Sir, Carbapenem resistance mediated by plasmid-encoded carbapenemases has emerged worldwide and become a major concern.1 The detection of the activity of carbapenemases has a strong impact on hospital infection control, because the detection of their presence can initiate measures to avoid potential outbreaks and lateral spread of the resistance. Although molecular detection by PCR is considered the gold standard for carbapenemase gene identification, some limitations are clearly recognized. Between them, false-negative results (the presence of a carbapenemase gene not tested in the PCR reaction, or mutations affecting annealing of primers) or the detection of inactive genes (i.e. no carbapenemase expression) can delay infection-control measures or, oppositely, initiate them when they are not required. A fast and accurate phenotypic method, the Carba NP test (CNPt), was developed; it detects carbapenemase activity with very high sensitivity and specificity and lower costs compared with those of PCR.2 This method is now being recommended in the CLSI guidelines for carbapenemase activity detection.3 However, recent studies have shown that this test has lower sensitivity particularly against isolates expressing β-lactamases with low carbapenemase activity, such as OXA-48-like, or expressing mucoid colonies.4,5 Another new test, the carbapenem inactivation method (CIM), has shown very promising results based on its sensitivity, specificity, low cost and easy interpretation.6 Briefly, the CIM consists of two steps: (i) incubation of a meropenem disc with the isolate to be tested; and (ii) incubation of this meropenem disc with the Escherichia coli ATCC strain. After this second incubation step, the presence of carbapenemase activity can be easily detected: the absence of an inhibition zone indicates enzymatic hydrolysis of meropenem during the first incubation step, whereas a ‘clear inhibition zone’ appears when the tested isolate does not express carbapenemase activity.6 The goal of this study was to compare the performance of the CIM and the CNPt against a panel of well-characterized enterobacteria.
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Tijet et al. (2015) studied this question.
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