PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Amorim S.L., Medeiros R.M.T. & Riet-Correa F. 2005. [Experimental poisoning by Manihot glaziovii (Euphorbiaceae) in goats.] Intoxicação experimental por Manihot glaziovii (Euphorbiaceae) em caprinos. Pesquisa Veterinária Brasileira 25(3):179-187. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: rmtmed@cstr.ufcg.edu.br Samples of fresh, dried and partially dried leaves of Manihot glaziovii Muell. Arg. were administered orally to Moxotó goats in single doses up to 12g/kg body weight (bw). The cyanide content of the plant samples was determined by the picrosodic paper test. The plant was collected from January to June 2004. When the goats with clinical signs were in lateral recumbency, they were treated intravenously with 50ml/100kg/bw of a 20% aqueous solution of sodium tiosulfate. Three experiments were performed. In Experiment 1, the plant was given immediately after collection to six goats; two ingested the plant after been ground and four ingested the plant without having been ground. In Experiment 2, the plant was maintained in the shade, in open air or inside plastic bags. The plastic bags were changed daily. The plant kept in plastic bags was given to 18 goats, 4, 8, 12, 16, 20, 24, 48, 72, 96 and 120 hours after collection. The plant kept in the open air was given to 13 goats, 4, 24, 48, 72 and 96 hours and 9, 10, 23 and 30 days after collection. In Experiment 3, the previously ground plant kept in the open air or inside plastic bags was administered 4, 8, 12, 16, 20, 24, 48, 72 and 96 hours after collection. Seventeen goats received the plant kept in plastic bags, and 16 goats the plant left in the open air. In Experiments 2 and 3, two or three goats were used for each period after collection, and the plant was given until the loss of its toxicity. Forty goats were used as controls for evaluation of the cardiac and respiratory frequencies. In Experiment 1, the ground and not ground plant had similar toxicity. In Experiment 2, the plant kept in the open air maintained its toxicity during the whole experiment (30 days), and the plant kept inside the plastic bags was toxic until 96 hours after collection. In Experiment 3, the ground plant, left in the open air or kept inside plastic bags, was toxic for 72 hours after collection. In all experiments clinical signs were characteristic of cyanide poisoning. All poisoned goats were treated successfully. In conclusion, Manihot glaziovii, which is used as forage in northeastern Brazil, should be ground and left for at least 96 hours in the open air before feeding to animals. The plant for preparing hay should be previously ground, and the hay should be given to animals also only 96 hours after its preparation.

• Poisonous plants plant poisoning Manihot glaziovii Euphorbiaceae cyanogenic plants hydrocyanic acid goats.

Abstract in Portuguese:

Amorim S.L., Medeiros R.M.T. & Riet-Correa F. 2005. [Experimental poisoning by Manihot glaziovii (Euphorbiaceae) in goats.] Intoxicação experimental por Manihot glaziovii (Euphorbiaceae) em caprinos. Pesquisa Veterinária Brasileira 25(3):179-187. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: rmtmed@cstr.ufcg.edu.br Samples of fresh, dried and partially dried leaves of Manihot glaziovii Muell. Arg. were administered orally to Moxotó goats in single doses up to 12g/kg body weight (bw). The cyanide content of the plant samples was determined by the picrosodic paper test. The plant was collected from January to June 2004. When the goats with clinical signs were in lateral recumbency, they were treated intravenously with 50ml/100kg/bw of a 20% aqueous solution of sodium tiosulfate. Three experiments were performed. In Experiment 1, the plant was given immediately after collection to six goats; two ingested the plant after been ground and four ingested the plant without having been ground. In Experiment 2, the plant was maintained in the shade, in open air or inside plastic bags. The plastic bags were changed daily. The plant kept in plastic bags was given to 18 goats, 4, 8, 12, 16, 20, 24, 48, 72, 96 and 120 hours after collection. The plant kept in the open air was given to 13 goats, 4, 24, 48, 72 and 96 hours and 9, 10, 23 and 30 days after collection. In Experiment 3, the previously ground plant kept in the open air or inside plastic bags was administered 4, 8, 12, 16, 20, 24, 48, 72 and 96 hours after collection. Seventeen goats received the plant kept in plastic bags, and 16 goats the plant left in the open air. In Experiments 2 and 3, two or three goats were used for each period after collection, and the plant was given until the loss of its toxicity. Forty goats were used as controls for evaluation of the cardiac and respiratory frequencies. In Experiment 1, the ground and not ground plant had similar toxicity. In Experiment 2, the plant kept in the open air maintained its toxicity during the whole experiment (30 days), and the plant kept inside the plastic bags was toxic until 96 hours after collection. In Experiment 3, the ground plant, left in the open air or kept inside plastic bags, was toxic for 72 hours after collection. In all experiments clinical signs were characteristic of cyanide poisoning. All poisoned goats were treated successfully. In conclusion, Manihot glaziovii, which is used as forage in northeastern Brazil, should be ground and left for at least 96 hours in the open air before feeding to animals. The plant for preparing hay should be previously ground, and the hay should be given to animals also only 96 hours after its preparation.

