AmpC β-lactamase-producing Enterobacterales: what a clinician should know

Meini, Simone; Tascini, Carlo; Cei, Marco; Sozio, Emanuela; Rossolini, Gian María

doi:10.1007/s15010-019-01291-9

Cited by 134 publications

(119 citation statements)

References 34 publications

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“…For Salmonella strain 7102.58, DDST results were also suspicious for the production of an inducible AmpC (see Fig. S2 in the supplemental material) (11). Both isolates were identified as Salmonella enterica subsp.…”

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First Clinical Case ofIn VivoAcquisition of DHA-1 Plasmid-Mediated AmpC in a Salmonella enterica subsp.entericaIsolate

Clément

Keller

Bernasconi

et al. 2019

Antimicrob Agents Chemother

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A pan-susceptible Salmonella enterica serovar Worthington isolate was detected in the stool of a man returning from Sri Lanka. Under ceftriaxone treatment, a third-generation cephalosporin (3GC)-resistant Salmonella Worthington was isolated after 8 days. Molecular analyses indicated that the two isolates were identical. However, the latter strain acquired a blaDHA-1-carrying IncFII plasmid probably from a Citrobacter amalonaticus isolate colonizing the gut. This is the first report of in vivo acquisition of plasmid-mediated resistance to 3GCs in S. enterica.

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confidence: 99%

“…However, the rapid emergence of 3GC-resistant (3GC-R) strains in human and nonhuman settings presents a public health concern (2,3). Most of these isolates produce extended-spectrum ␤-lactamases (ESBLs) or the plasmid-mediated AmpC (pAmpC) CMY-2 (4-7), whereas the DHA-1 pAmpC is rarely reported (8)(9)(10)(11)(12).…”

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confidence: 99%

First Clinical Case ofIn VivoAcquisition of DHA-1 Plasmid-Mediated AmpC in a Salmonella enterica subsp.entericaIsolate

Clément

Keller

Bernasconi

et al. 2019

Antimicrob Agents Chemother

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“…Our findings concur with this prior work, with 61.7% of isolates failing to amplify the bla CMY target, suggesting a lack of sensitivity in using cefoxitin as a screening tool for AmpC enzymes. In support of this hypothesis, AmpC has previously been reported as an underappreciated mechanism of 3GC-R due to a lack of standardized testing for its detection[35]. As such, molecular methods such as PCR that can detect other common and emerging acquired ampC gene families (e.g.…”

Section: Resultsmentioning

confidence: 99%

Molecular epidemiology of third-generation cephalosporin-resistant Enterobacteriaceae from Southeast Queensland, Australia

Stewart

Price

Schabacker

et al. 2020

Preprint

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27Third-generation cephalosporin-resistant (3GC-R) Enterobacteriaceae represent a major 28 threat to human health. Here, we captured 288 3GC-R Enterobacteriaceae clinical isolates 29 from 258 patients presenting at a regional Australian hospital over a 14-month period. 30Alongside routine mass spectrometry speciation and antibiotic sensitivity testing, isolates 31 were examined using a rapid (~40 min) pentaplex real-time PCR assay targeting the most 32 common extended spectrum β-lactamases (ESBLs; CTX-M-1 and CTX-M-9 groups, plus TEM, 33 SHV, and an internal 16S ribosomal DNA control). Additionally, AmpC CMY β-lactamase 34 prevalence was examined using a singleplex PCR. A subset of isolates, including all 3GC-R 35 isolates obtained from the intensive care unit, were subjected to whole-genome sequencing 36 (WGS) to assess transmission dynamics, the presence of unidentified resistance 37 determinants, and genotyping accuracy. Escherichia coli (80.2%) and Klebsiella pneumoniae 38 (17.0%) were dominant, with Klebsiella oxytoca, Klebsiella aerogenes and Enterobacter 39 cloacae infrequently identified. Ceftriaxone and cefoxitin resistance was identified in 97% 40 and 24.5% of E. coli and K. pneumoniae isolates, respectively. Consistent with global findings 41 in Enterobacteriaceae, the majority (98.3%) of isolates harbored at least one β-lactamase 42 gene, with 144 (50%) encoding blaCTX-M-1 group, 92 (31.9%) blaCTX-M-9 group, 48 (16.7%) blaSHV, 43 133 (46.2%) blaTEM, and 34 (11.8%) blaCMY genes. WGS of β-lactamase negative or 44 carbapenem-resistant isolates identified uncommon ESBLs and carbapenemases, including45 blaNDM and blaIMP, and confirmed all PCR-positive genotypes. No evidence of transmission 46 among intensive care unit patients was identified. We demonstrate that our PCR assays 47 enable the rapid and cost-effective identification of ESBLs in the hospital setting, which has 48 important infection control and therapeutic implications.49 52 determinants within and among bacterial populations [1]. Both infection and colonization 53 with these globally-disseminated organisms are associated with poor clinical outcomes and 54 death [2]. 3GC-R Enterobacteriaceae prevalence rates vary considerably among hospitals 55 and countries, with particularly high rates in India, Asia, and the Middle East [3]. Australia 56 has historically observed a relatively low frequency of 3GC-R Enterobacteriaceae. However, 57 this pattern may be changing, with an extended spectrum β-lactamase (ESBL) phenotype 58 detected in 13.3% of E. coli and 9.8% of K. pneumoniae in blood culture isolates in 2018 [4], 59 up from 2013 rates of 7.6% and 6.3%, respectively. Moreover, ceftriaxone resistance was 60 seen in 13.4% of E. coli and 9.4% of K. pneumoniae, with 86.3% and 82.6% containing CTX-M-61 type ESBL genes, respectively [4]. 62 63 AMR in 3GC-R Enterobacteriaceae is generally conferred by the presence of an ESBL or the 64 over-expression of a chromosomal or plasmid-borne AmpC β-lactamase; however, the 65 prevalence of these determinants var...

