Year: 2014

Infection Prevention 2014: Some highlights

Jon Otter (@jonotter) Conferences ,

ip2014

Another Infection Prevention Conference has been and gone; here are a few highlights. Worth noting that all of the submitted abstracts are published in an open access Journal of Infection Prevention supplement.

Opening talks

The now past-president Jules Storr kicked off the Conference with an inspiring talk on “real” leadership, which isn’t about CEOs and eminent professors. Real leadership inspires people to wash their hands in the dead of night when nobody’s looking. Roselinde Torres’ TED talk is worth a look (‘What it takes to be a great leader’) and ‘How to behave and why’ by the fantastically named Munro Leaf contains some leadership lessons from 1946!

Next up, IPS Patron Prof Didier Pittet challenged us to change our education methods to meet the changing (and dare I say somewhat fickle) needs of a rapidly changing world! Generation “We” (born 1980-2000, thus including me) require multimodal approaches to keep us engaged, and would probably rather watch a webinar than come to a conference! But, if you’d like to go ‘Old Skool’, there’s always Didier’s new book.

The highlight of the conference for me was Dr Jason Leitch’s address on developing a safety culture. A culture of safety has been embedded into other industries (e.g. airline, hotel and military) so why not healthcare? It’s a much quoted stat that a 747’s worth of people die from HCAI each [insert time period to suit your data]. So how many planes need to go down before we adopt a culture of safety? A culture of safety has a language to go with it – only the air traffic controller can say actually say “take-off”, and then only once. Perhaps only the IV nurse should be allowed to say “Catheter”, and only at the point of insertion!

Dr Michael Borg then took to the stage to parallel antibiotic resistance with Star Wars: a battle of intergalactic scale! Michael spent some time discussing the impressive reductions achieved in his hospital on multidrug-resistant A. baumannii, applying the principles of the ESCMID guidelines, with a particular focus on environmental issues. However, the new and more challenging threat comes from the carbapenem-resistant Enterobacteriaceae – aka the Death Star [note, pretty sure Dr Borg didn’t actually say that, but I think it’s a good fit with his analogy]. So what to do? Be an Ewok! Small and ostensibly insignificant, but surprisingly powerful as a collective force.

Cotteral Lecture – Dr Evonne Curran

Dr Evonne Curran delivered the Cotteral Lecture, entitled “The times they are a changing”. Reflecting on her thorough reviews of some older literature to write her outbreak columns on MRSA and CRE, Evonne reminded us how far we’ve come but how far we have yet to go. It wasn’t so long ago that we were questioning whether C. difficile was infectious (and now we’re asking a similar question from a different angle)! Equally, in 1990, installing one sink on a ward increased the number of sinks by 100%. Yet there can be no cause for complacency: we haven’t reached base camp for the CRE epi curve! Evonne didn’t quite finish on a song, but she did finish on a Hand Hygiene Haiku:

‘Five moments for hands

For infection prevention 

Essential for all’

Universal gloves and gowns

Dr Dev Anderson (Duke) gave an engaging lecture on the impressive ‘Benefits of Universal Gloves and Gowns’ (BUGG) study. This cluster randomized controlled trial design is likely to be the gold-standard assessment of infection prevention and control interventions. The problem with this powerful design is that studies need to be large to be powered appropriately. This study involved 20 ICUs and still failed to meet the primary end point (a reduction in MRSA / VRE acquisition). So will ICUs around the world be switching to universal gloves and gowns? On the basis of this study, combined with the well-publicized downsides of “contact precautions”, no. A targeted approach to contact precautions is better…

As if to reinforce the message of judicious use of gloves, Jennie Wilson’s talk highlighted that using gloves badly is worse than not using gloves at all! Some of the staff perceptions surrounding glove use were enlightening, including the classic: “when I wear gloves, I don’t need to wash my hands as often”. Hmmm.

CRE stream

Or should I say CPE stream? Or perhaps CPC is more to your fancy? This excellent stream kicked off with Dr Bharat Patel assisting in us in navigating the ‘acronym minefield’ that is multidrug-resistant Gram-negative bacteria. An informal poll of the audience prior to Dr Patel’s talk suggested that only a handful would be comfortable explaining the difference between CRE and CPE to a colleague. Hopefully, this was remedied by the talk!

Then, Dr Tara Palmore (NIH, USA), Dr Andrew Dodgson (Manchester) and Erika Grobler & Ogra Marufu (King’s College Hospital, London) provided a series of ‘views from the trenches’ of CRE prevention and control. Dr Palmore described the fascinating utility of whole genome sequencing to dissect the outbreak more or less in real time. She also highlighted the use of ‘monitors’ whose sole job it was to ensure compliance with hand hygiene and PPE at room entry and exit! Dr Dodgson described the ongoing CRE problems in Manchester. My key message from Dr Dodgson was not to bother with contact screening when you identify a new case: just go ahead and screen the whole ward – more than once. Finally, Erika and Ogra gave their perspective on control challenges. They are now screening all paediatric admissions to their hospital for CRE carriage, which is not a popular or easy policy, but they consider it to be a cornerstone of effective control. As we all wrestle to implement the principles of the Toolkit, this session provided useful advice from those in the know.

