Emergence of Antibiotic Resistance during Therapy for Infections Caused by
            <i>Enterobacteriaceae</i>
            Producing AmpC β-Lactamase: Implications for Antibiotic Use

Choi, Sang‐Ho; Lee, Jung Eun; Park, Su Jin; Choi, Seong–Jun; Lee, Sang‐Oh; Jeong, Jin‐Yong; Kim, Mina; Woo, Jun Hee; Kim, Yang Soo

doi:10.1128/aac.01083-07

Cited by 149 publications

(118 citation statements)

References 12 publications

(17 reference statements)

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“…also found that 19% of patients receiving broad-spectrum cephalosporins developed resistant Enterobacter isolates and that resistance was more likely to appear if the original isolate came from blood (156). A recent study evaluated 732 patients with infections due to Enterobacter spp., S. marcescens, C. freundii, or M. morganii (57). Resistance emerged in 11 of 218 patients (5%) treated with broad-spectrum cephalosporins, more often in Enterobacter spp.…”

Section: Clinical Relevance Chromosomal Ampc Enzymesmentioning

confidence: 99%

AmpC β-Lactamases

2009

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SUMMARY AmpC β-lactamases are clinically important cephalosporinases encoded on the chromosomes of many of the Enterobacteriaceae and a few other organisms, where they mediate resistance to cephalothin, cefazolin, cefoxitin, most penicillins, and β-lactamase inhibitor-β-lactam combinations. In many bacteria, AmpC enzymes are inducible and can be expressed at high levels by mutation. Overexpression confers resistance to broad-spectrum cephalosporins including cefotaxime, ceftazidime, and ceftriaxone and is a problem especially in infections due to Enterobacter aerogenes and Enterobacter cloacae, where an isolate initially susceptible to these agents may become resistant upon therapy. Transmissible plasmids have acquired genes for AmpC enzymes, which consequently can now appear in bacteria lacking or poorly expressing a chromosomal blaAmpC gene, such as Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis. Resistance due to plasmid-mediated AmpC enzymes is less common than extended-spectrum β-lactamase production in most parts of the world but may be both harder to detect and broader in spectrum. AmpC enzymes encoded by both chromosomal and plasmid genes are also evolving to hydrolyze broad-spectrum cephalosporins more efficiently. Techniques to identify AmpC β-lactamase-producing isolates are available but are still evolving and are not yet optimized for the clinical laboratory, which probably now underestimates this resistance mechanism. Carbapenems can usually be used to treat infections due to AmpC-producing bacteria, but carbapenem resistance can arise in some organisms by mutations that reduce influx (outer membrane porin loss) or enhance efflux (efflux pump activation).

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Section: Clinical Relevance Chromosomal Ampc Enzymesmentioning

confidence: 99%

AmpC β-Lactamases

2009

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“…is a major concern since it appears among ca. 10% to 20% of patients treated with broad-spectrum cephalosporins (35)(36)(37). Also, once selected, AmpC overproduction is stable, and approximately 30% to 40% of ECC isolates are currently resistant to third-generation cephalosporins worldwide (38,39).…”

mentioning

confidence: 99%

Complex Regulation Pathways of AmpC-Mediated β-Lactam Resistance in Enterobacter cloacae Complex

