In 1965 Reed et al. (21) reported an acute respiratory illness with systemic manifestations in 3 patients who raised pigeons as a hobby. Since that time, we have had the opportunity to study 9 additional patients. A number of these pigeon breeders had significant pulmonary changes on chest roentgenograms. It is the purpose of this communication to report these findings. Symptomatically and immunologically, pigeon breeder's disease appears to belong to a group of pathologic entities which include farmer's lung (7), bagassosis (5), mushroom picker's disease (4), maple bark stripper's disease (8, 10), and pituitary snuff taker's disease (18), all of which seem to involve a hypersensitivity reaction to a variety of inhaled organic dusts. Affected individuals develop specific precipitating antibodies in their sera to the materials associated with the respective disease. This is in contrast to the more common human hypersensitivity associated with skin sensitizing antibody but without precipitins (1). Eosinophilia, as found in Lömer's syndrome (16), is not a prominent feature. Exposure of susceptible individuals to pigeons or pigeon materials during handling of the birds or while taking care of pigeon lofts produces fever, chills, dyspnea, cough, generalized joint pains, and malaise within four to six hours. Diffuse, fine, crepitant rales are present on auscultation of the lungs and may persist for several days. The other symptoms usually clear in twelve to twenty-four hours, provided that contact with birds is avoided. The serum of all patients in this series contained high titers of specific precipitating antibodies to pigeon serum proteins and to antigens prepared from pigeon droppings. Intradermal injection of these pigeon antigens was followed by an Arthus-type of immunologic reaction in the skin (13). Roentgenographic Findings The most consistently observed pattern of pulmonary disease was a combination of coarsening of bronchovascular markings, fine sharp nodulations, and reticulation or honeycombing throughout the lung parenchyma consistent with an interstitial process (Figs. 1 and 2). In the acute phase there were superimposed, generalized, soft, patchy, ill-defined densities with a tendency to coalescence, characteristic of secondary alveolar involvement (11) (Figs. 4 and 5). All portions of the lungs were visibly involved in 6 patients. The distribution was predominantly perihilar in the other 2 individuals. There were no specific roentgenographic features to distinguish pigeon breeder's disease from the plethora of pulmonary disease entities with either similar interstitial involvement or mixed interstitial-alveolar involvement. Eight of the 12 patients reviewed had definite changes on the chest roentgenogram; 4 had normal findings in the presence of clinical and laboratory evidence of disease.