Polioencephalomalacia

Polioencephalomalacia (PEM), also referred to as cerebrocortical necrosis (CCN), is a neurological disease seen in ruminants that is caused by multiple factors, one of which is thiamine depletion in the body. Thiamine is a key chemical in glucose metabolism that, when deficient, is most threatening to neurological activity. In addition to altered thiamine status, an association with high sulfur intake has been observed as a potential cause of PEM. Other toxic or metabolic diseases (eg, acute lead poisoning, sodium toxicosis/water deprivation) can result in PEM as well.[1] Cattle, sheep, goat, and other ruminants that are diagnosed with PEM or pre-PEM suffer opisthotonus, cortical blindness, disoriented movement, and eventually fatality, if left untreated.[1] Current data shows that the onset of PEM can range from birth to late adulthood.[2]

Not to be confused with poliomyelitis.
star-gazing ewe with PEM
lateral recumbency and opisthotonos

Causes

Thiamine deficiency

Thiamine availability is controlled by the direct dietary consumption of thiamine. Thiamine availability is also regulated by thiaminases, which are enzymes that readily cleave thiamine molecules and inhibit essential thiamine-regulated pathways such as the metabolism of glucose.[3] Ruminants have working rumen microbes that synthesize thiamine molecules for the body; therefore, ruminants do not need to ingest thiamine rich foods for thiamine.[4] However, feed concentrates given to ruminants, specifically sheep and cattle, are often heavily stocked with thiaminases. The presence of thiaminases counter the production of thiamine by breaking them down, resulting in a futile cycle between rumen microbes and thiaminases. Eventually, when the rate of synthesis production can not exceed thiaminase intake, a state of thiamine deficiency will be reached. Thiaminase rich foods include different grains, fresh water fish, and ferns, all of which are often processed together to make feed concentrate.[5][6]

Overconsumption of glucose

Since glucose metabolism is regulated by thiamine, the overconsumption of glucose can also result in thiamine inadequacy.[7] When there is a sudden increase of glucose in the body, thiamine will be depleted so that thiamine is not available when the next round of glucose needs to be metabolized.

High sulfur intake

In light of recent research, high concentrations of sulfur intake have also been deemed responsible for PEM.[8][9] Sulfur is necessary for the synthesis of important sulfur-containing amino acids and their contribution to the synthesis of different hormones, enzymes, and structural proteins. The ruminant diet, especially that of cattle, can be overly concentrated with sulfur. In ruminants, the same rumen microbes that generate thiamine molecules reduce sulfur into toxic sulfides. Among the sulfide toxins is hydrogen sulfide, a gas compound that will compete with oxygen to bind with red blood cells and eventually enter the brain to disrupt neural activity.[10]

Clinical symptoms

Clinical signs of PEM are variable depending on the area of the cerebral cortex affected and may include head pressing, dullness, opisthotonos, central blindness, anorexia, muscle tremors, teeth grinding, trismus, salivation, drooling, convulsions, nystagmus, clonic convulsions, and recumbency.[11] Early administration of thiamine may be curative, but if the lesion is more advanced, then surviving animals may remain partially blind and mentally dull.

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See also
  • Cortical laminar necrosis[12]

References
  1. "Overview of Polioencephalomalacia - Nervous System". Merck Veterinary Manual. Retrieved 2019-12-02.
  2. "Thiamine deficiency induced polioencephomalacia (PEM) of sheep and cattle". 2017-05-27.
  3. Harper, Harold (1942). "Carbohydrate Metabolism in Thiamine Deficiency" (PDF). The Journal of Biological Chemistry. 142: 239–248 – via JBC.
  4. "Overview of Polioencephalomalacia - Nervous System - Merck Veterinary Manual". Merck Veterinary Manual. Retrieved 2017-05-27.
  5. Edmondson, Paul. "What is Thiaminase Poisoning - Insectivore". www.insectivore.co.uk. Retrieved 2017-05-27.
  6. Nollet, Leo M. L. (2004). Handbook of Food Analysis: Physical characterization and nutrient analysis. CRC Press. ISBN 9780824750367.
  7. Lahunta, Alexander de; Glass, Eric N.; Kent, Marc (2014-07-10). Veterinary Neuroanatomy and Clinical Neurology - E-Book. Elsevier Health Sciences. p. 440. ISBN 9781455748570.
  8. "Sulfur Toxicity | College of Veterinary Medicine". vetmed.iastate.edu.
  9. Hobson, P. N.; Stewart, C. S. (2012-12-06). The Rumen Microbial Ecosystem. Springer Science & Business Media. pp. 636–634. ISBN 9789400914537.
  10. "Dietary Sulfur in Ruminant Diets" (PDF). Westway Feed Products.
  11. "Merck Veterinary Manual". Merck Veterinary Manual. Retrieved 2017-06-17.
  12. Clinical Management of Polioencephalomalacia in goats S.Sivaraman,G.Vijayakumar,E.venkatesakumar, and K.K.Ponnuswamy Indian Veterinary Journal ,May, 2016, 93,(05) : 70-72"
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