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

## TL;DR

This study examines Pseudomonas aeruginosa strains from infections to understand their resistance to antibiotics and virulence factors.

## Contribution

The study identifies molecular arrangements linking virulence genes, β-lactamase genes, and resistance to β-lactamase inhibitors in P. aeruginosa.

## Key findings

- Most strains from healthcare and community infections had genes for proteases, phospholipases, and β-lactamase.
- Over 99% of strains were resistant to amoxicillin/clavulanic acid and ampicillin/sulbactam.
- Phylogroup 1 was more common than phylogroup 2 among the analyzed strains.

## Abstract

Background/Objectives: The emergence of hypervirulent Pseudomonas aeruginosa 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 P. aeruginosa strains isolated from patients with healthcare-associated infections and community-acquired infections. Methods: P. aeruginosa, 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. Results: In total, 124 P. aeruginosa 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 (aprA), phospholipases (pIcH and pIcN), elastases (lasA and lasB), rhamnolipids (rhLA), quorum-sensing system (lasI and rhII), and β-lactamase (blaoxa-4, blaoxa-1, and blaGES). 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). Conclusions: 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 P. aeruginosa should be improved.