Detecting and preventing carbapenem-resistant Enterobacteriaceae (CRE)
Late last week, the CDC issued new guidance for control of CRE. You can read my 2009 post for thoughts on their initial guidance. This update expands on that guidance, providing tailored recommendations for different settings, ranging from regions where no CRE have been reported to those in which CRE are common. The guidance also emphasizes regional control and the role of long term care (and “long term acute care”) in the epidemiology of CRE.
I think the new guidance is on the mark, and should be helpful as we struggle with how to respond to these bad bugs. As was the case back in 2009, my main concern relates to the screening recommendations. Not all CRE are created equal, and the test methods available to most laboratories are not good at differentiating among the really nasty (e.g. KPC- and NDM-producers) and the moderately nasty (e.g. chromosomal cephalosporinase + porin protein mutation). The former have much greater outbreak and local-regional spread potential, which is why the modified Hodge Test (MHT) has been used to single them out. But the MHT is not always easy to interpret, can have falsely positive and negative results, and seems to perform especially poorly in detecting certain carbapenemases (e.g. NDM). The CLSI has issued lower MIC breakpoints to better detect CRE, but these breakpoints are (appropriately) designed to guide therapy for individual patients, not to provide detailed information about resistance mechanisms for infection prevention or public health purposes. Lower breakpoints means more CRE detected, most of which do not carry mobile resistance elements like KPC and NDM. Do we respond to them in the same way (they are still resistant, after all….)?
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