Abstract in English:

Oliveira F.N., Rech R.R., Rissi D.R., Barros R.R. & Barros C.S.L. 2005. [Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds.] Intoxica-ção em suínos pela ingestão de sementes de Aeschynomene indica (Leg. Papilionoideae). Pesquisa Veterinária Brasileira 25(3):135-142. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

• Poisonous plants plant poisoning Aeschynomene indica Leguminosae Papilionoideae pathology diseases of the central nervous system diseases of swine.

Abstract in Portuguese:

Oliveira F.N., Rech R.R., Rissi D.R., Barros R.R. & Barros C.S.L. 2005. [Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds.] Intoxica-ção em suínos pela ingestão de sementes de Aeschynomene indica (Leg. Papilionoideae). Pesquisa Veterinária Brasileira 25(3):135-142. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

Abstract in English:

Brito M.F., Seixas J.N., Jabour F.F., Andrade G.B., Cunha B.R.M., França T.N. & Peixoto P.V. 2005. [About an outbreak of cumarin poisoning in cattle.] Sobre um surto de envenenamento por derivado cumarínico em bovinos. Pesquisa Veterinária Brasileira 25(3):143-149. Depto Epidemiologia e Saúde Pública, Instituto de Veterinária, UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: marilene@ufrrj.br An outbreak of cumarin poisoning which occurred in feedlot cattle in the county of Seropédica, Rio de Janeiro, is described. Three from 43 animal died. The main manifestations included bloody diarrhea, apathy, anorexia, sialorrhoe, incoordenation and dyspnoe. At post-mortem examinations there were mainly hemorrhages of varies forms and intensity in several organs, which also were seen at histopathological examination. Analysis for cumarin derivates of rumen, reticulum, omasum and abomasum contents, of liver and kidney samples, as well as of food collected from the trough, resulted positive for cumarin compounds which included warfarin, bromadiolone and brodifacoum. Feeding experiments with food stored at the property resulted negative. An intentional or accidental act could not be excluded. Animals that did not feed from the same trough did not get sick.

• umarin poisoning cattle.

Abstract in Portuguese:

Brito M.F., Seixas J.N., Jabour F.F., Andrade G.B., Cunha B.R.M., França T.N. & Peixoto P.V. 2005. [About an outbreak of cumarin poisoning in cattle.] Sobre um surto de envenenamento por derivado cumarínico em bovinos. Pesquisa Veterinária Brasileira 25(3):143-149. Depto Epidemiologia e Saúde Pública, Instituto de Veterinária, UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: marilene@ufrrj.br An outbreak of cumarin poisoning which occurred in feedlot cattle in the county of Seropédica, Rio de Janeiro, is described. Three from 43 animal died. The main manifestations included bloody diarrhea, apathy, anorexia, sialorrhoe, incoordenation and dyspnoe. At post-mortem examinations there were mainly hemorrhages of varies forms and intensity in several organs, which also were seen at histopathological examination. Analysis for cumarin derivates of rumen, reticulum, omasum and abomasum contents, of liver and kidney samples, as well as of food collected from the trough, resulted positive for cumarin compounds which included warfarin, bromadiolone and brodifacoum. Feeding experiments with food stored at the property resulted negative. An intentional or accidental act could not be excluded. Animals that did not feed from the same trough did not get sick.

Abstract in English:

