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1/42. Aerobiological analysis in a salami factory: a possible case of extrinsic allergic alveolitis by penicillium camembertii.

    A 39-year-old man was hospitalized with a history of fatigue, dyspnoea and low grade fever which seemed to be related to his working environment. The patient was employed in a salami factory, working near the area where the salami are seasoned with fungal inocula. Chest X-ray showed diffuse initial changes of reticulonodular pattern that disappeared after a brief course of steroids therapy. Precipitating antibodies to penicillium notatum and aspergillus fumigatus were found both in plasma and bronchoalveolar lavage fluid. This, together with the finding of a lymphocytic alveolitis with CD4 depletion and CD8 increase, suggested the possibility of extrinsic allergic alveolitis of fungal aetiology. Qualitative and quantitative monitoring with an impinger of both the working and outside environment for aerial fungal concentration demonstrated a very high level of contamination (up to 1.14x10(9) fungal propagules m-3 of air) and an inside/outside ratio from 21 to about 2000. penicillium camembertii was the most common species found in all the indoor sites (60-100% of the fungal load). The patient's BALF and serum both displayed precipitating antibodies to P. camembertii from the powder used for the inoculum and the air samples. These results together with the patient's working history gave some evidence of relationship between the indoor P. camembertii concentration and the patient's symptoms.
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2/42. hypersensitivity pneumonitis resulting from community exposure to canada goose droppings: when an external environmental antigen becomes an indoor environmental antigen.

    BACKGROUND: In the past, hypersensitivity pneumonitis has been attributed to occupational, agricultural, or home environmental exposure. OBJECTIVE: This report describes the first case of hypersensitivity pneumonitis due to community exposure to droppings from canada geese migrating through a suburban environment. METHOD: Clinical and serologic information was used in making the diagnosis of hypersensitivity pneumonitis. RESULTS: Serologic analysis demonstrated precipitating antibodies against goose droppings and against an extract made from washings from a filter taken from the patient's office. These studies also showed that the antigens in the office filter were goose dropping antigens. CONCLUSION: hypersensitivity pneumonitis can result from exposure to goose dropping antigens in the community that enter buildings through ventilation systems. This represents a new form of an old disease.
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3/42. hypersensitivity pneumonitis caused by fusarium napiforme in a home environment.

    BACKGROUND: We report a case of hypersensitivity pneumonitis (HP) in a 17-year-old male student caused by fusarium napiforme found in his home environment. methods: The patient was diagnosed according to history, chest radiograph, spirometry, high-resolution chest CT, and transbronchial lung biopsy. To identify the causative agent, cultured aeromolds were collected by the open-plate method. From the main fungi cultured, fungal antigens were prepared, and immunoblot analysis with the patient's serum and each fungal antigen was performed. RESULTS: Five fungal species were isolated from the patient's home. immunoblotting analysis with the patient's serum demonstrated more than 10 IgG-binding fractions to F. napiforme extract only, while little binding was noted with the other fungal antigens. CONCLUSIONS: We should be aware that HP may be caused by F. napiforme in the home environment.
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4/42. Extrinsic allergic alveolitis from a proteolytic enzyme.

    BACKGROUND: subtilisins are proteolytic enzymes of bacterial origin found in detergents. They are high-molecular-weight antigens and have been implicated in allergic rhinitis and asthma. OBJECTIVE: This report describes a case of extrinsic allergic alveolitis due to subtilisins in a liquid cleaner. methods: Clinical, radiologic, and serologic information were used to make the diagnosis. CASE REPORT: A 53-year-old woman developed respiratory symptoms while working with a cleaner containing subtilisins. Her symptoms intensified in the work environment and improved away from work. A computed tomography scan demonstrated alveolar and interstitial infiltrates with subsequent scarring. A pulmonary function study revealed a restrictive pattern with diminished diffusion capacity. Bronchoalveolar lavage showed lymphocytosis and all cultures were negative. Precipitating antibodies to the enzyme were found in the patient's serum. Her symptoms improved once she changed her occupation. CONCLUSIONS: The combination of the patient's clinical history, physical, laboratory, and radiologic findings support the diagnosis of extrinsic allergic alveolitis from the enzyme contained in the cleaner.
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5/42. hypersensitivity pneumonitis from ordinary residential exposures.

