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Year 2017 - Volume 37, Number 6
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xperimental and iatrogenic poisoning by sodium selenite in pigs, 37(6):561-569
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ABSTRACT.- Peixoto P.V., Oliveira K.D., França T.N., Driemeier D., Duarte M.D., Bezerra Jr P.S., Cerqueira V.D. & Amién A.G. 2017. Experimental and iatrogenic poisoning by sodium selenite in pigs. Pesquisa Veterinária Brasileira 37(6):561-569. Departamento de Nutrição Animal e Pastagem, Instituto de Zootecnia, Universidade Federal Rural do Rio de Janeiro, BR-465 Km 7, Seropédica, RJ 23890-000, Brazil. E-mail: peixotop@ufrrj.br
Following a case of iatrogenic selenium poisoning in a young pig, an experimental study was carry out. Sodium selenite was orally and parenterally administered to 13 pigs that were subdivided into three groups (G1, G2 and G3). The animals in groups G1 and G3 received sodium selenite intramuscularly (IM), G1 received a comercial formula, and G3 received sodium selenite mixed with distilled water at different dosages, and those in group G2 were fed commercial sodium selenite. Acute and subacute poisoning was observed in both groups, although the onset of clinical signs was slower in group G2. Only one pig (in group G1) that had received the highest dose showed a peracute course. Apathy, anorexia, dyspnea, vomiting, muscular tremors, proprioceptive deficit, ataxia and paresis of the hind limbs progressing to the front limbs evolving to tetraplegia were observed. Postmortem findings differed whether the animals received the injected (G1 and G3) or oral (G2) sodium selenite. The liver was moderately atrophic in some animals of G2. Some of the animals in groups G1 and G3 presented with lung edema. One pig in G3 had yellowish-brown areas in the ventral horns of the cervical intumescences of the spinal cord. The most important histological changes were present in the ventral horns of the cervical and lumbar intumescences of the spinal cord. In one animal, changes were present in the brainstem and mesencephalon. The initial lesion was a perivascular and astrocyte edema that progressing to lysis and death of astrocytes and neurons. In the chronic stage of the lesions, there were extensive areas of liquefaction necrosis with perivascular lymphocytic and histiocytic infiltration and occasional eosinophils. It seems that disruption of the blood-brain barrier due to astrocyte edema is the most likely mechanism of CNS lesion. |
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