Endobronchial Mass Due to MAC Infection Despite Macrolide Prophylaxis

Abstract

INTRODUCTION: Mycobacterium Avium Complex (MAC) is an ubiquitous bacteria known to cause lung disease in immunosuppressed individuals. Pulmonary involvement can range from asymptomatic colonization to diffuse parenchymal disease and cavitary lesions. We present the case of an AIDS patient recently started on antiretroviral therapy that developed a large polypoid endobronchial mass caused by MAC infection. CASE PRESENTATION: A 38 year old African American female presented to the hospital with one month history of progressive shortness of breath, non productive cough and recent onset hemoptysis. She has a four year history of HIV disease and previous intermittent exposure to antiretrovirals, with poor compliance. Her symptoms developed three weeks after starting therapy with raltegravir, efavirenz, emtricitabine, tenofovir as well as MAC prophylaxis with azythromycin. Her CD4 count at presentation was 31 cells/mcL compared to 2 cells/mcL six weeks earlier. Her initial chest radiograph showed patchy multilobular densities in the right lung. Chest CT showed a large right paratracheal mass extending into the lower trachea and right mainstem with infiltrates in the right upper and middle lobes. Bronchoscopy revealed a right sided tracheal polypoid mass extending to the main carina. Forceps biopsy was performed. The pathology report showed granulation-like tissue with abundant macrophages that contained numerous acid-fast bacilli and no evidence of malignancy. The large number of bacilli within macrophages suggested infection by MAC, which was confirmed by growth on bronchoalveolar lavage sample. She was started on combination therapy with ethambutol, azithromycin and levofloxacin. A follow-up chest CT, three weeks after, revealed marked decrease in the endotracheal mass. At four weeks after discharge patient reported no shortness of breath, occasional cough and no hemoptysis. DISCUSSION: Initiation of HAART induces immune reconstitution that is typically uneventful. We believe our patient developed immune reconstitution syndrome in response to MAC infection that was asymptomatic prior to HAART. Primary prophylaxis for MAC at the time HAART was initiated did not prevent the pulmonary manifestations. Her favorable outcome likely reflects further immune reconstitution as well as antibiotics. CONCLUSIONS: Tumor-like endobronchial masses due to MAC can develop as part of immune reconstitution even with macrolide prophylaxis. Onset of respiratory symptoms and pulmonary infiltrates within 2 to 4 weeks of initiation of antiretroviral therapy should prompt evaluation for mycobacterial disease.