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Serodiagnosis of misting fountains alveolitis
Abstract
Serological diagnosis of misting fountain alveolitis could best be established by using the water of patients fountains. The Ouchterlony technique was sufficient for the detection of IgG antibodies with 11 of 22 patients. In 10 sera, however, the more sensitive IgG ELISA was needed. Using known antigens, antibodies were found most frequently against Aureobasidium pullulans, Cephalosporium acremonium, and Pseudomonas aeruginosa. With 22 well-documented cases of misting fountains alveolitis and additional 13 cases, as far as we know, within the last two years, the present use of misting fountains is a serious health hazard in Germany.
A new ELISA is presented here, which detects the IgG antibodies against the antigens in the moldy water of misting fountains. In the sera of 30 of 32 patients suffering from humidifier lung from these new developed humidifiers, IgG antibodies were detected by this screening test. Positive results of this ELISA using coated pooled moldy humidifier water from 4 patients should be confirmed by the Ouchterlony test using patients humidifier water or by IgG tests against the single antigens of humidifier lung as Aureobasidium pullulans, Cephalosporium acremonium, Penicillia and other known molds and bacteria.
Our study aimed to elucidate the clinical role of Absidia corymbifera as an antigen of farmers lung. Using the ELISA technique, a total of 76 serum samples of patients with suggested farmers lung were investigated for IgG-antibodies against A. corymbifera as well as against Saccharopolyspora rectivirgula, Thermoactinomyces vulgaris, and Aspergillusfumigatus. Only 5 of 76 (7%) sera revealed antibodies against A. corymbifera, all of which presenting with at least one other positive antigen. We conclude that in Germany an investigation for IgG-antibodies against A. corymbifera does not improve the sensitivity of the diagnosis of farmers lung. However, this should be a focus of further research.
Following our previous study concerning IgG-antibodies against Absidia (Lichtheimia) corymbifera in sera of German farmers lung patients we looked for additional antigens in 30 sera of patients with suspected farmers lung. The sera also reacted with the antigens Erwinia herbicola, Thermoactinomyces sacchari, Thermoactinomyces dichotomicus, and Streptomyces albus. 17% of the sera reacted only with these, but not with the classical antigens. Therefore expanding the spectrum of farmers lung antigens may improve diagnostic sensitivity of farmers lung. However the clinical relevance of these additional antigens has to be determined by further studies.
We report about a 43-year-old man with dyspnoe due to an exogen allergic alveolitis/hypersensitivity pneumonitis caused by a biological detergent containing Bacteria subtilis. The diagnosis was confirmed by a reexposition at work, a specific provokation test and immunologic examinations. In the 70s the enzyme subtilisin was found to cause allergic reaction in its uncapsulated form in washing powder. This is, as far as we know, the second known case of an allergic alveolitis to Bacterium subtilis with subtilisin in an biological detergent and the first case to Bio-Circle Liquid®, a soluble-free cleaner used in industrial production. In his home the patient had contact with a contaminated ultrasound nebulizer for a long time. This humidifier may have induced the development of the immune reaction against Bacillus subtilis in the biological detergent.
We present a case report with follow up about an allergic alveolitis due to Bacillus subtilis. As main source of the allergen a biological detergent at the working place could be identified. An amplification by bacterial contamination of a room fontaine at home is very likely. A subclinical reactivation was detected by serial antibody titers and increases of C-reactive protein and lactatdehydrogenase (LDH).
Autoantibodies (ANA, ANCA) were found in 6 patients suffering from chronic extrinsic allergic alveolitis. Most patients had stopped antigen exposure. We discuss progress of the interstitial lung disease may not be caused by extrinsic allergic alveolitis alone but also by autoimmunity.
Hintergrund und Fragestellung: Die zunehmende Verwendung von Luftbefeuchtern im privaten Bereich, insbesondere von Kaltverneblern auf Ultraschallbasis, führt bei den so Exponierten gehäuft zu Fieber und pulmonalen Symptomen.
Patienten: Wir berichten über 14 Patienten (5 Frauen, 9 Männer, Durchschnittsalter 42,5 ± 17,4 Jahre). Alle benutzten einen Kaltvernebler auf Ultraschallbasis und litten unter Fieber, Husten und Atemnot.
Untersuchungsergebnisse: Bei 12 der Patienten wurde eine exogen-allergische Alveolitis (EAA) diagnostiziert, bei zwei ein „organic dust toxic syndrome” (ODTS) . Bei 10 Patienten wurde eine respiratorische Partialinsuffizienz in Ruhe oder bei Belastung, bei 9 eine restriktive Ventilationsstörung diagnostiziert. Bei 7 wurde das konventionelle Lungenröntgenbild als pathologisch befundet. Bei 6 von 8 Patienten, bei denen eine Computertomographie (CT) durchgeführt wurde, fanden sich für eine exogen-allergische Alveolitis (EAA) typische Veränderungen. Bei 8 der Untersuchten wurde mittels einer bronchoalveolären Lavage (BAL) eine lymphozytäre Alveolitis diagnostiziert. Bei 12 Betroffenen wurden Bakterien, Schimmelpilze und/oder Hefen im Befeuchterwasser nachgewiesen, bei 13 IgG-Antikörper gegen das Befeuchterwasser mittels Immundiffusion und/oder ELISA. 8 der Patienten wurden in der Klinik mit ihrem Befeuchterwasser provoziert, worauf alle Untersuchten reagierten.
Folgerungen: Diese Fälle zeigen, dass Befeuchter im häuslichen Umfeld Krankheiten verursachen können. Angesichts der zunehmenden Beliebtheit von Zimmerspringbrunnen sollten die EAA und ODTS bei Patienten mit Fieber und unklaren pulmonalen bzw. grippeartigen Symptomen in die Differenzialdiagnose einbezogen werden.
