PESQUISA VETERINÁRIA BRASILEIRA

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:

ABSTRACT.- Cunha P.H.J., Bandarra P.M., Dias M.M., Borges A.S. & Driemeier D. 2010. [Outbreak of polioencephalomalacia in cattle consuming high sulphur diet in Rio Grande do Sul, Brazil.] Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul. Pesquisa Veterinária Brasileira 30(8):613-617. Departamento de Medicina Veterinária, Escola de Veterinária, Universidade Federal de Goiás, Campus Samambaia, Cx. Postal 131, Goiânia, GO 74001-970, Brazil. E-mail: phcunhavet@yahoo.com.br 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% 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.

• Cerebrocortical necrosis polioencephalomalacia sulphur enxofre necrose cerebrocortical polioencefalomalacia

Abstract in Portuguese:

RESUMO.- Cunha P.H.J., Bandarra P.M., Dias M.M., Borges A.S. & Driemeier D. 2010. [Outbreak of polioencephalomalacia in cattle consuming high sulphur diet in Rio Grande do Sul, Brazil.] Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul. Pesquisa Veterinária Brasileira 30(8):613-617. Departamento de Medicina Veterinária, Escola de Veterinária, Universidade Federal de Goiás, Campus Samambaia, Cx. Postal 131, Goiânia, GO 74001-970, Brazil. E-mail: phcunhavet@yahoo.com.br 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% 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.

Abstract in English:

Abstract.- Raymundo D.L., Pavarini S.P., Bezerra Junior P.S., Antoniassi N.A.B., Brecht, B.S, Gomes M.J.P. & Driemeier D. 2010. [Acute myonecrosis by Clostridium septicum in horses.] Mionecrose aguda por Clostridium septicum em equinos. Pesquisa Veterinária Brasileira 30(8):637-640. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Two cases of acute necrotizing myositis caused by Clostridium septicum in horses are described. Both horses presented swelling of the right pelvic limb extending to the ventral abdominal region. The cut surface of the affected area revealed blood-stained edema and gas bubbles. The skeletal muscles of the caudal region of the thigh of the affect limbs had dark red discolored areas of blood-stained edema and crepitation; the deep musculature was dry. The main histopathological findings were swelling, vacuolation and hyaline and floccular necrosis of skeletal myofibers; in between myofibers there were hemorrhage, edema and large amounts of bacilli. In both cases, C. septicum was isolated from the edema fluid of muscular lesions.

• Clostridium septicum myonecrosis mionecrose

Abstract in Portuguese:

RESUMO.- Raymundo D.L., Pavarini S.P., Bezerra Junior P.S., Antoniassi N.A.B., Brecht, B.S, Gomes M.J.P. & Driemeier D. 2010. [Acute myonecrosis by Clostridium septicum in horses.] Mionecrose aguda por Clostridium septicum em equinos. Pesquisa Veterinária Brasileira 30(8):637-640. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Descrevem-se dois casos de miosite necrosante causada por Clostridium septicum em equinos. Os dois equinos apresentavam aumento de volume no membro pélvico direito e que se estendia para a região abdominal ventral. Ao corte, essa área era formada por edema sanguinolento e bolhas de gás. Os músculos esqueléticos da região caudal da coxa apresentavam áreas vermelho-escuras, crepitantes, com edema sanguinolento e, ao corte, as áreas mais profundas da musculatura tinham aspecto seco. As principais alterações histopatológicas observadas foram tumefação, vacuolização, necrose hialina e necrose flocular de fibras musculares esqueléticas. Entre as fibras, havia hemorragia, edema e grande quantidade de bacilos com tamanho de 3-6µm. Na coloração de Gram, os bacilos se apresentavam roxos (gram-positivos); quando impregnados pela prata (Warthin-Starry), se mostraram enegrecidos. Nos dois casos, C. septicum foi isolado, em ambiente anaeróbio, do líquido de edema das lesões musculares.

