A. N. Hamir

Neuropathological lesions in experimental lead toxicosis of dogs

Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.

Acid fast inclusions in tissues of dogs dosed with lead.

Liver, kidney and bone from dogs with experimental lead toxicosis were examined to study the frequency of occurrence of acid fast inclusions and the results were correlated with the lead content of these tissues. Light and electron microscopic studies revealed that bone and kidney had characteristic acid fast lead inclusions in 95 and 68 per cent of cases, respectively. Liver, although it had a high lead content, did not often show inclusions. For histopathological diagnosis of lead poisoning in dogs, we suggest that Ziehl-Nielsen stained sections of the epiphyseal area of long bone be examined for the presence of acid fast inclusions in osteoclasts.

Tissue lead distribution and pathological findings in lead exposed dogs maintained on fat and calcium modified diets

Abstract Five groups of dogs maintained on fat and calcium modified diets were given orally a lead salt mixture consisting of lead chloride, lead bromide and lead sulphate at a dose rate of 5 mg/kg/day for 24 days. All dogs were killed on day 25. Gross lesions were not seen in any but histopathological lesions consisting of acid-fast lead inclusions were seen in osteoclasts of nine dogs and in renal tubular epithelial cells of four dogs. Tissue lead concentrations (liver, kidney and bones) were greatly elevated in all groups except the group maintained on the commercial balanced diet and in that group, the lead levels were similar to those of the control dogs not receiving any lead. The results of the tissue lead concentrations in the latter two groups illustrates the suppressive effects of a balanced diet on gastrointestinal lead absorption in young dogs.