological abnormalities and high ruminal hydrogen sulfide concentration consistent with sulpur toxicosis in cattle.

• Cerebrocortical necrosis sulfur necrose cerebrocortical enxofre

Abstract in Portuguese:

RESUMO.- Cunha P.H.J., Badial P.R., Cagnini D.Q., Oliveira Filho J.P., Moraes L.F., Takahira R.K., Amorim R.L. & Borges A.S. 2011. [Experimental polioencephalomalacia in cattle induced by sulfur toxicosis.] Polioencefalomalacia experimental em bovinos induzida por toxicose por enxofre. Pesquisa Veterinária Brasileira 31(1):41-52. Departamento de Medicina Veterinária, Escola de Veterinária, Universidade Federal de Goiás, Rua 13 no.278, Apto 400, Plaza Residencial Sol de La Plaza, Setor Oeste, Goiânia, GO 74120-060, Brazil. E-mail: phcunhavet@yahoo.com.br O presente trabalho teve como objetivos avaliar os sinais clínicos, as concentrações do sulfeto de hidrogênio ruminal e as alterações anatomopatológicas associadas à intoxicação experimental por enxofre em bovinos. Foram utilizados dez bezerros mestiços leiteiros, sendo que quatro bovinos ingeriram ração sem sulfato de sódio (G1) e seis consumiram ração com sulfato de sódio (G2). Exames clínicos (temperatura retal, frequência cardíaca e respiratória e motricidade ruminal) e laboratoriais (hemograma, fibrinogênio, proteína plasmática, pH do fluido ruminal, concentração do sulfeto de hidrogênio ruminal, líquido cerebrospinal e histopatológico) foram realizados. A temperatura retal, frequência cardíaca, hemograma, fibrinogênio, proteína plasmática, pH do fluido ruminal e os valores do líquido cerebrospinal estavam dentro dos valores de referência para a espécie. Taquipnéia, hipomotricidade ruminal e elevados valores de sulfeto de hidrogênio ruminal foram observados nos bezerros do grupo G2. Um bezerro do grupo G2 apresentou sinais neurológicos e lesões histopatológicas de PEM. Dois animais de cada grupo foram eutanasiados. Lesões microscópicas foram observadas nos bezerros do G2. Histologicamente as alterações observadas foram necrose neuronal cortical e lesões hemorrágicas nos núcleos basais, tálamo, mesencéfalo, ponte e bulbo. O protocolo experimental constituído por uma dieta rica em carboidrato de alta fermentação, baixa quantidade de fibra efetiva e altos níveis de enxofre (0,52%) ocasionou alterações clinicas e histológicas e elevadas concentrações de sulfeto de hidrogênio ruminal compatíveis com quadro de intoxicação por enxofre.

Abstract in English:

Lima E.F., Riet-Correa F., Tabosa I.M., Dantas A.F.M., Medeiros J.M. & Sucupira Júnior G. 2005. [Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil.] Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(1):9-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br Seven outbreaks of polioencephalomalacia in goats and 3 in sheep are reported from the semiarid region of northeastern Brazil. Animals of different ages were affected in various seasons of the year. In 5 outbreaks the animals were supplemented with concentrate ration and in 5 others they were only grazing on pastures. In one outbreak sheep were supplemented with an energy-protein-mineral mixture containing 1.3% of sulfur flower. Clinical signs were characterized by blindness, depression, head pressing, circling, grinding of the teeth, incoordination, spastic paralysis, ataxia, depression of the palpebral and pupillary reflexes, lateral strabismus, nystagmus, and dilated pupils. Nine affected animals were treated with thiamine and dexamethasone; 7 of them recovered but 2 died. The diagnosis of the disease was based on the recovered animals after treatment and/or on the histologic lesions. The clinical course varied from 2 to 15 days. On three animals post-mortem examination was made. One had herniation of the cerebellum through the Foramen magnum and softening of the cerebral cortex. The cut surface of the cerebral cortex showed cavitation and yellowish discoloration. Another animal had only cerebellar herniation. In a third animal no gross lesions were observed. Histological changes in the 3 animals were laminar necrosis of the cerebral cortex, and in 2 malacia of the thalamus and the rostral colliculi was also observed. In 9 outbreaks the cause of the disease was not determined, but one was probably due to sulfur toxicosis caused by the high sulfur content of the energy-protein-mineral mixture containing 1.3% of sulfur flower (96% sulfur) and 30% chicken litter (0.39% sulfur).

• Polioencephalomalacia cortical necrosis goats sheep sulfur poisoning thiamine deficiency.

