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OCR for page 154
Cobalt
INTRODUCTION
Cobalt (Co) is in the same family in the periodic table as nickel and iron.
It makes up only 0.0023 percent of the earth's crust, where it usually
occurs with nickel or sulfide and arsenic ores. Industrially, cobalt is
used in alloy steel.
Although cobalt had been shown to be present in plant and animal
tissues, the first clear evidence that it was a dietary essential was in
1935 from Australian research into the cause of certain diseases of
cattle and sheep known as "coast disease" and "wasting disease"
(Underwood, 19771. There are cobalt-deficiency areas in a number of
different parts of the world. Cobalt is distributed widely in the animal
body, with the highest concentration in liver, bone' and kidney
(Underwood, 1977~. The only known function of the element in the
animal is its role as a component of vitamin By. Microbes use cobalt to
synthesize Bit.
ESSENTIALITY
Cobalt per se is a dietary essential for ruminants and horses, in which
it is incorporated into vitamin BE by gastrointestinal microbes. It is
essential in other animals as a component of vitamin Bit, but they have
more limited ability to synthesize vitamin Bit. In nonruminants vitamin
B,2 is absorbed from the lower digestive tract. The animals may also
ingest vitamin B,2 via coprophagy. Signs of cobalt deficiency in cattle
and sheep are loss of appetite, body weight loss, emaciation, and
154
OCR for page 155
Cobalt
155
anemia. The appearance is that of a starved animal. The dietary
requirement of cobalt for ruminants is 0.10 ppm, dry basis.
METABOLISM
Cobalt is not absorbed to a high degree by ruminants. In rats 80 percent
of orally administered cobalt appeared in the feces (Comaret al., 19461.
The element is used by microorganisms to synthesize vitamin B,2 in the
rumen of ruminants or in the cecum and colon of nonruminants. When
cobalt is injected or given orally in very large amounts, it accumulates
in the liver. Cobalt can replace zinc in certain proteolytic enzymes such
as pancreatic carboxypeptidase A (Vallee, 19741.
SOURCES
Cobalt is found in variable quantities in plants. Although most feeds are
adequate in cobalt, those grown in cobalt-deficient soils may be de-
ficient. Supplemental sources include cobalt oxide and salts such as
cobalt sulfate and cobalt chloride. The supplemental sources can be
administered by incorporating in feeds or mineral mixes, by drenching
with cobalt solutions, or use of cobalt '`bullets" composed of cobalt
oxide and finely divided iron. The bullets, administered orally, lodge
against the ruminoreticular fold to supply a steady amount of cobalt to
the rumina] digesta. Two problems have arisen from use of the bullets,
namely, regurgitation by the animal and coating of the pellets inside the
rumen with calcium phosphate (Underwood, 1977), which prevents
bioavailability of cobalt.
TOXICOSIS
Under practical conditions, cobalt deficiency in ruminants is more
likely than cobalt toxicosis. Nevertheless, in supplementation to pre-
vent a deficiency, accidental oversupplementation is possible,- which
will produce deleterious effects.
LOW LEVELS
Characteristic signs of chronic toxicosis for most species are reduced
feed intake and body weight, emaciation, anemia, hyperchromemia,
OCR for page 156
156 MINERAL TOLERANCE OF DOMESTIC ANIMALS
debility, and increased liver cobalt (Ely et al., 1948; Keener et al., 1949;
Becker and Smith, 1951; Turk and Kratzer, 1960~. The signs are similar
to those of cobalt deficiency except the elevated liver cobalt levels.
Addition of 2.88 ppm of cobalt to a diet of young pigs did not affect
performance (Kline et al., 19541.
HIGH LEVELS
Administration of large amounts of cobalt induces polycythemia in
simple-stomached animals (Underwood, 19771. The disturbance does
not occur in functional ruminants, but affects calves prior to rumen
development. The polycythemia is accompanied by hype~plasia of the
bone marrow, reticulocytosis, and increased blood volume. Toxic signs
from intravenous injection of 0.81 to 1.X0 mg/kg of body weight in
calves were lacrimation, salivation, dypsnea, incoordination, defeca-
tion, and urination (Dunn e' al., 19521. Oral administration of excessive
cobalt in cattle resulted in lack of appetite, decreased water consump-
tion, increased hemoglobin, red cell count and packed red cell volume,
and incoordination (Keener et al., 19491. Fatty infiltration of the liver,
slight pulmonary edema, and congestion and petechial to ecchymotic
hemorrhages in small intestine were reported in sheep that died of
cobalt toxicosis (Becker and Smith, 19511.
Adding cobalt in the form of cobalt chloride (CoCl2 6H2O) to the diet
at levels up to 200 ppm did not result in toxicosis in pigs fed a diet
adequate in iron (Huck and CIawson, 1976~. The addition of 400 or 600
ppm cobalt caused anorexia, growth depression, stiff-leggedness,
humped back, incoordination, and extreme muscular tremors. Serum
cobalt was increased and iron in serum was decreased by added cobalt.
FACTORS INFLUENCING TOXICITY
Increasing the protein level of the diet by feeding casein resulted in less
depression in growth rate of calves fed 200 mg cobalt per day, and the
calves fed the high-protein diet returned to normal gains in body weight
earlier (Ely et al., 19481. However, in calves fed 100 mg cobalt per day,
changing the protein content of the diet by addition of casein to the
grain mixture had no effect on cobalt toxicity. Administration of 500 mg
methionine intravenously to calves prior to injection with 50 or 75 mg
cobalt (0.6~1.85 mg/kg) prevented or decreased the severity of the
signs (Ely et al., 1953~. Ethylenediaminetetraacetate (EDTA), cystine, or
cysteine alleviated toxicosis in chicks fed 50 ppm cobalt (Turk and
Kratzer, 19601.
