2. Introduction
Selenium (Se) is an essential trace element for animals
and humans
Its potency as a nutrient and a toxicant is such that few
people have seen the pure element.
narrow margin between too little and too much
Daily requirement of selenium in diet
• 100 μg/kg DM for the beef cattle
• 300 μg/kg DM for dairy cows
Toxic dose 8-10mg/kg
3. Selenium (Se) is a metalloid that exists as various forms
• red amorphous powder
• reddish crystal or
• brown-black solid.
Selenium has four natural oxidation states:
• Selenide (+2)
• Elemental (0)
• Selenite (+4) and
• Selenate (+6)
Organic forms
• selenomethionine
• and selenocysteine
Inorganicform
7. EPIDEMIOLOGY
Marco Polo, in 1295, described chronic selenium poisoining
in horses ingesting certain plants .
Signs were :lose mane , tail hair and slough hooves
The first account of selenium poisoning in the U.S. was given
by Dr. T.C. Madison in 1856 . (horses ,Missouri river)
Poisoning is most common in grazing animals such as cattle,
sheep, and horses, which may forage on seleniferous
grasses, forbs or shrubs.
Poultry , swine are susceptible if given seleniferous grains or
diet.
8. Sources
Obligate indicator plants require (100 – 10000 ppm) for growth and survival.
accumulate selenium as water-soluble amino acid analogs of cysteine and
methionine. Eg Astralagus (locoweed) and Oonopsis (goldenweed).
Facultative indicator plants (25 – 100 ppm) . Eg Sideranthus and Atriplex
(saltbrush).
Non-accumulator plants may accumulate selenium upto 1-25ppm.
Feed supplements, injectable drugs, industrial and commercial sources and
seafood are the other sources of selenium.
Industrial and commercial sources include photoelectric cells, glass and
ceramics
Fish and shellfish(not toxic level)
9. Selenium containing plants
Plants preferentially accumulate inorganic forms and
transform into organic forms .
Inorganic forms of selenium is highly absorbed by plants
because this form readily dissolve in water and is less bound to
soil particles.
Barley, wheat, and alfalfa accumulate more than 5ppm
selenium
12. Mechanism of Action of Selenium toxicity
Selenium replaces Sulphur in amino acids such as Cysteine
and Methionine which results in synthesis of abnormal
structural and enzymatic proteins.
Depletion of intermediate substrate such as Glutathione
and S- adenosyl methionine which disturbs their
respective enzyme activities.
Production of free radicals by reaction of selenium with
thiols causing oxidative tissue damage.
The cytotoxic activity of Selenium results from pro-
oxidant catalytic activity of Selenide anions which
produce Superoxide ions, H2O2 and other metabolic
radicals.
13. Chronic Selenosis depresses ATP formation by reduction of
sulphydryl-containing enzymes such as Succinic acid
dehydrogenase and other dehydrogenases.
Tissue Ascorbic acid decreases due to increased oxidation
by ascorbic oxidases. This contributes to vascular damage
caused by selenosis.
GI lesions occur mainly due to irritant nature of Selenium.
14. Toxicity
Maximum tolerable dose for cattle, sheep and horse
range from 1 to 5 ppm while its daily requirement is
0.1 to 0.3 ppm in diet.
It may cause acute, subacute or chronic poisoning.
Selenious acid is the most toxic form of Selenium.
Acute poisoning: 1 to 5 mg/kg orally and 0.5 mg/kg
parenterally
Subacute poisoning: 3 ppm for 3 days or more
Chronic poisoning: 5-10 ppm Se for several weeks in
cattle, swine, horse
15.
16. Clinical Signs
Acute toxicity (Blind Staggers)
Lethargy, unresponsiveness, colic, bloat, dark watery
diarrhoea, quickened and weak heartbeats, dyspnoea,
frothing from nostrils, polyuria, cyanosis, weakness,
uncertain gait, prostration, coma and death in 1-2 days in
ruminants.
Poliomyelomalacia in swine
17. Subacute toxicity
Lowered conception rate and increase in a number of
piglets born dead.
