Case Presentation: A 58 year-old male with chronic obstructive pulmonary disease (COPD) and two recent admissions to an outside hospital for pneumonia presented with fever, chills, and a productive cough of three months duration. On admission, he was afebrile, tachycardic, and required his home two liters of supplemental oxygen. Physical exam was notable for coarse crackles in bilateral upper lobes. Laboratory studies demonstrated leukocytosis of 14.8/mm3. Chest radiograph showed biapical bullous changes with superimposed pleural and parenchymal scarring. The patient was admitted and started on intravenous vancomycin, pipercillin-tazobactam, and azithromycin. Chest computerized tomography scan showed large, bilateral, cavitary lesions and superinfection of apical bullae. Quantiferon testing and acid-fast bacilli smears were negative. On hospital day (HD) 2, the patient developed worsening cough, dyspnea, and fever of 39°C. On HD 3, he had worsening leukocytosis of 18.9/mm3 with elevation in erythrocyte sedimentation rate (ESR 53mm/hr) and C-reactive protein (CRP 152mg/L). Further history revealed that two days prior to his initial presentation, the patient had burned moldy hay and was exposed to a large amount of smoke. On HD 6, his sputum culture grew Aspergillus fumigatus. Antibiotics were transitioned to IV voriconazole, oral metronidazole, and oral trimethoprim-sulfamethoxazole. After 24 hours, the patient’s cough and dyspnea improved. WBC decreased to 16.8/mm3. He was transitioned to oral voriconazole and was discharged on a prolonged course. One month later, the patient followed up in clinic with resolution of symptoms and significant improvement in chest radiography.

Discussion: Chronic pulmonary aspergillosis (CPA) presents as an indolent course of fever, malaise, and productive cough in immunocompetent patients with underlying structural lung disease. The radiographic findings of CPA may not emerge in the early stages, and in our patient’s case, they were likely misidentified as the patient’s underlying disease. Early identification of this patient’s environmental exposure and increased clinical suspicion would have prevented delay in diagnosis, repeat hospitalizations, and unnecessary antimicrobial exposure.  Patients with untreated CPA have a five-year mortality approaching 80%, highlighting the importance of early and accurate diagnosis.

Conclusions: CPA may imitate other causes of pneumonia, especially in patients with underlying lung abnormalities. While untreated CPA is associated with high morbidity and mortality, it is under-recognized and thus incumbent upon the hospitalist to maintain a high index of suspicion when evaluating recurrent or difficult-to-treat pneumonia in patients with underlying structural lung disease. Hospitalized patients with chronic lung diseases and recurrent pneumonia should be evaluated for infection with Aspergillus spp starting with a detailed history and identification of environmental exposures.