Page 519 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
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486 SECTION | V Metals and Micronutrients
VetBooks.ir deficiency can cause poor growth, weakness, poor REFERENCES
immune function, poor reproductive function, and death.
Adams, A.W., Cunningham, F.E., Munger, L.L., 1975. Some effects on
In addition, sulfur-induced copper deficiency may play a
role in PEM (Gooneratne et al., 1989). Severe copper layers of sodium sulfate and magnesium sulfate in their drinking
water. Poult. Sci. 54, 707 714.
deficiency also causes myelin degeneration (enzootic
Ales, 1907. Case of poisoning by sulfur in the horse. Vet. J. 63, 524.
ataxia) in lambs, deer, and other ruminants (Cordy, 1971;
Amat, S., McKinnon, J.J., Olkowski, A.A., et al., 2013. Understanding
Faye et al., 1991; Audige et al., 1995). Sulfate-induced the role of sulfur-thiamine interaction in the pathogenesis of sulfur-
selenium deficiency can cause poor growth, weakness, induced polioencephalomalacia in beef cattle. Res. Vet. Sci. 95,
poor immune function, poor reproductive function, dam- 1081 1087.
age to the cardiac or skeletal muscles and death. Audige, L., Wilson, P.R., Morris, R.S., et al., 1995. Osteochondrosis,
skeletal abnormalities and enzootic ataxia associated with copper
deficiency in a farmed red deer (Cervus elaphus) herd. N. Zeal. Vet.
J. 43 (2), 70 76.
TREATMENT Beauchamp Jr, R.O., Bus, J.S., Popp, J.A., et al., 1984. A critical review
of the literature on hydrogen sulfide toxicity. Crit. Rev. Toxicol. 13,
Treatment for acute sulfur poisoning is predominantly
25 97.
supportive in nature, with removal of the causative mate-
Beke, G.J., Hironaka, R., 1991. Toxicity to beef cattle of sulfur in saline
rial, as well as administration of fluids and electrolytes.
well water: a case study. Sci. Total Environ. 101 (3), 281 290.
However, the human literature points to successful treat-
Bird, P.R., 1972. Sulfur metabolism and excretion studies in ruminants:
ment of acute hydrogen sulfide poisoning by induction of VII. Secretion of sulfur and nitrogen in sheep pancreatic and bile
methemoglobinemia with nitrite to allow for the forma- fluids. Aust. J. Biol. Sci. 25, 817 834.
tion of sulfmethemoglobin, similar to therapeutic proto- Bird, P.R., Moir, R.J., 1971. Sulfur metabolism and excretion studies in
cols for treatment of cyanide poisoning (Stine et al., ruminants. I. The absorption of sulfate in sheep after intraruminal or
1976; Peters, 1981). This type of therapy may also be intraduodenal infusions of sodium sulfate. Aust. J. Biol. Sci. 24,
beneficial in the treatment of subacute direct sulfur poi- 1319 1328.
soning. Since sulfides act on and split disulfide bridges, Block, R.J., Stekol, J.A., Loosli, J.K., 1951. Synthesis of sulfur amino
acids from inorganic sulfate by ruminants. II. Synthesis of cystine
the use of oxidized glutathione or other simple disulfide
and methionine from sodium sulfate by the goat and by the microor-
compounds could be protective or antidotal (Smith and
ganisms of the rumen of the ewe. Arch. Biochem. 33, 353 363.
Abbanat, 1966). The use of thiamine in the treatment of
Cordy, D.R., 1971. Enzootic ataxia in California lambs. J. Am. Vet.
PEM is beneficial, even though there is no overt thiamine
Med. Assoc. 158 (11), 1940 1942.
deficiency. The primary treatment of indirect mineral Dale, S.E., Ewan, R.C., Speer, V.C., et al., 1973. Copper, molybdenum,
deficiencies resultant from high sulfur intake would also and sulfate interaction in young swine. J. Anim. Sci. 37, 913 917.
include enhanced supplementation of copper and poten- Dougherty, R.W., Mullenax, C.H., Allison, M.J., 1965. Physiological phe-
tially selenium. In some cases in which limitation of nomena associated with eructation in ruminants. In: Dougherty, R.W.
water or forage sulfur intake is not possible, use of che- (Ed.), Physiology of Digestion in the Ruminant. Buttersworth,
lated copper and selenium becomes important in order to Washington, DC, p. 159.
bypass the sulfide binding/precipitation of essential Dow, C., Lawson, G.H.K., Todd, J.R., 1963. Sodium sulfate toxicity in
pigs. Vet. Rec. 75, 1052 1055.
minerals in the rumen and competitive inhibition of sele-
Edwin, E.E., Jackman, R., 1982. Ruminant thiamine requirement in ret-
nate from the intestinal tract.
rospect. Vet. Res. Commun. 5, 237 250.
In addition to direct treatment, management can play a
Faye, B., Grillet, C., Tessema, A., et al., 1991. Copper deficiency in
role in the prevention of sulfur poisoning. Testing of
ruminants in the Rift Valley of East Africa. Trop. Anim. Health
water and dietary materials will identify high sulfur prior Prod. 23 (3), 172 180.
to utilization. With this information, management strate- Friberg, L., Lener, J., 1986. Molybdenum. In: Friberg, L., Nordberg, G.F.,
gies can be utilized that would incorporate the sulfur at a Vouk, V.B. (Eds.), Handbook on the Toxicology of Metals, second
gradually increasing content in an attempt to allow for ed. Elsevier/North-Holland Biomedical Press, New York,
microbial adaptation. pp. 446 461.
Gooneratne, S.R., Olkowski, A.A., Klemmer, R.G., et al., 1989. High
sulfur related thiamine deficiency in cattle: a field study. Can. Vet.
J. 30, 139 146.
CONCLUDING REMARKS AND FUTURE Gould, D.H., 2000. Update on sulfur-related polioencephalomalacia. Vet.
DIRECTIONS Clin. North Am. Food Anim. Pract. 16, 481 496.
Gould, D.H., McAllister, M.M., Savage, J.C., et al., 1991. High sulfide
Although much is known about the different clinical dis- concentrations in rumen fluid associated with nutritionally induced
ease conditions that excessive sulfur can cause, treatment polioencephalomalasia. Am. J. Vet. Res. 52, 1164 1169.
remains only somewhat effective. Thus, it is important to Gould, D.H., Cummings, B.A., Hamar, D.W., 1997. In vivo indicators of
evaluate the use of nitrite- or disulfide-containing com- pathologic ruminal sulfide production in steers with diet-induced
pounds in the treatment of domestic animals. polioencephalomalacia. J. Vet. Diagn. Invest. 9, 72 76.