Fatal Canid Herpesvirus 1 Respiratory Infections in 4 Clinically Healthy Adult Dogs

Abstract

Four healthy adult dogs (Golden Retrievers aged 6 years and 9 years, Dalmatian aged 13 years, and Mastiff aged 5 years) developed clinical signs of acute respiratory disease and died within 2 to 7 days of onset of clinical signs. The lungs of the 3 dogs submitted for necropsy were diffusely and severely reddened due to hyperemia and hemorrhage. Microscopic lesions in all dogs were suggestive of acute viral or toxic respiratory damage and varied from acute severe fibrinonecrotic or hemorrhagic bronchopneumonia to fibrinous or necrotizing bronchointerstitial pneumonia. Necropsied dogs also had hemorrhagic rhinitis and tracheitis with necrosis. Virus isolation, transmission electron microscopy, and polymerase chain reaction were used to confirm the presence of canid herpesvirus 1 (CaHV-1) in the lung samples of these dogs. Lung tissues were negative for influenza A virus, canine distemper virus, canine parainfluenza virus, canine respiratory coronavirus, and canine adenovirus 2. Canid herpesvirus 1 has been isolated from cases of acute infectious respiratory disease in dogs but has only rarely been associated with fatal primary viral pneumonia in adult dogs. The cases in the current report document lesions observed in association with CaHV-1 in 4 cases of fatal canine herpesvirus pneumonia in adult dogs.

Viral molecular and pathological investigations ofCanid herpesvirus1 infection associated respiratory disease and acute death in dogs

“…Recently, CaHV-1 infection in clinically healthy adult dogs has been reported to cause severe acute respiratory problems [9], and hepatic necrosis without any respiratory signs [8]. However, the prevalence was quite rare.…”

“…CaHV-1 infection in adult to senior dogs was previously reported to cause mild respiratory symptoms that were localized and self-limited [21]. However, the evidence that CaHV-1 infection can induce a fatal systemic disease in adult dogs is increasing [9,16,20]. These fi ndings can be explained by immunocompromised conditions, including infection, disease, under stress and aging, which then resulted in viral reactivation and shedding.…”

“…In addition, damage to the respiratory epithelium and exfoliation of tissue debris that corresponded to tubular necrosis of the kidneys were also described. Some of the disseminated necrosis in several organs might have resulted from severe hypoxia due to viral pneumonia [9]. Compared with herpesvirus infections in other animals, most clinical signs after infection were involving the respiratory system according to its host cellular tropism and host restrictive property [1].…”

“…However, less specifi c alterations in puppies and other systemic disease involvement in older animals leads to diagnostic ambiguities and requires a specifi c method to confi rm the CaHV-1 infection, including immunohistochemistry, immunofl uorescence, virus isolation, electron microscopy, and molecular assays [9,22,26,27]. Typically, CaHV-1 infections are diffi cult to confi rm using immunohistochemistry, which has a lower sensitivity than PCR [28], because of the instability and fragility of the virus in storage [29].…”

“…After necropsy, the distinct lesion of CaHV-1 is seen as a generalized necrotizing and hemorrhagic disease, most obvious in the vital organs, such as the lung, liver, kidneys and spleen [8,9], although a similar fi nding is also evident in other organs, including the small intestine, adrenal glands, brain, heart, pancreas, stomach and eyes [10]. Eosinophilic intranuclear inclusion bodies might be present in the epithelial cells of the trachea, bronchi, lung, liver and kidneys, suggesting that inclusion bodies might be consistent with a fulminant CaHV-1 infection based on a high infection level of viral genomic DNA [11].…”