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Sulbactam is a plausible option for treatingAcinetobacter infections because of its intrinsic antibacterial activity against the members of theAcinetobacter genus, but the mechanisms of sulbactam resistance have not been fully studied inAcinetobacter baumannii . In this study, a total of 2,197 clinicalA. baumannii isolates were collected from 27 provinces in China. Eighty-eight isolates with various MICs for sulbactam were selected on the basis of their diverse clonality and underwent multilocus sequence typing (MLST), antimicrobial susceptibility testing, and resistance gene screening. The copy number and relative expression ofbla TEM-1D andampC were measured via quantitative PCR and quantitative reverse transcription-PCR, respectively. The genetic structure of multicopybla TEM-1D was determined using the whole-genome sequencing technology. The cefoperazone-sulbactam resistance rate of the 2,197 isolates was 39.7%. The rate of positivity forbla TEM-1D or ISAba1-ampC in the sulbactam-nonsusceptible group (64.91% and 78.95%, respectively) was significantly higher than that in the sulbactam-susceptible group (0% and 0%, respectively;P &lt; 0.001). The MIC of sulbactam (P &lt; 0.001) varied considerably between the groups expressingampC with or without upstream ISAba1 . Notably, the genetic structure of the multicopybla TEM-1D gene in strain ZS3 revealed thatbla TEM-1D was embedded within four tandem copies of the cassette IS26-bla TEM-1D -Tn3 -IS26 . Therefore,bla TEM-1D and ISAba1-ampC represent the prevalent mechanism underlying sulbactam resistance in clinicalA. baumannii isolates in China. The structure of the four tandem copies ofbla TEM-1D first identified may increase sulbactam resistance.

Molecular Epidemiology and Mechanism of Sulbactam Resistance in Acinetobacter baumannii Isolates with Diverse Genetic Backgrounds in China