The Pathologic Anatomy of Lead Poisoning in Dogs

Abstract

Absrract. Thirty-two dogs diagnosed as having lead poisoning were studied postmortem. Enlarged, pale staining nuclei of renal proximal tubular cells and hepatocytes were present in all affected dogs and frequently contained acid-fast inclusions. Bone changes consisting of persistent, thick cartilaginous trabeculae rimmed with bone caused radiopaque bands in the metaphyses of eight immature dogs. Brain lesions were characterized by vascular damage. Distended arterioles and capillaries were lined with swollen or necrotic endothelium and were often surrounded by hemorrhage and edema. These changes were associated with laminar necrosis in the cerebral cortex. Proliferation of new capillaries and gliosis occurred in dogs with chronic encephalopathies. Other changes included hyperplasia of bone marrow, metarubricytes in blood vessels, necrosis of occasional striated muscle fibers, decreased numbers of sperm and ovarian follicles, and peripheral neuropathy.Accidental lead poisoning in man has been known for at least 2,000 years. It is probable that domesticated animals suffered similarly for as many years because man shared numerous sources of lead with his animals. Knowledge of the extent and serious nature of lead poisoning in man and especially in domesticated and wild animals has only recently been acquired and is largely incomplete. With more research and diffusion of information, we should more readily recognize, and perhaps one day forestall this age-old, but preventable, disease.This report of pathologic changes in 32 dogs with lead intoxication is the sixth in a series of reports from a study of 236 dogs accidentally poisoned with lead. Other reports dealt with occurrence and source of exposure to lead [37] [5,11, 311; excessively red bone marrow [l, 131; hard, thickened, brittle bones [13]; and 'lead' lines in long bones [7]. In addition, congestion of the brain was reported by many authors.Microscopic lesions were most often reported in the kidneys, liver, and brain. Nephrosis [l, 11, 13, 21-23, 311, nephritis [15, 20, 23, 261, and eosinophilic inclusion bodies in renal and sometimes hepatic nuclei [13,15,22, 311 were common. Hepatic lesions described consisted of foci or zones of degenerative changes or necrosis [ 1 1, 15, 21, 22, 31, 331. In addition, periportal fibroplasia occurred in several dogs [l, 311. Neural lesions reported were degenerative changes of Purkinje cells [I 1, 22, 311, small hemorrhages [ll, 19, 311, edema [22], gliosis [9,18,19, 221, swelling of capillary endothelia [ 15, 191, proliferation of capillaries [6, 191, perivascular Materials and MethodsThe necropsy files (1959)(1960)(1961)(1962)(1963)(1964)(1965)(1966)(1967)(1968)(1969) of the Angel1 Memorial Animal Hospital were searched for case records of dogs in which the clinical diagnoses, hematologic data or lesions were consistent with lead intoxication. Final diagnoses of lead poisoning were established in 32 dogs by a combination of typical clinical and laboratory findings. Blood smears in all dogs examined (26) had excess ...

Pathobiological and Behavioral Effects of Lead Intoxication in the Infant Rhesus Monkey

“…In addition, the abnormal behaviors manifested during the neonatal period did not disappear as the animals grew older. Microscopic examination of the tissues of the central nervous system will establish if this retarded beEnvironmental Health Perspectives havioral development was related to lesions in the brain similar to those reported to occur in man and lower animals (8)(9)(10)(11)(12).…”

Effects of lead on collagen synthesis and renal function in the rat

“…The development of the cerebral cortex is retarded, ceteutum and cerebellum weightc arc diminished, and myelin formation is delayed (Michaelson and Sauerhoff 1974a). The brains of lead-poisoned dogs show changes similar to the above (Zook 1972). Suckling mice receiving lead through the milk develop a dose-responsive reduction in brain weight (Maker et al 1975).…”

“…These structures appear in liver parenchymal cells of children (Blackman 1936, Popoff et al 1963, dogs (Zook 1972), and rats (Moore and Goyer 1974) after their appearance in the kidney. Liver weight of rats is increased probably due to edema (Scoppa et al 1973).…”

“…Liver weight of rats is increased probably due to edema (Scoppa et al 1973). Some hemosiderosis is seen in the spleen of rabbits (Hass et al 1964) and in the liver of dogs, and many parenchy mal cells have enlarged nuclei (Zook 1972). In baboons, Kupffer cells are vacuolated, the rER is scanty and disorganized, and the mitochon dria are swollen with shrunken cristae.…”

“…Inclusions are also seen in the dog (Zook 1972). Inclusions contain about 90% of the lead in the kidney (Moore and Goyer 1974) sequestered in an insoluble, nondiffusible form until the ceil is shed into the urine (Goyer et al 1970a, 1970b, Goyer 1971.…”