polioencephalomalacia

thumb|"Torticollis|Star-gazing" ewe with PEM thumb|lateral recumbency and opisthotonos 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 (vitamin B1) 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. PEM may also be caused by other toxic or metabolic diseases such as: acute lead poisoning or salt poisoning. 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. Current data shows that the onset of PEM can range from birth to late adulthood.

== 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. Ruminants have working rumen microbes that synthesize thiamine molecules for the body; therefore, ruminants do not need to ingest thiamine rich foods for thiamine. 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.