A Case of Mycobacterium Avium-Intracellulare Following Initiation of Infliximab Therapy

Abstract

Purpose: Tumor necrosis factor (TNF)-α inhibitors have significantly impacted the treatment of inflammatory bowel disease and rheumatological disorders, but their use leaves patients susceptible to opportunistic infections. Mycobacterium avium-intracellulare (MAI) refers to two ubiquitous species, M. avium and M. intracellulare, collectively termed MAI. The mode of transmission is believed to be ingestion or inhalation. The bacterium is translocated across the epithelium of the gastrointestinal or respiratory tracts and infects resting macrophages. TNF-α is essential for macrophage activation, as well as granuloma formation and maintenance, all key components of host defense against intracellular pathogens. Thus, patients on TNF-α inhibitors are at increased risk of MAI infection, though exceedingly rare. Case Presentation: A 40 year-old Caucasian male recently diagnosed with ileocolonic Crohn's disease was started on infliximab after he failed to respond to 6-mercaptopurine, mesalamine, and prednisone. A negative PPD and chest x-ray were documented before initiating treatment. Six months later he presented with right-sided pleuritic chest pain and night sweats. He denied cough, sputum production, fevers or skin changes. He has a 13 pack-year tobacco history and is a truck driver with no international travel history. Examination was significant for fine crackles localized to the right upper lobe and was otherwise normal. CT-scan of the thorax revealed right upper lobe parenchymal destruction with cystic cavities. Bronchoscopy with bronchoalveolar lavage, performed to obtain a sputum specimen, was negative for acid-fast bacilli staining. Due to high clinical suspicion, infliximab was discontinued and four-drug tuberculosis therapy (isoniazid, pyrazinamide, ethambutol and rifampin) was initiated. Two weeks later, culture grew Mycobacterium avium-intracellulare with intermediate susceptibility to clarithromycin on testing. The patient remains off infliximab therapy and is completing a one-year course of ethambutol, rifampin and clarithromycin with repeat CT-scans every three months. Discussion: We report a rare case of Mycobacterium avium-intracellulare infection after initiation of TNF-α inhibitor therapy. Although it is uncommon, MAI must be in the differential diagnosis when a patient on anti-TNF-α therapy presents with new lung infiltrates.