Gardening Can Kill You
Abstract & Commentary
David A. Stevens, MD, FACP., Chief, Division of Infectious Diseases, Department of Medicine, Santa Clara Valley Medical Center, San Jose, CA; Professor of Medicine, Stanford University Medical School
Dr. Stevens reports no financial relationship relevant to this field of study.
Synopsis: A patient developed acute respiratory failure and died after exposure to dust while mulching in his garden. While attributed by the author to invasive disease by aspergillus, other considerations, such as extrinsic allergic alveolitis must be considered.
Source: Russell K, et al. Gardening can seriously damage your health. Lancet. 2008;371:2056.
As mentioned in the article by Russell et al, a patient was admitted to the hospital in the United Kingdom after a week's febrile respiratory illness; he had previously been in good health. Admission chest radiograph showed many nodules. His illness progressed to respiratory failure, with a radiographic picture of consolidation; he died a few days after admission. His history revealed his symptoms had started less than 24 hours after mulching in his garden, where he was exposed to clouds of dust. Sputum cultures in the hospital had grown Aspergillus fumigatus, and serum testing revealed a high serum Aspergillus galactomannan level and "significant" Aspergillus antibodies. He was given intravenous amphotericin B as a result of these findings.
This report was given attention in international media because of the implication of gardening causing aspergillosis. Russell et al stated that "inhalation of spores" can cause disease that "can be acute and invasive," and suggested that their patient had invasive disease ("Unlike most patients with acute, invasive aspergillosis, our patient did not seem to be immunosuppressed. . ."). However, Russell et al provide no evidence that their patient had invasive disease; the definitive basis for this would be documentation of tissue invasion, and suggestive support could be provided by radiographic evidence of cavitation or clinical evidence of hemorrhage. They indicate, correctly, that "acute aspergillosis, after contact with decayed plant matter," may occur and "may be considered an occupational hazard for gardeners," but I believe may incorrectly juxtapose this with their implication of "invasive disease." Of note, corticosteroids were apparently not given, which would be consistent with a working diagnosis of invasive aspergillosis.
Commentary
Most forms of acute aspergillosis that occur "after contact with decayed plant matter" are allergic forms of the disease, usually acute provocation of asthma. I believe the best pathophysiologic explanation of this patient's illness is as a variant of extrinsic allergic alveolitis. The pathophysiology is presumed similar to that entity when there is massive inhalation of Aspergillus spores, usually in farm environments. Symptoms are classically present within 24 hours, as was the case in this patient, and granulomas are found on biopsy. The classical entity of extrinsic allergic alveolitis is an unusual form of Aspergillus lung disease, and has been most associated with Aspergillus clavatus in malt workers. The patients develop dyspnea and fever four hours after exposure, and the clinical picture resembles the better-known "bird-fancier's lung" or "farmer's lung" (due to other allergens); diffuse micronodular infiltrates may be present at the time of symptoms. The patients have lgG precipitins and cell-mediated immune reactions against Aspergillus antigens, and granulomas are present on biopsy. Eosinophilia is not a feature. The scratch test is negative, though an intradermal test produces a reaction in four hours, with immunoglobulins and complement present on biopsy. Bronchial challenge, with antigen, as can be reproduced in the pulmonary function test laboratory, produces a reaction in four hours, with systemic symptoms and a restrictive defect, but without airway resistance. The entity can progress to irreversible fibrosis. Treatment of the acute or chronic form is uncertain, but corticosteroids have been used, and might be expected, to ameliorate inflammation, granulomas, and the cell-mediated component. It would be expected that antifungals would have no role in an allergic entity, but occasional cases have been described (Am Rev Resp Dis. 121:63), with a histopathology of granulomas with purulent microfoci, suggesting a tissue response to invasion; with a recommendation to use antifungals if the patient is unresponsive to steroid therapy.
Another possible explanation of this patient's illness is that he was a heterozygote for the congenital immuno-deficiency, chronic granulomatous disease (CGD), or had one of its genetic variants. A syndrome has been described in such persons (Clin Infect Dis. 45:673) of hypoxia, fever, and pulmonary infiltrates following inhalation of lots of Aspergillus from mulch. It is usually adult-onset, unlike the invasive pulmonary Aspergillus disease seen in children with classical CGD; the immunodeficiency may have been unknown prior to the exposure. The immunodeficiency is related to granulocyte failure to fire its NADPH oxidase enzyme, resulting in no effective cellular respiratory burst. In this type of "overwhelming mulch pneumonitis," the case fatality rate is 50%. The pathophysiology is suspected to be due to neutrophil damage from an ineffectual, but intense infiltration into the lung. Histopathology reveals dense neutrophil infiltration and pyogranulomas. Cavitation, vascular invasion, and hemorrhage do not occur and, as described, the serum galactomannan test is negative. The recommended therapy is corticosteroids and antifungals, and therapy with steroids must be sustained; premature tapering has been associated with exacerbations. The elevated galactomannan in the patient described could have been a false positive, such as from antibacterials given during the hospitalization.
These unusual entities need to be considered in the differential diagnosis of acute pneumonitis presenting after exposure to large quantities of Aspergillus spores.
As mentioned in the article by Russell et al, a patient was admitted to the hospital in the United Kingdom after a week's febrile respiratory illness; he had previously been in good health. Admission chest radiograph showed many nodules.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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