Pathology Case of the Month - Canada Goose and Bald Eagles

History:  

Case 1: An adult male 3320-g Canada Goose (Branta canadensis) was found dead on a golf course in Minnesota, US.  Another Canada Goose was observed listless and having trouble holding its head up.   

Case 2: An adult male 4260-g Bald Eagle (Haliaeetus leucocephalus) was found dead near a farm in North Dakota, US.  Prior to its death, the bird was unable to fly. 

Case 3: An adult male 2815-g Bald Eagle (Haliaeetus leucocephalus) was found alive on a farm in Minnesota, US.  It was standing on the side of the road and did not attempt to flee when approached.  It appeared to be choking and had greenish discharge from its nostrils and mouth.  The bird died en route to a rehabilitation facility. 

Gross Findings:  

Case 1: There was no subcutaneous, visceral and epicardial fat and pectoral muscle was atrophied, indicating emaciation.  The esophagus and proventriculus were distended and filled with duckweed (Fig. 1A).  The ventriculus contained 40 lead #9 (2.03 mm in diameter) pellets (Fig. 1B).  Intestines contained a moderate amount of thick tan to green digesta.  The gall bladder was moderately distended with dark green slightly viscous bile.   

Case 2: There was moderate subcutaneous and visceral fat, indicating good body condition.  However, serous atrophy of epicardial fat evidenced an acutely declining body condition.  A small amount of green fecal material was present in the feathers around the vent.  On the epicardium and extending into the myocardium were multiple white foci.  The esophagus contained a small amount of gray liquid.  The proventriculus was empty.  The ventriculus contained 23 #5 (3.05 mm in diameter) lead pellets (Fig. 1C)  Intestines contained a small amount of dark green creamy material.  The gall bladder was moderately distended with very viscous dark green to black bile (Fig. 1C).   

Case 3: There was minimal subcutaneous, visceral and mild epicardial fat, and pectoral muscle was severely atrophied and tacky, indicating poor body condition and dehydration.  Feathers of the right side of the head and tail tips were green.  Oral mucosa was multifocally green-tinged.  Bilaterally, conjunctivae were white.  Pale streaks were present in the myocardium (Fig. 1D) and on cut section multifocal tan foci extended into the myocardium.  The esophagus was empty.  The proventricular and ventricular mucosa was stained dark green and both the proventriculus and ventriculus were empty.  Intestines were diffusely green and contained green watery to thick material.  The gall bladder was severely distended with very viscous dark green bile.   

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Gross Diagnosis/es: 

1. Emaciation (Case 1) 
2. Serous atrophy of epicardial fat (Case 2) 
3. Poor body condition and dehydration (Case 3) 
4. Esophageal impaction (Case 1) 
5. Gall bladder distension with viscous bile (Cases 1–3) 
6. Bile staining (Cases 2,3) 
7. Ventriculus, lead pellets (Cases 1,2) 
8. Myocardial degeneration and necrosis, multifocal (Cases 2,3) 
9. Conjunctival pallor (Case 3) 

Laboratory Findings:  

Case 1: Liver lead level was 105.96 ppm, dry weight. 

Case 2: Liver lead level was 35.01 ppm, wet weight. 

Case 3: Liver lead level was 27.03 ppm, wet weight.   

 Disease: Lead poisoning (Plumbism) 

First report: The first report of lead poisoning in waterfowl in the US was in Texas in 1874. 

Distribution: Worldwide. 

Seasonality: Any time of year, but common after waterfowl hunting season where lead is not banned. 

Host range: Primarily waterfowl and raptors, but other avian species can be affected. 

Etiology: Lead ingestion.  Waterfowl ingest lead as grit or food particles while raptors consume lead-contaminated prey.  Sources include lead pellets, fishing sinkers, mine wastes, paint pigments, bullets, or other lead objects.  Lead shot in other tissues is not a source of lead poisoning (e.g. lead pellet in skeletal muscle of non-lethally shot bird). 

Pathogenesis: Ingested lead is dissolved by acid secreted by the proventriculus and mechanical grinding action in the ventriculus.  Lead is absorbed into the blood and deposited in liver and kidneys in acute poisoning and in bones in chronic poisoning.   

Lead affects a wide range of physiological and biochemical systems including the hematopoietic, vascular, nervous, renal, reproductive, skeletal, and immune systems.  Lead’s toxic mechanisms include: binding to calcium- and zinc-binding proteins, random hydrolysis of nucleic acids, and inducing RNA catalysis through activation of ribosomal 5S RNA, a natural leadzyme.  Lead poisoning interferes with several stages of heme synthesis.  It acts to inhibit delta-aminolevulinic acid dehydratase, heme synthetase, and the delivery of iron to the site of ferrochelatase action resulting in microcytic hypochromic anemia. 

Clinical signs: Reluctance to fly or weak flying, unsteady gait, bent neck during flight, change in tonal call, roof-shaped positioning of wings when standing, wing droop, fluid discharge from bill, losing fear of humans and easily captured, bile stained feces. 

Gross Lesions: Emaciation and pectoral muscle atrophy in chronic cases (although birds can be in good body condition with acute poisoning), bile staining of feathers around oral cavity or vent, facial edema, esophageal, proventricular or ventricular impaction, gall bladder distension with bright green or dark bile, bile staining of organs or gastrointestinal contents, lead pellets (non-magnetic) in proventriculus or ventriculus, pale foci on the heart, organ atrophy or pallor.  

Histologic lesions: Hepatocyte necrosis and Kupffer cell hemosiderosis, nephrosis and sloughing of renal tubular epithelium with variable acid-fast intranuclear inclusion bodies in proximal convoluted tubules, degeneration or necrosis of the heart, pectoral skeletal muscles and muscular tunics of the ventriculus, neuronal degeneration of the brain and meningeal edema, degenerative changes in peripheral nerves, hypocellular bone marrow with a marked decrease in mature erythrocytes and an increase in early and late polychromatic erythroblasts.  

Diagnosis: When other signs of lead poisoning are present: 

1. Liver lead values 2 < 6 ppm, wet weight and >3.0 and <20 ppm, dry weight are suggestive of subclinical lead poisoning 
2. Liver lead values 6–10 ppm, wet weight and >20.0 and <30. 0 ppm, dry weight are suggestive of clinical lead poisoning 
3. Liver lead values >10 ppm, wet weight and >30 ppm, dry weight are suggestive of severe clinical lead poisoning 

Public health concerns: No appreciable risk to human health. 

Management: 1) Deny birds the use of contaminated areas; 2) Carcass removal of lead contaminated animals to decrease secondary poisoning in raptors or scavengers. 

References: 

Maxie MG, Youssef S. 2007. Nervous system. In: Jubb, Kennedy & Palmer's Pathology of Domestic Animals, Vol. 1, 5th Ed., Maxie MG, editor, Saunders Ltd., New York, New York pp. 281–457. 

Pain DJ, Mateo R, Green RE. 2019. Effects of lead from ammunition on birds and other wildlife: A review and update. Ambio 48:935–953.  

Schmidt RE, Reavill DR, Phalen DN, editors. 2003. Pathology of pet and aviary birds. Blackwell Publishing Professional, Ames, Iowa, 234 pp.  

U.S. Geological Survey. 1999. Field manual of wildlife diseases: general field procedures and diseases of birds, https://pubs.usgs.gov/publication/itr19990001. Accessed April 2020.