Oral presentations

I didn’t make it to all of the oral presentations, but I was impressed by the ones that I saw. (Remember, you can view all of the accepted abstracts from the submitted oral and poster presentation in the Journal of Infection Prevention supplement.)

  • Donald Bunyan: E. coli bacteraemia in Scotland: nearly 50% classified as “community”; but how many of these were frequent fliers?
  • Angela Beal: Pulsed-xenon UV (Xenex): good reduction in total aerobic count, but less effective out of line of sight & 39% of sites VRE contaminated after process. Is this satisfactory?
  • John Chewins: spraying aqueous oxygen peroxide (aka ozone) onto chronic wounds less likely to withdraw from RCT due to infection and improves patient’s quality of life scores.
  • Jo Keward: introduction of semi-permanent Pods reduces missed isolation days by 60% on the Alder Hey HDU.
  • Andrea Whitfield: Service User Involvement in HCAI research: A necessary evil to get your grant or vital for top class research?

Use of disinfectants and HCAI – Dr David Weber

Dr Weber began by reviewing the compelling data that contaminated surfaces contribute to the transmission of some hospital pathogens. An age-old question is whether contamination of hands or surfaces is more important in transmission. A recent modeling study helps to answer this, suggesting that hands are generally more important, but that this will depend on pathogen and setting. Getting the best out of hospital cleaning and disinfection is a simple equation: ‘Product + Practice = Perfection’. The problem is the ‘practice’ part of that equation; it’s difficult to assure process repeatability. This is where new technologies such as automated room disinfection systems, and antimicrobial surfaces can come in most handy. Finally, Dr Weber pointed us towards the AJIC and ICHE recent special editions on all things environmental.

Ayliffe Lecture – Dr Stephanie Dancer

Dr Stephanie Dancer began the Ayliffe Lecture by reiterating a wish that I had earlier in the conference: for genetically modified visible microbes on surfaces! That way we’d all be able to see the long survival and low infectious dose exhibited by many hospital pathogens. As we come towards the end of antibiotics, we need to move from cure to prevention. Remember, mortality due to S. aureus bloodstream infection was once 80% and may be so again as we lose more antibiotics. We need intervention bundles (aka ‘intervention umbrellas’) but not all solutions are possible, practical, affordable or acceptable. A good dose of evidence and common sense is required to find and implement interventions that work!

The BIG debate: universal vs. targeted interventions (Dr Gould vs. Dr Otter)

I think that Dr Gould and I achieved our purpose of presenting both sides of the debate without coming to physical blows. I found myself on uncomfortable ground arguing for a “No” vote in Glasgow following the Scottish “In/Out” referendum. I think my decision to wear a bow tie (see image below) in recognition of Dr Gould’s signature neck-wear lightened the mood!

Figure: My choice of neck wear

Scotland debate

I’ve laid my arguments for targeted interventions out in a separate blog, but in short, universal interventions are appealing but fail to demonstrate short-term, long-term and cost-effectiveness. Targeted interventions have been shown to be effective in reducing transmission, preserve the activity of our precious antimicrobial agents, require less modification of human behaviour, and are cheaper and less resource-intensive. So, on balance, I favour targeted interventions for infection prevention and control.

Closing talks

Rose George gave an engaging talk ‘examining the unmentionables’. It’s eye-opening to think that 40% of the world population lacks adequate sanitation; open defecation is all too common with no privacy, dignity or safety! The flushing toilet, believe it or not, was voted the biggest medical advance of the last 200 years by the BMJ. Investing in sanitation makes financial sense too, with $1 invested in sanitation yields $6. You can see Rose’s TED talk here.

IPS Patron Tricia Hart and incoming president Heather Loveday rounded off the conference, exhorting us to examine our attitude and approach to infection and control. I left the conference feeling that IPS is in good hands with Heather at the helm.

Universal vs. targeted interventions in infection prevention and control: the case for a targeted strategy

Jon Otter (@jonotter) Conferences , , , ,

Today, I participated in a debate with Professor Ian Gould on universal vs. targeted interventions for infection prevention and control at Infection Prevention 2014. I was arguing for a targeted approach, and you can download my slides here, and you can listen to a recording of the talks here.

Universal interventions are appealing: they make no discrimination between patients, there’s a clear message for staff, and you have no way of knowing reliably who is colonized anyway! However, for me to get behind a universal intervention, it would have to demonstrate short-term, long-term and cost-effectiveness.

