INTRODUCTION: The spectrum of pulmonary infections caused by aspergillus species correlates well with the integrity of the host's immune system. Invasive pulmonary aspergillosis (IPA) characteristically affects patients with prolonged neutropenia, neutrophil dysfunction, hematopoetic stem cell transplantation (HSCT), patients receiving chemotherapy, solid organ transplantation, Acquired Immunodeficiency Syndrome, advanced chronic obstructive lung disease and chronic liver disease. Only two percent of cases in one review occur in immunocompetent and mildly immunocompromised patients. Pulmonary infarction, hemorrhage, tracheobronchitis, alveolar infiltrates, nodules and cavities are well notable features of IPA. We present a case of a patient with prostate cancer, presenting with IPA manifested by an endobronchial mass lesion.
CASE PRESENTATION: The patient was an 81-year-old man with hypertension, diabetes mellitus and prostate cancer diagnosed 20 years earlier and treated with radiation therapy. He had prostatectomy 9 months ago for locally advanced recurrence. He had hematuria, weight loss and a two week history of cough productive of clear sputum with streaks of blood. His medications included bicalutamide (casodex). He was a lifelong non-smoker. He appeared well-nourished. His temperature was 96 F, heart rate 74, respiratory rate 16, blood pressure 104/79. He had pale mucous membranes and oral thrush. Rectal exam revealed a firm mass. The remainder of the exam was normal. Lab data:Sodium 124, potassium 5.4, Bun 19, creatinine 1.1, glucose 189, wbc 9.1, hemoglobin 6.9, hematocrit 22, mcv 74, platelet count 449, PSA 36.13, albumin 2.9, AST 95, ALT 66, alkaline phosphatase 275, calcium 9.88 and cortisol 34.25. Urinalysis showed many white blood cells, red blood cells and bacteria. Blood gas on room air revealed a PH 7.43, Pco2 30, Po2 90 and sat 97%. CXR showed a mass in the right upper hemithorax arising from the pleura, a right pleural effusion, small bilateral nodules and left upper lobe collapse. CT of the chest also revealed subcarinal and left hilar lymph nodes, bilateral effusions and a left hilar mass compressing the descending pulmonary artery. There was an intrahepatic mass.Cystoscopy showed infiltration of the corpus carvernosa with prostate cancer. He declined chemotherapy. He developed respiratory failure and was intubated. Bronchoscopy revealed edematous right bronchial and left lower lobe segments. The left upper lobe orifice was occluded by a necrotic mass. The impressions were metastatic prostate cancer, another tumor and infection. Biopsy results showed a PSA negative cluster of atypical cells and aspergillus fumigatus. There were numerous aspergillus fumigatus and candida tropicalis hyphae on the bronchoalveolar lavage. Amphotericin was given but the patient's condition worsened and ventilatory support was discontinued at his family's request.
DISCUSSIONS: IPA was first described in 1953. It compromises more that 60% of mycoses found at autopsy and occurs in more that 10% of patients receiving HSCT. Mortality rates range between 30-90% in treated patients. It presents typically with mild hemoptysis, pleuritic chest pain and a cavitary lung lesion. Multiple nodules, wedge shaped halo and air-crescents are seen on CT. There is hematogenous spread due to blood vessel invasion. IPA is the most severe in the spectrum of infections arising from inhalation of aspergillus spores. They are ubiquitous in the soil, but can be found in hospital taps and shower heads. Intravenous voriconazole is now the treatment of choice. Literature search has revealed no prior report of invasive aspergillosis presenting endobronchially.
CONCLUSION: This case is an unusual presentation of IPA. Endobronchial metastasis from prostate cancer is exceedingly rare (one case report), but other radiographic features described above mimicked pulmonary metastases. Given the eight fold increase in incidence of IPA over the last two decades, this case underscores the importance of a heightened index of suspicion of IPA in patients without prototypical risk factors.
DISCLOSURE: Reverly John, None.