There is well-established evidence for the role of immediate and Arthus-type reaction involving precipitating antibodies in allergic bronchopulmonary aspergillosis.
Pepys et al (1968) reported four cases with asthma and pulmonary eosinophilia who had evidence of Type I and Type III allergy to
Candida albicans. Recently we have observed a patient whose clinical and immunological features might be attributable to the same mechanism. This report is believed to be the first case with the syndrome reported in Japan.
Patient Y. N., a 32-year-old female, gave a history of asthma for 2 years. She was admitted to our hospital in June 1973 for recurrent episodes of dyspnea and productive cough. Chest X-ray was negative. Bronchogram revealed no abnormality. The leukocyte count was 10, 500 with 8% eosinophils; sedimentation rate, 52mm/hr; smear of sputum revealed eosinophilia and cultures yielded growth of
C. albicans.
She reacted on Intradermal testing to
C. albicans and three other allergens, but did not to
Aspergillus fumigatus. A “dual” response was obtained with crude extract and mannan from
C. albicans group A, with appearance of wheal and flare at 30 minutes, followed at 5 hours by a diffuse edematous swelling. intradermal testing with the crude extract also gave induration and erythema at 24-72 hours. Agar-gel diffusion gave precipitation arcs to the crude extract and mannan A. She was underwent inhalation challenge with the crude extract (0.8mg). There was a moderate decrease in FVC and FEV
1.0 with dyspnea immediately after exposure. She developed progressive dyspnea, FEV
1.0 decreased to 47% of the pre-test level at 6 hours and 64% at 24 hours. Systemic reactions such as fever, malaise headache etc. were not remarkable, but accompanied by an increase at 24 hours in the white blood and eosiniphile count. Chest X-ray showed a definite infiltration in right upper lobe 24 and 48 hours after exposure, which disappeared by a week.
The inhalation test was repeated after 3 weeks with mannan A (3mg). The patient exhibited a “dual” asthmatic response, immediate followed by late type, reaching maximum severity at 6 hours, and the dyspnea gradually subsided and diasppeared by 24 hours.
During her stay in the hospital, chest X-ray Ead demonstrated fluctuating pulmonary infiltrations in right and left upper lobe, and bilateral lower lung fields accompanied by pleural effusion occasionally. She was placed on corticosteroids, bronchodilators and amphotericin B (by aerosol) with good response and discharged in April 1974.
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