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In veterinary medicine, lead is one of the most common causes of metallic poisoning in dogs and cattle.
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Poisoning in other species is limited because of reduced accessibility to lead, more selective eating habits or lowered susceptibility.
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Intake of lead causes acute and chronic toxicosis.
Sources of poisoning
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Lead poisoning can result when curious animals ingest lead-based paints.
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Lead in paints is available as lead tetraoxide, carbonate or sulphate.
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In cattle, many cases of lead poisoning are associated with seedling and harvesting activities.
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When used engine oil and battery disposal is handled improperly, it becomes a major source of lead poisoning.
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Vegetation grown in lead smelter areas where plants accumulate lead and contamination of vegetation on highways by exhaust fumes (petrol contains tetraethyl lead as contaminant) are other important sources of lead poisoning.
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Animals particularly sheep reported to acquire a taste for lead and insecticides (lead arsenate) may also result in lead poisoning in animals.
Clinical signs
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The prominent clinical signs are associated with the gastrointestinal and nervous systems.
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In cattle, signs appear within 24 hrs. of exposure and include ataxia, blindness, salivation, spastic twitching of eyelids, jaw champing, bruxism, muscle tremors and convulsions.
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Subacute lead poisoning, usually seen in sheep and older cattle is characterized by anorexia, rumen stasis, colic, dullness and transient constipation, frequently followed by diarrhoea, blindness, head pressing, bruxism, hyperesthesia and in coordination.
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Chronic lead poisoning which is occasionally seen in cattle, may produce syndrome that has many features in common with acute or subacute poisoning.
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In horses, lead poisoning usually produce a chronic syndrome characterized by weight loss, depression, weakness, colic, diarrhoea, laryngeal or pharyngeal paralysis (roaring) and dysphagia frequently resulting in aspiration pneumonia.
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In avian species, the prominent sings of lead toxicosis include anorexia, ataxia, loss of condition, wing and leg weakness, anaemia, gastrointestinal abnormalities including anorexia, colic, emesis and diarrhoea or constipation may be seen in dogs.
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Anxiety, hysterical barking, jaw champing, salivation, blindness, ataxia, muscle spasms, opisthotonus and convulsions may also be seen in intoxicated animals.
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Some dogs may shown CNS depression rather than excitation.
Post-mortem lesions
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Animals dying from acute lead poisoning may show few observable gross lesions.
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Oil or flakes of paint or battery may be seen in the GI tract.
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The irritant action of lead salts causes gastroenteritis.
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In the nervous system, congestion of cerebral cortex and flattening of cortical gyri are present.
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Histologically, endothelial swelling, laminar cortical necrosis and oedema of white matter may be evident.
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Tubular necrosis and degeneration of intranuclear acid fast inclusion bodies may be seen in the kidneys.
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Osteoporosis has been described in the affected lambs.
Diagnosis
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History
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Clinical signs
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Estimation of lead may be useful to evaluate excessive accumulation and to reflect the level or duration of exposure, severity and prognosis of toxicosis.
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Concentrations of lead in blood at 0.35 ppm against normal level of 0.05-0.25ppm (lead being ubiquitous in nature), liver or kidney cortex at 10 ppm are of diagnostic value in lead poisoning in most species.
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Haematologic abnormalities which are indicative of lead poisoning include anaemia, basophilic stippling of RBCs, anisocytosis, poikilocytosis, polychromasia and hypochromasia.
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Blood or urinary amino levulinic acid and protoporphyrin levels are sensitive indicators of lead exposure. In poisoned animals, ALA levels above 500mg / 100ml may be observed against the background (normal) level of 140mg / 100ml.
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