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ABSTRACT: The state of Santa Catarina is the largest national producer of onions. The consumption of onion (Allium cepa) by domestic animals can cause hemolytic anemia and hyperhemoglobinemia of Heinz bodies in erythrocytes. The epidemiological data and the pathological clinical picture were obtained during a visit to the property where the disease occurred. A herd of 54 beef cattle from a property in the municipality of Bom Retiro/SC, was placed in an onion crop, which had not been completely harvested because it was outside the desired standard for trade. The animals remained in this field for eight days. At the end of this period, all of them presented apathy, anorexia, brown urine and mucous membranes and an onion odor on expiration. The macroscopic changes observed were pale mucous membranes, blood with decreased viscosity and increased clotting time, liver with an evident lobular pattern and remains of onion in the rumen. The carcass gave off a strong onion odor. By histological analysis, there was central lobular coagulation necrosis in bridging in the liver. In the kidneys, there were intracytoplasmic hyaline droplets in tubular epithelial cells and a deposit of eosinophilic material in the lumen of the tubules. For the diagnosis of onion poisoning, epidemiological data associated with clinical signs, such as pale mucous membranes with evidence of hemoglobin pigmentation (brown mucosa) and hemoglobinuria, should be taken into account. This article seems to be the first report of onion poisoning in cattle in Brazil.

ABSTRACT: Scrapie is a contagious disease of sheep and goats caused by prions (PrPSc). This study described an outbreak of Scrapie in sheep in the state of Santa Catarina, Brazil. An 1-year and 3-month-old sheep developed clinical signs characterized by motor incoordination of the pelvic limbs, pruritus and alopecia for three days. The 38 sheep from the flock that were over 1 year of age underwent biopsies of the third eyelid and rectal mucosa, in addition to anti-PrPsc immunohistochemistry (IHC). Blood containing EDTA was collected for PRNP gene genotyping from these sheep. Of the 38, 16 (42.10%) had immunostaining againstPrPSc. IHC-positive animals were euthanized and necropsied, as well as lambs from positive mothers. Different organs of the 19 necropsied animals were collected in 10% buffered formalin for histopathological examination and anti-PrPSc IHC of the obex. The histopathology of the obex of the female with neurological signs presented discrete multifocal vacuolization of the cytoplasm of neurons and neuropil. The anti-PrPSc IHC showed that two out of the 19 obex samples had cytoplasmic immunostaining in neurons. The genotypes reported were ARQ/ARQ in 47.36%, ARR/ARQ in 36.84%, ARQ/VRQ in 10.52% and ARQ/VRR in 5.28%. The genotyping helps to identify susceptible animals and select animals more resistant to the development of Scrapie. The anti-PrPSc IHC from lymphoid biopsies, and genotyping demonstrated the high number of positive sheep classified in susceptible group.

Polysaccharide storage myopathy (PSSM) is a genetic disorder or by undetermined cause characterized by the abnormal accumulation of glycogen and polysaccharides in skeletal muscle fibers. The present report describes two Percheron horses, from different properties in the municipality of Pouso Redondo - SC, with locomotor clinical signs that started after work. The clinical signs observed were rigid gait, mainly of the pelvic limbs, muscle weakness, and recumbency. In the first case, the animal was diagnosed with severe multifocal rhabdomyonecrosis, moderate multifocal myoglobin nephrosis and severe diffuse transmural fibrinonecrotic gastritis. PSSM was confirmed by the presence of polysaccharide inclusions in myofiber sarcolemma visualized by periodic acid-Schiff (PAS) staining. In the second case, the horse presented two episodes of muscle disorder after work. The therapeutic protocol was based on penicillin, flunixin meglumine and fluid therapy with ringer lactate. An increase in creatine kinase (669.0 UI/L) and aspartate aminotransferase (669.0 UI/L) was observed in the serum biochemical evaluation. Research for mutation in the GYS1 gene was performed, with a positive heterozygote result. After rest and gradual recovery, the horse was only submitted to light work, with no return of the clinical condition since then. Thus, this report describes two cases of PSSM with distinct clinical evolution and diagnostic methods.

ABSTRACT: 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.

