PESQUISA VETERINÁRIA BRASILEIRA

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.

• Poisonous plants Crotalaria mucronata pyrrolizidine alkaloids interstitial pneumonia

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:

ABSTRACT.- Rozza D.B., Corrêa A.M.R., Leal J.S., Bandarra P.M., Guagnini F.S. & Djeison Lutier Raymundo D.L. & Driemeier D. 2007. [Experimental monensin poisoning in water buffaloes (Bubalus bubalis) and cattle.] Intoxicação experimental por monensina em búfalos e bovinos. Pesquisa Veterinária Brasileira 27(4):172-178. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Monensin is widely used as a feed additive to improve performance of livestock; however accidental poisoning by this ionophore compound has been reported in a number of animal species. Typical clinical signs and lesions of monensin poisoning were induced in water buffaloes dosed with single dosages of 15, 10, 7.5, and 5mg/kg of the compound. Only buffaloes dosed with 2.5 mg/kg (1 day) and 1mg/kg (7 days) survived. Clinical signs initiated about 6 h post-dosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the principal histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. In addition, this communication presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as health monitoring tools in the management of buffalo herds supplemented with monensin.

• Buffaloes cattle CK levels degenerative myopathy monensin toxicity monensin tolerance

Abstract in Portuguese:

ABSTRACT.- Rozza D.B., Corrêa A.M.R., Leal J.S., Bandarra P.M., Guagnini F.S. & Djeison Lutier Raymundo D.L. & Driemeier D. 2007. [Experimental monensin poisoning in water buffaloes (Bubalus bubalis) and cattle.] Intoxicação experimental por monensina em búfalos e bovinos. Pesquisa Veterinária Brasileira 27(4):172-178. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Monensin is widely used as a feed additive to improve performance of livestock; however accidental poisoning by this ionophore compound has been reported in a number of animal species. Typical clinical signs and lesions of monensin poisoning were induced in water buffaloes dosed with single dosages of 15, 10, 7.5, and 5mg/kg of the compound. Only buffaloes dosed with 2.5 mg/kg (1 day) and 1mg/kg (7 days) survived. Clinical signs initiated about 6 h post-dosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the principal histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. In addition, this communication presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as health monitoring tools in the management of buffalo herds supplemented with monensin.

Abstract in English:

ABSTRACT.- Oliveira K.D., França T.N., Nogueira V.A. & Peixoto P.V. 2006. [Diseases associated with selenium poisoning in animals.] Enfermidades associadas à intoxicação por selênio em animais. Pesquisa Veterinária Brasileira 27(4):125-136. Departamento de Nutrição Animal e Pastagem, Instituto de Zootecnia, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ 23890-000, Brazil. E-mail: krishna.oliveira@uvv.br Trough a critical literature review, the main data of selenium poisoning in domestic animals are presented. Epidemiological, clinical, anatomic and histopathological aspects attributed to Alkali Disease, Blind Staggers, acute poisoning and focal symmetrical poliomielomalacia of swine are discussed. The main objective of the paper is to clarify obscure points of selenium poisoning, as well to point out the risks that supplementation with this element can represent.

• Selenium poisoning alkali disease blind staggers focal symmetrical poliomielomalacia

Abstract in Portuguese:

ABSTRACT.- Oliveira K.D., França T.N., Nogueira V.A. & Peixoto P.V. 2006. [Diseases associated with selenium poisoning in animals.] Enfermidades associadas à intoxicação por selênio em animais. Pesquisa Veterinária Brasileira 27(4):125-136. Departamento de Nutrição Animal e Pastagem, Instituto de Zootecnia, Universidade Federal Rural do Rio de Janeiro, Seropédica, RJ 23890-000, Brazil. E-mail: krishna.oliveira@uvv.br Trough a critical literature review, the main data of selenium poisoning in domestic animals are presented. Epidemiological, clinical, anatomic and histopathological aspects attributed to Alkali Disease, Blind Staggers, acute poisoning and focal symmetrical poliomielomalacia of swine are discussed. The main objective of the paper is to clarify obscure points of selenium poisoning, as well to point out the risks that supplementation with this element can represent.

