RT Journal Article
T1 Interplay among Resistance Profiles, High-Risk Clones, and Virulence in the Caenorhabditis elegans Pseudomonas aeruginosa Infection Model
A1 Sanchez-Diener, Irina
A1 Zamorano, Laura
A1 Lopez-Causape, Carla
A1 Cabot, Gabriel
A1 Mulet, Xavier
A1 Pena, Carmen
A1 del Campo, Rosa
A1 Canton, Rafael
A1 Domenech-Sanchez, Antonio
A1 Martinez-Martinez, Luis
A1 Arcos, Susana C.
A1 Navas, Alfonso
A1 Oliver, Antonio
K1 Pseudomonas aeruginosa
K1 Caenorhabditis elegans
K1 Virulence
K1 Multidrug resistant
K1 Extensively drug resistant
K1 High-risk clones
AB The increasing prevalence of nosocomial infections produced by multidrug-resistant (MDR) or extensively drug-resistant (XDR) Pseudomonas aeruginosa is frequently linked to widespread international strains designated high-risk clones. In this work, we attempted to decipher the interplay between resistance profiles, high-risk clones, and virulence, testing a large (n = 140) collection of well-characterized P. aeruginosa isolates from different sources (bloodstream infections, nosocomial outbreaks, cystic fibrosis, and the environment) in a Caenorhabditis elegans infection model. Consistent with previous data, we documented a clear inverse correlation between antimicrobial resistance and virulence in the C. elegans model. Indeed, the lowest virulence was linked to XDR profiles, which were typically linked to defined high-risk clones. However, virulence varied broadly depending on the involved high-risk clone; it was high for sequence type 111 (ST111) and ST235 but very low for ST175. The highest virulence of ST235 could be attributed to its exoU(+) type III secretion system (TTSS) genotype, which was found to be linked with higher virulence in our C. elegans model. Other markers, such as motility or pigment production, were not essential for virulence in the C. elegans model but seemed to be related with the higher values of the statistical normalized data. In contrast to ST235, the ST175 high-risk clone, which is widespread in Spain and France, seems to be associated with a particularly low virulence in the C. elegans model. Moreover, the previously described G154R AmpR mutation, prevalent in ST175, was found to contribute to the reduced virulence, although it was not the only factor involved. Altogether, our results provide a major step forward for understanding the interplay between P. aeruginosa resistance profiles, high-risk clones, and virulence.
PB Amer soc microbiology
SN 0066-4804
YR 2017
FD 2017-09-15
LK http://hdl.handle.net/10668/19002
UL http://hdl.handle.net/10668/19002
LA en
NO Sánchez-Diener I, Zamorano L, López-Causapé C, Cabot G, Mulet X, Peña C, et al. Interplay among Resistance Profiles, High-Risk Clones, and Virulence in the Caenorhabditis elegans Pseudomonas aeruginosa Infection Model. Antimicrob Agents Chemother. 2017 Nov 22;61(12):e01586-17
NO We thank all the clinical microbiologists and clinicians participating in the REIPImulticenter study of P. aeruginosa bloodstream infections (PI08/0276) and the multi-center study of cystic fibrosis respiratory infections (PI12/00734). We also thank PilarSanchis and Guillem Frontera from IdisBa for statistical support.This work was supported by the Planes Nacionales de I D i 2008-2011/2013-2016and Instituto de Salud Carlos III, Subdirección General de Redes y Centros de Investi-gación Cooperativa, Ministerio de Economía y Competitividad, Spanish Network forResearch in Infectious Diseases (REIPI RD12/0015/0006, RD12/0015/004, RD16/0016/0004, RD16/0016/008, and RD16/0016/0011) and grants PI15/00088 and PI12/00734.This work was cofinanced by grants from the European Development Regional Fund “Away to achieve Europe” and operative program Intelligent Growth (2014-2020). I.S.-D.is the recipient of a P-FIS fellowship from Instituto de Salud Carlos III, Ministerio deEconomía y Competitividad.
DS RISalud
RD Apr 11, 2025