- High concentrations of sulfur can be toxic to cattle, decreasing performance as well as causing polioencephalomalacia.
- Cattle receiving additional sulfur were producing significantly more hydrogen sulfide.
- There was no correlation between sulfur treatment and hydrogen sulfide production.
What you need to know: High concentrations of sulfur can occur in things like distillers grains, and water sources. Sulfur can be toxic to cattle, expressed as decreased performance and polioencephalomalacia (PMC). The emergence of PMC starts with the ruminal conversion of sulfur into hydrogen sulfide, then eructation of gases into the sinuses, and absorption of these gases into the vasculature around the nasal cavities. These gases cause neurologic damage and brain swelling.
However unpleasant and costly sulfur toxicity is, there is much that is not understood about the mechanisms which produce the hydrogen sulfide gas nor what could be done to control production. Sulfo-reducing ruminal bacteria, or SRB for short, convert sulfur into hydrogen sulfide gas and are divided into two categories: assimilatory SRB (ASRB) and dissimilatory SRB (DSRB). A current hypothesis is that DSRB is the source of increases in hydrogen sulfide gases during high sulfur intake, which leads to polioencephalomalacia.
Twelve crossbred steers were separated into two groups, one that received low sulfur (0.19% S) and one that received high sulfur (0.39% S) through the addition of sodium sulfate into the ration. Each animal was fed their respective diet for 38 days and evaluated on days 0, 22, and 38 for ruminal hydrogen sulfide production. Ruminal fluid samples were also taken at these times to check for pH, ammonia nitrogen, volatile fatty acids, and microbes. The animals were also checked daily for any polioencephalomalacia symptoms.
Here is where things get interesting. Earlier, we talked about how the common hypothesis that dissimilatory sulfo-reducing ruminal bacteria (DSRB) were the cause of increased hydrogen sulfide gas production. We would, in turn, expect to see increases in the quantity of DSRB to match that of hydrogen sulfide production. However, this was not the case. The high-sulfur group was indeed producing significantly more hydrogen sulfide, but there was no significant correlation between the gas levels and the DSRB population. Additionally, there were no significant effects of the sulfur treatment on the diversity of the tested rumen microbiome.
The lack of observed polioencephalomalacia occurrence, or any change in feed intake, suggests that the sulfur content of the high sulfur treatment was not enough to impact the animals. The authors point to the fact that the makeup of old and new diets (moving from forage-based to concentrate-based) could "...increase ruminal H2S [hydrogen sulfide] concentration more slowly, allowing animals to adapt to high dietary S [sulfur] concentration and/or H2S concentration." They continue, stating, " Hence, it is possible that for PEM [polioencephalomalacia] development, adaptation time to high ruminal H2S concentration is as important as high ruminal H2S concentration itself."
What makes this paper notable is not what the researchers found specifically, but what they didn't find. These researchers did not find that DSRB count was causing elevated hydrogen sulfide, but instead that the hypothesis was an incomplete one. These findings suggest there is much more at play in the rumen production of hydrogen sulfide than we initially thought, including the magnitude of the role of DSRB.
Important to note:
- The low-sulfur diet had sulfur levels over the recommended concentrations. This was due to feedstuffs with high crude protein levels, which increased the total sulfur present. However, the concentrations were still much lower than the high-sulfur treatment.
Industry application: Although this paper didn't have an answer for avoiding sulfur toxicity or polioencephalomalacia, it offered some insightful information. When attempting to control sulfur toxicity in cattle, it is important to follow nutritional recommendations; however, this paper suggests that there may also be other factors at play, like ration transitions and diet composition.
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