Gross Findings: On external examination, caseous material is multifocally present adhered to the pharynx and to the buccal mucosa deep in the oral cavity (Fig 1A). On internal examination, there is abundant subcutaneous, visceral, and epicardial fat.  Many pinpoint tan foci are present in the liver (Fig 1B) and spleen, both of which are moderately enlarged. A small amount of fibrin is present on the liver capsule. The small intestinal content is cloudy, gelatinous, and contains light strands of fibrinous material; the serosal surface is diffusely red. The kidneys have an enhanced urate deposition pattern.

Histopathological Findings: There is multifocal ulceration and transmural necrosis of the pharynx and the buccal mucosa. Affected areas are covered by a thick mat of fibrin and necrotic cellular debris. Small numbers of epithelial cells in the intact pharyngeal mucosa contain eosinophilic intranuclear inclusions.  In the liver, there are numerous, randomly distributed, variably sized foci of acute hepatocellular necrosis, which are composed of a mixture of degenerate heterophils, fibrin, and necrotic cellular debris (Fig 1C). Occasional eosinophilic intranuclear inclusions are seen in intact hepatocytes adjacent to foci of necrosis (Fig 1D). Similar necrotic foci and viral inclusions are multifocally present in the spleen and in the wall of the cecae and esophagus.

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Morphologic Diagnosis: Acute, marked, multifocal necrotizing hepatitis and splenitis.

Disease: Herpesviral Inclusion Body Disease, Hepatosplenitis, Owl Herpes.

Etiology: Columbid herpesvirus-1 (CoHV-1), also known as Pigeon Herpesvirus.

Distribution: Hepatosplenitis in owls due to infection with CoHV-1 has been documented in North America, Australia, Asia, and Northern and Central Europe.

Seasonality: Transmission of CoHV-1 to owls occurs most commonly in the springtime, when the owls’ preferred food sources may be scarce and they are forced to prey on Rock Pigeons (Columba livia). Transmission of the virus amongst pigeons may occur year-round.  Viral shedding is most common in birds that are stressed and in close proximity to each other, such as on wintering or breeding grounds.

Host Range: Owl herpes has been previously described in Great-horned Owls and also in many other owl species, including Barking Owl (Ninox connivens) and Powerful Owl (Ninox strenua) in Australia, and Eurasian Eagle Owl (Bubo bubo), Ural Owl (Strix uralensis), Long-eared Owl (Asio otus), Snowy Owl (Bubo scandiacus) Little Owl (Athene noctua), and Boreal Owl (Aegolius funereus) in Europe. CoHV-1 has also been shown to cause hepatosplenitis in falcons and accipiters.

Transmission: CoHV-1 is an alphaherpesvirus that is endemic in Rock Pigeons (Columba livia). Infection in raptors is believed to occur most commonly when they feed on infected pigeons; however, virus may also spread between birds by direct or indirect contact with saliva or feces.

Clinical Signs: In owls, depression, anorexia, and leukopenia may be observed 2-5 days prior to death. In some cases, birds are found dead with no previous clinical signs. Unilateral keratitis/conjunctivitis may develop in surviving birds.

Pathology: Multifocal to coalescing areas of acute necrosis in the liver, spleen, and bone marrow are hallmarks of this disease. Grossly, these foci manifest as pinpoint to variably sized pale areas in the affected organ(s). Areas of necrosis may also be present in the pharynx and intestinal tract. On histopathology, eosinophilic intranuclear viral inclusions are seen in intact parenchymal or epithelial cells adjacent to foci of necrosis.

Diagnosis: A presumptive diagnosis of herpesviral inclusion body disease/hepatosplenitis may be made based on the presence of characteristic gross and histopathologic findings. A definitive diagnosis requires identification of CoHV-1 by PCR, sequencing, and/or virus isolation. 

Public Health Concerns: Herpesviruses of birds have not been associated with disease in humans.

Wildlife Population Impacts: Population impacts on owls have not been described.

Management: Rock pigeons should not be fed to owls, falcons or accipiters in rehabilitation or zoological facilities. Birds showing signs of illness and birds that are suspected to have been exposed to CoHV-1 should be separated from unaffected birds. Any bird that survives infection has the potential to shed virus in its feces or saliva, especially under stressful conditions. High levels of sanitation should be maintained to minimize disease transmission. Humans in contact with infected birds should not have any contact with other birds for seven days.

References:

• Gailbreath KL, Oaks JL. 2008. Herpesviral inclusion body disease in owls and falcons is caused by the pigeon herpesvirus (Columbid herpesvirus 1). J Wildl Dis. 44:427-433.
• Green RG, Shillinger JE. 1936. A virus disease of owls. Am J Pathol 12:405–410.
• Kaleta E, Docherty D. 2007. Avian herpesviruses. In: Infectious disease of wild birds. N. Thomas, D. Hunter, and C. Atkinson, eds. Blackwell Publishers, Ames, IA. pp. 63–86.
• Phalen DN, Holz P, Rasmussen L, Bayley C. 2011. Fatal columbid herpesvirus-1 infections in three species of Australian birds of prey. Aust Vet J. 89:193-6. doi: 10.1111/j.1751-0813.2011.00706.x. PMID: 21495992.
• Rose N, Warren AL, Whiteside D, Bidulka J, Robinson JH, Illanes O, Brookfield C. 2012. Columbid herpesvirus-1 mortality in great horned owls (Bubo virginianus) from Calgary, Alberta. Can Vet J. 53:265-8. PMID: 22942441; PMCID: PMC3280778
• Žlabravec Z, Krapež U, Slavec B, Vrezec A, Rojs O Z, Račnik J. 2018. Detection and Phylogenetic Analysis of Herpesviruses Detected in Wild Owls in Slovenia. Avian Dis. 62:397–403.