Abstract in English:
ABSTRACT.- Santos J.C.A., Riet-Correa F., Simões S.V.D. & Barros C.S.L. 2008. [Pathogenesis, clinical signs and pathology of diseases caused by hepatotoxic plants in ruminants and horses in Brazil.] Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil. Pesquisa Veterinária Brasileira 28(1):1-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: franklin.riet@pq.cnpq.br
Plants causing hepatic lesions in ruminants and horses constitute one important group of poisonous plants in Brazil. These plants can be placed in three major groups: plants causing acute liver necrosis; plants causing liver fibrosis; and plants causing hepatogenous photosensitization. For some of these plants the toxic principles are known. Cestrum parqui and Xanthium cavanillesi that cause acute liver necrosis contain carboxy-atractylosides. Senecio spp., Crotalaria spp., and Echium plantagineum that cause liver fibrosis contain pyrrolizidine alkaloids. As for the group of plants causing hepatogenous photosensibilization, Myoporum spp. contain furanosesquiterpenes, Lantana spp contain triterpenes, and Brachiaria spp. and Panicum spp. contain steroidal saponins. The clinical and pathologic features of the toxicosis caused by these phytotoxins, general mechanisms of production for the production of the clinical signs and the methods for diagnosis of hepatic failure in farm animals are reviewed.
Abstract in Portuguese:
ABSTRACT.- Santos J.C.A., Riet-Correa F., Simões S.V.D. & Barros C.S.L. 2008. [Pathogenesis, clinical signs and pathology of diseases caused by hepatotoxic plants in ruminants and horses in Brazil.] Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil. Pesquisa Veterinária Brasileira 28(1):1-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: franklin.riet@pq.cnpq.br
Plants causing hepatic lesions in ruminants and horses constitute one important group of poisonous plants in Brazil. These plants can be placed in three major groups: plants causing acute liver necrosis; plants causing liver fibrosis; and plants causing hepatogenous photosensitization. For some of these plants the toxic principles are known. Cestrum parqui and Xanthium cavanillesi that cause acute liver necrosis contain carboxy-atractylosides. Senecio spp., Crotalaria spp., and Echium plantagineum that cause liver fibrosis contain pyrrolizidine alkaloids. As for the group of plants causing hepatogenous photosensibilization, Myoporum spp. contain furanosesquiterpenes, Lantana spp contain triterpenes, and Brachiaria spp. and Panicum spp. contain steroidal saponins. The clinical and pathologic features of the toxicosis caused by these phytotoxins, general mechanisms of production for the production of the clinical signs and the methods for diagnosis of hepatic failure in farm animals are reviewed.
Abstract in English:
ABSTRACT.- Torres M.B.A.M. & Coelho K.I.R. 2008. Experimental poisoning by Senecio brasiliensis in calves: quantitative and semi-quantitative study on changes in the hepatic extracellular matrix and sinusoidal cells. Pesquisa Veterinária Brasileira 28(1):43-50. Laboratório de Patologia Veterinária, Universidade Federal do Paraná, Campus Palotina, Rua Pioneiro 2153, Jardim Dallas, Palotina, PR 85950-000, Brazil. E-mail: torres@ufpr.br
Extracellular matrix plays an important role in chronic hepatic lesions and has been studied in experimental intoxication models. However in cattle, studies on chronic disease have focused on the hepatocellular damage and extracellular matrix (ECM) changes are usually overlooked. There are no specific studies on the hepatic ECM in either normal or chronically damaged bovine liver. Thus an experimental model of hepatic toxicity model using Senecio brasiliensis poisoned calves was designed. Senecio brasiliensis contains pyrrolizidine alkaloids which cause either acute or chronic progressive dose dependent liver damage. Five calves were orally fed with 0.38g of dry leaves of S. brasiliensis/kg/day for 24 days. Liver needle biopsy specimens were obtained every 15 days for 60 days. Clinical signs of digestive complications appeared at 3rd week. One calf died on 45th day and four were evaluated up to 60th day. Biopsy samples were processed for routine light microscopy, immuno-histochemistry and transmission electron microscopy. From 30th day on progressive liver damage characterized by hepatocellular ballooning, necrosis, apoptosis and megalocytosis, centrilobular, pericellular and portal fibrosis were seen by light microscopy. Quantitative and semi-quantitative measurements of hepatic ECM components were performed before and after the onset of lesions. Morphometric analysis of total collagen and elastic fiber system was conducted. Total collagen and I and III collagen types progressively increased in throughout the liver of affected calves. Changes in location, amount and disposition of the elastic fiber system were also observed. Then numbers of Kupffer cells were significantly increased at 30th day and total numbers of sinusoidal cells were significantly increased at 45th and 60th days. Liver damage was progressive and irreversible even after the exposure to the plant was discontinued. Severe fibrotic lesions occurred mainly in portal tracts, followed by veno-occlusive and pericellular fibrosis. Collagen types I and III s were present in every normal and damaged liver, with predominance of type I. In affected calves the increase of total collagen and elastic fibers system paralleled the number of total sinusoidal cells.
