“…The underlying host-pathogen interaction mechanisms regulating the CF-characteristic microbial “switch” from S. aureus and H. influenzae to P. aeruginosa remain, however, controversial and incompletely understood, but probably involve pathogen-derived factors, such as pyocyanin and host-derived immune factors as well as environmental influences. In the era of commonly and early used inhaled antibiotics and prolonged patient survival, new “emerging” pathogens are increasingly detected in CF airway fluids, particularly fungi, such as Aspergillus fumigatus [ 2 , 26 ], Candida albicans [ 9 , 10 ], and Scedosporium species [ 22 ], and the bacteria Stenotrophomonas maltophilia [ 13 ], Achromobacter xylosoxidans [ 12 , 15 ], methicillin-resistant S. aureus (MRSA) [ 14 ], Burkholderia cepacia [ 11 , 25 ], and atypical mycobacteria (nontuberculous mycobacteria, NTMs) [ 1 , 23 ], which are often hard to treat in the clinics due to antibiotic resistance patterns [ 7 , 8 , 31 , 33 , 34 ]. Whereas the prevalence (or at least the detection rate) of these microbial species increases in most CF centers, their pathophysiological disease relevance for the outcome of CF lung disease remains controversial and poorly defined.…”