BMC veterinary research · 2015
Pulmonary alveolar proteinosis in a cat.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Szatmári Viktor, Teske Erik, Nikkels Peter G J, Griese Matthias, de Jong Pim A, Grinwis Guy, Theegarten Dirk, Veraa Stefanie, van Steenbeek Frank G, Drent Marjolein, Bonella Francesco
Аннотация
BACKGROUND: Pulmonary alveolar proteinosis is an extremely rare lung disease in animals and humans. It is characterized by the deposition of a large amount of phospholipoproteinaceous material in the alveoli. There are several possible etiologies, both congenital and acquired. Alveolar macrophages play an important role in the clearance of surfactant. This is the first report of pulmonary alveolar proteinosis in the feline species.
CASE PRESENTATION: Pulmonary alveolar proteinosis was diagnosed in an 8-month-old cat with chronic tachypnea, failure to thrive and finally respiratory distress. The diagnosis was based on the milky appearance of the bronchoalveolar lavage fluid taken under general anesthesia after bronchoscopy. Because of the worsening respiratory distress and development of anorexia the kitten was euthanized. Histopathology of the lungs showed alveoli and bronchi filled with eosinophilic material. Electron microscopy revealed lamellated intra-alveolar bodies. As the granulocyte-macrophage colony-stimulating factor was elevated in the serum and no autoantibodies against granulocyte-macrophage colony-stimulating factor were detected, a primary hereditary pulmonary alveolar proteinosis was suspected. The underlying cause was thought to be a dysfunction of the receptor of the granulocyte-macrophage colony-stimulating factor, however, a mutation in the genes encoding the alpha and beta chains of this receptor has not been found.
CONCLUSION: This is the first description of pulmonary alveolar proteinosis in a cat. This kitten is thought to have a primary hereditary pulmonary alveolar proteinosis with a possible defect in the signalling pathway of the receptor of the granulocyte-macrophage colony-stimulating factor. The imaging and pathologic findings are similar to those of humans.
CASE PRESENTATION: Pulmonary alveolar proteinosis was diagnosed in an 8-month-old cat with chronic tachypnea, failure to thrive and finally respiratory distress. The diagnosis was based on the milky appearance of the bronchoalveolar lavage fluid taken under general anesthesia after bronchoscopy. Because of the worsening respiratory distress and development of anorexia the kitten was euthanized. Histopathology of the lungs showed alveoli and bronchi filled with eosinophilic material. Electron microscopy revealed lamellated intra-alveolar bodies. As the granulocyte-macrophage colony-stimulating factor was elevated in the serum and no autoantibodies against granulocyte-macrophage colony-stimulating factor were detected, a primary hereditary pulmonary alveolar proteinosis was suspected. The underlying cause was thought to be a dysfunction of the receptor of the granulocyte-macrophage colony-stimulating factor, however, a mutation in the genes encoding the alpha and beta chains of this receptor has not been found.
CONCLUSION: This is the first description of pulmonary alveolar proteinosis in a cat. This kitten is thought to have a primary hereditary pulmonary alveolar proteinosis with a possible defect in the signalling pathway of the receptor of the granulocyte-macrophage colony-stimulating factor. The imaging and pathologic findings are similar to those of humans.