Page 518 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Sulfur Chapter | 35 485

VetBooks.ir been reported in sheep (Moshtaghi-Nia et al., 1989; Van maximum tolerable content of sulfur in the total diet is
In contrast, for sheep, beef cattle and dairy cattle the
Niekerk,
Niekerk
and
Van
1989a,b)
and
cattle
0.4% (NRC, 1985, 1988, 1996, 2001), while concentra-
(Wittenberg and Boila, 1988). High forage and water sul-
fur have also been associated with selenium deficiency tions slightly below this tolerable content (0.36%) have
(Ivancic and Weiss, 2001). Decreased serum and wool resulted in toxic effects (Gould et al., 1991). When 0.36%
selenium have been reported with increasing dietary sul- sulfur was fed in a high concentrate ration that slightly
fate (White and Somers, 1977; White, 1980). In addition, decreased rumen pH, which can enhance the formation of
increased soil sulfate inhibits plant uptake of selenium, hydrogen sulfide. In a review of the toxicology of sulfur
thereby increasing the potential for inducing a selenium in ruminants, it was stated that concentrations of sulfur
deficiency in ingesting herbivores (Newman and greater than 0.3% 0.4% may cause toxic effects
Schreiber, 1985), which may be an important mechanism (Kandylis, 1984). Since dietary toxicity of sulfur is not
in grazing animals. mutually exclusive to the various sulfur-containing com-
pounds, as different chemicals containing sulfur can have
the same clinical effects, total doses of sulfur/sulfate from
TOXICITY
both water and dietary material must be taken into
Toxicity of sulfur can be divided into three main catego- account when evaluating potential toxicity (Suttle, 1974).
ries that are likely to be encountered. The first is acute For example, water sulfate content of 500 mg/L would
oral poisoning. The second is subacute to chronic direct provide approximately half of the recommended maximal
toxicosis. And the third is subacute to chronic indirect daily intake for ruminants. In ruminants, the typical
toxicosis, as a secondary interference with other essential clinical presentation of subacute sulfur poisoning is
minerals that result in deficiencies. one of ataxia, weakness, blindness, recumbency, seizures,
Reports of acute oral sulfur poisoning are scarce in the and death.
literature. In a group of Holstein heifers, sulfur ingested Subacute ingestion of toxic doses of sulfate/sulfur has
at 0.85 3.8 g/kg body weight resulted in high morbidity been associated with Polioencephalomalacia (PEM), a
and moderate mortality (Gunn et al., 1987), while 20 hei- necrotizing lesion of the brain (Beke and Hironaka, 1991;
fers given 250 g sulfur in grain had high mortality (Julian Gould et al., 1991; Olkowski et al., 1992; Hamlen et al.,
and Harrison, 1975). Ewes fed a barley-sulfur mix 1993; McAllister et al., 1997). Gross and histologic
that provided approximately 40 45 g sulfur/ewe were lesions are primarily in the brain, but ruminal changes can
poisoned (White, 1964). Five horses administered 300 g be observed. Gross pathologic lesions include a darkening
sulfur succumbed to sulfur poisoning (Ales, 1907). of the rumen contents from precipitated sulfide salts,
Clinical and pathological manifestations of acute oral swelling of the cerebral hemispheres, softening of the
sulfur poisoning are similar across species (White, 1964; cerebral hemispheres, and yellow discoloration of the cor-
Julian and Harrison, 1975; Gunn et al., 1987). Abdominal tical gray matter. Histological lesions include necrosis of
pain, colic, rumen stasis, fetid diarrhea, dehydration, met- the cortical gray matter and occasional areas of necrosis
abolic acidosis, tachypnea, recumbency, and hydrogen in the thalamus or midbrain. The clinical condition can be
sulfide smell are expected clinical signs. Irritation, edema, an additive effect of the total sulfur in the diet and sulfate
and hemorrhage of the gastrointestinal tract and respira- in the drinking water (Beke and Hironaka, 1991). PEM
tory tract also should be expected. In addition, renal tubu- has been reported to be associated with high sulfur/sulfate
lar necrosis can be seen. ingestion in cattle (Beke and Hironaka, 1991; Gould
Monogastric animals are much less susceptible to the et al., 1991; Hamlen et al., 1993), pigs (Dow et al., 1963),
subacute direct and indirect toxic effects of excessive sul- and sheep (Olkowski et al., 1992). However, sodium ion
fur intake than ruminants. Pigs can tolerate 1000 mg/L poisoning in the pigs was likely the primary causative fac-
sulfur in the drinking water with only a mild cathartic tor, as the exposure was to sodium sulfate.
effect (Paterson et al., 1979), and 0.42% in the diet for The peak rumen production of hydrogen sulfide can
several months without adverse effects (Dale et al., 1973). be somewhat delayed from the time of initiating high sul-
Similarly, chicks had decreased growth rates at 1.2% fur intake. Peak rumen gas cap sulfide occurred at 1 3
dietary sulfur (Leach et al., 1960), and chickens had weeks after placing cattle on a high sulfur diet (Gould
decreased egg production, decreased feed intake and et al., 1997). But, continuing exposure resulted in a grad-
deaths at 4000 mg/L sulfate in their drinking water ual decline in the gas cap sulfide content. This would
(Adams et al., 1975). Since the indirect toxic effects of indicate an adaptation of the rumen microbes to favor
excessive sulfur, related to the interferences with other direct utilization of the sulfide or diminished rates of
essential minerals, are related to rumen conversion to sul- production.
fides, these effects are not observed in monogastric Subacute to chronic sulfur-induced mineral deficien-
animals. cies can result in severe health problems. Copper