Fecha de publicación: -- Fuente: PubMed "swarm" Int J Med Microbiol. 2026 Sep 26;323:151741. doi: 10.1016/j.ijmm.2026.151741. Online ahead of print.ABSTRACTPseudomonas aeruginosa (P. aeruginosa) is a common opportunistic pathogen that can rapidly evolve to adapt to diverse chronic infection microenvironments. Strains frequently isolated from chronic infections include mucoid strains, small-colony variants (SCVs), hypermutable strains, and antibiotic-resistant strains, which have been extensively researched. However, brown pigmented strains (here termed large-fragment-deletion brown strains, LFDBS) are also not uncommon in chronic infections. The production of this brown pigment is associated with large-scale genomic deletions containing hmgA, yet the adaptive repertoire of these strains and the underlying mechanisms remain incompletely elucidated, representing a significant gap relative to the better-characterized adaptive variants described above. In a previous study, we showed that P. aeruginosa PAO1r exhibited a brown colony phenotype, arising from a large-scale genomic deletion containing hmgA. In this study, we show that PAO1r is characterized by a reduced growth rate under static culture conditions, impaired swimming and swarming motility, enhanced biofilm formation, enhanced tolerance to DNA-damaging agents, and increased sensitivity to oxidative stress. Furthermore, these characteristics are shared by the two clinical LFDBS examined in this study. Further analysis indicates that the underlying mechanism of the reduced growth rate under static culture conditions and impaired swimming and swarming motility is attributed to c-di-GMP elevation resulting from phosphodiesterase gene co-deletion, which are characterized here for the first time. This study elucidates adaptive traits and the mechanisms underlying the persistence and recalcitrance of LFDBS in chronic infections. It deepens our understanding of P. aeruginosa evolutionary trajectories, and provides a theoretical foundation for the development of clinical treatment strategies targeting this distinct pathogen variant.PMID:42810128 | DOI:10.1016/j.ijmm.2026.151741