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C O N F E R E N C E 15 17 January 2018 Joint Pathology Center Veterinary Pathology Services WEDNESDAY SLIDE CONFERENCE 2017-2018 C o n f e r e n c e 15 17 January 2018 CASE I: S16-1796 (JPC 4101316). Signalment: 21-week-old, male, Eagle owl, Bubo bubo, avian. History: The animal’s general condition was reduced (sunken eyes, bristling of the feathers, anorexia) and got constantly worse over 3 days. The animal died subsequently despite treatment with glucose and activated charcoal. The animal originated from a falconry, was kept in an aviary with the possibility of free flight and was mostly fed Liver, owl. There are multiple well-demarcated areas of necrosis scattered through the liver parenchyma. (Photo on chicken and pigeons. courtesy of: Institute of Veterinary Pathology Vetsuisse- Faculty (University of Zurich), Winterthurerstrasse 268, Gross Pathology: The animal was in CH-8057 Zurich, Fax number +41 44 635 89 34, moderate body condition. The liver had a www.vetpathology.uzh.ch) light brown to beige color. On the surface, randomly distributed on all lobes, small (<1 Parasitological examination of feces: mm in diameter), sharply demarcated, Negative. whitish-yellowish foci were found. On the mucosa of the small intestine, randomly Microscopic Description: Liver: distributed, round, 2 mm in diameter, well Approximately 70% of the liver had demarcated, whitish-yellowish foci were multifocal to coalescing randomly detected. The spleen was considerably distributed foci of coagulative necrosis, swollen and showed a dark red to light violet characterized by hypereosinophilic color. Round, whitish-yellowish foci were hepatocytes with karyopyknosis and also detected on the surface of the spleen. karyorrhexis. The inflammatory response Laboratory results: surrounding foci of necrosis was minimal Bacteriological examination of liver and consisted of a few macrophages. Intra- (culture): Negative. nuclear eosinophilic inclusion bodies and 1 chromatin margination occurred in hepatocytes bordering the necrotic areas. Contributor’s Morphologic Diagnosis: Liver: Hepatitis, multifocal, acute, necrotizing, severe with intranuclear eosinophilic inclusion bodies within hepatocytes. Contributor’s Etiologic Diagnosis: Columbid herpesvirus 1 Liver, owl. Areas of largely coagulative necrosis are scattered throughout the section (delimited by arrows). The lack of inflammatory cells suggests an acute lesion. Contributor’s Comment: Gross and (HE, 168X) histologic lesions in this owl were highly suspicious of an infection with herpesvirus In owls, falcons, and eagles, the disease is and this was confirmed by the detection of known as hepatosplenitis. The disease the characteristic intranuclear inclusion usually has an acute to subacute course. bodies in hepatocytes bordering the necrotic Clinical signs are nonspecific, including foci. In addition to necrotizing hepatitis, weakness, anorexia and depression.7 necrotizing splenitis and necrotizing enteritis Characteristic gross lesions in falcons are was seen in this animal. The owl has been small white hepatic and splenic foci kept in an aviary and fed on chicken and representing necrosis and similar foci in the pigeons, the latter being the most likely bone marrow of falcons.3 Histologically, source of infection; pigeons are often areas of coagulative necrosis are detectable subclinically infected with columbid in the spleen, liver and bone marrow, Herpesvirus 1 that can cause disease in usually with only little associated owls.8 inflammation.3 Intranuclear eosinophilic inclusion bodies within hepatocytes or In 1932 in North America herpesvirus was macrophages bordering the necrotic areas first reported in owls and subsequently in can frequently be detected.3 Lesions caused prairie falcons (Falco mexicanus), American by CoHV-1 are not restricted to the liver and kestrels (Falco sparverius) and the peregrine spleen; often the small intestine and the falcon (Falco peregrinus).8 Originally kidney are also involved.6 The progression herpesvirus isolates from falcons and owls of the disease is associated with rapid virus have been considered as distinct viruses, multiplication and organ dysfunction. Most namely falconid herpesvirus 1 (FHV-1) and reported cases of disease in falcons and owls strigid herpesvirus 1 (StHV-1). However, involve prior documented or possible serologic studies showed cross-reactivity ingestion of pigeons or by direct contact among FHV-1, StHV-1 and columbid with the infected bird.4,8 herpesvirus-1 (CoHV-1) as well as that CoHV-1 and FHV-1 are indistinguishable In pigeons, Hhrpesvirus-induced disease and finally PCR studies confirmed that was first described in Rock Pigeons inclusion body hepatitis in falcons and owls (Columbia livia) and was called “inclusion is caused by columbid