Abstract in Portuguese:

Lima E.F., Riet-Correa F., Tabosa I.M., Dantas A.F.M., Medeiros J.M. & Sucupira Júnior G. 2005. [Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil.] Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(1):9-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br Seven outbreaks of polioencephalomalacia in goats and 3 in sheep are reported from the semiarid region of northeastern Brazil. Animals of different ages were affected in various seasons of the year. In 5 outbreaks the animals were supplemented with concentrate ration and in 5 others they were only grazing on pastures. In one outbreak sheep were supplemented with an energy-protein-mineral mixture containing 1.3% of sulfur flower. Clinical signs were characterized by blindness, depression, head pressing, circling, grinding of the teeth, incoordination, spastic paralysis, ataxia, depression of the palpebral and pupillary reflexes, lateral strabismus, nystagmus, and dilated pupils. Nine affected animals were treated with thiamine and dexamethasone; 7 of them recovered but 2 died. The diagnosis of the disease was based on the recovered animals after treatment and/or on the histologic lesions. The clinical course varied from 2 to 15 days. On three animals post-mortem examination was made. One had herniation of the cerebellum through the Foramen magnum and softening of the cerebral cortex. The cut surface of the cerebral cortex showed cavitation and yellowish discoloration. Another animal had only cerebellar herniation. In a third animal no gross lesions were observed. Histological changes in the 3 animals were laminar necrosis of the cerebral cortex, and in 2 malacia of the thalamus and the rostral colliculi was also observed. In 9 outbreaks the cause of the disease was not determined, but one was probably due to sulfur toxicosis caused by the high sulfur content of the energy-protein-mineral mixture containing 1.3% of sulfur flower (96% sulfur) and 30% chicken litter (0.39% sulfur).

Abstract in English:

ABSTRACT.- Marques A.P., Riet-Correa F., Soares M.P., Ortolani E.L. & Giuliodori M.J. 2003. (Sudden deaths in cattle associated with copper deficiency.] Mortes súbitas em bovinos associadas à carência de cobre. Pesquisa Veterinária Brasileira 23(1):21-32. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, Universidade Federal de Pelotas, 96010-900, Pelotas, RS, Brazil. An outbreak of sudden death was observed in cattle in southern Brazil. No significant gross or microscopic lesions were found in 1 O cattle at post-mortem examination. To test if the sudden deaths were caused by a toxic plant, 13 weeds were collected and given to rabbits at a total of 440 to 600 g per kg body weight within 7 days. Results were negative. Mean copper levels of the tiver in 10 cattle were very low (3.6± 1.6 ppm-dry matter) suggesting Cu deficiency as the cause of the disease. Five samples of pasture collected during the outbreak had normal levels of Cu (8.4±0.8 ppm-d.m.) and S (0.2%±0.03-d.m.), but high levels of Fe (522± 122 ppm-d.m.). One group of 10 heifers was supplemented with Cu subcutaneously. This group and a similar control group were maintained in the sarne area where the outbreak occurred. Serum levels of Cu, S, Fe, Mo and ceruloplasmin were determined bimonthly in both groups during one year. Mean serum levels of Cu (1.76± 1.06 to 10.34±3.1 μmol/1 for the control group and 3.86± 1.53 to 10.61 ± 1.34 μmol/1 for the treated group) and ceruloplasmin (6.59±3.93 to 18.61±4.14 mg/1 for the control group and 10.31±5.48 to 32.49±6.05 mg/1 for the treated group) were significantly higher in the supplemented group (P=0.0046 for Cu and P=0.0001 for ceruloplasmin), but they were below normal levels in most samples of both groups. Serum levels of Cu and ceruloplasmin were correlated (r=0.67; P=00.5). ln both groups serum levels of Fe (40.09±5.25 to 78.48±28.23 μmol/1) were higher than normal levels. Samples of forage were collected bimonthly for determination of Cu, Mo, S, Fe and protein in 7 points of the paddock where the outbreak occurred. Levels of Cu (1.36±0.56 to 4.76±1.15 ppm-d.m.) were below the normal ranges. The concentration of Mo (0.17±0.06 to 0.96±0.47 ppm-d.m.) was within normal ranges. Levels of S (0.21 ±0.04% to 0.5±0.17%) and Fe (172.92±62.64 to 437.24±205.44 ppm-d.m.) were occasionally within toxic level. Levels of protein varied from 7.77±2.6% to 13.16±3.02%. Six samples of water and six of submersed pastures were collected at the end of the experiment when the paddock was flooded. High levels of iron (169.23±83.49 ppm-d.m.) and S (0.06±0.03%) were found in the water. Levels of Fe and S in the submerse pasture were of 469.3±218.28 ppm and 0.19 ±0.05%, respectively. The results obtained suggest that the sudden deaths are due to Cu deficiency. Three factors seem to be responsible for the Cu deficiency: 1) high levels of iron in pastures and water; 2) occasionally low levels of copper in the pastures; and 3) the ingestion of S above the requirements due to the levels occasionally high in pastures and high in water. The outbreak reported is similar to other outbreaks of sudden deaths associated with low liver copper previously reported during winter in the sarne region of southern Brazil. This area is characterized by acid sandy soils with frequent flooding during this season. ln periodically flooded acid soils iron is solubilized and absorbed by the plants, decreasing the Cu content and increasing the Fe content of forage. This seems to be the main reason for Cu deficiency in the region.

