Intoxicação aguda por fluorsilicato de sódio em bovinos

• Autor(a) principal: Panziera, Welden
• Data de Publicação: 2018
• Outros Autores: Schwertz, Claiton Ismael, Silva, Fernando Soares da, Taunde, Paula Augusto, Pavarini, Saulo Petinatti, Driemeier, David
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/187799
• topic: Intoxicação por flúor; Gastroenteropatias; Bovinos; Montenegro (RS); Histopatologia; Pathology; Toxicology; Diseases of cattle; Digestive lesions; Fluoride

Background: Fluorine is a ubiquitous environmental element and fluoride poisoning in cattle is usually related to the ingestion of contaminated pastures or water, especially near industries, or mineral supplements with excessive amounts of this element. Cattle poisoning can be acute or chronic and is directly associated with the ingested dose and with the duration of exposure. The objective of this study is to report the epidemiological, clinical and anatomopathological aspects of an outbreak of acute sodium fluorosilicate intoxication in cattle. Case: Six 1-year-old, castrated male, mixed breed beef calves from a lot of 60 were found dead without previous clinical signs being observed. The calves died after ingesting a white, odorless, finely granular substance found by the owner near a road that intersected the property. The product was in an open package and identified as sodium fluorosilicate. Of the six dead calves, three were necropsied. Gross lesions were restricted to the digestive system and included varying degrees of hyperemia, hemorrhage, edema, and erosions in the pre-stomach and abomasum mucosae. The histological lesions observed in the three calves were characterized mainly by variable degenerative, necrotic and ulcerative changes in the epithelial lining of the forestomachs and abomasum. Partially (erosion) or totally (ulceration) bare lamina propria of forestomach papillae was covered by cellular debris and neutrophils. Multifocal lymphoid necrosis was seen in lymph nodes and spleen. Fluoride levels measured in the ruminal content of two necropsied calves were 55.2 and 9.17 mgF/kg of dry matter. After the diagnosis and discontinued exposure of the calves to the fluoride product, deaths ceased Discussion: The diagnosis of acute sodium fluorosilicate intoxication in cattle in this study was based on epidemiological, clinical, and anatomopathological findings, and in the determination of fluoride levels in ruminal content. The association of these data constitutes an important aid in suspecting and confirming the diagnosis of intoxication. The acute toxicity of fluoride, observed in the cattle of this study, is relatively rare. The intake of sodium fluorosilicate by cattle may have been favored by the absence of organoleptic properties of the product. The involvement of young cattle revealed an important epidemiological aspect of the condition, since cattle in this age group are the most predisposed to the intoxication due to their greater absorption capacity. The spontaneous ingestion of large amounts of sodium fluorosilicate by cattle of this study produced digestive morphological changes, characterized by variable hyperemia, hemorrhage, and necrosis in the forestomachs and abomasum. The proposed mechanism of lesions is associated with the acidic activity exerted by fluoride on the mucosa. Acute toxicosis must be differentiated from other conditions that cause acute digestive changes in ruminants such as Baccharis spp. poisoning, ruminal acidosis, arsenic poisoning and Baccharidastrum triplinervium intoxication. In these cases, the epidemiological and anatomopathological evidences are extremely important in the differentiation of each condition. Therefore, cattle practitioners should consider acute fluoride poisoning as a differential diagnosis in cattle presenting digestive signs or death without previous signs. Epidemiological, clinical, anatomopathological and the assessment of fluoride levels are important for the accurate diagnosis of this toxicosis.