Cattle Feeding: What Is Polioencephalomalacia?
04/27/2007 09:19AM
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Cause: Polioencephalomalacia is caused by a disturbance in thiamine metabolism. Thiamine is required for a number of important nervous system functions. This disease most commonly affects young, fast growing cattle on a high concentrate ration and may result from a thiamine-deficient diet, an increase in thiaminase (an enzyme that breaks down thiamine) in the rumen or an increase in dietary sulfates.
A thiamine-deficient diet is usually associated with an increase in the dietary concentrate:roughage ratio. When concentrates (feed grains such as corn) are increased and roughage (forage, cottonseed hulls, etc.) is decreased in the diet, rumen pH drops. This increases the numbers of thiaminase-producing bacteria in the rumen and decreases the amount of total useable thiamine. Thiaminase breaks down the form of thiamine that the animal could normally use. Some species of plants produce thiaminase and can cause a decrease in the useable amount of thiamine when consumed. Examples of these types of plants include kochia, bracken fern and equisetum.
A high sulfate diet can also inhibit an animal’s ability to properly utilize thiamine. Feeds such as molasses and corn gluten are often high in dietary sulfates. Some water sources can also contain a high amount of sulfur (i.e., “gyp” water). When these are consumed in excessive amounts, clinical signs of polioencephalomalacia can occur.
Cattle that are affected with this disease usually exhibit several signs of generalized neurological disease. These signs can include but are not limited to: blindness, inconsistent and uncoordinated movements, head pressing, “goose” stepping, lateral recumbency (lying with full lateral contact of the body trunk, head, neck and legs with the ground with the head, neck and legs usually extended), tetany (muscle spasms), convulsions with paddling motions and death. These signs usually exhibit sudden onset, with the animals typically having normal temperatures and rumen function.
Prevention: Preventative strategies should focus on the diet. Risk factors such as high concentrate rations or high sulfate diets should be avoided if possible. Thiamine can also be added to a feed ration or a free-choice mineral supplement at 3-10 ppm. However, this may not be cost effective in some instances.
Treatment: For successful recovery, early treatment is essential. Thiamine should be administered at 5-7 mg/lb (10-15 mg/kg) intravenously. The initial treatment should be followed with intramuscular injections twice daily with the same dosage for the next 2-3 days. If calves are not treated early in the disease process, they may show residual neurological effects indefinitely.
Source: University Of Arkansas Ag Extension