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“…Notably, cytoplasmic monitoring of the integrity of muropeptide recycling in response to the presence of cell wall‐targeting antibiotics (especially β‐lactams) controls β‐lactamase expression as a key resistance response of many Gram‐negative pathogens . The clinical importance of this connection cannot be overstated . The breadth of study of this β‐lactamase‐resistance response—from the molecular (antibiotic structure) to the macromolecular (protein‐ligand interaction, biochemical pathways) to the microbiological and the clinical—requires the medium of the comprehensive review .…”

Section: Abetting the β‐Lactam Antibiotics Against Gram‐negative Bactmentioning

confidence: 99%

“…216,217 The clinical importance of this connection cannot be overstated. [218][219][220] The breadth of study of this β-lactamase-resistance response-from the molecular (antibiotic structure) to the macromolecular (protein-ligand interaction, biochemical pathways) to the microbiological and the clinical-requires the medium of the comprehensive review. [221][222][223][224][225][226][227][228] Here, we focus on the involvement of a family of important enzymes-the lytic transglycosylases-in peptidoglycan recycling and β-lactamase induction.…”

Section: Abetting the β-Lactam Antibiotics Against Gram-negative Bamentioning

confidence: 99%

Constructing and deconstructing the bacterial cell wall

Fisher

Mobashery

2019

Protein Science

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The history of modern medicine cannot be written apart from the history of the antibiotics. Antibiotics are cytotoxic secondary metabolites that are isolated from Nature. The antibacterial antibiotics disproportionately target bacterial protein structure that is distinct from eukaryotic protein structure, notably within the ribosome and within the pathways for bacterial cell‐wall biosynthesis (for which there is not a eukaryotic counterpart). This review focuses on a pre‐eminent class of antibiotics—the β‐lactams, exemplified by the penicillins and cephalosporins—from the perspective of the evolving mechanisms for bacterial resistance. The mechanism of action of the β‐lactams is bacterial cell‐wall destruction. In the monoderm (single membrane, Gram‐positive staining) pathogen Staphylococcus aureus the dominant resistance mechanism is expression of a β‐lactam‐unreactive transpeptidase enzyme that functions in cell‐wall construction. In the diderm (dual membrane, Gram‐negative staining) pathogen Pseudomonas aeruginosa a dominant resistance mechanism (among several) is expression of a hydrolytic enzyme that destroys the critical β‐lactam ring of the antibiotic. The key sensing mechanism used by P. aeruginosa is monitoring the molecular difference between cell‐wall construction and cell‐wall deconstruction. In both bacteria, the resistance pathways are manifested only when the bacteria detect the presence of β‐lactams. This review summarizes how the β‐lactams are sensed and how the resistance mechanisms are manifested, with the expectation that preventing these processes will be critical to future chemotherapeutic control of multidrug resistant bacteria.

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AmpC β-lactamase-producing Enterobacterales: what a clinician should know

Cited by 134 publications

References 34 publications

First Clinical Case ofIn VivoAcquisition of DHA-1 Plasmid-Mediated AmpC in a Salmonella enterica subsp.entericaIsolate

First Clinical Case ofIn VivoAcquisition of DHA-1 Plasmid-Mediated AmpC in a Salmonella enterica subsp.entericaIsolate

Molecular epidemiology of third-generation cephalosporin-resistant Enterobacteriaceae from Southeast Queensland, Australia

Constructing and deconstructing the bacterial cell wall

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