A concise but powerful study has just been published in Archives of Internal Medicine, showing that the incidence of CP-CRE in clinical cultures has increased a whopping 69% between 2019 and 2023 in the USA, from 2.0 to 3.1 per 100,000 people.

This was a huge study co-ordinated by the CDC through a mandatory surveillance programme across 29 states and representing 35% of the entire population of the USA. Participating laboratories sent all of their CRE clinical isolates to the CDC for characterisation, and age-adjusted incidence rates were calculated.

The overall age-adjusted incidence rate increased more-or-less year on year from 2.0 in 2019 to 3.1 per 100,000 people in 2023. The incidence of NDM-producing CPE, and specifically NDM-producing Klebsiella sp. drove pretty much all of this increase. In fact, the incidence of NDM-producing CPE increased 461% over the study period!

There’s couple of really concerning elements to these findings. Firstly, the pace of change. To see this dramatic population-level increase in the incidence of CP-CRE over a 4 year period is nothing short of dramatic. Second, the fact that the metallo-beta-lactamase (MBL) NDM has become so established is a worry, given that MBL-CPE are even more difficult to treat and have worse outcomes than non-MBL CPE. Thirdly, this study included isolates from clincal cultures only (screens were excluded – I had to dig in the supplemental info to confirm this!). So, this does not show us the true extent of prevalence if we were to include colonisation.

We see a very different picture in the UK. The latest UKHSA epidemiological summary shows that the population rate of CPE is around 3 per 100,000 people – but this includes both screens and clinical cultures. The incidence of CPE in clinical cultures is around 0.9 per 100,000 people, more than 3x lower than in the USA. Now, we can’t directly compare these population-level estimates because the methodology behind them is different. But this is consistent with other studies suggesting that the prevalence of CPE in the UK is considerably lower than in the USA.

It’s notable that this study was undertaken over the pandemic years, so it’s possible that this had an impact on accelerating the progression of CPE. On the one hand, there was less social contact, and less international travel, so you may expect the pandemic to have slowed the spread of CPE rather than accelerated it. But we know that control of antimicrobial prescribing in general took a hit during the pandemic, so that could be a factor. Another possibility is that more pre-existing colonisation developed into infection during the pandemic years due to changes in population health (e.g. access to healthcare, changes in hospital care).

Finally, a note on nomenclature. I had quite a detailed discussion with some colleagues this week about how we classify “CPE”. I fully support the nomenclature used by the authors in this study, using “CP-CRE” (carbapenemase-producing carbapenem-resistant Enterobacterales) to differentiate it from from CRE (which may or may not be carbapenemase-producing). But fully acknowledge this is a bit fiddly, and gets even more fiddly if we go down the route of “NCP-CRE” (non-carbapenemase-producing CRE). Also, as somebody pointed out to me this week, NCP-CRE is a bit problematic because it assumes you have ruled out every single carbapenemase – so perhaps it should be “NKCP-CRE” (no known carbapenemase-producing CRE)! (I’m not serious about NKCP-CRE but I am serious about CP-CRE and NCP-CRE, in case you were wondering!)

The findings of this study really are salutary, and if the rate of change in the incidence of CPE continues, quite quickly we will see at least parts of the USA beginning to really suffer the consequences of the emergence of CPE.