Selenium is an essential trace element but also toxic in high amounts. It has a narrow margin between deficiency and toxicity. Sources of selenium include certain plants, feed supplements, and industrial products. Toxicity occurs when animals consume plants containing high selenium levels, typically over 8-10 mg/kg. Symptoms of acute selenium toxicity include neurological signs and death within days. Chronic toxicity impacts reproduction and causes anemia and garlic breath odor. Diagnosis involves tissue sampling and analysis. Treatment focuses on removing the toxic source and supporting the animal. Preventive measures include analyzing forage levels and using alternative grazing areas.

1. SELENIUM TOXICITY
Presented by:
Manisha Ghimire
B.V.Sc And AH
7th semester

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

5. Available in Nepal

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

10. locoweed
saltbush
Goldenweed

11. 2

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

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.

18. Chronic toxicity (Alkali Disease)
 Pronounced anemia
 A garlic odour from breathe occur.

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

24. Contraindications
 Dimercaprol: inhibits the recovery from Se poisoning.
 Vitamin E: synergistic action with Se.

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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27. Thank You!!