activity, etc. (Rosenfeld and Beath 1964; Davis et al. 2000).
4.3 Toxicopathology of Selenium in Different Domestic Animals
It is well‐known that all animals are susceptible to selenium poisoning. Grazing activity of sheep, cattle, horses that increases the rate of selenosis might be due to the consumption of forage of seleniferous grasses or shrubs, whereas poisoning that occurs in poultry or swine and other domestic animals is as a result of being given seleniferous grain or some other seleniferous food. Subtypes of toxicity to selenium are:i
i Acute intoxication:
This results from the ingestion of a lethal amount of primary‐indicator or other plants which contains high levels of selenium (several hundred ppm Se). As plants containing high levels of selenium are unpalatable, acute selenium intoxication is uncommon. However, it is usually associated with hungry animals that might eat these seleniferous plants.ii
ii Chronic intoxication:
Chronic selenium poisoning is a consequence of the consumption of toxic levels of selenium (5–40 ppm) in plants such as grass or grain where selenium is bound in plant protein and is fairly insoluble in water. However, it has been shown that this condition can be caused by feeding the element's inorganic salts. The seleniferous feed must be eaten for weeks or months to have its effect. The key symptoms of poisoning in cattle and horses include hair loss, emaciation, hoof malformations, and lameness. Perhaps the worst economic impact arising from seleniferous forage intake is lower reproduction.
Blind stagger type chronic selenium poisoning is said to be induced by organic selenium compounds. To show evidence of poisoning the animals will need to ingest highly toxic amounts of these plants over a significant period of time. The condition of blind staggers is described in three stages. The animal has some vision loss in the first stage, and wanders in circles, disregarding objects along its way. In the second stage, the signs in stage one reach extreme severity and the forelegs of the animal are weak and give way. In the third stage, oral activity is arrested. The mechanism of the tongue and swallowing becomes paralyzed, respiration is staggered and quickened, abdominal pain is evident, and the cornea becomes cloudy. The third stage occurs unexpectedly and death frequently follows within a couple of hours, usually due to respiratory arrest.
Toxicopathology relies on the concentration of selenium in blood and organs ranging from 1 to 5 ppm across the entire livestock in the seleniferous zone (O'Toole and Raisbeck 1995). The sub‐chronic and chronic toxicity of the Se causes pathological changes in the skeletal muscle, heart, liver, spleen, and kidney, as they are mostly accumulated at a higher level in these organs (Rosenfeld and Beath 2013). There are reports of histopathological changes such as disrupted endocardium layer, diffuse lung hemorrhages, parenchymal layer degeneration with focal necrosis in hepatic tissues, and nephritis (Faye and Seboussi 2008). Table 4.2 provides the recommended normal intake of selenium in animals per day.
4.3.1 Cattle
Toxicity in any animal depends on the different parameters or factors, such as forage organisms, animal feeding, and dietary components etc. Alkali disease or chronic cow toxicity occurs when 5–40 mg Se/kg BW diets are fed for several months. There is acute toxicity when eating feed, which contains 10–20 mg Se/kg BW (National Research Council [NRC] 1983). One research found that the feed conversion efficiency in young calves was affected by 10 mg Se/kg DM. The winter season is the most vulnerable to Se toxicity in dairy cattle, though handling Se‐enriched stall feed (Jenkins and Hidiroglou 1986; Ropstad et al. 1988). Se toxicity in animals has caused many symptoms, such as hair loss, coat roughness, dullness and lack of strength, emaciation, joint bone deterioration, higher respiration levels, weakness and lameness, hooves detachments, etc. (Ghosh et al. 1993; Rosenfeld and Beath 2013).
4.3.2 Sheep
Oral selenite exposure with 50 mg Se/day in sheep caused death after exposure for 72 days. Postmortem reports determined that lesions were observed in heart and lungs (Glenn et al. 1964a, 1964b). The seleniferous range caused severe eye deformation in growing lambs (Rosenfeld and Beath 1947). The erythrocytic lysis process was also reported after selenite exposure to sheep and this might explain the hematological changes in sheep due to chronic selenosis (Young et al. 1981).
Table 4.2 RDI of selenium ingestion for different animals.
Source: Adapted from Hosnedlova et al. (2017).
| Animal species | RDI of Se | References |
|---|---|---|
| Beef cattle | 100 μg/kg of FDM | National Research Council (NRC) (2001), Suttle (2010) |
| 0.20 mg/kg | McDowell (1992) | |
| Camel | 97–112 ng/ml | Zong‐Ping et al. (1994) |
| 25–53 ng/ml | Rahim (2005) | |
| Dairy cattle | 300 μg/kg of FDM | National Research Council (NRC) (2001), Suttle (2010) |
| 0.30 mg/kg | McDowell (1992) | |
| Donkeys | 2 mg/day | Geor et al. (2013) |
| 0.1–0.15 mg/100 kg BW | National Research Council (NRC) (2007) | |
| Goat | 0.1 mg/kg of FDM | Papazafeiriou et al. (2016) |
| Horses | 0.1 ppm of FDM | National Research Council (NRC) (2007), Pagan et al. (1999) |
| 0.10 mg/kg | McDowell (1992) | |
| Pigs | 0.15–0.30 mg/kg | Surai and Fisinin (2015) |
| Swine | 0.10–0.30 mg/kg | McDowell (1992) |
| Sheep | 0.1–0.2 mg/kg of FDM | National Research Council (NRC) (1985) |
| 0.10–0.20 mg/kg | McDowell (1992) |
BW – body weight; FDM – food dry matter; RDI – recommended daily intake.
Most of the studies indicated that toxicity in sheep and lambs was caused by 0.45–8 mg Se/kg LW (Caravaggi et al. 1970; Yaeger et al. 1998; Tiwary et al. 2006). Inorganic forms of Se caused toxicity in sheep and lambs. Giese (1984) found that most of the Se excreted via urine and feces after intravenous injection of high Se dose. The half‐life of Se in sheep is 14.7 days (Blodgett and Bevill 1987). Se toxicity in sheep and lamb caused respiratory problems, hair loss, cracks on hooves and horn, ataxia, and reduced feed intake. Myocardial