Abstract in Portuguese:
ABSTRACT.- Torres M.B.A.M. & Coelho K.I.R. 2008. Experimental poisoning by Senecio brasiliensis in calves: quantitative and semi-quantitative study on changes in the hepatic extracellular matrix and sinusoidal cells. Pesquisa Veterinária Brasileira 28(1):43-50. Laboratório de Patologia Veterinária, Universidade Federal do Paraná, Campus Palotina, Rua Pioneiro 2153, Jardim Dallas, Palotina, PR 85950-000, Brazil. E-mail: torres@ufpr.br
Extracellular matrix plays an important role in chronic hepatic lesions and has been studied in experimental intoxication models. However in cattle, studies on chronic disease have focused on the hepatocellular damage and extracellular matrix (ECM) changes are usually overlooked. There are no specific studies on the hepatic ECM in either normal or chronically damaged bovine liver. Thus an experimental model of hepatic toxicity model using Senecio brasiliensis poisoned calves was designed. Senecio brasiliensis contains pyrrolizidine alkaloids which cause either acute or chronic progressive dose dependent liver damage. Five calves were orally fed with 0.38g of dry leaves of S. brasiliensis/kg/day for 24 days. Liver needle biopsy specimens were obtained every 15 days for 60 days. Clinical signs of digestive complications appeared at 3rd week. One calf died on 45th day and four were evaluated up to 60th day. Biopsy samples were processed for routine light microscopy, immuno-histochemistry and transmission electron microscopy. From 30th day on progressive liver damage characterized by hepatocellular ballooning, necrosis, apoptosis and megalocytosis, centrilobular, pericellular and portal fibrosis were seen by light microscopy. Quantitative and semi-quantitative measurements of hepatic ECM components were performed before and after the onset of lesions. Morphometric analysis of total collagen and elastic fiber system was conducted. Total collagen and I and III collagen types progressively increased in throughout the liver of affected calves. Changes in location, amount and disposition of the elastic fiber system were also observed. Then numbers of Kupffer cells were significantly increased at 30th day and total numbers of sinusoidal cells were significantly increased at 45th and 60th days. Liver damage was progressive and irreversible even after the exposure to the plant was discontinued. Severe fibrotic lesions occurred mainly in portal tracts, followed by veno-occlusive and pericellular fibrosis. Collagen types I and III s were present in every normal and damaged liver, with predominance of type I. In affected calves the increase of total collagen and elastic fibers system paralleled the number of total sinusoidal cells.
Abstract in English:
ABSTRACT.- Boghossian M.R., Peixoto P.V., Brito M.F. & Tokarnia C.H. 2007. [Experimental poisoning by Crotalaria mucronata (Fabaceae) seeds in cattle.] Aspectos clínico-patológicos da intoxicação experimental pelas sementes de Crotalaria mucronata (Fabaceae) em bovinos. Pesquisa Veterinária Brasileira 27(4):149-156. Projeto Sanidade Animal Embrapa/UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: mailto:mubogho@hotmail.com
Experiments were performed to define the clinical and pathological picture of prolonged administration of the seeds of Crotalaria mucronata Desv. to cattle, in order to obtain additional information about this toxicosis. The ground seeds were administered orally to 9 bovines. Doses of 1g/kg/day, 2g/kg/day, 3g/kg/day each in one bovine, and 5g/kg/day in two of three bovines, given for 61- 63 days, did not cause poisoning. Doses of 5g/kg, in one bovine, 7.5g/kg in two bovines and 10g/kg in one bovine, given for 47-61 days, caused symptoms between 47 and 80 days after the first administration and caused death between 3 hours and 5 days after the onset of symptoms. The main clinical signs were positive venous pulse of the jugular vein, abdominal breath, tachycardia, loss of appetite, dry feces, sub-mandibular edema and weakness. Bovines that did not die, were slaughtered 8 or 9 months after first administration. At necropsy pulmonary paleness, hydropericardium, hydrothorax, hydroperitoneum, mesenteric edema, augmented hepatic consistency, discoloration of the liver, right cardiac ventricle dilatation and ruminal wall edema were seen. The main histological lesions were thickening of the alveolar walls and of the arterioles with narrowing of their lumen, and periarteriolar fibrosis, besides hepatic and cardiac lesions of minor importance. It is concluded, that the lesions caused by ingestion of the seeds of C. mucronata over a long period are caused by the difficulties of blood passage through the pulmonar vessels due to fibrosis and thickening of the arteriolar walls through the pneumotoxic action of the plant.
