Emerging resistance to ceftriaxone treatment owing to different ampD mutations in Enterobacter roggenkampii
Enterobacter cloacae
Broth microdilution
DOI:
10.1016/j.meegid.2022.105301
Publication Date:
2022-05-11T17:33:12Z
AUTHORS (4)
ABSTRACT
The Enterobacter cloacae complex is responsible for a variety of infections in hospitalized patients and resistant to β-lactam antibiotics owing the expression AmpC β-lactamase. We report emerging resistance roggenkampii exposed ceftriaxone explore mechanism underlying mutations this resistance.Three strains were derived from different samples one patient (blood liver abscess fluid). Antimicrobial susceptibility was evaluated by standard broth microdilution, while ampC determined via RT-PCR. Genetic relatedness pulsed-field gel electrophoresis (PFGE). Species identification comparative genome analysis performed sequencing. Mutation rate testing selection AmpC-derepressed mutants conducted mutation mechanism.E. F1247 susceptible third-generation cephalosporins (3GCs); F95 F1057, found blood sample on day 11 drainage fluid 25, resistant. 341- 642-fold higher respectively, than F1247. Three isolates same PFGE sequence types (ST1778) highly homologous (2 4 core single nucleotide polymorphism differences). Compared F1247, possessed 575 bp deletion, including 537 ampD, whereas F1057 harbored only amino acid (Leu140Pro ampD). rates exposure cefotaxime, ceftazidime, ceftriaxone, piperacillin-tazobactam, cefepime (1.90 ± 0.21) × 10-8, (3.18 0.43) (2.00 0.20) (2.92 0.29) 10-9, zero, respectively. In vitro-selected identified ampR, dacB.E. may develop vivo vitro upon 3GCs lesser extent piperacillin-tazobactam. should not be used as monotherapy E. infections. Therapy using or carbapenems preferred piperacillin-tazobactam treatment roggenkampii, especially if source control difficult.
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