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Hypersensitivity Pneumonitis Due to Molds in a Saxophone Player FREE TO VIEW

Flora Metzger, MD; Amaryllis Haccuria, MD; Gabriel Reboux, PhD; Nicole Nolard, MD; Jean-Charles Dalphin, MD, PhD; Paul De Vuyst, MD, PhD
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From the Department of Respiratory Disease (Drs Metzger and Dalphin) and the Department of Mycology (Dr Reboux), Jean Minjoz University Hospital, Besançon, France; Hôpital Erasme (Drs Haccuria and De Vuyst), Université libre de Bruxelles, Brussels, Belgium; and Scientific Institute of Public Health (Dr Nolard), Brussels, Belgium.

Correspondence to: Flora Metzger, MD, Department of Respiratory Disease, Jean Minjoz University Hospital, 3 bvd Alexander Fleming, 25030, Besançon, France; e-mail: fmetzger@chu-besancon.fr


For editorial comment see page 467

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(3):724-726. doi:10.1378/chest.09-2991
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This 48-year-old patient was evaluated for an interstitial pneumonia. An open-lung biopsy showed a pattern of nonspecific interstitial pneumonia. The CT scan appearance, showing mosaic ground-glass opacities in the ventilated parts of the lung, the centrolobular predominance of inflammation on the lung sections, and the presence of a lymphocytic alveolitis at BAL suggested a hypersensitivity pneumonitis. The patient was a white-collar worker and had no contact with pets, birds, drugs, or molds at home. He used to play the saxophone as a hobby. Two molds, Ulocladium botrytis and Phoma sp, were detected in the saxophone. Precipitating antibodies to these molds were present in his serum. An additional study confirmed the frequent colonization of saxophones with potentially pathogenic molds, such as Fusarium sp, Penicillium sp, and Cladosporium sp. Respiratory physicians should be aware of the risk of hypersensitivity pneumonitis in saxophone or perhaps other wind instrument players.

Figures in this Article

Hypersensitivity pneumonitis (HP) is an immunologically induced lung disease caused by repeated inhalation of agents in sensitized individuals. Causal antigens are various in nature, but the most commonly involved are microorganisms.1 To the best of our knowledge, only one case of HP has been described in a saxophonist, and this case was probably due to the inhalation of Candida albicans from his instrument.2 We report a well-documented case of HP in a saxophonist due to Phoma spp and Ulocladium botrytis in his instrument.

A 48-year-old nonsmoker presented with a progressive exertional dyspnea dating back 5 months. He had no relevant past history except bronchiectases in the lingula and the left lower lobe. He was an office clerk, had no occupational or domestic exposure to birds or molds, and took no medication. He had no extrapulmonary complaints. He had played the saxophone regularly since childhood.

At physical examination, inspiratory crackles were present at the right lung base. Room air oxygen saturation was 95% at rest but 86% after stair climbing. Pulmonary function tests revealed the following: total lung capacity 6.29 L, 78% predicted; vital capacity 3.34 L, 60% predicted; FEV1 2.05 L, 48% predicted; and CO transfer coefficient at 45% predicted. A CT scan demonstrated the presence of bilateral poorly defined micronodules and ground-glass patchy infiltrates that produced a mosaic pattern (Figs 1, 2) except in the lower part of the left lung.

Figure Jump LinkFigure 1. Initial CT scan. Mosaic pattern with poorly defined micronodules and ground-glass opacities contrasting with normal lung areas.Grahic Jump Location
Figure Jump LinkFigure 2. Initial CT scan. Mosaic pattern and previously-known bronchiectases.Grahic Jump Location

Laboratory tests showed no abnormalities. The search for autoantibodies was negative. BAL revealed a lymphocytic predominance with 1.070 × 103 cells/mL, 72% lymphocytes, 12% macrophages, 11% neutrophils, and 5% eosinophils. An open lung biopsy in the right upper lobe revealed a pattern of nonspecific interstitial pneumonia without granulomas or fibrosis (Fig 3). Mycologic samplings from the saxophone (mouthpiece and casket) revealed a fungal contamination with U botrytis and Phoma sp. Somatic antigens derived from these strains were made as previously described.3 Serum-specific antibodies were positive against these two fungal species. Respectively, eight and 11 bands were found by IgG Western blot for Ulocladium antigen and Phoma antigen.3 The final diagnosis was HP related to molds developed in the saxophone. A treatment with 32 mg/d methylprednisolone for 1 month, followed by a gradual tapering of the doses over a period of 3 months, was introduced in conjunction with regular drying of the saxophone after playing and cleaning with a disinfectant. Clinical symptoms, pulmonary function tests, and radiologic abnormalities improved within 2 months (Fig 4). After 2 months of hygiene measures, mycological samplings from the saxophone no longer revealed any mold colonization.

Figure Jump LinkFigure 3. Lung biopsy (hematoxylin and eosin stain, original magnification × 250). Uniform lymphocytic infiltration with predominance in centrolobular areas suggesting a nonspecific interstitial pneumonia pattern.Grahic Jump Location
Figure Jump LinkFigure 4. CT scan after 2 months of corticotherapy.Grahic Jump Location

Complementary investigations were conducted in 15 saxophonists who provided informed consent. According to the protocol approved by the ethics committee, they underwent a physical examination, respiratory function tests, and a CT scan of the lungs. Mycologic samplings were taken with an applicator in their saxophones and accessories. The results showed a fungal colonization in 13 out of 15 saxophones. Phoma sp was found in one instrument. The most frequently involved microorganisms were Fusarium oxysporum (7/15), Fusarium sp (6/15), Penicillium sp (6/15), C albicans (4/15), and Cladosporium sphaerospermum (3/15). Blood samples with search for precipitating antibodies were negative because no arc was observed by Ouchterlony double diffusion and < 2 arcs on electrosyneresis on cellulose acetate.3 We concluded that musicians had no significant sensitization against those molds. No additional case of HP was detected.

