Canine H3N8 influenza virus infection in dogs and mice.

An H3N8 influenza virus closely related to equine influenza virus was identified in racing greyhound dogs with respiratory disease in 2004 and subsequently identified in shelter and pet dogs. Pathologic findings in dogs spontaneously infected with canine influenza virus were compared with lesions induced in beagle and mongrel dogs following experimental inoculation with influenza A/canine/Florida/43/2004. BALB/c mice were inoculated with canine influenza virus to assess their suitability as an experimental model for viral pathogenesis studies. All dogs inoculated with virus developed necrotizing and hyperplastic tracheitis and bronchitis with involvement of submucosal glands as well as mild bronchiolitis and pneumonia. Viral antigen was identified in bronchial and tracheal epithelial cells of all dogs and in alveolar macrophages of several dogs. Many dogs that were spontaneously infected with virus also developed bacterial pneumonia, and greyhound dogs with fatal spontaneous infection developed severe pulmonary hemorrhage with hemothorax. Virus-inoculated BALB/c mice developed tracheitis, bronchitis, bronchiolitis, and mild pneumonia in association with viral antigen in airway epithelial cells and in type 2 alveolar epithelial cells. Virus was not detected in extrarespiratory sites in any animals. The results indicate that canine influenza virus infection consistently induces acute tracheitis and bronchitis in dogs. Mice may be a useful model for some pathogenesis studies on canine influenza virus infection.

Canine influenza virus replicates in alveolar macrophages and induces TNF-alpha.

Canine influenza virus (CIV) is a recently emergent pathogen of dogs that has caused highly contagious respiratory disease in racing Greyhounds, pet dogs, and shelter animals. Initial characterizations of CIV-induced respiratory disease suggested alveolar macrophages may be susceptible to virus infection. To investigate the role of the alveolar macrophage in the pathogenesis of CIV infection, primary alveolar macrophages were inoculated with CIV and studied from 0 to 48 hours later. Virus titers in alveolar macrophage culture supernatants increased significantly (P < .05, n = 7) from 3 to 24 hours following virus inoculation. Virus matrix gene expression was significantly increased (P < .05, n = 14) at 3, 6, and 12 hours after inoculation, peaking at 6,445-fold the level of RNA detectable immediately following inoculation. Virus-inoculated macrophages demonstrated significantly (P < .05, n = 5) decreased viability (30% trypan blue positive) by 12 hours after inoculation compared with mock-inoculated cells (5% trypan blue positive). By 12 hours after inoculation, tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) mRNA levels were significantly (P < .05, n = 11) increased over those immediately following inoculation. Only TNF-alpha protein levels were significantly increased (P < .05, n = 11) at 12 hours after inoculation. In conclusion, the results indicate that CIV replicates in canine alveolar macrophages and induces TNF-alpha expression and cell death.

Cervical hyperaesthesia in a Maltese Terrier with necrotising meningoencephalitis.

A 15-month-old female neutered Maltese Terrier was presented with a 12 hour history of low head carriage, reluctance to move and yelping when picked up. Physical examination was unremarkable apart from cervical hyperaesthesia. Twenty four hours after initial assessment there was significant clinical deterioration, with the dog exhibiting lateral cervical flexion and neurological abnormalities consistent with diffuse multifocal cerebral dysfunction. Cerebrospinal fluid analysis revealed a marked pleocytosis. Euthanasia was elected and gross necropsy findings included swelling of the right frontal cortex and a focal area of necrosis in the ventrolateral grey matter of the frontal cortex. Histological examination of the brain tissue revealed focal areas of necrosis and generalised non-suppurative inflammation consistent with a morphological diagnosis of necrotising encephalomyelitis.