• Cattle copper deficiency sudden death iron molibdenum sulfur Bovinos deficiência de cobre morte súbita ferro molibdênio enxofre

Abstract in Portuguese:

RESUMO.- Marques A.P., Riet-Correa F., Soares M.P., Ortolani E.L. & Giuliodori M.J. 2003. [Sudden deaths in cattle associated with copper deficiency.] Mortes súbitas em bovinos associadas à carência de cobre. Pesquisa Veterinária Brasileira 23(1):21-32. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, Universidade Federal de Pelotas, 96010-900, Pelotas, RS, Brazil. Foi estudado um surto de morte súbita em bovinos no sul do Rio Grande do Sul. Nos animais necropsiados não foram observadas lesões macroscópicas ou microscópicas significativas. Para testar se as mortes súbitas teriam sido causadas por plantas tóxicas, 13 espécies de plantas foram coletadas e administradas a coelhos num total de 440 a 600g/kg de peso vivo num período de 7 dias. Os resultados foram negativos. Os teores de cobre no fígado dos bovinos foram muito baixos (3,6±1,6 ppm-base seca) sugerindo que as mortes foram causadas por deficiência de cobre. Cinco amostras de pasto, coletadas no local do surto, apresentaram teores normais de Cu (8,4±0,8 ppm-bs) e S (0,2%±0,03%-bs), mas altos teores de Fe (522±122 ppm-bs). Um grupo de 10 novilhas foi suplementado com Cu subcutâneo. Este grupo e um grupo controle foram mantidos em área similar à da ocorrência do surto. Teores séricos de Cu, S, Fe, Mo e ceruloplasmina foram determinados bimensalmente durante um ano de experimento. Os teores médios de Cu (1,76±1,06 a 10,34±3,1 μmol/1 no grupo controle e 3,86± 1,53 a 10,61 ± 1,34 μmol/1 para o grupo suplementado) e ceruloplamina (6,59±3,93 a 18,61 ±4,14 mg/1 para o grupo controle e 10,35±5,48 a 32,49±6,05 mg/1 para o grupo suplementado) foram significativamente maiores no grupo suplementado (P=0,0046 para o Cu e P=0,0001 para a ceruloplasmina), mas a maioria das amostras tiveram teores abaixo do normal em ambos os grupos. Houve uma correlação entre os teores de Cu e os de ceruloplasmina (r=0,67, P=0,05). Em ambos os grupos os teores séricos de Fe (40,09±5,22 a 78,48±28,23 μmol/1) estiveram acima dos teores normais. Amostras de forragens foram coletadas bimensalmente em sete pontos do campo onde ocorreu o surto para determinação de Cu, Mo, S, Fe e proteína. Os teores de Cu (1,36±0,56 a 4,76±1,15 ppm-bs) estiveram abaixo dos requerimentos. Os teores de Mo (0,17±0,06 a 0,96±0,47 ppm-bs) estiveram dentro da normalidade. Valores de S (0,21 ±0,04% a 0,5±0, 17%) e Fe (172,92±62,64 a 437,24±205,44 ppm-bs) alcançaram, ocasionalmente, níveis tóxicos. Teores de proteína variaram de 7,77±2,6% a 13, 16±3,02%. Seis amostras de água e 6 amostras de pasto submerso foram coletadas no fim do experimento quando o campo estava inundado. Altos teores de Fe (169, 23±83,49 ppm) e S (0,06±0,03%) foram encontrados na água. Os teores de Fe e S no pasto submerso foram de 469,5±218,28 ppm e 0,19±0,05%, respectivamente. Os resultados obtidos sugerem que as mortes súbitas foram causadas por deficiência de Cu. Três fatores parecem ser responsáveis pela deficiência de Cu: 1) altos teores de Fe na pastagem e na água; 2) ocasionalmente baixos teores de Cu na pastagem; e 3) ingestão de S acima dos requerimentos, devido aos teores ocasionalmente altos na pastagem e na água. O surto descrito é similar a outros surtos de morte súbita em bovinos descritos no sul do Rio Grande do Sul durante o inverno, que foram, também, associados a baixos teores de cobre no fígado. As regiões onde ocorre a enfermidade são caracterizadas por solos arenosos e ácidos com inundações freqüentes durante o inverno. Em solos ácidos periodicamente inundáveis o ferro é solubilizado e absorvido pelas plantas, diminuindo o conteúdo de Cu na forragem e aumentando os teores de Fe. Esta parece ser a maior razão para a deficiência de cobre na região.