A rapid and simple method to detect ESBL in Enterobacter cloacae based on MIC of cefepime

Bastos, Marina de Souza; Menegucci, Thatiany Cevallos; Moreira, Rafael Renato Brondani; Garcia, Lourdes Botelho; Cardoso, Celso Luíz; Tognim, Maria Cristina Bronharo

doi:10.1590/0037-8682-0199-2014

Cited by 2 publications

(2 citation statements)

References 11 publications

(10 reference statements)

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“…ampC gene is frequently found on the chromosomes of non-fermenting bacteria such as Pseudomonas aeruginosa and some Enterobacteriaceae such as Enterobacter cloacae , Citrobacter freundii and Enterobacter asburiae [ 5 ]. ampC overexpression renders these pathogens resistant to penicillin, the first and second-generation cephalosporins, and β-lactam/β-lactamase inhibitors [ 14 ], as well as carbapenems, especially with porin loss [ 3 , 15 ]. The overproduction of AmpC is the major cause of ECC's cephalosporin resistance [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Cefazolin and imipenem enhance AmpC expression and resistance in NagZ-dependent manner in Enterobacter cloacae complex

et al. 2022

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Background Enterobacter cloacae complex (ECC) is a common opportunistic pathogen and is responsible for causing various infections in humans. Owing to its inducible chromosomal AmpC β-lactamase (AmpC), ECC is inherently resistant to the 1st- and 2nd- generation cephalosporins. However, whether β-lactams antibiotics enhance ECC resistance remains unclear. Results In this study, we found that subinhibitory concentrations (SICs) of cefazolin (CFZ) and imipenem (IMP) can advance the expression of AmpC and enhance its resistance towards β-lactams through NagZ in Enterobacter cloacae (EC). Further, AmpC manifested a substantial upregulation in EC in response to SICs of CFZ and IMP. In nagZ knockout EC (ΔnagZ), the resistance to β-lactam antibiotics was rather weakened and the effect of CFZ and IMP on AmpC induction was completely abrogated. NagZ ectopic expression can rescue the induction effects of CFZ and IMP on AmpC and increase ΔnagZ resistance. More importantly, CFZ and IMP have the potential to induce the expression of AmpR's target genes in a NagZ-dependent manner. Conclusions Our findings suggest that NagZ is a critical determinant for CFZ and IMP to promote AmpC expression and resistance and that CFZ and IMP should be used with caution since they may aggravate ECC resistance. At the same time, this study further improves our understanding of resistance mechanisms in ECC.

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Section: Introductionmentioning

confidence: 99%

Cefazolin and imipenem enhance AmpC expression and resistance in NagZ-dependent manner in Enterobacter cloacae complex

et al. 2022

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“…ampC genes are frequently found on the chromosomes of non-fermenting bacteria (such as Pseudomonas aeruginosa) and several family members of Enterobacteriaceae (for instance Enterobacteriaceae) [17,18]. ampC overexpression renders these pathogens resistant to penicillin, the rst and second-generation cephalosporins, and β-lactam/β-lactamase inhibitors [19], as well as carbapenems, especially with porin loss [20,21]. The overproduction of AmpC is the major cause of EC's cephalosporin resistance [22].…”

Section: Introductionmentioning

confidence: 99%

Cefazolin and Imipenem Enhance AmpC Expression and Resistance in NagZ-Dependent Manner in Enterobacter Cloacae

Yang¹,

Wang²,

Zhong³

et al. 2021

Preprint

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Background: Enterobacter cloacae (EC) is a commonly occurring opportunistic pathogen and is responsible for causing various infections in humans. Owing to its inducible chromosomal AmpC β-lactamase (AmpC), EC is inherently resistant to the 1st- and 2nd- generation cephalosporins. However, whether β-lactams antibiotics enhance EC resistance remains unclear.Results: In this study, we found that subinhibitory concentrations (SICs) of cefazolin (CFZ) and imipenem (IMP) are able to advance the expression of AmpC and improve its resistance towards β - lactams through NagZ in EC clinical isolate. Our work indicate that AmpC manifested a substantial upregulation in EC in response to SICs of CFZ and IMP. In nagZ knockout EC (ΔnagZ), we found that the resistance to β - lactam antibiotics was rather weakened and the effect of CFZ and IMP on induction of AmpC was completely abrogated. Ectopic expression of NagZ can rescue the induction effect of CFZ and IMP on AmpC and enhance resistance in ΔnagZ. More importantly, CFZ and IMP have the potential to bring about the target genes expressions of AmpR in a NagZ-dependent manner.Conclusions: Our findings show that NagZ is a critical determinant for CFZ and IMP to promote AmpC expression and improve resistance and that CFZ and IMP should be used with caution since they may aggravate EC resistance. At the same time, this study further improves our understanding of resistance mechanisms in EC.

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A rapid and simple method to detect ESBL in Enterobacter cloacae based on MIC of cefepime

Cited by 2 publications

References 11 publications

Cefazolin and imipenem enhance AmpC expression and resistance in NagZ-dependent manner in Enterobacter cloacae complex

Cefazolin and imipenem enhance AmpC expression and resistance in NagZ-dependent manner in Enterobacter cloacae complex

Cefazolin and Imipenem Enhance AmpC Expression and Resistance in NagZ-Dependent Manner in Enterobacter Cloacae

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