To the Editor: Recent advances in the understanding of antimycobacterial immune response have led to descriptions of predisposing conditions to dissemination of nontuberculous mycobacteria (NTM) infection. The interferongamma (IFN-γ)/interleukin-12 (IL-12) axis is a critical pathway for intracellular killing of mycobacteria (online Technical Appendix Figure, http://wwwnc. cdc. gov/EID/article/22/6/15-1860-Techapp. pdf)(1). We report a case of disseminated NTM infection in a woman from Laos who showed IFN-γ autoantibodies. We also conducted a literature review to review similar cases. A previously healthy 50-year-old woman from Laos was referred to Hospices Civils de Lyon, France, for fever and generalized lymphadenopathies; pathological examination revealed a nonnecrotizing granuloma. Culture yielded Mycobacterium fortuitum. After a 3-month azithromycin/ciprofloxacin regimen, symptoms resolved. A few months later, a computed tomography scan showed persistence of enlarged mediastinal lymph nodes; biopsy disclosed nonspecific sinus histiocytosis. Mycobacterial cultures were negative. One month later, the patient reported intense dorsal spine pain. She was diagnosed with multifocal vertebral osteomyelitis, and tissue specimens tested positive for M. intracellulare. Azithromycin/ciprofloxacin was prescribed again. At 6 months, lesions worsened, and epidural abscess led to spinal cord compression, requiring decompressive laminectomy. Postoperative cultures were positive for M. intracellulare. Treatment was changed to azithromycin, rifabutin, ethambutol, and amikacin for 2 weeks, then rifabutin and moxifloxacin, which led to clinical improvement.

The patient experienced 2 episodes of thoracic herpes zoster concomitantly to each episode of illness. The recurrent NTM infection led us to investigate her immune status. Results of standard immunologic tests (leukocyte, serum level of immunoglobulin isotypes, and T-, B-, and NK0cell counts) and in vitro T-cell proliferation were normal; HIV testing was negative. Given its critical role in Mycobacteria clearance by host cells, we used IFN-γ whole-blood activation to investigate further. IFN-γ plasma level was undetectable, excluding complete forms of IFN-γ R1/R2. IL-12 p40 subunit plasmatic level was decreased, but the IL-12 receptor was present and functional. In addition, both BCG and IL-12 stimulations failed to trigger IFN-γ production. Ultimately, the detection of IFN-γ autoantibodies in high levels explained these abnormalities. Antimycobacterial treatment was continued for 2 years, then changed to azithromycin suppressive therapy; IFN-γ autoantibodies remained positive at the time of this report, 2 years after azithromycin initiation.