PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

ABSTRACT.- Anjos B.L., Irigoyen L.F., Piazer J.V.M., Brum J.S., Fighera R.A. & Barros C.S.L. 2009. [Experimental acute poisoning by bracken fern (Pteridium aquilinum) in cattle.] Intoxicação experimental aguda por samambaia (Pteridium aquilinum) em bovinos. Pesquisa Veterinária Brasileira 29(9):753-766. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, Santa Maria, RS 97105-900, Brazil. E-mail: claudioslbarros@uol.com.br This experiment was design to address the following points in relation to the acute poisoning by bracken fern (Pteridium aquilinum) in cattle: 1) the severity of the thrombocytopenia in different stages of the intoxication and its relationship to possible deficits in the secondary hemostasis, 2) the relationship between neutropenia and the morphological signs of septicemia occasionally found at necropsy, and 3) the mechanism of anemia and its relationship with blood loss, medium life of erythrocytes and the progress of the disease. The fresh green upper parts of P. aquilinum were fed to four mixed breed calves with average age of 18 months and weights ranging from 190 to 215 kg. A calf of similar age and weight was kept together with the other four under the same conditions, except for the ingestion of P. aquilinum. The four fern-fed calves died with typical features of acute bracken fern poisoning after being fed with the plant for 53-58 days daily doses of 8.0, 8.6, 10.2, and 10.6g/kg body weight totaling at the end of the experiment, respectively, 59.3%, 63.3%, 47.4%, and 47.5% of bracken fern in relation to their body weight. The disease was characterized by fever up to 42.5°C and varying degrees of hemorrhages observed clinically, at necropsy and on histological examination. Death occurred 6-7 days after the onset of fever. The hematological changes consisted mainly of marked thrombocytopenia and neutropenia. Two of the four affected calves had mild anemia. The deficits in secondary hemostasis were mild in each case. There were no significant changes thus permitting to rule out the role of secondary hemostasis in the pathogenesis of the hemorrhages in the bracken fern poisoning. The measurement of fibrin degradation products in the serum showed conflicting results and did no allow for a solid conclusion regarding the role of disseminated intravascular coagulation in the pathogenesis of the hemorrhages in fern poisoning. The cytology and the histopathology of bone marrow from the four poisoned calves revealed marked decrease in the numbers of hematopoietic cells from the three marrow lineages, which characterizes marrow failure due to aplasia; it was concluded that the events of the primary hemostasis due to thrombocytopenia are responsible for the hemorrhages. In blood culture from three affected calves there was growth of Klebsiella oxytoca, Staphylococcus hyicus and Staphylococcus aureus, indicating that septicemia, facilitated by neutropenia could have a role in the death of cattle acutely poisoned due to the ingestion of P. aquilinum. Additional points of the interest in the acute experimental poisoning by bracken fern in cattle reported here were the development of hematuria and the so called laryngeal form.

• Poisonous plants bracken fern Pteridium aquilinum plant poisoning plantas tóxicas samambaia intoxicação por planta

Abstract in Portuguese:

RESUMO.- Anjos B.L., Irigoyen L.F., Piazer J.V.M., Brum J.S., Fighera R.A. & Barros C.S.L. 2009. [Experimental acute poisoning by bracken fern (Pteridium aquilinum) in cattle.] Intoxicação experimental aguda por samambaia (Pteridium aquilinum) em bovinos. Pesquisa Veterinária Brasileira 29(9):753-766. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, Santa Maria, RS 97105-900, Brazil. E-mail: claudioslbarros@uol.com.br Este experimento foi delineado para investigar os seguintes pontos em relação à intoxicação aguda por samambaia (Pteridium aquilinum) em bovinos: 1) a intensidade da trombocitopenia em diferentes momentos da intoxicação e sua relação com possíveis déficits na hemostasia secundária, 2) a relação da neutropenia com as manifestações morfológicas de septicemia ocasionalmente observadas na necropsia, e 3) o mecanismo da anemia e sua relação com a perda de sangue, a vida média eritróide e a evolução da doença. As hastes superiores mais verdes de P. aquilinum foram administradas a quatro bovinos sem raça definida, com idade média de 1,5 ano e pesos entre 190-215 kg. Um bovino de idade e peso semelhantes foi usado como controle e, exceto por não ter recebido P. aquilinum, foi mantido nas mesmas condições que os outros quatro. Os quatro bovinos que receberam a planta morreram com quadro característico da intoxicação aguda por samambaia após receberem durante 53-58 dias, doses diárias de 8,0, 8,6, 10,2 e 10,6g/kg de peso corporal, que totalizaram, ao final do experimento, respectivamente, 112,7, 107,6, 85,7, 90,15 kg da planta, o que corresponde, respectivamente, a 59,3%, 63,3%, 47,4%, 47,5% da planta em relação ao peso dos bovinos. A doença caracterizou-se por febre de até 42,5°C e diversos graus de hemorragias observadas clinicamente, na necropsia e na histopatologia. A morte ocorria 6-7 dias após o início do quadro febril. As alterações hematológicas revelaram trombocitopenia e neutropenia acentuadas. Em dois dos quatro bovinos havia anemia leve. Não houve variações significativas nos tempos de coagulação dos bovinos intoxicados, quando avaliados os fatores de coagulação (secundária), excluindo-se assim a possibilidade da participação de distúrbios da hemostasia secundária na patogênese das hemorragias nessa intoxicação. A determinação dos produtos da degradação da fibrina no soro revelou dados conflitantes, não permitindo concluir se a coagulação intravascular disseminada tem participação na patogênese das hemorragias nessa intoxicação. A citopatologia e histopatologia da medula óssea dos quatro bovinos intoxicados revelaram acentuada diminuição no número de células hematopoéticas das três linhagens medulares, caracterizando insuficiência medular por aplasia; conclui-se que apenas eventos da hemostasia primária devidos a trombocitopenia são responsáveis pelas hemorragias. Na hemocultura de três dos bovinos intoxicados houve crescimento de Klebsiella oxytoca, Staphylococcus hyicus e Staphylococcus aureus, indicando que a septicemia, facilitada pela neutropenia, pode ter participação na causa da morte de bovinos na intoxicação aguda pela ingestão de P. aquilinum. Aspectos adicionais de interesse na reprodução da intoxicação aguda por samambaia em bovinos deste relato incluem o desenvolvimento de hematúria na doença aguda e a apresentação da chamada forma laríngea da doença.

Abstract in English:

Langohr I.M., Gava A. & Barros C.S.L. 2005. [Poisoning in cattle by Baccharidastrum triplinervium (Asteraceae).] Intoxicação por Baccharidastrum triplinervium (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 25(4):235-238. Animal Disease Diagnostic Laboratory, Purdue University, 406 South University, West Lafayette, IN 47907, Estados Unidos. E-mail: ilangohr@purdue.edu An outbreak of poisoning by Baccharidastrum triplinervium in cattle from Paraná, Brazil, is described. The disease occurred during a severe drought in early summer. The onset of clinical signs was two days after 50 cows and 8 heifers had been introduced into a pasture with high density of B. triplinervium that showed signs of having been consumed by the animals. Fifteen animals (9 cows and 6 heifers) got sick. Of these 15, two cows and four heifers died after a clinical course of 12-60 hours. Clinical signs included depression, ruminal atony, moderate bloat, marked dehydration, mild diarrhea and anorexia. The animals were restless, laying down and getting up constantly, remaining progressively longer periods in sternal recumbency. Once in that position, the animals had an extended head or the head turned to one of the sides of the body, and were groaning. Additionally, the cows had an abrupt fall in milk yield. The remaining affected cattle presented milder clinical signs and were partially back to their feed on the day following the onset of the clinical signs. The milk production was back to normal values within one week. The main gross lesions observed in two necropsied cows were in the forestomachs and abomasum, consisting of edema of the ruminal wall, as well as of diffuse reddening of the mucosae of the rumen, reticulum, abomasum and of some of the omasal folds. The main histological lesions included multifocal ballooning degeneration and necrosis of the lining epithelium of the rumen, associated with neutrophilic infiltrate. The diagnosis was based on the epidemiological data and on the experimental reproduction of the disease by force-feeding 3 bovine with the aeral fresh parts (20 and 30g/kg) of B. triplinervium. Chemical analysis of dried material from B. triplinervium harvested at the site of the outbreak was negative for macrocyclic trichothecenes.

• Poisonous plants Baccharidastrum triplinervium Asteraceae plant poisoning diseases of cattle pathology.

