RESUMO

Background: Polioencephalomalacia (PEM) is a neurological disease in ruminants, which is characterized by malacia of brain gray matter. Thiamine deficiency and sulfur intoxication are the most common causes of PEM in sheep. Affected animals present signs of cerebrocortical syndrome, including amaurosis, ataxia, head pressing, mental depression, seizures, and opisthotonus. The neurological examination aims to determine the neurolocalization of the lesions and advanced imaging techniques are useful for confirming the affected area(s) in the central nervous system. The aim of this study is to describe clinical features and ante-mortem diagnosis using magnetic resonance imaging (MRI) in a sheep with PEM. Case: A 18-month-old male Dorper sheep from a flock started receiving concentrate 7 days before. According to the owner, no clinical signs of abnormality were observed on the previous morning. However, in the afternoon, the animal became selfisolated and did not follow the flock to the sheepfold. The following day, he was found in recumbency. Physical examination revealed lateral recumbency, rectal temperature 39.5ºC, 52 bpm, 120 bpm, congested mucous membranes, capillary refill time 1 s, ruminal (4/5 min) and intestinal hypomotility. The assessment of the central nervous system revealed a decreased level of consciousness, focal seizures, opisthotonus, and absence of menace response. The following differential diagnoses were listed: PEM, head trauma, focal symmetrical encephalomalacia, bacterial encephalitis, and rabies. Treatment was composed of dexamethasone [0.2 mg/kg - i.v., SID (1st-3rd day), 0.1 mg/kg, i.v., SID (4th-6th day), and 0.05 mg/kg, i.v., SID (7th-9th day)]; mannitol [1 g/kg - i.v. and diazepam 0.4 mg/kg, i.v. single dose at admission]; vitamin B1 [10 mg/kg - i.m., SID], furosemide [1 mg/kg - i.v., SID for 3 days] and sulfadoxine/trimethoprim [30 mg/kg - i.m., SID for 10 days]. After the initial treatment, the patient showed mild clinical improvement; however, the amaurosis was still present. Magnetic resonance imaging of the brain was performed on the 2nd day of hospitalization, showing a symmetrical hypersignal in the parietal and occipital cortices, in the axial and sagittal sequences weighted in T2 and FLAIR. Discussion: This study aimed to describe the clinical signs and MRI findings in a sheep with PEM. In this case, the sudden change to the feed composition probably led to ruminal dysbiosis, inhibition of thiamine-producing microorganisms and proliferation of bacteria that synthesize thiaminase. Thiamine therapy proved to be effective and capable of reverting the clinical signs. The decrease in the level of consciousness, cortical blindness, and opisthotonus are due to alterations in the parietal cortex, in the occipital cortex, and in the cerebellum, respectively, which were demonstrated by hypersignal areas in the MRI. Therefore, the neurolocalization of the lesion based on neurologic examination and the MRI findings were related. The physicochemical and cytological evaluations of the cerebrospinal fluid, and dosage of thiamine and the concentration of hydrogen sulphide in the rumen were not performed. However, the response to thiamine treatment associated with the neurologic examination and MRI findings helped in determining the diagnosis. Additionally, MRI can be used as a useful tool for the ante mortem diagnosis of PEM.

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RESUMO

Background: Perinatal mortality in sheep is determined by death between 60 days of gestation and 28 days postpartum. The starvation / hypothermia complex was characterized by lambs that walked, but did not feed. Polioencephalomalacia (PEM) is a descriptive term that indicates the morphological diagnosis for necrosis with softening of the gray matter in the brain. There are no data available in the literature relating PEM to the starvation / hypoglycemia / hypothermia complex in small ruminants. Thus, the objective of this work is to report a case of polyioencephalomalacia related to the starvation / hypoglycemia / hypothermia and septicemia complex in a newborn sheep. Case: A 5-day-old sheep female mixed race (Dorper x Santa Inês), 3.0 kg, from a rural property in the Federal District, was sent to the Veterinary Pathology Laboratory of the University of Brasília, for a necropsy. Organ fragments were collected and fixed in a 10 % buffered formalin solution, routinely processed for histology and stained with Hematoxylin and Eosin (HE). Additionally, swabs from the meninges, eyeballs and navels were collected for bacteriology. The animal came from twin pregnancies and was weak since birth. With three days of life, it presented apathy, weakness, difficulty in breastfeeding, difficulty in walking, and decubitus in a self-auscultation position. After 2 days of evolution the lamb died. Macroscopically, eyeball opacity, omphalophlebitis and congested brain were observed. Microscopically in the frontal cortex, the leptomeninge was markedly thickened by a large number of neutrophils and, to a lesser extent, macrophages, lymphocytes and plasmocytes, associated with aggregates of free eosinophilic rods or in the cytoplasm of macrophages. In the underlying gray substance, the neurópilo was observed containing...(AU)

