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

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.

Polioencephalomalacia Caused by Thiamine Deficiency in Sheep of Basrah Province, Iraq.

“…Since neurons need a lot of carbohydrates as an energy source necessary for nerve function [5], the depletion of carbohydrate sources might cause alterations in the mechanism of action of all nervous system parts, but final neuronal death, especially cortical region might suspect [9]. Thereby, damage to the brain cells may be responsible for the demonstration of the symptoms [10].…”

“…Although Sulfur-induced polioencephalomalacia has been recognized in the last 30 tears, the role that sulfur plays in polioencephalomalacia is still not clearly defined [10]. It has been proposed that lesion development has an association with the inhalation of eructed H2S from the rumen.…”

Polioencefalomalacia asociada a exceso de azufre dietético en bovinos de engorde a corral

“…Si bien la PEM por exceso de S dietético, proveniente de GD, agua de bebida y/o forraje, ha sido diagnosticada en Norteamérica (Amat et al, 2013), Reino Unido, Brasil (Sant' Ana y Barros, 2010), Nueva Zelanda y Australia (McKenzie et al, 2009), no existen antecedentes nacionales al respecto, pese al difundido y creciente suministro de GD a bovinos de EC. Pensando que esta etiología haya sido subestimada, es recomendable el monitoreo del contenido de S total en las dietas de EC, especialmente en aquellas que incluyan GD, considerando también al S aportado por el agua de bebida.…”

“…Polioencefalomalacia (PEM) es un término patológico que se refiere al reblandecimiento de la sustancia gris del encéfalo (necrosis cerebro-cortical) (Gould, 2000). En bovinos se ha asociado a múltiples causas, tales como: déficit dietético de fibra, deficiencia de tiamina, exceso de azufre (S) dietético, intoxicación con plomo e intoxicación con sal (Amat et al, 2013;Dore y Smith, 2017). Si bien puede haber casos en los que es impo-sible determinar su etiología, la nutrición generalmente desempeña un rol clave en el desarrollo de este trastorno (Dore y Smith, 2017).…”

Notes from the Field: Death of a Farm Worker After Exposure to Manure Gas in an Open Air Environment — Wisconsin, August 2016

“…The sulfur concentration in a tested syrup sample (collected the day of the visit, stored in a refrigerator, and tested on January 20, 2017) was 1.53% of dry matter; 18–20 pounds of syrup were fed per day to each animal. At the recommendation of a cattle nutritionist, the farmer was providing thiamine supplementation to prevent polioencephalomalacia, a neurologic disease of ruminants that has been associated with thiamine status and high sulfur intake ( 4 ). Previous laboratory tests of the herd’s mixed feed analyzed on September 16, 2016, found a sulfur concentration of 0.44% of diet dry matter.…”