Polioencephalomalacia

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Not to be confused with poliomyelitis, a disease that affects humans.

Polioencephalomalacia (PEM) literally means softening of the cerebrocortical grey matter distributed in a laminar (layered) pattern. It is also called Laminar cortical necrosis or Cortical necrosis. PEM is a sporadic disease of unknown cause occurring in cattle, sheep and goats. PEM is most commonly seen in cattle at 6-18 months of age when fed concentrate rations. Sheep are usually affected at 2-7 months of age.

The lesion is associated with thiamine deficiency or a disturbance in thiamine metabolism. Ruminants are supplied with thiamine by synthetic activity of ruminal bacteria. PEM most commonly develops in cattle fed carbohydrate-rich and roughage-poor rations, which leads to subclinical lactic acidosis and hence an alteration in ruminal microflora. Other mechanisms for disturbances in thiamine deficiency include;

- Destruction of thiamine within the gastrointestinal tract (for example by thiaminases in bracken fern)

- Inactivation of thiamine by excess sulfates or sulfides or elemental sulfur

- Production of inactive thiamine analogues

- Decreased thiamine absorption

- Increased faecal excretion of thiamine

Clinical signs of PEM include head pressing, dullness, central blindness, anorexia, muscle tremors, teeth grinding, salivation, convulsions, nystagmus, and recumbency.^[1] Early administration of thiamine may be curative but if the lesion is more advances then surviving animals may remain partially blind and mentally dull.