Abstract in Portuguese:
ABSTRACT.- Boghossian M.R., Peixoto P.V., Brito M.F. & Tokarnia C.H. 2007. [Experimental poisoning by Crotalaria mucronata (Fabaceae) seeds in cattle.] Aspectos clínico-patológicos da intoxicação experimental pelas sementes de Crotalaria mucronata (Fabaceae) em bovinos. Pesquisa Veterinária Brasileira 27(4):149-156. Projeto Sanidade Animal Embrapa/UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: mailto:mubogho@hotmail.com
Experiments were performed to define the clinical and pathological picture of prolonged administration of the seeds of Crotalaria mucronata Desv. to cattle, in order to obtain additional information about this toxicosis. The ground seeds were administered orally to 9 bovines. Doses of 1g/kg/day, 2g/kg/day, 3g/kg/day each in one bovine, and 5g/kg/day in two of three bovines, given for 61- 63 days, did not cause poisoning. Doses of 5g/kg, in one bovine, 7.5g/kg in two bovines and 10g/kg in one bovine, given for 47-61 days, caused symptoms between 47 and 80 days after the first administration and caused death between 3 hours and 5 days after the onset of symptoms. The main clinical signs were positive venous pulse of the jugular vein, abdominal breath, tachycardia, loss of appetite, dry feces, sub-mandibular edema and weakness. Bovines that did not die, were slaughtered 8 or 9 months after first administration. At necropsy pulmonary paleness, hydropericardium, hydrothorax, hydroperitoneum, mesenteric edema, augmented hepatic consistency, discoloration of the liver, right cardiac ventricle dilatation and ruminal wall edema were seen. The main histological lesions were thickening of the alveolar walls and of the arterioles with narrowing of their lumen, and periarteriolar fibrosis, besides hepatic and cardiac lesions of minor importance. It is concluded, that the lesions caused by ingestion of the seeds of C. mucronata over a long period are caused by the difficulties of blood passage through the pulmonar vessels due to fibrosis and thickening of the arteriolar walls through the pneumotoxic action of the plant.
Abstract in English:
Karam F.S.C., Soares M.P., Haraguchi M., Riet-Correa F., Méndez M.C. & Jarenkow J.A. 2004. [Epidemiological aspects of seneciosis in southern Rio Grande do Sul, Brazil.] Aspectos epidemiológicos da seneciose na região sul do Rio Grande do Sul, Brasil. Pesquisa Veterinária Brasileira 24(4):191-198. Laboratório de Toxicologia, Faculdade de Medicina Veterinária, URCAMP, Bagé, RS 96400-110, Brazil. E-mail: fernando@alternet.com.br
Seneciosis is the main cause of livestock mortality due to poisonous plants in the State of Rio Grande do Sul, Brazil. This paper presents epidemiological data of 24 outbreaks in cattle and one in horses, diagnosed by the Regional Diagnostic Laboratory at Pelotas University in southern Rio Grande do Sul, from 1998 to 2000. Additionally, data of 54 outbreaks which occurred in 1978-1997 were analyzed. The farms where outbreaks occurred in 1998-2000 were visited to obtain clinical and epidemiological data and to verify the presence of Senecio spp. Eleven outbreaks (45.83%) affected cattle up to 3 years of age, and 13 (54.16%) cattle over 3 years. Nine (37.5%) outbreaks affected females and 15 (62.5%) males. Ten (41.66%) outbreaks occurred in spring, 4 (16.66%) in summer, 5 (20.83%) in autumn, and 5 (20.83%) in winter. Morbidity rate was estimated with 4.92% and case fatality with 95.59%. The predomionating Senecio species were S. brasiliensis on 12 farms (57.14%), S. selloi on 10 (47.61%), S. oxyphyllus on 6 (28.57%), S. heterotrichius on 3 (14.28%), and S. leptolobus on 1 farm (4.76%). The main clinical signs were progressive emaciation, incoordination, diarrhea, tenesmus, rectal prolapse and aggressiveness. The clinical manifestation periods of affected cattle observed during the farm visits, or of cattle sent for post-mortem examination,were 24-96 hours in 4 outbreaks (16.66%), 4-7 days in 7 (29.16%), 1-2 weeks in 4 (16.66%), 2-3 weeks in 2 (8.33%), 1-2 months in 2 (8.33%), and 2-3 months in 1 outbreak (4.16%). In 4 outbreaks (16.66%) the clinical manifestation period was not established. In outbreaks with longer clinical manifestation periods some animals showed photosensitization. The main necropsy findings were a hard and enlarged liver, distended gall bladder, edema of the mesenterium and abomasum, and increased amount of liquid in the cavities. Histopathological findings were fibroplasia, megalocytosis and biliary ductal proliferation of the liver, and spongy degeneration of the cerebral white matter. Samples of different Senecio species, in different seasons, were analyzed for detection of pyrrolizidine alkaloids (PAs) by thin layer chromatography. Retrorsine was found in Senecio brasiliensis, S. heterotrichius, S. selloi and S. oxyphyllus. In S. brasiliensis and S. heterotrichius one and two more non-identified PAs were detected, respectively. The total PAs concentration by spectrophotometric method was 0.25% for S. brasiliensis, 0.19% for S. heterotrichius, 