We’ll be publishing the results of the vote on whether or not we can halve HA-GNBSI by 2021 later this week. Right now, it looks like Martin is heading for a comfortable, if somewhat depressing victory (“No, we can’t halve GNBSI by 2021”) but there’s still time to ride a wave of positivity and vote with me that “Yes, we can halve GNBSI by 2021”. So, I thought that now would be an appropriate time to review the recent JHI paper that both Martin and I referred to, providing some enhanced epidemiological data on E. coli BSIs in England.
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?
The Department of Health announced last week their intention to halve the rate of E. coli BSI by 2020. Whilst this is a move that should be embraced, it will be an enormous challenge to achieve. The reduction that has been delivered with MRSA BSI could be seen as a model for success (and I suspect that if you were a politician, you would see it this way). However, it is vital to recognise that E. coli BSI and, more broadly, Gram-negative BSI (GNBSI) are not the same as MRSA BSI, and will require a different reduction strategy.
Take a look at these three stories on intensive poultry production and antimicrobial resistance in India published yesterday on the Bloomberg website. In accordance with what the movie industry does, these articles should be accompanied by a warning: “These articles contains scenes that some readers may find disturbing”. As the editor of the articles said in an email to colleagues that forwarded it to me: “I think you’ll agree that these are important stories and deserve attention (and hopefully a response from the appropriate authorities and the community).” Obviously, I do agree.
I attended the first EMBRACE seminar today at Imperial College London. EMBRACE (Engineering, Medicine, Natural Sciences and Physical Sciences Bridging Research in Antimicrobial resistance: Collaboration and Exchange) is a gap-bridging collaborative aiming to bring together Engineers, Scientists, Doctors, and others to find new ways to address AMR and tackle HCAI. I thought I’d share some of my highlights from the seminar.
I am becoming increasingly interested in colistin resistance in CPE, not least because of this work that we will be presenting on colistin resistance in CPE at ECCMID in a few months time. I have been brushing up on how colistin resistance occurs in CPE, and why it is important, so thought I’d share my findings. I started with a pubmed search for “colistin resistance mechanism” on 12/02/16 and this is what I found (85 hits from the initial search):
Colistin is an old class (discovered during WWII) of cationic antibiotic. Colistin (polymyxin E) is a polypeptide bactericidal agent and is one of the two clinically available forms of polymyxin agents (polymyxin B and polymyxin E). Colistin interacts with lipopolysaccharide in the outer membrane, resulting in a leaky and ultimately dead bacterial cell.1 Issues with presumed nephrotoxicity have kept colistin very much on the top shelf, but the emergence of CPE has brought colistin down a shelf or two – and we are learning that the nephrotoxicity tradionally associated with colisin may not be so bad afterall.1