Clinical and pathological aspects and cerebellar lectin binding in cattle poisoned with Solanum fastigiatum var. fastigiatum and Solanum bonariense

Microscopic and lectin histochemical studies were performed using the cerebella of 33 natural cases of Solanum fastigiatum var. fastigiatum intoxication in the cattle from southern Brazil and 2 natural and 4 experimental cases of Solanum bonariense from Uruguay. The following biotinylated lectins were used in both cases: WGA, sWGA, BS-I, Con-A, RCA-I, DBA, and UEA-I, with the addition of LCA in S. fastigiatum poisoning cases. Histologically, the lesions consisted of fine vacuolization, distention of portions of the Purkinje cells, axonal spheroids measuring 14-50 m in the granular cell layer and adjacent white matter and, proliferation of the Bergmann?s glia. Lectin histochemistry revealed strong reactivity of stored material in Purkinje neurons with the lectins sWGA, Con-A, and LCA in S. fastigiatum cases. A similar pattern was found in S. bonariense cases with a most intense reactions to WGA, and less intense reaction to Con-A, whereas BS-I and RCA-I binding was absent to poor in these neurons in all the cases studied.Lectin reactivity in Purkinje cells between cases was independent of cell damage (from mild to severe loss of neurons). Both S. fastigiatum and S. bonariense have similar lectin binding,  suggesting a similar pathogenesis. Since comparable binding patterns have been described in animals poisoned with swainsonine-containing plants, perhaps the toxins in these plants contain related glycosidaseinhibiting toxins or inhibit glycoprotein and lysosomal metabolism through some related mechanism. The results of this study showed that in spontaneous poisoning by S. fastigiatum and S. bonariense in the cattle, the pattern of lectin binding is similar to those observed in S. fastigiatum experimental conditions.Fil: Sant’Ana, Fabiano J.F.. Universidade Federal de Santa Catarina; BrasilFil: Barbeito, Claudio Gustavo. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Nishida, Fabian. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Gimeno, Eduardo Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias; ArgentinaFil: Verdes, José M.. Universidad de la República. Facultad de Ciencias; UruguayFil: Moraña, Antonio. Universidad de la República; UruguayFil: Barros, Claudio S.L.. Universidad de la República; Urugua

Granuloma micótico nasal bovino

A case of mycotic bovine nasal granuloma in a 10 year-old Jersey cow, produced by Drechslera halodes is presented. Histopathological sections showed abundant hyaline and pigmented extra and intracellular fungal structures together with a polymorphic cellular granuloma formed by neutrophils, lymphocytes, plasmocytes, histiocytes and giant cells of the Langhans type. It is the first case of mycotic bovine nasal granuloma recognized in Uruguay although this disease seems to be frequent according to the opinion of veterinarian specialists. Another similar clinical case also in a Jersey cow from the same dairy house with an intense cellular infiltrate rich in eosinophils without granulomatous image, together with extracellular hyaline and fuliginous fungal forms, is also referred for comparative purposes. Geotrichum sp. was isolated. The need of an early diagnosis and treatment of the disease is stressed.É apresentado caso de granuloma micótico nasal bovino, em vaca Jersey, com 10 anos de idade, produzido por Drechslera halodes. Cortes histopatológicos mostraram abundantes estruturas fúngicas hialinas e pigmentadas extra e intracelulares junto com granuloma polimorfo celular formado por neutrófilos, linfócitos, plasmócitos, histiócitos e células gigantes de Langhans. É o primeiro caso de granuloma micótico nasal bovino diagnosticado no Uruguai embora esta doença pareça ser freqüente de acordo com a opinião de veterinários especializados. Outro caso clínico semelhante, também em vaca Jersey da mesma fazenda de criação de gado leiteiro, com intenso infiltrado celular rico em eosinófilos, sem imagem granulomatosa, junto com formas fúngicas fuliginosas hialinas extra celulares é também relatado para fins de comparação. Geotrichum sp. foi isolado. A necessidade de diagnóstico precoce e tratamento da doença é enfatizada

A novel pathogenic mechanism for cerebellar lesions produced by Solanum bonariense in cattle