Abstract in Portuguese:

Langohr I.M., Gava A. & Barros C.S.L. 2005. [Poisoning in cattle by Baccharidastrum triplinervium (Asteraceae).] Intoxicação por Baccharidastrum triplinervium (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 25(4):235-238. Animal Disease Diagnostic Laboratory, Purdue University, 406 South University, West Lafayette, IN 47907, Estados Unidos. E-mail: ilangohr@purdue.edu An outbreak of poisoning by Baccharidastrum triplinervium in cattle from Paraná, Brazil, is described. The disease occurred during a severe drought in early summer. The onset of clinical signs was two days after 50 cows and 8 heifers had been introduced into a pasture with high density of B. triplinervium that showed signs of having been consumed by the animals. Fifteen animals (9 cows and 6 heifers) got sick. Of these 15, two cows and four heifers died after a clinical course of 12-60 hours. Clinical signs included depression, ruminal atony, moderate bloat, marked dehydration, mild diarrhea and anorexia. The animals were restless, laying down and getting up constantly, remaining progressively longer periods in sternal recumbency. Once in that position, the animals had an extended head or the head turned to one of the sides of the body, and were groaning. Additionally, the cows had an abrupt fall in milk yield. The remaining affected cattle presented milder clinical signs and were partially back to their feed on the day following the onset of the clinical signs. The milk production was back to normal values within one week. The main gross lesions observed in two necropsied cows were in the forestomachs and abomasum, consisting of edema of the ruminal wall, as well as of diffuse reddening of the mucosae of the rumen, reticulum, abomasum and of some of the omasal folds. The main histological lesions included multifocal ballooning degeneration and necrosis of the lining epithelium of the rumen, associated with neutrophilic infiltrate. The diagnosis was based on the epidemiological data and on the experimental reproduction of the disease by force-feeding 3 bovine with the aeral fresh parts (20 and 30g/kg) of B. triplinervium. Chemical analysis of dried material from B. triplinervium harvested at the site of the outbreak was negative for macrocyclic trichothecenes.

Abstract in English:

Barbosa J.D., Oliveira C.M.C., Duarte M.D., Peixoto P.V. & Tokarnia C.H. 2005. [Experimental and natural poisoning by Ipomoea asarifolia (Convolvulaceae) in buffaloes and other ruminants.] Intoxicações experimental e natural por Ipomoea asarifolia (Convolvulaceae) em búfalos e outros ruminantes. Pesquisa Veterinária Brasileira 25(4):231-234. Escola de Medicina Veterinária, Campus Castanhal, Universidade Federal do Pará, Rua Maximino Porpino 1000, Castanhal, PA 68743-080, Brazil. E-mail: tokarnia@ufrrj.br Ipomoea asarifolia R. et Schult. is a plant responsible for occasional outbreaks of poisoning in cattle, sheep and goats. Its oral administration to cattle and buffalos showed that the buffalo is as susceptible as cattle. One to 4 daily doses of 10-20g/kg caused similar symptoms in both species, as incoordination, muscular twiching and swaying of the head and anterior part of the body (pendular movement). In buffaloes the signs of incoordination were observed to a smaller extent. There is no report yet on natural poisoning by I. asarifolia in buffaloes, possibly because cases are not being noticed.

• Poisonous plants Ipomoea asarifolia Convolvulaceae plant poisoning buffaloes bovines sheep goats.

Abstract in Portuguese:

Barbosa J.D., Oliveira C.M.C., Duarte M.D., Peixoto P.V. & Tokarnia C.H. 2005. [Experimental and natural poisoning by Ipomoea asarifolia (Convolvulaceae) in buffaloes and other ruminants.] Intoxicações experimental e natural por Ipomoea asarifolia (Convolvulaceae) em búfalos e outros ruminantes. Pesquisa Veterinária Brasileira 25(4):231-234. Escola de Medicina Veterinária, Campus Castanhal, Universidade Federal do Pará, Rua Maximino Porpino 1000, Castanhal, PA 68743-080, Brazil. E-mail: tokarnia@ufrrj.br Ipomoea asarifolia R. et Schult. is a plant responsible for occasional outbreaks of poisoning in cattle, sheep and goats. Its oral administration to cattle and buffalos showed that the buffalo is as susceptible as cattle. One to 4 daily doses of 10-20g/kg caused similar symptoms in both species, as incoordination, muscular twiching and swaying of the head and anterior part of the body (pendular movement). In buffaloes the signs of incoordination were observed to a smaller extent. There is no report yet on natural poisoning by I. asarifolia in buffaloes, possibly because cases are not being noticed.