Before getting into the details of my argument, it is worth defining what we mean by ‘universal’ or ‘targeted’ interventions (see Table 1, below). It’s important to note that an intervention can be targeted either to an individual (e.g. chlorhexidine given to decolonize the skin of a patient known to be colonized with MRSA) or targeted to a population (e.g. chlorhexidine given to all patients in high risk settings, such as the ICU). Screening is an interesting one. It’s easy to mistake screening as a universal strategy when it’s applied to all patients (as is common in the NHS), but it’s fundamentally a targeted strategy to identify patients for an intervention (such as isolation and / or decolonization). A truly universal strategy has no need of screening.

Table 1: defining universal and targeted interventions.universal vs. targeted definitions_cropped

Short-term effectiveness

Short-term effectiveness can be difficult to measure. What is the standard for demonstrating short-term effectiveness? Most common interventions lack accepted standards for demonstrating short-term effectiveness, and the results may well be different as setting and pathogen varies. However, there are some universal approaches that have effectively failed at the first hurdle and not demonstrated even short-term effectiveness. For example, ‘selective’ digestive decontamination has been applied to try to decolonize carriers of resistant Gram-negatives. Although this clearly has some impact, and reduces colonization, it seems to temporarily suppress the level of resistant bacteria in the gut flora, not decolonize the patient. Similarly, the use of universal gloves and gowns failed to meet the primary endpoint in a cluster randomized controlled study (the BUGG study).

Long-term effectiveness

A number of universal strategies that have demonstrated some level of short-term effectiveness fail in terms of long-term effectiveness due to the promotion of bacterial resistance (or reduced susceptibility). For example, selective digestive decontamination on a group of patients resulted in a sharp increase in gentamicin resistance, and perhaps more worryingly an increase in colistin resistance. Furthermore, a microbiomic analysis of a patient undergoing selective digestive decontamination identified a seven-fold increase in the abundance of aminoglycoside resistance genes in the ‘resistome’.

Another way in which universal strategies that are effective in the short-term may fail in the long-term is due to reliance on human beings to maintain compliance with protocols. This is relatively easy during studies, where staff have both support and scrutiny to drive performance. When the spotlight is off and they’re on their own, performance is less impressive. We can see this type of “reverse Hawthorne effect” in compliance with contact precautions, and in hand and environmental hygiene.

Cost effectiveness

Once a strategy has demonstrated both short-term and long-term effectiveness, it must demonstrate cost effectiveness before widespread adoption. Even if you disagree with me and consider screening to be a universal strategy for MRSA when applied to all patients at the time of admission, it has failed to demonstrate cost-effectiveness in almost all scenarios. Economic analysis using the standard threshold of £30,000 per Quality Adjusted Life Year (QALY) has shown that screening all admissions for MRSA is not effective for teaching or acute hospitals at current, high or low prevalence. Universal screening was only cost-effective for specialist hospitals (the vast minority), and then only at some levels of MRSA prevalence. For this reason, the Department of Health is going to reverse its recommendation for universal screening of all hospital admissions.

Summary

I can’t think of a single universal intervention that has demonstrated short-term, long-term and cost effectiveness (see Table 2). Decolonization using chlorhexidine comes close, but almost all studies of this intervention have been performed in an ICU setting, where this intervention is applied to a targeted population. I would be uncomfortable about using chlorhexidine for daily bathing of all hospital patients due to the risk of promoting reduced bacterial susceptibility.

Table 2: short-term, long-term and cost-effectiveness of universal interventions.universal vs targeted debate summary_cropped

Targeted interventions have been shown to be effective in reducing transmission, preserve the activity of our precious antimicrobial agents, require less modification of human behaviour, and are cheaper and less resource-intensive. So, on balance, I favour targeted interventions for infection prevention and control.

How to assess scientific posters: a practical guide

Jon Otter (@jonotter) Conferences , ,

Posters are a hugely important part of scientific congresses. The submitted abstracts that get accepted as oral presentations are always only a fraction of the science available at conferences. And which abstracts get selected as oral presentations are, to a degree, at the whim of the abstract assessment committee and procedures. So, there will be some gems amongst the posters that have the potential to change practice.

I gave a talk at IPS today: a practical guide to assessing scientific posters. You can download my slides here. But they will only tell part of the story. The idea was for the session to be a practical workshop to arm those who are new to infection prevention and control with the tools to maximize their conference experience in terms of accessing submitted science.

I covered the publication process: concept -> research -> abstract -> poster -> paper -> “post-publication peer review”. It was interesting to think in more detail about what makes a good poster. Clearly, first and foremost, a poster must be visual. If it doesn’t look good visually, then it’s not a good poster. That said, what looks “good” is somewhat subjective, but I think some basic themes emerge in terms of visual presentation:

  • Eye catching – draws the viewer in
  • Graphical, not text based
  • Not cluttered
  • Good use of colour
  • Clear ‘flow’ from one section to the next
  • Key findings communicated clearly
  • Contains more detailed information for those that want it
  • Correct size for the board (check the guidelines!)
  • Not an essay / epic; it’s designed to stimulate discussion
  • No intricate fonts that are difficult to read
  • Watch out for fuzzy low-res graphics
  • You can’t include all your data – be selective

And then there’s the scientific content. Really, this is the same question as what makes a good abstract or, indeed paper. The following criteria may be useful in this regard:

Table: what makes a good poster (or abstract, or paper) in terms of content?How to assess a poster_cropped

So, I hope the participants found this session useful.

