Increasing prevalence of ESBL-producing Enterobacteriaceae in Europe

TLDR

Extended‑spectrum β‑lactamases (ESBLs) have risen across Europe, shifting from TEM/SHV‑producing Klebsiella outbreaks in the 1990s to predominantly CTX‑M‑producing Escherichia coli community infections driven by clonal spread and co‑selection with other antibiotics. The study calls for ongoing surveillance of epidemic clones carrying multiple β‑lactamases and emerging fluoroquinolone/aminoglycoside resistance mechanisms.

Abstract

Extended-spectrum beta-lactamases (ESBLs) have been increasingly reported in Europe since their first description in 1983. During the 1990s, they were described mainly as members of the TEM- and SHV-beta-lactamase families in Klebsiella pneumoniae causing nosocomial outbreaks. Nowadays, they are mostly found in Escherichia coli that cause community-acquired infections and with increasing frequency contain CTX-M enzymes. Dissemination of specific clones or clonal groups and epidemic plasmids in community and nosocomial settings has been the main reason for the increase in most of the widespread ESBLs belonging to the TEM (TEM-24, TEM-4, TEM-52), SHV (SHV-5, SHV-12) and CTX-M (CTX-M-9, CTX-M-3, CTX-M-14 or CTX-M-15) families in Europe. Co-selection with other resistances, especially to fluoroquinolones, aminoglycosides and sulfonamides, seems to have contributed to the problem. The emergence of epidemic clones harbouring several beta-lactamases simultaneously (ESBLs, metallo-beta-lactamases or cephamycinases) and of new mechanisms of resistance to fluoroquinolones and aminoglycosides warrants future surveillance studies.