Aguirre J.I., Gomar M.S., Igal, S., Quiroga M.A., Portiansky E.L & Gimeno E.J. 2005. Bone changes caused by experimental Solanum malacoxylon poisoning in rabbits. [Alterações ósseas causadas na intoxicação experimental por Solanum malacoxylon em coelhos.] Pesquisa Veterinária Brasileira 25(1):34-38. Institute of Pathology “Prof. Dr. Bernardo Epstein”, School of Veterinary Sciences, National University of La Plata, P.O.Box 296, (1900) La Plata, Argentina. E-mail: ejgimeno@fcv.unlp.edu.ar The aim of this study was to describe the bone changes observed after a daily oral administration of the calcinogenic plant Solanum malacoxylon (syn. S. glaucophyllum) (Sm) during 9 days. The Sm-poisoned rabbits had an increase of bone resorption in the endosteal surface of the cortical zone and also in the surface covered by osteoblasts of the primary and secondary spongiosa of the trabecular bone compartment. Moreover, the epiphyseal growth plates in long bones appeared narrower than in the control rabbits, with reduction of the proliferative and hyperthrophic chondrocyte zones. The electron microscopic study revealed a significant decrease of proteoglycans in the hyperthrophic chondrocyte zone evidenced by a significant reduction of rutenium red positive granules in the poisoned rabbit. Altogether, these data suggest that cell differentiation may play a pivotal role in the pathogenesis of Sm-induced bone lesions.

• Solanum malacoxylon S. glaucophyllum calcinogenic plant rabbit bone tissue growth plate.

Abstract in Portuguese:

Aguirre J.I., Gomar M.S., Igal, S., Quiroga M.A., Portiansky E.L & Gimeno E.J. 2005. Bone changes caused by experimental Solanum malacoxylon poisoning in rabbits. [Alterações ósseas causadas na intoxicação experimental por Solanum malacoxylon em coelhos.] Pesquisa Veterinária Brasileira 25(1):34-38. Institute of Pathology “Prof. Dr. Bernardo Epstein”, School of Veterinary Sciences, National University of La Plata, P.O.Box 296, (1900) La Plata, Argentina. E-mail: ejgimeno@fcv.unlp.edu.ar The aim of this study was to describe the bone changes observed after a daily oral administration of the calcinogenic plant Solanum malacoxylon (syn. S. glaucophyllum) (Sm) during 9 days. The Sm-poisoned rabbits had an increase of bone resorption in the endosteal surface of the cortical zone and also in the surface covered by osteoblasts of the primary and secondary spongiosa of the trabecular bone compartment. Moreover, the epiphyseal growth plates in long bones appeared narrower than in the control rabbits, with reduction of the proliferative and hyperthrophic chondrocyte zones. The electron microscopic study revealed a significant decrease of proteoglycans in the hyperthrophic chondrocyte zone evidenced by a significant reduction of rutenium red positive granules in the poisoned rabbit. Altogether, these data suggest that cell differentiation may play a pivotal role in the pathogenesis of Sm-induced bone lesions.

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:

Seitz A.L., Colodel E.M., Barros S.S. & Driemeier D. 2005. [Experimental poisoning by Sida carpinifolia (Malvaceae) in sheep.] Intoxicação experimental por Sida carpinifolia (Malvaceae) em ovinos. Pesquisa Veterinária Brasileira 25(1):15-20. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS 91540-000, Brazil. E-mail: alseitz@terra.com.br. Seven sheep received dry crushed Sida carpinifolia L.f. One of them died at 18 and other at 53 days of the experiment. Four others were euthanatized and necropsied at 30, 45, 75 and 100 days. For one sheep the supply of S. carpinifolia was interrupted on the 80th day of the experiment, and 70 days later the animal was euthanized and necropsied. The minimal amount of the dry plant consumed was 11 g/kg and the maximum was 30 g/kg. The progression of clinical findings was similar in six animals with slight diarrhea at 20 days of experiment. Neurological signs were observed at 25 days and included ataxia with dysmetria, muscle tremors of the head, atypical postural reactions, frequent falls, sluggish of movements, difficulty in grazing and swallowing. These signs were enhanced when the animals were forced to walk. Four of the animals presented progressive emaciation. The sheep whose supply of the plant was interrupted recovered gradually, and 11 days after the animal returned to normal. During necropsy, only enlarged mesenteric lymph nodes were observed. The histological alterations were more significant in the central nervous system, with multiple and severe cytoplasmic distention and vacuolation which affects specially Purkinje cells of the cerebellum, neurons of cerebral cortex, thalamus, midbrain and the ventral horn of spinal cord. Axonal spheroids in the brain, more frequently in the granular layer of cerebellum were also observed. The cytoplasmic vacuolation was also found in pancreatic acinar cells, renal tubules, thyroid follicular epithelium, hepatocytes and macrophages of lymphoid organs. The ultrastructural lesions observed were cytoplasmic vacuolation, some surrounded by membranes in Purkinje cells of cerebellum and thyroid follicular cells. The sheep, which had S. carpinifolia withdrawn from its diet for 70 days, had no significant histological alterations.

• Toxic plants plant poisoning Sida carpinifolia Malvaceae lysosomal storage disease swainsonine electronic microscopy.

