Genetic Analysis of Virulence and β-Lactamase Determinants Related to β-Lactamase Inhibitors in Pseudomonas aeruginosa Strains from Nosocomial Infections

<b>Background/Objectives</b>: The emergence of hypervirulent <i>Pseudomonas aeruginosa</i> strains resistant to β-lactamase inhibitor antibiotics is a critical health problem as they impede the treatment of infections. The objective of this study was to determine the different molecular arrangements of the virulence genotype related to β-lactamase genotype and the resistance phenotype to a combination of β-lactam antibiotics and β-lactamase inhibitors, and the phylogroups in <i>P. aeruginosa</i> strains isolated from patients with healthcare-associated infections and community-acquired infections. <b>Methods</b>: <i>P. aeruginosa,</i> virulence genes, β-lactamase genes and phylogroups were identified using polymerase chain reaction. Resistance to β-lactam antibiotics and β-lactamase inhibitors was determined using the disk diffusion method. The MIC determination of ticarcillin/clavulanic acid and piperacillin/tazobactam was performed using the MIC test strip for antimicrobial susceptibility testing. <b>Results</b>: In total, 124 <i>P. aeruginosa</i> strains from patients with healthcare-associated (67/124) and community-acquired infections (57/124) were analyzed. Most strains from patients with healthcare-associated infections and community-acquired infections harbored genes for proteases (<i>aprA</i>), phospholipases (<i>pIcH</i> and <i>pIcN</i>), elastases (<i>lasA</i> and <i>lasB</i>), rhamnolipids (<i>rhLA</i>), quorum-sensing system (<i>lasI</i> and <i>rhII</i>), and β-lactamase (<i>bla_oxa-4</i>, <i>bla_oxa-1</i>, and <i>bla_GES</i>). In total, 100% (124/124) and 99.1% (123/124) of the strains isolated from patients with healthcare-associated and community-acquired infections were resistant to the β-lactamase inhibitor antibiotics, amoxicillin/clavulanic acid and ampicillin/sulbactam, respectively, while 54% (67/124) of the strains were resistant to piperacillin/tazobactam. Phylogroup 1 (22/124) was detected more frequently among the strains in relation to phylogroup 2 (8/12). <b>Conclusions</b>: We demonstrated different association profiles of virulence genotype related to the β-lactamase genotype, the β-lactamase inhibitor resistome, phylogroups, and clinical origin of the strains. Therefore, medical treatment regimens against infections caused by <i>P. aeruginosa</i> should be improved.