PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Poisoning by Trema micrantha commonly causes hepatocellular necrosis in cattle, sheep, and goats and edema and cerebral hemorrhage in horses. This plant can cause toxic pneumopathy in sheep, and there is only one report of the natural form and one of the experimental form in the State of Rio Grande do Sul. This study aimed to report an outbreak of the respiratory form of natural poisoning by T. micrantha in sheep. Six sheep developed clinical respiratory signs after consumption of the plant and four of them died and two recovered after treatment with dexamethasone. The sheep presented tachypnea, noisy breathing, edema of the face, eyelids, and vulva, and subcutaneous emphysema on the face and neck. Necropsy (Sheep 2, 3, and 4) showed uncollapsed, heavy, diffuse red lungs with evident costal impressions and a moderate amount of serosanguineous fluid flowed at section. The liver had a moderate diffuse evident lobular pattern. The histopathology of the lungs of the three necropsied sheep showed congestion and edema with the formation of hyaline membranes within accentuated diffuse alveoli, in addition to thickening of the alveolar septa due to mild to moderate diffuse type II pneumocyte hyperplasia and also mild to moderate diffuse infiltrate of macrophages, lymphocytes, plasma cells, and neutrophils in the lumen of alveoli, bronchi, and bronchioles. Sheep 3 also showed type II pneumocytes with enlarged and hyperchromatic nuclei, sometimes binucleated with evident nucleoli, and, in some regions, the pneumocytes were desquamated to the alveolar lumen forming small syncytia and mild multifocal hyperplasia in the bronchial epithelium. The anti-cytokeratin IHC evaluation showed marked diffuse intracytoplasmic staining in hyperplastic type II pneumocytes in the bronchiolar epithelium of the three evaluated sheep. The liver of the three sheep had mild multifocal centrilobular necrosis. It seems to be the second report of spontaneous poisoning by T. micrantha in sheep developing lung lesions described in Brazil and the first in the State of Santa Catarina.

• Toxic plant pneumotoxicosis Trema micrantha sheep interstitial pneumonia hepatotoxic Brazil

Abstract in Portuguese:

A intoxicação por Trema micrantha, comumente causa em bovinos, ovinos e caprinos necrose hepatocelular e, edema e hemorragia cerebral em equinos. Essa planta em ovinos pode causar pneumopatia tóxica, existindo descrição apenas de um relato da forma natural e um da forma experimental no estado do Rio Grande do Sul. O objetivo deste trabalho é relatar, um surto, da forma respiratória de intoxicação natural por T. micranta em ovinos. Seis ovinos desenvolveram sinais clínicos respiratórios após o consumo da planta e destes quatro morreram e dois após o tratamento com dexametasona se recuperaram. Os ovinos apresentaram taquipneia, respiração ruidosa, edema de face, pálpebras, vulva e enfisema subcutâneo na face e pescoço. Na necropsia (Ovinos 2, 3 e 4) observou-se pulmões não colabados, pesados, vermelhos difusos com impressões costais evidentes e ao corte fluindo moderada quantidade de líquido serosanguinolento. O fígado apresentava padrão lobular evidente difuso moderado. Na histopatologia, em pulmões dos três ovinos necropsiados havia congestão e edema com formação de membranas hialinas no interior de alvéolos difusos acentuados, além de espessamento dos septos alveolares devido a hiperplasia de pneumócitos tipo II difuso discreta à moderada, havia ainda, infiltrado de macrófagos, linfócitos, plasmócitos e neutrófilos difuso discreto a moderado no lúmen de alvéolo, brônquios e bronquíolos. No Ovino 3, observou-se ainda pneumócitos tipo II com núcleos aumentados e hipercromáticos, por vezes binucleados com nucléolos evidentes, e em algumas regiões estes pneumócitos estavam descamados para a luz alveolar formando pequenos sincícios e no epitélio de brônquios havia hiperplasia multifocal discreta. A avaliação IHQ anti-citoqueratina demonstrou marcação intracitoplasmática difusa acentuada em pneumócitos tipo II hiperplásicos no epitélio bronquiolar dos três ovinos avaliados. No fígado dos três ovinos havia necrose centrolobular multifocal discreta. Este parece ser o segundo relato da intoxicação espontânea por T. micrantha em ovinos desenvolvendo lesões pulmonares, descrito no Brasil e o primeiro no estado de Santa Catarina.

• Planta tóxica pneumotoxicose Trema micrantha ovinos pneumonia intersticial hepatotóxica Brasil.

