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I will assume that this question is regarding carbapenem resistance in gram-negative rods. The most likely mechanisms of carbapenem resistance are either production of a carbapenemase (e.g., KPC, OXA, or metallo-beta-lactamase) or the combination of a cephalosporinase (e.g., AmpC-type enzyme or ESBL) and loss of a porin in the outer membrane.
To my knowledge, of these mechanisms, the detection of carbapenem resistance is most troublesome for KPC-producers. The isolates may test susceptible to some carbapenems, specifically imipenem and meropenem, regardless of the method used to test susceptibility. The most sensitive indicator of the KPC enzyme is ertapenem susceptibility (any method works here including automated methods). KPC-producers are also characteristically very resistant to extended-spectrum beta-lactamases. The KPC enzyme has been reported in several species of Enterobacteriaceae, but occurs most commonly in Klebsiella pneumoniae.
Isolates of Enterobacteriaceae, especially isolates of K. pneumoniae that are resistant to extended-spectrum cephalosporins and non susceptible to ertapenem should be suspected of a carbapenemase. The carbapenemase activity could be confirmed by either PCR for the most likely gene, which in the U.S. is blaKPC, or a carbapenemase could be confirmed by a phenotypic test like the carbapenem inactivation assay {Yigit et al. 2001. AAC 45:1151}.
It is not clear that ertapenem resistance equals meropenem or imipenem resistance especially if the mechanism of ertapenem resistance a combination of a cephalosporinase with porin loss {Woodford et al. 2007. Int J Antimicrob Agent 29:456}.
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