Extended-spectrum beta-lactamase-producing Enterobacteriaceae: what are the threats?

Abstract

Extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae, emerged in the 1980s and followed two epidemiological waves. The first one was characterized by the emergence and diffusion of TEM and SHV-derived ESBL in Enterobacteriaceae mainly including Klebsiella pneumoniae and Enterobacter aerogenes in the hospital setting. Infection control implemented in the 1990s in high-risk wards like the intensive care units resulted in a remarkable decrease in ESBL-producing K. pneumoniae and prevented the increase of ESBLproducing E. aerogenes. The second wave, which occurred at the end of the 1990s, was characterized by the emergence of a new ESBL type, the CTX-M enzymes and their spread in Escherichia coli. CTX-M-producing E. coli strains, also resistant to several antibiotic families other than β-lactams, were identified in the community- and hospital-acquired infections. CTX-M-producing E. coli isolates were shown to partly belong to clones (ST131, ST95, ST69, ST393, ST405, and ST10) corresponding to the E. coli fecal dominant population in humans. CTX-M spread in E. coli species, which represent the enterobacterial symbiotic partners of humans with daily excretion of 10²⁰ colony forming units (CFU), resulted in a new fecal peril and a bottomless reservoir of CTX-M for the other enterobacterial species that permanently or intermittently colonize the human digestive tract.