Polioencephalomalacia

 

Pathology:

Polioencephalomalacia (PEM), also known as cerebrocortical necrosis, is a disease characterized by a disturbance of the central nervous system. The brain of infected animals becomes inflamed and swollen, and eventually becomes necrotic. Diagnosis is usually done by performing a necropsy on the brain of the dead animal. Dead gray matter will fluoresce under a Wood's lamp.

Causes:

PEM sometimes occurs on high grain diets, and diets that include plants high on thiaminases and sulfur. Thiaminases are enzymes found in a few plants, such as bracken fern, and the raw flesh and viscera of certain fish and shellfish. When ingested these enzymes split thiamin (Vitamin B1), an important compound in energy metabolism, and render it inactive. Normally ruminants are fairly resistant to thiamin deficiency since rumen microbes provide the animal with sufficient amounts of thiamin. However, the ingestion of thiaminases will lead to deficiency. Additionally, young growing ruminants, especially cattle and sheep, fed high-grain diets are especially susceptible. Diets high in grains can encourage the growth of certain thiaminase-producing bacteria in the rumen. These bacteria, including Clostridium sporogenes and a few species of Bascillus can produce enough thiaminases to induce thiamin deficiency. A thiamine-analogue is also produced within the rumen if there is excess sulfur, which may replace thiamine in important metabolic reactions in the brain. When thiamine is deficient, key tissues that require large amounts of thiamine, such as the brain and heart, are the first to show lesions.

Clinical signs:

This usually occurs suddenly. Affected sheep stand or sit alone, are blind and arch their necks back and stare upwards and become "star gazers", the medical name for this being opishotonus. They are disoriented, lose their appetite, and they do not want to drink. Temperature and respiratory rate are usually normal but the heart rate may be depressed. Excitement may be seen but is usually replaced with dullness. Normally only a few individuals are affected. The animal may go down on its side with its head thrown back. The legs may be rigidly extended and convulsions may occur. Animals with PEM will often press their head against a wall or post. If not treated on time, most animals with PEM will die within 48 hours.

   

Photo used with permission of Cornell University

Treatment and prevention:

Sheep suffering from polioencephalomalacia generally respond very well to treatment if caught early. They can be successfully treated with 200 to 500 mg of thiamin injected intravenously, intramuscularly, or subcutaneously. Because thiamine is water-soluble, it is quickly eliminated from the body through the kidneys and, therefore there is little risk of overdosing. Dexamethasone is often administered along with thiamine to reduce brain swelling. Although recovery is usually quick, if significant brain damage has occurred, the recovered sheep rarely regain satisfactory levels of productivity. Therefore, very early treatment is critical. If a case of PEM is diagnosed in a herd of sheep, it is advisable to inject the remaining animals with thiamine as prevention. Drinking water should be tested for sulfur contents, sources of thiaminases, if any, should be removed and animals should be introduced to grain diets in steps to avoid a sudden increase in thiaminases-producing bacteria in the rumen.

 

References:

Sheep Production Handbook, Oct. 1988.  Sheep Industry Development Program, INC. Pg 7-8.

http://www.inform.umd.edu/EdRes/Topic/AgrEnv/ndd/goat/METABOLIC_AND_NUTRITIONAL_DISEASES.html

http://www.ansci.cornell.edu/plants/toxicagents/ 

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