Abstract in English:

ABSTRACT.- Soares M.P., Quevedo P.S. & Schild A.L. 2008. [Perreyia flavipes larvae poisoning in cattle in southern Rio Grande do Sul, Brazil.] Intoxicação por larvas de Perreyia flavipes em bovinos na região sul do Rio Grande do Sul. Pesquisa Veterinária Brasileira 28(3):169-173. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, Universidade Federal de Pelotas, Campus Universitário s/n, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br Three outbreaks of poisoning by Perreyia flavipes Konow, 1899 (Hymenoptera: Pergidae) in cattle during July and August 2006 in southern Brazil are reported. The morbidity rate was 0.8%, 6.2% and 33% on the 3 farms, respectively. Fatality rate was 100%. Clinical signs were depression, jaundice, recumbence, pedaling movements and death in 24-48 hours. The liver was enlarged with increased lobular pattern, the mesenteric lymph nodes were edematous and Peyer patches of the small gut were depressed. Petechial hemorrhages and ecchymosis were observed in the mesentery and abomasum. On histologic examination the liver showed centrolobular or massive necrosis. Hemosiderosis and necrosis of the germinative centers of lymph nodes, white pulp of the spleen and Peyer patches were also observed. The poisoning occurred probably due to an intense drought in October-December 2005, when the insect stayed as a cocoon underground. The dry conditions probably avoided a higher number of adult sawflies to emerge from the cocoons, what resulted in greater egg production. The large amount of decaying grass due to almost normal rain fall during summer seemed to have provided favorable environmental conditions for the development of larvae in winter.

• Perreyia flavipes sawfly epidemiology bovine hepatic necrosis

Abstract in Portuguese:

ABSTRACT.- Soares M.P., Quevedo P.S. & Schild A.L. 2008. [Perreyia flavipes larvae poisoning in cattle in southern Rio Grande do Sul, Brazil.] Intoxicação por larvas de Perreyia flavipes em bovinos na região sul do Rio Grande do Sul. Pesquisa Veterinária Brasileira 28(3):169-173. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, Universidade Federal de Pelotas, Campus Universitário s/n, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br Three outbreaks of poisoning by Perreyia flavipes Konow, 1899 (Hymenoptera: Pergidae) in cattle during July and August 2006 in southern Brazil are reported. The morbidity rate was 0.8%, 6.2% and 33% on the 3 farms, respectively. Fatality rate was 100%. Clinical signs were depression, jaundice, recumbence, pedaling movements and death in 24-48 hours. The liver was enlarged with increased lobular pattern, the mesenteric lymph nodes were edematous and Peyer patches of the small gut were depressed. Petechial hemorrhages and ecchymosis were observed in the mesentery and abomasum. On histologic examination the liver showed centrolobular or massive necrosis. Hemosiderosis and necrosis of the germinative centers of lymph nodes, white pulp of the spleen and Peyer patches were also observed. The poisoning occurred probably due to an intense drought in October-December 2005, when the insect stayed as a cocoon underground. The dry conditions probably avoided a higher number of adult sawflies to emerge from the cocoons, what resulted in greater egg production. The large amount of decaying grass due to almost normal rain fall during summer seemed to have provided favorable environmental conditions for the development of larvae in winter.

Abstract in English:

Abstract.- Raymundo D.L., Bezerra Junior P.S., Bandarra P.M., Pedroso P.M.O., Oliveira E.C., Pescador C.A. & Driemeier D. 2008. Spontaneous poisoning by larvae of Perreyia flavipes (Pergidae) in sheep. Pesquisa Veterinária Brasileira 28(1):19-22. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Avenida Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br From a flock of 175 Texel sheep 25 animals died after consumption of a sawfly larvae subsequently identified as Perreyia flavipes. The disease occurred in June-July 2006 on a farm located in the county of Encruzilhada do Sul, Rio Grande do Sul, Brazil. Although there were 11 cattle in the same paddock, none of them was affected. High numbers of compact masses containing up to 150 larvae were scattered in the paddock where the animals were grazing. Most affected sheep showed severe apathy during 24-36 h before death, but weakness, muscular tremors and depression were also observed. Necropsy was performed on six sheep and the main macroscopic lesions were hemor-rhages in the subcutaneous tissues, endocardium, gallbladder wall, and abomasal mucosa. In all animals was found hydrothorax, hydropericardium, ascites, and mild jaundice. Edema in the abomasal folds, mesentery, perirenal tissues, and gallbladder wall were also seen. The livers were yellowish with disseminated pinpoint hemorrhages in the parenchyma and had an enhanced lobular pattern. Perreyia flavipes larval body fragments and heads were found in the forestomach contents of the six sheep. Feces were scant, dry and formed balls coated by mucus and streaks of blood. Similar contents were also present at the end of the cecum. Prominent microscopic lesions included severe and diffuse periacinar or massive necrosis of hepatocytes associated with multifocal random hemorrhages. Diffuse necrosis of lymphoid follicles in lymph nodes and Peyer´s patches, lymphoid depletion and necrosis in germinative centers of the spleen, and diffuse vacuolization in the renal tubular epithelia were also seen.