Abstract in English:

ABSTRACT.- Lucioli J., Furlan F.H., Mezaroba S., Bechtold S.L., Gava A. & Traverso S.D. 2007. [Acute sodium fluorsilicate poisoning in cattle in the state of Santa Catarina.] Intoxicação aguda por fluorsilicato de sódio em bovinos no Estado de Santa Catarina. Pesquisa Veterinária Brasileira 27(1):49-52. Laboratório de Patologia Animal, Departamento de Clínica e Patologia, Faculdade de Veterinária, UDESC, Avenida Luís de Camões 2090, Lages, SC 88520-000, Brazil. E-mail: a2sdt@cav.udesc.br An acute poisoning with sodium fluorsilicate in six cattle is reported, as well as the experimental reproduction by oral administration of the compound to two bovines. Clinical manifestations of the natural poisoning include muscle tremors, hypersalivation, groaning and rapid death. In the experimental poisoning lateral recumbency, dyspnea, tetanic spasms and paddling was also observed. The main necropsy findings were reddening, edema and ulceration of the ruminal and abomasal mucosa. Histopathological findings were necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration of the submucosal and muscular layers. Tubular renal necrosis, liver portal necrosis and necrosis of the lymphoid tissues was also noted. The sodium fluorsilicate caused clinical signs at a dose of 300mg/kg, and death from 400mg/kg on.

• Sodium fluorsilicate poisoning cattle pathology

Abstract in Portuguese:

ABSTRACT.- Lucioli J., Furlan F.H., Mezaroba S., Bechtold S.L., Gava A. & Traverso S.D. 2007. [Acute sodium fluorsilicate poisoning in cattle in the state of Santa Catarina.] Intoxicação aguda por fluorsilicato de sódio em bovinos no Estado de Santa Catarina. Pesquisa Veterinária Brasileira 27(1):49-52. Laboratório de Patologia Animal, Departamento de Clínica e Patologia, Faculdade de Veterinária, UDESC, Avenida Luís de Camões 2090, Lages, SC 88520-000, Brazil. E-mail: a2sdt@cav.udesc.br An acute poisoning with sodium fluorsilicate in six cattle is reported, as well as the experimental reproduction by oral administration of the compound to two bovines. Clinical manifestations of the natural poisoning include muscle tremors, hypersalivation, groaning and rapid death. In the experimental poisoning lateral recumbency, dyspnea, tetanic spasms and paddling was also observed. The main necropsy findings were reddening, edema and ulceration of the ruminal and abomasal mucosa. Histopathological findings were necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration of the submucosal and muscular layers. Tubular renal necrosis, liver portal necrosis and necrosis of the lymphoid tissues was also noted. The sodium fluorsilicate caused clinical signs at a dose of 300mg/kg, and death from 400mg/kg on.

Abstract in English:

ABSTRACT.- Barros C.S.L., Castilhos L.M.L., Rissi D.R., Kommers G.D. & Rech R.R. 2007. [Liver biopsy for the diagnosis of Senecio brasiliensis (Asteraceae) poisoning in cattle.] Biópsia hepática no diagnóstico da intoxicação por Senecio brasiliensis (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 27(1):53-60. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Liver lesions caused by Senecio spp. poisoning in cattle are progressive and deaths may occur many months after the plant is ingested. Laboratory tests of liver function are not always reliable indicators of subclinical affected animals. Liver biopsy could be useful to identify cattle with hepatic lesions but without clinical signs and would have also a prognostic value since it is generally believed that hepatic lesions will eventually cause liver failure and death. Such animals could be picked out by liver biopsy before clinical signs develop and be sent to slaughter, minimizing economic losses. This study was aimed to evaluate the liver biopsy as a diagnostic and prognostic tool in cases of Senecio spp. poisoning in cattle. An outbreak of Senecio brasiliensis was diagnosed in dairy calves which ingested hay contaminated by 5-10% of this Senecio species. Liver biopsy using a Menghini needle by right transthoracic approach was carried out in 135 calves that ingested the contaminated hay. Biopsed calves were followed up for 26 months after the biopsy. Seventeen biopsied calves had typical lesions of Senecio spp. poisoning (positive calves) and 118 had histologically normal livers (negative calves). Hepatic lesions of positive calves included fibrosis, hepatomeglocytosis, and biliary hyperplasia. Fifteen out of the 17 positive calves died with typical clinical signs of Senecio spp. poisoning within 17-149 days after the biopsy; 13 of those were necropsied and had typical gross and histopathological lesions of Senecio spp. poisoning. Two positive calves were clinically normal at the end of the post-biopsy observation period. The prognostic value (sensibility) of the test was considered high since 88.23% of the positive calves died. The specificity of the test was considered very high (99.16%) since only one of the 118 negative calves died in the observation period. In none of the biopsed calves a negative effect related to the biopsy technique was observed.

