Morrissey, Ian;
Bouchillon, Samuel K.;
Hackel, Meredith;
Biedenbach, Douglas J.;
Hawser, Stephen;
Hoban, Daryl;
Badal, Robert E.
Evaluation of the Clinical and Laboratory Standards Institute phenotypic confirmatory test to detect the presence of extended-spectrum β-lactamases from 4005 Escherichia coli, Klebsiella oxytoca, Klebsiella pneumoniae and Proteus mirabilis isolates
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Medientyp:
E-Artikel
Titel:
Evaluation of the Clinical and Laboratory Standards Institute phenotypic confirmatory test to detect the presence of extended-spectrum β-lactamases from 4005 Escherichia coli, Klebsiella oxytoca, Klebsiella pneumoniae and Proteus mirabilis isolates
Beteiligte:
Morrissey, Ian;
Bouchillon, Samuel K.;
Hackel, Meredith;
Biedenbach, Douglas J.;
Hawser, Stephen;
Hoban, Daryl;
Badal, Robert E.
Beschreibung:
<jats:p>A subset of <jats:italic>Escherichia coli</jats:italic>, <jats:italic>Klebsiella oxytoca</jats:italic>, <jats:italic>Klebsiella pneumoniae</jats:italic> and <jats:italic>Proteus mirabilis</jats:italic> isolates collected for the Study for Monitoring Antimicrobial Resistance Trends that were positive for the Clinical and Laboratory Standards Institute (CLSI) extended-spectrum β-lactamase (ESBL) phenotypic confirmatory test (<jats:italic>n</jats:italic> = 3245) or had an ertapenem MIC of ≥0.5 µg ml<jats:sup>−1</jats:sup> (<jats:italic>n</jats:italic> = 293), or both (<jats:italic>n</jats:italic> = 467), were analysed for ESBL genes. Most ESBL phenotype <jats:italic>E. coli</jats:italic> or <jats:italic>K. pneumoniae</jats:italic> possessed an ESBL gene (95.8 and 88.4 %, respectively), and this was 93.1 % if carbapenem-non-susceptible <jats:italic>K. pneumoniae</jats:italic> were removed. This rate was lower for <jats:italic>P. mirabilis</jats:italic> (73.4 %) and <jats:italic>K. oxytoca</jats:italic> (62.5 %). Virtually all ESBL-positive isolates (99.5 %) were cefotaxime non-susceptible [CLSI or European Committee on Antimicrobial Susceptibility Testing (EUCAST) breakpoints)]. Fewer isolates (82 %) were ceftazidime non-susceptible (CLSI breakpoints). In addition, 21.1 % of <jats:italic>E. coli</jats:italic>, 25 % of <jats:italic>K. oxytoca</jats:italic> and 78.7 % of <jats:italic>P. mirabilis</jats:italic> isolates were ceftazidime susceptible but ESBL positive. This suggests that CLSI breakpoints for ceftazidime are too high to detect ESBLs. The lower EUCAST breakpoints detected ESBLs in <jats:italic>E. coli</jats:italic> and <jats:italic>K. oxytoca</jats:italic> better, but 59.6 % of ESBL-positive isolates of <jats:italic>P. mirabilis</jats:italic> were ceftazidime susceptible. For isolates with ertapenem MICs ≥0.5 µg ml<jats:sup>−1</jats:sup>, more accurate ESBL phenotype analysis was observed for <jats:italic>E. coli</jats:italic> and <jats:italic>K. pneumoniae</jats:italic> (sensitivity >95 % for both, specificity 94.4 and 54.1 %, respectively). If carbapenemase-positive <jats:italic>K. pneumoniae</jats:italic> were excluded, the specificity increased to 78 %. The positive predictive values for the ESBL phenotypic test with <jats:italic>E. coli</jats:italic> and <jats:italic>K. pneumoniae</jats:italic> were 97.6 and 81.8 %, respectively, and negative predictive values were 75.9 and 95.2 %, respectively. We therefore suggest that it would be prudent to confirm phenotypic ESBL-positive <jats:italic>P. mirabilis</jats:italic>, <jats:italic>K. pneumoniae</jats:italic> and <jats:italic>K. oxytoca</jats:italic> with molecular analysis.</jats:p>