Molecular Epidemiology of<i>Mycobacterium abscessus</i>, with Focus on Cystic Fibrosis

Jönsson, Bodil; Gilljam, M.; Lindblad, Anders; Ridell, Malin; Wold, Agnes E.; Welinder‐Olsson, Christina

doi:10.1128/jcm.02592-06

Cited by 186 publications

(190 citation statements)

References 42 publications

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“…The emergence of MABSC in CF patients is estimated to have occurred in the mid-1990s [35] and was probably multifactorial. This period saw major improvements in the microbiological methods for isolating MABSC and other NTM [13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Inhaled therapies, azithromycin andMycobacterium abscessusin cystic fibrosis patients

Catherinot¹,

Roux²,

Vibet³

et al. 2012

Eur Respir J

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Cystic fibrosis (CF) patients are at particularly high risk of developing lung disease caused by Mycobacterium abscessus complex (MABSC). Over the last 10 years, changes in CF treatment, with increasing use of inhaled therapies and low-dose azithromycin, have been accompanied by an increase in the prevalence of MABSC infections in CF patients. There is therefore some concern about the role of new CF treatments in the emergence of MABSC infections.We addressed this issue by means of a case-control study including 30 MABSC-positive cases and 60 nontuberculous mycobacteria-negative CF controls matched for age, sex and centre. We also compared practices at the CF centres with the highest prevalence of MABSC with those at the other centres.No positive association was found between MABSC lung disease and the use of inhaled therapies or low-dose azithromycin in the 4 years preceding MABSC isolation. These treatments were not significantly more frequently used at the CF centres with the highest MABSC prevalence rates.In conclusion, there is no evidence for a link between M. abscessus complex lung disease and inhaled therapies or low-dose azithromycin in patients with CF.

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Section: Discussionmentioning

confidence: 99%

Inhaled therapies, azithromycin andMycobacterium abscessusin cystic fibrosis patients

Catherinot¹,

Roux²,

Vibet³

et al. 2012

Eur Respir J

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“…102 Among 14 NTMinfected individuals with CF included in a study in Sweden, a shared strain was found only in 1 pair of siblings. 228 However, a recent report from the United States described the use of rep-PCR and PFGE typing to show the apparent spread of a strain of M. abscessus subsp. massiliense from a chronically infected adult with CF to 4 others attending the same clinic in Seattle.…”

Section: Iiia5 Nontuberculous Mycobacteriamentioning

confidence: 99%

Infection Prevention and Control Guideline for Cystic Fibrosis: 2013 Update

Saiman

Siegel

LiPuma

et al. 2014

Infect. Control Hosp. Epidemiol.

352

382

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The 2013 Infection Prevention and Control (IP&C) Guideline for Cystic Fibrosis (CF) was commissioned by the CF Foundation as an update of the 2003 Infection Control Guideline for CF. During the past decade, new knowledge and new challenges provided the following rationale to develop updated IP&C strategies for this unique population:1. The need to integrate relevant recommendations from evidence-based guidelines published since 2003 into IP&C practices for CF. These included guidelines from the Centers for Disease Control and Prevention (CDC)/Healthcare Infection Control Practices Advisory Committee (HICPAC), the World Health Organization (WHO), and key professional societies, including the Infectious Diseases Society of America (IDSA) and the Society for Healthcare Epidemiology of America (SHEA). During the past decade, new evidence has led to a renewed emphasis on source containment of potential pathogens and the role played by the contaminated healthcare environment in the transmission of infectious agents. Furthermore, an increased understanding of the importance of the application of implementation science, monitoring adherence, and feedback principles has been shown to increase the effectiveness of IP&C guideline recommendations.2. Experience with emerging pathogens in the non-CF population has expanded our understanding of droplet transmission of respiratory pathogens and can inform IP&C strategies for CF. These pathogens include severe acute respiratory syndrome coronavirus and the 2009 influenza A H1N1. Lessons learned about preventing transmission of methicillin-resistant Staphylococcus aureus (MRSA) and multidrug-resistant gram-negative pathogens in non-CF patient populations also can inform IP&C strategies for CF.

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“…M. abscessus lung disease is highly prevalent in patients with cystic fibrosis (CF) and is becoming a major issue for most CF centers worldwide (3)(4)(5)(6). Although M. abscessus is an RGM, it can persist and cause lung disease with caseous lesions (7).…”

mentioning

confidence: 99%

Mycobacterium abscessus cording prevents phagocytosis and promotes abscess formation

Bernut

Herrmann

Kissa

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

302

493

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Mycobacterium abscessus is a rapidly growing Mycobacterium causing a wide spectrum of clinical syndromes. It now is recognized as a pulmonary pathogen to which cystic fibrosis patients have a particular susceptibility. The M. abscessus rough (R) variant, devoid of cell-surface glycopeptidolipids (GPLs), causes more severe clinical disease than the smooth (S) variant, but the underlying mechanisms of R-variant virulence remain obscure. Exploiting the optical transparency of zebrafish embryos, we observed that the increased virulence of the M. abscessus R variant compared with the S variant correlated with the loss of GPL production. The virulence of the R variant involved the massive production of serpentine cords, absent during S-variant infection, and the cords initiated abscess formation leading to rapid larval death. Cording occurred within the vasculature and was highly pronounced in the central nervous system (CNS). It appears that M. abscessus is transported to the CNS within macrophages. The release of M. abscessus from apoptotic macrophages initiated the formation of cords that grew too large to be phagocytized by macrophages or neutrophils. This study is a description of the crucial role of cording in the in vivo physiopathology of M. abscessus infection and emphasizes cording as a mechanism of immune evasion.morphotype | pathogenesis | granuloma | innate immunity T he rapidly growing mycobacterium (RGM) Mycobacterium abscessus (M. abscessus) is an emerging pathogen that infects a wide spectrum of tissues in humans, including lungs, skin, and soft tissues (1, 2). M. abscessus lung disease is highly prevalent in patients with cystic fibrosis (CF) and is becoming a major issue for most CF centers worldwide (3-6). Although M. abscessus is an RGM, it can persist and cause lung disease with caseous lesions (7).M. abscessus exists as two variants: rough (R) and smooth (S). Ex vivo and in vivo studies have described the hypervirulence phenotype of the R versus the S morphotype (8, 9), and epidemiological studies have confirmed the persistence and acute respiratory syndromes caused by the R morphotype (4, 10, 11). The major difference between the R and S variants is the loss of a surface-associated glycopeptidolipid (GPL) (12). Analysis of the pathogenicity of M. abscessus has been hampered by the lack of genetic tools and the restricted panel of cellular/animal models. However, new genetic tools, including conditional gene expression, recently have been applied to both the S and R morphotypes (13, 14), but developing new animal models amenable to the manipulation of the host response is still challenging. The M. abscessus genome harbors a mercury-resistance plasmid sharing 99% identity with an episome from the slowgrowing fish pathogen Mycobacterium marinum, indicating that these species have exchanged this plasmid in a shared ecosystem (15). M. abscessus has been described in wild and captive fish species (16,17), and hand infections caused by M. abscessus have been reported in healthy fish handlers (18), sug...

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Molecular Epidemiology ofMycobacterium abscessus, with Focus on Cystic Fibrosis

Cited by 186 publications

References 42 publications

Inhaled therapies, azithromycin andMycobacterium abscessusin cystic fibrosis patients

Inhaled therapies, azithromycin andMycobacterium abscessusin cystic fibrosis patients

Infection Prevention and Control Guideline for Cystic Fibrosis: 2013 Update

Mycobacterium abscessus cording prevents phagocytosis and promotes abscess formation

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