PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

ABSTRACT.- Barbosa R.C., Riet-Correa F., Lima E.F., Medeiros R.M.T., Guedes K.M.R, Gardner D.R., Molyneux R.J. & Melo L.E.H. 2007. Experimental swainsonine poisoning in goats ingesting Ipomoea sericophylla and Ipomoea riedelii (Convolvulaceae). Pesquisa Veterinária Brasileira 27(10):409-414. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande. Campus de Patos, 58700-000 Patos, Paraíba, Brazil. E-mail: franklin.riet@pq.cnpq.br Ipomoea sericophylla and Ipomoea riedelii cause a glycoprotein storage disease in goats. This paper reports the experimental poisoning in goats by dried I. sericophylla and I. riedelii containing 0.05% and 0.01% swainsonine, respectively. Three groups with four animals each were used. Group 1 received daily doses of 2g/kg body weight (bw) of dried I. sericophylla (150mg of swainsonine/kg). Goats from this group had clinical signs 36-38 days after the start of ingestion. Group 2 received dried I. riedelii daily doses of 2g/kg of I. riedelii (30mg of swainsonine/kg) for 70 days. No clinical signs were observed, therefore the swainsonine dose was increased to 60mg/kg for another 70 days. Goats from Group 2 had clinical signs 26-65 days after increase in swainsonine dose to 60mg/kg. Group 3 was used as control. In these experiments the minimum toxic dose was 60mg/kg which represents 0.0004% of the dry matter in goats ingesting 1.5% bw of the dry matter. For goats ingesting 2%-2.5% bw of dry matter this dose would be 0.00024%-0.0003% of the dry matter. After the end of the experiment two goats were euthanized and another six were observed for recovery of clinical signs. Four goats that continued to consume swainsonine containing plant for 39-89 days after the first clinical signs had non reversible signs, while two goats that ingested the plant for only 15 and 20 days after the first clinical signs recovered completely. These and previous results indicate that irreversible lesions due to neuronal loss occur in goats that continue to ingest the plants for about 30 days after the first clinical signs. Clinical signs and histological lesions were similar to those reported previously for goats poisoned by swainsonine containing plants. No significant alterations were found in packed cell volume, red and white blood cell counts, hemoglobin and mean corpuscular hemoglobin concentrations, mean corpuscular volume, and serum levels of glucose, total protein, and albumin, and the serum activities of gamma glutamyl transferase and aspartate aminotransferase. Swainsonine concentration of 0.05% in I. sericophylla and 0.01% in I. riedelii are different from samples of these plants used in previous experiments, which contained 0.14% and 0.5% swainsonine, respectively, demonstrating a wide variation in the toxicity of different samples.

• Poisonous plants plant poisoning lysosomal storage disease swainsonine goats Ipomoea sericophylla Ipomoea riedelii

Abstract in Portuguese:

ABSTRACT.- Barbosa R.C., Riet-Correa F., Lima E.F., Medeiros R.M.T., Guedes K.M.R, Gardner D.R., Molyneux R.J. & Melo L.E.H. 2007. Experimental swainsonine poisoning in goats ingesting Ipomoea sericophylla and Ipomoea riedelii (Convolvulaceae). Pesquisa Veterinária Brasileira 27(10):409-414. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande. Campus de Patos, 58700-000 Patos, Paraíba, Brazil. E-mail: franklin.riet@pq.cnpq.br Ipomoea sericophylla and Ipomoea riedelii cause a glycoprotein storage disease in goats. This paper reports the experimental poisoning in goats by dried I. sericophylla and I. riedelii containing 0.05% and 0.01% swainsonine, respectively. Three groups with four animals each were used. Group 1 received daily doses of 2g/kg body weight (bw) of dried I. sericophylla (150mg of swainsonine/kg). Goats from this group had clinical signs 36-38 days after the start of ingestion. Group 2 received dried I. riedelii daily doses of 2g/kg of I. riedelii (30mg of swainsonine/kg) for 70 days. No clinical signs were observed, therefore the swainsonine dose was increased to 60mg/kg for another 70 days. Goats from Group 2 had clinical signs 26-65 days after increase in swainsonine dose to 60mg/kg. Group 3 was used as control. In these experiments the minimum toxic dose was 60mg/kg which represents 0.0004% of the dry matter in goats ingesting 1.5% bw of the dry matter. For goats ingesting 2%-2.5% bw of dry matter this dose would be 0.00024%-0.0003% of the dry matter. After the end of the experiment two goats were euthanized and another six were observed for recovery of clinical signs. Four goats that continued to consume swainsonine containing plant for 39-89 days after the first clinical signs had non reversible signs, while two goats that ingested the plant for only 15 and 20 days after the first clinical signs recovered completely. These and previous results indicate that irreversible lesions due to neuronal loss occur in goats that continue to ingest the plants for about 30 days after the first clinical signs. Clinical signs and histological lesions were similar to those reported previously for goats poisoned by swainsonine containing plants. No significant alterations were found in packed cell volume, red and white blood cell counts, hemoglobin and mean corpuscular hemoglobin concentrations, mean corpuscular volume, and serum levels of glucose, total protein, and albumin, and the serum activities of gamma glutamyl transferase and aspartate aminotransferase. Swainsonine concentration of 0.05% in I. sericophylla and 0.01% in I. riedelii are different from samples of these plants used in previous experiments, which contained 0.14% and 0.5% swainsonine, respectively, demonstrating a wide variation in the toxicity of different samples.

Abstract in English:

ABSTRACT.- Antoniassi N.A.B., Ferreira E.V., Santos C.E.P., Campos J.L.E., Nakazato L. & Colodel E.M. 2007. [Spontaneous Ipomoea carnea subsp. fistulosa (Convolvulaceae) poisoning of cattle in the Brazilian Pantanal.] Intoxicação espontânea por Ipomoea carnea subsp. fistulosa (Convol-vulaceae) em bovinos no Pantanal Matogrossense. Pesquisa Veterinária Brasileira 27(10):415-418. Departamento de Clínica Médica Veterinária, Faculdade de Agronomia e Medicina Veterinária, Universidade Federal de Mato Grosso, Cuiabá, MT 78068-900, Brazil. E-mail: moleta@ufmt.br A spontaneous Ipomoea carnea subsp. fistulosa (canudo, algodoeiro) poisoning of cattle in the county of Poconé, Brazilian Pantanal, is reported. The investigation began after 12 cattle had died from a flock of 500 animals maintained in an extensive area intensely infested by I. carnea subsp. fistulosa with scarce availability of other fodder plants. The deaths occurred from June to September of 2006. Clinical signs were loss of weight and neurological deficits with hypermetry and incoordination. No significant gross lesions were observed at postmortem examination of one bovine. Histological changes comprised widespread cytoplasmic vacuolation of neurons, cells of the thyroid, kidney and pancreas. Cattle with similar clinical picture, that had been removed from the area invaded by I. carnea subsp. fistulosa and placed into areas with native and Brachiaria sp. pasture, recovered clinically within 15 days.

• Poisonous plants Ipomoea carnea subsp. fistulosa plant poisoning storage diseases cattle

Abstract in Portuguese:

ABSTRACT.- Antoniassi N.A.B., Ferreira E.V., Santos C.E.P., Campos J.L.E., Nakazato L. & Colodel E.M. 2007. [Spontaneous Ipomoea carnea subsp. fistulosa (Convolvulaceae) poisoning of cattle in the Brazilian Pantanal.] Intoxicação espontânea por Ipomoea carnea subsp. fistulosa (Convol-vulaceae) em bovinos no Pantanal Matogrossense. Pesquisa Veterinária Brasileira 27(10):415-418. Departamento de Clínica Médica Veterinária, Faculdade de Agronomia e Medicina Veterinária, Universidade Federal de Mato Grosso, Cuiabá, MT 78068-900, Brazil. E-mail: moleta@ufmt.br A spontaneous Ipomoea carnea subsp. fistulosa (canudo, algodoeiro) poisoning of cattle in the county of Poconé, Brazilian Pantanal, is reported. The investigation began after 12 cattle had died from a flock of 500 animals maintained in an extensive area intensely infested by I. carnea subsp. fistulosa with scarce availability of other fodder plants. The deaths occurred from June to September of 2006. Clinical signs were loss of weight and neurological deficits with hypermetry and incoordination. No significant gross lesions were observed at postmortem examination of one bovine. Histological changes comprised widespread cytoplasmic vacuolation of neurons, cells of the thyroid, kidney and pancreas. Cattle with similar clinical picture, that had been removed from the area invaded by I. carnea subsp. fistulosa and placed into areas with native and Brachiaria sp. pasture, recovered clinically within 15 days.

Abstract in English:

ABSTRACT.- Rech R.R., Rissi D.R., Rodrigues A., Pierezan F., Piazer J.V.M., Kommers G.D. & Barros C.S.L. 2006. [Poisoning by Solanum fastigiatum (Solanaceae) in cattle: epidemiology, clinical signs and morphometry of cerebellar lesions.] Intoxicação por Solanum fastigiatum (Solanaceae) em bovinos: epidemiologia, sinais clínicos e morfometria das lesões cerebelares. Pesquisa Veterinária Brasileira 26(3):183-189. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Nineteen cases of Solanum fastigiatum (Solanaceae) poisoning in cattle from three municipalites in the State of Rio Grande do Sul, Brazil, occurring from 2003 to 2005, are described. Morbidity and mortality rates were respectively 6.7% and 3.4%. Average age of affected cattle was five-year-old (2 to 8-year-old) and duration of clinical courses was 3-18 months. Clinical signs observed in all affected cattle were cerebellar deficits characterized by hypermetry, incoordination, falls, muscle tremors, transitory seizures and wide base stance. One affected bovine had encephalic traumatic subdural hemorrhage and another had gross atrophy of the cerebellum. Histologically, lesions were restricted to the cerebellum and consisted of partial or complete vacuolation of the perikaria of Purkinje neurons with occasional axonal spheroids in the granular cell layer and in the white matter of the cerebellum. In advanced cases there were extensive loss of cerebellar Purkinje neurons and proliferation of the Bergmann’s glia. The morphometric evaluation of the numbers of Purkinje neurons and of the thickness of the cerebellar molecular layer indicated decreased numbers of Purkinje neurons with consequent decrease in the molecular layer thickness.

• Poisonous plants Solanum fastigiatum Solanaceae lysosomal storage diseases central nervous system diseases of cattle neuropathology

Abstract in Portuguese:

ABSTRACT.- Rech R.R., Rissi D.R., Rodrigues A., Pierezan F., Piazer J.V.M., Kommers G.D. & Barros C.S.L. 2006. [Poisoning by Solanum fastigiatum (Solanaceae) in cattle: epidemiology, clinical signs and morphometry of cerebellar lesions.] Intoxicação por Solanum fastigiatum (Solanaceae) em bovinos: epidemiologia, sinais clínicos e morfometria das lesões cerebelares. Pesquisa Veterinária Brasileira 26(3):183-189. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Nineteen cases of Solanum fastigiatum (Solanaceae) poisoning in cattle from three municipalites in the State of Rio Grande do Sul, Brazil, occurring from 2003 to 2005, are described. Morbidity and mortality rates were respectively 6.7% and 3.4%. Average age of affected cattle was five-year-old (2 to 8-year-old) and duration of clinical courses was 3-18 months. Clinical signs observed in all affected cattle were cerebellar deficits characterized by hypermetry, incoordination, falls, muscle tremors, transitory seizures and wide base stance. One affected bovine had encephalic traumatic subdural hemorrhage and another had gross atrophy of the cerebellum. Histologically, lesions were restricted to the cerebellum and consisted of partial or complete vacuolation of the perikaria of Purkinje neurons with occasional axonal spheroids in the granular cell layer and in the white matter of the cerebellum. In advanced cases there were extensive loss of cerebellar Purkinje neurons and proliferation of the Bergmann’s glia. The morphometric evaluation of the numbers of Purkinje neurons and of the thickness of the cerebellar molecular layer indicated decreased numbers of Purkinje neurons with consequent decrease in the molecular layer thickness.

