Not all carbapenem-resistant Pseudomonas aeruginosa strains are alike: tailoring antibiotic therapy based on resistance mechanisms

Abstract

Purpose of review: To correlate the resistance mechanisms and the susceptibility to new antibiotics in Pseudomonas aeruginosa .

Recent findings: Definition of antibiotic resistance in Pseudomonas aeruginosa is still debated. Carbapenem-resistant Pseudomonas aeruginosa (CRPA) and difficult-to-treat resistant Pseudomonas aeruginosa (DTR-PA) are used but which of them better correlate with the risk of mortality remains debated. Mechanisms underlying resistance in Pseudomonas aeruginosa are complex and may be combined, resulting in unpredictable phenotype and cross-resistance. Thus, not all CRPA are alike and tailoring antibiotic therapy on resistance mechanisms is challenging.

Summary: Current guidelines recommend the use of new antipseudomonal agents for CRPA or DTR-PA infections but they don't provide specific information on how tailoring antibiotic therapy on underlying resistance mechanisms. This review may be useful to understand which mechanisms are involved in CRPA and may have practical implications helping clinicians to select an appropriate antibiotic regimen. Several antibiotics are now available for Pseudomonas aeruginosa but their rational use is important to avoid development of future resistance. The knowledge of local epidemiology and most common resistance mechanisms may guide empirical therapy, but targeted antibiotic therapy should be re-evaluated as soon as susceptibility testing profile is available and selected according to Pseudomonas aeruginosa phenotype.

Box 1

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FIGURE 1

Scenarios of antibiotic resistance in Pseudomonas aeruginosa and underling mechanisms. ∗Resistance to: cefalosporins, fluoroquinolones, piperacillin/tazobactam, carbapenems (contemporary presence defines DTR-PA). ∗∗Cefepime/zidebactam, cefepime/taniborbactam, aztreonam/avibactam. MBL, metallo-β-lactamases; PBP, nonessential penicillin binding protein.