PESQUISA VETERINÁRIA BRASILEIRA

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:

Nobre V.M.T., Riet-Correa F., Barbosa Filho J.M., Dantas A.F.M., Tabosa I.M. & Vasconcelos J.S. 2004. [Poisoning by Crotalaria retusa (Fabaceae) in Equidae in the semiarid region of Paraíba.] Intoxicação por Crotalaria retusa (Fabaceae) em eqüídeos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 24(3):132-143. Depto Clínicas Veteri-nárias, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: verônica.nobre@uol.com.br From 2000 to 2003 eight cases of poisoning by Crotalaria retusa L. were observed in horses on 8 farms in the semiarid region of Paraíba and Ceará. C. retusa was found in all farms. The main clinical signs were characteristic of hepatic encephalopathy, with dullness or hyperexcitability, head pressing, compulsive walking or circling and, occasionally, violent uncontrollable galloping. Decreased cranial nerve reflexes, ataxia and weakness were also observed. Other clinical signs were anorexia, weight loss, photosensitization and jaundice. The clinical manifestation period varied from 4 to 40 days, but most horses had a previous history of weight loss. At necropsy the livers were hard, with irregular surface and white areas mixed with dark red areas and increased lobular pattern. Mild jaundice, ascitis, hydropericardium and hydrothorax were also observed. Edema and moderate congestion were seen in the lungs. Histologic changes of the liver were characterized by fibrosis, mainly periportal, megalocitosis and bile duct cell proliferation. Multifocal areas of centrilobular or midzonal hemorrhages were also observed. Centrilobular hemorrhagic necrosis was present in two horses. Alzheimer type II astrocytes were observed, isolated or in groups, mainly in the caudate nucleus and cortex in 4 horses. The poisoning was experimentally produced in 1 adult horse and 3 adult donkeys. The horse received daily 100 g of C. retusa seeds and died 52 days after the beginning of the experiment. The dried whole C. retusa was mixed with grass and given to the 3 experimental donkeys at daily doses of 10g/kg, 5g/kg and 2.5g/kg, respectively. The donkey treated with 5g per kg died 48 days after beginning of the experiment and the other two were sacrificed at 120 days. Clinical signs and pathology were similar to those observed in spontaneous cases, but Alhzeimer type II astrocytes were observed only in the donkey that died 48 days after the beginning of ingestion of the plant material. The concentration of monocrotaline in the whole plant given to the donkeys was 0.5%.

• Poisonous plants plant poisoning Crotalaria retusa Fabaceae hepatic cirrhosis horse pirrolizidine alkaloids.

Abstract in Portuguese:

Nobre V.M.T., Riet-Correa F., Barbosa Filho J.M., Dantas A.F.M., Tabosa I.M. & Vasconcelos J.S. 2004. [Poisoning by Crotalaria retusa (Fabaceae) in Equidae in the semiarid region of Paraíba.] Intoxicação por Crotalaria retusa (Fabaceae) em eqüídeos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 24(3):132-143. Depto Clínicas Veteri-nárias, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: verônica.nobre@uol.com.br From 2000 to 2003 eight cases of poisoning by Crotalaria retusa L. were observed in horses on 8 farms in the semiarid region of Paraíba and Ceará. C. retusa was found in all farms. The main clinical signs were characteristic of hepatic encephalopathy, with dullness or hyperexcitability, head pressing, compulsive walking or circling and, occasionally, violent uncontrollable galloping. Decreased cranial nerve reflexes, ataxia and weakness were also observed. Other clinical signs were anorexia, weight loss, photosensitization and jaundice. The clinical manifestation period varied from 4 to 40 days, but most horses had a previous history of weight loss. At necropsy the livers were hard, with irregular surface and white areas mixed with dark red areas and increased lobular pattern. Mild jaundice, ascitis, hydropericardium and hydrothorax were also observed. Edema and moderate congestion were seen in the lungs. Histologic changes of the liver were characterized by fibrosis, mainly periportal, megalocitosis and bile duct cell proliferation. Multifocal areas of centrilobular or midzonal hemorrhages were also observed. Centrilobular hemorrhagic necrosis was present in two horses. Alzheimer type II astrocytes were observed, isolated or in groups, mainly in the caudate nucleus and cortex in 4 horses. The poisoning was experimentally produced in 1 adult horse and 3 adult donkeys. The horse received daily 100 g of C. retusa seeds and died 52 days after the beginning of the experiment. The dried whole C. retusa was mixed with grass and given to the 3 experimental donkeys at daily doses of 10g/kg, 5g/kg and 2.5g/kg, respectively. The donkey treated with 5g per kg died 48 days after beginning of the experiment and the other two were sacrificed at 120 days. Clinical signs and pathology were similar to those observed in spontaneous cases, but Alhzeimer type II astrocytes were observed only in the donkey that died 48 days after the beginning of ingestion of the plant material. The concentration of monocrotaline in the whole plant given to the donkeys was 0.5%.