RESUMO: Claviceps purpurea é o fungo associado ao ergotismo. Esta é uma enfermidade causada pela ingestão de escleródios chamados de ergot, que contém alcalóides que atuam em receptores adrenérgicos, dopaminérgicos e seratoninérgicos causando efeito direto em vasos sanguíneos, musculatura lisa e sistema nervoso central e autônomo. Descrevem-se dados epidemiológicos, sinais clínicos e lesões de uma enfermidade de bovinos caracterizada por hipertermia, taquicardia, taquipneia e ulcerações na coroa do casco de bovinos. Entre 2000 e 2014 foram diagnosticados 13 surtos, três da forma distérmica, sete da forma gangrenosa e três da forma convulsiva. Porém, em cinco destes sete surtos, nos locais onde esses animais pastoreavam havia alta incidência de inflorescências de Sporobolus indicus conhecido como “capim-mourão”, infectadas por um fungo com coloração enegrecida, identificado como Bipolaris sp. A enfermidade foi reproduzida experimentalmente em cinco bovinos com a administração destas inflorescências. Os bovinos em experimentação receberam inflorescências de S. indicus respectivamente nas doses diárias de 0,1g/kg, 0,2g/kg, 0,2g/kg, 0,26g/kg e 0,34g/kg por um período de 4, 7, 9 e 30 dias. Após três a sete dias de ingestão das inflorescências infectadas, quatro dos cinco bovinos apresentaram diarreia e manifestaram taquicardia, taquipneia e hipertermia em algum período durante a ingestão. Estes sinais coincidiram com os dias mais quentes deste período. Um bovino manifestou hiperemia na coroa do casco e perda de pêlos da extremidade da cauda. Baseado na reprodução experimental é possível afirmar que o capim Sporobolus indicus infectado pelo fungo Bipolaris sp é capaz de causar diarreia, hipertermia, taquicardia, taquipneia, hiperemia na coroa do casco e perda de pêlos da extremidade da cauda.

ABSTRACT: Polioencephalomalacia (PEM) is the morphological characterization for softening of brain gray matter, and excess sulfur intake is one of its main causes. This study describes an outbreak of this disease in 1-to-3-month-old calves in a farm located in Santa Catarina state, Brazil. The herd consisted of 27 Jersey male calves whose diet was composed of initial feed, ground whole corn, and mineral salt. From this herd, 10 animals became ill, showing signs of apathy, anorexia and blindness, evolving to generalized weakness and death. Necropsy was performed in three of these animals, which showed flattening of the cerebral convolutions in addition to softened, yellowish areas in the cerebral cortex. Histopathological examination revealed deep laminar necrosis associated with perineuronal and perivascular edema, as well as neurons with wrinkled, eosinophilic, or vacuolated cytoplasm. The following sulfur doses were observed: 8,010mg/kg in corn, 6,385mg/kg in initial feed, 1,060mg/kg in mineral salt and 2.3mg/L in water, reaching dose values far above the accepted, totaling a daily intake of approximately 6,533.5mg sulfur/animal/day. As differential diagnosis, lead was dosed in the kidneys and liver of the three calves, with negative results. Also, the calf that sickened last was treated with 20mg/kg thiamin and 0.2mg/kg dexamethasone (IM; QID) for three days and eventually recovered. According to anatomopathological findings, excess sulfur intake and therapeutic diagnosis, sulfur poisoning was suggested as the cause of PEM in these 1-to-3-month-old calves. Occurrence of PEM is rare in calves at such a young age.

RESUMO: Tifton 68 (Cynodon nlemfuensis Vanderyst) é uma gramínea cultivada na região sul do Brasil, responsável por manifestações clínicas superagudas de dispneia, dificuldade de deglutição, tremores musculares, timpanismo e decúbito em bovinos. A morte ocorre rapidamente após o início dos primeiros sinais e não são encontradas alterações macro e microscópicas significativas. O presente estudo descreve os aspectos epidemiológicos, clínicos e lesionais da intoxicação espontânea por tifton 68 que ocorreu nos municípios de Rio do Sul, Pouso Redondo, Taió e Rio do Campo, estado de Santa Catarina, Brasil, nos anos de 1996, 1997, 1998 e 2010, respectivamente. Experimentalmente foram avaliadas a presença de ácido cianídrico nas folhas verdes e secas desta planta, através do teste do papel picrossódico e a reversão da intoxicação pela utilização de uma solução antídoto específica de tiossulfato de sódio e nitrito de sódio. A reprodução experimental consistiu na administração de folhas verdes de tifton 68 para dois bovinos com doses a partir de 10,3g/kg. O quadro de intoxicação cianogênica foi confirmado pela imediata resposta ao tratamento intravenoso com a solução antídoto. As amostras da planta verde forneceram resposta positiva ao teste do papel picrossódico. O feno de tifton 68 não demonstrou qualquer toxicidade, mesmo em altas doses (18 e 27g/kg), sendo seguro para a alimentação de bovinos.