INTRODUCTION: Pseudomonas infection is a risk factor for allergic bronchopulmonary aspergillosis (ABPA) in patients with cystic fibrosis(CF), possibly related to increased release of aspergillus fumigatus antigens. The role of pseudomonas in the course of ABPA in non-CF patients is unknown. We present a case of severe ABPA, cavitary pseudomonas pneumonia, and hemodynamically significant hemoptysis requiring lobectomy.
CASE PRESENTATION: A 52-year-old lifetime nonsmoking man presented emergently with hemoptysis. He had a vague history of childhood asthma, and a ten year history of “COPD” characterized by chronic cough and purulent sputum, partially responsive to antibiotics and brief courses of corticosteroids. Evaluation one year ago showed a computerized chest tomogram with severe bronchiectasis, normal serum immunoglobulins, alpha-1 antitrypsin level (MM phenotype), and normal sweat chloride. ABPA was diagnosed with sputum culture positive for aspergillus fumigatus, aspergillus anti-IgE of 34.5kU/L (3699% reference), and a total IgE of 1260 kU/l. Oral prednisone and voriconazole improved symptoms, decreased IgE (140 kU/l), and increased FEV1 from 0.69 to 1.2 liters. Sputum cultures during exacerbations showed nocardia asteroides, methicillin sensitive staphylococcus aureus, and stenotrophomonas, each specifically treated. Two months before admission, while continuing on voriconazole and prednisone, the patient developed a new thick-walled left upper lobe cavitary lesion. Bronchoalveolar lavage showed a pan-sensitive pseudomonas aeruginosa treated with six weeks of intravenous antibacterial therapy. One week after discontinuing antipseudomonal therapy he developed low grade fever and new bright red hemoptysis which resolved with embolization of both upper lobe bronchial arteries. Recurrent hemoptysis three weeks later(one week before admission) prompted a repeat embolization focused on neovascularization surrounding the left cavity. On presentation he was in mild respiratory distress, tachycardic, coughing up bright red blood with a 4 gm/dl drop in hemoglobin. Intubation with a double lumen ET tube demonstrated persistent left sided airway hemorrhage; at one week he underwent successful left upper lobectomy. Pathologic diagnosis was characteristic of ABPA with no evidence of invasive fungal infection: an 8x7x5 cm cavity containing necrotic fragments and hemorrhage, lined by granulation tissue with a thick fibrous capsule. The parenchyma demonstrated extensive obstructive pneumonia, bronchiectasis, bronchopneumonia and emphysema, and fungal elements within the bronchial lumen surrounded by acute and chronic inflammation. Acid fast and auramine rhodamine mycobacterial stains were negative.
DISCUSSIONS: Although early treatment with oral corticosteroid therapy was delayed in this patient due to an atypical presentation and years of erratic uncoordinated treatment associated with a disadvantageous social situation, he improved markedly on ABPA therapy. The intrapulmonary cavity and associated florid inflammation lesion prompted an initial radiological suspicion of invasive aspergillosis, but surgical pathology showed only ABPA. We speculate that the interaction of pseudomonas and aspergillus observed in CF patients may also occur in non CF patients.
CONCLUSION: ABPA can be missed in patients presenting as adult chronic bronchitis. Massive hemoptysis can occur and lobectomy is lifesaving in this unusual setting. Prolonged antipseudomonal therapy may be required in patients with ABPA similar to CF patients, and suggest the possibility that an interaction between the pseudomonas infections and aspergillus enhanced the inflammatory response, mimicking invasive aspergillus infections. While antibiotic treatment for 6 weeks was considered sufficient for cavitary pneumonia, we now would consider prolonged antibacterial treatment as for a lung abscess.
DISCLOSURE: Marina Dolina, None.