Tending the human microbiome

Jon Otter (@jonotter) Antibiotic resistance , , ,

Atomic antibiotics

This isn’t hot off the press (a 2012 review article by Tosh & McDonald) but it’s probably more important now than when first published, given our rapid advances in understanding of the importance of the microbiome in human health over the last year or two.

A couple of clear principles emerge from the review:

  • A happy, healthy human microbiome is characterized by diversity (both in terms of number of different species, and diversity within the species), and composed mainly of bacteria that we’re not familiar with – Fermicutes and Bacteroidetes).
  • Antibiotics have a profound and sustained effect on the human microbiome (even those that are typically associated with no or few side effects). This results in a reduction in both diversity and change in composition, which is bad news for human health. In particular, this leave the gut more open to colonization with unwanted intruders aka antibiotic resistant bacteria.

The future of anti-infective therapy according to Tosh and McDonald is in:

(1)     Developing and using more microbiome-sparing antimicrobial therapy. The idea of ‘selective digestive decontamination’ flies in the face of this objective.

(2)     Developing techniques to maintain and restore indigenous microbiota. A lot of progress has been made here, for example, in the case of faecal microbiota transplantation (FMT) for the treatment of recurrent CDI.

(3)     Discovering and exploiting host protective mechanisms normally afforded by an intact microbiome.

Rather than obliterate our microbiome with overuse of antibiotic “Atomic bombs”, we need to carefully tend individual and collective microbiomes in order to make them resistant to the increasing queue of antibiotic resistant colonizers!

Article citation: Tosh PK, McDonald LC. Infection control in the multidrug-resistant era: tending the human microbiome. Clin Infect Dis 2012;54:707-713.

Image credit: Modified from ‘Mushroom cloud‘.

Not all resistant Gram-negative bacteria are created equal: Enterobacteriaceae vs. non-fermenters

Jon Otter (@jonotter) Acinetobacter, CRE, Epidemiology , , , , ,

apples and oranges

Apples and oranges. They’re both more or less spherical and classified as fruits, and that’s about whether the similarity ends. It’s the same for antibiotic-resistant Enterobacteriaceae (e.g. Klebsiella pneumoniae) and non-fermenters (e.g. Acinetobacter baumannii): they both share the same basic shape (more or less) and classification (Gram-negative), and that’s about where the similarity ends (see the Table below):

Table: Comparing the epidemiology of resistant Enterobacteriaceae and non-fermenters.3M webinar QA Not all created equal_table

I gave a webinar yesterday as part of a three part series on resistant Gram-negatives. You can download the slides here, and access the recording here (although you’ll have to register to do so). I am increasingly hearing people talking about ‘carbapenem-resistant organisms’ (CRO), used as a catch-all term to encompass both the Enterobacteriaceae and the non-fermenters. As you can see from the comparison table able, this doesn’t make a lot of sense given the key differences in their epidemiology. Indeed, MRSA is a CRO, so why don’t we lump that together with the Enterobacteriaceae and non-fermenters? Carbapenem-resistant Enterobacteriaceae and carbapenem-resistant non-fermenters are both emerging problems, but they are not the same problem.

I asked a few questions of the audience, which I’ve summarised below:

Figures: Questions asked of around 150 webinar participants, mainly from the USA.3M webinar QA Not all created equal Q13M webinar QA Not all created equal q23M webinar QA Not all created equal q3

I was not surprised that so few people felt comfortable explaining the difference between the Enterobacteriaceae and non-fermenters – and this rather justified the whole thrust of the webinar! I was a little surprised that the ‘prevalence’ of the two groups of resistant bacteria were so similar; I was expecting the Enterobacteriaceae to be more common (although I admit this wasn’t a brilliantly worded question). In terms of control interventions, it’s true that we still don’t really know what works to control resistant Gram-negative bacteria. But it does seem likely that the control interventions will be different for Enterobacteriaceae and non-fermenters, and this did come across in the responses. Hand hygiene was selected by most people (which makes sense), with screening & isolation, and stewardship more commonly selected for Enterobacteriaceae, and cleaning / disinfection for the non-fermenters.