• Poisonous plants Senecio brasiliensis Asteraceae liver biopsy diseases of cattle pathology

Abstract in Portuguese:

ABSTRACT.- Barros C.S.L., Castilhos L.M.L., Rissi D.R., Kommers G.D. & Rech R.R. 2007. [Liver biopsy for the diagnosis of Senecio brasiliensis (Asteraceae) poisoning in cattle.] Biópsia hepática no diagnóstico da intoxicação por Senecio brasiliensis (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 27(1):53-60. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Liver lesions caused by Senecio spp. poisoning in cattle are progressive and deaths may occur many months after the plant is ingested. Laboratory tests of liver function are not always reliable indicators of subclinical affected animals. Liver biopsy could be useful to identify cattle with hepatic lesions but without clinical signs and would have also a prognostic value since it is generally believed that hepatic lesions will eventually cause liver failure and death. Such animals could be picked out by liver biopsy before clinical signs develop and be sent to slaughter, minimizing economic losses. This study was aimed to evaluate the liver biopsy as a diagnostic and prognostic tool in cases of Senecio spp. poisoning in cattle. An outbreak of Senecio brasiliensis was diagnosed in dairy calves which ingested hay contaminated by 5-10% of this Senecio species. Liver biopsy using a Menghini needle by right transthoracic approach was carried out in 135 calves that ingested the contaminated hay. Biopsed calves were followed up for 26 months after the biopsy. Seventeen biopsied calves had typical lesions of Senecio spp. poisoning (positive calves) and 118 had histologically normal livers (negative calves). Hepatic lesions of positive calves included fibrosis, hepatomeglocytosis, and biliary hyperplasia. Fifteen out of the 17 positive calves died with typical clinical signs of Senecio spp. poisoning within 17-149 days after the biopsy; 13 of those were necropsied and had typical gross and histopathological lesions of Senecio spp. poisoning. Two positive calves were clinically normal at the end of the post-biopsy observation period. The prognostic value (sensibility) of the test was considered high since 88.23% of the positive calves died. The specificity of the test was considered very high (99.16%) since only one of the 118 negative calves died in the observation period. In none of the biopsed calves a negative effect related to the biopsy technique was observed.

Abstract in English:

ABSTRACT.- Nóbrega Jr J.E., Riet-Correa F., Medeiros R.M.T. & Dantas A.F.M. 2006. [Poisoning by Sorghum halepense (Poaceae) in cattle in the Brazilian semiarid.] Intoxicação por Sorghum halepense em bovinos no semi-árido. Pesquisa Veterinária Brasileira 26(4):201-204. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.com.br An outbreak of poisoning by Sorghum halepense (L.) Pers. in cattle in the Brazilian semiarid is reported. Nine cattle were introduced 15 days after the first rains into a paddock where the plant was sprouting and had 25-30cm high. Clinical signs of dyspnea, anxiety, muscular tremors and incoordination appeared 15 minutes after the animals began to graze. Two of them died within about 3 hours. The others recovered. Cyanotic mucosa, dark muscles, lung edema and hemorrhages, and leaves of the plant in the rumen were observed at necropsy. The plant was positive for the picrosodic paper test. S. halepense from another farm of occurrence of the poisoning was transplanted into two pots. The picrosodic paper test was performed fortnightly in the plants growing in one of them. The plant was positive for cyanide in all growth stages; during the first 45 days the test was positive within 1 minute, but after day 60 within 3 minutes. Thirty days after the plant had been transplanted into one of the pots, it was administered to a goat at a dose of 11.8g/kg, causing clinical signs of HCN poisoning. The animal recovered after the intravenous administration of 5mL/10kg body weight of a 20% sodium thiosulfate solution. In the Brazilian semiarid S. halepense is frequently found invading the border of ponds and irrigated crops, and is used as forage during the dry season.

