Occurrence of plasmidic AmpC type β-lactamase-mediated resistance in Escherichia coli: report from the SENTRY Antimicrobial Surveillance Program (North America, 2004)

Deshpande, Lalitagauri M.; Jones, Ronald N.; Fritsche, Thomas R.; Sader, Hélio S.

doi:10.1016/j.ijantimicag.2006.07.025

Cited by 45 publications

(29 citation statements)

References 14 publications

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“…Both of these pAmpC genes have previously been detected in E. coli in the United States and have been implicated in ESBL screenpositive, confirmatory testing-negative reports (5). Phenotypic screening with APB detected 20 of 22 amplification-confirmed pAmpC genes and three apparent false-positive results, lending support to this method of screening.…”

Section: Discussionmentioning

confidence: 61%

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Unreliable Extended-Spectrum β-Lactamase Detection in the Presence of Plasmid-Mediated AmpC in Escherichia coli Clinical Isolates

Robberts¹,

Kohner²,

Patel

2009

J Clin Microbiol

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The emergence of extended-spectrum ␤-lactamase (ESBL) and plasmid-mediated AmpC (pAmpC) enzymes in Escherichia coli raises concern regarding accurate laboratory detection and interpretation of susceptibility testing results. Twenty-six cefpodoxime ESBL screen-positive, cefoxitin-resistant E. coli clinical isolates were subjected to clavulanate ESBL confirmatory testing employing disk augmentation, Etest, and the BD Phoenix NMC/ID-132 panel. Phenotypic pAmpC production was assessed by boronic acid disk augmentation. ESBL and pAmpC genes were detected by gene amplification and sequencing. ESBL genes (SHV and/or CTX-M-type genes) were detected in only 7/26 ESBL screen-positive isolates. Of 23 aminophenylboronic acid screen-positive isolates, pAmpC genes were detected in 20 (CMY-2 or FOX-5 genes). High incidences of false-positive ESBL confirmatory results were observed for both clavulanate disk augmentation (9/19) and BD Phoenix (5/19). All were associated with the presence of pAmpC genes with or without TEM-1. Etest performed poorly, as the majority of interpretations were nondeterminable. In addition, false-negative ESBL confirmatory results were observed in isolates possessing concomitant ESBL and pAmpC genes for Etest (four of five), BD Phoenix (three of five), and disk augmentation (one of five). The results indicate poor performance of currently employed ESBL confirmatory methods in the setting of concomitant pAmpC. Some isolates with pAmpC and ESBL genes fell within the susceptible category to extended-spectrum cephalosporins, raising concern over currently employed breakpoints.Ambler class A extended-spectrum ␤-lactamase (ESBL) genes in Escherichia coli are well documented. Possible ESBL production has been reported to occur in up to 9% of European E. coli isolates (15). In addition, chromosomal Ambler class C AmpC genes have been mobilized and are now being disseminated on plasmids, reminiscent of the early dissemination and evolution of ESBLs (11). Increasingly, reports document the detection of plasmid-mediated AmpC resistance (pAmpC) in E. coli (4,6,12). Data from the SENTRY antimicrobial surveillance program for North America show that 19/65 ESBL screen-positive E. coli isolates harbored pAmpC (5).The ESBL hydrolytic spectrum includes the oxyimino-cephalosporins and monobactams but not 7-␣-methoxy-cephalosporins (cephamycins) and is inhibited by clavulanate, sulbactam, and tazobactam. The broader spectrum of the AmpC enzymes includes the cephamycins, and AmpC enzymes are not inhibited by clavulanate, sulbactam, or tazobactam. The Clinical and Laboratory Standards Institute (CLSI) recommends that antimicrobial susceptibility testing include screening for ESBL production in E. coli, employing cefpodoxime, ceftazidime, aztreonam, cefotaxime, or ceftriaxone, followed by phenotypic confirmation with clavulanate (3).ESBL screening results are reviewed to select for those organisms that need phenotypic ESBL confirmation, as recommended by CLSI, and results are issued with the aim of preventing inappropriate u...