    A previously healthy woman developed hypersensitivity pneumonitis of such severity that she required chronic systemic corticosteroid therapy for symptom control. Detailed investigation of her workplace and home environments revealed fungi in her typical suburban home, to which she had specific serum precipitating antibodies. Efforts to remove mold from the home were unsuccessful in relieving symptoms, and moving to another residence was the only intervention that allowed her to be withdrawn from corticosteroid therapy. hypersensitivity pneumonitis is commonly associated with occupational or avocational exposures, such as moldy hay in farmers or bird antigen in bird breeders. We propose that hypersensitivity pneumonitis may occur in north america, as it does in japan, from domestic exposures alone.
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6/42. Organic antigen-induced interstitial lung disease: diagnosis and management.

    BACKGROUND: Traditionally, chronic idiopathic interstitial pneumonia/fibrosis (IIP/F) had included usual interstitial pneumonia, desquamative interstitial pneumonia, and nonspecific interstitial pneumonia (NSIP). More recent classifications have included bronchiolitis obliterans-organizing pneumonia (BOOP), respiratory bronchiolitis-associated interstitial lung disease, and acute interstitial pneumonia. Some chronic eosinophilic pneumonias (CEP)/pulmonary infiltrate with eosinophilia (PIE) have obvious causes, but many lack an identifiable etiology. We felt that hypersensitivity pneumonitis (HP) was being underdiagnosed and was hidden within this large heterogeneous group of interstitial lung disorders of unrecognized cause. OBJECTIVE: We sought to prove that detailed environmental histories and investigations would reveal causative contaminations in the home or workplace of some patients with idiopathic interstitial lung disease and remediation of the contamination would stabilize the disorder. methods: Consecutive cases of IIP/F were investigated. patients were identified by compatible signs and symptoms, roentgenographic studies, pulmonary function tests, and lung biopsies. They were further evaluated with detailed environmental histories, serologic tests, and investigation into the suspected causative environment. Environmental and specific antigen challenges were done in some cases. Remediation of contaminations or moving into another environment were the methods used as therapy. RESULTS: Eighty-six consecutive patients with IIP/F were evaluated. Twelve patients were subsequently diagnosed with specific causes for interstitial lung disease. Fifty-seven of 74 patients were identified by clinical evaluation and lung biopsy with HP, CEP/PIE, NSIP, BOOP, UIP, and nonclassifiable morphologic patterns. Seventeen patients were not biopsied or had an inadequate transbronchial biopsy but had consistent findings radiographically and clinically of idiopathic interstitial lung disease. Contamination of the home was causative in 69 of 74 and the workplace in 3 of 74 cases. There were 9 positive and 33 negative environmental challenges with 4 positive and 1 negative specific challenges. Fifty of 74 (67%) patients are receiving no treatment and are free of active disease after remediation of the environmental contamination, with a mean survival of 8.2 years. CONCLUSIONS: Our data show that UIP, BOOP, NSIP, CEP/PIE, and nonclassifiable morphologic patterns represent a spectrum of interstitial lung disease that may be caused by inhalation of organic dusts in the home or workplace as described with HP. Remediation of, or moving from the contamination, can lead to arrest of the active inflammatory process and stability of the lung disorder.
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7/42. Humidifier lung: possible contribution of endotoxin-induced lung injury.

    A 56-year-old man was admitted with cough, fever, myalgia, and arthralgia. Chest computed tomography demonstrated bilateral diffuse ground-glass opacities predominantly in the upper lungs. Subpleural non-segmental consolidation was observed in the late phase. hypersensitivity pneumonitis was suspected, and an environmental provocation test with the incidental use of a home ultrasonic humidifier was positive. Unlike typical hypersensitivity pneumonitis, serum KL-6 levels were normal. Although several microorganisms were isolated from the humidifier water, there was no evidence for immune sensitization. We detected high amounts of endotoxin in the humidifier water, which may have contributed to the lung injury of this patient.
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8/42. hypersensitivity pneumonia-nonspecific interstitial pneumonia/fibrosis histopathologic presentation: a study in diagnosis and long-term management.

