Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/11405
Kpi, a chaperone-usher pili system associated with the worldwide-disseminated high-risk clone Klebsiella pneumoniae ST-15.
Gato, Eva | Vázquez-Ucha, Juan Carlos | Rumbo-Feal, Soraya | Álvarez-Fraga, Laura | Vallejo, Juan A | Martínez-Guitián, Marta | Beceiro, Alejandro | Ramos Vivas, Jose | Sola-Campoy, Pedro J ISCIII | Perez-Vazquez, Maria Dolores ISCIII | Rodiño-Janeiro, Bruno Kotska | Romero, Antonio | Poza, Margarita | Bou, Germán | Pérez, Astrid | Oteo, Jesús ISCIII
Proc Natl Acad Sci U S A . 2020 Jul 21;117(29):17249-17259.
Control of infections caused by carbapenem-resistant Klebsiella pneumoniae continues to be challenging. The success of this pathogen is favored by its ability to acquire antimicrobial resistance and to spread and persist in both the environment and in humans. The emergence of clinically important clones, such as sequence types 11, 15, 101, and 258, has been reported worldwide. However, the mechanisms promoting the dissemination of such high-risk clones are unknown. Unraveling the factors that play a role in the pathobiology and epidemicity of K. pneumoniae is therefore important for managing infections. To address this issue, we studied a carbapenem-resistant ST-15 K. pneumoniae isolate (Kp3380) that displayed a remarkable adherent phenotype with abundant pilus-like structures. Genome sequencing enabled us to identify a chaperone-usher pili system (Kpi) in Kp3380. Analysis of a large K. pneumoniae population from 32 European countries showed that the Kpi system is associated with the ST-15 clone. Phylogenetic analysis of the operon revealed that Kpi belongs to the little-characterized γ2-fimbrial clade. We demonstrate that Kpi contributes positively to the ability of K. pneumoniae to form biofilms and adhere to different host tissues. Moreover, the in vivo intestinal colonizing capacity of the Kpi-defective mutant was significantly reduced, as was its ability to infect Galleria mellonella The findings provide information about the pathobiology and epidemicity of Kpi+K. pneumoniae and indicate that the presence of Kpi may explain the success of the ST-15 clone. Disrupting bacterial adherence to the intestinal surface could potentially target gastrointestinal colonization.
GI tract colonization | Klebsiella pneumoniae | ST-15 high-risk clone | chaperone-usher pili system | pathogenesis
A549 Cells | Animals | Anti-Bacterial Agents | Bacterial Adhesion | Biofilms | Carbapenems | Cell Line | Disease Models, Animal | Drug Resistance, Multiple, Bacterial | Epithelial Cells | Europe | Female | Fimbriae, Bacterial | Gene Deletion | Genes, Bacterial | Humans | Klebsiella Infections | Klebsiella pneumoniae | Mice | Mice, Inbred BALB C | Molecular Chaperones | Multilocus Sequence Typing | Operon | Phylogeny
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