Summary
Background and objective: Recently an increasing number of patients presented with febrile and respiratory symptoms associated with exposure to a new type of domestic ultrasonic humidifier.
Patients and methods: We report on 14 patients (5 females, 9 males; average age 42.5 17.4 years) with recurrent episodes of fever, cough and dyspnea after repeated exposure to ultrasonic misting fountains at home.
Results: A diagnosis of extrinsic allergic alveolitis (humidifier lung: 12 patients) or toxic alveolitis (humidifier fever: 2 patients) was made on the basis of the history and the clinical, radiological, laboratory and immunological findings. 10 patients had a partial respiratory insufficiency at rest or on exercise, 9 had a restrictive ventilatory abnormality. The chest x-ray was abnormal in 7 patients. Of 8 patients in whom computed tomography was done 6 had typical changes of an exogenous allergic alveolitis. Bronchoalveolar lavage revealed lymphocytic alveolitis in 8 patients. In 12 patients bacteria, moulds and/or yeasts were demonstrated in the humidier fluid which they had used. 13 patients had IgG antibodies to the humidier fluid. 8 patients were subjected to inhalative challenge tests to their own ultrasonic misting fountain: all of them had positive reactions.
Conclusions: These cases demonstrate the potential of ultrasonic humidifying devices to cause illness in the home. In view of their increasing popularity, humidifier lung and humidifier fever should be considered in the differential diagnosis of patients with unexplained pulmonary or flu-like illness with fever.
There have been several recent reports of pulmonary disease resulting from exposure to Mycobacterium avium complex in indoor hot tubs. The disease is thought to be due either to infection or extrinsic allergic alveolitis (EAA). In this report we describe the case of a patient who developed episodes of fever, dyspnea and cough 4-6 hours after cleaning his indoor swimming pool. A diagnosis of EAA was made on finding a restrictive lung function pattern with gas exchange abnormalities, a predominant lymphocytosis in the bronchoalveolar lavage, diffuse ground-glass opacities in the lower lobes on high-resolution computer tomography, and specific IgG antibody activity to the swimming pool water. There was no precipitin reaction or specific IgG antibody activity to microbes extracted from the water. Interestingly, the water contained Mycobacterium avium complex (MAC) in huge amounts and in this case the histopathological features of the lung biopsy specimens differed from those seen in typical EAA, but were similar to those described in "hot tub lung" caused by mycobacteria. Solely by avoidance of cleaning the swimming pool, without any pharmacological treatment, the patient recovered completely within three months. To the best of our knowledge, this is the first report of EAA possibly associated with MAC exposure in a swimming pool environment.
The aim of our study was to evaluate clinical diagnoses in symptomatic persons exposed to aerosols from humidifiers or air conditioners. In addition, we tried to identify the causative antigens. Results of clinical investigations, including inhalation challenge tests, demonstrated a typical hypersensitivity pneumonitis (humidifier lung) in 9 persons and isolated systemic symptoms without significant changes in lung function and chest x-rays (humidifier fever) in 3 persons. Microbiological studies revealed a variety of fungi and bacteria in the water supplies of humidifiers and air conditioners at patients' workplaces. The detection of 4 members of the order Sphaeropsidales (Deuteromycotina), not previously associated with humidifier-induced diseases, is of special interest. By means of an improved polystyrene tube-immunoradiometric assay, high concentrations of IgG antibodies against extracts prepared from water of patients' humidifier systems were found in all cases. In addition, patients demonstrated low concentrations of IgG antibodies against thermophilic Actinomycetes, and usually also against various fungi, such as Alternaria tenuis, Aureobasidium pullulans, Penicillium notatum, Aspergilli, and fungi of the order Sphaeropsidales, which were isolated and cultured from humidifier water supplies. The much higher concentrations of antibodies against humidifier/air conditioner water extracts seem to result from sensitization to a variety of antigens from different fungi and bacteria. For in vivo and in vitro diagnostic tests in humidifier-induced lung diseases, we especially recommend using extracts from water systems installed at the corresponding workplaces.
An outbreak of hypersensitivity pneumonitis in a textile plant was attributed on epidemiological grounds to a chilled water air-conditioning system where a slime was growing in the chilled water sump and on demister vanes. All of the patients and about 80% of their asymptomatic co-workers had strongly positive precipitin tests to extracts of the slime. An adaptation of a radioiodinated staphylococcal protein A solid-phase radioimmunoassay was applied to monitor antigen and specific antibody. To control the outbreak, a variety of cleaning and water treatment measures were taken between 1977 and 1979 to reduce the amount of antigen in the water and in the air. The amount of slime in the water was greatly reduced though the antigen content per gram of slime did not change. Airborne antigen in the affected work areas decreased progressively.
A 22-year-old woman developed recurrent episodes of fever, cough and dyspnea after repeated exposure to a misting fountain at home. A diagnosis of extrinsic allergic alveolitis (EAA) was made by detection of serum antibodies against the fountain water, by culture of Bacillus subtilis, Mucor racemosus, Mucor mucedo, and Saccharomyces cerevisiae from the water, and by detection of specific IgG antibodies against Bacillus subtilis and the Mucores. The diagnosis was confirmed by a restrictive lung function pattern, and a highly increased total cell count with a lymphocytosis of 39 % in the bronchoalveolar lavage. An inhalation challenge with the misting fountain resulted in a positive reaction. Because this humidifier system has recently become widespread at home, clinicians should be aware of this specific type of EAA which may be called "misting fountain alveolitis".