Clinical signs in the Snow Geese included shaking from side to side, swimming in circles, and lethargy. Two Snow Geese and a Trumpeter Swan, submitted along with the Mallard, were diagnosed with Avian Influenza Virus (AIV). The Mallard Duck was negative for AIV.

Gross Findings: There were no significant external findings. There was a scant amount of subcutaneous, fat and a fair amount of cervical, visceral, and epicardial fat. Pectoral muscle was mildly atrophied and tacky (dehydration). Kidneys were red and orange with a prominent reticular pattern.

Histopathology: Glomerular mesangium was often effaced by amorphous, eosinophilic, acellular material (Fig. 1A). A similar material was present in the interstitium and occasionally in medullary cones (Fig. 1B). The material stained light red to orange with a Congo red stain (Figs. 1C, D) and showed apple-green birefringence under polarized light (Figs. 1E, F). There was scattered osseous metaplasia and mineralization in the renal parenchyma. Similar amorphous eosinophilic material was observed in the wall of splenic arterioles, surrounding follicles in the thyroid glands, and within the adrenal gland.

Sources/Usage: Public Domain. View Media Details

Etiologic diagnosis: Renal, splenic, thyroidal, and adrenal amyloidosis

Nomenclature: Amyloid and amyloidosis are classified according to the amyloid fibril protein “A” followed by the fibril protein precursor. In animals, at least eight amyloid precursors are known. For example, AL-amyloid represents amyloid derived from immunoglobulin light chain and AA-amyloid refers to amyloid derived from serum A-amyloid protein (SAA).

Etiology: More than 25 types of proteins are known to aggregate, insolubilize, and deposit in tissue as ß-pleated sheets of amyloid fibril protein. Systemic amyloidosis can be due to AL-amyloidosis, AA-amyloidosis, or familial amyloidosis. The most common form of amyloid in birds is AA-amyloid. It is a common cause of amyloidosis in waterfowl and an important cause of death in Anseriformes. AA-amyloidosis may be secondary and associated with chronic inflammation (e.g. mycobacteriosis or pododermatitis) or neoplasia, or it may be idiopathic. AA-amyloidosis in birds can be familial with a copy of the SAA gene in the duck genome that can be expressed in the absence of inflammation. Experimental intravenous or oral administration of amyloid has shown transmissibility in avian species.

Disease: Amyloidosis is a group of protein misfolding diseases characterized by the deposition of amyloid in one or more tissues.

Distribution: Worldwide.

Host range: Humans, domestic animals, and wildlife. For avian species, the highest incidence is seen in Anseriformes (especially Anatidae), Gruiformes, and Phoenicopteriformes, but amyloidosis occurs in most avian orders.

Pathogenesis: The mechanisms that allow the proteins to form amyloid fibrils are not well understood. Amyloidosis occurs when proteins misfold and deposit as fibrils in tissues.

Clinical signs: Clinical signs vary according to which organs are affected and to what extent, so are generally non-specific. For instance, local amyloid deposition may not cause clinical signs, while renal or hepatic deposition may result in renal or hepatic failure.

Pathology: Grossly, organs may be enlarged and firm with pallor or discoloration. Hepatic or splenic fracture with coelomic hemorrhage can occur. Microscopically, amyloid is palely eosinophilic, homogenous, acellular and is deposited extracellularly. It stains orange to red with Congo red and exhibits apple green birefringence under polarized light. A study in waterfowl reported liver, spleen, adrenal gland, kidney, and thyroid gland as the most common sites of amyloid deposition.

Diagnosis: Amyloid is identified by microscopy with Congo red staining and apple green birefringence under polarized light. Thioflavin T stain attaches to amyloid fibrils and is visible with fluorescent microscopy. Identifying the type of amyloid requires immunohistochemistry, TEM, and genetic studies.

Wildlife population impacts: Amyloidosis is not considered to have a significant impact on wildlife population health.

Management: Management of this disease in wildlife is not practical.

References:

• Fenton H, McManamon R and Howerth EW. 2018. Anseriformes, Ciconiiformes, Charadriiformes, and Gruiformes. In: Pathology of Wildlife and Zoo Animals. Terio KA, McAloose D, and St. Leger J., editors. Elsevier, California, pp. 697–721. https://doi.org/10.1016/B978-0-12-805306-5.00029-8.
• Landman WJM, Gruys E, Gielkens ALJ. 1998. Avian amyloidosis. Avian Pathol: 27: 437–449. https://doi.org/10.1080/03079459808419367.
• Tanaka S, Dan C, Kawano H, Omoto M, Ishihara T. 2008. Pathological study on amyloidosis in Cygnus olor (mute swan) and other waterfowl. Med Mol Morphol 41: 99–108. https://doi.org/10.1007/s00795-008-0401-3.
• Woldemeskel M. 2012. A concise review of amyloidosis in animals. Vet Med Int: Article ID 427296: 1–11. https://doi.org/10.1155/2012/427296.