Introduction

• Cause: exposure to lead in paint, vehicle batteries, contaminated soil or plants and other sources.
• Signs: blindness, behavioral change, head pressing, sudden death.
• Diagnosis: blood lead concentration.
• Treatment: supportive care, removal from source and chelation therapy, if practical.
• Prognosis: poor in animals with neurological signs.

Pathogenesis

Etiology

• Cattle can be exposed to multiple sources of lead including the following:
  • Old lead paint e.g. on buildings where the paint is deteriorating or recycled wood materials.
  • Discarded lead batteries.
  • Ash from burnt lead-containing materials.
  • Lead foreign bodies e.g. lead shot, lead solder.
  • Contaminated soils or plants in areas close to battery recycling plants or previously used for shooting (e.g. clay pigeon shooting) or mining.

Predisposing factors

General

• Previous exposure and therefore elevated lead body burden.

Specific

• Young age.

Pathophysiology

• Lead has no biological role.
• Lead has multiple biochemical effects.
• It interferes with many enzyme systems, particularly those containing sulfhydryl groups. This produces multiple effects including impaired haem synthesis and demyelination of peripheral nerves.
• Lead ions are similar in size to calcium ions and so can antagonize or mimic the biological action of calcium.
• The exact nature of the effect on the central nervous system is unknown, but probably involves interference with intracellular calcium function.
• Lead also alters vitamin D metabolism and affects cell membrane stability.

Timecourse

• Variable, clinical signs may occur a few days after exposure but can be insidious in onset.  
• Sudden death may be the first reported clinical sign.

Epidemiology

• Cases of lead poisoning are common in the spring and summer following turnout into pasture.

Diagnosis

Treatment

Prevention

Outcomes