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:

ABSTRACT.- Colodel E.M., Driemeier D., Loretti A.P., Gimeno E.J., Traverso S.D., Seitz A.L. & Zlotowski P. 2002. [Clinical and pathological aspects of Sida carpinifolia poisoning in goats in Rio Grande do Sul.] Aspectos clínicos e patológicos da intoxicação por Sida carpinifolia (Malvaceae) em caprinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 22(2):51-57. Setor de Patologia Veterinária, Depto Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. This report includes the clinical and pathological studies of a lysosomal storage disease which spontaneously occurred in three flocs of goats e after consumption of Sida carpinifolia, the predominant plant in the paddocks where the animals were grazing. In the outbreaks a total of 25 out of 51 animals were affected. Post-mortem examination was performed on 11 goats. The disease was experimentally induced by dosing goats with Sida carpinifolia. The plant was administered in natura or dried to 3 animals. No clinical or pathological changes were observed in one goat dosed with Sida rhombifolia ad libidum during 40 days. Clinical signs of the poisoning were ataxia, hypermetria, muscle tremors in the head and neck and disorders of deglutition. The clinical signs were exacerbated by movement. After the surviving animals had been moved to other pastures and stopped eating the plant, clinical signs were still observed during 24 months. At necropsy, no significant gross lesions were observed. Microscopic lesions included various degrees of vacuolization in the cytoplasm of neurons and glial cells. Similar lesions were observed in the acinar pancreatic cells, hepatocytes, proximal convoluted tubular cells, follicular epithelial cells of the thyroid gland and macrophages oflymph nodes. In the surviving animals, mild neuronal cytoplasmic vacuolization was observed, and few cells were eosinophilic and shrunken. In these cases neurons, especially Purkinje cells, had disappeared. Through the histochemical study of the cerebellar sections, the lysosomal storage disease was characterized as an alpha-mannosidosis. The vacuoles within the Purkinje cells strongly reacted with lectins of Concanavalia ensiformis, Triticum vulgaris and succinylated Triticum vulgaris. The pattern observed in this investigation is similar to those seen in other poisonings by swainsonine-containing plants.

• Sida carpinifolia Malvaceae lysosomal storage disease a-mannosidosis goats lectins doença de armazenamento lisossomal a-manosidose caprinos lectinas.

Abstract in Portuguese:

RESUMO.- Colodel E.M., Driemeier D., Loretti A.P., Gimeno E.J., Traverso S.D., Seitz A.L. & Zlotowski P. 2002. [Clinical and pathological aspects of Sida carpinifolia poisoning in goats in Rio Grande do Sul.] Aspectos clínicos e patológicos da intoxicação por Sida carpinifolia (Malvaceae) em caprinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 22(2):51-57. Setor de Patologia Veterinária, Depto Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. Este trabalho inclui os estudos clínicos e patológicos da doença de armazenamento lisossomal induzida pelo consumo espontâneo de Sida carpinifolia. A enfermidade foi observada em três rebanhos, que juntos eram compostos por 51 caprinos, dos quais, 25 foram afetados e 11 necropsiados. Nos três surtos, S. carpinifolia era a vegetação predominante nos piquetes ocupados pelos animais. Clinicamente, a doença caracterizou-se por distúrbios neurológicos que consistiam de ataxia, hipermetria, posturas anormais, tremores musculares afetando principalmente as regiões da cabeça e pescoço, dificuldade para ingestão de alimentos e quedas freqüentes. Estes sinais clínicos eram exacerbados pela movimentação. Em alguns animais, embora com um quadro clínico estabilizado, as alterações neurológicas persistiram durante 24 meses após sua retirada dos piquetes infestados por S. carpinifolia. A doença foi reproduzida administrando-se S. carpinifolia, in natura ou seca à sombra, para 3 caprinos. Um caprino recebeu Sida rhombifolia, ad libidum, por 40 dias e não desenvolveu alterações clínicas ou patológicas. Na necropsia não havia alterações. Microscopicamente, as principais alterações foram distensão e vacuolização citoplasmáticas em neurônios e, em menor intensidade, em células da glia do sistema nervoso central. Alterações similares foram observadas em células acinares pancreáticas, hepatócitos, células tubulares renais, células foliculares epiteliais da tireóide e macrófagos de órgãos linfóides. Nos animais que não mais ingeriam S. carpinifolia por períodos de um mês ou mais, observou-se uma diminuição da vacuolização citoplasmática de neurônios, que apresentavam citoplasma eosinofilico e aspecto enrugado. Nestes casos, notou-se também desaparecimento neuronal especialmente em células de Purkinje e gliose local. Em cortes cerebelares, esta doença de armazenamento foi caracterizada como ?-manosidose pelo estudo histoquímico por lectinas. Os vacúolos nas células de Purkinje reagiram fortemente com as lectinas Concanavalia ensiformis, Triticum vulgaris e Triticum vulgaris succinilado. O padrão obtido neste estudo é similar ao encontrado em intoxicação por plantas que apresentam swainsoniana como princípio tóxico.

Abstract in English:

The ultrastructural changes in the cerebellum of 2 calves experimentally poisoned with Solanum sp. and 1 calf poisoned with Solanum fastigiatum var. fastigiatum are described. The lesions induced were basically the sarne in all three animals. The perikarya of the Purkinje cells contained numerous lipid inclusions similar to those found in the inherited or induced neurolipidoses. These inclusions seemed to derive from the endoplasmic reticulum from which the lamellar bodies, vesiculo-membranous bodies, cytoplasmic membranous bodies and dense bodies take their origin. Similar changes occurred in the axys cylinders and dendrites of these cells. The morphological evidence suggests that the lipidic inclusions are the result of the formation of lipid complexes resistant to metabolism, rather than a lysosomal defect such as occurs in the inherited lipidoses.

• Plant poisoning Solanum fastigiatum var. fastigiatum Solanum sp. storage diseases cerebellar degeneration induced neurolipidoses

Abstract in Portuguese:

Três terneiros foram experimentalmente intoxicados, dois com Solanum sp. e um com Solanum Jastigiatum var. fastigiatum. Foram estudadas as alterações ultraestruturais induzidas no cerebelo. As lesões foram basicamente as mesmas para os três animais. O citoplasma das células de Purkinje continha numerosas inclusões lipídicas semelhantes àquelas encontradas nas neurolipidoses hereditárias ou induzidas. Essas inclusões parecem derivar do retículo endoplasmático de onde se originam os corpos lamelares, corpos vesículo-membranosos, corpos citoplasmático-membranosos e corpos densos. Lesões semelhantes ocorreram nos axônios e dentritos dessas células. As evidências morfológicas sugerem que as inclusões lipídicas são o resultado da formação de complexos lipídicos resistentes ao metabolismo, ao invés de resultarem de um defeito lisossômico, tal como ocorre nas lipidoses hereditárias.

