Veterinary Medicine and
Animal Sciences

Veterinary Medicine and Animal Sciences

ISSN 2054-3425
Review

A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Samat Amat1*, Andrew A. Olkowski2, Metin Atila3 and Tyler J. O'Neill4

*Correspondence: Samat Amat saa647@mail.usask.ca

1. Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada.

Author Affiliations

2. Department of Animal and Poultry Science, College of Agriculture and Bioresources, University of Saskatchewan, Saskatoon, SK S7N 5A8, Canada.

3. Department of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada.

4. Dalla Lana Faculty of Public Health, Division of Epidemiology, University of Toronto, Toronto, ON M5T 3M7, Canada.

Abstract

Polioencephalomalacia (PEM), also known as cerebrocortical necrosis, is an important neurologic disease that affects ruminants. Thiamine deficiency and sulfur (S) toxicity have been well recognized as major etiological factors. The mechanism of thiamine deficiency associated PEM has been well elucidated. However, the role of S in PEM pathogenesis remains unclear, although the relationship between S toxicity and PEM has been established for 3 decades. The development of S-induced malacic lesions is believed to be independent of thiamine deficiency, since blood thiamine levels in affected individuals remain in the range of normal animals. However, cattle affected by S-induced PEM frequently respond to thiamine treatment in early disease stages. Thiamine supplementation is reported to reduce the incidence and severity of S-induced PEM. This suggests a possible metabolic relationship between excess S intake and thiamine in the development of malacic lesions. Such an association is further supported by recent studies reporting that high dietary S may increase the metabolic demand for thiamine pyrophosphate (TPP), a critical cofactor in several metabolic pathways. Systemic failure to synthesize metabolically requisite levels of TPP in the brain may be an important precursor in the pathogenesis of S-induced PEM. There is increasing evidence of the importance of thiamine in the pathogenesis of S-induced PEM. Thus, understanding the potential role of S-thiamine interaction in the development of malacic lesions is important step to determine the mechanism of S-induced PEM. The objective of this article is to provide an overview of thiamine deficiency and S toxicity associated PEM, and to discuss the potential role of S-thiamine interaction in the pathogenesis of S-induced PEM in ruminants.

Keywords: Polioencephalomalacia, sulfur, thiamine, interaction, malacic lesions, ruminants

ISSN 2054-3425
Volume 1
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