0.03% for S. oxyphyllus, and 0.03% for S. selloi. The highest PAs concentration occurred in winter (June/July). No alkaloids were found in samples of S. leptolobus. These results show that S. brasiliensis is the most important cause of seneciosis in southern Rio Grande do Sul. Additional data obtained dealt with 54 outbreaks of PAs poisoning in 1978-1997. During this period, 7 outbreaks (12.96%) affected cattle up to 3 years of age, 39 (72.22%) cattle over 3 years, and 3 outbreaks (5.55%) affected cattle of different ages. In 5 outbreaks (9.25%) the age was not informed. Seven outbreaks (12.96%) affected males, 39 (72.22%) females, 3 (5.55%) both sexes, and in 5 outbreaks (9.25%) the sex was not informed. Twenty-three outbreaks (42.59%) occurred in spring, 9 (16.66%) in summer, 9 (16.66%) in autumn, and 13 (24.07%) in winter. The greater number of outbreaks during 1998-2000 (24 outbreaks in 3 years) in regard to 1978-1997 (54 outbreaks in 20 years) is probably due to a decrease of more than 50% in the number of sheep in the region.
Abstract in Portuguese:
Karam F.S.C., Soares M.P., Haraguchi M., Riet-Correa F., Méndez M.C. & Jarenkow J.A. 2004. [Epidemiological aspects of seneciosis in southern Rio Grande do Sul, Brazil.] Aspectos epidemiológicos da seneciose na região sul do Rio Grande do Sul, Brasil. Pesquisa Veterinária Brasileira 24(4):191-198. Laboratório de Toxicologia, Faculdade de Medicina Veterinária, URCAMP, Bagé, RS 96400-110, Brazil. E-mail: fernando@alternet.com.br
Seneciosis is the main cause of livestock mortality due to poisonous plants in the State of Rio Grande do Sul, Brazil. This paper presents epidemiological data of 24 outbreaks in cattle and one in horses, diagnosed by the Regional Diagnostic Laboratory at Pelotas University in southern Rio Grande do Sul, from 1998 to 2000. Additionally, data of 54 outbreaks which occurred in 1978-1997 were analyzed. The farms where outbreaks occurred in 1998-2000 were visited to obtain clinical and epidemiological data and to verify the presence of Senecio spp. Eleven outbreaks (45.83%) affected cattle up to 3 years of age, and 13 (54.16%) cattle over 3 years. Nine (37.5%) outbreaks affected females and 15 (62.5%) males. Ten (41.66%) outbreaks occurred in spring, 4 (16.66%) in summer, 5 (20.83%) in autumn, and 5 (20.83%) in winter. Morbidity rate was estimated with 4.92% and case fatality with 95.59%. The predomionating Senecio species were S. brasiliensis on 12 farms (57.14%), S. selloi on 10 (47.61%), S. oxyphyllus on 6 (28.57%), S. heterotrichius on 3 (14.28%), and S. leptolobus on 1 farm (4.76%). The main clinical signs were progressive emaciation, incoordination, diarrhea, tenesmus, rectal prolapse and aggressiveness. The clinical manifestation periods of affected cattle observed during the farm visits, or of cattle sent for post-mortem examination,were 24-96 hours in 4 outbreaks (16.66%), 4-7 days in 7 (29.16%), 1-2 weeks in 4 (16.66%), 2-3 weeks in 2 (8.33%), 1-2 months in 2 (8.33%), and 2-3 months in 1 outbreak (4.16%). In 4 outbreaks (16.66%) the clinical manifestation period was not established. In outbreaks with longer clinical manifestation periods some animals showed photosensitization. The main necropsy findings were a hard and enlarged liver, distended gall bladder, edema of the mesenterium and abomasum, and increased amount of liquid in the cavities. Histopathological findings were fibroplasia, megalocytosis and biliary ductal proliferation of the liver, and spongy degeneration of the cerebral white matter. Samples of different Senecio species, in different seasons, were analyzed for detection of pyrrolizidine alkaloids (PAs) by thin layer chromatography. Retrorsine was found in Senecio brasiliensis, S. heterotrichius, S. selloi and S. oxyphyllus. In S. brasiliensis and S. heterotrichius one and two more non-identified PAs were detected, respectively. The total PAs concentration by spectrophotometric method was 0.25% for S. brasiliensis, 0.19% for S. heterotrichius, 0.03% for S. oxyphyllus, and 0.03% for S. selloi. The highest PAs concentration occurred in winter (June/July). No alkaloids were found in samples of S. leptolobus. These results show that S. brasiliensis is the most important cause of seneciosis in southern Rio Grande do Sul. Additional data obtained dealt with 54 outbreaks of PAs poisoning in 1978-1997. During this period, 7 outbreaks (12.96%) affected cattle up to 3 years of age, 39 (72.22%) cattle over 3 years, and 3 outbreaks (5.55%) affected cattle of different ages. In 5 outbreaks (9.25%) the age was not informed. Seven outbreaks (12.96%) affected males, 39 (72.22%) females, 3 (5.55%) both sexes, and in 5 outbreaks (9.25%) the sex was not informed. Twenty-three outbreaks (42.59%) occurred in spring, 9 (16.66%) in summer, 9 (16.66%) in autumn, and 13 (24.07%) in winter. The greater number of outbreaks during 1998-2000 (24 outbreaks in 3 years) in regard to 1978-1997 (54 outbreaks in 20 years) is probably due to a decrease of more than 50% in the number of sheep in the region.