• Poisonous plants Sorghum halepense cyanogenic glycosides plant poisoning cattle

Abstract in Portuguese:

ABSTRACT.- Nóbrega Jr J.E., Riet-Correa F., Medeiros R.M.T. & Dantas A.F.M. 2006. [Poisoning by Sorghum halepense (Poaceae) in cattle in the Brazilian semiarid.] Intoxicação por Sorghum halepense em bovinos no semi-árido. Pesquisa Veterinária Brasileira 26(4):201-204. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.com.br An outbreak of poisoning by Sorghum halepense (L.) Pers. in cattle in the Brazilian semiarid is reported. Nine cattle were introduced 15 days after the first rains into a paddock where the plant was sprouting and had 25-30cm high. Clinical signs of dyspnea, anxiety, muscular tremors and incoordination appeared 15 minutes after the animals began to graze. Two of them died within about 3 hours. The others recovered. Cyanotic mucosa, dark muscles, lung edema and hemorrhages, and leaves of the plant in the rumen were observed at necropsy. The plant was positive for the picrosodic paper test. S. halepense from another farm of occurrence of the poisoning was transplanted into two pots. The picrosodic paper test was performed fortnightly in the plants growing in one of them. The plant was positive for cyanide in all growth stages; during the first 45 days the test was positive within 1 minute, but after day 60 within 3 minutes. Thirty days after the plant had been transplanted into one of the pots, it was administered to a goat at a dose of 11.8g/kg, causing clinical signs of HCN poisoning. The animal recovered after the intravenous administration of 5mL/10kg body weight of a 20% sodium thiosulfate solution. In the Brazilian semiarid S. halepense is frequently found invading the border of ponds and irrigated crops, and is used as forage during the dry season.

Abstract in English:

ABSTRACT.- Carvalho N.M., Alonso L.A., Cunha T.G., Ravedutti J., Barros C.S.L. & Lemos R.A.A. 2006. [Poisoning of cattle by Tetrapterys multiglandulosa in Mato Grosso do Sul, Brazil.] Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul. Pesquisa Veterinária Brasileira 26(3):139-146. Departamento de Medicina Veterinária, Universidade Federal de Mato Grosso do Sul, Avenida Senador Filinto Müller 2443, Caixa Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br Two outbreaks of poisoning by Tetrapterys multiglandulosa in cattle and the experimental reproduction of the toxicosis in sheep are described. Both outbreaks occurred on the same farm in the municipality of Bataiporã, state of Mato Grosso do Sul, Brazil. The first outbreak occurred in July-October 2004 and involved a cattle population at risk of 290 pregnant cows, which were introduced into a 60 hectare pasture with a legal reservation area heavily infested by T. multiglandulosa. Of these, 230 cows (79.3%) aborted, had stillbirths or delivered weak calves that died few days after birth. Seven cows died, and one cow and a 10-day-old calf were necropsied. The second outbreak occurred in September-October 2005, 40 days after 285 2-year-old heifers were introduced into the same pasture infested by T. multiglandulosa and where the first outbreak had occurred in the previous year. Nine heifers got sick and died, and three of then were necropsied. Clinical signs of affected cattle, including a 10-day-old calf, were marked lethargy, loss of weight with distension of the abdomen (ascites), subcutaneous dependant edema, distended and pulsating jugular veins, dyspnea and cardiac arrhythmia. Necropsy findings included a round and dilated heart with whitish and firm areas in the myocardium, and changes related to cardiac failure such as cavitary edema, nutmeg liver, pulmonary edema, a large blood clot in the left ventricle. Histopathological changes included necrosis and fibrosis in the myocardium, chronic passive hepatic centrolobular congestion, pulmonary edema, and spongy degeneration in the white matter of the brain. Experimental sheep died 29 (Sheep 1) and 35 (Sheep 2) days after being fed average daily doses of T. multiglandulosa corresponding to 14g/kg (Sheep 1) and 7,5 g/kg (Sheep 2) per day. Clinical signs were observed from the 7th day (Sheep1) and the 4th day (Sheep 2) of the experiment and included tachycardia, arrhythmia, lethargy and head pressing. Necropsy and histopathologic findings in both experimental sheep were very similar to those observed in affected cattle of the two spontaneous outbreaks.

