Abstract. An aflatoxicosis outbreak affected 65 dogs from 9 different farms after they were fed diets with cooked corn meal as a common ingredient. Of the dogs, 60 died. Numerous dogs died on additional farms, but those dogs were not included in the study. The farmers acquired the contaminated maize products, in the form of whole corn grain or as corn meal, from the same supplier. The corn product was mixed with meat that was left over from home or commercial rations to form corn polenta, which was fed to the dogs. Necropsy was performed on 3 dogs. Two of the dogs died after a few days of refusing food, showing anorexia, polydipsia, icteric mucous membranes, hematemesis, hematochezia, or melena, and bleeding of the skin, eye, ear, and mouth. The primary necropsy findings included jaundice, hemorrhages in several organs, and yellowish enlarged liver with enhanced lobular pattern. The dog that experienced chronic ascites had a yellowish liver with reduced volume, irregular surface, and increased consistency. The main histological findings included hepatocyte fatty degeneration, biliary duct hyperplasia, cholestasis and, in the chronic case, hepatic fibrosis. High-performance liquid chromatography analysis of the corn meal from 2 affected farms revealed 1,640 ppb and 1,770 ppb of aflatoxin B 1 , respectively. The current study demonstrates an additional way that dogs can be exposed to, poisoned, and killed by aflatoxin.

Congenital Neospora caninum infection was diagnosed in two Saanen goat kids from two distinct herds with a history of abortion and weak newborn goat kids in the Southern region of the State of Minas Gerais, Brazil. The first kid was weak at birth, had difficulty to rise and was unable to nurse. Gross lesions of porencephaly and hydrocephalus ex vacuo were seen. Multifocal necrosis, gliosis and non-supurative encephalitis were observed in the brain. Several parasitic cysts with a thick wall that reacted strongly only with polyclonal antiserum to Neospora caninum were seen in the cerebral cortex, brain stem and cerebellum. The second kid was born from a Neospora caninum seropositive mother that aborted in the last pregnancy. It was born without clinical signs. The diagnosis of neosporosis was based on antibody titer of 1:800 to N. caninum by indirect fluorescence antibody test obtained from blood collected before the goat kid ingested the colostrum and Neospora caninum DNA was detected by polymerase chain reaction and sequenced from placenta. This is the first report of neosporosis in goats in the southeast region of Brazil.

Trema micrantha, a fast-growing tree distributed throughout the Americas, produces palatable leaves that have been associated with hepatic necrosis and acute death when consumed by livestock. This report describes fatal pulmonary disease of sheep triggered by consumption of Trema micrantha. Affected sheep had severe progressive dyspnea for a few days before death. Subcutaneous and mediastinal emphysema, reddened lungs, interalveolar septal thickening, and diffuse type II pneumocyte proliferation were the main pathological findings. After ingesting 77.5 and 102.5 g/kg (divided in 3 doses, at 30-day intervals) of T. micrantha leaves, 2 additional sheep developed the same condition. These findings indicate that T. micrantha toxicosis should be considered in the differential diagnosis of ovine respiratory disease.

Descreve-se um surto de intoxicação por salinomicina em bovinos. De um grupo de 46 novilhas Simmental, 13 morreram após manifestação de incoorde-nação, andar rígido, diarréia, emagrecimento, tremores musculares, cansaço após pequenos movimentos, dispnéia e, ocasionalmente, urina escura. Os animais eram encontrados mortos ou morriam subitamente quando movimentados. As lesões macroscópicas consistiam basicamente de áreas pálidas no miocárdio, hemorragias subepicárdicas, hidropericárdio, hidrotórax, congestão e edema pulmonar e, em alguns casos, edema de declive e fígado de noz-moscada. Os principais achados microscópicos foram lesões multifocais de necrose e perda de fibras miocárdicas, que eram substituídas por tecido conjuntivo fibroso. Cerca de 9 dias antes do início da mortandade, as novilhas tinham sido medicadas para eimeriose, com um premix contendo 6% de salinomicina.

