Understanding the role of sulfur–thiamine interaction in the pathogenesis of sulfur-induced polioencephalomalacia in beef cattle

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

“…Neville et al, [48] reported that ruminants exposed to elevated dietary S (0.65% or 0.83% DM) exhibited relatively high H 2 S gas ranging from 2000 to 8000 ppm, but did not show clinical signs of PEM. Similarly, Amat et al, [11] did not observe any clinical or histopathological changes associated with PEM in beef heifers fed high dietary S (0.62% S, DM), despite the elevated ruminal H 2 S level (2296 ppm). However, it has been reported that cattle with clinical signs of PEM have lower ruminal H 2 S than those clinically normal steers (H 2 S > 2000 ppm) [46].…”

“…Gould et al, [35] also induced PEM in Holstein steers by feeding an experimental diet with added sodium sulfate (NaSO 4 ). Case reports of S-induced PEM have been reported feedlots globally [1,11,[38][39][40].…”

“…Because the levels of total thiamine in blood or brain tissue of affected animals appear to be in the range of normal animals [35], or even elevated [23,36], it is commonly believed that the pathogenesis of S-induced PEM lesions is independent of thiamine deficiency [71]. Interestingly, thiamine therapy has effectively improved the clinical status of animals affected by S-induced PEM [11,72]. This suggests an associated metabolic relationship between excess S intake and thiamine in the development of malacic lesions.…”

“…To date, however, there is no convincing evidence to support the theory that the concentration of inhaled H 2 S from the rumen is high enough to induce PEM lesions. Furthermore, cattle affected by S-induced PEM frequently respond to thiamine treatment [9][10][11], and thiamine supplementation decreased the incidence and severity of S-induced PEM [12]. In this context, it is difficult to reconcile possible direct association between inhaled H 2 S and thiamine deficiency that may explain pathogenesis of necrotic lesions in the cerebral cortex.…”

“…The sulfite ion is a strong nucleophile and has the capacity to destroy thiamine [13]. Thus, thiamine deficiency appears to be a plausible risk factor involved in the etiology of PEM associated with excessive intake of S. A recent study by Amat et al, [11] reported reduced thiamine pyrophosphate (TPP), an active form of thiamine involved as a co-factor in several key Veterinary Medicine and Animal Sciences ISSN 2054-3425 doi: 10.7243/2054-3425-1-1 metabolic pathways, in the brains of S-induced PEM affected cattle, suggesting a more complex metabolic relationship between S and thiamine in the development of malacic lesions than previously postulated. 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.…”