Abstract in Portuguese:

Seitz A.L., Colodel E.M., Barros S.S. & Driemeier D. 2005. [Experimental poisoning by Sida carpinifolia (Malvaceae) in sheep.] Intoxicação experimental por Sida carpinifolia (Malvaceae) em ovinos. Pesquisa Veterinária Brasileira 25(1):15-20. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS 91540-000, Brazil. E-mail: alseitz@terra.com.br. Seven sheep received dry crushed Sida carpinifolia L.f. One of them died at 18 and other at 53 days of the experiment. Four others were euthanatized and necropsied at 30, 45, 75 and 100 days. For one sheep the supply of S. carpinifolia was interrupted on the 80th day of the experiment, and 70 days later the animal was euthanized and necropsied. The minimal amount of the dry plant consumed was 11 g/kg and the maximum was 30 g/kg. The progression of clinical findings was similar in six animals with slight diarrhea at 20 days of experiment. Neurological signs were observed at 25 days and included ataxia with dysmetria, muscle tremors of the head, atypical postural reactions, frequent falls, sluggish of movements, difficulty in grazing and swallowing. These signs were enhanced when the animals were forced to walk. Four of the animals presented progressive emaciation. The sheep whose supply of the plant was interrupted recovered gradually, and 11 days after the animal returned to normal. During necropsy, only enlarged mesenteric lymph nodes were observed. The histological alterations were more significant in the central nervous system, with multiple and severe cytoplasmic distention and vacuolation which affects specially Purkinje cells of the cerebellum, neurons of cerebral cortex, thalamus, midbrain and the ventral horn of spinal cord. Axonal spheroids in the brain, more frequently in the granular layer of cerebellum were also observed. The cytoplasmic vacuolation was also found in pancreatic acinar cells, renal tubules, thyroid follicular epithelium, hepatocytes and macrophages of lymphoid organs. The ultrastructural lesions observed were cytoplasmic vacuolation, some surrounded by membranes in Purkinje cells of cerebellum and thyroid follicular cells. The sheep, which had S. carpinifolia withdrawn from its diet for 70 days, had no significant histological alterations.

Abstract in English:

García y Santos M.C., Schild A.L., Barros S.S., Riet-Correa F., Elias F. & Ramos A.T. 2004. [Perinatal lesions in cattle experimentally poisoned by Ateleia glazioviana (Leg. Papilionoideae).] Lesões perinatais em bovinos na intoxicação experimental por Ateleia glazio-viana (Leg.Papilionoideae). Pesquisa Veterinária Brasileira 24(3):178-184. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Cx.Postal 354, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br Leaves of Ateleia glaziovian Baill., dried in a 100o C oven for 16-20 hours, were given to seven crossbred cows, always as bolus. Two of them received 9 g/kg at 4 months of pregnancy. Three cows in the 8th month of pregnancy received daily doses of 1-2 g/kg of the leaves, until a total amount of 10, 21 and 28 g/kg/bw was reached. Two 8-month-pregnant cows were fed 15.5 and 18 g/kg of the dried leaves. Two 4-month-pregnant cows were fed 35 g/kg of green leaves of A. glazioviana. The cow treated with 21 g/kg of the dry plant material showed clinical signs of poisoning and delivered a stillborn calf. No clinical signs were observed in the other cows. The calves from cows that received 9, 15.5 and 28 g/kg of the dried leaves showed weakness and suckling difficulties, and were killed. Whitish areas and thickening of the right ventricle wall of the heart were observed in the stillborn calf. Thickening of the wall of the right ventricle was also observed in the calf delivered by the cow treated with 28g/kg of dry plant. The other calves had no gross lesions. The histological changes in all necropsied calves were characterized by tumefaction and vacuolization of muscle fibers and proliferation of fibrous tissue, similar as occurred in spontaneous cases of fibrosis of the heart muscle in cattle poisoned by A. glazioviana. PAS stained slides revealed positive granules in the cardiomyocytes more evident than those of the control calf. The stillborn calf had mild spongiosis of the white matter of the cerebellum, thalamus and rostral colliculi. The ultrastructural pathology revealed cardiac fibers with large glycogen storage within myofibril bundles, which showed loss of bundles and disappearance of whole sarcomers. Mild glycogen storage was observed in a control calf.

• Poisonous plants plant poisoning Ateleia glazioviana Leguminosae Papilionoideae abortion cardiac fibrosis glycogenosis.