In this report we present a well-documented case of HP in a saxophone player. In the previously reported case of HP in a musician, presumed to be due to C albicans,2 there was no CT scan, BAL, or pathologic data. The present diagnosis of HP is based on a combination of several factors. The clinical feature is compatible with a subacute form of HP.4 BAL showed a lymphocytic alveolitis. CT scan showed a classic radiologic HP presentation of ground-glass opacities shadowing areas of normal lung, creating a mosaic pattern. What was particularly interesting on CT scan was the lack of involvement of the zones with the bronchiectases, much less ventilated, which reinforces the diagnosis of an inhalational origin of lung disease. Although lung biopsy in HP classically shows lymphocytic infiltration and granulomas, histologic pattern of nonspecific interstitial pneumonia has been described in recognized HP.5 Ultimately, the sensitization of the musician against the molds found in his saxophone is important evidence for HP.

The additional study on saxophonists showed that saxophones are frequently colonized by fungal species and constitute a source of potentially inhalable and pathogenic molds. Indeed, cases of HP due to Fusarium sp, Penicillium sp, and Cladosporium sp have been reported. The lack of sensitization of the musicians may be explained by too poor a level of exposure or too short a contact with the molds, since it is known that a long exposure is necessary to stimulate an immune response.6

We present a case of HP in a saxophonist due to the inhalation of molds from his instrument and an additional investigation that emphasizes the fact that musicians may be a population at risk for immunologically induced lung disease. Physicians should be aware of this potential disease in subjects who play a wind instrument.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

HP

hypersensitivity pneumonitis

Girard M, Lacasse Y, Cormier Y. Hypersensitivity pneumonitis. Allergy. 2009;643:322-334. [CrossRef] [PubMed]
 
Lodha S, Sharma OP. Hypersensitivity pneumonitis in a saxophone player. Chest. 1988;936:1322. [CrossRef] [PubMed]
 
Reboux G, Piarroux R, Roussel S, Millon L, Bardonnet K, Dalphin JC. Assessment of four serological techniques in the immunological diagnosis of farmers’ lung disease. J Med Microbiol. 2007;56pt 10:1317-1321. [CrossRef] [PubMed]
 
Richerson HB, Bernstein IL, Fink JN, et al. Report of the Subcommittee on Hypersensitivity Pneumonitis Guidelines for the clinical evaluation of hypersensitivity pneumonitis. J Allergy Clin Immunol. 1989;845 pt 2:839-844. [CrossRef] [PubMed]
 
Lima MS, Coletta EN, Ferreira RG, et al. Subacute and chronic hypersensitivity pneumonitis: histopathological patterns and survival. Respir Med. 2009;1034:508-515. [CrossRef] [PubMed]
 
Cormier Y, Bélanger J, Durand P. Factors influencing the development of serum precipitins to farmer’s lung antigen in Quebec dairy farmers. Thorax. 1985;402:138-142. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. Initial CT scan. Mosaic pattern with poorly defined micronodules and ground-glass opacities contrasting with normal lung areas.Grahic Jump Location
Figure Jump LinkFigure 2. Initial CT scan. Mosaic pattern and previously-known bronchiectases.Grahic Jump Location
Figure Jump LinkFigure 3. Lung biopsy (hematoxylin and eosin stain, original magnification × 250). Uniform lymphocytic infiltration with predominance in centrolobular areas suggesting a nonspecific interstitial pneumonia pattern.Grahic Jump Location
Figure Jump LinkFigure 4. CT scan after 2 months of corticotherapy.Grahic Jump Location

Tables

References

Girard M, Lacasse Y, Cormier Y. Hypersensitivity pneumonitis. Allergy. 2009;643:322-334. [CrossRef] [PubMed]
 
Lodha S, Sharma OP. Hypersensitivity pneumonitis in a saxophone player. Chest. 1988;936:1322. [CrossRef] [PubMed]
 
Reboux G, Piarroux R, Roussel S, Millon L, Bardonnet K, Dalphin JC. Assessment of four serological techniques in the immunological diagnosis of farmers’ lung disease. J Med Microbiol. 2007;56pt 10:1317-1321. [CrossRef] [PubMed]
 
Richerson HB, Bernstein IL, Fink JN, et al. Report of the Subcommittee on Hypersensitivity Pneumonitis Guidelines for the clinical evaluation of hypersensitivity pneumonitis. J Allergy Clin Immunol. 1989;845 pt 2:839-844. [CrossRef] [PubMed]
 
Lima MS, Coletta EN, Ferreira RG, et al. Subacute and chronic hypersensitivity pneumonitis: histopathological patterns and survival. Respir Med. 2009;1034:508-515. [CrossRef] [PubMed]
 
Cormier Y, Bélanger J, Durand P. Factors influencing the development of serum precipitins to farmer’s lung antigen in Quebec dairy farmers. Thorax. 1985;402:138-142. [CrossRef] [PubMed]
 
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