Update on the Epidemiology of Pulmonary Nontuberculous Mycobacterial Infections

Kendall, B.; Winthrop, Kevin

doi:10.1055/s-0033-1333567

Cited by 195 publications

(189 citation statements)

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“…The incidence of pulmonary nontuberculous mycobacterial (PNTM) disease is increasing in many regions of the world (1)(2)(3). PNTM disease frequently occurs in slender middleaged and older females (4).…”

Section: Introductionmentioning

confidence: 99%

Changes in cholesterol level correlate with the course of pulmonary nontuberculous mycobacterial disease

Hong

Yang

et al. 2016

J. Thorac. Dis.

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Background: Nutritional assessment is important in patients with pulmonary nontuberculous mycobacterial (PNTM) disease. The therapeutic effect of a cholesterol-rich diet in tuberculosis (TB) patients has been demonstrated, but the role of cholesterol in PNTM disease is unclear. This study evaluated the sequential changes in nutritional markers, including cholesterol, total lymphocyte count and visceral fat volume, according to the PNTM disease course. Methods:This was an age-, sex-and number of comorbid diseases-matched case-control analysis of 89 patients with PNTM disease and 356 controls, who were participants in a Korean national survey. Conclusions: These findings suggest that the change in cholesterol level may be a marker of disease progression in patients with PNTM disease. Results

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Section: Introductionmentioning

confidence: 99%

Changes in cholesterol level correlate with the course of pulmonary nontuberculous mycobacterial disease

Hong

Yang

et al. 2016

J. Thorac. Dis.

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“…The continuing high global incidence of and death due to tuberculosis infections [1] and the dramatic increase in pulmonary NTM disease globally over the past three decades [2] underscores the need to further understand the complex host immune responses to mycobacterial exposure in order to develop effective prophylactic and therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Restoration of innate immune activation accelerates Th1‐cell priming and protection following pulmonary mycobacterial infection

et al. 2014

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The immune mechanisms underlying delayed induction of Th1-type immunity in the lungs following pulmonary mycobacterial infection remain poorly understood. We have herein investigated the underlying immune mechanisms for such delayed responses and whether a selected innate immune-modulating strategy can accelerate Th1-type responses. We have found that, in the early stage of pulmonary infection with attenuated Mycobacterium tuberculosis (M.tb H37Ra), the levels of infection in the lung continue to increase logarithmically until days 14 and 21 postinfection in C57BL/6 mice. The activation of innate immune responses, particularly DCs, in the lung is delayed. This results in a delay in the subsequent downstream immune responses including the migration of antigen-bearing DCs to the draining lymph node (dLN), the Th1-cell priming in dLN, and the recruitment of Th1 cells to the lung. However, single lung mucosal exposure to the TLR agonist FimH postinfection is able to accelerate protective Th1-type immunity via facilitating DC migration to the lung and draining lymph nodes, enhancing DC antigen presentation and Th1-cell priming. These findings hold implications for the development of immunotherapeutic and vaccination strategies and suggest that enhancement of early innate immune activation is a viable option for improving Th1-type immunity against pulmonary mycobacterial diseases.Keywords: DCs r Delayed Th1 immunity r FimH r Mycobacterium r Tuberculosis Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionPulmonary mycobacterial infection is mainly caused by Mycobacterium tuberculosis (M.tb), the causative agent of tuberculosis (TB), and by other slow growing less virulent nontuberculous Correspondence: Dr. Zhou Xing e-mail: xingz@mcmaster.ca mycobacterial (NTM) species including M. avium and M. kasasii. The continuing high global incidence of and death due to tuberculosis infections [1] and the dramatic increase in pulmonary NTM disease globally over the past three decades [2] underscores the need to further understand the complex host immune responses to mycobacterial exposure in order to develop effective prophylactic and therapeutic strategies.Protective immunity against mycobacterial infection requires the presence of a robust adaptive Th1-type response at the site of Eur. J. Immunol. 2014Immunol. . 44: 1375Immunol. -1386 infection. Upon exposure to the bacterium, mycobacteria is taken up by sentinel APCs such as DCs and delivered to the draining lymph node (dLN) [3,4]. On arrival, these APCs present mycobacterial antigen to naive T cells within the dLN, thereby priming the antigen-specific T cells to a Th1 phenotype and stimulating their expansion [5]. The Th1 cells are then recruited back to the site of infection, and the secretion of Th1 cytokines such as IFN-γ by these cells is critical to activation of infected APCs to control bacterial growth [6]. However, one of the defining characteristics of host defense toward mycobacterial patho...

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“…However, these measures have their own limitations and may over-or underestimate disease burden (1,2,9). The chronic and slowly progressive nature of the disease, with required treatment of at least 12-18 months, leads to costly prescription medications and recurring hospital visits as a result of relapse or reinfection (10)(11)(12)(13)(14).…”

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confidence: 99%

The Burden of Pulmonary Nontuberculous Mycobacterial Disease in the United States

et al. 2015

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Rationale: State-specific case numbers and costs are critical for quantifying the burden of pulmonary nontuberculous mycobacterial disease in the United States.Objectives: To estimate and project national and state annual cases of nontuberculous mycobacterial disease and associated direct medical costs.Methods: Available direct cost estimates of nontuberculous mycobacterial disease medical encounters were applied to nontuberculous mycobacterial disease prevalence estimates derived from Medicare beneficiary data (2003)(2004)(2005)(2006)(2007). Prevalence was adjusted for International Classification of Diseases, 9th Revision, undercoding and the inclusion of persons younger than 65 years of age. U.S. Census Bureau data identified 2010 and 2014 population counts and 2012 primary insurance-type distribution. Medical costs were reported in constant 2014 dollars. Projected 2014 estimates were adjusted for population growth and assumed a previously published 8% annual growth rate of nontuberculous mycobacterial disease prevalence. Measurements and Main Results:In 2010, we estimated 86,244 national cases, totaling to $815 million, of which 87% were inpatient related ($709 million) and 13% were outpatient related ($106 million). Annual state estimates varied from 48 to 12,544 cases ($503,000-$111 million), with a median of 1,208 cases ($11.5 million). Oceanic coastline states and Gulf States comprised 70% of nontuberculous mycobacterial disease cases but 60% of the U.S. population. Medical encounters among individuals aged 65 years and older ($562 million) were twofold higher than those younger than 65 years of age ($253 million). Of all costs incurred, medications comprised 76% of nontuberculous mycobacterial disease expenditures. Projected 2014 estimates resulted in 181,037 national annual cases ($1.7 billion).Conclusions: For a relatively rare disease, the financial cost of nontuberculous mycobacterial disease is substantial, particularly among older adults. Better data on disease dynamics and more recent prevalence estimates will generate more robust estimates.Keywords: cost analysis; epidemiology; nontuberculous mycobacteria; pulmonary

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Update on the Epidemiology of Pulmonary Nontuberculous Mycobacterial Infections

Cited by 195 publications

References 42 publications

Changes in cholesterol level correlate with the course of pulmonary nontuberculous mycobacterial disease

Changes in cholesterol level correlate with the course of pulmonary nontuberculous mycobacterial disease

Restoration of innate immune activation accelerates Th1‐cell priming and protection following pulmonary mycobacterial infection

The Burden of Pulmonary Nontuberculous Mycobacterial Disease in the United States

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