A genomic study of 44 isolates of CPE from various species identified between 2008 and 2010, mainly from the Northwest of England, has concluded that plasmids played a key role in the early dissemination of CPE.
I came to ECCMID 2017 with a very specific question: do we need to think beyond ‘same-bug-same-gene’ horizontal transmission from a practical IPC view point in order to address the threat of IPC? The answer, unfortuantely, is yes!
The risk of interspecies transmission of carbapenemase genes is a real concern. We can barely get our heads around many different types of carbapenemase in a whole host of Gram-negative bacteria (compare the relative simplicity of methicillin resistance in S. aureus: a single gene, in a single species). Throw in interspecies horizontal transmission of carbapenemases and things get really tricky! Do we implement different control strategies to try to interrupt the transmission of carbapenemases (in contrast to the organisms themselves)? Could you have a multispecies outbreak of a carbapenemase on your hands and not even realise it?