Intoxication with Solanum bonariense in cattle causes cerebellar cortical degeneration with perikaryal vacuolation, axonal swelling, and death primarily of Purkinje cells, with accumulation of electron-dense residual storage bodies in membrane-bound vesicles. The pathogenesis of this disease is not fully understood. Previously, we proposed that inhibition of protein synthesis in Purkinje cells among other altered metabolic pathways could lead to cytoskeletal alterations, subsequently altering cell-specific axonal transport. In the present study, immunohistochemical and histochemical methods were used to identify neuronal cytoskeletal alterations and axonal loss, demyelination, and astrogliosis in the cerebellum of intoxicated bovines. Samples of cerebellum from 3 natural and 4 experimental cases and 2 control bovines were studied. Immunoreactivity against neurofilament (NF)-200KDa confirmed marked loss of Purkinje neurons, and phospho-NF protein, β-tubulin, and affinity reaction against phalloidin revealed an altered perikaryal distribution of neuronal cytoskeletal proteins in the remaining Purkinje cells in intoxicated cattle. Reactive astrogliosis in every layer of the cerebellar cortex was also observed with anti–glial fibrillary acidic protein immunohistochemistry. In affected cattle, demyelination and axonal loss in the cerebellar white matter, as well as basket cell loss were demonstrated with Klüver–Barrera and Bielschowsky stains, respectively. Based on these results, we propose that neuronal cytoskeletal alterations with subsequent interference of the axonal transport in Purkinje cells may play a relevant role in the pathogenesis of this neurodegenerative disorder, and also that demyelination and axonal loss in the cerebellar white matter, as well as astrogliosis in the gray matter, likely occur secondarily to Purkinje cell degeneration and death.Facultad de Ciencias Veterinaria

A novel pathogenic mechanism for cerebellar lesions produced by Solanum bonariense in cattle

Intoxication with Solanum bonariense in cattle causes cerebellar cortical degeneration with perikaryal vacuolation, axonal swelling, and death primarily of Purkinje cells, with accumulation of electron-dense residual storage bodies in membrane-bound vesicles. The pathogenesis of this disease is not fully understood. Previously, we proposed that inhibition of protein synthesis in Purkinje cells among other altered metabolic pathways could lead to cytoskeletal alterations, subsequently altering cell-specific axonal transport. In the present study, immunohistochemical and histochemical methods were used to identify neuronal cytoskeletal alterations and axonal loss, demyelination, and astrogliosis in the cerebellum of intoxicated bovines. Samples of cerebellum from 3 natural and 4 experimental cases and 2 control bovines were studied. Immunoreactivity against neurofilament (NF)-200KDa confirmed marked loss of Purkinje neurons, and phospho-NF protein, β-tubulin, and affinity reaction against phalloidin revealed an altered perikaryal distribution of neuronal cytoskeletal proteins in the remaining Purkinje cells in intoxicated cattle. Reactive astrogliosis in every layer of the cerebellar cortex was also observed with anti–glial fibrillary acidic protein immunohistochemistry. In affected cattle, demyelination and axonal loss in the cerebellar white matter, as well as basket cell loss were demonstrated with Klüver–Barrera and Bielschowsky stains, respectively. Based on these results, we propose that neuronal cytoskeletal alterations with subsequent interference of the axonal transport in Purkinje cells may play a relevant role in the pathogenesis of this neurodegenerative disorder, and also that demyelination and axonal loss in the cerebellar white matter, as well as astrogliosis in the gray matter, likely occur secondarily to Purkinje cell degeneration and death.Facultad de Ciencias Veterinaria

Cerebellar Cortical Degeneration in Cattle Poisoned With Solanum spp. in South America: An Epidemiological, Clinicopathological, Pathological, and Toxicological Review

Cattle that consume Solanum bonariense L (= Solanum fastigiatum Willd.) or Solanum paniculatum L. develop a typical cerebellar cortical degeneration characterized by periodic episodes of ataxia, hypermetria, hyperesthesia, head and thoracic limb extension, opisthotonus, nystagmus, and falling to the side or backward. Histological lesions include vacuolation, degeneration, and loss of Purkinje cells. Axonal spheroids, microcavitations, and other changes of Wallerian degeneration in cerebellar granular layer and white matter are also observed. Neurotoxic compounds in Solanum spp. causing neurologic dysfunction in ruminants were not definitively elucidated. The same Solanaceae species are extensively used with culinary purposes or for the treatment of liver and gastrointestinal disorders as hangovers in humans. In the present paper, we review the epidemiology, clinical signs, and pathological hallmarks of poisoning by Solanum —S. bonariense L. (=S. fastigiatum Willd.) and S. paniculatum—with emphasis in histopathology, ultrastructural, and lectin- and immuno-histochemical changes in spontaneous and experimentally poisoned cattle in South America. The current knowledge of the pathogenesis of these bovine cerebellar cortical degenerations is discussed, and some advances in botanical and toxicological aspects of these Solanaceae species are presented, taking into account the potential risk of human poisoning.Fil: Verdes, Jose M.. Universidad de la República; UruguayFil: Riet Correa, Franklin. Federal University of Campina Grande; BrasilFil: Medeiros, Rosane M.T.. Federal University of Campina Grande; BrasilFil: Moraña, Antonio. Universidad de la República; UruguayFil: Battes, Daniel. Universidad de la República; UruguayFil: Dehl, Virginia. Universidad de la República; UruguayFil: Borteiro, Claudio. Universidad de la República; UruguayFil: Gimeno, Eduardo Juan. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Sant’Ana, Fabiano J.F.. Universidade Federal de Goiás; BrasilFil: Barros, Claudio S.L.. Federal University of Santa Maria; BrasilFil: Barros, Servero S.. Federal University of Santa Maria; Brasi

