Thennoactinomyces vulgaris, extract from wood dust, and concentrated water in the air conditioner, which was set in the mushroom cultivating room by counter immunoelectrophoresis. (Fig 1 and Table 1) In the macrophage migration inhibition test by Harringtons agarose method using lymphocytes from patients peripheral blood and guinea pigs peritoneal macrophages, macrophage migration added with mushroom spore antigen was markedly inhibited compared with those without the antigen (Fig 1b). There was no manifest inhibition when other contaminants were added. Eight to 12 hours after provocative inhalation test using 0.55 mg proteins of the mushroom spore extract on the patient, a high fever, cough, dyspnea on exertion, and fatigue developed with leukocytosis, positive reaction of CRP, and accele-relation of BSR. Hypoxemia, decrease of %Dco, and increase of the nodular shadows in both lung fields were also observed. However, inhalation using other contaminants (Thennoactinomyces vulgaris, Micropolyspora faeni, and wood dusts extract) on the patient did not provoke any symptoms and signs (Table 2). other
The patients clinical and laboratory findings and the results of provocative inhalation tests show that the disease in this case is compatible with hypersensitivity pneumonitis. There were several reports concerning hypersensitivity pneumonitis among mushroom workers. Offending allergens in these cases were mostly organic dusts containing thermophilic actinomycetes arising from the compost in which the mushrooms were grown. In this case, mushroom spores, organic dusts, wood dust, and other contaminants in the air conditioner were suspected as allergenic substances. It is suggested that the allergen in this case was not several contaminants or wood dusts but the mushroom spore itself because precipitins and MIF were detected only to mushroom spores extract but not to other contaminants. Also, inhalation with spore extract could provoke typical symptoms and signs of the hypersensitivity pneumonitis, but other substances could not. The reason why mushroom spores induced the disease seems to be due to indoor cultivation. In this method, spores will stagnate in the cultivating room and easily be inhaled by the workers. Another reason appears to be the size of the mushroom spores. They are too small to reach to alveoli of the human lung. We have reported similar cases of the disease due to the spores of another land of mushroom which was cultivated by an indoor method. Nos ter, in West Germany, also reported a similar case. Immunologic mechanism contributing to this hypersensitivity pneumonitis was postulated to be due to combined type III and type IV allergic reactions like those to farmers lung and pigeon breeders lung because precipitins and MIF for the proper allergen were detected, although the precise mechanism was to be clarified. This presentation points out that hypersensitivity pneumonitis may occur in workers who are engaged in indoor mushroom cultivation, and spores as well as molds can provoke the disease.
Table 1 — Serum Precipitim by Counterimmunoelectrophoresis
|Pholiota nameko extract||+|
|Water of air conditioner||—|
Table 2 — Provocative Inhalation Tests using Suspect Antigens
|AgInhalation||Mushroom Spore Extract||Thennoacti nomyces vulgaris||Micropolysporafaeni|
|Body temperature (C)||36.7||39.1*||36.6||36.6||36.6||36.7|
|Dyspnea, cough||–||+ *||–||–||–||–|
Figure 1a. (top) Precipitants in counterimmunoelectrophoresis. Precipitating lines were observed between the wells filled with the antigen (upper portion) and the wells filled with various dilutions of the patients serum (lower portion). Figure 1b. Macrophage migration inhibition test by Harringtons method. Migration added with the antigen (right side) was inhibited (34%) compared with that of without antigen (left side).
Tags: dyspnea cough, hypersensitivity pneumonitis, micropolyspora faeni