Infection with highly pathogenic avian influenza (HPAI) H5N1 in an Ontario dog
Josepha DeLay, Davor Ojkic, Yohannes Berhane, Carissa Embury-Hyatt, Cindy Boeve
Animal Health Laboratory, University of Guelph, Guelph, ON (DeLay, Ojkic); National Center for Foreign Animal Disease, Canadian Food Inspection Agency, Winnipeg, MB (Berhane, Embury-Hyatt); Ritson Veterinary Clinic, Oshawa, ON (Boeve)
AHL Newsletter 2023;27(3):26.
In March 2023, a 9-year-old castrated male golden retriever dog was lethargic and hyporexic 48 hours after scavenging on a Canada goose carcass. The dog presented to a veterinarian 72 hours after exposure, at which time it was pyrexic (T 40.2 C / 104.4 F) and was treated with antibiotics. The dog developed diarrhea and acute respiratory distress later that same day, and died before further intervention was possible.
The dog was submitted to the AHL for postmortem examination. Due to an ongoing highly pathogenic H5N1 avian influenza (HPAI) outbreak in Ontario, and a history of exposure to a wild bird carcass, the dog’s body was tested for influenza A virus prior to examination. An H5 subtype influenza A virus was detected by PCR in oropharyngeal swabs. Infection of the goose carcass with H5 influenza A virus was also confirmed. Based on the results of screening tests in both the dog and the scavenged goose, infection of the dog with HPAI was considered likely. As a result, enhanced biosecurity measures and personal protective equipment (PPE) were used for the postmortem exam of the dog.
Gross lesions in the dog targeted lung and adrenal glands. Red discoloration and rubbery consistency involved 85% of right lung and 15% of left lung. The left adrenal gland was small and difficult to locate; the right adrenal gland could not be definitively identified. Histologically, there was acute suppurative pleuritis with minimal alveolar hemorrhage, necrosuppurative tracheobronchial lymphadenitis, and severe bilateral adrenocortical atrophy. In lung, a thin segmental to continuous band of neutrophils and macrophages was present in the pleura. In some sites, few similar inflammatory cells extended into subpleural alveoli. Focal necrosis and fibrin exudation was present in one tracheobronchial lymph node. Bilaterally in adrenal glands, cortices were thin and consisted only of zona glomerulosa. Zona fasciculata and zona reticularis were replaced by a narrow band of plump macrophages.
Influenza A virus was detected in lung and brain by PCR. Similar to initial oropharyngeal swab PCR results, the PCR product was typed as H5. Further testing for HPAI was carried out by the Canadian Food Inspection Agency (CFIA) due to the reportable disease requirements for this pathogen. CFIA confirmed H5N1 avian influenza virus in lung and spleen by virus isolation.
Histologic lesions in lung and lymph node of this dog, consisting of suppurative pleuritis and fibrinonecrotizing lymphadenitis, were not typical of influenza and were more suggestive of a bacterial etiology. Bacterial culture from lung yielded moderate growths of E.coli and Klebsiella pneumoniae, and minimal growth of Staphylococcus hominus. However, immunohistochemical (IHC) procedures carried out both at the AHL and by CFIA laboratories, and using 2 different influenza A virus-specific antibodies, confirmed the presence of influenza virus antigen in association with lesions in both lung and tracheobronchial lymph node. Viral antigen was also detected in brain, although there was no microscopic evidence of inflammation or necrosis in this site. In addition, influenza virus nucleic acid was detected in lung, tracheobronchial lymph node, and tonsil by in situ hybridization (ISH).
Sporadic infection with HPAI has been reported in humans, but human-to-human transmission has not been documented. Human cases are most often considered sporadic spill-over events in workers involved in culling activities. In wild and domestic carnivores, including dogs and cats, exposure to the virus is assumed or confirmed to be associated with ingestion of infected birds. In the dog in this report, infection with HPAI was confirmed and is considered significant with regards to the cause of the dog’s death, especially in the context of clinical evidence of pyrexia. Lung lesions associated with influenza virus infection were atypical for this pathogen in mammals but were nonetheless significant. Neurotropism and significant lesions in the central nervous system (CNS) are described in many cases of HPAI infection in other species. Although CNS infection in this dog was confirmed by IHC, no associated microscopic lesions were evident.
Concurrent bilateral adrenocortical atrophy in this dog likely resulted in some degree of adrenocortical insufficiency. The relative contribution to death from both acute infection with HPAI and chronic adrenocortical atrophy / insufficiency is difficult to determine without benefit of antemortem adrenocortical function testing. The cause of adrenocortical atrophy in dogs is often undetermined (idiopathic), although an immune-mediated pathogenesis is suggested. AHL
References
1. Alkie TN, et al. Characterization of neurotropic highly pathogenic avian influenza H5N1 viruses with novel genome constellations and mammalian adaptive mutations in free-living mesocarnivores in Canada. Emerg Microbes Infect. 2023;12: 548555.
2. Songserm T, et al. Fatal avian influenza A H5N1 in a dog. Emerg Infect Dis 2006;12:1744-1745.
3. Sillman S. Highly pathogenic avian influenza in mammals: A case report of 2 domestic cats. University of Nebraska – Lincoln. 2023. https://vbms.unl.edu/VDC/documents/HPAI_Cats.pdf.