Polioencephalomalacia: Difference between revisions

From WikiMD's Wellness Encyclopedia

CSV import
 
CSV import
 
Line 34: Line 34:
[[Category:Neurological disorders]]
[[Category:Neurological disorders]]
{{Veterinary-med-stub}}
{{Veterinary-med-stub}}
<gallery>
File:Moraedje_gris_do_cervea_berbis_loucant_e_hôt.jpg|Polioencephalomalacia
File:Berbis_moraedje_gris_cervea_djus_forsitindaedje_cô.jpg|Polioencephalomalacia
</gallery>

Latest revision as of 01:23, 18 February 2025

Polioencephalomalacia (PEM) is a neurological disease found in ruminants, characterized by the softening of the grey matter in the cerebral cortex. It is also known as cerebrocortical necrosis (CCN) and is most commonly observed in cattle, sheep, and goats. PEM is associated with a deficiency or imbalance of certain nutrients, particularly thiamine (vitamin B1), and is often linked to high-concentrate diets that lead to a reduction in thiamine production or an increase in thiamine destruction in the rumen.

Etiology[edit]

The primary cause of PEM is a deficiency in thiamine. Thiamine is essential for glucose metabolism in the brain. Without it, there is an accumulation of lactate and pyruvate, leading to an increase in intracranial pressure and, subsequently, cerebral necrosis. Factors that can lead to thiamine deficiency include:

  • Consumption of high-concentrate diets low in thiamine
  • Overgrowth of thiaminase-producing bacteria in the rumen, which destroy thiamine
  • Ingestion of plants containing thiaminase, such as bracken fern
  • Sulfur toxicity, which can interfere with thiamine absorption

Clinical Signs[edit]

Clinical signs of PEM can vary but often progress through several stages:

  • Early Stage: Animals may appear blind, exhibit aimless wandering, and press their heads against objects.
  • Intermediate Stage: There may be increased salivation, grinding of the teeth, and convulsions.
  • Advanced Stage: Animals often lie down, unable to stand, showing severe opisthotonos (arching of the back due to muscle contraction), and may die if not treated promptly.

Diagnosis[edit]

Diagnosis of PEM is based on clinical signs, dietary history, and response to thiamine treatment. Laboratory tests can confirm thiamine deficiency, and post-mortem examinations typically reveal softening and yellowing of the cerebral cortex.

Treatment and Prevention[edit]

Treatment involves the administration of thiamine, either orally or intravenously, depending on the severity of the condition. Recovery can be rapid if treatment is initiated early. Prevention focuses on ensuring a balanced diet, avoiding high-risk feeds, and monitoring sulfur levels in the diet and water.

Epidemiology[edit]

PEM can occur worldwide, affecting both domestic and wild ruminants. Outbreaks are often related to dietary changes, particularly in intensive farming systems where high-concentrate diets are common.

See Also[edit]

Stub icon
   This article is a veterinary medicine–related stub. You can help WikiMD by expanding it!