Cerebellar Cortical Degeneration in Cattle Poisoned with <i>Solanum</i> spp. in South America: An Epidemiological, Clinicopathological, Pathological, and Toxicological Review

Cattle that consume Solanum bonariense L (= Solanum fastigiatum Willd.) or Solanum paniculatum L. develop a typical cerebellar cortical degeneration characterized by periodic episodes of ataxia, hypermetria, hyperesthesia, head and thoracic limb extension, opisthotonus, nystagmus, and falling to the side or backward. Histological lesions include vacuolation, degeneration, and loss of Purkinje cells. Axonal spheroids, microcavitations, and other changes of Wallerian degeneration in cerebellar granular layer and white matter are also observed. Neurotoxic compounds in Solanum spp. causing neurologic dysfunction in ruminants were not definitively elucidated. The same Solanaceae species are extensively used with culinary purposes or for the treatment of liver and gastrointestinal disorders as hangovers in humans. In the present paper, we review the epidemiology, clinical signs, and pathological hallmarks of poisoning by Solanum —S. bonariense L. (=S. fastigiatum Willd.) and S. paniculatum—with emphasis in histopathology, ultrastructural, and lectin- and immuno-histochemical changes in spontaneous and experimentally poisoned cattle in South America. The current knowledge of the pathogenesis of these bovine cerebellar cortical degenerations is discussed, and some advances in botanical and toxicological aspects of these Solanaceae species are presented, taking into account the potential risk of human poisoning.Facultad de Ciencias Veterinaria

Cerebellar Cortical Degeneration in Cattle Poisoned with <i>Solanum</i> spp. in South America: An Epidemiological, Clinicopathological, Pathological, and Toxicological Review

Cattle that consume Solanum bonariense L (= Solanum fastigiatum Willd.) or Solanum paniculatum L. develop a typical cerebellar cortical degeneration characterized by periodic episodes of ataxia, hypermetria, hyperesthesia, head and thoracic limb extension, opisthotonus, nystagmus, and falling to the side or backward. Histological lesions include vacuolation, degeneration, and loss of Purkinje cells. Axonal spheroids, microcavitations, and other changes of Wallerian degeneration in cerebellar granular layer and white matter are also observed. Neurotoxic compounds in Solanum spp. causing neurologic dysfunction in ruminants were not definitively elucidated. The same Solanaceae species are extensively used with culinary purposes or for the treatment of liver and gastrointestinal disorders as hangovers in humans. In the present paper, we review the epidemiology, clinical signs, and pathological hallmarks of poisoning by Solanum —S. bonariense L. (=S. fastigiatum Willd.) and S. paniculatum—with emphasis in histopathology, ultrastructural, and lectin- and immuno-histochemical changes in spontaneous and experimentally poisoned cattle in South America. The current knowledge of the pathogenesis of these bovine cerebellar cortical degenerations is discussed, and some advances in botanical and toxicological aspects of these Solanaceae species are presented, taking into account the potential risk of human poisoning.Facultad de Ciencias Veterinaria

A novel pathogenic mechanism for cerebellar lesions produced by Solanum bonariense in cattle