Abstract in English:

ABSTRACT.- Costa R.A., Schild C., Silveira C.S., Macías-Rioseco M., Mirazo S., Maya L., Clariget J. & Riet-Correa F. 2018. Acute and chronic bovine pulmonary edema and emphysema in Uruguay. [Edema e enfisema pulmonar agudo e crônico em bovinos do Uruguai.] Pesquisa Veterinária Brasileira 38(10):1929-1934. Instituto Nacional de Investigación Agropecuaria, Estación Experimental INIA La Estanzuela, Ruta 50 Km 11, Colonia del Sacramento, Colonia, Uruguay. E-mail: frcorrea@inia.org.uy An outbreak of pulmonary edema and emphysema with acute and chronic cases is reported in a farm in Uruguay. In a herd of 40 Hereford steers, 20 died. The deaths began four days after a change of paddock, from an old pasture of Avena sativa to a lush growing pasture of the same grass. Acutely affected animals showed severe dyspnea, sialorrhea, cough, and subcutaneous edema, and died within 72 hours. Chronically affected steers showed dyspnea, respiratory noises, weight loss, and intolerance to exercise. The deaths began four days after the change of paddock. Ten days after the first death, the steers were withdrawn from the pasture, but continued dying throughout the following 40 days. Twenty animals died and six were necropsied. Grossly, the lungs were diffusely armed and glistening, with reddish and crepitant cut surface, and presented alveolar septae sharply distended by edema and emphysema. There was subpleural emphysema with air blebs distributed across the pleural surface. Presence of Dictyocaulus viviparus was observed in three steers. In some animals, the trachea was diffusely reddish with presence of pink foam; in some others, there was bloody liquid in the tracheal lumen. Histologic examination showed severe diffuse alveolar and interstitial emphysema, hyaline membranes adhered to the alveolar wall, thickening of the interlobular septae with proliferation of type II pneumocytes, and moderate-to-severe multifocal histiocytic, neutrophilic and eosinophilic infiltrate. In the trachea, there was submucosal hemorrhage and moderate multifocal eosinophilic and lymphocytic infiltrate. The steers with chronic signs presented similar lung lesions, but multifocal pulmonary fibrosis and cardiac dilatation were also observed. The diagnosis of acute bovine pulmonary emphysema and edema (ABPE) was based on the occurrence of the disease after introduction of the herd in a lush green pasture, on the characteristic gross and histologic lesions, and on the absence of other toxic or infectious agents causing similar lesions. Cattle raisers should be alert to the risks of occurrence of this disease after the introduction of the herds into paddocks with green and lush pastures.

• Pulmonary edema pulmonary emphysema cattle Uruguay L-tryptophan 3-methylindole fog fever atypical interstitial pneumonia bovine pathology Edema pulmonar enfisema pulmonar bovinos Uruguai L-triptofano 3-metil-indol fog fever pneumonia intersticial atípica bovino patologia.

Abstract in Portuguese:

RESUMO.- Costa R.A., Schild C., Silveira C.S., Macías-Rioseco M., Mirazo S., Maya L., Clariget J. & Riet-Correa F. 2018. Acute and chronic bovine pulmonary edema and emphysema in Uruguay. [Edema e enfisema pulmonar agudo e crônico em bovinos do Uruguai.] Pesquisa Veterinária Brasileira 38(10):1929-1934. Instituto Nacional de Investigación Agropecuaria, Estación Experimental INIA La Estanzuela, Ruta 50 Km 11, Colonia del Sacramento, Colonia, Uruguay. E-mail: frcorrea@inia.org.uy Descreve-se um surto de edema e enfisema pulmonar com casos agudos e crônicos em bovinos em uma criação semi-intensiva no Uruguai. De um lote de 40 novilhos da raça Hereford morreram 20. As mortes começaram quatro dias após uma mudança de alimentação, de uma pastagem mais velha de Avena sativa, para uma pastagem recentemente plantada de aveia que estava em brotação. Os animais afetados apresentaram sinais clínicos agudos de dispneia, sialorreia, tosse e alguns desenvolveram edema subcutâneo, morrendo em até 72 horas. Outros novilhos mais cronicamente afetados apresentaram dispneia, ruídos respiratórios, perda de peso e intolerância ao exercício. As mortes começaram quatro dias após a mudança de pastagens. Dez dias após a primeira morte, os novilhos foram retirados do pasto, mas morreram ainda durante 40 dias mais. Ao total, morreram vinte animais e seis foram necropsiados. Nas necropsias dos animais mortos na fase aguda os pulmões estavam difusamente armados e brilhosos e ao corte de coloração avermelhada e crepitante, com os septos alveolares acentuadamente distendidos por edema e enfisema. Havia enfisema subpleural caracterizado por bolhas de ar distribuídas pela superfície pleural. Em três bovinos havia ainda presença de Dictyocaulus viviparus. Alguns animais apresentaram a traqueia difusamente avermelhada com espuma de coloração rósea ou liquido sanguinolento livre na luz traqueal. Histologicamente havia edema e enfisema alveolar e intersticial difuso severo, membranas hialinas espessas aderidas à parede alveolar, espessamento dos septos interlobulares com proliferação de pneumócitos tipo II e infiltrado inflamatório histiocítico, neutrofílico e eosinofílico multifocal moderado a severo. Na traqueia havia hemorragias na submucosa e infiltrado eosinofílico e linfocítico multifocal. Os novilhos com sinais crônicos apresentaram lesões pulmonares semelhantes, entretanto, foram observadas também, fibrose pulmonar multifocal e dilatação cardíaca. O diagnóstico de EEPAB baseou-se na ocorrência da doença após a introdução do rebanho em uma pastagem viçosa em brotação, nas características macroscópicas e histológicas e na ausência de outros agentes tóxicos ou infecciosos que causam lesões semelhantes. Se alerta para os riscos da ocorrência desta enfermidade, quando houver mudanças de pastagens.