Abstract in English:

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

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

Abstract in Portuguese:

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

Abstract in English:

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

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

Abstract in Portuguese:

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

Abstract in English:

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

• umarin poisoning cattle.

Abstract in Portuguese:

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

Abstract in English:

Riet-Correa G., Terra F.F., Schild A.L., Riet-Correa F. & Barros S.S. 2005. [Experimental poisoning by Tetrapterys multiglandulosa (Malpighiaceae) in sheep.] Intoxicação experimental por Tetrapterys multiglandulosa (Malpighiaceae) em ovinos. Pesquisa Veterinária Brasileira 25(2):91-96. Curso de Medicina Veterinária, Campus de Castanhal, UFPA, Castanhal, PA 68740-080, Brazil. E-mail: griet@ufpa.br Cardiac fibrosis was observed in a calf showing dullness, weakening and respiratory insufficiency in a farm in the state of São Paulo, where cardiac insufficiency, abortion and nervous signs in cattle were associated with the ingestion of Tetrapterys multiglandulosa. The objectives of this paper were to determine the susceptibility of sheep to the intoxication by T. multiglandulosa, to describe the clinical and pathological characteristics of the intoxication, and to evaluate the possibility of using sheep as an experimental species for toxicological studies with this plant. In a previous experiment to determine the toxicity of T. multiglandulosa to be used in sheep, the green plant was given to a steer at the dose of 22g per kg body weight (g/kg/bw), daily, during 9 days. After 9 days the steer showed nervous signs, and on the 12thday was euthanatized. No gross lesions were observed at necropsy. Status spongiosus was observed on the deeper layers of the cerebral cortex and subcortical white matter. Six male sheep were divided in three groups of two sheep each. Group 1 (Sheep 1 and 2) received daily doses of 6 g/kg/bw of the dry plant, during 30 days; Group 2 (Sheep 3 and 4) received daily doses of 3 g/kg/bw, during 60 days; and Group 3 was the control group. Sheep 1 was euthanatized 30 days after the start of the ingestion. Only cardiac arrhythmia was observed clinically, and no lesions were observed at necropsy. Sheep 2, 3 and 4 had also cardiac arrhythmia from day 9, 12 and 18, respectively. From day 52 they started to show depression, reluctance to move and incoordination. Clinical signs got gradually worst and the sheep were euthanatized on days 60, 70 and 80, when clinical signs were marked, and the animals will die at any moment. Hydrothorax, hydropericardium, ascites, nutmeg appearance of the liver and hard whitish myocardium, mainly in the interventricular septum and left ventricle, were observed at necropsy. Histologically, the heart of Sheep 2, 3 and 4 had areas of fibrosis associated with mononuclear cell infiltration. No lesions were found in the heart of Sheep 1. The 4 treated sheep had status spongiosus in different areas of the cerebrum and brain stem, mainly of the deep layers of the cerebral cortex and subcortical white matter. Status spongiosus were also observed in the cerebellar white matter and cervical medulla. In the later the vacuolization was moderate in the white matter and mild in the grey matter. Status spongiosus were mild in Sheep 1 and moderate to severe in Sheep 2, 3 and 4. On electron microscopy it was observed that the status spongiosus is due to an intramyelinic edema. No gross or histologic lesions were observed on the two control sheep, which were euthanized on day 80 after the start of the experiment.

• etrapterys multiglandulosa Malpighiaceae cardiac fibrosis status spongiosus nervous system sheep.

Abstract in Portuguese:

Riet-Correa G., Terra F.F., Schild A.L., Riet-Correa F. & Barros S.S. 2005. [Experimental poisoning by Tetrapterys multiglandulosa (Malpighiaceae) in sheep.] Intoxicação experimental por Tetrapterys multiglandulosa (Malpighiaceae) em ovinos. Pesquisa Veterinária Brasileira 25(2):91-96. Curso de Medicina Veterinária, Campus de Castanhal, UFPA, Castanhal, PA 68740-080, Brazil. E-mail: griet@ufpa.br Cardiac fibrosis was observed in a calf showing dullness, weakening and respiratory insufficiency in a farm in the state of São Paulo, where cardiac insufficiency, abortion and nervous signs in cattle were associated with the ingestion of Tetrapterys multiglandulosa. The objectives of this paper were to determine the susceptibility of sheep to the intoxication by T. multiglandulosa, to describe the clinical and pathological characteristics of the intoxication, and to evaluate the possibility of using sheep as an experimental species for toxicological studies with this plant. In a previous experiment to determine the toxicity of T. multiglandulosa to be used in sheep, the green plant was given to a steer at the dose of 22g per kg body weight (g/kg/bw), daily, during 9 days. After 9 days the steer showed nervous signs, and on the 12thday was euthanatized. No gross lesions were observed at necropsy. Status spongiosus was observed on the deeper layers of the cerebral cortex and subcortical white matter. Six male sheep were divided in three groups of two sheep each. Group 1 (Sheep 1 and 2) received daily doses of 6 g/kg/bw of the dry plant, during 30 days; Group 2 (Sheep 3 and 4) received daily doses of 3 g/kg/bw, during 60 days; and Group 3 was the control group. Sheep 1 was euthanatized 30 days after the start of the ingestion. Only cardiac arrhythmia was observed clinically, and no lesions were observed at necropsy. Sheep 2, 3 and 4 had also cardiac arrhythmia from day 9, 12 and 18, respectively. From day 52 they started to show depression, reluctance to move and incoordination. Clinical signs got gradually worst and the sheep were euthanatized on days 60, 70 and 80, when clinical signs were marked, and the animals will die at any moment. Hydrothorax, hydropericardium, ascites, nutmeg appearance of the liver and hard whitish myocardium, mainly in the interventricular septum and left ventricle, were observed at necropsy. Histologically, the heart of Sheep 2, 3 and 4 had areas of fibrosis associated with mononuclear cell infiltration. No lesions were found in the heart of Sheep 1. The 4 treated sheep had status spongiosus in different areas of the cerebrum and brain stem, mainly of the deep layers of the cerebral cortex and subcortical white matter. Status spongiosus were also observed in the cerebellar white matter and cervical medulla. In the later the vacuolization was moderate in the white matter and mild in the grey matter. Status spongiosus were mild in Sheep 1 and moderate to severe in Sheep 2, 3 and 4. On electron microscopy it was observed that the status spongiosus is due to an intramyelinic edema. No gross or histologic lesions were observed on the two control sheep, which were euthanized on day 80 after the start of the experiment.

Abstract in English:

Rissi D.R., Rech R.R., Fighera R.A., Cagnini D.Q., Kommers G.D. & Barros C.S.L. 2005. [Spontaneous Baccharis coridifolia poisoning in cattle.] Intoxicação espontânea por Baccharis coridifolia em bovinos. Pesquisa Veterinária Brasileira 25(2):111-114. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two outbreaks of Baccharis coridifolia poisoning in cattle in southern Brazil are described. Cases occurred when stressed, hungry and thirsty cattle brought from pastures free of B. coridifolia were placed into pastures heavily infested by this poisonous plant. In the two outbreaks morbidity was 21.73% and 22.51% and lethality was virtually 100%. Clinical signs included mild bloat, instability of hind limbs, muscle tremors, dry muzzle, dry feces or diarrhea, polydipsia and restlessness. Consistent necropsy findings included dehydration, large amounts of ruminal fluid, reddening and erosions of the mucosae of the forestomachs. Degeneration and necrosis of the lining epithelium of the forestomachs and of lymphoid tissue were the main histopathological changes encountered.

• Poisonous plants Baccharis coridifolia Asteraceae diseases of cattle pathology.

Abstract in Portuguese:

Rissi D.R., Rech R.R., Fighera R.A., Cagnini D.Q., Kommers G.D. & Barros C.S.L. 2005. [Spontaneous Baccharis coridifolia poisoning in cattle.] Intoxicação espontânea por Baccharis coridifolia em bovinos. Pesquisa Veterinária Brasileira 25(2):111-114. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two outbreaks of Baccharis coridifolia poisoning in cattle in southern Brazil are described. Cases occurred when stressed, hungry and thirsty cattle brought from pastures free of B. coridifolia were placed into pastures heavily infested by this poisonous plant. In the two outbreaks morbidity was 21.73% and 22.51% and lethality was virtually 100%. Clinical signs included mild bloat, instability of hind limbs, muscle tremors, dry muzzle, dry feces or diarrhea, polydipsia and restlessness. Consistent necropsy findings included dehydration, large amounts of ruminal fluid, reddening and erosions of the mucosae of the forestomachs. Degeneration and necrosis of the lining epithelium of the forestomachs and of lymphoid tissue were the main histopathological changes encountered.

