Abstract
The MERINO trial has seemingly laid to rest the question: 'Are carbapenems the preferred therapy for ESBL-producing infections?' It has, however, brought another important question to the forefront: 'How do we know when we have an ESBL-producing infection?' A commonly used approach is the interpretation that non-susceptibility to third-generation cephalosporins (e.g. ceftriaxone MICs of ≥2 mg/L) is an accurate proxy for ESBL production. We believe that relying on antibiotic susceptibility results alone to predict ESBL production in clinical isolates is fraught with issues. Rather, we believe accurate molecular assays that detect a comprehensive range of ESBL genes, along with other relevant β-lactamase genes, are well within the reach of existing technology and necessary to optimize patient care. Herein, we elaborate on why the current approach for determining whether an organism is likely to be an ESBL producer (i) is inaccurate; (ii) encourages carbapenem overuse; (iii) ignores the potential for ESBL production in other Enterobacterales species; and (iv) promotes the silent epidemic of ESBL transmission.