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.
MRSA
Time to go shopping for a UVC system?
It is great to see the long-awaited ‘Benefits of Terminal Room Disinfection’ (BETR-D) randomised controlled trial of a UVC automated room decon (ARD) system published, in the Lancet, no less! This study firms up the importance of environmental contamination in transmission, and demonstrates additional benefit of UVC over and above enhanced conventional methods for VRE, maybe for MRSA, but not for C. difficile.
All BSIs are expensive, not just antimicrobial resistant ones
Eurosurveillance have recently published a study from the TIMER group evaluating the impact of antimicrobial resistance on hospital mortality, excess length of stay (LOS), and cost of BSI in European hospitals. The study highlights the high cost of BSIs, especially when antimicrobial resistant.
Reducing Gram-negative BSI…by accident
We have precious little data on what works to prevent the transmission of MDR-GNR. An interesting article published recently in CID provides invaluable data that an infection control programme aimed at reducing MRSA (and succeeding) was also effective in reducing GNR BSI!
LA-MRSA: The Never-ending Sequel
Over the last years, we have been getting used to the fact, that commercial pig, veal, and chicken farms, as well as horse breeding, is associated with a risk of animal to human transmission of livestock-associated Methicillin-resistant Staphylococcus aureus (LA-MRSA). In the line of suspects, chicken were the last to be conformed as true source of LA-MRSA. Van Duijkeren et al (J Antimicrob Chemother 2016;71:58-62) investigated addition feathered suspects, namely dugs and turkeys.
First of all lets get Donald & friends of the list of suspects. In only one of 10 duck farms that were investigated, MRSA was found in the samples from the animals and duck houses. None of the humans living or working on duck farms, nor any part of their residence, was MRSA-positive. It therefore seems save to conclude that ducks pose no danger for transmission of LA-MRSA.
Unfortunately, the story about turkeys seems to be different. Overall, 3 of the 10 turkey farms harbored MRSA. In addition, MRSA was found in 16% of the humans and 31% of the farmhouse samples. The highest risk was seen among the turkey farmers themselves (45.5% MRSA-positive), but employees and family members (6.3%) weren’t free of risk, either. Significant risk factors found by the investigators were: having physical contact with the animals and visiting poultry houses.
In 2 out of 3 frams in which MRSA was found among the animals and the humans, whole genome mapping showed >95% homology, corroborating the strong evidence for animal-to-human transmission of MRSA on turkey farms.
English HCAI and AMR data at your Fingertips
PHE have just launched an interactive database for HCAI and AMR data from England using their ‘Fingertips’ platform. The HCAI data in the module has been available for years, but was buried in pretty dense Excel spreadsheets so tricky to visualise. The Fingertips platform makes data extraction and visualisation so easy even I can do it (example below).
Community MRSA preys on the poor and deprived
As you can probably tell from the title, this post comes with a warning: it presents some rather “un-PC” data, but I’ll do my best to deliver it calmly and dispassionately! My old research team from KCL have just published a paper in PLOS Medicine on the association between social and material deprivation, and MRSA.
I’ve been interested in the dynamic between hospital-associated (HA) and community-associated (CA) MRSA for years (not least because it was the subject of my PhD thesis). I wrote a review several years ago on how community MRSA should be seen as a genotypic phenomenon with epidemiological implications. Using this framework, it is possible to get your head around CA strains of MRSA beginning to cause hospital-acquired infections. The aim of this study was to use a large collection of MRSA from across several regions of London to explore the transmission dynamics and epidemiological associations of HA and CA types of MRSA.
Reflections from Infection Prevention 2015 Part I: Beating the bugs
Infection Prevention 2015, the annual conference of IPS, was held in Liverpool this year. I’m delighted to say that the abstracts from the submitted science are published Open Access in the Journal of Infection Prevention. This first instalment of my report will be “bug-focussed”, followed by another two on different themes:
Part I: Beating the bugs
Part II: Improving the systems
Part III: Thinking outside the box
Opening lectures
The conference kicked off with fellow ‘Reflections’ blogger Prof Andreas Voss. By Andreas’ own admission, he was given a curve-ball of a title: ‘CRE, VRE, C. difficle or MRSA: what should be the priority of infection prevention?’ [No idea where that could have come from…] Andreas developed a framework for grading the priority of our microbial threats, accounting for transmissibility, virulence, antibiotic resistance, at-risk patients, feasibility of decolonisation, cost, and impact of uncontrolled spread. And the result? Any and all microbes that cause HCAI should be a priority of infection prevention. Even those that seem to have less clinical impact (such as VRE) are good indicators of system failure. If we focus too much on one threat, we risk losing sight of the bigger picture.
What is the fitness cost of mupirocin resistance?
Jon posted a blog last week on mupirocin resistance in MRSA. This week, guest blogger Dr Gwen Knight (bio below) writes about a companion paper also published in the Journal of Antimicrobial Chemotherapy, which models mupirocin resistance…
It is a truth universally acknowledged, that acquiring most mechanisms of drug resistance incurs a fitness cost to the host bacterium. Determining the size of this cost and the impact that this cost will have on the spread of drug resistance is difficult. Is a 10% reduction in growth rate in the laboratory enough to stop resistance spreading in a hospital?
Mupirocin use drives mupirocin resistance…or does it?
I’ve blogged before that mupirocin resistance is an inevitable consequence of mupirocin use. Whilst I still think that this is true, my old colleagues from GSTT / KCL have just published an article suggesting that mupirocin resistance in MRSA has more to do with clonal variation than with mupirocin use.
The study is part of an ambitious project to sequence the genome of around 1000 MRSA isolates from across Central and South-East London (Guy’s and St. Thomas’, King’s, and Lewisham). Each isolate was then tested for phenotypic high (HMR) and low (LMR) mupirocin resistance, the genome was scoured for the genetic determinants known to be associated with mupirocin resistance, and clone was derived from the genome sequence. Risk factors for both HMR and LMR were then explored.
Reflections on Infection Prevention and Control 