Intoxication with Solanum bonariense in cattle causes cerebellar cortical degeneration with perikaryal vacuolation, axonal swelling, and death primarily of Purkinje cells, with accumulation of electron-dense residual storage bodies in membrane-bound vesicles. The pathogenesis of this disease is not fully understood. Previously, we proposed that inhibition of protein synthesis in Purkinje cells among other altered metabolic pathways could lead to cytoskeletal alterations, subsequently altering cell-specific axonal transport. In the present study, immunohistochemical and histochemical methods were used to identify neuronal cytoskeletal alterations and axonal loss, demyelination, and astrogliosis in the cerebellum of intoxicated bovines. Samples of cerebellum from 3 natural and 4 experimental cases and 2 control bovines were studied. Immunoreactivity against neurofilament (NF)-200KDa confirmed marked loss of Purkinje neurons, and phospho-NF protein, β-tubulin, and affinity reaction against phalloidin revealed an altered perikaryal distribution of neuronal cytoskeletal proteins in the remaining Purkinje cells in intoxicated cattle. Reactive astrogliosis in every layer of the cerebellar cortex was also observed with anti–glial fibrillary acidic protein immunohistochemistry. In affected cattle, demyelination and axonal loss in the cerebellar white matter, as well as basket cell loss were demonstrated with Klüver–Barrera and Bielschowsky stains, respectively. Based on these results, we propose that neuronal cytoskeletal alterations with subsequent interference of the axonal transport in Purkinje cells may play a relevant role in the pathogenesis of this neurodegenerative disorder, and also that demyelination and axonal loss in the cerebellar white matter, as well as astrogliosis in the gray matter, likely occur secondarily to Purkinje cell degeneration and death.Facultad de Ciencias Veterinaria

A novel pathogenic mechanism for cerebellar lesions produced by Solanum bonariense in cattle

Intoxication with Solanum bonariense in cattle causes cerebellar cortical degeneration with perikaryal vacuolation, axonal swelling, and death primarily of Purkinje cells, with accumulation of electron-dense residual storage bodies in membrane-bound vesicles. The pathogenesis of this disease is not fully understood. Previously, we proposed that inhibition of protein synthesis in Purkinje cells among other altered metabolic pathways could lead to cytoskeletal alterations, subsequently altering cell-specific axonal transport. In the present study, immunohistochemical and histochemical methods were used to identify neuronal cytoskeletal alterations and axonal loss, demyelination, and astrogliosis in the cerebellum of intoxicated bovines. Samples of cerebellum from 3 natural and 4 experimental cases and 2 control bovines were studied. Immunoreactivity against neurofilament (NF)-200KDa confirmed marked loss of Purkinje neurons, and phospho-NF protein, β-tubulin, and affinity reaction against phalloidin revealed an altered perikaryal distribution of neuronal cytoskeletal proteins in the remaining Purkinje cells in intoxicated cattle. Reactive astrogliosis in every layer of the cerebellar cortex was also observed with anti–glial fibrillary acidic protein immunohistochemistry. In affected cattle, demyelination and axonal loss in the cerebellar white matter, as well as basket cell loss were demonstrated with Klüver–Barrera and Bielschowsky stains, respectively. Based on these results, we propose that neuronal cytoskeletal alterations with subsequent interference of the axonal transport in Purkinje cells may play a relevant role in the pathogenesis of this neurodegenerative disorder, and also that demyelination and axonal loss in the cerebellar white matter, as well as astrogliosis in the gray matter, likely occur secondarily to Purkinje cell degeneration and death.EEA BalcarceFil: Verdes, José Manuel. Universidad de la República. Facultad de Veterinaria; Uruguay. Instituto de Investigaciones Biológicas Clemente Estable; UruguayFil: Márquez, Mercedes. Universitat Autònoma de Barcelona. Veterinary Faculty. Department of Animal Medicine and Surgery; EspañaFil: Calliari, Aldo. Universidad de la República. Facultad de Veterinaria; Uruguay. Instituto de Investigaciones Biológicas Clemente Estable; UruguayFil: Battes, Daniel. Universidad de la República. Facultad de Veterinaria; Uruguay.Fil: Moraña, José Antonio. Universidad de la República. Facultad de Veterinaria; Uruguay.Fil: Gimeno, Eduardo Juan. Universidad Nacional de La Plata, Facultad de Ciencias Veterinarias; ArgentinaFil: Odriozola, Ernesto Raul. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Balcarce; ArgentinaFil: Giannitti, Federico. Instituto Nacional de Investigaciones Agropecuarias. La Estanzuela, Colonia; UruguayFil: Guerrero, Florentina. Universidad de Santiago de Compostela. Facultad de Veterinaria. Departments of Anatomy and Animal Production; EspañaFil: Fidalgo, Luis Eusebio. Universidad de Santiago de Compostela. Facultad de Veterinaria. Veterinary Clinical Sciences; EspañaFil: Pumarola, Martí. Universitat Autònoma de Barcelona. Veterinary Faculty. Department of Animal Medicine and Surgery; Españ