• Poisonous plants Tetrapterys multiglandulosa Malpighiaceae plant poisoning cardiomiopathy abortion diseases of cattle pathology

Abstract in Portuguese:

ABSTRACT.- Carvalho N.M., Alonso L.A., Cunha T.G., Ravedutti J., Barros C.S.L. & Lemos R.A.A. 2006. [Poisoning of cattle by Tetrapterys multiglandulosa in Mato Grosso do Sul, Brazil.] Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul. Pesquisa Veterinária Brasileira 26(3):139-146. Departamento de Medicina Veterinária, Universidade Federal de Mato Grosso do Sul, Avenida Senador Filinto Müller 2443, Caixa Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br Two outbreaks of poisoning by Tetrapterys multiglandulosa in cattle and the experimental reproduction of the toxicosis in sheep are described. Both outbreaks occurred on the same farm in the municipality of Bataiporã, state of Mato Grosso do Sul, Brazil. The first outbreak occurred in July-October 2004 and involved a cattle population at risk of 290 pregnant cows, which were introduced into a 60 hectare pasture with a legal reservation area heavily infested by T. multiglandulosa. Of these, 230 cows (79.3%) aborted, had stillbirths or delivered weak calves that died few days after birth. Seven cows died, and one cow and a 10-day-old calf were necropsied. The second outbreak occurred in September-October 2005, 40 days after 285 2-year-old heifers were introduced into the same pasture infested by T. multiglandulosa and where the first outbreak had occurred in the previous year. Nine heifers got sick and died, and three of then were necropsied. Clinical signs of affected cattle, including a 10-day-old calf, were marked lethargy, loss of weight with distension of the abdomen (ascites), subcutaneous dependant edema, distended and pulsating jugular veins, dyspnea and cardiac arrhythmia. Necropsy findings included a round and dilated heart with whitish and firm areas in the myocardium, and changes related to cardiac failure such as cavitary edema, nutmeg liver, pulmonary edema, a large blood clot in the left ventricle. Histopathological changes included necrosis and fibrosis in the myocardium, chronic passive hepatic centrolobular congestion, pulmonary edema, and spongy degeneration in the white matter of the brain. Experimental sheep died 29 (Sheep 1) and 35 (Sheep 2) days after being fed average daily doses of T. multiglandulosa corresponding to 14g/kg (Sheep 1) and 7,5 g/kg (Sheep 2) per day. Clinical signs were observed from the 7th day (Sheep1) and the 4th day (Sheep 2) of the experiment and included tachycardia, arrhythmia, lethargy and head pressing. Necropsy and histopathologic findings in both experimental sheep were very similar to those observed in affected cattle of the two spontaneous outbreaks.

