Disseminated Mycobacterium avium complex infection presenting as superior vena cava syndrome in a patient with anti-interferon-gamma autoantibody: a case report

Abstract

Background: Superior vena cava (SVC) syndrome is primarily associated with malignancy, with infectious etiologies being less common. Tuberculosis is the most common infectious cause of SVC syndrome (SVCS). There has been no report of SVCS caused by nontuberculous mycobacteria (NTM). Here, we present a case of SVCS caused by disseminated Mycobacterium intracellulare in a patient who was previously healthy and subsequently tested positive for anti-interferon gamma autoantibodies. Case presentation: A 38-year-old woman with no significant past medical history presented with a 3-month history of fever, progressive dyspnea, productive cough, and weight loss. She also reported a one-year history of ulcerative wounds on her right ankle and chest wall. On examination, she exhibited fever, tachycardia, tachypnea, facial and bilateral upper extremity edema, and cervical lymphadenopathy. Chest computed tomography revealed a 4-cm right paratracheal mass, causing SVC obstruction, and suspicious lytic lesions in the thoracic bones. Radiologic imaging of the right ankle showed an osteolytic lesion. Tissue specimens from lymph node biopsy and ankle wound demonstrated positive staining for acid-fast bacilli. While awaiting culture results, an anti-interferon gamma autoantibody assay was performed and returned positive. Mycobacterial culture subsequently identified M. intracellulare. Empiric therapy for NTM infection was initiated with imipenem and azithromycin. Following species identification, treatment was switched to a combination of azithromycin, rifampin, ethambutol, and levofloxacin. Clinical symptoms and imaging findings gradually resolved following the treatment. Conclusion: Nontuberculous mycobacterial (NTM) disease is a rare cause of superior vena cava syndrome. In cases of disseminated NTM infection, a thorough evaluation for associated underlying conditions, particularly adult-onset immunodeficiency (AOID), linked to anti-IFN-γ autoantibodies, is essential.