Alveolar macrophages are the main target cells in feline calicivirus-associated pneumonia.

Feline calicivirus (FCV) is a pathogen of felids and one of the most common causative agents of feline upper respiratory disease (URD). Reports of natural FCV pneumonia in the course of respiratory tract infections are sparse. Therefore, knowledge on the pathogenesis of FCV-induced lung lesions comes only from experimental studies. The aim of the present study was to assess the type and extent of pulmonary involvement in natural respiratory FCV infections of domestic cats and to identify the viral target cells in the lung. For this purpose, histology, immunohistochemistry and RNA-in situ hybridisation for FCV and relevant cell markers were performed on diagnostic post-mortem specimens collected after fatal URD, virulent systemic FCV or other conditions. All groups of cats exhibited similar acute pathological changes, dominated by multifocal desquamation of activated alveolar macrophages (AM) and occasional type II pneumocytes with fibrin exudation, consistent with diffuse alveolar damage (DAD). In fatal cases, this was generally seen without evidence of epithelial regeneration. In cats without clinical respiratory signs, type II pneumocyte hyperplasia was present alongside the other changes, consistent with the post-damage proliferative phase of DAD. FCV infected and replicated in AM and, to a lesser extent, type II pneumocytes. This study shows that lung involvement is an infrequent but important feature of FCV-induced URD. AM are the main viral target cell and pulmonary replication site, and their infection is associated with desquamation and activation, as well as death via apoptosis.

Paraneoplastic syndrome in haemophagocytic histiocytic sarcoma in a dog.

A case of metastatic splenic haemophagocytic histiocytic sarcoma (HHS) in a 6-year-old neutered male flat-coated retriever is described. The main clinical findings were hypoalbuminaemia and regenerative anaemia. The diagnosis was based on histological features and expression of CD11d by the neoplastic cells. Tumour cells were shown to produce interleukin (IL)-6, to phagocytose erythrocytes and to take up albumin, as demonstrated by immunohistochemistry and ultrastructural examination. Quantitative polymerase chain reaction identified increased IL-6 gene expression in affected organs. These findings suggest that neoplastic cells are responsible for the clinical features of HHS, by removing erythrocytes and albumin from the blood and releasing cytokines, such as IL-6.