Abstract in English:

ABSTRACT.- Seixas J.N., Peixoto P.V., Armién A.G., Jabour F.F. & Brito M.F. 2006. [Clinical and pathogenetic aspects of abamectin poisoning in calves.] Aspectos clínicos e patogenéticos da intoxicação por abamectina em bezerros. Pesquisa Veterinária Brasileira 26(3):161-166. Pro-jeto Sanidade Animal Embrapa/UFRRJ, Km 47, Seropédica, RJ 23890-000, Brazil. E-mail: josiseixas@ufrrj.br Clinic-pathological aspects and the pathogenesis of experimental abamectin poisoning were studied, after subcutaneous administration of different abamectin doses in 9 calves, as well as the clini-cal and pathological aspects of 74 cases of the iatrogenic poisoning with this drug in cattle, which occurred in the states of Rio Grande do Sul, Pará, Maranhão, Paraíba and Mato Grosso do Sul. From the 9 calves submitted to experimental administration of single doses, 5 calves died (4 calves received doses 6-10 times higher than recommended, and one received the therapeutic daily dose during 11 days). Abamectin poisoning induces neurological dysfunctions, characterized by an initial phase of hyperexcitability, followed by widespread muscular hypotony and progressive depression. No macroscopic or microscopic alterations were observed in the central nervous system or in any other organ. It is concluded that abamectin is an antihelmintic which should be used with restriction, because of the risks leading to death when used in young calves, even in therapeutic doses.

• Abamectin poisoning neurological alterations calves

Abstract in Portuguese:

ABSTRACT.- Seixas J.N., Peixoto P.V., Armién A.G., Jabour F.F. & Brito M.F. 2006. [Clinical and pathogenetic aspects of abamectin poisoning in calves.] Aspectos clínicos e patogenéticos da intoxicação por abamectina em bezerros. Pesquisa Veterinária Brasileira 26(3):161-166. Pro-jeto Sanidade Animal Embrapa/UFRRJ, Km 47, Seropédica, RJ 23890-000, Brazil. E-mail: josiseixas@ufrrj.br Clinic-pathological aspects and the pathogenesis of experimental abamectin poisoning were studied, after subcutaneous administration of different abamectin doses in 9 calves, as well as the clini-cal and pathological aspects of 74 cases of the iatrogenic poisoning with this drug in cattle, which occurred in the states of Rio Grande do Sul, Pará, Maranhão, Paraíba and Mato Grosso do Sul. From the 9 calves submitted to experimental administration of single doses, 5 calves died (4 calves received doses 6-10 times higher than recommended, and one received the therapeutic daily dose during 11 days). Abamectin poisoning induces neurological dysfunctions, characterized by an initial phase of hyperexcitability, followed by widespread muscular hypotony and progressive depression. No macroscopic or microscopic alterations were observed in the central nervous system or in any other organ. It is concluded that abamectin is an antihelmintic which should be used with restriction, because of the risks leading to death when used in young calves, even in therapeutic doses.

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:

ABSTRACT.- Barros R.R., Irigoyen L.F., Kommers G.D., Rech R.R., Fighera R.A. & Barros C.S.L. 2006. [Poisoning by Ramaria flavo-brunnescens (Clavariaceae) in cattle.] Intoxicação por Ramaria flavo-brunnescens (Clavariaceae) em bovinos. Pesquisa Veterinária Brasileira 26(2):87-96. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two oubreaks of poisoning by the mushroom Ramaria flavo-brunnescens are reported in cattle from two farms located in the municipalities of Santa Maria and São Gabriel, state of Rio Grande do Sul, during April-May 2005. Out of a total of 180 yearling calves that had access to a pasture with eucalyptus woods, 19 were affected and 10 died. The clinical courses were 8-15 days and clinical signs included depression, weight loss, dehydration, drooling, loosening and loss of the long hairs of the tip of the tail, smoothening of the dorsal surface of the tongue with occasional ulceration, loosening of the corneal encasement of horns, hard and ball-shaped feces covered with a film of mucous, hypopion, hyphema and corneal opacity. Two calves had leucocytosis due to mild regenerative left shift. Nine calves were necropsied. Necropsy findings confirmed the clinical observation and additionaly included fibrinonecrotic esophagitis, mainly in the distal third of the esophageal mucosa. Histopathological changes in the skin of the tail included orthokeratotic hyperkeratosis; hair folicles with irregular contours, thickening of the tricolemmal keratin layer with occasional formation of keratin plugs, and degeneration and necrosis of the outer root sheath. At the laminar region of the hooves, there was hyperplasia of the top of epidermal laminae with irregular keratinization and retention of nuclei; several epidermal laminae were shortened and fused. There was hemorrhage, fibrin and neutrophilic infiltrate in the dermal laminae. In the mucosa of the tongue there was thinning of the covering epithelium, atrophy and loss of filiform papillae, multifocal areas of dyskeratosis, and spongiosis of the basal cell layer. In some parts the epithelium was lost and the surface consisted of granulation tissue and mixed inflammatory cell infiltrate. The esophageal mucosae of six calves had varying degree of epithelial necrosis and inflammation. The loss of the covering epithelium revealed an underneath area of granulation tissue with heavy inflammatory infiltrate composed predominantly of neutrophils and macrophages. In six calves there were focal symmetric bilateral areas of malacia observed at the level of obex in the medulla oblongata and affecting the white matter and parts of the dorsal nucleus of the vagus and of the hypoglossal nucleus. The epidemiology, clinical signs, pathology, and pathogenesis of poisoning by R. flavo-brunnescens in cattle are discussed.