Abstract in Portuguese:

García y Santos M.C., Schild A.L., Barros S.S., Riet-Correa F., Elias F. & Ramos A.T. 2004. [Perinatal lesions in cattle experimentally poisoned by Ateleia glazioviana (Leg. Papilionoideae).] Lesões perinatais em bovinos na intoxicação experimental por Ateleia glazio-viana (Leg.Papilionoideae). Pesquisa Veterinária Brasileira 24(3):178-184. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Cx.Postal 354, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br Leaves of Ateleia glaziovian Baill., dried in a 100o C oven for 16-20 hours, were given to seven crossbred cows, always as bolus. Two of them received 9 g/kg at 4 months of pregnancy. Three cows in the 8th month of pregnancy received daily doses of 1-2 g/kg of the leaves, until a total amount of 10, 21 and 28 g/kg/bw was reached. Two 8-month-pregnant cows were fed 15.5 and 18 g/kg of the dried leaves. Two 4-month-pregnant cows were fed 35 g/kg of green leaves of A. glazioviana. The cow treated with 21 g/kg of the dry plant material showed clinical signs of poisoning and delivered a stillborn calf. No clinical signs were observed in the other cows. The calves from cows that received 9, 15.5 and 28 g/kg of the dried leaves showed weakness and suckling difficulties, and were killed. Whitish areas and thickening of the right ventricle wall of the heart were observed in the stillborn calf. Thickening of the wall of the right ventricle was also observed in the calf delivered by the cow treated with 28g/kg of dry plant. The other calves had no gross lesions. The histological changes in all necropsied calves were characterized by tumefaction and vacuolization of muscle fibers and proliferation of fibrous tissue, similar as occurred in spontaneous cases of fibrosis of the heart muscle in cattle poisoned by A. glazioviana. PAS stained slides revealed positive granules in the cardiomyocytes more evident than those of the control calf. The stillborn calf had mild spongiosis of the white matter of the cerebellum, thalamus and rostral colliculi. The ultrastructural pathology revealed cardiac fibers with large glycogen storage within myofibril bundles, which showed loss of bundles and disappearance of whole sarcomers. Mild glycogen storage was observed in a control calf.

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:

Oliveira C.M.C., Barbosa J.D., Macedo R.S.C., Brito M.F., Peixoto P.V. & Tokarnia C.H. 2004. [A comparative study of the toxicity of Palicourea juruana (Rubiaceae) to buffalo and cattle.] Estudo comparativo da toxidez de Palicourea juruana (Rubiaceae) para búfalos e bovinos. Pesquisa Veterinária Brasileira 24(1):27-30. Escola de Medicina Veterinária, Campus Castanhal, Universidade Federal do Pará, Rua Maximino Porpino 1000, Castanhal, PA 68743-080, Brazil. E-mail: tokarnia@ufrrj.br An experimental study was performed to establish the toxicity of Palicourea juruana for buffaloes and to add new data on the toxicity of this plant for cattle. The clinical and pathological pictures were similar, but a comparison of the lethal doses for buffaloes (1-2g/kg) and cattle (0.25g/kg) shows that the buffalo is at least 4 times more resistant. In experiments performed 10 years earlier with the fresh leaves - collected on the same farm in July, at the beginning of the dry season, only 2 months later than in this second experimental series - the lethal dose for cattle was 2 g/kg. No explanation was found for the extremely high toxicity of the plant observed in the present study.

• Plant poisoning Palicourea juruana Rubiaceae cattle buffaloes.

Abstract in Portuguese:

Oliveira C.M.C., Barbosa J.D., Macedo R.S.C., Brito M.F., Peixoto P.V. & Tokarnia C.H. 2004. [A comparative study of the toxicity of Palicourea juruana (Rubiaceae) to buffalo and cattle.] Estudo comparativo da toxidez de Palicourea juruana (Rubiaceae) para búfalos e bovinos. Pesquisa Veterinária Brasileira 24(1):27-30. Escola de Medicina Veterinária, Campus Castanhal, Universidade Federal do Pará, Rua Maximino Porpino 1000, Castanhal, PA 68743-080, Brazil. E-mail: tokarnia@ufrrj.br An experimental study was performed to establish the toxicity of Palicourea juruana for buffaloes and to add new data on the toxicity of this plant for cattle. The clinical and pathological pictures were similar, but a comparison of the lethal doses for buffaloes (1-2g/kg) and cattle (0.25g/kg) shows that the buffalo is at least 4 times more resistant. In experiments performed 10 years earlier with the fresh leaves - collected on the same farm in July, at the beginning of the dry season, only 2 months later than in this second experimental series - the lethal dose for cattle was 2 g/kg. No explanation was found for the extremely high toxicity of the plant observed in the present study.

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%.