The present study describes clinical, gross and histopathological findings of PEM following an abrupt change of diet in two ranches housing 2750 dairy and 2300 beef cattle.
As a result of severe PEM, 256 cattle died or were slaughtered.
Clinical findings included circling, hypersensitivity, excessive salivation, hypermetria, incoordination, blindness and death. The first clinical signs occurred in beef calves (6–8 months old) at a holding facility.
Clinical signs of the disorder continued intermittently during the 5-month period in both ranches and were more evident in calves and lactating dairy cows.
The affected cattle did not respond to thiamine injections.
Clinical signs disappeared gradually following removal of barley malt sprouts from the diet.
Although macroscopic lesions were not apparent in the brain tissues of some animals, histopathology typical of PEM was found in most cases: spongiosis in the neuropil and neuronal necrosis, haemorrhage, capillary hyperplasia, fibrinoid degeneration in arterioles, multifocal liquefaction necroses in the grey matter and abundance of gitter cells with vacuolar large cytoplasm.
Sulphide in rumen fluid of a clinically affected animal was measured as 1.55 mg/dl, which is considerably higher than that collected from two control cows (mean 0.21 mg/dl).
The total sulphur content of the diet containing barley malt sprouts was estimated to be 0.45%, which is also higher than the National Research Council (NRC) maximum tolerable levels.
In conclusion, PEM can result from excess barley malt sprout intake because of its higher sulphur content. Clinical signs may occur shortly after the intake of barley malt sprout as outbreaks with a higher number of deaths or as an ongoing periodic condition.
Source: Kul, O., Karahan, S., Basalan, M. & Kabakci, N. (2006): Polioencephalomalacia in Cattle: A Consequence of Prolonged Feeding Barley Malt Sprouts. In: Journal of Veterinary Medicine Series A 53 (3), 123-128.
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