Vulnerability to Nontuberculous Mycobacterial Lung Disease or Systemic Infection Due to Genetic/Heritable Disorders

Chan, Edward D.

doi:10.1007/978-3-319-93473-0_4

Cited by 5 publications

(5 citation statements)

References 100 publications

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“…Isolated NTM lung disease may occur de novo in normal lungs but is more likely to develop in those with pre-existing bronchiectasis or COPD. The three most common genetic disorders associated with bronchiectasis are CF, AAT deficiency, and PCD (3,4). Other disorders known to be associated with bronchiectasis include Williams-Campbell syndrome (cartilage defect), Mounier-Kuhn syndrome (elastin defect resulting in marked airway dilatation), and Sjogren's syndrome (dry, inspissated mucus leading to bronchiectasis) as well as sequelae from suboptimally treated pyogenic bacterial pneumonia or tuberculosis.…”

Section: Discussionmentioning

confidence: 99%

Non-tuberculous mycobacterial lung disease due to multiple “minor” risk factors: an illustrative case and a review of these “lesser elements”

Moon

Guillaumin²,

Chan

2020

J Thorac Dis

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Section: Discussionmentioning

confidence: 99%

Non-tuberculous mycobacterial lung disease due to multiple “minor” risk factors: an illustrative case and a review of these “lesser elements”

Moon

Guillaumin²,

Chan

2020

J Thorac Dis

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“…Typically, these two species are both reported as "MAC," but their environmental sources differ, and there is evidence indicating differential pathogenicity and clinical disease severity between the two species [6,7]. Since MAC is ubiquitous in the environment and exposure is likely unavoidable, it is apparent that some form of host susceptibility must also be present for MAC lung disease to occur [3,4,8]. In that context, pulmonary MAC disease occurs primarily in patients with structural lung disease, especially bronchiectasis and emphysema, without demonstrable systemic immune suppression [3,4,8].…”

Section: Introductionmentioning

confidence: 99%

“…Since MAC is ubiquitous in the environment and exposure is likely unavoidable, it is apparent that some form of host susceptibility must also be present for MAC lung disease to occur [3,4,8]. In that context, pulmonary MAC disease occurs primarily in patients with structural lung disease, especially bronchiectasis and emphysema, without demonstrable systemic immune suppression [3,4,8]. Pathophysiologic questions are further complicated because MAC lung disease can evolve in two forms, either fibro-cavitary disease similarly to pulmonary tuberculosis (TB), or as a more indolent infection associated radiographically with nodules and bronchiectasis (nodular/bronchiectatic disease) [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

A marmoset model for Mycobacterium avium complex pulmonary disease

et al. 2023

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Rationale Mycobacterium avium complex, is the most common nontuberculous mycobacterial respiratory pathogen in humans. Disease mechanisms are poorly understood due to the absence of a reliable animal model for M. avium complex pulmonary disease. Objectives The objectives of this study were to assess the susceptibility, immunologic and histopathologic responses of the common marmoset (Callithrix jacchus) to M. avium complex pulmonary infection. Methods 7 adult female marmosets underwent endobronchial inoculation with 108 colony-forming units of M. intracellulare and were monitored for 30 or 60 days. Chest radiograph was assessed at baseline (prior to infection) and at the time of sacrifice (30 days for 3 animals and 60 days for 4 animals), and bronchoalveolar lavage cytokines, histopathology and cultures of the bronchoalveolar lavage, lungs, liver and kidney were assessed at time of sacrifice. Serum cytokines were monitored at baseline and weekly for 30 days for all animals and at 60 days for those alive. Group differences in serum cytokine measurements between those that tested positive versus negative for the M. intracellulare infection were assessed using a series of linear mixed models. Measurements and main results Five of seven animals (two at 30 days and three at 60 days of infection) had positive lung cultures for M. intracellulare. Extra-pulmonary cultures were positive in three animals. All animals appeared healthy throughout the study. All five animals with positive lung cultures had radiographic changes consistent with pneumonitis. At 30 days, those with M. intracellulare lung infection showed granulomatous inflammation, while at 60 days there were fewer inflammatory changes but bronchiectasis was noted. The cytokine response in the bronchoalveolar lavage fluid was uniformly greater in the animals with positive M. intracellulare cultures than those without a productive infection, with greater levels at 30-days compared to 60-days. Similarly, serum cytokines were more elevated in the animals that had positive M. intracellulare cultures compared to those without a productive infection, peaking 14–21 days after inoculation. Conclusion Endobronchial instillation of M. intracellulare resulted in pulmonary mycobacterial infection in marmosets with a differential immune response, radiographic and histopathologic abnormalities, and an indolent course consistent with M. avium complex lung infection in humans.

