PESQUISA VETERINÁRIA BRASILEIRA

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:

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%.

Abstract in English:

Faccini J.L.H., Santos A.C.G. & Bechara G.H. 2004. [Bovine demodicosis in the state of Paraíba, northeastern Brazil.] Demodicose bovina no Estado da Paraíba. Pesquisa Veterinária Brasileira 24(3):149-152. Depto Parasitologia Animal, Instituto de Veterinária, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ 23890-000, Brazil. E-mail: faccini@ufrrj.br Cases of bovine demodicosis caused by Demodex bovis were reported in a Sindhi herd from December 1989 to January 1992. Both localized and generalized forms were diagnosed. This is the first report of the generalized form in Brazil. In the first two years, demodicosis was diagnosed only in cattle < 2 years old, whereas animals of all ages were positive in the last two years. Prevalence varied from 20.4% (11/54) to 53.1% (26/49) and 13.2% (12/91) to 14.8% (9/61) for cattle < 2 years old and > 2 years old, respectively. Clinical signs varied from a few small nodules to a thickened skin with soft large nodules in the localized and generalized forms, respectively. Main microscopic features of the nodules in the generalized form consisted of acanthosis with hyperqueratosis, chronic sebaceous adenitis, subcutaneous muscular necrosis, focal cellular degeneration of the epidermis basal layer and presence of large number of mites inside the lumen of dilated hair follicles. In addition, a chronic perifoliculitis was observed, characterized by lymphoplasmocytic infiltrate which also contained macrophages and neutrophils. It is suggested that poor nutrition and stress due to prolonged drought probably contributed to the increase of susceptibility of the herd to mite infestation.

• Demodex bovis demodicosis cattle pathology Brazil.

Abstract in Portuguese:

Faccini J.L.H., Santos A.C.G. & Bechara G.H. 2004. [Bovine demodicosis in the state of Paraíba, northeastern Brazil.] Demodicose bovina no Estado da Paraíba. Pesquisa Veterinária Brasileira 24(3):149-152. Depto Parasitologia Animal, Instituto de Veterinária, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ 23890-000, Brazil. E-mail: faccini@ufrrj.br Cases of bovine demodicosis caused by Demodex bovis were reported in a Sindhi herd from December 1989 to January 1992. Both localized and generalized forms were diagnosed. This is the first report of the generalized form in Brazil. In the first two years, demodicosis was diagnosed only in cattle < 2 years old, whereas animals of all ages were positive in the last two years. Prevalence varied from 20.4% (11/54) to 53.1% (26/49) and 13.2% (12/91) to 14.8% (9/61) for cattle < 2 years old and > 2 years old, respectively. Clinical signs varied from a few small nodules to a thickened skin with soft large nodules in the localized and generalized forms, respectively. Main microscopic features of the nodules in the generalized form consisted of acanthosis with hyperqueratosis, chronic sebaceous adenitis, subcutaneous muscular necrosis, focal cellular degeneration of the epidermis basal layer and presence of large number of mites inside the lumen of dilated hair follicles. In addition, a chronic perifoliculitis was observed, characterized by lymphoplasmocytic infiltrate which also contained macrophages and neutrophils. It is suggested that poor nutrition and stress due to prolonged drought probably contributed to the increase of susceptibility of the herd to mite infestation.

Abstract in English:

ABSTRACT.- Medeiros R.M.T., Riet-Correa F., Tabosa I.M., Silva Z.A., Barbosa R.C., Marques A.V.M.S. & Nogueira F.R.B. 2003. [Nitrate and nitrite poisoning in cattle caused by the ingestion of Echinochloa polystachya and Pennisetum purpureum in the semiarid region of the state of Paraíba.] Intoxicação por nitratos e nitritos em bovinos por ingestão de Echinochloa polystachya (capim-mandante) e Pennisetum purpureum (capim-elefante) no sertão da Paraíba. Pesquisa Veterinária Brasileira 23(1):17-20. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: rmtmed@cstr.ufpb.br Three outbreaks ofnitrate poisoning are reported from the semiarid region ofthe state of Paràíba, northeastem Brazil. One outbreak caused by Echinochloa polystachya (capim-mandante) and two others caused by Pennisetum purpureum (capim-elefante) occurred at the end ofthe dry season, after the first raios. ln one ofthe outbreaks caused by Pennisetum purpureum part of the pasture had been fertilized with cattle manure. Five out of 11 cattle died on one farm, 27 out of81 on another, and 3 out of9 on a third one. Clinicai sigos were anorexia, respiratory distress, teeth grinding, depression or hyperexitability, tremors, abdominal contractions, salívation, nasal discharge, uncoordinated gait, cyanosis, and finally recumbency. Nitrates and nitrites in the blood of affected cattle and pastures were determined by the diphenylamine test. It is suggested that the main reason for nitrate accumulation in the grasses was the prolonged draught followed by rain. ln one ofthe outbreaks caused by Pennisetum purpureum, another reason was probably the fertilization of the soil with cattle manure.

• Nitrate poisoning Echinochloa polystachya Pennisetum purpureum capim-elefante capim-mandante Intoxicação por nitratos.

Abstract in Portuguese:

RESUMO.- Medeiros R.M.T., Riet-Correa F., Tabosa I.M., Silva Z.A., Barbosa R.C., Marques A.V.M.S. & Nogueira F.R.B. 2003. [Nitrate and nitrite poisoning in cattle caused by the ingestion of Echinochloa polystachya and Pennisetum purpureum in the semiarid region of the state of Paraíba.] Intoxicação por nitratos e nitritos em bovinos por ingestão de Echinochloa polystachya (capim-mandante) e Pennisetum purpureum (capim-elefante) no sertão da Paraíba. Pesquisa Veterinária Brasileira 23(1):17-20. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: rmtmed@cstr.ufpb.br Descrevem-se três surtos de intoxicação por nitratos e nitritos em bovinos na região semi-árida do estado da Paraíba, nordeste do Brasil. O primeiro surto foi causado por Echinochloa polystachya (capim-mandante) e os demais por Pennisetum purpureum (capim-elefante) e ocorreram após um período prolongado de seca, após o início das primeiras chuvas. Em um dos surtos causado por Pennisetum purpureum, uma parte da área onde estava o pasto que continha níveis altos de nitratos havia sido fertilizada com esterco de bovino. No primeiro surto morreram 5 bovinos de um total de 11, no segundo morreram 21 de um total de 81 e no terceiro morreram 3 de um total de 19 bovinos. Os sinais clínicos se caracterizaram por anorexia, dispnéia, ranger de dentes, depressão ou hiperexitabilidade, tremores, contrações abdominais, salivação, corrimento nasal, andar cambaleante, mucosas cianóticas e, finalmente, decúbito. A presença de nitratos e nitritos foi detectada no sangue dos animais e nos pastos por meio da prova de difenilamina. Parece que o principal fator que determinou a concentração de altos níveis de nitratos nas plantas foi a ocorrência de chuvas depois de um longo período de seca. Outro fator importante no surto causado por Pennisetum purpureum foi a fertilização do solo com esterco.