needs, but with a higher proportion of sulfide as an outcome. Sulfide is readily absorbed through the rumen wall reaching the bloodstream. Sulfide binds the haemoglobin, creating sulfhaemoglobin that reduces the ability to carry oxygen to tissues. Sulfide also affects energy production at the cell level, causing cell damage. Deaths have been reported from acute sulfide toxicity, as the liver plays an essential role in sulfide detoxication, which impairs liver function. The formation of H2


S in the rumen depends on two main fac-


tors: the excess of S, which will serve as a substrate for sul- fur-reducing bacteria (SRB) and the ruminal pH. A lower pH in the rumen will result in a great proportion of sulfide as H2


S.


PEM originating from the respiratory system


PEM is a disease characterised by damage to the brain’s grey matter leading to neurological dysfunction. Multiple causes can lead to PEM, such as thiamine deficiency, water depriva- tion, lead toxicity, sodium toxicity and S toxicity. PEM caused by S toxicity is a consequence of the accumula- tion of H2


S in the rumen produced by rumen bacteria and


Table 1 – Sulfur content of ruminant feedstuff.


Feed


Barley malt sprouts, dehydrated Beet pulp, w/molasses, dehydrated Corn, distillers grains, dehydrated Corn gluten meal, 60% Molasses, beet Rapeseed meal


Whey, dehydrated


Sulfur, % DM basis 0.85 0.42 0.46 0.72 0.60 1.25 1.12


Conclusion Sulfur is an essential nutrient for ruminal bacteria that is often supplemented in ruminant diets. Nevertheless, the increased use of feedstuff containing high S levels raises concerns re- garding mineral absorption, reduced feed intake and fibre di- gestibility affecting animal performance. Sulfur contribution of individual feedstuffs and feed addi- tives has to be taken into account during formulation to manage the exposure of ruminants to high sulfur diets. Addi- tionally, it should not be forgotten to quantify S content. The control of the S content in the animal’s drinking water can also give insights about how much it is contributing as a source of S to ruminants.


▶ DAIRY GLOBAL | Volume 8, No. 2, 2021 27


then eliminated through eructation, as illustrated in Figure 1. It is estimated that 60% of the eructed gas is inhaled by the animal. Once breathed in, H2


S crosses the pulmonary barrier and reaches the brain. H2S disturbs the oxidative process that


generates ATP, the molecule responsible for carrying energy within the cell, causing cellular anoxia and death by apopto- sis. The brain is the most affected organ as it has a high ener- gy demand for oxygen, especially in the grey matter due to its many synapses.


Additional concern of S excess The excess of S can also compromise the absorption of trace minerals in ruminants. In the rumen, free Molybdenum (Mo) and S form complexes called thiomolybdates that bind strongly to Copper (Cu), preventing it from being absorbed. The Cu deficiency caused by the interaction with S and Mo is called a secondary deficiency. Even if Cu is supplied at appro- priate levels in the diet, the animals would be deficient as the complexation in the rumen would prevent its uptake by the animal.


Sulfur contribu- tion of individu- al feedstuffs and feed additives has to be taken into account during formula- tion to manage the exposure of ruminants to high sulfur diets.


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