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%.
Abstract in Portuguese:
Nobre V.M.T., Riet-Correa F., Barbosa Filho J.M., Dantas A.F.M., Tabosa I.M. & Vasconcelos J.S. 2004. [Poisoning by Crotalaria retusa (Fabaceae) in Equidae in the semiarid region of Paraíba.] Intoxicação por Crotalaria retusa (Fabaceae) em eqüídeos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 24(3):132-143. Depto Clínicas Veteri-nárias, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: verônica.nobre@uol.com.br
From 2000 to 2003 eight cases of poisoning by Crotalaria retusa L. were observed in horses on 8 farms in the semiarid region of Paraíba and Ceará. C. retusa was found in all farms. The main clinical signs were characteristic of hepatic encephalopathy, with dullness or hyperexcitability, head pressing, compulsive walking or circling and, occasionally, violent uncontrollable galloping. Decreased cranial nerve reflexes, ataxia and weakness were also observed. Other clinical signs were anorexia, weight loss, photosensitization and jaundice. The clinical manifestation period varied from 4 to 40 days, but most horses had a previous history of weight loss. At necropsy the livers were hard, with irregular surface and white areas mixed with dark red areas and increased lobular pattern. Mild jaundice, ascitis, hydropericardium and hydrothorax were also observed. Edema and moderate congestion were seen in the lungs. Histologic changes of the liver were characterized by fibrosis, mainly periportal, megalocitosis and bile duct cell proliferation. Multifocal areas of centrilobular or midzonal hemorrhages were also observed. Centrilobular hemorrhagic necrosis was present in two horses. Alzheimer type II astrocytes were observed, isolated or in groups, mainly in the caudate nucleus and cortex in 4 horses. The poisoning was experimentally produced in 1 adult horse and 3 adult donkeys. The horse received daily 100 g of C. retusa seeds and died 52 days after the beginning of the experiment. The dried whole C. retusa was mixed with grass and given to the 3 experimental donkeys at daily doses of 10g/kg, 5g/kg and 2.5g/kg, respectively. The donkey treated with 5g per kg died 48 days after beginning of the experiment and the other two were sacrificed at 120 days. Clinical signs and pathology were similar to those observed in spontaneous cases, but Alhzeimer type II astrocytes were observed only in the donkey that died 48 days after the beginning of ingestion of the plant material. The concentration of monocrotaline in the whole plant given to the donkeys was 0.5%.
Abstract in English:
The toxicity of 5 species of Senecio was studied' experimentally in cattle and chicks. The chicks were fed during 60 days with a ration containing 5% of dry plant. All Senecio species were toxic in the following sequence of toxicity: S. brasiliensis, S. heterotrichius, S. cisplatinus, S. selloi and S. leptolobus. To cattle the plants were administrated at 22.5, 45, 90 and 180g per kg of body weight in a period from 15 to 39 days. S. leptolobus was not toxic at these doses. The other 4 species were toxic indicating its paiticipation in the occurrence of seneciosis in cattle in southem Brazil. The determination of the alkaloid content showed integerrimine and retrorsine (0.31 % of dry weight) in S. brasiüensis and S. heterotrichius (0.19%); retrorsine and senecionine in S. cisplatinus (0.16%) and S. selloi (0.10%) and neosenkirkine and florosenine in S. leptolobus (0.005%). Integerrimine, retrorsine, mixtures of integerrimine-retrorsine and neosenkirkine-florosenine were fed to chicken at 50mg per kg of food during 45 days; The mixture of necisenkirkine-florosenine was less toxic than the others. The alkaloids showed less toxicity than the dried plants, due probably to the loss of alkaloids during extraction or drying procedure or storage contions of the plants.
