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Updated: Feb 6, 2026

Trans-vivo Delayed Type Hypersensitivity Assay for Antigen Specific Regulation
Published on: May 2, 2013
[FAMILIAL OCCURRENCE OF SUMMER-TYPE HYPERSENSITIVITY PNEUMONITIS IN DEFECTIVE HOME]
Kohei Watanabe1, Ryota Ohtoshi1, Toshihiro Hayashi1
1Itabashi Chuo Medical Center.
A 53-year-old-woman presented our hospital with 1 month history of exertional dyspnea and mild fever. When examined, temperature was 37.2℃ and her respiratory rate of 22/min with an O2 saturation of 95% (02 4L/min), the rest of her vital signs were normal. The Chest X-ray was significant for ground-grass attenuation, and computed tomography showed diffuse nodular lesions bilaterally. She reported that the floorboard in the living room had been rotten last two months, and her husband was admitted to another hospital with similar symptoms the day before. We suspected that she and her husband have familial hypersensitivity pneumonitis although their children who live in the same house don't have any symptoms. After the admission, her respiratory status improved without treatment. The trans-bronchial lung biopsy specimens showed lymphocytic infiltration in alveolar area, and epithelioid cell granuloma consisted of CD68-positive macrophages. These findings corresponded to subacute hypersensitivity pneumonitis. The bronchoalveolar lavage revealed predominant lymphocytes of 92%, with a low CD4/8 ratio of 0.39. Serum anti-Trichosporon asahii antibodies were positive. With the result of positive environmental challenge test in her house, which showed elicited dyspnea and temperature increase up to 38℃ a few hours after she came back home, the patient was diagnosed as having summer-type hypersensitivity pneumonitis. Her husband was also diagnosed as the same disease, and symptoms improved with antigen avoidance and prednisolone. The patient was discharged to her relative's place for the moment of house repair. The patient's symptoms did not recur after her house was repaired.
A 53-year-old-woman presented our hospital with 1 month history of exertional dyspnea and mild fever. When examined, temperature was 37.2℃ and her respiratory rate of 22/min with an O2 saturation of 95% (02 4L/min), the rest of her vital signs were normal. The Chest X-ray was significant for ground-grass attenuation, and computed tomography showed diffuse nodular lesions bilaterally. She reported that the floorboard in the living room had been rotten last two months, and her husband was admitted to another hospital with similar symptoms the day before. We suspected that she and her husband have familial hypersensitivity pneumonitis although their children who live in the same house don't have any symptoms. After the admission, her respiratory status improved without treatment. The trans-bronchial lung biopsy specimens showed lymphocytic infiltration in alveolar area, and epithelioid cell granuloma consisted of CD68-positive macrophages. These findings corresponded to subacute hypersensitivity pneumonitis. The bronchoalveolar lavage revealed predominant lymphocytes of 92%, with a low CD4/8 ratio of 0.39. Serum anti-Trichosporon asahii antibodies were positive. With the result of positive environmental challenge test in her house, which showed elicited dyspnea and temperature increase up to 38℃ a few hours after she came back home, the patient was diagnosed as having summer-type hypersensitivity pneumonitis. Her husband was also diagnosed as the same disease, and symptoms improved with antigen avoidance and prednisolone. The patient was discharged to her relative's place for the moment of house repair. The patient's symptoms did not recur after her house was repaired.
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