Sulfur Toxicity in Feedlot Cattle

By John J. Wagner, Ph.D.
Professor & General Manager, Southeast Colorado Research Center
Colorado State University, Lamar, Colorado

The Need for Sulfur

Sulfur is an important component of many functions in the body and is an essential nutrient for beef cattle.  It is an important part of the amino acids methionine, cysteine, and cystine.  The B-vitamins thiamine and biotin also contain sulfur.  Rumen microbes require sulfur for their normal growth and metabolism.  A large portion of the sulfur found in typical feedlot diets is a component of the natural protein and most practical diets are adequate in sulfur.  However, feeding diets high in non-protein nitrogen or high in rumen undegradable intake protein may reduce the amount of sulfur available for rumen microorganisms, thus increasing the need of supplemental sulfur.  The requirement for sulfur (National Research Council) is 0.15% of diet dry matter and maximum tolerable level is listed as 0.40% of diet dry matter (NRC, 1996).

Sources of Sulfur

Total sulfur intake from all feed and water sources must be considered when evaluating nutritional programs for sulfur adequacy or excess.  Typical diet components for feedlot cattle (including corn, alfalfa hay, and corn silage) contain relatively low to moderate concentrations of sulfur.  Under most circumstances, typical combinations of these feeds generally used for cattle pose little or no danger for sulfur toxicity.  Several feeds, especially co-products from grain milling (wet or dry) industries may be high in sulfur.  As these products are included in the diet, sulfur concentration generally increases, resulting in a rise in the risk of sulfur toxicity.

Sulfur concentrations in water can vary tremendously.  In 1999, the National Animal Health Monitoring System conducted a study of feedlots with greater than 1,000 head capacity (NAHMS 2000).  Two–hundred and sixty-three feedlots from 10 states supplied water samples for analysis.  Approximately 77% of the samples contained less than 300 ppm sulfate, 15% of the samples contained 300 to 999 ppm sulfate, and 8% of the samples registered greater than 1,000 ppm sulfate.  If a feedlot steer consumes approximately 10 gallons of water daily, sulfate intake from water is 4, 40 and 120 g per day if the water contained 100, 1,000, or 3,000 ppm sulfate.  Sulfate is approximately one-third sulfur.  Therefore, sulfur intake from water by the steer would be 1.3, 13.0, 40 g per head daily, respectively.  If the steer was consuming 19.8 lb. of dry matter daily that contained 0.12% sulfur, total sulfur intake expressed as a percent of dietary dry matter intake would be 0.13, 0.26 or 0.56%, respectively.  It is highly likely that the steer consuming 3,000 ppm sulfate would experience some degree of sulfur toxicity.  At 100 or 1,000 ppm the likelihood of sulfur toxicity is reduced considering the base diet was assumed to contain 0.12% sulfur.  However, if the base diet contained 30% wet distillers grains on a dry matter basis, and if the distillers grains contained 0.60% sulfur, an additional 0.14% [(0.60 – 0.13) x 0.30] sulfur would be added to the diet.  In this instance, the steer consuming 1,000 ppm sulfate water is now at risk of developing sulfur toxicity.  Early in the growth of the ethanol industry, several feedlots that had successfully used marginal quality water (or about 1,000 ppm sulfate) for many years started to experience sulfur problems only after the addition of distillers grains in the diet.

Manifestation of Sulfur Toxicity

Elemental sulfur is considered one of the least toxic minerals; however, hydrogen sulfide, a product of sulfate metabolism in the rumen, is as toxic as cyanide (NRC, 2000).  The manifestation of sulfur toxicity in feedlot cattle is often a condition called polioencephalomalacia (PEM), which is characterized by necrosis of the cerebral cortex.  Symptoms of the condition include blindness, poor coordination, lethargy, and seizures.  Very often affected cattle are observed standing in the corner of the pen like a saw horse with all four feet spread to the extreme corners of their body.  Pen riders, doctors, and other feedlot personnel often refer to cattle exhibiting these signs as “brainers.”  This colorful name is appropriate when one considers that PEM literally means softening (malacia) of the gray matter (polio) of the brain (encephalo).

A number of research findings have linked PEM outbreaks to thiamin status, including a reduction in the activity of a thiamin diphosphate dependent enzyme (transketolase) in blood and an increase in the levels of thiaminases in the gastrointestinal tract.  PEM has been induced by feeding thiamin antagonists.  Researchers have demonstrated that calves recover from early symptoms of PEM if high doses of thiamin are administered.  The large body of evidence that associates PEM with thiamin status has led to the often erroneous assumption that outbreaks of PEM are the result of altered thiamin status and intravenous thiamin administration is often automatically used to treat cattle with PEM.  The addition of 100 to 200 mg of thiamin per head daily is often added to diets of cattle perceived to be at risk of developing PEM.