Assuntos

RESUMO

Background: Perinatal mortality in sheep is determined by death between 60 days of gestation and 28 days postpartum. The starvation / hypothermia complex was characterized by lambs that walked, but did not feed. Polioencephalomalacia (PEM) is a descriptive term that indicates the morphological diagnosis for necrosis with softening of the gray matter in the brain. There are no data available in the literature relating PEM to the starvation / hypoglycemia / hypothermia complex in small ruminants. Thus, the objective of this work is to report a case of polyioencephalomalacia related to the starvation / hypoglycemia / hypothermia and septicemia complex in a newborn sheep. Case: A 5-day-old sheep female mixed race (Dorper x Santa Inês), 3.0 kg, from a rural property in the Federal District, was sent to the Veterinary Pathology Laboratory of the University of Brasília, for a necropsy. Organ fragments were collected and fixed in a 10 % buffered formalin solution, routinely processed for histology and stained with Hematoxylin and Eosin (HE). Additionally, swabs from the meninges, eyeballs and navels were collected for bacteriology. The animal came from twin pregnancies and was weak since birth. With three days of life, it presented apathy, weakness, difficulty in breastfeeding, difficulty in walking, and decubitus in a self-auscultation position. After 2 days of evolution the lamb died. Macroscopically, eyeball opacity, omphalophlebitis and congested brain were observed. Microscopically in the frontal cortex, the leptomeninge was markedly thickened by a large number of neutrophils and, to a lesser extent, macrophages, lymphocytes and plasmocytes, associated with aggregates of free eosinophilic rods or in the cytoplasm of macrophages. In the underlying gray substance, the neurópilo was observed containing...

Assuntos

RESUMO

The present study aimed to describe epidemiological, clinical, laboratorial, and pathological findings of polioencephalomalacia (PEM) in ruminants from the semi-arid region of Rio Grande do Norte, Brazil. A total of seven ruminants (five sheep, one cattle, and one goat) with pathological diagnosis of PEM were included. Four cases were associated with thiamine deficiency, on account of chronic ruminal acidosis caused by diets rich in carbohydrate, with mainly concentrates, ground soybean hulls, and melon. Three ruminants from an outbreak of petroleum poisoning presented macro and microscopic lesions consistent with changes of malacia and edema in deep structures of the brain, as described in ruminants with PEM associated with sulfur intoxication. Major macroscopic changes included congestion of cerebral vessels, edema, and herniation of the cerebellum. The most observed microscopic lesions, among all assessed cases, were laminar and segmental neuronal necrosis at different regions of the brain, spongiosis, nuclear pyknosis, and red nucleus neurons. Cerebrospinal fluid analysis revealed nonspecific alterations, requiring its association with epidemiological, clinical, and pathological findings, as the results described here are similar to those reported in toxic diseases with neurological manifestations, such as botulism.

O presente trabalho objetiva descrever os achados epidemiológicos, clínicos, laboratoriais e patológicos de casos de polioencefalomalácia (PEM) em ruminantes na região semiárida do Rio Grande do Norte. Sete ruminantes (cinco ovinos, um bovino e um caprino) com diagnóstico patológico de PEM foram incluídos. Quatro casos foram associados à deficiência de tiamina devido acidose láctica ruminal crônica por oferta de alimentação rica em carboidratos, destacando-se os concentrados, casca de soja triturada e melão. Três ruminantes de um surto de intoxicação por petróleo apresentaram lesões macro e microscópicas condizentes com alterações de malácia e edema em estruturas profundas do encéfalo, descritas em ruminantes com PEM associada à intoxicação por enxofre. As principais alterações macroscópicas incluíram congestão dos vasos cerebrais, edema e conificação do cerebelo. Em todos os casos avaliados, as lesões microscópicas mais observadas foram a necrose neuronal laminar e segmentar em diferentes regiões do encéfalo, espongiose, picnose nuclear e a presença de neurônios vermelhos. A análise do líquido cefalorraquidiano revelou alterações inespecíficas, sendo necessário sua associação aos achados epidemiológicos, clínicos e patológicos, pois os resultados aqui descritos são semelhantes aos relatados em doenças tóxicas com manifestações neurológicas, como o botulismo.