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Section: Discussionmentioning

confidence: 61%

“…Increasingly, reports document the detection of plasmid-mediated AmpC resistance (pAmpC) in E. coli (4,6,12). Data from the SENTRY antimicrobial surveillance program for North America show that 19/65 ESBL screen-positive E. coli isolates harbored pAmpC (5).…”

mentioning

confidence: 99%

Unreliable Extended-Spectrum β-Lactamase Detection in the Presence of Plasmid-Mediated AmpC in Escherichia coli Clinical Isolates

Robberts¹,

Kohner²,

Patel

2009

J Clin Microbiol

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“…We detected fewer ESBL producers (13,14) but a higher proportion of MDR isolates (23,39,45). Not surprisingly, the resistance rates were the highest in NA isolates.…”

Section: Discussionmentioning

confidence: 71%

Major Differences Exist in Frequencies of Virulence Factors and Multidrug Resistance between Community and Nosocomial Escherichia coli Bloodstream Isolates

et al. 2010

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Escherichia coli is a major cause of bloodstream infections and death due to sepsis. It is the most frequent Gram-negative bacterial pathogen recovered from cultures of blood from both community-acquired and nosocomial cases. We set out to determine the relationships between E. coli virulence factors (VFs), phylogenetic groups, and antibiotic resistance and whether bacteremia cases had a community, health care-associated. or nosocomial origin. Isolates from consecutive episodes of E. coli bacteremia in 303 patients presenting to a university hospital were screened for their VFs, phylogenetic group, and antibiotic resistance. The majority of VFs present in the collection were equally distributed between antibiotic-susceptible and multiple-drugresistant (MDR) isolates, but the overall VF score was higher for isolates of community and health careassociated origin than those of nosocomial origin (P ‫؍‬ 0.0002 and P ‫؍‬ 0.0172, respectively); the papA, papG allele II, hlyA, and hek VFs were more prevalent in this cohort. Most isolates belonged to phylogenetic group B2, which harbored a greater proportion of antibiotic-susceptible isolates than MDR isolates (P ‫؍‬ 0.04). The community, health care-associated, or nosocomial origin of E. coli bacteremia determines the virulence capacity of an isolate better than the phylogenetic group does. This study provides new insights into the relationships between the pathogenesis and epidemiology of E. coli bacteremia.Escherichia coli is a leading cause of bloodstream infections worldwide, and the associated rate of mortality is high (32). Extraintestinal pathogenic E. coli (ExPEC) is the predominant cause of these invasive infections, which often originate from the urinary tract. They possess a wide variety of specialized virulence factors (VFs) responsible for pathogenesis outside the gastrointestinal tract, including diverse adhesins, invasins, and protectins (48). ExPEC isolates are generally concentrated within phylogenetic group B2 and, to a lesser extent, group D, whereas less virulent and commensal E. coli isolates belong to groups A and B1 (25,29,37). However, the minimal requirements for bacterial invasion of the bloodstream have yet to be determined.Bacteremic isolates harbor a significantly greater repertoire of VFs than gastrointestinal tract commensal E. coli isolates (46), and where their molecular and epidemiological environments have been further analyzed, it appears that antibioticsusceptible and -resistant ExPEC isolates are fundamentally different bacterial populations (19,21,23,25,27,37,38,42,43,50). Antibiotic-susceptible strains mostly derive from phylogenetic group B2 and are associated with higher VF prevalences than antibiotic-resistant strains, which are typically associated with shifts toward groups D and A. This decreased prevalence of VFs within resistant strains has been suggested to be a possible trade-off between resistance and virulence in ExPEC (8). An important epidemiological consideration is whether community-acquired (CA) or health care-asso...

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“…The isolates which susceptible to cefepime and resistant to cefoxitine were consider as an AmpC-producer isolate [13].…”

Section: Phenotypic Detection Of Ampcmentioning

confidence: 99%

Phenotypic and Molecular Characterization of Plasmid Mediated AmpC among Clinical Isolates of Klebsiella pneumoniae Isolated from Different Hospitals in Tehran

Azimi¹

2015

JCDR

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Occurrence of plasmidic AmpC type β-lactamase-mediated resistance in Escherichia coli: report from the SENTRY Antimicrobial Surveillance Program (North America, 2004)

Cited by 45 publications

References 14 publications

Unreliable Extended-Spectrum β-Lactamase Detection in the Presence of Plasmid-Mediated AmpC in Escherichia coli Clinical Isolates

Unreliable Extended-Spectrum β-Lactamase Detection in the Presence of Plasmid-Mediated AmpC in Escherichia coli Clinical Isolates

Major Differences Exist in Frequencies of Virulence Factors and Multidrug Resistance between Community and Nosocomial Escherichia coli Bloodstream Isolates

Phenotypic and Molecular Characterization of Plasmid Mediated AmpC among Clinical Isolates of Klebsiella pneumoniae Isolated from Different Hospitals in Tehran

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