Abstract
In 1959, E. Pestalozzi, who worked for the Allergy Unit of the Department of Dermatology of the University Hospital Zurich, was the first to describe the syndrome as a febrile group disease in a model carpenters workshop caused by inhalation of humidifier water contaminated with moulds [1]. 6 cases of humidifier disease were diagnosed and clarified in the same hospital in 1969 and 1970. Those cases were compiled in an unpublished medical inaugural doctoral thesis (University of Zurich 1973). Always in the afternoon of a working day, i.e. approximately 6 - 8 hours after they had started work, the patients (5 males and 1 female) suffered from nausea, exhaustion, fever with shivering, sweating, dyspnoa, cough, expectoration and gastrointestinal problems. During the episodes, the blood sedimentation rate was increased, blood count showed a leukocytosis, in 3 cases Roentgen thorax was pathologic. In 2 of these cases, basal on both sides increased markings, and in the 3rd case 3 - 4 mm sized shadow spots in the whole lung could be detected. The diagnosis was confirmed by the fact that the symptoms vanished after the humidifier in the working place was turned off or removed from the working place but returned at once when the humidifier was turned on again. In the humidifier water, several different mould and bacteria species could be cultivated. Intracutaneous and inhalative provocation tests were carried out with extracts from the humidifier water. In 3 patients, the inhalation test (in 1 case with Alcaligenes faecalis, in 2 cases with Pseudomonas fluorescens) provoced a delayed early reaction with an increase in fever, nausea, partially with pains in the limbs and cough. Leukocytosis could be shown in the laboratory. In a 4th patient, the inhalation ofMonilia extract (Hollister-Stier) led to a severe immediate reaction with cough, severe dyspnea, FEV 1 decrease and general nausea, so that an intensive emergency therapy was necessary. Pathogenetically, a Type III hypersensitivity reaction was postulated, although no precipitins could be shown in the immunoelectrophoresis. In 4 cases, the precipitin reaction against hey extracts was, however, positive. In contrast to Pestalozzis initial observations, the fact that only 1 worker diseased under the same exposition conditions speaks against a toxic reaction or an infectious disease. Also, on account of the literature, the humidifier disease was considered to be a syndrome of different etiology but with probably homogeneous pathogenesis.
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