Assuntos

RESUMO

The present study aimed to describe epidemiological, clinical, laboratorial, and pathological findings of polioencephalomalacia (PEM) in ruminants from the semi-arid region of Rio Grande do Norte, Brazil. A total of seven ruminants (five sheep, one cattle, and one goat) with pathological diagnosis of PEM were included. Four cases were associated with thiamine deficiency, on account of chronic ruminal acidosis caused by diets rich in carbohydrate, with mainly concentrates, ground soybean hulls, and melon. Three ruminants from an outbreak of petroleum poisoning presented macro and microscopic lesions consistent with changes of malacia and edema in deep structures of the brain, as described in ruminants with PEM associated with sulfur intoxication. Major macroscopic changes included congestion of cerebral vessels, edema, and herniation of the cerebellum. The most observed microscopic lesions, among all assessed cases, were laminar and segmental neuronal necrosis at different regions of the brain, spongiosis, nuclear pyknosis, and red nucleus neurons. Cerebrospinal fluid analysis revealed nonspecific alterations, requiring its association with epidemiological, clinical, and pathological findings, as the results described here are similar to those reported in toxic diseases with neurological manifestations, such as botulism.(AU)

O presente trabalho objetiva descrever os achados epidemiológicos, clínicos, laboratoriais e patológicos de casos de polioencefalomalácia (PEM) em ruminantes na região semiárida do Rio Grande do Norte. Sete ruminantes (cinco ovinos, um bovino e um caprino) com diagnóstico patológico de PEM foram incluídos. Quatro casos foram associados à deficiência de tiamina devido acidose láctica ruminal crônica por oferta de alimentação rica em carboidratos, destacando-se os concentrados, casca de soja triturada e melão. Três ruminantes de um surto de intoxicação por petróleo apresentaram lesões macro e microscópicas condizentes com alterações de malácia e edema em estruturas profundas do encéfalo, descritas em ruminantes com PEM associada à intoxicação por enxofre. As principais alterações macroscópicas incluíram congestão dos vasos cerebrais, edema e conificação do cerebelo. Em todos os casos avaliados, as lesões microscópicas mais observadas foram a necrose neuronal laminar e segmentar em diferentes regiões do encéfalo, espongiose, picnose nuclear e a presença de neurônios vermelhos. A análise do líquido cefalorraquidiano revelou alterações inespecíficas, sendo necessário sua associação aos achados epidemiológicos, clínicos e patológicos, pois os resultados aqui descritos são semelhantes aos relatados em doenças tóxicas com manifestações neurológicas, como o botulismo.(AU)

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RESUMO

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.

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.

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RESUMO

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.(AU)

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.(AU)

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RESUMO

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.

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.

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RESUMO

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.(AU)

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.(AU)

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RESUMO

Neste trabalho descreve-se surto de polioencefalomalacia em bovinos decorrente da ingestão de dieta com excessiva concentração de enxofre em uma propriedade no Rio Grande do Sul. O lote era composto por 30 bezerros, mantidos em um piquete com azevém (Lolium multiflorum) e suplementados com ração e sal mineral. Seis bezerros morreram e dois deles foram necropsiados; amostras de tecido hepático para dosagem de chumbo e fragmentos do sistema nervoso central para histopatológico foram colhidos. Um dos bezerros foi examinado antes da morte e sinais neurológicos encefálicos foram constatados. Foi estabelecido o teor de enxofre nos componentes da dieta e água, a produção de sulfeto de hidrogênio ruminal em cinco bovinos do mesmo lote e realizada PCR de um bloco de parafina para detecção de DNA do herpevirus bovino tipo 5. O consumo total de enxofre foi de 0,38 por cento da matéria seca fornecida aos animais e as dosagens de sulfeto de hidrogênio ruminal em animais do mesmo lote variaram de 1.000 a 2.500ppm. Os achados histopatológicos indicaram necrose laminar do córtex cerebral. Não foi detectado chumbo na amostra de tecido hepático e não foi identificado DNA do herpesvirus bovino tipo 5 no encéfalo. O quadro clínico de síndrome cerebrocortical associado aos elevados valores do sulfeto de hidrogênio ruminal, alta ingestão de enxofre na dieta e os achados histopatológicos permitem estabelecer o excesso de enxofre como causador da polioencefalomalacia.

