NAVLE Nervous

Bovine Polioencephalomalacia Study Guide

Polioencephalomalacia (PEM), also known as cerebrocortical necrosis (CCN), is an important non-infectious neurological disease of ruminants characterized by necrosis of the cerebral cortex.

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.

High-YieldOn the NAVLE, PEM questions frequently test your ability to recognize the classic clinical presentation (stargazing, cortical blindness, dorsomedial strabismus) and appropriate treatment with thiamine. Remember that PEM is NOT the same as polio in humans - it is not infectious!
Etiology Mechanism Risk Factors
Thiamine Deficiency Reduced thiamine synthesis by rumen microbes or destruction by thiaminase enzymes High-concentrate, low-fiber diets; ruminal acidosis; rapid feed changes
Sulfur Toxicosis Excess ruminal hydrogen sulfide (H2S) production causing direct neurotoxicity High-sulfur water (greater than 2000 ppm); distillers grains; brassica forages
Thiaminase-Containing Plants Thiaminase I enzyme destroys thiamine and creates antagonistic analogs Bracken fern (Pteridium aquilinum); horsetail; nardoo fern; kochia
Drug-Induced Amprolium acts as thiamine antagonist; some anthelmintics act as thiaminase cofactors Amprolium overdose; levamisole; thiabendazole treatment

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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