Author: Jon Otter (@jonotter)

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.

Isolation: the enemy of CRE

Jon Otter (@jonotter) CRE , , , ,

isolation enemy cre

Pat Cattini (Matron / Lead Specialist Nurse Infection Prevention and Control, Royal Brompton and Harefield NHS Foundation Trust) and I recently teamed up to present a webinar entitled: ‘Introduction to the identification and management of carbapenem-resistant Enterobacteriaceae (CRE)’. You can download our slides here, and here’s the recording:

The webinar covered the following ground:

  • Why the fuss?
  • What are CRE?
  • Who do we screen?
  • How do we screen?
  • What happens if someone is positive?
  • Key questions

CRE represent a combination of anitibiotic resistance, mortality and potential for rapid spread, so we need to be proactive in our approach to the detection and management of carriers. We simply can’t afford for CRE to become established in the same way that MRSA did, so now is the time of opportunity to develop the most effective prevention strategy. The recently published Public Health England Toolkit is useful, but it’s a set of tools to help construct a local policy, not a one-size-fits-all CRE policy. We hope that this webinar will assit you in developing your local CRE policies and plans.

Oh, and look out for the Premiere of ‘ISOLATION: THE ENEMY OF CRE’ (a Pat Cattini film)…

My close shave with viral haemorrhagic fever (VHF)

Jon Otter (@jonotter) Ebola, Viruses , , , ,

ebolaAs the outbreak of Ebola continues unabated in Sierra Leone and Liberia (1323 cases and 729 deaths as of July 27), I thought it would be an opportune moment to share a close shave that I had with the closely related Lassa viral haemorrhagic fever (VHF) virus in 2009.

A patient was transferred from Mali to a London hospital with a diagnosis of malaria. The case was initially thought to represent a low risk of VHF (to be fair, Lassa had never been reported in Mali, and the patient came with a diagnosis of malaria). This led to the potential exposure of 123 healthcare workers and visitors, and a busy week for the infection prevention and control team to follow each of these individuals. The useful risk assessment now available from Public Health England may have helped to reduce the number of people exposed.

The patient died in a negative pressure ICU room on the day of admission. At that time, there were no clear recommendations about how to decontaminate the room, so I was involved in developing a decontamination plan with the hospital. Due to the rarity of VHF in the UK, the plan took a week to be authorized by the Health and Safety Executive. This meant that by the time it came to decontaminating the room, the bags of blood-soaked clinical waste, spots of blood on the bed, and used consumables on the floor had been festering for a week. Not ideal.

Our decontamination plan included the use of hydrogen peroxide vapour (HPV) for terminal room disinfection due to the risk that VHF viruses can survive when protected by blood for several weeks on surfaces. This is borne out by some sampling during an outbreak that found intact RNA from the Ebola virus on blood contaminated fomites (although not on fomites that were not contaminated with blood). It’s reassuring that the Department of Health / Health and Safety Executive guidelines published a few years after this case also recommend the use of fumigation for terminal decontamination of hospital rooms.

I ended up being tasked with setting up the HPV equipment that was used to decontaminate the room. We decided it would be better to clean the room after the decontamination to provide some protection to the cleaners. This meant that I was the first person to enter the room after the body of the patient had been removed. I will never forget donning my Tyvek suit, gloves and face-fitted FFP3 mask (see below!). It was exciting: I felt a lot like Dustin Hoffman in Outbreak (the movie that got me interested in medical microbiology in the first place). But it was also frightening. The most frightening part was collecting the bags of clinical waste and consumables from the floor, knowing that they were still likely harbouring live Lassa fever virus. To think that one slip could have infected me with a deadly virus for which there is no treatment…

Lassa PPE me

Figure: Me kitted out in PPE (and looking somewhat apprehensive)

There is legitimate concern that we may see cases of Ebola in the UK and USA in this globalized, interconnected world. If so, then we need to be prepared, and some have questioned our state of readiness. We are fortunate to have comprehensive guidelines from the Department of Health / Health and Safety Executive, including clear guidance on how to decontaminate a room following a case of VHF.

My close shave with VHF has given me a great deal of respect and, frankly, veneration for the brave healthcare workers who are risking their lives on the front line in bringing the current outbreak of Ebola under control.

Photo: Ebola courtesy of Phil Moyer and CDC/Cynthia Goldsmith.

Preventing HCAI: go long or go wide?

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

quarterbackThere seems to be a general movement away from targeted, pathogen-based precautions (principally screening and isolation) in the USA. This changing professional opinion was clear from the recent SHEA conference, where several leading experts gave what amounted to a collective justification for abandoning contact precautions for MRSA.

