Selenium

Selenium is similar to sulphur and may replace sulphur in amino acids. Elemental selenium is insoluble in water. • Selenite is extremely toxic and selenate is soluble and toxic. In Ireland, selenium toxicity is known as dog murrain.

Sources:

• Plants have diverse tendencies to accumulate selenium. Eg : Astralagus, oonopsis,Sideranthus, Atriplex.
• Feed supplements, injectable drugs, industrial and commercial sources and seafood are the other sources of selenium.
• Cattle, sheep and horses may graze selenium-containing plants. Swine and poultry may develop toxicosis after consuming grains raised in seleniferous soil. Some of the medicated shampoos also contain selenium.
• Industrial and commercial sources include photoelectric cells, glass and ceramics.
• Fish and shellfish can accumulate selenium that exists naturally in the ocean. But the accumulation is not to a toxic level.

Toxokinetics:

Absorption: Small intestine is the primary absorption site; no absorption takes place in the stomach and rumen.

Distribution: Plasma proteins transport absorbed selenium.

Metabolism:  Selenium is metabolized both by reduction and methylation.

Excretion:  Urine is the major route of excretion in monogastric animals.  Ruminants excrete significant amounts of selenium in the faeces as well.

Mechanism of action: 3-10mg per Kg body weight is lethal for large animals.

• Glutathione depletion and lipid peroxidation are probable important factors in toxicosis.
• Selenium replaces sulphur in amino acids (cysteine and methionine), possibly affecting some essential proteins.
• Chronic selenosis depresses adenosine triphosphate formation possibly by inhibition of sulphydryl enzymes.
• Tissue ascorbic acid levels fall, possibly contributing to the vascular damage caused by selenosis.

CLINICAL SYMPTOMS

  Acute:

• Due to ingestion of obligate indicator plants clinical signs are noticed in 1 – 2 hours and animals may die between 2 hours to seven days.
• Symptoms include colic, bloat, dark watery diarrhoea, polyuria, fever, mydriasis, uncertain gait, peculiar rooted-to-one-spot stance with head and ears lowered, fast and weak pulse, pale and cyanotic mucous membrane, blood tinged froth from the nostrils, prostration and death.

  Subacute (Blind staggers) :

• Poor appetite, staring coat, wander aimlessly, circling, disregarding obstacles and stumbling over them or walking through them.
• Subnormal temperature, emaciation, swollen eyelids, near blindness. Salivation, lacrimation, severe abdominal pain, inability to swallow, complete paralysis, collapse and death have also been reported.

Chronic (Alkali disease)

• Lameness, hoof and hair abnormalities, partial blindness, paresis, in-coordination, emaciation and lethargy .
•  Hoof begins to shed. Shedding is incomplete and old hoof fuses with new hoof and form abnormally long rocker shaped hoof.
• In horses there will be loss of long hair from the mane and tail will occur.
• In cattle, there will be a rough coat, dullness and lack of vitality and emaciation with deprived appetite.

Diagnosis:

 Diagnosis is based on clinical signs and estimation of selenium in whole blood and liver.

Treatment:

• Strychnine sulphate 2-5mg/Kg Bd. Wt. Of I/M or S/C.
• Sodium arsenite / Arsenic trioxide: 0.2-0.5 mg/Kg Bd. Wt. Orally.
• High protein diet can prevent selenium poisoning.
• Use of saline purgatives.
• Acetylcysteine a substitute for glutathione may be effective.