Abstract in English:

Dutra I.S., Döbereiner J. & Souza A.M. 2005. [Botulism in beef and dairy cattle fed with poultry litter.] Botulismo em bovinos alimentados com cama de frango. Pesquisa Veterinária Brasileira 25(2):115-119. Depto Apoio, Produção e Saúde Animal, Curso de Medicina Veterinária, Universidade Estadual Paulista (Unesp), Rua Clóvis Pestana 793, Araçatuba, SP 16065-080, Brazil. E-mail: isdutra@fmva.unesp.br Outbreaks of botulism caused by type C and D of the botulinum toxin are frequent in Brazil, and are associated with bone chewing and ingestion of contaminated food and water. This paper reports the epidemiological, clinical, pathological and laboratorial aspects of 7 outbreaks of botulism in beef and dairy cattle fed with poultry litter, which occurred in the states of São Paulo and Minas Gerais, 1989-2000. Five outbreaks occurred in beef cattle herds, raised in confinement or under pasture conditions and supplemented with poultry litter, and 2 outbreaks occurred in dairy farms. From o total of 1,535 cattle supplemented regularily with poultry litter 455 animals (29.64%) died within 2 to 4 weeks. Morbidity and mortality varied from 3.47 to 100% in the 7 outbreaks. In one of the farms the lethality was 60.52%, and in others more than 88.43%, reaching 100% in three farms. Clinical signs were progressive paralysis, difficulties in moving, decubitus, normal alertness, decreased muscular tonus of tongue and tail, sialorrhoe and dyspnoe. At post-mortem examination of 30 cattle no noteable changes were observed. Spores of Clostridium botulinum were found in poultry litter samples collected on 7 farms. In liver, ruminal and intestinal fluid samples from 30 necropsied cattle botulinum toxin of type C (5) and D (9) or of the CD complex (1) were found in at least one of the samples collected from 15 animals, which confirms the clincial, pathological and epidemiological diagnosis of botulism.

• Botulism cattle poultry litter.

Abstract in Portuguese:

Dutra I.S., Döbereiner J. & Souza A.M. 2005. [Botulism in beef and dairy cattle fed with poultry litter.] Botulismo em bovinos alimentados com cama de frango. Pesquisa Veterinária Brasileira 25(2):115-119. Depto Apoio, Produção e Saúde Animal, Curso de Medicina Veterinária, Universidade Estadual Paulista (Unesp), Rua Clóvis Pestana 793, Araçatuba, SP 16065-080, Brazil. E-mail: isdutra@fmva.unesp.br Outbreaks of botulism caused by type C and D of the botulinum toxin are frequent in Brazil, and are associated with bone chewing and ingestion of contaminated food and water. This paper reports the epidemiological, clinical, pathological and laboratorial aspects of 7 outbreaks of botulism in beef and dairy cattle fed with poultry litter, which occurred in the states of São Paulo and Minas Gerais, 1989-2000. Five outbreaks occurred in beef cattle herds, raised in confinement or under pasture conditions and supplemented with poultry litter, and 2 outbreaks occurred in dairy farms. From o total of 1,535 cattle supplemented regularily with poultry litter 455 animals (29.64%) died within 2 to 4 weeks. Morbidity and mortality varied from 3.47 to 100% in the 7 outbreaks. In one of the farms the lethality was 60.52%, and in others more than 88.43%, reaching 100% in three farms. Clinical signs were progressive paralysis, difficulties in moving, decubitus, normal alertness, decreased muscular tonus of tongue and tail, sialorrhoe and dyspnoe. At post-mortem examination of 30 cattle no noteable changes were observed. Spores of Clostridium botulinum were found in poultry litter samples collected on 7 farms. In liver, ruminal and intestinal fluid samples from 30 necropsied cattle botulinum toxin of type C (5) and D (9) or of the CD complex (1) were found in at least one of the samples collected from 15 animals, which confirms the clincial, pathological and epidemiological diagnosis of botulism.

Abstract in English:

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

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

Abstract in Portuguese:

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