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.
We now know that CPE is firmly embedded in the Northwest of England: a fairly recent point prevalence study of CPE carriage in the inpatient population in a large Manchester hospital found that 11% of patients were colonised or infected. But how did we get to this point? Did this arise from clonal dissemination of successful strains, horizontal gene transfer within and between species, or a bit of both?
In order to answer this question, a team including researchers from PHE and a Manchester hospital got 44 old KPC-producing CPEs (from 2008-2010) out of the freezer and sequenced their carbapenemase-bearing plasmids.
The 44 CPE included 24 K. pneumoniae, 7 E. coli, and 2 Enterobacter sp, which harboured KPC-2 (n=33), KPC-3 (n=9), and KPC-4 (n=2). The epidemiology of the large outbreak in Manchester is unusual – and different to other parts of the world. Instead of being dominated by a single K. pneumoniae clone (ST258), the picture is polyspecies and polyclonal within K. pneumoniae: in this study, only 7/19 K. pneumoniae isolates from the Northwest were from the ST258 clonal group. 84% of the CPE carried their carbapenemase on the same plasmid class (IncFIIK2). Most of these plasmids (93%) were closely related to the archetypal KPC-encoding plasmid associated with K. pneumoniae elsewhere in the world (pKpQIL). Some of the differences between the archetypal pKpQIL and the plasmid identified in the study may be associated with more efficient horizontal transfer of carbapenemases.
So, this is a small group of isolates, and the selection criteria for the group isn’t made clear. However, it does support the idea that horizontal spread of carbapememases is vital in understanding the epidemiology of CPE.