Q&A

Following the webinar, the audience asked a few interesting questions:

  1. Can you get chlorhexidine resistant organisms? A number of studies have hinted that reduced susceptibility to chlorhexidine may be an emerging problem, (for example Batra, Otter, Lee and Suwantarat). But increases in bacterial MICs (for Gram-positive bacteria at least) appear to be a long way below the applied concentration. However, it’s worth noting that the measured CHG skin concentration in one study (15-312 mg/L before the daily bath and 78-1250 mg/L after the daily bath) was much lower than the applied CHG concentration (10,000 mg/L). This is around the CHG MIC for some Gram-negatives and potentially brings the subtly reduced susceptibility to CHG reported in MRSA into play. On balance though, the rationale and data on reduced susceptibility are cautionary but not enough to recommend against universal use in the ICU given the clinical upside.
  2. Do you think we should be doing universal chlorhexidine bathing? On our ICU in London, we have been using universal chlorhexidine decolonization for a decade combined with targeted screening and isolation, and have seen a dramatic reduction in the spread of MRSA. So yes, I think we should be doing universal chlorhexidine bathing, but the need to monitor carefully for the emergence of clinically-relevant reduced susceptibility.
  3. Can we discontinue contact precautions for CRE? The short answer is no. Quite a few studies have found that gut colonization with CRE typically lasts for at least 6 months to >1 year. And those that become spontaneously ‘decolonised’ sometimes revert to colonized, suggesting that they weren’t really decolonized at all – it’s just that their load of CRE at the time of sampling had fallen below the limit of detection. So I favour a “once positive, always positive” approach to CRE colonization.
  4. Which disinfectant would you recommend for resistant Gram–negatives? It does seem that the non-fermenters (and in particular A. baumannii) are “more environmental” than the Enterobacteriaceae. However, the Enterobacteriaceae (including CRE – especially K. pneumoniae) can survive on dry surfaces for extended periods. Therefore, I think enhanced disinfection – especially at the time of patient discharge – is prudent for both groups. Consider using bleach or hydrogen peroxide-based liquid disinfectants, and terminal disinfection may be a job for automated room disinfection systems, such as hydrogen peroxide vapour.
  5. Should we use objective tools to monitor cleaning? Effective tools are available to objectively monitor cleaning (e.g. ATP and fluorescent dyes), and these have been shown to improve surface hygiene. Therefore, we should all now be using these tools to performance manage our cleaning processes.

Image credit: ‘Apples and oranges’.

Acinetobacter contamination: is anywhere safe?

Jon Otter (@jonotter) Acinetobacter, Contamination , , , ,

A study from New York City describes an environmental survey of contamination with antibiotic-resistant Gram-negative bacteria on surfaces in the community. The authors hypothesise that resistant Gram-negatives could be carried by staff, patients and visitors beyond the confines of the hospital.

Almost 500 environemntal samples were collected from surfaces in the public areas of six hospitals and surrounding communities (<1 mile from the hospital) (443 samples), with a further surfaces from communities >1.5 miles from any hospital as a control (50 samples). A total of 70 GNR were identified (Figure), mostly fairly inoccousous species from a human disease viewpoint. However, some potential human pathogens were identified (Table).

Figure: breakdown of Gram-negative rods identified from surfaces in public areas of the hospital and surrounding community.GNR contam

Table: potential human pathogens identified from surfaces in public areas of the hospital and surrounding community.

n % Species
15 3.0 Acinetobacter baumannii
3 0.6 Citrobacter freundii
2 0.4 Escherichia coli
2 0.4 Stenotrophomonas maltophilia
1 0.2 Enterobacter cloacae

Some other important findings:

  • All of the A. baumannii isolates were resistant to ceftazidime, and one was resistant to imipenem (i.e. carbapenem-resistant). Eleven of the 15 were clonally related to one another and to a patient isolate from one of the hospitals.
  • One of the S. maltophilia isolates carried an integron-encoded VIM carbapenemase, which is potentially transmissible to other Gram-negative species (including Enterobacteriaceae).  
  • Each sample was cultured in an enrichment broth, and the broth was probed for the presence of a range of beta-lactamase genes (including ESBLs and carbapenemases). No beta-lactamases were detected (other than the S. maltophilia isolate). I suspect the picture would have been rather difference in New Dehli!
  • Although the survey included both surfaces in public areas of hospitals and in the community, it seems that most of the A. baumannii were identified on surfaces in the community.

So, is it a surprise to see environmental contamination with antibiotic-resistant Gram-negatvies on touch-surfaces in the community? Not really, A. baumannii in particular can survive on surfaces for ages, and ‘mimics’ Gram-positive bacteria in terms of its environmental longevity (i.e. months / years). That said, I performed a similar study looking for MRSA on touch surfaces in the community in London, and didn’t find any. More importantly, do we need to do anything about this? As the authors state, A. baumannii can be virtually impossible to eliminate from hospital surfaces without resorting to hydrogen peroxide vapour. So is it time to roll hydrogen peroxide vapour into your local Pizza Hut? Clearly not. You’d hope that cleaning and disinfection protocols, which should deal with this sort of contamination, are already established in these public places, but it would be prudent to reinforce these basic hygienic practices. Also, I agree with the authors that these findings represent and opportunity for the promotion of hand hygiene in the community.