The update of the SHEA Compendium of Strategies to Prevent Healthcare-Associated Infections in Acute Care Hospitals is accompanied by a commentary from a group of leading US figures titled ‘Approaches for preventing HCAI: Go long or go wide’. In the commentary, the authors weigh the evidence and opinion for so-called ‘vertical’ (aka targeted) vs. ‘horizontal’ (aka universal) interventions (Table).

go wide or longTable: Go long or go wide? Examples of targeted and universal interventions (adapted from Wenzel & Edmond, via Septimus et al.).

The commentary outlines the potential drawbacks of targeted approaches (such as fewer visits from healthcare workers and feelings of isolation), but doesn’t spend a lot of time discussing the potential drawbacks of universal approaches. For example, “isolation fatigue”, where a procedure loses its impact if it has to be applied to every patient. And then there’s the possibility of resistance when performing universal decolonization. This is particularly worrysome when using antibiotics, but could also be a problem when using biocides such as chlorhexidine.

I’m not ready to abandon pathogen-based targeted interventions just yet. Conceptually, it just does not make sense. If you have a patient with MRSA and a respiratory virus, chances are they will become a ‘super-spreader’. Those who favour universal approaches do make some provision for exceptional cases that really should be identified and isolated via a ‘syndromic’ approach to isolation: crudely, only isolate patients when they’re oozing. However, this syndromic approach would likely miss our ‘super-spreading’ patient, which may well result in an MRSA outbreak – that we could all do without.

Furthermore, if you have a patient who is colonized with CRE, are you brave enough to take no special precautions, as would be the case for a ‘universal only’ approach? The success of this strategy would depend on a high level of compliance with standard precautions such as hand hygiene and environmental cleaning and disinfection. Whilst sound in theory, this just doesn’t happen in the trenches; your facility is above average if your hand hygiene compliance rate is the right side of 40%. Whilst still not 100%, hand hygiene compliance is higher when patients are placed in isolation, most likely because there’s a stronger psychological trigger to comply with hand hygiene.

It’s important to note that targeted and universal approaches are by no means mutually exclusive. For example, 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, should we go long or go wide in the prevention of HCAI? The answer is both. We should optimize case for all patients, which means careful standard precations with liberal application of chlorhexidine and tight restriction of antibiotics. But we should also identify those with communicable pathogens and segregate them from others. In this regard, we have the weight of history on our side.

Image: Jeff Weese.

How to write a conference abstract…and beyond!

Jon Otter (@jonotter) Conferences ,

ACIPC

The Australasian College for Infection Prevention and Control (ACIPC) asked me to give a webinar on writing a conference abstract for an infection prevention and control conference. I thought it would be useful to share the slides (which you can download here), and let you know how it went.

So why bother submitting an abstract to a conference? It’s all about the big speakers on the big stage, right? Wrong. Submitted abstracts delivered through oral and poster presentation is the life blood of the science underpinning our infection prevention and control practice. There’s a useful PLOS blog along these lines here.

It can be pretty daunting to prepare an abstract for a conference if you’ve not done it before, or had a bad experience in the past. So the idea of the webinar was to provide a step-by-step guide to producing a winning conference abstract.

There are a number of hurdles to overecome to get your abstract accepted. You need to tick the ethics box, be transparent with conflicts of interest, decide on appropriate authorship before getting down to the abstract itself. Follow the ‘house rules’ of the conference carefully to avoid your abstract being rejected simply because it’s in the wrong format.

The title of your abstract is especially important; it will be all that many people will read (particularly if it’s bad). I’ve included some illustrations of titles that I think are good, and some that are not so good. The ones in the ‘not so good’ category are by no means bad: these are accepted abstracts from a scientific conference. It’s just that if the authors thought again about a creative, engaging, informative title, I think they’d come up with something difference. (I should add here, that my abstract titles tend to default to really dull because I’m not brave enough to do anything more creative, so who am I to talk!)

When it comes to writing the abstract itself, the following ‘Dos and Don’ts’ should help:

dos and donts

Once the abstract is accepted, it will be time to produce the poster or prepare the slides. Both posters and slides to illustrate talks should be just that – a visual illustration. For me, the text of the abstract should suffice for the text of the poster and, to a lesser degree, the slides. Save the dense text for the paper that should follow.

Finally, if you have any queries about an abstract for a conference, get in touch with the conference organisers. Behind the impersonal abstract submission site will be living, breathing human beings who would love to support you in disseminating your findings for the good of the community.