STUDIES ON THE PATHOGENESIS OF PANCREATIC ALTERATIONS IN ZINC TOXICOSIS IN DUCKLINGS. (VOLUMES I AND II) (HISTOPATHOLOGY, CLINICOPATHOLOGIC, ULTRASTRUCTURAL PATHOLOGY)

EVELYN ANNE KAZACOS, Purdue University

Abstract

Pancreatic lesions due to zinc toxicosis have been reported in various animals but the descriptions of the histopathologic changes were limited to chronically-injured pancreata. The purposes of this study were to determine the minimum dietary level of zinc needed to produce pancreatic lesions, study the sequential morphological alterations of the pancreas and assess clinicopathologic parameters indicative of pancreatic damage. The toxic effects of varying levels of dietary zinc in ducklings were examined. Weakness, decreased feed intake and body weights, and pancreatic lesions were observed in ducklings fed dietary zinc at levels of (GREATERTHEQ) 2000 ppm Zn for 4 weeks. A high mortality rate was noted at dietary levels (GREATERTHEQ) 3000 ppm Zn. Grossly, the pancreas was atrophic, white, firm and nodular. The microscopic pancreatic alterations in birds fed 2000 ppm consisted of acinar degeneration, necrosis, atrophy and interstitial fibrosis. The pancreatic changes were more destructive in ducklings fed 3000-8000 ppm Zn. Chronic changes were not observed in pancreata of birds fed 9000-10,000 ppm Zn because of high mortality in these groups early in the study. The sequential clinicopathologic and morphologic alteration of the pancreas in ducklings fed 2500 ppm Zn were examined to evaluate this toxicity as a model of pancreatic injury. Mean serum amylase activities were significantly increased between days 3-10, which corresponded to the development of marked pancreatic alterations. The PCV, Hb and MCV of zinc-fed birds were low and were suggestive of iron deficiency anemia. Histologically, acinar cells had cytoplasmic vacuolation at day 3, followed by progressive acinar cell degeneration, necrosis and atrophy. Islets and ducts were unaffected and inflammatory cell infiltration was minimal. Fibrosis was first observed at day 10. By day 17, many pancreata had chronic damage with branching, duct-like structures that were embedded in abundant fibrous tissue. Ultrastructurally, acinar cells with early alterations had numerous, variable-size crinophagic and autophagic vacuoles. Alterations in the RER appeared later and included dilatation, vesiculation, degranulation and sequestration. Some damaged cells were necrotic with swollen mitochondria and pyknotic nuclei. The branching, duct-like structures in chronically-injured pancreata consisted of markedly atrophic acinar cells; these alterations are similar to those described previously in other pancreatic diseases in man and experimental animals.

Degree

Ph.D.

Subject Area

Veterinary services

COinS