Abstract in Portuguese:
Com o objetico de determinar a toxicidade de espécies de Senecio existentes na região, cinco espécies desse gênero de planta foram administradas experimentalmente a frangos e bovinos. Para os frangos; que receberam a planta dessecada misturada a 5% na ração durante 60 dias, todas as espécies resultaram tóxicas na seguinte ordem de toxicidade: Senecio brasiliensis, S. heterotrichius, S. cisplatinus, S. selloi e S. leptolobus. Aos bovinos, as plantas acima mencionadas foram administradas dessecadas nas doses de 22,5, 45, 90 e 180g/kg de peso vivo. S. leptolobus não resultou tóxico nas doses utilizadas, e as outras 4 espécies foram tóxicas, o que evidencia que elas provavelmente participam na etiologia da seneciose em bovinos da região, de vez que tem sido encontradas com evidências de terem sido consumidas. Foi realizada a determinação química do conteúdo de alcaloides das espécies de Senecio utilizadas, observando-se integerrimina e retrorsina em Senecio brasiliensis (0.31% da matéria seca) e S. heterotrichius (0,19%); retrorsina e senecionina em S. cisplatinus (0,16%) e S. selloi (0,10%) e neosenkirkina e florosenina em S. leptolobus (0,005%). Integerrimina, retrorsina, misturas de integerrimina e retrorsina e neosenkirkina e florosenina foram administradas a frangos, durante 45 dias, na dose de 50mg/kg de ração, sendo que as intoxicações provocadas pelos alcalóides foram menos graves que as induzidas pelas plantas dessecadas, o que, provavelmente, foi devido à perda de alcalóides durante o processo de extração e/ou durante a dessecação e armazenagem das plantas.
Abstract in English:
In experimental studies with Senecio brasiliensis (Spreng.) Lessing, 12 eighteen-months-old sheep were force-fed orally or by ruminal canula, the dried aerial parts of the plant collected during sprouting. Two sheep of the sarne age were used as controls. Plant related death occurred in 4 animals fed amounts of the plant corresponding to 15, 18 and 60 percent of their body weight. Another animal died of an unrelated disease. All animals remained in good condition throughout the experiment. Clinical signs, lasting from 1 to 5 days, and observed only in those animals that went on to die, were: depression, loss of appetite, loss of rumination, drooling of thick saliva, jaundice, and dark urine. The most important necropsy findings included jaundice, enlarged livers with accentuation of the lobular pattem, and darkened kidneys. Microscopically there was liver cell degeneration and necrosis associated with varying degrees of cholestasis, bile duct hyperplasia, hepatomegalocytosis and fibroplasia, although proliferative and megalocytic lesions were never very marked. The most prominent lesion in the kidneys were tubular nephrosis with the presence of bile pigment in the renal tubular epithelium and tubular lumina, and hyalin casts in the tubular lumina. Copper levels were high (800 and 950 ppm) in two of the dead animals and normal (349 and 159) in the other two. The clinical-pathological syndrome presented by the four animals which died suggests a form of chronic hepatogenous copper poisoning, secondary to pyrrolizidine alkaloidosis. The animals which did not die did not show clinical signs, and were sacrificed and necropsied at least 120 days after the last plant feeding. None of the sacrificed animals presented gross lesions, although some revealed milder microscopic liver changes similar to those above described. It was concluded that sheep are more resistant to the effects of Senecio brasiliensis than cattle. The results of theis study suggest that the use of sheep to control the plant, in order to preventt S. brasiliensis poisoning in cattle, would not be safe.