An outbreak of polioencephalomalacia in cattle caused by ingestion of high sulphur diet, in Rio Grande do Sul, Brazil is described. One group of 30 calves was kept in Italian ryegrass (Lolium multiflorum) pasture and supplemented with concentrate and minerals. Six calves died, necropsy was performed in two of them and liver samples (for lead determination) and fragments of central nervous system were collected. Clinical and neurological examination was performed in one calf and confirmed brain involvement. Sulphur content on dietary components and water, ruminal hydrogen sulfide production in five calves of the same group and PCR from formalin-fixed paraffin-embedded cerebral tissues to detect bovine herpesvirus 5 DNA was perfomed. The total sulphur intake was 0.38 percent dry matter and the values of ruminal sulfide concentration ranged from 1,000 to 2,500ppm. Lead It was not detected in the liver samples and PCR was negative for bovine herpesvirus 5. The brain lesions were characterized by laminar neuronal necrosis. The clinical signs of cerebrocortical syndrome associated with high ruminal sulfide values, elevated intake of dietary sulphur and histological lesions confirmed that the excess of sulphur caused the polioencephalomacia in these calves.

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RESUMO

Neste trabalho descreve-se surto de polioencefalomalacia em bovinos decorrente da ingestão de dieta com excessiva concentração de enxofre em uma propriedade no Rio Grande do Sul. O lote era composto por 30 bezerros, mantidos em um piquete com azevém (Lolium multiflorum) e suplementados com ração e sal mineral. Seis bezerros morreram e dois deles foram necropsiados; amostras de tecido hepático para dosagem de chumbo e fragmentos do sistema nervoso central para histopatológico foram colhidos. Um dos bezerros foi examinado antes da morte e sinais neurológicos encefálicos foram constatados. Foi estabelecido o teor de enxofre nos componentes da dieta e água, a produção de sulfeto de hidrogênio ruminal em cinco bovinos do mesmo lote e realizada PCR de um bloco de parafina para detecção de DNA do herpevirus bovino tipo 5. O consumo total de enxofre foi de 0,38 por cento da matéria seca fornecida aos animais e as dosagens de sulfeto de hidrogênio ruminal em animais do mesmo lote variaram de 1.000 a 2.500ppm. Os achados histopatológicos indicaram necrose laminar do córtex cerebral. Não foi detectado chumbo na amostra de tecido hepático e não foi identificado DNA do herpesvirus bovino tipo 5 no encéfalo. O quadro clínico de síndrome cerebrocortical associado aos elevados valores do sulfeto de hidrogênio ruminal, alta ingestão de enxofre na dieta e os achados histopatológicos permitem estabelecer o excesso de enxofre como causador da polioencefalomalacia.(AU)

An outbreak of polioencephalomalacia in cattle caused by ingestion of high sulphur diet, in Rio Grande do Sul, Brazil is described. One group of 30 calves was kept in Italian ryegrass (Lolium multiflorum) pasture and supplemented with concentrate and minerals. Six calves died, necropsy was performed in two of them and liver samples (for lead determination) and fragments of central nervous system were collected. Clinical and neurological examination was performed in one calf and confirmed brain involvement. Sulphur content on dietary components and water, ruminal hydrogen sulfide production in five calves of the same group and PCR from formalin-fixed paraffin-embedded cerebral tissues to detect bovine herpesvirus 5 DNA was perfomed. The total sulphur intake was 0.38 percent dry matter and the values of ruminal sulfide concentration ranged from 1,000 to 2,500ppm. Lead It was not detected in the liver samples and PCR was negative for bovine herpesvirus 5. The brain lesions were characterized by laminar neuronal necrosis. The clinical signs of cerebrocortical syndrome associated with high ruminal sulfide values, elevated intake of dietary sulphur and histological lesions confirmed that the excess of sulphur caused the polioencephalomacia in these calves.(AU)

Assuntos