fbpx
Wikipedia

Polioencephalomalacia

January 01, 1970

Not to be confused with poliomyelitis.

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 diseaes such as: acute lead poisoning or salt poisoning.[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]

"Star-gazing" ewe with PEM
lateral recumbency and opisthotonos

Causes edit

Thiamine deficiency edit

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 edit

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 edit

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 edit

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.

See also edit

References edit

  1. ^ a b "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". 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"

External links edit

 
Wikimedia Commons has media related to Polioencephalomalacia in ruminants.

January 01, 1970
polioencephalomalacia, confused, with, poliomyelitis, also, referred, cerebrocortical, necrosis, neurological, disease, seen, ruminants, that, caused, multiple, factors, which, thiamine, depletion, body, thiamine, vitamin, chemical, glucose, metabolism, that, . Not to be confused with poliomyelitis 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 diseaes such as acute lead poisoning or salt poisoning 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 Star gazing ewe with PEM lateral recumbency and opisthotonos Contents 1 Causes 1 1 Thiamine deficiency 1 2 Overconsumption of glucose 1 3 High sulfur intake 2 Clinical symptoms 3 See also 4 References 5 External linksCauses editThiamine deficiency edit 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 edit 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 edit 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 editClinical 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 See also editCortical laminar necrosis 12 References edit a b Overview of Polioencephalomalacia Nervous System Merck Veterinary Manual Retrieved 2019 12 02 Thiamine deficiency induced polioencephomalacia PEM of sheep and cattle 2017 05 27 Harper Harold 1942 Carbohydrate Metabolism in Thiamine Deficiency PDF The Journal of Biological Chemistry 142 239 248 via JBC Overview of Polioencephalomalacia Nervous System Merck Veterinary Manual Merck Veterinary Manual Retrieved 2017 05 27 Edmondson Paul What is Thiaminase Poisoning Insectivore www insectivore co uk Retrieved 2017 05 27 Nollet Leo M L 2004 Handbook of Food Analysis Physical characterization and nutrient analysis CRC Press ISBN 9780824750367 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 Sulfur Toxicity College of Veterinary Medicine vetmed iastate edu Hobson P N Stewart C S 2012 12 06 The Rumen Microbial Ecosystem Springer Science amp Business Media pp 636 634 ISBN 9789400914537 Dietary Sulfur in Ruminant Diets PDF Westway Feed Products Merck Veterinary Manual Retrieved 2017 06 17 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 External links editPolioencephalomalacia Disease Caused by a Deficiency of Thiamine at tvsp org http ag ansc purdue edu sheep ansc442 Semprojs 2002 neurological polio htm http www merckvetmanual com mvm index jsp cfile htm bc 102000 htm nbsp Wikimedia Commons has media related to Polioencephalomalacia in ruminants Retrieved from https en wikipedia org w index php title Polioencephalomalacia amp oldid 1221593473, wikipedia, wiki, book, books, library,

article

, read, download, free, free download, mp3, video, mp4, 3gp, jpg, jpeg, gif, png, picture, music, song, movie, book, game, games.