Abstract

To the Editor:

I am grateful to Lin et al¹ for their contribution to the knowledge of nontuberculous mycobacterial infections. However, I would like to make one comment. When assessing immunocompetence, we need to ask ourselves what are we looking for. It is well known that patients with deficiency of interferon gamma-IL12/R pathway (also known as Mendelian susceptibility to mycobacterial disease–MSMD) are prone to pulmonary and extrapulmonary infections caused by slow-growing nontuberculous mycobacteria. Patients with defects in the interferon gamma pathway are predisposed to mycobacterial diseases, while those with defects in the IL-12 pathway are frequently threatened by nontyphoid salmonellosis. Tuberculosis has been described in both of these signaling pathway defects. These disorders are genetically different but immunologically similar as impaired IFNgamma-mediated immunity is the common pathogenic mechanism accounting for mycobacterial infection in all patients.² The severity of the histological and clinical phenotype depends on the type of genetic defect. Genetic analysis of the IFNgamma/IL-12 pathway should improve our understanding of the human immune response to mycobacteria and help us elucidate the genetic bases of tuberculosis.³ In the patient reported, the assay to rule out this defect had not been performed. This is why when assessing immunocompetence in extrapulmonary infections by Mycobacterium szulgai, we should first rule out IFNgamma-IL12/R pathway defects.