• Liver necrosis Perreyia flavipes sawfly larval poisoning sheep

Abstract in Portuguese:

Abstract.- Raymundo D.L., Bezerra Junior P.S., Bandarra P.M., Pedroso P.M.O., Oliveira E.C., Pescador C.A. & Driemeier D. 2008. Spontaneous poisoning by larvae of Perreyia flavipes (Pergidae) in sheep. Pesquisa Veterinária Brasileira 28(1):19-22. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Avenida Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br From a flock of 175 Texel sheep 25 animals died after consumption of a sawfly larvae subsequently identified as Perreyia flavipes. The disease occurred in June-July 2006 on a farm located in the county of Encruzilhada do Sul, Rio Grande do Sul, Brazil. Although there were 11 cattle in the same paddock, none of them was affected. High numbers of compact masses containing up to 150 larvae were scattered in the paddock where the animals were grazing. Most affected sheep showed severe apathy during 24-36 h before death, but weakness, muscular tremors and depression were also observed. Necropsy was performed on six sheep and the main macroscopic lesions were hemor-rhages in the subcutaneous tissues, endocardium, gallbladder wall, and abomasal mucosa. In all animals was found hydrothorax, hydropericardium, ascites, and mild jaundice. Edema in the abomasal folds, mesentery, perirenal tissues, and gallbladder wall were also seen. The livers were yellowish with disseminated pinpoint hemorrhages in the parenchyma and had an enhanced lobular pattern. Perreyia flavipes larval body fragments and heads were found in the forestomach contents of the six sheep. Feces were scant, dry and formed balls coated by mucus and streaks of blood. Similar contents were also present at the end of the cecum. Prominent microscopic lesions included severe and diffuse periacinar or massive necrosis of hepatocytes associated with multifocal random hemorrhages. Diffuse necrosis of lymphoid follicles in lymph nodes and Peyer´s patches, lymphoid depletion and necrosis in germinative centers of the spleen, and diffuse vacuolization in the renal tubular epithelia were also seen.

Abstract in English:

ABSTRACT.- Domingues-F.L.M., Ferreira J., Lopes F.M., Tymoszczenko A. & Gioso M.A. 2007. The effect of timing temporary cements to treat induced pulp necrosis in the teeth of dogs. Revista Pesquisa Veterinária Brasileira 27(2):85-88. Departamento de Cirurgia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando de Marques de Paiva 87, Bloco 8-superior, Cidade Universitária, São Paulo, SP 05508-000, Brazil. E-mail: lesliedf@usp.br During endodontic therapy (pulpectomy, root canal debridement and root canal filling) microbiological management is a major concern. Bacteria present in dentine tubules, apical foramina and apical delta are causally related to failure of the procedure. Studies have shown that during single session endodontic treatment bacteria remain within dental structures. The aim of the present study was to evaluate endodontic treatment performed as two sessions, using temporary endodontic dressing materials for different periods in four groups of experimental dogs. A total of 80 roots of second and third upper premolar teeth and second, third and fourth lower premolar teeth were divided into four groups. The pulp chamber was opened with burrs and the pulp exposed for 60 days to induce pulpal inflammation and necrosis. Groups II, III and IV were treated with calcium hydroxide plus camphorated paramono-chlorophenol (PMCC) for 7, 15 and 30 days, respectively. In all groups, the root canals were filled with zinc oxide-eugenol and gutta-percha cones. Clinical and radiographical measurements were performed every 2 weeks. After 60 days a small block section containing the teeth, surrounding periapical tissues and the periodontium was removed for histological and microbiological study. Histological analysis revealed intense inflammatory response in all groups. Microbiological analysis showed microbial reduction inversely proportional to the period of time that the intracanal temporary medicament was left in place.

• Apical delta endodontic gutta-percha camphorated paramonochlorophenol microorganisms dogs

Abstract in Portuguese:

ABSTRACT.- Domingues-F.L.M., Ferreira J., Lopes F.M., Tymoszczenko A. & Gioso M.A. 2007. The effect of timing temporary cements to treat induced pulp necrosis in the teeth of dogs. Revista Pesquisa Veterinária Brasileira 27(2):85-88. Departamento de Cirurgia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando de Marques de Paiva 87, Bloco 8-superior, Cidade Universitária, São Paulo, SP 05508-000, Brazil. E-mail: lesliedf@usp.br During endodontic therapy (pulpectomy, root canal debridement and root canal filling) microbiological management is a major concern. Bacteria present in dentine tubules, apical foramina and apical delta are causally related to failure of the procedure. Studies have shown that during single session endodontic treatment bacteria remain within dental structures. The aim of the present study was to evaluate endodontic treatment performed as two sessions, using temporary endodontic dressing materials for different periods in four groups of experimental dogs. A total of 80 roots of second and third upper premolar teeth and second, third and fourth lower premolar teeth were divided into four groups. The pulp chamber was opened with burrs and the pulp exposed for 60 days to induce pulpal inflammation and necrosis. Groups II, III and IV were treated with calcium hydroxide plus camphorated paramono-chlorophenol (PMCC) for 7, 15 and 30 days, respectively. In all groups, the root canals were filled with zinc oxide-eugenol and gutta-percha cones. Clinical and radiographical measurements were performed every 2 weeks. After 60 days a small block section containing the teeth, surrounding periapical tissues and the periodontium was removed for histological and microbiological study. Histological analysis revealed intense inflammatory response in all groups. Microbiological analysis showed microbial reduction inversely proportional to the period of time that the intracanal temporary medicament was left in place.

Abstract in English:

Amorim S.L., Oliveira A.C.P., Riet-Correa F., Simões S.V.D., Medeiros R.M.T. & Clementino I.J. 2005. [Nutritional muscular dystrophy in sheep in Paraíba.] Distrofia muscular nutricional em ovinos na Paraíba. Pesquisa Veterinária Brasileira 25(2):120-124. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB Brazil. E-mail: riet@cstr.ufcg.edu.br 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.

• Nutritional muscular dystrophy muscular segmental necrosis selenium and vitamine E deficiency sheep.

Abstract in Portuguese:

Amorim S.L., Oliveira A.C.P., Riet-Correa F., Simões S.V.D., Medeiros R.M.T. & Clementino I.J. 2005. [Nutritional muscular dystrophy in sheep in Paraíba.] Distrofia muscular nutricional em ovinos na Paraíba. Pesquisa Veterinária Brasileira 25(2):120-124. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB Brazil. E-mail: riet@cstr.ufcg.edu.br 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.

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:

Traverso S.D., Correa A.M.R., Schmitz M., Colodel E.M. & Driemeier D. 2004 [Experimental poisoning by Trema micrantha (Ulmaceae) in cattle.] Intoxicação experi-mental por Trema micrantha (Ulmaceae) em bovinos. Pesquisa Veterinária Brasileira 24(4):211-216. Setor de Patologia Veterinária, Depto Patologia Clínica Veterinária, Faculdade de Veteriná-ria, UFRGS, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@vortex.ufrgs.br Leaves of Trema micrantha were orally given to 13 cattle. Ten animals received green leaves in a single dose, two animals received green leaves in fractionated doses, and one received the dried leaves in a single dose. Eight animals showed clinical signs and six of them died. Clinical signs were observed 16 hours after administration and included apathy, anorexia, drooling, progressive weakness, coma and death. Neurological signs as pressing the head against obstacles and head shaking were observed in four animals . Death occurred between 67 and 153 hours after the end of plant ingestion. The main gross lesions were observed in the liver, and included friable consistency, pronounced lobular pattern and areas of haemorrhages. The liver of one bovine was homogeneously dark reddened. Petechial hemorrhages in serosal membranes and edema in the gall bladder were frequently seen. Pale kidneys with red spots in the cortex were observed in one animal. Microscopically, the most striking lesion in the liver was massive coagulative necrosis, associated with centrolobular haemorrhages, observed in four animals. In the liver of one bovine centrolobular necrosis was observed . Tubular renal necrosis was noted in two animals. Additional microscopic lesions were found in the central nervous system of five bovines, especially in the frontal cortex, and included perineuronal and perivascular edema with basophilia and retraction of the neurons. T T. micrantha caused clinical signs with 50g/kg and death with doses of 54g/kg or higher. The fractionated administration of the green leaves as well as the dried leaves did not cause poisoning.

• Poisonous plants plant poisoning Trema micrantha Ulmaceae cattle liver necrosis.

