Mupirocin use drives mupirocin resistance…or does it?

mupirocin

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.

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Reconsidering the burden of CRE screening

 

swabs

Shortly after the PHE Toolkit was published, I blogged some crude sums to size the burden of CRE admission screening a la Toolkit. I’m pleased to report that colleagues at Imperial have done a much better job of this, published in a letter in the Journal of Infection. The study provides some evidence that the recommendation in the PHE CRE Toolkit to perform pre-emptive isolation of suspected carriers whilst obtaining three negative screens is simply not feasible. The team then compare an alternate strategy – of applying the Tookit triggers to admissions to high risk specialties only (intensive care, nephrology, cardiothoracic surgery, neurosurgery and oncology).

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We need to work together to reduce CRE and other pathogens

Some fascinating modelling from the CDC Vital Signs programme suggests that a co-ordinated, multi-facilitiy approach will be much more effective than each hospital doing its own prevention interventions.

The team first estimated the burden of key infections in the US: CRE, multi-resistant  P. aeruginosa, invasive MRSA and CDI combined were responsible for 310,000 infections in 2011, which would increase 10% to 340,000 over 5 years. However, with an ‘aggressive’ national intervention, this could be reduced to below 200,000 by 2019. It would be a huge undertaking to implement and co-ordinate a national campaign in the US, where there is so much heterogeneity in the way that hospitals are structured and funded. But if anybody can do it, the CDC can!

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It’s transmission doc, but not as we know it

A groundbreaking study just published in PLOS Genetics provides new insight into the transmission dynamics of bacteria in the ICU setting using WGS. The ambitious authors performed WGS on virtually all bacterial isolates from ICUs in a US hospital for a year. The first surprise was that 12% of the bacteria considered clinically relevant were previously undescribed.

The next – and perhaps biggest – surprise was that whilst transmission of the usual suspect pathogens (MRSA, VRE etc) was rare, 9% of the other bacteria were shared by multiple patients, often with overlapping admissions (see the figure below). This suggests that there is a fair bit of transmission going on under the radar in the ICU setting.

Figure: Clonal lineages extending across multiple patients.

WGS ICU timeline

This study reminds me of one published in CID a few years ago showing that outbreaks of resistance probably occur regularly and usually undetected across multiple species.

So, is it time to start using WGS for all bacteria identified in the clinical laboratory? Not quite yet I don’t think: the analytical methods have not yet caught up with the sequencing technology. But this study is a glimpse of the future, no doubt about it.

Should we throw out the chlorhexidine with the bathwater?

Noto chg

Following hot on the heels of a series of studies showing that daily bathing using chlorhexidine reduces the risk of HCAI, a recent study suggests that chlorhexidine daily bathing does not reduce HCAI. The headline finding is that chlorhexidine bathing did not reduce HCAI. Before throwing out the chlorhexidine with the bathwater, it’s worth considering the limitations of the study.

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Is CRE lurking in nursing homes?

Nursing home CRE

They say that things come in threes, so following hot on the heels of blogs about MRSA and other MDROs in nursing homes, I was struck by a recent outbreak report of CRE associated with nursing homes the Netherlands.

Following the admission of a patient from a Greek ICU, a nosocomial transmission of CRE (ST258 KPC K. pneumoniae) occurred. By the way, this occurred despite the hospital recognising the risk of CRE at the time of admission from the Greek ICU, perform an admission screening and implementing pre-emptive contact precautions. Then the index patient was transferred to a nursing home, where subsequent transmission occurred to four other patients.

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How much chlorhexidine actually makes it to a patient’s skin?

CHG

There has been much impressive research of late around the use of chlorhexidine daily bathing to reduce the burden of skin contamination and protect patients from infection. This is quickly becoming en vogue, especially for ICU settings in the USA. But what is compliance like with this intervention, and how do you measure compliance? The studies that have measured compliance previous have said “Yes, this patient was given a chlorhexidine wash today”, but have rarely gone so far as to measure the actual concentration of chlorhexidine on the patient’s skin.

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How can we stop nursing homes nurturing MRSA?

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There is an emerging feeling that we need to start spreading the focus of infection prevention and control beyond acute hospitals. There has always been a sense that standards of infection control outside of acute settings are, shall we say, “different” to acute hospitals (aka non-existent) so it’s great to see a study of an infection control intervention in nursing homes.

The study was a cluster randomised controlled trial of MRSA screening, decolonisation and enhanced environmental disinfection vs. standard precautions in 104 of 157 nursing homes in a Swiss region. The authors chose a rather unusual, pragmatic endpoint of the prevalence of MRSA colonisation after 12 months.

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CRE winging its way around the world

aeroplane

CRE are known to be adept at hitchhiking around the world, hence the focus on cross-border transmission in Europe. A startling example of this comes in a report from Poland result from the terrorist shootings in Tunisia. Two Polish nationals seriously injured in the shootings were repatriated following a 10-day stay in a hospital in Tunis, Tunisia. A grand total of four CREs were identified from the two patients!

Three of these were identified at the time of admission, so almost certainly originated in Tunisia. The fourth CRE was identified 10 days after repatriation to Poland. The authors suggest that the most likely explanation for this is poor sensitivity of admission screening. I venture, however, that it’s more likely due to in-hospital transmission in Poland, since the two patients were treated by the same staff.

Nonetheless, the most troublesome finding here is that at least three separate CREs were imported into Poland by just two patients. Can anybody find me a paper on the prevalence and epidemiology of CRE in Tunisia? No? Thought not. The implication here is that CRE is already far more established than feared in Tunisia and many other parts of the world!

Image: Aeroplane.

Biofilms make the hospital environment far from ‘inanimate’

biofilm

Anybody doubting that biofilms really do exist on dry hospital surfaces needs to read this study: biofilms are there, they are complex, and they are common. A landmark study by the same Australian Vickery group published in 2012 first identified biofilms on a handful of dry hospital surfaces in an ICU. But this study is far more comprehensive and convincing.

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