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Sixteen captive adult horned vipers (Vipera ammodytes ammodytes) were submitted for necropsy examination following a 2-week history of lethargy, anorexia and dyspnoea. Gross lesions included widespread haemorrhage, serosanguineous effusions in the body cavities and multiple pinpoint white to yellow foci in the liver. Microscopically, there was multifocal hepatic coagulative necrosis associated with intranuclear acidophilic inclusion bodies in sinusoidal endothelial cells. Similar endothelial lesions were observed in the myocardium, fat bodies, kidneys and spleen. Transmission electron microscopy revealed numerous virions (100-110 nm) in the nuclei of endothelial cells and intracytoplasmic enveloped virions (140-150 nm) were also found. The gross and histological findings and the ultrastructural features of the intranuclear inclusions and viral particles were consistent with herpesviral infection. To the best of our knowledge, these are the first reported cases of a lethal herpesvirosis in horned vipers and the second report in snakes.

EQUINE INFECTIOUS ANAEMIA VIRUS-INDUCED PULMONARY INTERSTITIAL DAMAGE: WHAT ABOUT AEROSOL TRANSMISSION? P. Bolfa*, J.L. Cadore y, J.F. Mornex z, C. Catoi*, A. Gal*, M. Taulescu* and C. Lerouxz *Pathology Department, University of Agricultural Sciences and Veterinary Medicine, Cluj-Napoca, Romania, yInternal Medicine Department, VetAgro Sup, Marcy-l’Etoile and zUMR754 INRA University Lyon 1, Retrovirus and Comparative Pathology, France Introduction: Equine infectious anaemia (EIA) is considered a blood-borne disease primarily transmitted iatrogenically or by haematophagous insects and the virus infects cells of the monocyte/ macrophage lineage. Alternative routes of transmission have not been explored, although there is evidence that EIA was spread via aerosolized particles during the 2006 EIA virus (EIAV) outbreak in Ireland. Materials and Methods: Haematoxylin and eosin-stained sections of lung from 77 EIAV seropositive Romanian horses were scored based on lymphocyte infiltration, (peri) bronchiolar inflammation and thickness of the alveolar septa. Immunolabelling for p26 EIAV capsid protein expression and smooth muscle actin was performed. Results: 52% of the EIAV-positive horses displayed a mild inflammation around the bronchi; 22%, moderate inflammation with inflammatory cells inside the wall and epithelial bronchiolar hyperplasia; and 6.5%, moderate to severe inflammation, with destruction of the bronchiolar epithelium and accumulation of smooth muscle cells within the pulmonary parenchyma. Interestingly, EIAV p26 was expressed in the cytoplasm of cells compatible by morphology and localization with alveolar and bronchiolar epithelial cells. Conclusions: The observed lesions were compatible with the interstitial diffuse pneumonia observed during other lentiviral infections. The presence of EIAV capsid in lung epithelial cells suggests that EIAV might be responsible for the bronchointerstitial damage observed. THE NOVEL HUMAN CORONAVIRUS EMC CAUSES DISEASE IN MACAQUES BUT NOT IN FERRETS J.M.A. van den Brand, L. Wiersma, S.L. Smits, L. Provacia, V.S. Raj, A.D.M.E. Osterhaus, T. Kuiken and B.L. Haagmans Viroscience Lab, Erasmus MC, Rotterdam, The Netherlands Introduction: In 2012 a novel human coronavirus (HCoV-EMC) causing lower respiratory tract infection was discovered in human patients. The clinical course of the disease was similar to that seen in severe acute respiratory syndrome (SARS). However, the virulence and pathogenesis of the virus is not yet known and no animal models for human disease have been established. Materials and Methods: Cynomolgus macaques and ferrets were inoculated with HCoV-EMC. At 1 or 4 days after inoculation the animals were killed and pathological, immunohistochemical, in-situ hybridization, virological and serological analyses were performed on samples from those animals. To determine the presence of the receptor for the HCoV-EMC dipeptidyl peptidase 4 (DDP4) in different cell types of the respiratory tissue, immunohistochemical analysis was used. Results: HCoV-EMC caused mild respiratory disease in macaques, with non-ciliated bronchiolar epithelial cells as important target cells. Ferrets were not productively infected. Conclusions: Our results confirm HCoV-EMC as the cause of respiratory disease in a non-human primate model. This suggests that the cynomolgus macaque is a suitable experimental animal species to model this disease in man.

A 2-year-old female llama ( Lama glama), from a private zoological park, with anorexia, ataxia, dyspnea, ascites, and emaciation, was necropsied. Gross inspection, and cytological, histological, and immunohistochemical analyses were performed. A firm, white, multinodular mass, 25 cm in diameter was found in the liver parenchyma. Similar nodules up to 3 cm were found in lymph nodes, lung, diaphragm, and peritoneum. Histologically, the affected organs were replaced by an infiltrative growth of undifferentiated neoplastic cells. Immunohistochemically, neoplastic cells were positive for pancytokeratin (panCK), CK20, and CK19, and negative for thyroid transcription factor 1, CK7, and carcinoembryonic antigen. A diagnosis of poorly differentiated metastatic cholangiocarcinoma was made.