Abstract in Portuguese:

Traverso S.D., Correa A.M.R., Schmitz M., Colodel E.M. & Driemeier D. 2004 [Experimental poisoning by Trema micrantha (Ulmaceae) in cattle.] Intoxicação experi-mental por Trema micrantha (Ulmaceae) em bovinos. Pesquisa Veterinária Brasileira 24(4):211-216. Setor de Patologia Veterinária, Depto Patologia Clínica Veterinária, Faculdade de Veteriná-ria, UFRGS, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@vortex.ufrgs.br Leaves of Trema micrantha were orally given to 13 cattle. Ten animals received green leaves in a single dose, two animals received green leaves in fractionated doses, and one received the dried leaves in a single dose. Eight animals showed clinical signs and six of them died. Clinical signs were observed 16 hours after administration and included apathy, anorexia, drooling, progressive weakness, coma and death. Neurological signs as pressing the head against obstacles and head shaking were observed in four animals . Death occurred between 67 and 153 hours after the end of plant ingestion. The main gross lesions were observed in the liver, and included friable consistency, pronounced lobular pattern and areas of haemorrhages. The liver of one bovine was homogeneously dark reddened. Petechial hemorrhages in serosal membranes and edema in the gall bladder were frequently seen. Pale kidneys with red spots in the cortex were observed in one animal. Microscopically, the most striking lesion in the liver was massive coagulative necrosis, associated with centrolobular haemorrhages, observed in four animals. In the liver of one bovine centrolobular necrosis was observed . Tubular renal necrosis was noted in two animals. Additional microscopic lesions were found in the central nervous system of five bovines, especially in the frontal cortex, and included perineuronal and perivascular edema with basophilia and retraction of the neurons. T T. micrantha caused clinical signs with 50g/kg and death with doses of 54g/kg or higher. The fractionated administration of the green leaves as well as the dried leaves did not cause poisoning.

Abstract in English:

Cattani C.S.O., Colodel E.M., Traverso S.D., Correa A.M.R., & Driemeier D. 2004. [Experimental poisoning by Dodonea viscosa (Sapindaceae) in cattle.] Intoxicação experimental por Dodonea viscosa (Sapindaceae) em bovinos. Pesquisa Veterinária Brasileira 24(1):31-34. Depto Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Bairro Agronomia, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. E-mail: moleta@terra.com.br The leaves of Dodonea viscosa were force fed to five bovines. Four received the leaves in fresh green stage and the fifth dried ones. Clinical signs were observed in four of the bovines that died; the fifth did not show signs of poisoning. The fresh green plant was proved to be toxic from a dose of 25g/kg on. Dried leaves fed at the dose of 30 g/kg were also toxic. All the animals that died showed clinical signs from 13h30min to 45h after the ingestion of the plant and and death followed within about 48h. The clinical course lasted for about 8h30min until death. The main symptoms where apathy, anorexia, slight tenesmus, muscle trembling, difficulties to keep consciousness, pressing the head against obstacles, lateral recumbency, paddling movements, coma and death. The most significant macroscopic alterations were observed in the liver, with accentuation of the lobular pattern, dark-red areas interspersed with yellowish areas. Petechiae were found in serosal membranes of the abdominal and thoracic organs as well as the intestines. The main microscopic change was hepatic centrolobular coagulative necrosis, associated with congestion and hemorrhages.

• Dodonea viscosa diseases of cattle plant poisoning hepatocellular necrosis.

Abstract in Portuguese:

Cattani C.S.O., Colodel E.M., Traverso S.D., Correa A.M.R., & Driemeier D. 2004. [Experimental poisoning by Dodonea viscosa (Sapindaceae) in cattle.] Intoxicação experimental por Dodonea viscosa (Sapindaceae) em bovinos. Pesquisa Veterinária Brasileira 24(1):31-34. Depto Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Bairro Agronomia, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. E-mail: moleta@terra.com.br The leaves of Dodonea viscosa were force fed to five bovines. Four received the leaves in fresh green stage and the fifth dried ones. Clinical signs were observed in four of the bovines that died; the fifth did not show signs of poisoning. The fresh green plant was proved to be toxic from a dose of 25g/kg on. Dried leaves fed at the dose of 30 g/kg were also toxic. All the animals that died showed clinical signs from 13h30min to 45h after the ingestion of the plant and and death followed within about 48h. The clinical course lasted for about 8h30min until death. The main symptoms where apathy, anorexia, slight tenesmus, muscle trembling, difficulties to keep consciousness, pressing the head against obstacles, lateral recumbency, paddling movements, coma and death. The most significant macroscopic alterations were observed in the liver, with accentuation of the lobular pattern, dark-red areas interspersed with yellowish areas. Petechiae were found in serosal membranes of the abdominal and thoracic organs as well as the intestines. The main microscopic change was hepatic centrolobular coagulative necrosis, associated with congestion and hemorrhages.