    BACKGROUND: Nonspecific interstitial pneumonia/fibrosis (NSIP) has been classified a form of idiopathic interstitial pneumonia/fibrosis. We have shown that cases of NSIP without demonstrable serum precipitins may be caused by inhalation of high levels of mold and/or bacteria in closed environments. OBJECTIVE: We report a patient with a clinical and histopathologic diagnosis of NSIP without serum precipitins caused by a microbial contamination in her home. Her case was converted from an acute to an insidious clinical presentation by inadequate remediation. A prolonged avoidance-challenge technique demonstrated that this case of NSIP was a form of hypersensitivity pneumonia that was reversible by effective remediation. methods: The patient was identified by compatible signs and symptoms, roentgenographic studies, pulmonary function tests, and a transbronchial lung biopsy. She was further evaluated with a detailed environmental history, serologic tests, and investigation of the home environment. An environmental avoidance and challenge technique was performed to confirm cause and effect and to determine that remediation had been effective. RESULTS: review of the biopsy showed NSIP and failed to reveal any non-caseating granuloma formation. Investigation of the home revealed a cladosporium species contamination of the air conditioning system and penicillium species beneath an entryway carpet. serum precipitins to commercial antigens of common mold to the south texas area were negative. Avoidance and challenge techniques confirmed the home as the causative environment in this case of NSIP. The patient has been free of signs and symptoms and has taken no medication for interstitial lung disease over the past 30 months. CONCLUSIONS: Some cases of NSIP may be caused by inhalation of microbial antigen(s) in a closed environment. An environmental challenge technique was an effective method to determine the causative environment and confirm that remediation had been effective. Inadequate remediation may lead to symptomatic improvement, but may convert a patient from an acute to an insidious presenter. The environmental challenge obviates a need for specific challenges to determine specific causation. Remediation of or moving from an environmental contamination to achieve reversibility or prevent progression was the treatment of choice to avoid use of long-term immunosuppressive agents.
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ranking = 5
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9/42. Evaluation of hypersensitivity pneumonitis among workers exposed to metal removal fluids.

    hypersensitivity pneumonitis (HP) was identified among employees in an automobile parts manufacturing facility. Mycobacteria immunogenum (MI) was identified as a metal removal fluid (MRF) contaminant at this facility and had been identified as a contaminant in other facilities where HP had occurred. We therefore questioned whether measurement of MI-specific cell-mediated immunity would be associated with HP in this facility. We also questioned whether measures of cell-mediated immunity would be more informative about the presence of HP than evaluation of serum anti-MI antibody levels. Workers were categorized for exposure and disease status by questionnaire and review of medical records. Cell-mediated immunity to MI was assessed by measuring in vitro secretion of cytokines (interleukin 8, tumor necrosis factor alpha, and interferon-gamma) from peripheral blood mononuclear cells or anticoagulated whole blood induced by culture with MI antigen. serum antibodies against MI were also measured. Six study participants met our survey definition for HP and 48 did not. As has been reported for various agents causing HP, serum antibody levels against MI were increased in both exposed workers and workers with HP. serum antibodies did not distinguish between the two. When expressed as a percentage of secretion induced by lipopolysaccharide, MI induced a significant increase in interleukin-8 secretion in exposed participants' whole blood cultures. There were trends for increased MI-induced secretion of interferon-gamma by peripheral blood mononuclear cells from both exposed workers and workers with HP. However, these trends did not attain statistical significance. Thus, several measures of immunity to MI distinguished between exposed and unexposed workers but not between workers with and without HP. These evaluations of cell-mediated immunity were not more informative than measurement of serum antibodies. As was done at this facility, institution of a comprehensive safety and health plan for MRF is necessary to eliminate (or minimize) health effects related to occupational exposures in the machining environment.
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10/42. dapsone-induced hypersensitivity pneumonitis mimicking pneumocystis carinii pneumonia in a patient with AIDS.

    Interstitial pneumonitis, often related to infectious etiologies, occurs commonly in hiv-infected patients. However, hypersensitivity pneumonitis from noninfectious etiologies, including environmental stimuli or drug exposure, is an unusual etiology of interstitial pneumonitis in hiv-infected patients. We report a patient with AIDS who developed a dapsone-induced hypersensitivity pneumonitis mimicking pneumocystis carinii (PCP) pneumonia. We believe drug-induced hypersensitivity pneumonitis should be considered in the differential diagnosis of interstitial pneumonia in hiv-infected patients in whom infectious etiologies have been ruled out.
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