The authors use strong words to describe NYC as ‘plagued’ with resistant Gram-negative bacteria, and a ‘dismal failure to control A. baumannii.’ If this epidemic continues, we can expect to see the focus of the problem – and the target for our interventions – shift from the acute hospital setting to encompass the community.

Ebola: PPE and paranoia

Jon Otter (@jonotter) Ebola , , , ,

The contrast in the stringency of the CDC and UK Department of Health / Health and Safety Executive guidelines for infection prevention and control when dealing Ebola virus disease (EVD) patients is striking. This is particularly acute with regard to recommendations for Personal Protective Equipment (PPE) and terminal disinfection. Having recently reviewed both documents for a webinar on Ebola infection prevention and control (you can download the slides here, by the way), I thought I’d share the contrast:

Table: PPE and disinfection recommendations for dealing with patients with Ebola virus disease. Source: US CDC patient and environmental guidelines, and UK Department of Health. (Please note – this summary chart is designed to be illustrative rather than definitive.)Ebola ppe table

So is there any reason why the level of PPE and type of terminal disinfection required should be any different depending on which side of the Atlantic you happen to be? None whatsoever. So why the discrepancy? It’s difficult to say. This difference in recommendations has prompted the question of “To CDC or not to CDC” in terms of PPE for Ebola, and an opinion piece in Annals of Internal Medicine justifying the CDC approach. It is probably true that the level of PPE recommended by CDC is enough to block transmission, and that the risk of environmental contamination is low enough such that fumigation is not necessary. Probably. But is that good enough when Ebola is on the line? It is certainly true that you can be wearing all the PPE in the world but if you put in on incorrectly, don’t take care of it during use or remove it carelessly you will put yourself at risk.

When I came to decontaminate a room using hydrogen peroxide vapour following a case of Lassa fever in London some years ago, I wore all the PPE that I could lay my hands on (see below)!

Me illustrating the “belt and braces” (aka paranoid) approach to PPE (a la UK, not CDC recommendations).Lassa PPE me_annotated

Did this level of PPE match the risk of exposure to viable Ebola? Perhaps not, but it certainly made me feel a whole lot more secure about entering the room to do the job!

Journal Roundup August 2014: seeking your input

Jon Otter (@jonotter) Roundup , , , , ,

Fist bumpThe August edition of the Journal of Hosptial Infection Journal Roundup is now available, featuring:

  • A whopping five-fold increase in the detection of CRE in 25 US community hospitals.
  • MALDI-TOF as a new frontier for rapid detection of carbapenemase activity.
  • More on fist bumping instead of hand shaking. (Would you like a fist bump greeting from your doctor? No thanks!)
  • Triclosan-impregnated stitches would be cost-effective if they were only a little bit effective, but turns out they’re not effective at all.
  • The new ‘crAssphage bacteriophage’, C. difficile biofilms, and increasing rates of antibiotic resistance – all in the human gut microbiome.
  • Some hope for Ebola drug and vaccine targets.
  • How to reduce the number of sickies that children take from school (through effective school-based immunization programmes).
  • Thoughtful analysis on S. aureus outbreaks of old with lessons for now.
  • Reviews of CRE mortality, global antibiotic use, microbial hitchhikers, overdiagnosis & overtreatment, useless reporting of science in the mainstream media, and whether biocide use drives biocide resistance.

I’ve written three editions of the Journal of Hosptial Infection Roundup now (June, July and August), so there’s a few examples to review. You can read about my methods for producing the Roundup in the blog accompanying the June edition. I thought that now would be a good time to get some feedback, specifically:

  • Is the title right? A few people have expected it to be an overview of articles in the Journal of Hospital Infection only.
  • Is the length about right? (Do you fall asleep reading it or find yourself begging for more?)
  • Is the depth right? Or would you like to read more about less articles, or less about more articles?

Any feedback that you have would be most appreciated. Please either submit a comment below or email me.

Photo credit: ‘Fist bump’.

CRE and friends: Q&A

Jon Otter (@jonotter) CRE , , , ,

the end of antibiotics_smallI gave the first in a three part webinar series for 3M last night, and you can download the slides here. Also, you can access the recording here (although you will need to register to do so).

The webinar was attended by >200 participants from across the US. I tried to outline the three pronged threat of multidrug-resistant Gram-negative rods (especially CRE) in terms of high levels of antibiotic resistance, stark mortality (for invasive disease) and the potential for rapid spread (including the prospect of establishing a community reservoir). Then, I gave an overview of the US and European picture in terms of CRE prevalence. Finally, I discussed the diagnostic challenges and options.

The most interesting part for me was the response to the questions that I threw out to the audience (see Figure below).

