LEAD Poisoning in Farm Animals

LEAD Poisoning

Lead Poisoning is also called Plumbism, it occurred due to Accidental ingestion of sources of lead metal or
compounds or ingestion of feed or grazing pasture containing excessive lead.

Lead Poisoning in farm animals

Sources of lead of Lead Poisoning:

• Discarded lead batteries
• Lead based paints
• Industrial sources of lead
• Pastures near motor vehicle
• highways/smelters
• Crank case oil/grease

Epidemiology:

• One of the most common poisoning in farm animals, especially young cattle
• Natural curiosity, licking habit, lack of oral discrimination of cattle
• Horse more selective in eating habit
• Buffalo have high tolerance than cattle
• Morbidity 10 30 case fatality 100
• 24 V battery mixed with feed of 80 heifers, 55 were died or destroyed on human grounds.
• Toxic levels of acute lead toxicity
• Varies between species & composition of compound
  • Calves 400-600 mg/Kg
  • Adult cattle 600 800 mg/kg
  • Goats 400 mg/Kg
  • Horses less than for ruminants (survived after having 1000 mg/Kg
• Biological half life of lead in blood is 9 weeks

Pathogenesis:

• Lead acetate is very soluble and more toxic than lead oxide or solid lead sheeting.
• Only small portion of lead is absorbed from the alimentary tract b/c of formation in GIT insoluble lead complexes excreted in feces.
• the remaining lead absorbed some is excreted in bile, milk and urine.
• acute poisoning Deposition occur in tissues (liver, renal cortex and Medulla)
• Chronic poisoning deposition in bones.
• Toxic effects manifested in 3 ways
  • • Lead encephalopathy
      ingestion of large doses of lead
    • Gastroenteritis (irritation)
      (ingestion of moderate doses)
    • Degeneration of peripheral nerves
      long term ingestion of small amounts
• Encephalopathy and lesions in peripheral nerve degeneration due to degeneration of NS tissue
• Lead localizes in cytoplasm of capillary endothelial cells development of edema.
• Basic lesion is likely to be vascular with basic change in transport b/t blood and brain.
• Blue “Lead line” does not occur in ruminants as in man and dogs
• Lead line is deposit of lead sulfide formed by the combination of lead with sulfide from tarter
• Lead is transferred against placental barrier
• Anemia occur in chronic lead poisoning
  • • Shortened erythrocyte lifespan
    • Impaired heme synthesis
      Lead inhibit heme synthetase enzyme combineprotoporphyrin and iron to make heme.

CLINICAL SIGNS of Lead Poisoning:

• Per acute cases death without clinical signs
  • • Acute Form
      • Sudden onset of signs & short course 12-24 hrs
      • Staggering gait
      • Muscle tremors (head and neck)
      • Champing of jaws (chewing gum fits) and frothing
      • Snapping of eyelids, rolling of eyes and bellowing
      • Blindness ,
      • Cervical, facial, auricular twitching
      • Falling tonic clonic convulsions till death
      • Hyperesthesia to touch and sound
      • Increased respiration and heart rates
      • Mania and frenzy
      • Death due to respiratory failure
    • Sub acute form
      • Animal remain alive for 3 4 days
      • Dullness
      • Complete anorexia
      • Blindness
      • Abnormalities of gait (incoordination, staggering, sometimes circling)
      • Muscle tremors and hyperesthesia
      • Grinding of teeth
      • Hypersalivation may occur
      • Mild abdominal pain
      • Alimentary tract dysfunction
      • Death occur by misadventure (waterhole, trap in fence)

DIAGNOSIS of Lead Poisoning:

• History
• Determination of lead in blood, feces, milk, urine
• Whole blood lead level in normal ruminants is 0.05-0.25 ppm
• Poisoning >0.35 ppm, death at 1.0 ppm

Differential diagnoses:

Differential diagnosis Lead Poisoning given below;

• Hypomagnesaemic tetany (staggers)
• Polioencephalomalacia
• Rabies

TREATMENT of Lead Poisoning:

• Calcium versinate (CaEDTA) 6.6% solution @ 1ml/Kg in divided doses 2-3 times daily for 3-5 days
• Thiamine HCl @ 25 mg/Kg plus CaEDTA @ 110 mg/Kg

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