Abstract in Portuguese:
Num estudo experimental com Senecio brasiliensis (Spreng.) Lessing, 12 ovinos de 18 meses de idade receberam, por via oral ou por fistula ruminal, as partes aéreas dessecadas da. planta colhida durante a brotação. Dois animais da mesma idade foram usados como controle. A morte devido a planta ocorreu em 4 animais que receberam quantidades da planta correspondentes a 15, 18 e 60 por cento de seus pesos corporais. Um 5º animal morreu de doença intercorrente. Todos os animais permaneceram em bom estado de nutrição durante todo o experimento. Sinais clínicos, que foram observados apenas nos animais que morreram, tiveram uma evolução de 1 a 5 dias e incluíam apatia, anorexia, parada da ruminação, salivação abundante e viscosa e icterícia. Os achados de necropsia mais importantes encontrados nesses animais foram de icterícia, fígado aumentado e com acentuação do padrão lobular e rins de coloração escura. Microscopicamente, havia degeneração e necrose hepatocelulares associadas a vários graus de bilestase, hiperplasia de duetos biliares, hepatomegalocitose e fibroplasia, embora as lesões proliferativas e de megalocitose nunca fossem muito marcantes. Nos rins, as lesões microscópicas mais proeminentes eram de nefrose tubular com presença de pigmento biliar no citoplasma das células epiteliais e na luz dos túbulos e de cilindros hialianos na luz dos túbulos. Dentre os animais que morreram os níveis de cobre estavam elevados (800 e 950 ppm) no fígado de dois animais e não elevados (349 e 159 ppm) em dois outros. A síndrome clínico patológica apresentada por quatro animais que morreram sugere uma forma de intoxicação hepatógena crônica por cobre, secundária à intoxicação por alcalóides pirrolizidínicos encontrados na planta. Os animais que não morreram espontaneamente também não apresentaram sinais clínicos e foram sacrificados e necropsiados, no mínimo, 120 dias após a última administração da planta. Nenhum desses animais sacrificados mostrou lesões macroscópicas, embora alguns mostrassem alterações hepáticas histológicas menos acentuadas, mas semelhantes as acima descritas. Conclui-se que os ovinos são mais resistentes a ação do S. brasiliensis do que os bovinos. No entanto, os resultados desse experimento sugerem que não é seguro o uso de ovinos para o controle da planta, a fim de prevenir a intoxicação por S. brasiliensis em bovinos.
Abstract in English:
Ten outbreaks of poisoning by Senecio spp. which occurred in the State of Rio Grande do Sul, Southern Brazil, from 1978 to 1985, are described. Thirteen post-mortem examinations were performed and addicionally 5 materials sent in were examined. The disease affected cows, steers, heifers and calves. Clinical signs characterized by diarrhea, rectal tenesmus, incoordination and agressiveness, were observed 1 to 4 days before death. Other manifestations of the disease in some animals were progressive weight loss, dermatitis of the nose and subcutaneous edemas. Gross and microscopic pathology were characteristic of the intoxication by pyrrolizidine alkaloids. The gallbladder showed, in few cases, nodules measuring 2 to 3 mm distributed in the whole mucosa. The central nervous sistem showed spongy degeneration of the white matter, in the border between this and the grey matter and sometimes in the grey matter. In every farm in which the disease occurred variable amounts of Senecio brasiliensis, S. selloi, S. heterotrichius, S. cisplatinus and S. leptolobus were present. The first 4 species are experimentally toxic for cattle and chicks. Most outbreaks occurred between July and August. Considering that the intoxication is progressive and that the clinical signs appeared many months after the ingestion of the plant, it is possible that comsumption occurs between May and August, period in which the plant is growing and the disponibility of pasture is considerably decreased. Sheep were not present in any farm in which the disease was diagnosed.
Abstract in Portuguese:
Descrevem-se 10 surtos de intoxicação por Senecio spp. em bovinos no Rio Grande do Sul, ocorridos no período 1978-1985, sendo realizadas 13 necropsias e adicionalmente processados 5 materiais enviados. A doença afetou vacas, novilhos, novilhas e terneiros. Os sinais clínicos eram observados 1 a 4 dias antes da morte, caracterizando-se por diarréia, tenesmo retal, incoordenação e agressividade. Também observou-se, em alguns animais, perda de peso progressiva; lesões de dermatite no focinho; ascite e edemas subcutâneos. As lesões macroscópicas e histológicas observadas eram características de intoxicação por alcalóides pirrolizidínicos. A vesícula biliar apresentou, em 3 casos, nódulos de 2 a 3 mm, distribuídos em toda a mucosa. No sistema nervoso central observaram-se lesões de espongiose, na substância branca, no limite entre esta e a substância cinzenta, e, às vezes, na substância cinzenta. Em todos os estabelecimentos onde ocorreu a doença existiam quantidades variáveis de Senecio brasiliensis, S. selloi, S. heterotrichius, S. cisplatinus e S. leptolobus. As 4 primeiras espécies são tóxicas experimentalmente para bovinos e frangos. A maioria dos surtos ocorreram entre julho e janeiro. Considerando que o efeito da intoxicação é progressivo, e que os sinais clínicos podem aparecer vários meses após a ingestão da planta, é provável que a ingestão ocorra entre os meses de maio e agosto, período em que a planta está em brotação e a disponibilidade de pastagem diminui consideravelmente. Em nenhum dos estabelecimentos afetados existiam ovinos.
