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This chapter focuses on the diagnosis and management of pulmonary infections caused by nontuberculous mycobacteria (NTM), a large group of species of the genus Mycobacterium that can cause disease in humans and that are distinct from other classic mycobacterial pathogens, such as M. leprae, M. ulcerans, and species of the M. tuberculosis complex. Despite the diversity of this group of pathogens, the clinical presentation and diagnostic approach to most pulmonary NTM infections is similar, and the vast majority of disease is caused by a handful of species, including those of the M. avium (MAC) and M. abscessus (MAb) complexes, as well as M. kansasii and M. xenopi. Management differs according to species, extent of disease, and susceptibility patterns. We describe here the epidemiology and pathogenesis of pulmonary NTM infections and a general diagnostic approach. We then proceed to the treatment regimens used for common NTMs and discuss the nuances associated with management in special populations.


There are 192 known species of the genus Mycobacterium.1 Of these, several are M. tuberculosis complex species that cause tuberculosis in humans, while M. leprae causes leprosy and M. ulcerans causes Buruli ulcer. Most of the remainder are known as nontuberculous mycobacteria (NTM), which are environmental organisms typically found in soil and water. Together, they constitute the greatest source of pulmonary mycobacterial infection in developed nations. Most human pulmonary NTM disease is caused by species of the M. avium and M. abscessus complexes, as well as M. kansasii and M. xenopi; others, such as M. gordonae, are generally considered contaminants.2 The relative contributions of each species responsible for infection may vary geographically.3–5 Overall, prevalence has increased by up to 8.2% per year in recent decades, representing up to 48 cases per 100,000 in the United States as of 2012.2,6

Among risk factors for pulmonary NTM disease that predispose to infection, a common theme is underlying structural lung abnormalities that impede physiologic airway clearance or ciliary function. Notable among these underlying diagnoses are bronchiectasis, chronic obstructive pulmonary disease, pneumoconiosis, and pulmonary alveolar proteinosis. Cystic fibrosis, including the presence of cystic fibrosis transmembrane conductance regulator (CFTR) changes not associated with clinical cystic fibrosis, and α1-antitrypsin deficiency are two genetic conditions that predispose to pulmonary NTM infection.7,8 Additional associations that have been observed are listed in Table 131-1. Although immunodeficiency is a risk factor for both pulmonary and disseminated NTM infections,9 the vast majority of pulmonary NTM infection occurs in the absence of known immunodeficiency.

TABLE 131-1Common Risk Factors and Associations with Pulmonary NTM Infection

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