Birds show low hatchability and embryos are usually
deformed without beaks and with ropy feathers.
19. Clinical Pathology
Non significant alterations were recorded in mean values
of Hb, PCV, TLC and TEC
20. Postmortem Findings
Acute toxicoses causes congestion of organs,
gastroenteritis, renal necrosis and hemorrhages,
hydrothorax, pulmonary edema, pale cardiac muscles,
etc.
In subacute form, congestion and necrosis of liver and
renal medulla, epicardial petechiae, abomasal and
intestinal ulceration, erosion of articular surfaces
(particularly tibia) occur.
Transverse lines of abnormal growth occurs in hooves,
cardiomyopathy and chronic fibroses or cirrhosis occurs.
21. Diagnosis
History of feeding in selenium rich soil
Sign and symptoms
definitive diagnosis is based on assessments of selenium concentrations
in serum, blood, tissue, feed, forage, and supplements.
Glutathione peroxidase activity can be used to diagnose selenium
deficiency, but is less useful in the diagnosis of selenium toxicosis.
The liver and kidneys are the most common postmortem samples used
for selenium analysis.
Kidney selenium concentrations are higher than liver concentrations;
however, in cases of toxicosis, this ratio can be reversed
The liver selenium concentration increases rapidly after parenteral
selenium supplementation.
22. Treatment
Saline purgatives such as magnesium sulphate to eliminate
selenium from gut.
Acute Selenosis
Oxygen therapy and treatment of pulmonary edema.
Acetylcysteine as substitute of depleted glutathione at
the loading dose of 140mg/kg body weight by I.V route
followed by 70 mg/kg daily in 4 divided doses.
Subacute and chronic selenosis
Addition of substances in the diet that antagonise or
inhibit toxic effects of Se. Examples: linseed oil meal,
arsenic, silver, copper, and cadmium.
Treatment of soil to reduce Se uptake
25. Prevention and Control
Intensive sampling of herbage for Se analysis can be used
to identify the most dangerous parts of the farm.
Graze the less dangerous fields.
Application of sulfur-containing materials e.g. sulfate of
ammonia or gypsum, can reduce the levels of Se in
herbage.
If signs of toxicity arise on winter feed, additional safe
feed should be used to dilute the toxic feed and the oral
sulfate-dosing regime can be tried.
Se should be removed from all mineral supplements of
concentrate rations used on Se toxic farms.
If other measures can not be used, cattle should be
grazed in preference to horses in potentially toxic areas
26. References
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of the American Medical Association, 275(14), 1087.
https://doi.org/10.1001/jama.1996.03530380029025
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& Holt, T. (2011). Acute selenium toxicosis in polo ponies. Journal of Veterinary Diagnostic
Investigation, 23(3), 623–628. https://doi.org/10.1177/1040638711404142
4)D.K. Grewal, S. N. S. R. and C. S. R. (2016). Grewal, D.K., et al. "Chronic selenosis in dairy
animal--a study of clinical observations and haematological profile. 17.
5)K. J. JENKINS and M. HIDIROGLOU. (1972). A REVIEW OF SELENIUM/VITAMIN E RESPONSIVE
PROBLEMS IN LIVESTOCK: A CASE FOR SELENIUM AS A FEED ADDITIVE IN CANADA. 52.
6)Lynn F. James and James L. Shupe. (1984). Selenium poisoining in Livestock.
7)Mézes, M. and B. K. (2009). (n.d.). Prooxidant mechanisms of selenium toxicity –.
8)PAM Rogers(1), S. A. G. F. R. C. & J. M. (n.d.). Selenium toxicity in farm animals: treatment
and prevention.
9)“Preventing Selenium Poisoning in Growing and Fattening Pigs” by R. C. Wahlstrom, L. D.
Kamstra et al. (n.d.). Retrieved May 19, 2023, from
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Animal Practice, 36(3), 775–789. https://doi.org/10.1016/J.CVFA.2020.08.013 11)Selenium