• Intoxicação por planta Solanum fastigiatum var.fastigiatum Solanum sp. doença de armazenamento degeneração cerebelar neurolipidose induzida

Abstract in English:

The evolution of lesions caused by Solanum fastigiatum var. fastigiatum in the central nervous system of cattle was studied experimentally in 7 calves. The doses used varied from 75 to 1,163 g/kg of body weight, administered in periods from 15 to 620 days. Initial alterations were characterized by vacuolation of Purkinje cells and the presence of axonal spheroids in the cerebellar granular layer. Later there was a loss of Purkinje cells which were replaced by astroglia. Axonal spheroids suffered wallerian degeneration and, as a consequence microcavitation and proliferation of astroglia were observed. Simultaneously with the degenerative process, perivascular cuffing, consisting mainly of macrophages, was observed. The reversibility of the lesions was studied in four calves, two of which received 440 g/kg of body weight while the other two received 350 g/kg. One of the animals which received 440 g/kg during 140 days and another which received 350 g/kg during 107 days were slaughtered at the end of plant administration. The remaining two animals were maintained without the plant for an additional 113 and 63 days, respectively, and then slaughtered. This study showed that lesions in the pericaryon and axons of Purkinje cells, are slowly reversible, and that some spheroids probably originating from the lost Purkinje cells, suffer wallerian degeneration. The lesions observed, as well as their evolution, are similar to those described in storage diseases. The fact that these alterations are slowly reversible points to the possibility thant the disease occurs as a consequence of an enzymatic inhibition or from the presence of a slowly hydrolyzed substance in the plant. In order to study the susceptibility to the intoxication by Solanum fastigiatum var. fastigiatum, three sheep were fed 430 g/kg of body weight in a period of 202 to 370 days, while six rabbits, six guinea pigs and eight rats received 10% of the plant in a commercial feed during 120 days. Of all species tested, only sheep were susceptible to the intoxication showing lesions similar to those observed in calves.

• Toxic plants Solanaceae Solanum fastigiatum catte sheep rabbits guinea pigs rats cerebellar degeneration wallerian degeneration storage diseases induced lipidosis

Abstract in Portuguese:

Foi estudada a evolução das lesões do sistema nervoso central causadas por Solanum fastigiatum var. fastigiatum em 7 bovinos. Utilizaram-se doses que variaram de 75 g/kg de peso a l.163 g/kg de peso administradas num período entre 15 e 620 dias. As alterações iniciais caracterizaram-se por vacuolização das células de Purkinje e presença de esferóides axonais localizados na substância branca cerebelar. Posteriormente, ocorreu o desaparecimento de células de Purkinje, sendo substituídas por astroglia. Os esferóides axonais sofreram degeneração walleriana, observando-se, em conseqüência, microcavitações e proliferação de astroglia. Simultaneamente ao processo degenerativo, observou-se acúmulo perivascular constituído principalmente por macrófagos. A reversibilidade das lesões foi estudada em 4 bovinos, dois dos quais receberam 440 g/kg de peso, os outros dois, 350 g/kg de peso. Um dos bovinos que receberam 440 g/kg de peso durante 140 dias e outro que recebeu 350 g/kg durante 107 dias, foram sacrificados após o final da administração da planta, e os outros dois animais foram mantidos sem a planta por 113 e 63 dias, respectivamente, e, posteriormente, sacrificados. Este estudo demonstrou que as lesões do pericário e axônios são lentamente reversíveis, e alguns esferóides, pertencentes provavelmente às células de Purkinje já desaparecidas, sofrem degeneração walleriana. As lesões observadas, bem como sua evolução são similares às descritas nas doenças do armazenamento; o fato de que essas alterações sejam lentamente reversíveis indica a possibilidade de que a enfermidade ocorra em conseqüência de uma inibição enzimática ou da presença de uma substância lentamente hidrolisável contida na planta. Para o estudo da suscetibilidade à intoxicação por Solanum fastigiatum var. fastigiatum, foram utilizados 3 ovinos que receberam 430 g/kg de peso, num período de 202 a 370 dias, e 6 coelhos, 6 cobaias e 8 ratos, que receberam planta a 10% misturada em ração comercial durante 120 dias. Das espécies utilizadas, somente os ovinos foram sensíveis à intoxicação por esta planta, mostrando lesões similares às observadas em bovinos.

• Plantas tóxicas Solanaceae Solanum fastigiatum bovinos ovinos coelhos cobaias ratos degeneração cerebelar degeneração walleriana enfermidades do armazenamento lipidose induzida