Pseudomonas aeruginosa is a major cause of chronic respi-ratory infections (CRI) in patients with underlying diseases such as cystic fibrosis, bronchiectasis, or chronic obstructive pulmonary disease (COPD) (1, 6, 7). The establishment of P. aeruginosa CRI is driven by the acquisition of an important number of adaptive mutations required for long-term persis-tence (10, 12). Among them, the hallmark of P. aeruginosa CRI is the conversion to the mucoid phenotype that drastically increases the organism’s resistance to clearance by the immune system and antimicrobial treatments (2). Antimicrobial resis-tance development in this setting is frequent, although so far it is generally driven by mutations in chromosomal genes and not by the horizontal acquisition of resistance determinants (4, 8, 9). In June 2007, a mucoid multidrug-resistant (MDR) P.
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