PEDIATRICS Vol. 39 No. 6 June 1967, pp. 904-915
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PIGEON BREEDER'S LUNG IN CHILDREN

E. Richard Stiehm M.D.1, Charles E. Reed M.D.2, and William H. Tooley M.D.3

1 The Department of Pediatrics, University of Wisconsin Medical School, Madison, Wisconsin
2 The Department of Medicine, University of Wisconsin Medical School, Madison, Wisconsin
3 The Department of Pediatrics, University of California School of Medicine, San Francisco, California

Diffuse interstitial pneumonitis associated with the prolonged exposure to pigeons is described in five boys ages 7 to 15. The clinical characteristics include a gradual onset of cough, shortness of breath, and weight loss; in three cases, acute onset of fever, chills, cough, and muscle aches occurred within 12 hours after heavy exposure. Physical findings consisted only of occasional rales and wheezes. The chest x-rays in four cases showed a diffuse interstitial pneumonitis. A lung biopsy in one case disclosed interstitial inflammation, round cell infiltration, and giant cell formation. The patients improved when the birds were removed. One severely ill boy was treated successfully with steroids.

Pulmonary function studies disclosed diminished vital capacity, absent or minimal airway obstruction, and a variable defect in diffusing capacity. Their sera contained normal or elevated complement levels, increased ggrG and ggrA globulin, and precipitating antibody to extracts of pigeon feathers, droppings, and plasma. Levels of precipitating antibody, measured by a new radial diffusion technique, tended to correlate with the severity of the disease and the degree of exposure to pigeons. Antibody levels fell progressively when pigeons were removed from the environment.

Except that the specific antigens differ, pigeons breeder's lung, Farmer's lung, bagassosis, maple bark stripper's disease and other similar syndromes are identical. They all differ sharply from allergic bronchial asthma in the symptoms and the mechanisms of the hypersensitivity. The histopathology of the biopsy, the elevated serum complement, and the absence of disease in some exposed individuals who have precipitins favor the interpretation that the pathogenesis of this illness is a delayed hypersensitivity to the inhaled antigens; but participation of an Arthus-type reaction cannot be excluded.

Submitted on October 31, 1966
Accepted on December 2, 1966




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