Abstract in English:
An outbreak of poisoning by Echium plantagineum is described in the county of Bagé, State of Rio Grande do Sul, Brazil. From a group of 77 Holstein calves, bom in April and May, 1981, 28 animals died between June and May of the following year as a consequence of the poisoning. Clinical signs were characterized by anorexia, tenesmus and rectal prolapse, and in some cases diarrhea, ataxia and ptyalism. The animals died after a course which varied from one to seven days. Some of the surviving calves showed retarded growth, and in three cases photosensitivity. Photosensitization was also observed in some adult cattle. Gross pathological changes were: a small hard liver, an enlarged gallblader with an edematous wall, edemas in the mesentery; intestine and abomasum, and fluid in the body cavities. Main histological lesions were: megalocytosis, fibrosis and proliferation of bile duct cells in the liver, and spongy degeneration of the nervous tissue localized mainly in the white matter. The disease was reproduced experimentally in chickens with a plant sample collected on the farm where the outbreak occurred. The plant was dried and mixed at 0%, 2.5% and 5% with the ration for 50 days, with five replications and two chickens per replication. The mean final weight of the gróup coosuming 5% of plant was significantly lower than that of the other groups at necropsy; seven chickens from de sarne group showed subcutaneous edema, fluid in body cavities, a yellow liver and enlarged gallblader. Histological studies of both groups that consumed E. plantagineum showed megalocytosis, fibrosis and proliferation of bile duct cells in the liver; the alteration was more marked in the 5% group. In a similar experiment, E. plantagineum, collected in the county of Pelotas, was given to chickens at 0% and 5% with the rationfor 60 days. Mean weights of both groups were similar and histological lesions were not observed. This experiment demonstrated the variable toxicity of the plant. The disease was also reproduced in cattle. Two calves consumed the plant, collected in 1981 on the farm where the disease occured. The plant was dried and mixed at 10% with the ration during 80 days. Another two calves consumed the plant, collected on the sarne farm in 1982, during 38 days, after which they were to pasture for 50 days and then returned to consume the plant during another 38 days. The histological studies of liver biopsies, collected 30 days after the end of plant consumption, showed megalocytosis in the four animals. One calf from the first experiment anq one from the second died at 167 and 187 days, respectively, after the end of the plant consumption. They showed lesions characteristic of poisoning by pyrrolizidine alkaloids, similar to those alterations observed in spontaneous disease.
Abstract in Portuguese:
Descreve-se um surto de intoxicação por Echium plantagineum ocorrido no município de Bagé, Rio Grande do 'Sul, no qual, de um total de 77 terneiros de raça Holandês, nascidos em abril e maio de 1981, morreram 28 entre junho de 1981 e abril de 1982. Os sinais clínicos caracterizaram-se por anorexia, tenesmo e prolapso retal, em alguns casos diarréia, ataxia e sialorréia; a morte ocorria após um curso variável de 1 a 7 dias. Alguns terneiros, que não morreram, apresentaram desenvolvimento retardado, e em 3 casos fotossensibilização. No gado adulto também se observaram casos de fotossensibilização. Nas necropsias observou-se diminuição do tamanho do fígado e aumento de sua consistência, aumento da vesícula biliar com edema da parede, edemas no mesentério, abomaso e intestino e líquido nas cavidades. As lesões histológicas do fígado caracterizaram-se por megalocitose, fibrose e proliferação de células dos duetos biliares; o sistema nervoso central apresentava lesões de espongiose localizadas principalmente na substância branca. A doença foi reproduzida experimentalmente em frangos que receberam a planta, colhida no local do surto, secada e misturada a 0%, 2,5% e 5% na ração, durante 50 dias, em um experimento com 5 repetições e 2 frangos por repetição. No grupo que recebeu a planta a 5%, a média de peso foi significativamente menor que a dos outros grupos; 7 frangos desse grupo apresentaram lesões macroscópicas caracterizadas por edema subcutâneo, líquido nas cavidades, fígado amarelado e vesícula biliar aumentada. Na histologia do fígado dos 2 grupos que receberam E. plantagineum observou-se megalocitose, fibrose e proliferação de células dos duetos biliares; essas alterações foram mais marcadas nos frangos que receberam a planta a 5%. Em outro experimento, E. platagineum, colhido no município de Pelotas, foi administrado a frangos a 0% e 5% durante 60 dias, não se observando diferença nas médias de peso dos dois grupos, nem lesões histológicas de significação, o que evidencia a variação de toxicidade da planta. A doença foi reproduzida experimentalmente também em bovinos, sendo que 2 terneiros receberam, durante 80 dias, a planta colhida no ano de 1981 no local onde ocorreu o surto, secada e misturada a 10% na ração; outros 2 terneiros receberam a planta, colhida no mesmo local no ano de 1982, durante 38 dias, ficaram a campo por 50 dias e novamente receberam a planta por 38 dias. No estudo de biopsias de fígado, realizadas 30 dias após finalizada a administração da planta, os 4 animais apresentaram megalocitose. Um terneiro do primeiro experimento e um do segundo morreram, respectivamente, aos 167 e 187 dias após terem finalizado o consumo da planta, apresentando lesões macroscópicas e histológicas características de intoxicação por alcalóides pirrolizidínicos, similares às observadas em casos espontâneos.