β-lactam resistance in Pseudomonas aeruginosa is mediated by multiple mechanisms in most clinical isolates.

MARTÍNEZ E, ESCOBAR PÉREZ J, MÁRQUEZ C, VILACOBA E, CENTRÓN D, LEAL AL, SAAVEDRA C, SAAVEDRA SY, TOVAR C, VANEGAS N, STOKES HW.

Journal of Global Antimicrobial Resistance

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2013

2213-7165

Background β-lactam resistance is driven by a number of mechanisms in Pseudomonas aeruginosa clinical isolates. While several are relatively well understood, how they act cooperatively in pathogenic strains is less clear. In some isolates, resistance profiles cannot always be explained by identifying the role of the common resistance determining pathways, suggesting that other mechanisms may be important. Methods Pathogenic P. aeruginosa isolates from four countries were characterized by PCR, quantitative expression analysis for the presence and activity of several pathways that influence antibiotic resistance has been performed. In addition, culture experiments were conducted to test how random transposition of the insertion sequence IS26 during growth may influence resistance to some antibiotics. Results In most strains antibiotic resistance was being driven by changes in multiple pathways and by the presence or absence of genes acquired by Lateral Genetic Transfer. Changes in chromosomal pathways included over-expression of AmpC and two efflux pumps. Also, gain or loss of IS26 at some chromosomal locations, most notably oprD, could influence resistance to carbapenems. Conclusions P. aeruginosa pathogenic strains are evolving to become multidrug resistant in more complex and multifactorial ways. This is being influenced by single strains acquiring changes in numerous known pathways as well as by newly emerging resistance mechanisms in this species.