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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Bibliographic Details
Published inJournal of cystic fibrosis Vol. 23; no. 1; pp. 58 - 64
Main Authors VanDevanter, D.R., LiPuma, J.J., Konstan, M.W.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.01.2024
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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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content type line 23
ISSN:1569-1993
1873-5010
DOI:10.1016/j.jcf.2023.09.011