I am currently involved in some research that requires a clear distinction between CPE (i.e. Enterobacteriaceae that produce a carbapenemase) and non-carbapenemase-producing CRE. Since ‘non-carbapenemease-producing carbapenem-resistant Enterobacteriaceae’ is a bit of a mouthful, I need to come up with some sort of acronym. I would appreciate your thoughts on the scheme set out below:
You can read more thoughts on acronyms for carbapenem-resistant bacteria in a previous post here.
The analytical lab methods that we use to grow antibiotic-resistant bacteria make a big difference in terms of recovery. However, ‘pre-analytical’ factors are just as important in determining the sensitivity of prevalence studies. We are used to the idea of studies to work out the most sensitive anatomical site to sample for detecting colonisation with antibiotic-resistant bacteria. However, there are other ‘pre-analytical’ factors that may skew the findings of prevalence studies. A study from my old research group at KCL highlights how staff and patient choices, behaviours, and demographics can be pre-analytical factors that could skew prevalence studies.
I posted a blog a couple of years ago (was it really that long!) on a fascinating study suggesting that only 1/5 of S. aureus in hospital patients is hospital-acquired. My key conclusion from that study was that the number of potential sources for S. aureus that the team investigated was inadequate to draw any firm conclusions (they didn’t include staff, surfaces, or visitors). I concluded that ‘the next frontier of transmission mapping must be a more comprehensive evaluation of other potential sources…’. The authors must have been reading, because this study from the same group was published recently in Lancet ID, which is a more comprehensive evaluation of other potential sources.
I blogged on mcr-1 (colistin resistance) in China last week, to share the latest reassuring data. Well, the paper on which todays’ blog is printed will be used to wrap tomorrows’ market fish (typical Dutch expression). Nicolle Stoesser (Oxford) send me the latest news, coming from a Nature Microbiology study providing evidence for the potential of spread of carbapenamases by flies and birds. Not reassuring at all, and potentially with major consequences. Continue reading
My previous blog on “mcr-1 and the end of the world” evoked responses on the important effects of colistin resistance on patient outcome, referring to a new study in CID with the following abstract closure: “Importantly, mortality was increased in patients with colistin-resistant isolates.” The wording is correct, but I’m afraid that it will be interpreted incorrectly. Continue reading
This post provides a briefing on the current status of the Mycobacterium chimaera issue related to heater-cooler units (HCUs) used in cardiothoracic surgery. You can download some accompanying slides here. Also, I found this recent ICHE review on the subject very helpful to bring me up to speed.
If you read this, you may well be concerned about antibiotic resistance and consider reducing the burden of disease caused by AMR as one of your professional goals. Broad attention helps us to fight the problem: it creates awareness and funds for research. So, how do we cope with data that may jeopardize these ambitions (raising awareness fort he problem AMR)? Here is the eaxmple of mcr-1. Continue reading
Tabloids have repeatedly warned the people for superbugs on chicken meat, after researchers had convincingly shown that the chicken filets that we buy are contaminated with ESBL-producing bacteria, mainly E. coli. Widely considered a public health threat, it was a decisive argument to insist on reductions in antibiotic use in the agricultural industry in the Netherlands. Yet, whether meat contamination constitutes a risk for human health is unknown. This was now quantified, with surprising results. Continue reading
A PNAS paper on the genomic diversity of carbapenemase producing bacteria in the US reports strong evidence of carbapenamase (an enzyme produced by bacteria that breaks down carabapenem antibiotics) activity but no sign of a carbapenemase gene. This provides a timely reminder that we are only really scratching the surface in our understanding of carbapenemases and how they work.
A new Lancet ID study suggests that restriction of fluoroquinolone usage has been the main driver of the national reduction in C. difficile infection in England. This paper is challenging in terms of some of the accepted approaches to controlling the transmission of C. difficile: if it’s all about reducing fluoroquinolones (and antimicrobials in general) and nothing to do with these measures, then why invest so much time and energy in isolation of symptomatic cases, cleaning and disinfection etc?
Reflections on Infection Prevention and Control 