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.- Fighera R.A., Rozza D.B., Piazer J.V., Copetti M.V., lrigoyen L.F. & Barros C.S.L. 2003. [Interstitial pneumonia in cattle fed moldy sweet potatoes (Ipomoea batatas).] Pneumonia intersticial em bovinos associada à ingestão de batata-doce (lpomoea batatas) mofada. Pesquisa Veterinária Brasileira 23(4):161-166. Depto Patologia, Universidade Federal de Santa Maria, 97105- 900 Santa Maria, RS, Brasil. E-mail: claudioslbarros@uol.com.br Cases of respiratory disease were diagnosed in five out of 23 cattle (21. 7%) after they wete fed moldy damaged sweet potatoes (lpomoea batatas) on a small farm in the county of São Vicente do Sul, state of Rio Grande do Sul, Brazil. Of those five cattle, three died spontaneously and another one was euthanatized for necropsy while showing advanced respiratory clinicai signs. The disease manifested itself approximately 24 hours after the ingestion of the sweet potatoes and lasted from 1 to 4 days. Clinicai signs included dyspnea (labored breathing and abdominal respiration), tachypnea, extended neck with Iow carriage of the head and rhythmical flaring of the nostrils. Two cows were necropsied. Necropsy findings included distended pale and rubbery lungs which failed to collapse when the thorax was open, and marked pulmonar interstitial emphysema and edema. Lymphoid hyperplasia was observed in the hilar nodes and spleen. Histologically, the lesions were those of interstitial pneumonia. Alveolar septa were thickened by fibroblasts and inflammatory cells, and there was hypertrophy and hyperplasia of type li pneumocytes; the interlobular septa were distended by edema and emphysema. The culture of the moldy sweet potatoes yielded Fusarium solani and Fusarium oxysporum.

• Toxic diseases mycotoxicoses respiratory diseases interstitial pneumonia diseases of cattle sweet potatoes lpomoea batatas Intoxicações micotoxicoses doenças respiratórias pneumonia intersticial doenças de bovinos batata-doce.

Abstract in Portuguese:

RESUMO.- Fighera R.A., Rozza D.B., Piazer J.V., Copetti M.V., lrigoyen L.F. & Barros C.S.L. 2003. [Interstitial pneumonia in cattle fed moldy sweet potatoes (Ipomoea batatas).] Pneumonia intersticial em bovinos associada à ingestão de batata-doce (lpomoea batatas) mofada. Pesquisa Veterinária Brasileira 23(4):161-166. Depto Patologia, Universidade Federal de Santa Maria, 97105- 900 Santa Maria, RS, Brasil. E-mail: claudioslbarros@uol.com.br Uma doença respiratória foi diagnosticada em cinco dentre 23 bovinos (21, 7%) após terem sido alimentados com batata-doce (lpomoea batatas) mofada em uma pequena propriedade rural em São Vicente do Sul, Rio Grande do Sul, Brasil. Três dos cinco bovinos afetados morreram espontaneamente, e o quarto foi sacrificado para necropsia quando mostrava sinais clínicos respiratórios avançados. A manifestação clínica iniciara cerca de 24 horas após a ingestão das batatasdoces e a evolução clínica foi de 1 a 4 dias. Os sinais clínicos incluíam dispnéia (respiração laboriosa e abdominal), taquipnéia, pescoço estendido com cabeça baixa e dilatação ritmada das narinas. Dois bovinos foram necropsiados. Os achados de necropsia incluíam pulmões distendidos, pálidos e de consistência borrachenta, que não colapsavam quando o tórax era aberto; enfisema e edema acentuados eram evidentes no pulmão. Os linfonodos e o baço apresentavam alterações características de hiperplasia linfóide. Histologicamente, as lesões eram típicas de pneumonia intersticial. Os septos alveolares estavam espessados por fibroblastos e células inflamatórias, havia hipertrofia e hiperplasia de pneumócitos tipo II; os septos interlobulares estavam distendidos por edema e enfisema. A cultura de amostras das batatas-doces mofadas produziu Fusarium solani e F. oxysporum.