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Acute lung injury after exposure to Stachybotrys chartarum
ARTICLE IN PRESS Respiratory Medicine Extra (2007) 3, 74–75
respiratory MEDICINE Extra
CASE REPORT
Acute lung injury after exposure to Stachybotrys chartarum Cyrus Shariat, Harold R. Collard Department of Medicine, San Francisco General Hospital, University of California San Francisco, San Francisco, CA (CS, HRC), USA Received 21 February 2007; accepted 23 March 2007
KEYWORDS Stachybotrys chartarum; Acute lung injury; Diffuse alveolar damage; Mold
Summary An association between exposure to Stachybotrys chartarum, a ubiquitous environmental mold, and respiratory disease in humans has been suggested but remains poorly defined [Hossain MA, Ahmed MS, Ghannoum, MA. Attributes of Stachybotrys chartarum and its association with human disease. J Allergy Clin Immunol 2004; 113: 200–08]. We report a patient who presented with acute respiratory failure and histopathological evidence of diffuse alveolar damage shortly after exposure to S. chartarum in her home. & 2007 Published by Elsevier Ltd.
A 63-year-old woman with limited scleroderma and no known pulmonary disease was in her usual state of health until her water-damaged bathroom wall was removed. The following day, she developed a dry cough. She had no dyspnea, fever, chills, or night sweats. One month later, her bathtub was removed to reveal a large area of black mold. The patient swept and vacuumed the area, and subsequently developed progressive cough and dyspnea. The patient was a non-smoker, was taking no new medications, and had no recent sick contacts, other significant new exposures or travel history. She had clinically
Abbreviations: BAL, bronchoalveolar lavage; CT, computed tomography; S. chartarum, Stachybotrys chartarum Corresponding author. Tel.: +1 916 397 1331. E-mail addresses: [email protected] (C. Shariat), [email protected] (H.R. Collard). 1744-9049/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.rmedx.2007.03.001
stable limited scleroderma with no history of pulmonary fibrosis or gastroesophageal dysmotility In the emergency room, the patient was afebrile with a respiratory rate of 28 and an oxygen saturation of 69% on room air. The physical examination revealed diffuse inspiratory crackles. Laboratory workup revealed a leukocytosis of 16,300 cells/mm3. A CT scan of the chest demonstrated airspace consolidation involving all lobes (Fig. 1). The patient was started empirically on levofloxacin and high dose solumedrol and admitted to the intensive care unit. The patient worsened, and on the fourth day of hospitalization underwent a core needle biopsy of the left lower lobe which demonstrated alveolar septal thickening, type II pneumocyte hyperplasia and hyaline membrane formation consistent with acute lung injury. On the seventh day of hospitalization, she was intubated for progressive hypoxemia. No infectious etiology was identified. Intravenous cyclophosphamide was added to her regimen.
ARTICLE IN PRESS Acute lung injury after exposure to Stachybotrys chartarum
Figure 1 Computed tomography scan of the chest demonstrates diffuse consolidation consistent with acute lung injury.
She gradually improved, was extubated after two and a half weeks and was discharged from the hospital three weeks later on oral prednisone and cyclophosphamide. Since discharge, the patient has completely avoided her home. Her dyspnea has continued to improve. Cultures of the black mold from her bathroom grew Stachybotrys chartarum. Assays for mycotoxin production were not performed.
Discussion An association between respiratory illness and indoor mold, particularly in moisture damaged buildings, has been suggested.1 Recently, there have been lawsuits filed for health injury as a result of exposure to toxic mold in residential or office buildings. S. chartarum, popularly known as black mold, has been the most frequently cited fungus.1 Importantly, a direct causal relationship between S. chartarum and human disease has been difficult to prove. S. chartaram is a ubiquitous environmental fungus generally found in soil and strata that are rich in cellulose. The species is known to produce a variety of mycotoxins which are thought to be potential causes of pulmonary disease.1 In the 1940s, a respiratory syndrome called ‘‘stachybotrytoxicosis’’ was ascribed to S. chartaram, occurring in people in contact with moldy straw.1 A building-associated pulmonary disease has also been de-
75 scribed with exposure to S. chartarum.2,5 In the early 1990s, a cluster of 10 cases of idiopathic pulmonary hemosiderosis in infants from Cleveland, OH was reported and linked to toxigenic S. chartarum.2 Although this report furthered the notoriety of S. chartarum, the Center for Disease Control ultimately concluded that the evidence for a causal relationship was insufficient.2 Animal studies have demonstrated S. chartarum to cause pulmonary injury. A one-time intratracheal exposure to S. chartarum caused severe pulmonary inflammation in rats which was detectable in BAL (broncheoalveolar lavage) fluid.4 Mice exposed intranasally to spores of S. chartarum had a dose-dependent increase in inflammatory cells in BAL fluid as well as an induction of pro-inflammatory cytokines and chemokine mRNA in the lung.3 Alternative diagnoses seem unlikely in this case. While infectious pneumonia was not thoroughly investigated with bronchoaveolar lavage cultures, the patient’s history was atypical and the patient worsened on antibiotics. Although one case of diffuse alveolar damage in scleroderma has been published, scleroderma lung disease seems equally unlikely.6 Given the patient’s known exposure to S. chartarum, the time course of her illness, the biological plausibility of lung injury based on animal models, and the lack of reasonable alternative etiologies, we suggest that this is a case of acute lung injury caused by exposure to S. chartarum. This case underscores the need for further in-depth studies using objective markers of disease, relevant animal models and careful examination of confounding factors in order to better define the relationship between S. chartarum and pulmonary disease.
