Abstract
Abstract Polioencephalomalacia as a result of sulphur excess is a growing problem in cattle and sheep, mainly in young, growing animals. It is common in different regions of the world. The disease develops favoured by certain conditions such as sustained provision of feed and water with high sulphur content, use of dietary supplements containing sulphur, and a habitat with high hydrogen sulphide concentration. Pathogenesis of the disease is complex, but very important are oxidative-antioxidative imbalance, dysfunction of vessels, and secondary cerebral cortex ischaemia as a result of direct and/or indirect action of sulphur metabolites, namely hydrogen sulphide, sulphides, and sulphites. Clinical signs and changes in the cerebral cortex in the form of degenerative necrotic lesions are similar to those observed in polioencephalomalacia caused by vitamin B1 deficiency, and lead and salt intoxication. Highly increased sulphur content (more than 0.3-0.4 of dry matter) in the diet is the basis for differential diagnosis, as well the high concentration of hydrogen sulphide in gas and sulphides in rumen fluid. In prophylaxis and treatment the most important measure is to limit sulphur intake and in acute cases to neutralise low pH in rumen and administer vitamin B1 injections.
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