• Poisonous plants Ramaria flavo-brunnescens Clavariaceae plant poisoning mushroom poisoning keratinization defect focal symmetric encephalomalacia diseases of cattle pathology.

Abstract in Portuguese:

ABSTRACT.- Barros R.R., Irigoyen L.F., Kommers G.D., Rech R.R., Fighera R.A. & Barros C.S.L. 2006. [Poisoning by Ramaria flavo-brunnescens (Clavariaceae) in cattle.] Intoxicação por Ramaria flavo-brunnescens (Clavariaceae) em bovinos. Pesquisa Veterinária Brasileira 26(2):87-96. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two oubreaks of poisoning by the mushroom Ramaria flavo-brunnescens are reported in cattle from two farms located in the municipalities of Santa Maria and São Gabriel, state of Rio Grande do Sul, during April-May 2005. Out of a total of 180 yearling calves that had access to a pasture with eucalyptus woods, 19 were affected and 10 died. The clinical courses were 8-15 days and clinical signs included depression, weight loss, dehydration, drooling, loosening and loss of the long hairs of the tip of the tail, smoothening of the dorsal surface of the tongue with occasional ulceration, loosening of the corneal encasement of horns, hard and ball-shaped feces covered with a film of mucous, hypopion, hyphema and corneal opacity. Two calves had leucocytosis due to mild regenerative left shift. Nine calves were necropsied. Necropsy findings confirmed the clinical observation and additionaly included fibrinonecrotic esophagitis, mainly in the distal third of the esophageal mucosa. Histopathological changes in the skin of the tail included orthokeratotic hyperkeratosis; hair folicles with irregular contours, thickening of the tricolemmal keratin layer with occasional formation of keratin plugs, and degeneration and necrosis of the outer root sheath. At the laminar region of the hooves, there was hyperplasia of the top of epidermal laminae with irregular keratinization and retention of nuclei; several epidermal laminae were shortened and fused. There was hemorrhage, fibrin and neutrophilic infiltrate in the dermal laminae. In the mucosa of the tongue there was thinning of the covering epithelium, atrophy and loss of filiform papillae, multifocal areas of dyskeratosis, and spongiosis of the basal cell layer. In some parts the epithelium was lost and the surface consisted of granulation tissue and mixed inflammatory cell infiltrate. The esophageal mucosae of six calves had varying degree of epithelial necrosis and inflammation. The loss of the covering epithelium revealed an underneath area of granulation tissue with heavy inflammatory infiltrate composed predominantly of neutrophils and macrophages. In six calves there were focal symmetric bilateral areas of malacia observed at the level of obex in the medulla oblongata and affecting the white matter and parts of the dorsal nucleus of the vagus and of the hypoglossal nucleus. The epidemiology, clinical signs, pathology, and pathogenesis of poisoning by R. flavo-brunnescens in cattle are discussed.