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 for 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. Table 1 lists sulfur
concentration found in several common feed ingredients. 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 3000 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
(≈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
(Figure 1). 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 by-passing 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 feedyard 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 (Table 2). 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 (Figure 2). 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
from 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. Feedyards 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 thiamin 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.
Figure
1. Steer exhibiting classic symptoms of PEM. (Photo
courtesy of Dr. Guy Loneragan, West Texas A&M University and Dr.
John Wagner, Southeast Colorado Research Center, Colorado State
University.)
Click
image to enlarge
|
Table 1. Sulfur concentration in feeds
typically fed to feedlot cattle. |
|
Feed
commodity |
NRC, 1996 |
Practical Rangea |
|
Alfalfa hay |
0.28 |
0.21 – 0.54 |
|
Corn silage |
0.12 |
0.10 – 0.20 |
|
Corn grain |
0.13 |
0.11 – 0.17 |
|
Corn gluten
feed |
0.47 |
0.40 – 0.75 |
|
Corn gluten
meal |
0.90 |
0.80 – 1.20 |
|
Condensed
Corn Distillers Solubles |
0.40 |
1.00 – 2.23 |
|
Wet Corn
Distillers Grains plus solubles |
0.44 |
0.35 – 0.90 |
|
Soybean meal |
0.46 |
0.35 – 0.60 |
aBased
on the author’s experience.
|
Table 2.
Effect of water sulfate concentration on feedyard performance
and carcass merit. |
|
|
Treatment |
|
|
Period |
136 |
291 |
583 |
1219 |
2360 |
SEMa |
|
Average daily gain, lb |
|
|
|
|
|
|
D 0 to 28 |
5.20 |
5.36 |
4.72 |
4.89 |
4.30 |
0.13 |
|
D 29 to 56 |
5.14 |
4.78 |
5.42 |
4.56 |
4.65 |
0.15 |
|
D 57 to 84 |
4.76 |
4.76 |
4.67 |
4.83 |
4.91 |
0.07 |
|
D 85 to 116 |
3.95 |
3.90 |
4.23 |
4.39 |
4.32 |
0.07 |
|
D 0 to 116 |
4.76 |
4.69 |
4.76 |
4.67 |
4.54 |
0.07 |
|
|
|
|
|
|
|
|
|
Daily dry
matter intake, lb |
|
|
|
|
|
|
D 0 to 28 |
16.13 |
18.87 |
17.81 |
16.18 |
16.53 |
0.33 |
|
D 29 to 56 |
22.70 |
26.01 |
24.46 |
22.48 |
22.92 |
0.51 |
|
D 57 to 84 |
23.80 |
25.57 |
24.24 |
24.02 |
23.58 |
0.29 |
|
D 85 to 116 |
24.02 |
24.91 |
24.46 |
24.02 |
24.46 |
0.35 |
|
D 0 to 116 |
21.60 |
23.80 |
22.70 |
21.69 |
21.86 |
0.33 |
|
|
|
|
|
|
|
|
|
Feed:gain |
|
|
|
|
|
|
|
D 0 to 28 |
3.13 |
3.45 |
3.33 |
3.33 |
3.85 |
0.16 |
|
D 29 to 56 |
4.35 |
5.56 |
5.26 |
5.00 |
5.00 |
0.27 |
|
D 57 to 84 |
5.00 |
5.26 |
5.26 |
5.00 |
4.76 |
0.24 |
|
D 85 to 116 |
6.25 |
6.67 |
5.88 |
5.56 |
5.88 |
0.32 |
|
D 0 to 116 |
4.35 |
5.00 |
4.76 |
4.55 |
4.76 |
0.13 |
|
|
|
|
|
|
|
|
|
Final weight, lb |
1203 |
1196 |
1204 |
1191 |
1180 |
9.30 |
|
HCWb |
767 |
768 |
768 |
758 |
751 |
6.47 |
|
Dressing % |
63.78 |
64.23 |
63.75 |
63.65 |
63.61 |
0.16 |
|
Fat depth, in. |
0.55 |
0.56 |
0.61 |
0.62 |
0.55 |
0.03 |
|
Yield gradec |
3.55 |
3.54 |
3.59 |
3.47 |
3.32 |
0.13 |
|
Marblingd |
5.07 |
5.08 |
5.15 |
5.08 |
5.02 |
0.07 |
|
Ch & Pre |
50.0 |
48.9 |
61.7 |
53.2 |
38.3 |
|
| |
|
|
|
|
|
|
|
aStandard
Error of the Mean.
bHot
carcass weight, LB.
cCalculated
from carcass measurements.
dMarbling
score units, 5.00 = Small00.
ePercentage
of individual carcasses grading low choice or higher.

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