Hypersensitivity Pneumonitis owed t...

Hypersensitivity Pneumonitis owed to Mushroom (Pholiota nameko) Spores (*1)

Hypersensitivity pneumonitis has been described in newly come years as an occupational hazard of mushroom workers. [1-8] Thermophilic fungi were speculation to be responsible for hypersensitivity pneumonitis among mushroom workers. In this article, we demonstrate a hypersensitivity pneumonitis possibly befitting to the inhalation of the spores of the mushroom named Pholiota nameko.

MUSHROOM CULTIVATION METHODS

The edible mushroom Pholiota nameko is cultivated indoors in all seasons in Japan. Wet copse dust is used instead of fertilizing mixture In a small, windowless building which is kept at high temperature and humidity at air conditioner, many mushrooms advance on the surface of the package which consists of a mixture of the mushroom spawns and thicket dust. When they are grown the cultivating compass is filled with the spores and/or oidiospores of the mushroom. Workers who harvest the mushroom easily inhale the spores. As the size of the spores are 4 to 6 [mu] they can reach the terminal areas of the lung Workers in the building may also be expos to other contaminants so as molds. These contaminants in this growing regularity are less than those in the outdoor system because compost is not used and mold do not increase as readily.

CASE REPORT

A 52-year-old man started work in a mushroom-cultivating building which was mainly relate toed with harvesting the P nameko mushroom. Seven years later, he noticed arid cough, dyspnea on exertion, and slight febrile affection several hours after work. These symptoms became thus market that he required admission to a hospital for common month. At the close of this time, his condition had improved. However, in succession return to his former work, these symptoms appeared again. In October 1984 he visited our hospital. in succession admission, auscultation of his chest revealed slight crepitations in the lower parts. Chest roentgenogram demonstrated diffuse, fine, granular shadows upon both lower lung fields. The BSR was slightly increased, and CRP was positive. Leukocytosis was not construct Mantoux reaction was negative. Pulmonary function studies showed a slight decrease of diffusion capacity. Histologic findings of the lung on transbronchial biopsy revealed granulomatous alveolitis compatible with that of hypersensitivity pneumonitis; thickening of alveoli fit to infiltration of plasma confined apartments lymphocytes, giant cells, and infiltration of macrophage-like small cavitys into the alveolar lumen. Manifest increase of lymphocyte was observ in the BALF; total confined apartments were 2.5 X 10 [7] 82 percent of them were lymphocyte 13 percent were macrophages, and others were neutrophilis and eosinophils. Precipitins against the mushroom spore extract were descryed but not against Micropolyspora faeni, Thermoactinomyces vulgaris, extract from grove dust, and concentrated water in the air conditioner, which was station in the mushroom cultivating apartment by counter immunoelectrophoresis. (Fig 1 and Table 1) In the macrophage migration inhibition proof by Harrington's agarose method [9] using lymphocyte from patient's peripheral vital fluid and guinea pig's 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 trial using 0.55 mg proteins of the mushroom spore extract forward the patient, a high agitation cough, dyspnea on exertion, and fatigue expanded with leukocytosis, positive reaction of CRP and accelerelation of BSR Hypoxemia, decrease of %Dco and increase of the modular shadows in the couple lung fields were also observ However, inhalation using other contaminants (Thermoactinomyces vulgaris, Micropolyspora faeni, and timber dusts extract) on the patient did not incense any symptoms and signs (Table 2)

DISCUSSION

The patient's clinical and laboratory findings and the ensues of provocative inhalation tests present to view 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 for the greatest part organic dusts containing thermophilic actinomycetes arising from the manure in which the mushrooms were grown In this case, mushroom spores, organic dusts, timber dust, and other contaminants in the air conditioner were suspected as allergenic substances. It is glance ated that the allergen in this case was not several contaminants or timber-land dusts but the mushroom spore itself because precipitins and MIF were finded only to mushroom spores extract unless not to other contaminants. Also, inhalation with spore extract could offend typical symptoms and signs of the hypersensitivity pneumonitis, still other substances could not. The reason wherefore mushroom spores induced the disease looks to be due to indoor cultivation. In this system spores will stagnate in the cultivating scope and easily be inhaled at 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 owing to the spores of another kind of mushroom which was cultivated at an indoor method. [10] Noster, [11] in West Germany, also reported a similar case. Immunologic mechanism contributing to this hypersensitivity pneumonitis was postulated to be befitting to combined type III and protoplast IV allergic reactions like those to farmer's lung and pigeon breeder's lung [12] because precipitins and MIF for the exact allergen were detected, although the precise mechanism was to be clarified. This presentation points gone out that hypersensitivity pneumonitis may appear in workers who are engaged in indoor mushroom cultivation, and spores as well as mold can work into a passion the disease.