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“…Typically, these two species are both reported as "MAC," but their environmental sources differ, and there is evidence indicating differential pathogenicity and clinical disease severity between the two species (6,7). Since MAC is ubiquitous in the environment and exposure is likely unavoidable, it is apparent that some form of host susceptibility must also be present for MAC lung disease to occur (3,4,8). In that context, pulmonary MAC disease occurs primarily in patients with structural lung disease, especially bronchiectasis and emphysema, without demonstrable systemic immune suppression (3,4,8).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Marmoset Model for Mycobacterium avium Complex Pulmonary Disease

Peters

Maselli

Mangat

et al. 2021

Preprint

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RationaleMycobacterium avium complex, is the most common nontuberculous mycobacterial respiratory pathogen in humans. Disease mechanisms are poorly understood due to the absence of a reliable animal model for M. avium complex pulmonary disease.ObjectiveAssess the susceptibility, immunologic and histopathologic responses of the common marmoset (Callithrix jacchus) to M. avium complex pulmonary infection.Methods7 adult female marmosets underwent endobronchial inoculation with 108 colony-forming units of M. intracellulare and were monitored for 30 or 60 days. Prior to infection, chest radiograph and serum cytokines were assessed; serum cytokines were also monitored weekly for 30 days. At sacrifice 30 days (3 animals) or 60 days (4 animals) after infection, chest radiograph, serum and bronchoalveolar lavage cytokines, histopathology, and cultures of the bronchoalveolar lavage, lungs, liver, and kidney were analyzed.Measurements and Main ResultsFive of seven animals (two at 30 days and three at 60 days of infection) had positive lung cultures for M. intracellulare. Extra-pulmonary cultures were positive in three animals. All animals appeared healthy throughout the study. All five animals with positive lung cultures had radiographic changes consistent with pneumonitis. At 30 days, those with M. intracellulare lung infection showed granulomatous inflammation while at 60 days there was less inflammatory change, but bronchiectasis was noted. The cytokine response in the bronchoalveolar lavage fluid was uniformly greater in the animals with positive M. intracellulare cultures than those without a productive infection with greater levels at 30-days compared to 60-days. Similarly, serum cytokines were more elevated in the animals that had positive M. intracellulare cultures compared to those without a productive infection, peaking 14-21 days after inoculation.ConclusionEndobronchial instillation of M. intracellulare resulted in pulmonary mycobacterial infection in marmosets with a differential immune response, radiographic and histopathologic abnormalities, and an indolent course consistent with M. avium complex lung infection in humans.

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Vulnerability to Nontuberculous Mycobacterial Lung Disease or Systemic Infection Due to Genetic/Heritable Disorders

Cited by 5 publications

References 100 publications

Non-tuberculous mycobacterial lung disease due to multiple “minor” risk factors: an illustrative case and a review of these “lesser elements”

Non-tuberculous mycobacterial lung disease due to multiple “minor” risk factors: an illustrative case and a review of these “lesser elements”

A marmoset model for Mycobacterium avium complex pulmonary disease

Marmoset Model for Mycobacterium avium Complex Pulmonary Disease

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