Abstract

Five bottlenose dolphins (three females and two males) were diagnosed with an acute lead intoxication. Despite clinical efforts, three females died within 10 to 30 days after diagnosis. CBC showed normal red blood cell (RBC) count in all animals. Less than 48 hours before death, Female 1 showed severe normocytic normochromic anemia, mildly regenerative, and high count of nucleated red blood cells (NRBC) (4%). All the animals had platelet and white blood cell count within normal limits. However, Female 3 showed neutrophilic leukocytosis for the last 15 days of life. Blood smears showed moderate anisocytosis and polychromasia of RBC in Female 1, and band neutrophils in Female 3. Basophilic stippling of erythrocytes was not observed in blood smears. Necropsies of the three carcasses, immediately performed, revealed: severe icteric discoloration of subcutis, blubber, and internal organs; almost complete absence of blood in the aorta and organs; collection of fluid in the lungs; cerebral edema; and signs of gastritis with different grades of ulceration, splenic hypoplasia, and adrenal cortex hyperplasia with reduction of the medulla.

Histologically, the most relevant alterations were: increased pale striations in the myocardium in the absence of Zenker’s necrosis with unaltered coronary vessels; injured areas in the hepatic and renal parenchyma with clumps of amorphous blue-staining material observed with Mallory technique in the cytoplasm of the degenerating cells, confirming the presence of lead; and lead-induced intra-nuclear inclusions bodies (IBs) present in approximately 20% of the injured hepatocytes and renal proximal convoluted lining cells. The kidneys presented a portion of collecting tubules engulfed focally, and the lumens of others were reduced in size. Necrosis was observed in a few hepatic cells and the renal tubular epithelium, but inflammatory cells or fibrosis were not identified. Congestion of the liver and a moderate degree of hemosiderosis with absence of marked liver damage were common in all dolphins examined. The lungs exhibited focal thickening of the interstitial connective tissue that occasionally became more extensive encroaching upon the alveolar walls. In the central nervous system, the most prominent degenerative changes were related to Purkinje cells, associated with small hemorrhages, edema, gliosis, swelling and proliferation of the capillary endothelium, interspersed perivascular cuffing, and cerebral neuronal degeneration. Histologic tissue changes can be of considerable diagnostic value in suspected cases, and IBs within renal and hepatic epithelia may be considered diagnostic (except in the case of suspected bismuth intoxication¹) in dolphins. The distribution of degenerative changes and vascular lesions in the gastric epithelium and in the cerebellar and cerebral cortex (neurons and glia) might also suggest ischemia as the cause of the major gastrointestinal and CNS lesions. The excess of hepatic and splenic hemosiderosis and erythrophagocytosis observed are correlated with the decreased life span of erythrocytes caused by lead. Finally, a total depletion of the red marrow with severe myelophthisis was also observed. Bone marrow partly occupied by adipose tissue, with almost complete absence of stem cells from the myeloid and erythroid lineage, indicated a total absence of regenerative phenomena in the erythropoietic marrow.

Literature cited

1.  Wachstein, M. Studies on inclusion bodies. Amer. J. clin. Path. 19: 609–614 (1946)