Experimental poisoning by narasin was induced in 13 sheep through oral administration of the drug. Six sheep died, three were killed in extremis and four recovered. The onset of clinical signs was 2 hours to 7 days after the administration of the drug, and the clinical course lasted from 7 hours to 14 days. Initially there were laborious breathing, tachypnea, fever and ruminal atony. These signs were followed by incoordinated gait, stiffness, reluctance to move and changes in frequency and intensity of cardiac sounds. Grunting, grinding of teeth, myoglobinuria, and sternal and lateral recumbency were also observed. One sheep had sudden death. Necropsy findings were observed in seven of the sheep that died and consisted of pale areas in the skeletal muscles and myocardium. More frequently affected muscles were masseter, semitendinosus, sternocephalicus, brachiocephalicus, extrinsec muscles of the tongue, pectoral, supraspinatus and teres major. Hydropericardium, edema of the lungs and the wall of the gall bladder were also observed. Ocasionally the cut surface of the lymph nodes was reddened and moist. In one sheep there was edema surrounding the esophagus and within the cervical muscles; in another one there was a bolus of partially chewed food in the oral cavity. Histologically, the pale areas in the skeletal muscles and myocardium corresponded to multifocal or focal extensive degeneration and necrosis of myofibers; these lesions were sometimes associated with processes of regeneration in skeletal muscles and reparation in the myocardium. The histological muscle lesions were more pronounced in the tongue and muscles of the limbs.INDEX TERMS: Narasin, ionophore antibiotics, sheep, pathology, toxicosis.SINOPSE.-Intoxicação pelo antibiótico ionóforo narasina foi induzida experimentalmente em 13 ovinos; desses, seis morreram espontaneamente, três foram sacrificados in extremis e quatro se recuperaram. O início dos sinais clínicos ocorria entre 2 horas e 7 dias após a administração da droga e persistiam por 7 horas a 14 dias. Inicialmente havia respiração ofegante e entrecortada, taquipnéia, febre, redução temporária do apetite ou anorexia e atonia ruminal seguidos de alterações no andar, como arrastar das pinças, apoio sobre os 1 Aceito para publicação em 25 de abril de 1997.Parte da tese de mestrado do primeiro autor. Defendida no Curso de Pós-Graduação (CPG) em Medicina Veterinária, área de concentração em patologia, Universidade Federal de Santa Maria (UFSM), em 29 de janeiro de 1997. Trabalho financiado pelo CNPq, projeto 530198/93-2.2 CPG em Medicina Veterinária, área de concentração em patologia, Centro de Ciências Rurais, UFSM, 97119-900 Santa Maria, Rio Grande do Sul.3 Departamento de Patologia, UFSM. Bolsista do CNPq (350938/91-1).boletos dos membros posteriores, incoordenação, rigidez, relutância em movimentar-se e alteração na frequência e intensidade dos sons cardíacos. Ocorriam também gemidos, ranger de dentes, urina acastanhada e decúbito esternal ou lateral. Um animal apresentou morte súbita. Alteraç...

We report tuberculosis in a stranded South American sea lion (Otaria byronia) in Brazil caused by Mycobacterium pinnipedii, a member of Mycobacterium tuberculosis complex.

Este estudo teve como objetivo determinar a prevalência e achados anatomopatológicos de tumores primários e metastáticos do coração ou de tecidos da base do coração, diagnosticados em caninos do Sul de Minas Gerais. O diagnóstico foi realizado mediante análise histopatológica e imuno-histoquímica das neoplasias. Durante os anos de 1994-2009, foram realizadas 2397 necropsias em caninos. Neoplasias no coração foram detectadas em 31 cães (1,29%), onde, sete (22,58%) eram primárias e 24 (77,42%) metastáticas. As neoplasias diagnosticadas como primárias do coração foram o hemangiossarcoma (1/7) e o mixoma (1/7); e como primárias da base do coração o quimiodectoma (3/7) e o carcinoma de tireoide ectópica (2/7). A frequência foi maior em cães machos (5/7), da raça Boxer (3/7) e com idade média de 9,7±1,88 anos. Nas neoplasias metastáticas, a frequência foi maior em fêmeas (15/24), em cães da raça Rottweiler (7/24) e a idade média foi de 7,5±3,23 anos, sendo o linfoma de células T a neoplasia metastática de maior ocorrência (7/27).

Descreve-se um surto de intoxicação por monensina em avestruzes e equinos em uma propriedade no Rio Grande do Sul. Oito dias antes do aparecimento dos primeiros sinais clínicos, uma ração comercial formulada para bovinos, cuja composição incluía monensina (177ppm), foi introduzida na dieta dos animais. Três equinos manifestaram dificuldade de movimentação, cólica, sudorese e decúbito permanente; dois morreram em 48 horas após o inicio dos sinais. Três avestruzes adoeceram, dois apresentaram decúbito esternal permanente, o outro estava apático e relutante ao movimento. Dois avestruzes morreram 15 e 30 dias após o início dos sinais. Nas necropsias dos equinos, observou-se miocárdio com palidez multifocal, hemorragia no endocárdio e no epicárdio (principalmente ao redor dos vasos coronarianos) e musculatura esquelética com áreas branco-amareladas bilaterais e focalmente extensas. Essas alterações corresponderam histologicamente, à miopatia e cardiomiopatia necróticas. Nos avestruzes, músculos esqueléticos difusamente pálidos e com múltiplos pequenos pontos brancos corresponderam à necrose segmentar polifásica, com alterações necróticas e regenerativas