Guérin

Isnard

Cattoir

et al. 2015

Antimicrob Agents Chemother

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bEnterobacter cloacae complex (ECC), an opportunistic pathogen causing numerous infections in hospitalized patients worldwide, is able to resist ␤-lactams mainly by producing the AmpC ␤-lactamase enzyme. AmpC expression is highly inducible in the presence of some ␤-lactams, but the underlying genetic regulation, which is intricately linked to peptidoglycan recycling, is still poorly understood. In this study, we constructed different mutant strains that were affected in genes encoding enzymes suspected to be involved in this pathway. As expected, the inactivation of ampC, ampR (which encodes the regulator protein of ampC), and ampG (encoding a permease) abolished ␤-lactam resistance. Reverse transcription-quantitative PCR (qRT-PCR) experiments combined with phenotypic studies showed that cefotaxime (at high concentrations) and cefoxitin induced the expression of ampC in different ways: one involving NagZ (a N-acetyl-␤-D-glucosaminidase) and another independent of NagZ. Unlike the model established for Pseudomonas aeruginosa, inactivation of DacB (also known as PBP4) was not responsible for a constitutive ampC overexpression in ECC, whereas it caused AmpC-mediated high-level ␤-lactam resistance, suggesting a posttranscriptional regulation mechanism. Global transcriptomic analysis by transcriptome sequencing (RNA-seq) of a dacB deletion mutant confirmed these results. Lastly, analysis of 37 ECC clinical isolates showed that amino acid changes in the AmpD sequence were likely the most crucial event involved in the development of high-level ␤-lactam resistance in vivo as opposed to P. aeruginosa where dacB mutations have been commonly found. These findings bring new elements for a better understanding of ␤-lactam resistance in ECC, which is essential for the identification of novel potential drug targets.

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“…Increased incidence of nosocomial infections and broad resistance to third generation cephalosporins, penicillins and quinolones are a serious problem. However, fourth generation antimicrobials remain effective for treatment but with serious side effects [29]. Aminoglycosides, quinolones, trimethoprim/sulphamethoxazole, and carbapenems displayed good activity against Gram-negative pathogens including Enterobacter species [30].…”

Section: Assessment Of Antimicrobial Susceptibilitymentioning

confidence: 99%

Characterization of Phenotype and Genotype of Biofield Treated Enterobacter aerogenes

Jana¹,

Trivedi²,

Branton³

2015

Transl Med (sunnyvale)

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Enterobacter aerogenes (E. aerogenes) has been commonly described as a versatile opportunistic pathogen in hospital infections. The aim of the present work was to evaluate the impact of biofield treatment on E. aerogenes for its phenotypic and genotypic characteristics. E. aerogenes bearing ATCC 13048 (American Type Culture Collection) was procured from Bangalore Genei, in sealed pack and divided into control and treated groups. Treated group was subjected to Mr. Trivedi's biofield treatment and analyzed for antimicrobial susceptibility, minimum inhibitory concentration (MIC), biochemical reactions, and biotype using automated MicroScan Walk-Away ® system. In addition, treated group of E. aerogenes was evaluated for DNA polymorphism by Random Amplified Polymorphic DNA (RAPD) and 16S rDNA sequencing to establish the phylogenetic relationship of E. aerogenes with different closely related bacterial species. Antimicrobial susceptibility results showed an alteration of 14.28% among twenty-eight tested antimicrobials. Similarly, 15.65% tested antimicrobials showed an alteration in MIC values. Chloramphenicol showed improved sensitivity i.e. resistant to susceptible after biofield treatment, with the support of decreased MIC by two folds (i.e. >16 to ≤8 µg/mL). Norfloxacin also showed decrease MIC by two folds (i.e. 8 to ≤4 µg/mL) as compared to control. Biofield treatment showed an impact on biochemical reactions (9.09%) followed by a change in biotype number (7770 5272) in treated group with respect to control (7770 5372). Using RAPD analysis, sample showed an average range of 4 to 42% of polymorphism, while 16S rDNA study showed that treated sample was detected as Kluyvera cryocrescens (GenBank Accession Number: AM184245) with 97% identity of gene sequencing data, which was nearest homolog species to Enterobacter aerogenes strain: C1111 (Accession No. AB244467). These results suggest that Mr. Trivedi's unique biofield treatment can alter the antimicrobial sensitivity pattern, thus it can be used as alternate energy medicine in future.

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Emergence of Antibiotic Resistance during Therapy for Infections Caused by Enterobacteriaceae Producing AmpC β-Lactamase: Implications for Antibiotic Use

Cited by 149 publications

References 12 publications

AmpC β-Lactamases

AmpC β-Lactamases

Complex Regulation Pathways of AmpC-Mediated β-Lactam Resistance in Enterobacter cloacae Complex

Characterization of Phenotype and Genotype of Biofield Treated Enterobacter aerogenes

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