Longitudinal bacterial prevalence in cystic fibrosis airways: Fact and artifact
•CF airways are prone to opportunistic infections that can drive local inflammation.•Prevalence changes were studied from 2001-2019 for 7 CF bacterial opportunists.•Overall opportunist prevalence generally fell as population health improved.•Year-to-year prevalence change rates differed across organ...
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Published in | Journal of cystic fibrosis Vol. 23; no. 1; pp. 58 - 64 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.01.2024
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Subjects | |
Online Access | Get full text |
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Summary: | •CF airways are prone to opportunistic infections that can drive local inflammation.•Prevalence changes were studied from 2001-2019 for 7 CF bacterial opportunists.•Overall opportunist prevalence generally fell as population health improved.•Year-to-year prevalence change rates differed across organisms and birth cohorts.•More people changed infection status yearly than was suggested by prevalence change.
Opportunistic bacterial infection is a hallmark of cystic fibrosis (CF) lung disease and early mortality. Poorly characterized prevalence changes have accompanied two decades of health improvements, with CFTR modulators likely to further affect infection epidemiology.
Bacterial prevalence change trends across birth cohorts were assessed with linear regression using 2001–2019 US CF Foundation Patient Registry data. Informative missingness was assessed, as was age-to-age infection status.
Bacterial prevalence constantly changed from 2001 to 2019, with changes differing across birth cohorts. Informative censoring affected prevalence change for some organisms. Age-to-age infection status changes were greater than net changes in bacterial prevalence and varied by age.
CF infection epidemiology changed over two decades and will continue to do so. Understanding how modulators affect infection epidemiology will require creative designs for longitudinal prevalence change studies emphasizing prevalence changes independent of effects on lung biology. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1569-1993 1873-5010 |
DOI: | 10.1016/j.jcf.2023.09.011 |