References 1. Hossain MA, Ahmed MS, Ghannoum MA. Attributes of Stachybotrys chartarum and its association with human disease. J Allergy Clin Immunol 2004;113:200–8. 2. Kuhn DM, Ghannoum MA. Indoor mold, toxigenic fungi, and Stachybotrys chartarum: infectious disease perspective. Clin Microbiol Rev 2003;16:142–72. 3. Ochiai E, Kamei K, Hiroshima K, et al. The pathogenicity of Stachybotrys chartarum. Jpn J Med Mycol 2005;46:109–17. 4. Rao CY, Burge HA, Brain JD. The time course of responses to intratracheally instilled toxic Stachybotrys chartarum spores in rats. Mycopathologia 2000;149:27–34. 5. Hodgson MJ, Morey P, Leung WY, et al. Building-associated pulmonary disease from exposure to Stachybotrys chartarum and Aspergillus versicolor. J Occup Environ Med 1998;40(3):241–9. 6. Fujita J, Yoshinouchi T, Ohtsuki Y, et al. Non-specific interstitial pneumonia as pulmonary involvement of systemic sclerosis. Ann Rheumatic Dis 2001;60:281–3.
respiratory MEDICINE Extra
CASE REPORT
Acute lung injury after exposure to Stachybotrys chartarum Cyrus Shariat, Harold R. Collard Department of Medicine, San Francisco General Hospital, University of California San Francisco, San Francisco, CA (CS, HRC), USA Received 21 February 2007; accepted 23 March 2007
KEYWORDS Stachybotrys chartarum; Acute lung injury; Diffuse alveolar damage; Mold
Summary An association between exposure to Stachybotrys chartarum, a ubiquitous environmental mold, and respiratory disease in humans has been suggested but remains poorly defined [Hossain MA, Ahmed MS, Ghannoum, MA. Attributes of Stachybotrys chartarum and its association with human disease. J Allergy Clin Immunol 2004; 113: 200–08]. We report a patient who presented with acute respiratory failure and histopathological evidence of diffuse alveolar damage shortly after exposure to S. chartarum in her home. & 2007 Published by Elsevier Ltd.
A 63-year-old woman with limited scleroderma and no known pulmonary disease was in her usual state of health until her water-damaged bathroom wall was removed. The following day, she developed a dry cough. She had no dyspnea, fever, chills, or night sweats. One month later, her bathtub was removed to reveal a large area of black mold. The patient swept and vacuumed the area, and subsequently developed progressive cough and dyspnea. The patient was a non-smoker, was taking no new medications, and had no recent sick contacts, other significant new exposures or travel history. She had clinically
Abbreviations: BAL, bronchoalveolar lavage; CT, computed tomography; S. chartarum, Stachybotrys chartarum Corresponding author. Tel.: +1 916 397 1331. E-mail addresses: [email protected] (C. Shariat), [email protected] (H.R. Collard). 1744-9049/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.rmedx.2007.03.001
stable limited scleroderma with no history of pulmonary fibrosis or gastroesophageal dysmotility In the emergency room, the patient was afebrile with a respiratory rate of 28 and an oxygen saturation of 69% on room air. The physical examination revealed diffuse inspiratory crackles. Laboratory workup revealed a leukocytosis of 16,300 cells/mm3. A CT scan of the chest demonstrated airspace consolidation involving all lobes (Fig. 1). The patient was started empirically on levofloxacin and high dose solumedrol and admitted to the intensive care unit. The patient worsened, and on the fourth day of hospitalization underwent a core needle biopsy of the left lower lobe which demonstrated alveolar septal thickening, type II pneumocyte hyperplasia and hyaline membrane formation consistent with acute lung injury. On the seventh day of hospitalization, she was intubated for progressive hypoxemia. No infectious etiology was identified. Intravenous cyclophosphamide was added to her regimen.
