Lead-induced encephalopathy in dogs fed high fat, low calcium diets.

Growing, mongrel dogs were fed high fat (22%), low calcium (.1%) semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity. Seizures were observed in 44% of the lead toxic dogs and microscopic encephalopathy was observed in 89% of the lead toxic dogs. The encephalopathy was characterized by bilaterally symmetrical areas of vacuole formation involving the neuropile especially in a laminar pattern at the tips of the gyri of the cerebral cortex. The spongy state was accompanied by capillary activation and gliosis. These lesions are similar to those reported in accidental lead toxicoses in other species but previous efforts to experimentally induce these lesions in young dogs fed low-calcium, normal-fat (16%) purified diets have been unsuccessful.