In vitro activity of ceftolozane/tazobactam, ceftazidime/avibactam and cefiderocol against clinical isolates of non-aeruginosa Pseudomonas.

Abstract

Background: Although less virulent than Pseudomonas aeruginosa, non-aeruginosa Pseudomonas (NAP) are opportunistic pathogens that cause invasive infections, mainly in immunosuppressed or intensive care patients. MDR strains of NAP are increasingly isolated, especially MBL-producing isolates.

Objectives: We evaluated the activity of cefiderocol, ceftazidime/avibactam and ceftolozane/tazobactam against a collection of clinical isolates of NAP, which was voluntarily enriched with resistant strains.

Methods: We retrospectively determined the MICs of cefiderocol, ceftazidime/avibactam and ceftolozane/tazobactam in 71 NAP clinical isolates. Most isolates of our collection were not susceptible to meropenem (75%) or ceftazidime (45%).

Results: Among the first-line β-lactam-resistant isolates, the strains for which no carbapenemase was detected were susceptible to ceftolozane/tazobactam or ceftazidime/avibactam, except for one isolate. These latter associations were more active against P. fluorescens isolates than against other NAP. Most isolates (94%) of our collection were susceptible to cefiderocol, with a median MIC of 0.25 mg/L. In particular, the 19 carbapenemase-producing strains, including 15 VIM-producing strains, were susceptible to cefiderocol. Cefiderocol MICs were higher for P. fluorescens complex isolates (MIC50 = 2 mg/L) than for P. putida complex isolates (MIC50 = 0.25 mg/L). Resistance to cefiderocol was detected in only four isolates, of which three P. fluorescens complex isolates remained susceptible to ceftolozane/tazobactam and ceftazidime/avibactam.

Conclusions: Ceftolozane/tazobactam and ceftazidime/avibactam may be of interest as second-line β-lactams against non-carbapenemase-producing strains. Cefiderocol was highly active against NAP of our collection, especially MBL-producing isolates. Further studies are needed to correlate in vitro susceptibility of NAP to cefiderocol and clinical responses.