Figure: response to the questions from the 200 or so participants.

CRE and friends charts q1

CRE and friends charts q2

CRE and friends charts q3

I was somewhat saddened but not especially surprised that the difference between CRE and CPE was not clear in the minds of most participants. I appreciate that this may be in part due to the fact that ‘CPE’ seems to be used more commonly in Europe than in the US. But this is an international problem, so we need to get our terminology straight in our globalised world.

It was encouraging to hear that most US hospitals have had no CRE, or only one or two cases. However, 11% of the participants see CRE regularly, with cases unconnected to outbreaks. This is a concern, and suggests that CRE has become established in these areas. Indeed, a recent study from 25 Southeastern US community hospitals reports a 5-fold increase in the prevalence of CRE since 2008, suggesting that CRE is becoming established in some parts of the US.

Most participants didn’t know which method was used by their clinical laboratory to detect CRE. I’m not sure whether or not this is a problem. You’d hope that laboratorians to know that they’re doing!

Q&A

The webinar included time for a Q&A from the audience, which covered the following:

  • “How long to resistant Gram-negatives survive on surfaces?” This depends on which Gram-negative you’re talking about. Non-fermenters, especially Acinetobacter baumannnii, have remarkable survival properties measured in months and years. Enterobacteriaceae have a somewhat lower capacity to survive on dry surfaces, but it can still be measured in weeks and months, rather than hours and days.
  • “How important is the environment in the transmission of resistant Gram-negatives?” Again, this depends on which Gram-negative you’re talking about. For A. baumannii the answer is probably “very important” whereas for the Enterobacteriaceae the answer is more like “quite important”.
  • “What would you recommend for terminal disinfection following a case of CRE?” I would recommend the hospitals usual “deep clean” using either a bleach or hydrogen peroxide disinfectant, and consideration of using an automated room disinfection system. I would not be happy with a detergent or QAC clean; we can’t afford to leave an environmental reservoir that could put the next patient at risk.
  • “Are antibiotic-resistant Gram-negative bacteria also likely to be resistant to disinfectants” There’s been a lot of discussion on this issue, but the short answer is no. I’d expect an antibiotic-resistant Enterobacteriaceae isolate to be as susceptible to disinfectants as a corresponding antibiotic-susceptible isolate.  
  • “Should patients with CRE be left to the end of surgical lists, and are is special instrument reprocessing required?” There is no need to implement special instrument reprocessing – follow your usual procedures here. Should CRE patients be left to the end of surgical lists? It would be prudent if possible, but don’t lose sleep over it.
  • “Are any special decontamination measures necessary for endoscopes?” A number of outbreaks of CRE have been reported associated with endoscopy. However, usual endoscope reprocessing methods should be sufficient to deal with CRE, provided they are done correctly!
  • “How do you lessen your chances of acquiring CRE?” Healthy individuals lack the risk factors for CRE infection (although CRE can occasionally cause infections in the community). Thus, the personal protective equipment (PPE) specified for contact precautions (gloves and gowns) combined with rigorous hand hygiene are sufficient to protect healthcare workers.
  • “Are toilet seats in India safe?” What a question! I guess we’re talking about an organism with gastrointestinal carriage, so it’s probably that contamination of the toilet seat will occur. It may be prudent to clean or disinfect toilet seats in India before using them. Either that, or squat!
  • “Can you expand on isolation protocols?” Firstly, ensure that patients infected or colonized with CRE are assigned a single room (not so relevant in the US, but important in healthcare elsewhere). Then, make sure you have appropriate policy and supply of PPE (principally gloves and gowns). Consider implementing ‘enhanced precautions’, including a restriction of mobile devices. Finally, consider cohorting patients and staff to the extent possible. You can read more about NIH’s approach to isolation here.
  • “Can patients who are colonized with CRE be deisolated?” This is a tricky one, which is basically an evidence free zone and hence an area of controversy. Longitudinal studies show that carriage of CRE can persist for months or even years, so it makes sense to continue isolation for the duration of a hospitalization and not bother with repeated swabbing. At the time of readmission, it makes sense to take a swab to see whether colonization continues. If not, then it may be rational to deisolate them – perhaps after a confirmatory swab. I wish I could be more decisive here, but the evidence is scant.

Do please let me know if you have anything to add to this Q&A!  

Are contaminated hands more important than contaminated surfaces?

Jon Otter (@jonotter) Contamination , , , , ,

Cast your minds back to the 2010 HIS conference in Liverpool and Drs Stephanie Dancer and Stephan Harbarth debating the relative importance of contaminated hands vs. surfaces in the transmission of MDROs. I don’t remember the details of the debate, but I do remember the surprising lack of evidence on both sides. Back then, we had no real way to quantify the contribution of the environment to the transmission of MDROs, or to measure the relative importance of contaminated hands vs surfaces. The evidence has evolved to the extent that a group of US researchers have published a paper modeling the relative contribution of contaminated hands vs surfaces to the transmission of MDROs. I like the paper very much, and the authors should be congratulated for breaking new ground in understanding transmission routes of MDROs.

