Endobronchial obstructive lesions in patients with HIV are uncommon. However, a marked worsening of clinical findings even after a definitive diagnosis and treatment has commenced is much more unusual.
A 31 year old male with HIV with a recent history of incarceration presented to an outside hospital with fever, syncope, and an abnormal chest x-ray. He was admitted and treated for pneumonia then subsequently discharged to home. His fevers recurred thus he was readmitted to our institution with a persistent consolidation in the left upper lobe. Sputum smears were positive for acid fast bacilli. He was started on INH, rifampin, ethambutol, and pyrazinamide. Antiretrovirals were started 3 weeks later with improved CD4 counts and decreased viral load. After 2 months, despite compliance with anti-mycobacterial & anti-retroviral therapies, he presented with chest pain, shortness of breath, and hemoptysis. Chest CT showed progressive LUL consolidation and volume loss with a suspicion for an obstructive endobronchial lesion. Bronchoscopy was performed revealing several sessile polypoid endobronchial lesions at the main carina and left mainstem bronchus. Endobronchial biopsies were and and histopathology showed granulomatous inflammation with numerous acid fast bacilli consistent with mycobacteria. Initial sputum culture and subsequent respiratory cultures revealed Mycobacterium kansasii sensitive to rifampin.
Mycobacterium kansasii is the second most common cause of nontuberculous mycobacterial disease in the US. Clinical presentation parallels that of tuberculosis with findings including upper lobe parenchymal cavitary infiltrates. Endobronchial lesions are very unusual for M. kansasii but a few case reports have been published with this finding. The unique feature of this case is the patient’s clinical worsening after initiation of anti-mycobacterial agents. Such clinical course & manifestations may be related to immune reconstitution inflammatory syndrome (IRIS). IRIS is a clinical syndrome demonstrating a paradoxical worsening of preexisting infections following initiation of highly active antiretroviral therapy (HAART). It is most associated with M. tuberculosis but has not yet been reported in M. kansasii. The 2007 ATS/IDSA Statement on the diagnosis, prevention, and treatment of nontuberculous mycobacterial disease recommends treatment of M. kansasii with rifampin, ethambutol, and isoniazid for a duration that should include 12 months of negative sputum cultures. Patients with severe immunodeficiency with CD4 counts of <50 who begin HAART within the first 2 months of anti-mycobacterial treatment are considered at high risk for developing IRIS. However, this risk may be necessary to avoid developing other opportunistic infections. Management of this syndrome is supportive and HAART is generally continued. Corticosteroid therapy may be considered in severe life-threatening manifestations of IRIS.
This case report highlights two important unique features: (1) Mycobacterium kansasii pulmonary disease commonly presents with cavitary parenchymal infiltrates but may also present with obstructing endobronchial lesions. (2) Immune reconstitution inflammatory syndrome (IRIS) should be considered in severely immunosuppressed patients recently started on HAART wherein there is paradoxical worsening of clinical features.
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