Pseudomonas spp. are ubiquitous microorganisms that exhibit intrinsic and acquired resistance to many antimicrobial agents. Pseudomonas aeruginosa is the most studied species of this genus due to its clinical importance. In contrast, the Pseudomonas fluorescens complex consists of environmental and, in some cases, pathogenic opportunistic microorganisms. The records of antimicrobial-resistant P. fluorescens are quite scattered, which hinders the recognition of patterns. This review compiles published data on antimicrobial resistance in species belonging to the P. fluorescens complex, which were identified through phylogenomic analyses. Additionally, we explored the occurrence of clinically relevant antimicrobial resistance genes in the genomes of the respective species available in the NCBI database. Isolates were organized into two categories: strains isolated from pristine sites and strains isolated from human-impacted or metal-polluted sites. Our review revealed that many reported resistant phenotypes in this complex might be related to intrinsic features, whereas some of them might be ascribed to adaptive mechanisms such as colistin resistance. Moreover, a few studies reported antimicrobial resistance genes (ARGs), mainly β-lactamases. In-silico analysis corroborated the low occurrence of transferable resistance mechanisms in this Pseudomonas complex. Both phenotypic and genotypic assays are necessary to gain insights into the evolutionary aspects of antimicrobial resistance in the P. fluorescens complex and the possible role of these ubiquitous species as reservoirs of clinically important and transmissible ARGs.
Bibliographical noteKAUST Repository Item: Exported on 2022-09-14
Acknowledged KAUST grant number(s): BAS/1/1096-01-01
Acknowledgements: This study was financed by Coordenação de Aperfeiçoamento de Pessoal de Nível Superior– Brasil (CAPES)–Finance Code 001; Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), and Programa Antártico Brasileiro (PROANTAR). This study was also financed in part by INPRA (CNPq 465718/2014-0; FAPERGS17/2551-0000514-7) and CAPES Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) grant # E-26/211.554/2019. The APC was funded by KAUST Baseline Grant (BAS/1/1096-01-01).