herpesvirus-1.3 body disease” or “inclusion body hepatitis”.3 Herpesvirus is prevalent in the pigeon population and has little to no effect on the 2 health of this species. Pigeons, especially breeding pigeons when feeding regurgitated those kept in captivity, are common crop milk during the first weeks of life of subclinical carriers of the virus. However, the squabs.5 Contact during courtship, disease occurs in squabs aged ten to sixteen preening and mutual feeding of adult pairs weeks. Clinical signs such as depression, during mating does not result in virus anorexia, conjunctivitis, oral and pharyngeal transmission. Ingested virus replicates in the ulceration, dyspnea, and diarrhea with a oropharynx region, followed by short-term duration of a few hours to as long as one viremia and virus multiplication in all week are reported, but not always present. internal organs. Squabs show severe Histological lesions include hepatic and epithelial lesions in the pharynx, esophagus splenic necrosis as reported in owls and and crop. Infection by pigeon herpesvirus falcons. In addition upper respiratory tract only rarely results in clinically overt forms inflammation with ulceration and upper of disease in adults and adult pigeons gastrointestinal tract inflammation with usually do not present any clinical signs ulceration is described. Epithelial and except depression, anorexia or parenchymal cells bordering the necrotic conjunctivitis.5 Exact data on the prevalence areas contain eosinophilic intranuclear of herpesvirus disease in pigeons is not inclusions.3,4 available. Numerous reports provide evidence for the presence of the pigeon The disease is transmitted to squads by herpesvirus in all European countries and chronically infected male and female many pigeon lofts. Pigeon herpesvirus has Liver, owl. At the edge of the areas of necrosis, degenerating hepatocytes often contain a single eosinophilic intranuclear inclusions. (HE, 400X) 3 been detected in all breeds of domestic herpesviruses are more resistant to chemical pigeons (Columba livia f. domestica), feral disinfectants.2 pigeons, and other members of the family Columbidae.5 The main differential for liver and intestinal lesions in raptors with prominent in- JPC Diagnosis: Liver: Hepatitis, tranuclear inclusion bodies would be necrotizing, random, multifocal to adenovirus. However, most of these animals coalescing, moderate with intranuclear are subclinically infected and diagnosis is eosinophilic viral inclusion bodies, Eagle often made at necropsy.2 owl (Bubo bubo), avian. Conference participants noted that there was Conference Comment: Hepatosplenitis some slide variation with mixed colonies of caused by herpesvirus in owls (OHV) and bacteria in areas of necrosis on some slides falcons (FHV) are genetically similar and (presumed postmortem overgrowth) and are both pathogenic for owls, ring-necked intranuclear inclusion bodies in bile duct doves (Streptopelia sp.) and kestrels epithelial cells. (Eurasian and American).2 In a comprehensive review of OHV, Drs. Contributing Institution: Burtscher and Sibalin reviewed the wide Institute of Veterinary Pathology spectrum of hosts affected and identified the Vetsuisse-Faculty (University of Zurich) tawny owl and barn owl as being resistant.1 Winterthurerstrasse 268, CH-8057 Zurich Herpesviral disease in birds of prey is often Fax number +41 44 635 89 34 Peracute, resulting in rapid fatalities. www.vetpathology.uzh.ch However, subclinical cases do occur and are characterized by lethargy, anorexia, References: diarrhea, and a progressive leukopenia. 1. Burtscher H, Sibalin M. Herpesvirus Gross lesions include hepatomegaly and stringis: host spectrum and distribution splenomegaly with pharyngeal and intestinal in infected owls. J Wildl Dis. lesions in owls. Microscopically, there is 1975;11(2):164-169. hepatic necrosis with prominent intranuclear 2. Cooper JE. Infectious diseases, inclusion bodies most prominent at the edge excluding macroparasites. In: Birds of of the necrotic tissue.2 Prey Health & Disease. 3rd ed. Oxford, UK: Blackwell Science Ltd.; 2002:101- The virus is often spread through infected 102. pigeons,as in this case, and is a risk to both 3. Gailbreath K, Oaks L. Herpesviral captive and free-living birds of prey around inclusion body disease in owls and the world. Diagnosis is usually based on falcons is caused by the pigeon gross lesions and identification of the herpesvirus (Columbid herpesvirus-1). J characteristic eosinophilic intranuclear in- Wildlife Dis. 2008;44:427-433. clusion bodies microscopically which are 4. Kaleta E, Docherty D. Avian pathognomonic for this disease.9 There is no herpesviruses. In: Thomas N, Hunter D, successful treatment for viral hepatitis and eds. Infectious Disease of Wild Birds. most often
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