Extended-spectrum β-lactamases (ESBLs) have emerged as one of the most consequential antimicrobial resistance mechanisms of the 21st century. Among Class A β-lactamases which include TEM, SHV, CTX-M, VEB, and GES families CTX-M has risen to global dominance, with over 450 variants documented in the Beta-Lactamase Database (BLDB). The CTX-M designation reflects both its substrate profile (cefotaxime hydrolysis) and its geographic origin (Munich), where the first isolate was recovered from the ear of a 4-month-old child with otitis media. Over the last two decades, blaCTX-M-15 and blaCTX-M-14 have displaced other genotypes and become the predominant CTX-M alleles worldwide.
Historical Aspect First Discovery
The founding clinical event of CTX-M history centers on a cefotaxime-resistant Escherichia coli isolate recovered in Germany in 1989. This isolate was phenotypically distinct from TEM- and SHV-type ESBL producers, displaying a markedly enhanced capacity to hydrolyze cefotaxime over ceftazidime a substrate preference that would define the entire CTX-M family. Concurrent, independent emergence was simultaneously noted in France and South America, pointing to a geographically distributed yet biochemically convergent resistance evolution.