Further demise of the penny
An adult pied imperial pigeon was submitted to the AHL for postmortem examination. The bird was found dead, with green mucus draining from the oral cavity. Postmortem examination revealed the bird to be in thin body condition. Internally, the most striking finding was an enlarged and dilated gizzard lined by thickened, soft and friable koilin with multiple erosions, containing bright green mucus and a single, extensively eroded 1999 Canadian penny (Fig. 1). In addition to ventriculitis, histology revealed enteritis, as well as hemosiderophages in the liver, extensive tubular degenerative changes in the kidneys, and to a lesser extent, the pancreas. Trace mineral analysis of the pancreas revealed zinc levels of 2,400 µg/g, well into the toxic range (1,000-3,500 µg/g), confirming the diagnosis of zinc toxicosis.
Although dietary zinc intake is required for various physiologic processes including the function of numerous metalloenzymes, excessive intake of the heavy metal can have detrimental effects. Zinc toxicosis is well-documented in mammalian and bird species, particularly in inquisitive psittacines chewing on the surfaces of galvanized metal cages (“new wire disease”) or ingesting cage accessories, hardware, and metallic toys. Clinical signs are often nonspecific and include depression, lethargy, anorexia, weight loss, regurgitation, anemia, PU/PD, ataxia, paresis, anemia, and sudden death. The pancreas appears to be a major target organ of Zn toxicity, although other target organs include the kidney, gastrointestinal tract, and liver.
This large pigeon was able to ingest a coin, and it certainly chose the wrong one! Prior to 1997, Canadian pennies were composed of 98% copper with traces of tin and zinc. From 1997-1999, pennies were composed of 98% zinc with a copper plating, and from 2000 onwards of 94% steel, with a copper plating. Unfortunately for this bird, the minting date sealed its fate.
Figure 1. Eroded 1999 penny in the ventriculus of a pied imperial pigeon.
A case of duck viral enteritis
In April 2017, a mature Muscovy duck hen from a hobby flock was submitted for postmortem to the AHL-Kemptville lab under the Small Flock Disease Surveillance project. The duck was from a small farm with 19 ducks of various breeds, 3 turkeys, 30 laying hens, and 5 quail. Each bird species was kept separately, both in outside pens in the day and in separate sheds at night. The hen had been eating and seemed healthy, but was found dead. The day after the hen was submitted, the 2 other Muscovy ducks died but were not submitted.
At postmortem, the hen was in good body condition, with generalized tissue congestion and petechiation of abdominal fat and epicardium. There was multifocal to confluent severe acute necrosis and ulceration of the mucosa of the esophagus. The small intestinal, large intestinal, and cecal content was dark fluid, and the intestinal lymphoid tissue (annular bands) was transmurally congested and dark red.
Histology revealed severe acute necrotizing esophagitis, enteritis characterized by villus atrophy, acute crypt necrosis and multifocal secondary bacterial infection, severe acute lymphoid necrosis of intestinal annular bands (Fig. 1)and spleen, mild multifocal hepatic and bile duct necrosis. Eosinophilic intranuclear inclusion bodies were seen in esophageal squamous and glandular epithelial cells, gut crypt epithelium, reticular cells in lymphoid tissue, bile duct epithelial cells, and hepatocytes. PCR was negative for Newcastle disease (APMV-1) and influenza A viruses.
The gross lesions and histopathology are typical of duck viral enteritis (DVE, duck plague), caused by species Duck herpesvirus 1 (DHV-1). The PCR test for DHV-1, conducted by Texas A&M Veterinary Medical Diagnostic Laboratory, was positive (esophagus, lung, spleen). Anecdotally, DVE is rarely diagnosed in Ontario in wild or captive ducks.
Domestic ducks can be infected by direct contact with wild birds or contact with the contaminated environment, commonly water. Recovered birds may carry the virus in its latent form, and viral reactivation may be the cause of outbreaks. Wild birds can be asymptomatic carriers, shedding virus intermittently for years. Some birds have a short period of nonspecific illness followed by death. Breeder ducks can have sudden high mortality. As infection moves through the flock, more signs are seen, including a severe drop in production, anorexia, thirst, depression, weakness, nasal and ocular discharges, diarrhea, and sometimes neurologic signs. Young ducklings can have severe diarrhea with some blood, and die rapidly. Morbidity and mortality can be very high, and Muscovy ducks seem to be more susceptible than other duck breeds.
Figure 1. Small intestine annular bands showing mucosal hemorrhage and lymphoid necrosis. H&E.