The model simulates patient-to-patient transmission in a 20-bed ICU. The values of the parameters that were used to build the model were sensible on the whole, although baseline hand hygiene compliance was set at 57-85% (depending on staff type and whether at room entry or exit), which seems rather generous when baseline environmental cleaning compliance was set at 40%. Also, the increased risk from the prior room occupant for MRSA and VRE was set at 1.4 (odds ratio) for both, whereas it probably should be higher for VRE (at least >2) based on a number of studies.

100 simulations were run for each pathogen, evaluating the impact of step-wise changes in hand hygiene or terminal cleaning compliance. The key finding is that improvements in hand hygiene compliance are more or less twice as effective in preventing the transmission of MDR A. baumannii, MRSA or VRE, i.e. a 20% improvement in terminal cleaning is required to ‘match’ a 10% improvement in hand hygiene compliance. Also, the relationship between improved terminal cleaning and transmission is more or less linear, whereas the relationship with hand hygiene shows relatively more impact from lower levels of hand hygiene compliance (see Figure, below). Thus, the line for improving hand hygiene or terminal cleaning would intercept and indeed cross over at around 40 or 50% improvement. The implication here is that hand hygiene is more important at low levels of compliance, whereas terminal cleaning is more important at high levels of compliance (although don’t forget the difference in the baseline compliance ‘setpoint’.

hand v env Figure. The impact of percentage improvement in hand hygiene or terminal cleaning on the transmission of MDROs. Dotted line represents my not-very-scientific extrapolation from eyeballing the data.

The study raises some important issues for discussion:

  • It had not struck me before that the level of compliance with hand hygiene and environmental cleaning are nearly identical, on average, with only around 40% of hand hygiene opportunities met and 40% of environmental surfaces cleaned if human beings are left to their own devices. Both of these figures can be improved considerably with concerted effort, but the sustainability of these improvements without continued effort is rather disappointing.
  • The models address MRSA, VRE and MDR A. baumannii transmission. It’s a little strange that C. difficile was not included, since most consider this to be the ‘most environmental’ hospital pathogen.
  • The study only modeled the impact of terminal cleaning, whereas daily cleaning seems likely to also be an important factor (which is acknowledged as a limitation in the discussion). This seems especially important in light of data that touching a contaminated surface carries approximately the same risk of hand contamination as touching an infected or colonized patient.
  • I am not certain that this assumption makes logical sense: ‘thoroughness of cleaning of 40% implies that, given a single cleaning opportunity, there is a 40% probability that the room will be cleaned sufficiently well to remove all additional risk for the next admitted patient’. This would be true if cleaning was performed to perfection 4 times out of 10, whereas it is actually performed with 40% efficacy 10 times out of ten! To this end, it would be interesting to insert the various automated room disinfection systems into the model to evaluate and compare their impact. Indeed, hydrogen peroxide vapour has been shown to mitigate and perhaps even reverse the increased risk from the prior room occupant (for VRE at least).
  • In the introduction, the authors comment that ‘A randomized trial comparing improvements in hand hygiene and environmental cleaning would be unethical and infeasible.’ I see what they’re saying here, in that it would be unethical by modern standards to investigate the impact of no hand hygiene or no environmental cleaning (although this has been done for hand hygiene), but it would be useful, feasible and ethical to perform a cluster RCT of improving hand hygiene and environmental cleaning. It would look something like the classic Hayden et al VRE study, but with an RCT design.
  • How useful is mathematical modeling in informing decisions about infection prevention and control practices? This is not the first mathematical model to consider the role of the environment. For example, researchers have used models to evaluate the relative importance of various transmission routes including fomites for influenza. But a model is only as good as the accuracy of its parameters.
  • Does this study help us to decide whether to invest in increasing hand hygiene or terminal cleaning? To an extent yes. If you have awful compliance with both hand hygiene and terminal cleaning at your facility, this study suggests that improving hand hygiene compliance will yield more improvement than improving terminal cleaning (for A. baumannii, MRSA and VRE at least). However, if you have high levels of compliance with hand hygiene and terminal cleaning, then improving terminal cleaning will yield more.

In general, this study adds more evidence to the status quo that hand hygiene is the single most effective intervention in preventing the transmission of HCAI. However, in a sense, the hands of healthcare workers can be seen as high mobile surfaces that are often contaminated with MDROs and rarely disinfected when they should be!

Article citation: Barnes SL, Morgan DJ, Harris AD, Carling PC, Thom KA. Preventing the transmission of multidrug-resistant organisms: modeling the relative importance of hand hygiene and environmental cleaning interventions. Infect Control Hosp Epidemiol 2014; 35: 1156-1162.