Massive pulmonary alveolar lipoproteinosis in an English Bulldog

Introduction: A 7-year-old, male English bulldog with a history of juvenile idiopathic epilepsy treated with phenobarbital and bromide developed sudden severe dyspnoea with respiratory arrest 12 h after admission. Thoracic radiographs revealed abnormal alveolar and interstitial patterns. Materials and Methods: Necropsy examination was performed and tissues were processed routinely. Sections of lung were stained by PAS, von Kossa's stain and Congo red. Selected lung samples were submitted for transmission electron microscopy (TEM). Results: There was marked hepatomegaly with a friable consistency of the liver, mitral valve endocardiosis and pulmonary oedema with disseminated 1–8 mm umbilicated lesions in the apical, accessory and right principal lung lobes. Microscopically, alveoli (60–80%) were filled with pale eosinophilic, amorphous to granular PAS-positive, von Kossa- and Congo red-negative material associated with macrophages and neutrophils. Interstitial fibrosis and mineralization were moderate. Myocardial septal and right ventricle fatty infiltration was present. TEM revealed short lamellar 3.125 nm fascicles at 6.25 nm periodic distance and compatible with accumulation of surfactant. Conclusions: Differentials diagnoses included alveolar proteinosis, lipidosis and hyalinosis. The conjunction of lesions was suggestive of alveolar lipoproteinosis/phospholipidosis. Association with mineralization and inflammation explained the dyspnoea. The alveolar storage could have derived from chronic administration of bromide