Case of Pseudomembranous Necrotizing Tracheobronchial Aspergillosis in an Immunocompetent Host
A 44-year-old Korean male presented with a fever, non-productive cough, and myalgias for 10 days. For the previous 5 years, he had been treated for hypertension with an angiotensin-converting enzyme inhibitor. Prior to admission, he was treated with oral quinolone for 7 days by the outpatient department, but his condition progressively worsened with resting dyspnea, a productive cough, and a fever for 2 days before admission to the Wonkwang University Hospital, Iksan, Korea. The patient was a 30-pack-a-year ex-smoker, and had no history of previous respiratory diseases nor a specific family history.\nOn admission, he had a temperature of 38.6℃, blood pressure of 120/80 mmHg, heart rate of 90 b.p.m, and respiratory rate of 30 breaths/min. Chest auscultation was significant for bilateral inspiratory coarse, crackles and end-expiratory wheezing around the perihilar areas. Arterial blood gas values on room air were: pH 7.343, PaCO2 41.2 mmHg, PaO2 59.2 mmHg, and SaO2 90.7%. The WBC was 19,580/mm3 (neutrophils 82.5%); the ESR was 71 mm/h; and the C-reactive protein was 184.6 mg/L. The percentage of hemoglobin A1c in the blood was 5.8%. The blood urea nitrogen was 32.4 mg/dL and the creatinine was 1.32 mg/dL. The random glucose of capillary blood on admission was 117 mg/dL. A chest X-ray obtained on admission demonstrated bilateral bronchial wall thickening with perihilar area and lower lobe predominance (). The results of the initial sputum stains and sputum and blood cultures were all negative. The HIV test also was negative.\nThe patient received empirical therapy with cefoperazone/sulbactam and vancomycin for 4 days, but rapidly deteriorated with a high fever, increasing dyspnea, and hypoxemia. He developed respiratory failure with severe CO2 retention, and was admitted to the intensive care unit and mechanically ventilated. On the fifth day of therapy, chest CT and fiberoptic bronchoscopy were performed because of a rapidly increasing respiratory acidosis with hypoxemia in contrast to the chest X-ray lesions. A chest CT scan revealed only bilateral peribronchial infiltrates with patent bronchi and no consolidation of the parenchyma (). A bronchoscopy demonstrated extensive whitish exudative membranes covering the trachea and both mainstem bronchi (). The endobronchial biopsy specimens and bronchial washing fluid revealed Aspergillus species without parenchymal invasion (). A high fever persisted and 2 days later the patient developed refractory septic shock and hypoxemia. Despite using IV amphotericin B and supportive care, acute deterioration followed with refractory hypoxemia and oliguria, resulting in a fatal cardiac arrest on the fifth day of the intensive care unit stay. We could not perform a post-mortem examination because of the refusal of his family members.