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Arsenic constitutes one of the most important toxicological hazards to farm animals.
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However, poisoning is relatively less frequent due to decreased use of arsenicals as pesticides, ant baits and wood preservatives.
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Toxicity varies with factors such as oxidation state of arsenic, solubility, species of animal involved and duration of exposure.
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Arsenic poisoning is caused by different types of inorganic and organic arsenical compounds.
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Drinking water containing more than 0.25% arsenic is considered potentially toxic, especially to large animals.
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Herbivores are commonly poisoned because they eat contaminated forage.
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The inadvertent use of arsenicals (lead arsenate) owing to its resemblance with other preparations (lime) causes toxicity in dairy cattle.
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Deaths in sheep due to dipping in arsenical preparations has been on record.
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Lead arsenate in baits intended for insects.
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Dogs are occasionally poisoned either maliciously or after being injected intravenously for therapeutic purpose due to overdosing.
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Swine and fowl are rarely poisoned.
Clinical signs
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Poisoning due to arsenic is usually acute with major effects on gastrointestinal tract and cardiovascular system.
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Because of its direct effect on capillaries, there is transudation of plasma, loss of blood and hypovolemic shock.
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In acute cases, profuse watery diarrhoea (rice water) sometimes tinged with blood is characteristic along with sever colic, dehydration, weakness, depression, weak pulse and cardiovascular collapse.
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The onset is rapid and signs are usually seen within few hours (or upto 24 hr).
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In peracute poisoning animals may simply be found dead.
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In subacute cases, the animals may live for several days.
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Signs of poisoning include colic, anorexia, depression, staggering, weakness, diarrohea with blood and/or mucosal shreds in faeces, polyuria and then anuria, dehydration, thirst, partial paralysis of hind limbs, trembling, stupor, cold extremities, subnormal temperature and convulsions (occasionally).
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Chronic cases are rare and are characterized by wasting, poor condition, thirst, brick-red mucous membranes, normal temperature and a weak and irregular pulse.
Post-mortem lesions
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In peracute toxicosis, no significant lesions may be seen.
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Inflammation and reddening of GI mucosa (local or diffuse) may occur, followed by oedema, rupture of blood vessels and necrosis of epithelial and subepithelial tissue.
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Necrosis may progress to perforation of gastric or intestinal wall.
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GI contents are often fluid, foul smelling and blood tinged.
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They may contain shreds of epithelial tissue.
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There is diffuse inflammation of liver, kidneys and other visceral organs.
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Liver may have fatty degeneration and necrosis and kidneys have tubular damage.
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Lungs may be oedematous and congested.
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In case of cutaneous exposure the skin may exhibit necrosis and be dry or leathery.
Diagnosis
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History
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Clinical signs
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Chemical examination of arsenic in tissues (liver or kidney) or stomach contents provides confirmation. However, it is difficult to state a diagnostic level of arsenic in animal tissues. Liver and kidneys of normal animals rarely contain > 1 ppm arsenic (wet weight basis); toxicity being associated with a concentration of >3 ppm. The determination of arsenic in stomach contents is of value usually within first 24-28 hrs. after ingestion. The concentration of arsenic in urine can be high for several days (upto 14 days) after ingestion.
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History of sudden onset of severe colic, bloody/watery diarrhoea containing mucosal shreds along with post-mortem finding of gastroenteritis and degenerative changes in liver and kidney may be suspected as a case of arsenic poisoning.
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No other metal or metalloid causes such a speedy onset of gastrointestinal (GI) damage.
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