Nontuberculous mycobacteria represent over 190 species and subspecies that are present throughout the environment, and a subset of these include pathogens that can lead to infection in humans. In the United States, NTM disease rates are three- to fivefold higher than tuberculosis rates.[12,13] NTM infections can be subdivided into pulmonary and extrapulmonary infections. Patients with pulmonary infections are most likely to have MAC infection, whereas those with extrapulmonary disease may also have infection with Mycobacterium abscessus, Mycobacterium chelonae, and Mycobacterium fortuitum. Both slow-growing nontuberculous mycobacteria, including MAC and Mycobacterium kansasii, and rapidly growing nontuberculous mycobacteria, including M abscessus, can cause pulmonary infections. Because NTM infection can be insidious and therefore difficult to diagnose, it may not be immediately recognized as a cause of pulmonary symptoms in an affected individual.
Owing to the ubiquitous nature of nontuberculous mycobacteria, no risk factors for exposure are known. Routine screening for NTM infection is not recommended; however, further evaluation should be pursued in a patient with an unexplained cough, including chest CT and bronchoscopy. Although NTM infections may occur in immunocompetent individuals, those at higher risk include:
Patients in these high-risk groups are more likely to have progression of NTM infection and increased mortality rates. Oral and inhaled glucocorticoid therapies have also been reported as a risk factor for NTM infection.
Patients with rheumatoid arthritis may be at higher risk for infections owing to an increase in the production of CD28-null T cells that can downregulate antigen-presenting cell activity. Because of the systemic inflammatory nature of the disease, patients with rheumatoid arthritis often have pulmonary involvement as part of their disease process, which separately increases the risk for NTM pulmonary infection.
Beyond pathogenetic immune dysregulation and underlying pulmonary disease, immunosuppressive therapies lead to further reduction in immunity. TNF inhibitors are biologic agents used to treat patients with autoimmune conditions, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, psoriasis, and inflammatory bowel disease. TNF inhibitors are often the first class of biologic agents prescribed for patients with these conditions. To date, there are five reference drugs (etanercept, infliximab, adalimumab, golimumab, and certolizumab pegol) and over a dozen biosimilar products that fall under the category of TNF inhibitors.
These biologic agents lead to immunosuppression and increased risk for various opportunistic infections. In particular, TNF blockade increases the risk for granulomatous infections, including tuberculosis and NTM infections. TNF is a proinflammatory cytokine that is necessary for the formation and maintenance of granulomas, which are important for host defense against mycobacterial infections. TNF stimulates macrophages in granulomas to release interferon-gamma, which activates macrophages to kill mycobacteria. TNF blockade therefore reduces immunity against mycobacterial infection.
A study using the US Food and Drug Administration MedWatch database through 2007 identified a total of 59 cases of NTM pulmonary infection in the setting of TNF inhibitor therapy. MAC was the most common nontuberculous mycobacteria identified and was associated with pulmonary infection in older women with rheumatoid arthritis. Of the patients in the study, 65% were also receiving prednisone and 55% were also receiving methotrexate. A follow-up study in 2013 found that NTM infections were five to 10 times more likely in patients with rheumatoid arthritis on TNF inhibitor therapy than in those who were not taking TNF inhibitors. The same study found that NTM infections were more common than tuberculosis in the United States.
According to the American Thoracic Society and Infectious Diseases Society of America guidelines, the diagnosis of NTM infection is made in the setting of pulmonary or systemic symptoms, imaging findings of nodular or cavitary opacities on chest radiography, or high-resolution chest CT demonstrating bronchiectasis and bronchial wall thickening with multiple small centrilobular nodules, with exclusion of other diagnoses. Microbiologic evidence of NTM must be present and consist of either (1) a positive acid-fast bacilli culture on two sputum samples or one bronchial wash/bronchoalveolar lavage sample or (2) lung biopsy with mycobacterial histologic features with a positive culture on biopsy, sputum, or bronchial sample.
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