NAVLE Nervous

Ovine and Caprine Polioencephalomalacia Study Guide

Polioencephalomalacia (PEM), also known as cerebrocortical necrosis (CCN), is a common, potentially fatal neurological disease affecting sheep and goats worldwide.

Overview and Clinical Importance

Polioencephalomalacia (PEM), also known as cerebrocortical necrosis (CCN), is a common, potentially fatal neurological disease affecting sheep and goats worldwide. The term "polio" in this context refers to gray matter (Greek: polios = gray), "encephalo" refers to brain, and "malacia" means softening. This disease has absolutely no relationship to the viral poliomyelitis affecting humans.

PEM is characterized by necrosis of the cerebral cortex, leading to neurological dysfunction. In small ruminants, the disease often has a shorter course with fewer survivors compared to cattle, making early recognition and treatment critical. Mortality rates range from 50-90% if untreated.

High-YieldPEM in sheep and goats has a more rapid clinical course and higher mortality than in cattle. Early thiamine administration is essential for survival.
Cause Mechanism Risk Factors
Thiamine Deficiency Reduced ruminal thiamine synthesis or increased thiaminase production by bacteria (Clostridium sporogenes, Bacillus thiaminolyticus) High-concentrate/low-fiber diets, ruminal acidosis, rapid diet changes, amprolium or levamisole administration
Sulfur Toxicosis Excess dietary sulfur leads to ruminal hydrogen sulfide (H2S) production, which is absorbed and causes direct neurotoxicity or secondary thiamine deficiency High-sulfur water, distillers grains, sulfur-containing plants (mustard, turnips), sulfur supplements

Etiology and Pathophysiology

Primary Causes

PEM is a pathological diagnosis representing the common endpoint of several conditions. The two primary mechanisms are:

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