Talk:Polioencephalomalacia

message: Hello, I am interested in making some changes and additions onto the slurry pit page. The following is a draft of what I'd like to add along with its references.
Introduction to Polioencephalomalacia
Polioencephalomalacia (PEM), also referred to as cerebrocortical necrosis (CCN), is a neurological disease seen in ruminants that generally results from disrupted thiamine production in the body. Thiamine is a key chemical in glucose metabolism, and because the brain outcompetes all other organs in energy consumption, thiamine deficiency is most threatening to neurological activity. Cattles, sheep, goat, and other ruminants that are diagnosed with PEM or pre-PEM suffer opishotonus, cortical blindness, disoriented movement, and fatility, if left untreated. There is not a proven correlation between age and the onset of PEM, and current diagnosis records reveal infected ruminants of all ages. [1]
Thiamine Regulation
Thiamine availability is regulated by the direct dietary consumption of thiamine and thiaminases, which are enzymes that readily cleave thiamine molecules and inhibit essential thiamine-regulated pathways such as the metabolism of glucose. [2]
In the special case of animals with rumen, ruminants have working rumen microbes that synthetize thiamine molecules without pre-ingesting thiamine rich foods. [3]However, feed concentrates given to livestock ruminants, specifically sheep and cattle, are often heavily stocked with thiaminases, which counter the production of thiamine. As a result thiaminases and rumen microbes work conjointly in a futile cycle, eventually reaching a state of thiamine deficiency. Thiaminase rich foods include different grains, fresh water fish, and plants, usually ferns, which are often processed together to make feed concentrate. [4][5]
Since glucose metabolism is regulated by thiamine, the overconsumption of glucose can also result in thiamine inadequacy.[6] By substituting food concentrates made up of complex fibers by simple carbohydrates, thiamine is equilibrated to break down excess carbohydrates until the rumen system is depleted of thiamine. In fact, PEM was first seen in the 19th century when ruminants were fed byproducts of sugar refining.
Sulfur Intake
In light of recent research, high concentrations of sulfur intake has also been deemed responsible for PEM.[7][8] 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 obstructs oxidation by competing with oxygen sites and eventually disrupting neural function.[9]
1. "Thiamine deficiency induced polioencephomalacia (PEM) of sheep and cattle". www.agric.wa.gov.au. Retrieved 2017-05-27.
2. Harper, Harold (1942). "Carbohydrate Metabolism in Thiamine Deficiency" (PDF). The Journal of Biological Chemistry. 142: 239–248 – via JBC.
3. "Overview of Polioencephalomalacia - Nervous System - Merck Veterinary Manual". Merck Veterinary Manual. Retrieved 2017-05-27.
4. Edmondson, Paul. "What is Thiaminase Poisoning - Insectivore". www.insectivore.co.uk. Retrieved 2017-05-27.
5. Nollet, Leo M. L. (2004). Handbook of Food Analysis: Physical characterization and nutrient analysis. CRC Press. .
6. Lahunta, Alexander de; Glass, Eric N.; Kent, Marc (2014-07-10). Veterinary Neuroanatomy and Clinical Neurology - E-Book. Elsevier Health Sciences. p. 440. .
7. "Sulfur Toxicity | College of Veterinary Medicine". vetmed.iastate.edu. Retrieved 2017-05-27.
8. Hobson, P. N.; Stewart, C. S. (2012-12-06). The Rumen Microbial Ecosystem. Springer Science & Business Media. pp. 636–634. .
9. "Dietary Sulfur in Ruminant Diets" (PDF). Westway Feed Products. 2015. Retrieved May 27, 2017.  — Preceding unsigned comment added by Joycexiong55 (talk • contribs) 18:04, 27 May 2017 (UTC)
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