Hypersensitivity pneumonitis develops following sensitization to innumerable organic aerosols and chemical antigens, many found ubiquitously. An illustrative case is presented, demonstrating atypical hypersensitivity pneumonitis resulting from a commonly found organism.
A 55 year-old woman with no smoking history reported five years’ progressive exertional dyspnea. Shortly preceding the onset of her dyspnea, she abruptly developed a minimally productive cough, which persisted until her presentation. Multiple courses of antibiotics and β-agonists failed to relieve her symptoms, which varied over time. She denied fevers or sweats, and no ill-contacts were identified. No relevant occupational or environmental exposure history was elicited. Examination revealed only trace, scattered wheezes on forced expiration. Pulmonary function testing demonstrated low-normal lung volumes with a diffusing capacity of 53% predicted, but no inducible airflows obstruction. High resolution CT images demonstrated mosaic attenuation of both lungs, with regional air trapping, scattered ground glass infiltrates, and mild lymphadenopathy. Chronic interstitial pneumonia was seen on lung biopsy, with non-necrotizing granulomata, bronchiolitis, and multinucleated giant cells. Pseudozyma was cultured from the biopsy specimen. The patient was treated with corticosteroids for Pseudozyma-induced hypersensitivity pneumonitis, with prompt symptomatic, radiographic and gas exchange improvement.DISCUSSION: Fungal organisms are among the more typical precipitants of immune-mediated lung injury. The fungal order Ustilaginales, including Pseudozyma/Tilletiopsis species, contains the phytopathogenic corn and grain smuts which cause crop losses worldwide. Yet, despite their ubiquity, these organisms have rarely been reported to induce hypersensitivity pneumonitis. While antigen avoidance was impossible, this patient responded favorably to corticosteroid therapy.
The intriguing rarity of corn and grain smut-induced lung injury may eventually offer insight into the pathogenesis of hypersensitivity pneumonitis. It also reminds clinicians that the absence of an obvious exposure history cannot exclude the diagnosis of hypersensitivity pneumonitis, due to its countless causes.
S.E. Evans, None.