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 May 16, 2005
Pigeon-breeder's Disease
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This is the common term for "hypersensitivity pneumonitis" (or extrinsic allergic alveolitis) denoting nonatopic, non-asthmatic, allergic pulmonary disease. Hypersensitivity pneumonitis is manifested mainly as occupational disease, in which exposure to inhaled organic agents leads to acute and eventually chronic pulmonary disease.


Attacks of chills, fever, and cough with shortness of breath can occur in persons closely associated with birds such as pigeons and parakeets. In some patients, the onset is slow rather than acute. The symptoms are due to antigenic substances in the birds' excreta. Symptoms usually subside when exposure to the birds ceases. Associated forms of the disease include bird breeder disease, bathtub refinisher's lung, mushroom picker disease, mushroom worker's lung, laboratory technician's lung, pituitary snuff-taker's lung, plastic worker's lung, epoxy resin lung, maltworker's lung, maple bark stripper's disease, bagassosis, wheat weevil disease, farmer's lung, ventilation pneumonitis, and cheese-worker's lung. Antibodies directed against the inhaled agent can be identified in serum. Acute illness is characterized by sudden onset of malaise, chills, fever, cough, shortness of breath, and nausea 4 to 8 hours after exposure to the offending agent. This may occur after the patient has left work or even at night and thus may mimic paroxysmal nocturnal dyspnea. A subacute hypersensitivity pneumonitis syndrome has been described that is characterized by the insidious onset of chronic cough and slowly progressive dyspnea, anorexia, and weight loss. Chronic respiratory insufficiency and the appearance of pulmonary fibrosis on radiographs may or may not occur after repeated exposure to the offending agent. Acute hypersensitivity pneumonitis is characterized by interstitial infiltrates of lymphocytes and plasma cells, with noncaseating granulomas in the interstitium and air spaces. Diffuse fibrosis is the hallmark of the subacute and chronic phases.


Symptoms generally include dyspnea, wheezing, and dry coughs that seem to shake the entire body. Additional symptoms may include chills, sweating, aching, and fatigue. Most cases involve typical episodes that are mild and short and may be misdiagnosed. The chronic disease that develops with prolonged exposure to the irritant may be characterized by fever, rales, cyanosis, and, possibly, expectoration of blood. Bibasilar crackles, tachypnea, tachycardia and occasionally cyanosis are present. Small nodular densities sparing the apexes (tips) and bases of the lungs are noted on chest x-ray. Pulmonary function studies reveal restrictive dysfunction and reduced diffusing capacity. Laboratory studies reveal an increase in the white blood cell count with a shift to the left, hypoxemia, and the presence of precipitating antibodies to the offending agent in serum.


Identification and, if possible, avoidance of the irritant are the initial concerns of treatment. In an occupational setting, improved ventilation and air filtering masks are recommended for mild symptoms. If permanent lung changes have not occurred, corticosteroids and avoidance measures often reduces severity and may resolve acute symptoms. Corticosteroids also may be tried in persistent cases. A change of occupation may be necessary. Treatment of hypersensitivity pneumonitis consists of identification of the offending agent, avoidance of further exposure, and, in severe cases, oral corticosteroids (prednisone, 0.5 mg/kg) daily as a single morning dose, tapered to nil over 4 to 6 weeks.


Do any tests need to be done to rule out any other disease? What treatment do you recommend? If the irritant is eliminated, will the disease subside on its own? How long will it take for the symptoms to disappear? If avoidance of the irritant is impossible, what is the best treatment? Has any permanent damage been done? Will any medication be prescribed? What are the side effects? Will this disease now make the body prone to pulmonary problems?

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