Bovine Polioencephalomalacia Study Guide
Overview and Clinical Importance
Polioencephalomalacia (PEM), also known as cerebrocortical necrosis (CCN), is an important non-infectious neurological disease of ruminants characterized by necrosis of the cerebral cortex. The term derives from Greek: polio (gray) + encephalo (brain) + malacia (softening), literally meaning softening of the gray matter of the brain.
PEM is a common neurological disorder affecting cattle, sheep, goats, deer, and camelids worldwide. In cattle, it most commonly affects calves aged 6-18 months, particularly those on high-concentrate diets or in feedlot settings. The condition represents a pathological end point resulting from several distinct etiologies, most notably thiamine (Vitamin B1) deficiency and sulfur toxicosis.
Etiology and Pathophysiology
Primary Causes of PEM
Pathophysiology of Thiamine Deficiency
Thiamine pyrophosphate (TPP), the active form of thiamine, serves as an essential cofactor for three critical enzymes in glucose metabolism:
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