Production Animal Clinical Toxicology

Chemicals | Pathogenesis | Clinical Signs | Clinical Pathology | Necropsy | Diagnosis | Treatment

Return to Production Animal Clinical Toxicology Index

Chemicals

Compounds

• lead tetroxide (red lead) - paint, plumbing
• lead carbonate (white lead) - paint, lino, asphalt
• lead oxides, sulphides - motor and vehicle emissions
• lead arsenate - garden sprays

Sources

• batteries, paint, putty, solder, sump oil and filters, mine tailings

Pathogenesis

• lead ions inhibit enzyme systems containing free sulphydryl groups
• main sites - bone marrow, brain, kidney
• bone marrow - affects pathway for haem synthesis
• d-aminolevulinic acid dehydratase and ferro chelatase are inhibited resulting in accumulation of d-aminolevulinic acid and prophyrin
• anaemia a consequence
• reduced Hb formation
• increased immature red cells, red cell fragility
• brain - lead induces increased capillary permeability
• oedema, laminar malacia and cavitation
• kidney
• lead forms insoluble complexes with protein in epithelial cells
• epithelium becomes dystrophic and intranuclear inclusions develop

Clinical Signs

cattle

• acute - more common in calves
• sudden death of some animals
• champing, staggering, rolling of eyes
• tonic-clonic convulsions
• opisthotonus, muscle tremor especially head and neck
• hyperaesthesia, excitability, aggression
• blindness
• head pressing, stiff, jerky gait
• subacute - more common in adults
• dullness, inappetence
• apparent blindness
• incoordination, circling
• muscle tremors, hyperaesthesia
• abdominal pain
• ruminal atony, constipation

sheep

• similar to subacute signs in cattle

horses

• not common
• roaring caused by paralysis of recurrent laryngeal nerve
• pharyngeal paralysis - recurrent choke
• regurgitation through nostrils
• paralysis, abdominal pain, convulsions

Clinical Pathology

• blood smears for nucleated erythrocytes and/or basophilic stippling
• d-aminolevulinic acid levels in urine
• blood lead levels
• blood zinc protoporphrin levels
• necropsy: liver, kidney lead levels

Necropsy

• acute
• cases may have no specific lesions
• subacute
• gastroenteritis
• brain oedema - cerebrocortical softening, yellow discolouration, cavitation

Diagnosis

• history
• clinical signs
• clinical pathology

Treatment

• calcium disodium EDTA
• convulsions controlled by use of CNS depressants