ARTICLE IN PRESS Acute lung injury after exposure to Stachybotrys chartarum
Figure 1 Computed tomography scan of the chest demonstrates diffuse consolidation consistent with acute lung injury.
She gradually improved, was extubated after two and a half weeks and was discharged from the hospital three weeks later on oral prednisone and cyclophosphamide. Since discharge, the patient has completely avoided her home. Her dyspnea has continued to improve. Cultures of the black mold from her bathroom grew Stachybotrys chartarum. Assays for mycotoxin production were not performed.
Discussion An association between respiratory illness and indoor mold, particularly in moisture damaged buildings, has been suggested.1 Recently, there have been lawsuits filed for health injury as a result of exposure to toxic mold in residential or office buildings. S. chartarum, popularly known as black mold, has been the most frequently cited fungus.1 Importantly, a direct causal relationship between S. chartarum and human disease has been difficult to prove. S. chartaram is a ubiquitous environmental fungus generally found in soil and strata that are rich in cellulose. The species is known to produce a variety of mycotoxins which are thought to be potential causes of pulmonary disease.1 In the 1940s, a respiratory syndrome called ‘‘stachybotrytoxicosis’’ was ascribed to S. chartaram, occurring in people in contact with moldy straw.1 A building-associated pulmonary disease has also been de-
75 scribed with exposure to S. chartarum.2,5 In the early 1990s, a cluster of 10 cases of idiopathic pulmonary hemosiderosis in infants from Cleveland, OH was reported and linked to toxigenic S. chartarum.2 Although this report furthered the notoriety of S. chartarum, the Center for Disease Control ultimately concluded that the evidence for a causal relationship was insufficient.2 Animal studies have demonstrated S. chartarum to cause pulmonary injury. A one-time intratracheal exposure to S. chartarum caused severe pulmonary inflammation in rats which was detectable in BAL (broncheoalveolar lavage) fluid.4 Mice exposed intranasally to spores of S. chartarum had a dose-dependent increase in inflammatory cells in BAL fluid as well as an induction of pro-inflammatory cytokines and chemokine mRNA in the lung.3 Alternative diagnoses seem unlikely in this case. While infectious pneumonia was not thoroughly investigated with bronchoaveolar lavage cultures, the patient’s history was atypical and the patient worsened on antibiotics. Although one case of diffuse alveolar damage in scleroderma has been published, scleroderma lung disease seems equally unlikely.6 Given the patient’s known exposure to S. chartarum, the time course of her illness, the biological plausibility of lung injury based on animal models, and the lack of reasonable alternative etiologies, we suggest that this is a case of acute lung injury caused by exposure to S. chartarum. This case underscores the need for further in-depth studies using objective markers of disease, relevant animal models and careful examination of confounding factors in order to better define the relationship between S. chartarum and pulmonary disease.
References 1. Hossain MA, Ahmed MS, Ghannoum MA. Attributes of Stachybotrys chartarum and its association with human disease. J Allergy Clin Immunol 2004;113:200–8. 2. Kuhn DM, Ghannoum MA. Indoor mold, toxigenic fungi, and Stachybotrys chartarum: infectious disease perspective. Clin Microbiol Rev 2003;16:142–72. 3. Ochiai E, Kamei K, Hiroshima K, et al. The pathogenicity of Stachybotrys chartarum. Jpn J Med Mycol 2005;46:109–17. 4. Rao CY, Burge HA, Brain JD. The time course of responses to intratracheally instilled toxic Stachybotrys chartarum spores in rats. Mycopathologia 2000;149:27–34. 5. Hodgson MJ, Morey P, Leung WY, et al. Building-associated pulmonary disease from exposure to Stachybotrys chartarum and Aspergillus versicolor. J Occup Environ Med 1998;40(3):241–9. 6. Fujita J, Yoshinouchi T, Ohtsuki Y, et al. Non-specific interstitial pneumonia as pulmonary involvement of systemic sclerosis. Ann Rheumatic Dis 2001;60:281–3.