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For the past 40 years, the approach to studying infections in the airways of persons with cystic fibrosis (CF) has largely parallelled that taken in the study of other human infectious diseases. A microorganism (the causative agent) recovered in culture from an infected site is studied in isolation using a variety of in vitro and in vivo models intended to approximate some facet of the human infection. Although this strategy has yielded a wealth of information regarding microbial virulence factors and pathogenic mechanisms for many human infections, its limitations, when applied to the chronic, polymicrobial infections that typify CF, are becoming increasingly obvious. We now appreciate that respiratory tract infection in CF most often involves diverse communities of opportunistic bacterial species that are well adapted to the peculiarities of this niche. We have, furthermore, come to understand that species within this community are not merely living unaffected by their microbial neighbours, but rather, are actively engaged with each other. And we are steadily decoding the rules and mechanisms that govern this microbial concert.
Given this expanding understanding of infection in CF, it seems reasonable to shift our attention towards a conceptual framework that considers the airway microbial community as the ‘pathogenic unit.’ Adoption of this framework leads to several relevant but unanswered questions. How are these communities structured? Are they relatively static or dynamic? Are changes in the community stochastic or canonical? What drives changes in community structure, and how do these …
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