The results from efforts to treat or prevent PEM with thiamin are mixed.  Much of the confusion surrounding thiamin therapy may be attributed to the fact that high sulfate intake may induce PEM through either one of, or a combination of, two distinct mechanisms.  High sulfate intake has been shown to reduce duodenal thiamin flow and sulfite, a product of sulfate reduction, can destroy thiamin in the rumen resulting in thiamin deficiency.  This form of sulfate induced PEM may respond to thiamin therapy or may be prevented by thiamin supplementation.  However, an alternative mechanism through which sulfate causes PEM may be involved particularly if sulfate intake is extremely high.

Sulfides inhibit cytochrome C, an enzyme of the electron transport chain.  It has been proposed that rumen generated sulfides escaped detoxification in the liver and were responsible for sulfate induced PEM.  High sulfate intake results in extreme concentrations of hydrogen sulfide in the rumen gas cap.  These sulfides are inhaled during eructation, absorbed into the blood stream in the lung, and transported to the brain, thus bypassing the liver.  In addition, it has also been suggested that the high amounts of sulfides absorbed through the rumen wall and transported to the liver may overwhelm the capacity of the liver to detoxify sulfide.  Thus, a portion of these sulfides may also reach the brain.  Cattle experiencing PEM caused by the inhibition of cytochrome C will not respond to thiamin therapy.

Cattle consuming high sulfate water do not necessarily need to show symptoms of PEM to experience reduced feed yard performance.  Feedlot steers were provided with water of various sulfate concentrations ranging from 136 to 2, 360 ppm.  No clinically apparent symptoms of PEM were reported and performance by all steers in the study was outstanding.  However, increasing water sulfate concentration resulted in linear decreases in daily gain, gain to feed ratio, final weight, hot carcass weight, and dressing percentage.  Sulfate concentration by period interactions were evident for dry matter intake, average daily gain, and feed efficiency.  Water sulfate concentration also influenced water intake.  The effect of water sulfate on performance was greatest during the early periods of the trial and less evident toward trial completion.  Water intake differences were greatest during the periods of the greatest performance reduction and not evident during the last period.  The trial was started during the early summer (July 16) and ambient temperatures were greatest during this time.  It appears that extreme water sulfate concentrations inhibit water intake by nearly 18%.  It is possible that performance reductions observed for cattle consuming high sulfate water in summer may actually be a function of reduced ability of the cattle to effectively combat heat stress.

Nutritional Interventions

In addition to supplemental thiamin, several other nutritional manipulations have been proposed to help control sulfur-induced PEM.  Colorado State University scientists demonstrated up to a 37% reduction in the rate of hydrogen sulfide production from an in vitro fermentation system with the addition of nitrate.  Other researchers demonstrated a 77% reduction in hydrogen sulfide production when an in vitro system was treated with molybdenum and a 71% reduction in hydrogen sulfide production when the system was treated with 9, 10-anthraquinone.  Hydrogen sulfide production rate was reduced by over 75% when an in vitro system was exposed to clinoptilolite, a form of zeolite.  Feeding high levels of ammonium nitrate, molybdenum, or zeolite often reduced the hydrogen sulfide concentration in the rumen gas cap, but did not improve feedlot performance by steers consuming high sulfate water (> 2,000 ppm) in experiments conducted at the Southeast Colorado Research Center in the late 1990s.

Management Recommendations

  1. Sample all sources of water and evaluate for sulfate concentration.  Blending water for various sources to reduce the sulfate concentration to less than 1,000 ppm may reduce the risk of sulfur induced PEM and lost performance.
  2. Sample all co-product feed ingredients and analyze for sulfur.
  3. Make certain total (water plus feed) dietary sulfur intake expressed as a percentage of dry matter intake is less than 0.40%.
  4. Avoid stacking sulfur risk factors.  Feed yards forced to use marginal or poor quality water may simply not be able to successfully utilize grain milling co-products.  Likewise, simultaneous use of several high-sulfur grain milling co-products should be avoided.
  5. Logic may suggest the elimination of high sulfur trace mineral sources such as copper or zinc sulfate from the diet.  However, the amount of sulfur contributed to the diet by trace mineral source is minimal compared with the sulfur contribution from grain milling co-products or marginal to poor quality water.
  6. Thiamin supplementation or intravenous thiamin administration may provide some measure of success in managing PEM if thiamine metabolism is compromised in the rumen.  However, thiamin therapy or supplementation will likely be of limited value if exposure to hydrogen sulfide is excessive.
  7. To date, despite modest successes in laboratory in vitro systems and non-research based testimonials to the contrary, no dietary modifications have been shown to effectively control PEM or improve performance in feedlot cattle exposed to high sulfur intake.  References available upon request from Dr. Wagner.