Page 506 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Selenium Chapter | 33 473

VetBooks.ir Subcutaneous LD 50 of selenium is 1 mg/kg in lambs and weight daily for 128 days in dairy cows (Ellis et al.,
1997; Lawler et al., 2004). Differences in susceptibility to
1.9 mg/kg in adult cattle (Grace, 1994). In 2009, 21
chronic selenium poisoning may be a product of historical
horses from Venezuela that were in Florida for an inter-
national polo match died from selenium overdose exposure, variability in rumen microbial population
(Florida Department of Agriculture and Consumer and/or age-associated susceptibility. As stated previously,
Services, 2009; Desta et al., 2011). The selenium was certain microbes can reduce selenium to nonbioavailable
misformulated in a compounded intravenous vitamin- forms, resulting in decreased systemic absorption. Pigs
mineral product, resulting in a 100 fold overdose and an develop chronic selenosis with exposure to selenium as
IV selenium exposure of 4 5 mg/kg BW. The horses low as 8 mg/kg of diet (Goehring et al., 1984; Mahan and
developed clinical signs within hours of the administra- Magee, 1991; Stowe and Herdt, 1992). And horses
tion and died within 3 18 h. exposed to 20 mg Se/kg DM for 3 weeks developed
Clinical manifestation of acute selenium poisoning lesions (Stowe and Herdt, 1992).
begins as early as 8 10 h, but can be delayed for up to Clinical signs of chronic selenosis include depression,
36 h (Franke and Moxon, 1936; NRC, 1983; Raisbeck, weakness, emaciation, anemia, hair loss, hoof abnormali-
2000; Tiwary et al., 2006; Davis et al., 2012). Onset as ties, anorexia, diarrhea, weight loss, lameness, reproductive
early as 1.5 h occurred with IV exposure (Desta et al., failure, and death (Rosenfeld and Beath, 1964; O’Toole and
2011). Early in the clinical syndrome, one can detect the Raisbeck, 1995; Underwood and Suttle, 1999; Raisbeck,
garlicky smell of dimethylselenide on the breath. Clinical 2000; Davis et al., 2014; Davis, 2016). Hoof wall abnor-
signs that follow include respiratory distress, restlessness malities are frequently identified in cattle, horses and pigs,
or lethargy, head down, droopy ears, anorexia, gaunt and include swelling of the coronary band, hoof deformities
appearance, salivation, watery diarrhea, fever, sweating, and/or separation and sloughing of the hoof wall. Hair loss
tachycardia, teeth grinding, stilted gait, tetanic spasms, from the base of the tail and switch in cattle, horses and
and/or death. Clinical signs tend to progress quickly after mules is sometimes referred to as “bobtail disease.”
they are first observed. Gross and histologic lesions Interestingly, sheep do not develop the alopecia or hoof
include systemic congestion, pulmonary edema, skeletal lesions that are seen in cattle, but they have decreased wool
muscle necrosis, myocardial necrosis, and petechial growth rates. In pigs, goats and horses, there may be a gen-
hemorrhages in and on the myocardium. eral alopecia (Franke, 1934). Pigs also develop neurologic
“Blind staggers” has historically been associated with signs of paralysis (Goehring et al., 1984).
subacute to chronic selenium poisoning. However, this Pathologic lesions of chronic selenium poisoning are
association was due to its occurrence in known selenifer- generally related to hoof lesions and to the effects of
ous areas. The areas with seleniferous soils also tend to starvation (Raisbeck, 2000). Lesions of nephritis, hepatic
have highly alkaline soils with high potential for exces- cirrhosis, and myocardial necrosis can be expected. In
sive sulfur exposure. It has been stated that blind staggers pigs, bilateral malacia of the gray matter in the spinal
cannot be reproduced with pure selenium compounds cord can be seen.
alone and likely involves other factors, such as alkaloid Reproductive abnormalities are seen (Davis and Hall,
poisoning, starvation or polioencephalomalasia (O’Toole 2017; Davis, 2016) in several species when excessive
and Raisbeck, 1995). However, one can still find refer- selenium is ingested. Field reports indicate that reproduc-
ences that tie it to selenium (Underwood and Suttle, 1999; tive performance can be reduced without the other typical
NRC, 2005). signs of alkali disease at 5 10 ppm Se in diet (Olson
Chronic selenosis, often referred to as “alkali disease,” et al., 1970), but direct experimental evidence in large
is the result of long-term ingestion of seleniferous forages animals has been lacking (Raisbeck, 2000). A recent set
(NRC, 1983, 2005; Raisbeck, 2000). High selenium of studies found failure of conception occurred in ewes
intake is generally for greater than 30 days and, due to fed 10 and 30 ppm plant origin selenium, while abnormal
plant selenium content, is usually associated with faculta- sperm and sperm motility occurred in rams fed 25 ppm
tive accumulators, not indicator plants, although chronic plant origin selenium (Davis, 2016). Decreased concep-
selenosis can also be reproduced by long-term feeding of tion rate and an increased fetal resorption rate in cattle,
high inorganic selenium (Kaur et al., 2003). Calves were sheep and horses were observed when they were fed natu-
chronically poisoned with selenite at 0.25 mg/kg body ral diets containing 20 50 mg Se/kg diet (Harr and Muth,
weight daily for 16 weeks. In a similar study in yearlings, 1972). Both rats exposed to 3 ppm Se as seleniferous
selenium as selenite at 0.8 mg/kg/day and as seleno- wheat (Musnell et al., 1936) and mice exposed to 3 ppm
methionine at 0.28 mg/kg/day resulted in alkali disease selenate in their drinking water (Schroeder and
(O’Toole and Raisbeck, 1995). However, other studies Mitchener, 1972b) had abnormally low rates of concep-
did not produce alkali disease with selenium doses as tion. Both deficiencies and excesses of selenium have
high as 11.9 mg/kg of diet in feeders or 118 mg/kg body been shown to adversely affect spermatogenesis, motility