Robert E. Schmidt, DVM, PhD, DACVP∗rschmidt@zooexotic.com and Drury R. Reavill, DVM, DABVP (Avian Practice), DACVP,     Zoo/Exotic Pathology Service, 7647 Wachtel Way, Citrus Heights, CA 95610, USA

∗Corresponding author.

Although not well described, occasional reports of avian exocrine and endocrine pancreatic disease are available. This article describes the lesions associated with common diseases of the avian pancreas reported in the literature and/or seen by the authors.

Keywords

Avian pancreas

Exocrine

Endocrine

Pathology

Infectious disease

Noninfectious disease

Proliferative disease

Key points

Diseases of the pancreas can affect the exocrine pancreas, the endocrine pancreas, or both. Diseases and lesions of these tissues are infrequently described in birds. This article describes the diseases/lesions of both the exocrine and endocrine pancreas in the general categories of noninfectious, infectious, and neoplastic/proliferative conditions.

Exocrine pancreas noninfectious disease

Prolonged caloric deficiency in birds will lead to pancreatic atrophy.1 Grossly, the change may not be significant; but histologically, there is acinar epithelial atrophy associated with normal islets of Langerhans. Atrophy can also be the end result of a variety of problems, including the following:

The degree of pancreatic atrophy can vary but is characterized grossly by a small and possibly irregular pancreas and histologically by a variable loss of zymogen granules, with shrinkage of acinar cells. The cells usually have clear cytoplasm. Acini are irregular, and acinar lumens may be difficult to see (Fig. 1). Atrophy has been described in several species.3,4

The pancreas is the target organ in cases of zinc toxicity.5 Gross lesions may not be noticeable. However, slight parenchymal mottling is occasionally seen; in chronic disease, the pancreas is atrophied. Acutely, the primary microscopic lesion is vacuolation and degranulation of acinar cells (Fig. 2). Necrosis of individual cells may also be present. Minimal mononuclear inflammatory infiltrates may be seen. In chronic disease, the appearance is similar to that described earlier, with the potential addition of interstitial fibrosis.

Rarely other toxicities have involved the pancreas. Levamisole toxicity in kiwis (Apteryx mantelli) resulted in acute pancreatic degeneration and necrosis, among other lesions in the lungs and liver. It was thought that kiwis are sensitive to the drug.6

Acute pancreatic necrosis is seen in psittacine birds, particularly Quaker parakeets.7 Many of these birds die suddenly. Gross lesions include a firm pale pancreas, variable hemorrhage, and adjacent fat necrosis characterized by firm yellow-white foci (Fig. 3). In one cockatoo, a marked serous and serosanguineous effusion was reported. Histologic changes are caused by acute coagulation necrosis of pancreatic acini, hemorrhage within the pancreatic lobules, and multifocal necrosis of mesenteric adipose tissue (Fig. 4). One of the causes of the lesions may be a high-fat diet, but the exact cause has not been determined.

Fat accumulation in the pancreatic acinar cells sometimes accompanies severe fatty liver disease, as is sometimes seen in Amazon parrots. This change is usually not grossly visible.

Pancreatic fibrosis of undetermined cause is also seen infrequently. Grossly, the pancreas is firm and irregular; microscopically, interstitial fibrosis replaces normal acini (Fig. 5).8

Infectious disease

Viral and bacterial agents reported to cause pancreatitis include the following:

Paramyxovirus can cause chronic pancreatitis, particularly in Neophema sp and small passerine birds. Affected pancreases are firm and irregular. A variable lymphoplasmacytic and histiocytic inflammatory response and lymphoid follicle formation characterize the lesion (Fig. 6). Fibrosis is seen in some cases.

Herpesvirus,15 polyomavirus, poxvirus, and adenovirus usually induce pancreatic necrosis and variable inflammation as part of a systemic disease process. Etiologic specificity is determined by finding characteristic intranuclear inclusion bodies (Figs. 7 and 8).

Influenza A virus causes pancreatic lesions in both experimental and natural disease.16–18 Grossly, the pancreas is hemorrhagic and necrotic; acute necrosis is seen histologically.16

Several bacterial agents have been associated with pancreatitis.15

Gross lesions vary from none to hemorrhage and necrosis, and there may be a purulent exudate in cases of bacterial pancreatitis. Bacterial infection is histologically characterized by necrosis, fibrin deposition, and a primarily heterophilic response, whereas infection with Chlamydophila psittaci results in a nonsuppurative pancreatitis. The pancreas can also be involved in cases of systemic mycobacteriosis, although infrequently.19

Parasitic pancreatitis can follow the plugging of pancreatic ducts by nematodes or trematodes.2,20 Grossly, pancreatic ducts are thickened and prominent; the pancreas has a roughened appearance (Fig. 9). Trematodiasis may result in be brown-black pigmentation. Histologically, the pancreatic ducts are dilated and contain the parasites in the duct. Inflammatory changes are minimal to mild. Pancreatic trematodiasis is seen almost exclusively in Amboina king parrots.

Cryptosporidiosis of the pancreatic ducts has been reported in ostriches.21 Grossly, the birds were emaciated and had atrophic-appearing pancreases. Microscopically, the organisms were present associated with ductal epithelium.

There was some necrosis and lymphoplasmacytic inflammation.

Proliferative and neoplastic disease

Bile and pancreatic duct hyperplasia and papilloma formation is seen in some birds with internal papillomatosis (PsHV 3).22 They may accompany bile and pancreatic duct changes or occur independently of them.

Pancreatic ductular neoplasia may also be associated with PsHV 3.23,24 Morphologically, low-grade papillary adenocarcinoma is occasionally seen. These tumors are composed of moderately undifferentiated cells within acinarlike...