OCR for page 157
Cobalt
157
Addition of 200 ppm iron, 400 ppm manganese, and 400 ppm zinc
alleviated the growth depression in swine caused by adding 400 ppm
cobalt and partially restored feed intake and growth from adding 600
ppm cobalt (Huck and CIawson, 19761. Feeding O.5 or 1.0 percent
methionine alleviated the toxicosis caused by feeding 600 ppm cobalt.
I
TISSUE LEVELS
There are only limited data concerning the effect of feeding excessive
cobalt on tissue levels of the mineral. Oral administration of cobalt to
cattle increased cobalt in liver and kidney up to over 10-fold (Keener e'
al., 1949~. The levels were 2.1 to 15.4 ppm in liver and 1.9 to 5.4 ppm
in kidney, dry basis. Levels for control animals were 0.44 to 0.85 ppm
for liver and 0.26 to 0.41 ppm, dry basis, for kidney. Liver cobalt in
swine was increased by all levels of cobalt supplementation, the level
being generally proportional to the supplemental level (Huck and Claw-
son, 19761. The effect of supplementing 200, 400, and 600 ppm cobalt
on cobalt in liver, spleen, kidney, and heart was studied by these
workers. Cobalt was increased in these tissues by supplementation.
MAXIMUM TOLERABLE LEVELS
Cattle tolerated cobalt at a level of 66 mg/100 kg (Keener et al., 1949)
and sheep tolerated up to 352 mg/100 kg (Becker and Smith, 1951~. The
66 mg/100-kg level would mean 26 ppm if the dry matter intake is
assumed to be 2.5 percent of body weight. Thus, 10 ppm appears safe.
No signs of toxicosis were observed in chicks fed diets with 4.7 ppm
cobalt, and severe toxicosis was observed at 50 ppm (Turk and Kratzer,
1960~. In swine 200 ppm cobalt produced no adverse effect (Huck and
CIawson, 19761. It appears that swine and poultry should be able to
tolerate 10 ppm.
SUMMARY
Cobalt is a dietary essential for ruminants, which use it for the synthesis
of vitamin Be. Nonruminants are usually fed vitamin Be rather than
cobalt, since they possess only limited capacity to use the mineral to
advantage in meeting their vitamin Be requirement. Sources of cobalt
in addition to amounts in feedstuffs are cobalt oxide and salts of cobalt.
OCR for page 158
158 MINERAL TOLERANCE OF DOMESTIC ANIMALS
A deficiency is more likely to occur than toxicosis. Signs of toxicosis
are polycythemia in simple-stomached animals, and reduced feed
intake and body weight, emaciation, anemia, debility, increased hemm
Robin and packed cell volume, and elevated liver cobalt in ruminants.
Toxic levels appear to be at least 300 times the requirement, so the
likelihood of a problem appears remote. Also, increased protein or
methionine administration appears to help in protecting against cobalt
toxicosis.
OCR for page 159
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Cobalt
REFERENCES
161
Andrews, E. D. 1965. Cobalt poisoning in sheep. N.Z. Vet. J. 13:101.
Becker, D. E., and S. E. Smith. l9Sl. The level of cobalt tolerance in yearling sheep. J.
Anim. Sci. 10:266.
Comar, C. L., G. K. Davis, and R. F. Taylor. 1946. Cobalt metabolism studies: Radim
active cobalt procedures with rats and cattle. Arch. Biochem. 9:149.
Dunn, K. M., R. E. Ely, and C. F. Huffman. 1952. Alleviation of cobalt toxicity in calves
by methionine administration. J. Anim. Sci. 11:326.
Ely, R. E., K. M. Dunn, and C. F. Huffman. 1948. Cobalt toxicity in calves resulting from
high oral administration. J. Anim. Sci. 7:239.
Ely, R. E., K. M. Dunn, C. F. Huffman, C. L. Comar, and G. K. Davis. 1953. The effect
of methionine on the tissue distribution of radioactive cobalt injected intravenously into
dairy calves. J. Anim. Sci. 12:394.
Muck, D. W., and A. J. Clawson. 1976. Excess dietary cobalt in pigs. J. Anim. Sci.
43:1231.
Keener, H. A., G. P. Percival, and K. S. Marrow. 1949. Cobalt tolerance in young dairy
cattle. J. Dairy Sci. 32:527.
Kline, E. A., J. Kostelic, G. C. Ashton, P. G. Homeyer, L. Quinn, and D. V. Catron.
1954. The effect of the growth performance of young pigs of adding cobalt, vitamin BE
and antibiotics to semipurif~ed rations. J. Nutr. 53:543.
Turk, J. L., Jr., and F. H. Kratzer. 1960. The effects of cobalt in the diet of the chicks.
Poult. Sci. 39:1302. (Abstr.)
Underwood, E. J. 1977. Trace Elements in Human and Animal Nutrition, 4th ed. Aca-
demic Press, New York.
Vallee, B. L. 1974. The entatic properties of cobalt carboxypeptidase and cobalt procar-
boxypeptidase. In W. G. Hoekstra, J. W. Suttie, H. E. Ganther, and W. Mertz, eds.
Trace Element Metabolism in Animals2, p. 5. University Park Press, Baltimore, Md.
Representative terms from entire chapter:
body weight
