PEDIATRICS Vol. 105 No. 5 May 2000, p. e71
From the Division of Allergy and Immunology, Department of Pediatrics, University of South Florida, St Petersburg, Florida.
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ABSTRACT |
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Opinions expressed in commentaries are those of the authors and not necessarily those of the American Academy of Pediatrics or its Committees. Commentaries are not peer-reviewed.
Key words: hypersensitivity pneumonitis.
In this month's Pediatrics electronic pages,
Sarvaas et al1 report on a family with extrinsic
allergic alveolitis, also known as hypersensitivity pneumonitis (HP),
to pigeon serum proteins. HP is an interstitial lung disease caused by
an abnormal immunologic response to any of a wide variety of antigens
of chemical or biologic nature, most commonly inhaled antigens of
fungi, bacteria, and animal proteins of avian, bovine, porcine, or
murine origin.2,3 The symptoms are usually intense and
include nonproductive cough, dyspnea, chills, fever, myalgia, and
malaise. End-expiratory rales over the lower lung fields are commonly
noted. Chest radiograph usually shows parenchymal nodular densities,
reticulation, and coarse bronchovascular markings. Exacerbations are
often associated with prostration and marked leukocytosis and thus
mimic acute pulmonary infection. The immunologic reaction affects
primarily the interstitium and alveoli and comprises both the
cell-mediated (T cells) and humoral immunity (specific immunoglobulin G
[IgG] antibodies in immune complexes). The diagnosis is
supported by the demonstration of high titers of serum-precipitating
antibodies specific to the causative antigen. Systemic corticosteroid
therapy brings rapid symptomatic relief. Early detection and total
avoidance of the offending agent are associated with complete recovery. Chronic low-grade exposure might be associated with minimal symptoms but can slowly lead to pulmonary fibrosis and irreversible loss in lung
function.
Most cases of HP are related to heavy occupational exposure. HP caused
by inhaled avian serum proteins in bird droppings is commonly called
bird-breeder's lung or bird-fancier's disease. Of special interest in
the report by Sarvaas et al1 is that the antigen source
was wild city pigeons nesting outside the family's house. The initial
unawareness of such information resulted in the misdiagnosis and rapid
death of the first affected family member The report by Sarvaas et al1 highlights the difficulty in
suspecting HP outside the occupational setting and the potential
gravity of missing the diagnosis. In my experience, for example, it was
easy to clinically suspect and serologically confirm HP in a patient
who had multiple hospitalizations for acute pulmonary illness and his
environmental history revealed the presence of 58 birds of various
species in his house. Only after repeated counseling did his wife
(reluctantly) give away 52 birds and keep 6! On the other hand, HP was
not suspected in a colleague of mine, an allergist, who for several
months had a distressing cough, the cause of which was not clear, and
the chest radiograph showed minimal findings. He did not respond to multiple courses of various antibiotics. His symptoms tended to occur
more at work, were worse on Mondays, and markedly improved after he
went on vacation for 2 weeks. He seriously considered moving to another
job. His symptoms were especially exacerbated whenever he entered a
particular room in the clinic that has a full-blowing air conditioner
vent. Inspection of the air conditioning unit, which was on the roof
just above our clinic area, revealed the presence of several pigeon
nests at the intake vent. It was only after the custodian had
exterminated those nests and cleaned the vents that my colleague's
symptoms rapidly improved. Testing his serum for precipitating
antibodies to avian serum proteins showed high titer to pigeon serum
albumin. It is quite possible that the abundance of wild pigeons in
certain cities might be causing HP more than is being realized. Another
unusual case of HP, that was difficult to recognize, was that caused by
inhaled soybean antigens in a scientist who was working on developing a
veterinarian diet using soybean flour as one of the
ingredients.4
The corollary is that it would be prudent to consider HP in patients
who have pulmonary disease of unknown cause. Young age or the lack of
history of exposure to a conventional source of an organic inhalant
should not deter the physician from pursuing detailed information about
the patient's environment, which may include inspection. A high index
of suspicion might lead to the culprit. It would be prudent to
institute a trial of avoidance of the suspected factors while arranging
to perform the relevant tests. The importance of expertise in carrying
out those tests cannot be overemphasized.5
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the mother. Within a few
months of the mother's death, her 5 children developed severe
respiratory illness that required hospitalization. Antibiotics did not
ameliorate the symptoms and extensive evaluation did not reveal the
nature of their illness. Inspection of the family's house did not
reveal any source of toxic or infectious agents. It was striking,
however, to observe the abundance of pigeons nesting on the back of the
house. Only then did the children mention that they often helped their
mother manually clean the fire escape of bird droppings and feathers. Testing the children's sera showed high titers of IgG antibodies to
pigeon proteins, supporting the diagnosis of HP. Systemic
corticosteroid therapy resulted in striking recovery and the pigeon
nests were eliminated.
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FOOTNOTES |
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Received for publication Jan 12, 2000; accepted Jan 13, 2000.
Address correspondence to Sami L. Bahna, MD, DrPH, Division of Allergy and Immunology, Department of Pediatrics, University of South Florida, All Children's Hospital, 801 Sixth St South, St Petersburg, FL 33701. E-mail: bahnas{at}allkids.org
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ABBREVIATIONS |
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HP, hypersensitivity pneumonitis; IgG, immunoglobulin G.
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