vasculitis were found after exposing lambs with 8 mg Se/kg LW (Gupta et al. 1982; Tiwary et al. 2006).
4.3.3 Pigs
Miller and Williams (1940) reported that oral selenite intoxication with swine body weight of 13–23 mg Se/kg caused paresis, tremor, vomiting, anorexia, diarrhea, and depression (Figure 4.1). 10 ppm of sowing exposure results in toxicity, shown by reduced design rate, litter size, and piglet weight (Wahlstrom and Olson 1959). A study by Diehl et al. (1975) reported that 2.0 and 1.2 mg/kg body weight administration caused muscle tetany, increased plasma glutamic oxaloacetic transaminase (GOT) activity, and clinical signs of tremor, ataxia, etc. As observed in sheep and calves, acute and chronic Se toxicity has also emerged in young pigs. Acute Se toxicity in young lambs following selenosis manifested similar symptoms (Shortridge et al. 1971). Chronic Se toxicity induced sluggishness, lack of energy, emaciation, hair roughness, hair loss, sluggishness of hooves, damage to the liver, heart failure, etc. (Underwood 1979).
Figure 4.1 (a and b) Symptoms of selenosis in pigs (unthriftiness (a) and separation of the hoofs from the skin (b)).
(Source: Adapted from Wahlstrom et al. (1956)).
Toxicity varies according to the pigs’ genetic difference. Some of the studies have reported that pigs’ susceptibility to Se toxicity varied depending on pigs’ hair color (Wahlstrom and Olson 1959; Wahlstrom et al. 1984). Red‐haired pigs were more prone to Se toxicity than black‐ or white‐haired pigs (Wahlstrom et al. 1984). 4–8 mg Se/kg DM exerts Se toxicity in pigs in food grains; that also depends on the composition of food and other factors such as duration of exposure (Palmer et al. 1983; Goehring et al. 1984a; Goehring et al. 1984b). One study of a maize‐soybean diet with 8 mg Se/kg DM impaired appetite and growth within five weeks of exposure. However, for the same time duration this concentration in wheat and oats had no effect on the pigs (Goehring et al. 1984a; Goehring et al. 1984b). 12 mg Se/kg DM of feed caused hoof lesions in pigs, as in dairy cattle and horses (Goehring et al. 1984b). The concentration in pigs with 5, 10, and 25 mg Se/kg DM for 120 days resulted in hoof lesion, edema, hyperemia, extreme spinal cord lesions, paralysis of the body, emaciation, postnecrotic atrophic liver cirrhosis, and lumbal poliomyelomalacia, etc. and inflammation (Goehring et al. 1984b; O'Toole and Raisbeck 1995). Feeding meal diets of corn‐soybean along with 5 ppm of Se in swine results reduced growth and feed intake. The most influential measure of toxicity to Se is decreased growth rate. Up to 8.3 ppm Se addition in swine feed did not cause any health effects but after 12 ppm Se meal exposure caused hoof lesions (Mahan and Moxon 1980; Wahlstrom et al. 1984; Goehring et al. 1984b). The same diagnosis of hoof lesions was also published for Harrison et al. (1983) after exposure to Se. Poulsen et al. (1989) reported that after suckling the growth rate was stunted by exposure to Se, because the milk produced lower rates of Se than the feed received. They also reported that 16 mg of inorganic Se/kg feed along with diets based on barley produced no health hazards such as sow conception, number of piglets born, mortality rate, etc. But after Se supplementation, there was a tendency to lower piglet body weight as the colostrum and milk contained Se.
A higher dose of Se in feed also decreased feed intake, circular dark band on hoofs, and rate of gain following piglet weaning (Wahlstrom and Olson 1959; Goehring et al. 1984b; Mahan and Moxon 1984; Poulsen et al. 1989). Kim and Mahan (2001a) reported Se supplementation in swine muscle ad internal organs such as heart, kidney, liver etc. caused the higher Se accumulation. They also reported that inorganic Se caused serious swine problems. They came to this conclusion after feeding 0.3–10 ppm Se to the swine with organic and inorganic form Se. Results showed that exposure of 7–10 ppm Se for prolonged periods caused selenosis due to organic Se exposure after alteration of reproductive performance. On the other hand, inorganic Se during lactation period caused detrimental effects in the progeny (Kim and Mahan 2001b).
