Relationship between sulfur, thiamine and polioencephalomalacia

a review

Authors

  • G. A. Niles Oklahoma Animal Disease Diagnostic Laboratory, Oklahoma State University, P.O. Box 7001, Stillwater, OK 74076-7001
  • S. E. Morgan Oklahoma Animal Disease Diagnostic Laboratory, Oklahoma State University, P.O. Box 7001, Stillwater, OK 74076-7001
  • W. C. Edwards Oklahoma Animal Disease Diagnostic Laboratory, Oklahoma State University, P.O. Box 7001, Stillwater, OK 74076-7001

DOI:

https://doi.org/10.21423/bovine-vol36no2p93-99

Keywords:

acidosis, cerebrocortical necrosis, clinical aspects, differential diagnosis, drug therapy, hydrogen sulfide, lesions, metabolism, poisoning, polioencephalomalacia, reviews, rumen bacteria, rumen gases, sulfur, thiamin, thiaminase, toxicity, vitamin deficiencies

Abstract

Thiamine deficiency has been classically described as the cause of ruminant polioencephalomalacia (PEM). More recently excess dietary sulfur has been shown to be a major cause of PEM. This paper reviews the relationship between PEM and thiamine metabolism in mature cattle, thiaminase in plants, rumen acidosis and excess dietary sulfur. Signs of PEM caused by lead poisoning, water deprivation-sodium ion toxicity and sulfur toxicosis are clinically and microscopically indistinguishable. Diagnosis of sulfur-induced PEM relies on ruling out other diseases, and demonstrating elevated dietary sulfur intake. Total sulfur intake from both feed and water must be determined when investigating an outbreak of PEM in cattle.

Cover image of Volume 36, No.2 of the Bovine Practitioner: a photo of the Wisconsin State Capitol taken across Lake Monona at night

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Published

2002-06-01

Issue

Vol. 36, No. 2 (2002 June)

Section

Articles

How to Cite

Relationship between sulfur, thiamine and polioencephalomalacia: a review. (2002). The Bovine Practitioner, 36(2), 93-99. https://doi.org/10.21423/bovine-vol36no2p93-99