Encefalomalacia focal simétrica em suínos causada por ingestão de sementes de Aeschynomene indica

• Autor(a) principal: Oliveira, Fabiano Nunes de
• Data de Publicação: 2005
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Manancial - Repositório Digital da UFSM
• dARK ID: ark:/26339/0013000013pq1
• Texto Completo: http://repositorio.ufsm.br/handle/1/10003
• topic: Medicina veterinária; Intoxicação por planta; Encefalomalacia focal simétrica; Aeschynomene indica; Fabaceae; Doença de suínos; Doença do sistema nervoso central; Patologia; Suíno; CNPQ::CIENCIAS AGRARIAS::MEDICINA VETERINARIA

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 soy bean bran, 5% comercial premix with minerals and vitamins and 20% of broken rice contaminated with 40% of A. indica seeds. Although all 100 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 start of the 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 necropsied in the premises. The intoxication was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pig C-E) of A. indica seeds and in one adult 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 start of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of encephalic leptomeninges of all pigs, large amounts of A. indica seeds in the stomach and small intestine of Pigs C-E and, reddening of the intestinal wall and bloody intestinal content. 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 capillary endothelia in several nuclei and in the telencephalic cortex. In the Pig F, fed a ration with 16,5% of A. indica seeds the lesions were similar in distribution but more severe. In swine fed rations containing 10% and 15% of A. indica in the ration, histopathological changes in the brain consisted of discreet 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 from 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 is responsible for this neurological condition in swine and that the clinical outcome and pathological changes are dose-dependent.