4.3.4 Poultry
Seleniferous region has impacted on the poultry industry after poor hatchability, embryo deformities, malformed toes, legs, wings, etc. (Franke 1934; Franke et al. 1936; Franke and Tully 1936; Moxon 1937). However, it has been also reported that the toxicity of Se in poultry or any other animals depends upon the other several factors which are intimately associated with the nature of diet, gender of animals, any co‐exposure of other elements to the animals, etc. (Levander 1972). Selenate injection with 0.6–0.8 ppm in the air sac of poultry eggs before incubation caused the teratogenic effects on the developing embryo, such as malformed upper beak, missing eyes and legs, and stunted growth (Franke et al. 1936). The same type of results were reported by Sukra et al. (1976) and Khan and Gilani (1980). Poley et al. (1941) indicated that 4.0 and 10 ppm Se application by dietary grains caused lower growth rates for chicks. 15 ppm dietary application culminated in decreasing hatchability to zero (Poley et al. 1937). Trelease and Beath (1949) recorded Se toxicity embryo deformities, the toxicity caused by various chemicals exposure growing turkeys administered with 20 ppm Se in regular rations. 9.0 ppm Se application on laying turkey hens caused few embryonic malformations but this increased at 15.0 ppm Se application (Carlson et al. 1951).
One study reported that insertion of Se as selenious acid with 0.4 ppm into the yolk before the incubation caused toxicity and produced malformed embryos (Ridgway and Karnofsky 1952). Layed eggs of poultry reared after dieting with 8.0 ppm Se from wheat caused induction for necrosis in growing embryo, especially in the brain, spinal cord, and upper beak, and also decreased the growth of the embryo (Gruenwald 1958). This study was also supported by the findings of Rosenfeld and Beath (2013). Latshaw (1975) studied unequal distribution of injected Se in eggs, such as higher concentration in yolk than the albumen part of the eggs. Selenite injection of 18 pg Se/egg into the yolk caused abnormal changes in hematological profile after 19 days and a propensity toward malformed embryo formation was reported (Landauer 1940; Kury et al. 1967). One study reported that 2.0 ppm dietary Se did not produced any defective effects in the laying hens in terms of growth and egg laying, but administration of 8.0 ppm caused a reduction of egg laying and stunted body growth (Thapar et al. 1969). Ort and Latshaw (1978) administered 5, 7, and 9 ppm Se in laying hens. Results reported that a 5 ppm dose caused the reduce hatchability, a 7 ppm dose caused reduced egg weights, and a 9 ppm caused zero egg production. Selenite in a Torula yeast diet to chicks increased the chicks' mortality rate (El‐Begearmi and Combs Jr 1982).
Mertz and Underwood (1986) found that application of 8 ppm Se in diet caused higher bioavailability of Se in feathers. Supplementing emus with 1.4 ppm Se caused reduced hatchability from 52% to 40% with fatal egg deformities (Kinder et al. 1995). Another study reported that 2.0 ppm Se from the administration of selenite by drinking water has no effect on chick growth patterns (Cantor et al. 1984). Drinking Se‐containing 300 μgSe/l agricultural drainage water caused embryonic death and death of adult birds (Ohlendorf 1989). Kumar et al. (2018) conducted a study on the effects of sodium selenite on adult White Leghorn broiler birds. For 42 days they administered sodium selenite with 15 and 30 ppm. Results indicated that histopathological changes occurred in the liver, kidney, lungs, heart, and intestine (Figure 4.2a–d). There were diminished amounts of hemoglobin, packed volume of cells, ALT, and AST.
In one study, the following concentrations of inorganic selenium and selenized yeast were given to chickens: 0, 2, 5, 10, 15, 20, or 30 mg Se/kg for six months. Concentration with 10, 15, 20, or 30 mg Se/kg feed induced some pathological changes, such as renal edema; higher rates of dystrophy cells were found in renal tubules (Todorović et al. 2004). Ort and Latshaw (1978) found that 5 mg Se/kg administration reduced hatchability and deformed embryos (absence of eyes, beaks, wing and feet irregularities). Another research suggested that 4 mg Se decreases the appetite of deformed eggs in
