disinfection

Is deliberately seeding hospital rooms with Bacillus spores a good idea? No, I don’t think so either!

Jon Otter (@jonotter) Contamination , ,

A fascinating Italian/Belgian multicentre study introduces us to the idea of “biocontrol” for problematic surface contamination. They test using “live” cleaning products that deliberately seed hospital surfaces with Bacillus species spores in an attempt to reduce the ecological space for pathogenic microbes through a “competitive exclusion” approach. Ridiculous as it sounds, there’s some logic to this idea. We’re just beginning to understand the potential of complementing a depleted microbiome in human health, so perhaps the same theory goes for the “environmentome”?

The study design is on the one hand impressive and ambitious, with more than 20,000 surfaces samples collected from the three hospitals. However, it is also messy and confusing, with different intervention and sampling protocols in the three hospitals. In particular, it’s a real shame that areas were not randomized to receive the “live” vs. conventional cleaning agents. It seems clear that this was not a carefully planned multicentre study using a standardized protocol – it reads more like three separate studies shoe-horned together.

That said, the results are impressive. Areas treated with the “live” cleaning agents were significantly less likely to be contaminated with coliforms, S. aureus, Candida albicans, with a more moderate impact on C. difficile. However, it’s difficult to determine the scale of the reduction since the relative rather than actual load reductions are reported.

A neat sub-experiment at one of the hospitals is perhaps the most convincing part of the study, where conventional and “live” cleaning agents were alternated (Figure). You can clearly see that the microbial load tracked downwards when the “live” agent was used, and rebounded when the conventional agent was reinstated.

vandini bacillus sporesFigure: Bacterial load of coliforms (black circles) and S. aureus (white circles). Black arrow = beginning of the “live” cleaning agent; black dotted arrow = conventional cleaning agent.

Notwithstanding the impressive reductions, this approach is ringing some alarm bells:

  • Do we really know what we’re doing by deliberately seeding the hospital environment with bacterial spores? Almost all microbes can be pathogenic to immuno-compromised patients. Plus, whilst you know what you’re putting down, you don’t know what it will become when exposed to the selective pressure of hospitals. The authors did take a look at this, using antibiotic susceptibility testing and a PCR assay to show that Bacillus species identified from the original cleaning agents and from hospitals surfaces during study did not differ in their carriage of antibiotic resistance genes. However, this is only scratching the surface of a complex risk.
  • Where do all the pathogens go? Having an environment that is full of Bacillus spores does not make a scrap of difference to the amount of pathogens that are shed into the environment. So, either the Bacillus spores somehow reduce the amount of time that these pathogens survive on surfaces, or offer them a more complex hiding place. I suspect the latter is more likely.
  • Related to this, recent work has identified established biofilms on dry hospital surfaces with important implications. Won’t a daily dose of Bacillus spores only serve to promote the buildup of this biofilm?
  • The authors proffer some potential reasons for the lower bacterial counts, including competition for nutrients and quorum sensing to destabilize biofilms. I think these are very unlikely, because they rely on the Bacillus spores germinating on the surfaces. I suspect that the spores remain firmly as spores, and the reductions are explained by occlusion and competition for space.
  • Ethics can be a pain, but it’s there for a reason – to prevent our patients from unnecessary harm. The outcome of their ethical submission was surprising: “The two Ethics Committees stated that a formal authorization was not necessary because the probiotic products would not be directly administered to patients but exploited for cleaning of hospital surfaces only.” Applying a soup of Bacillus species spores to a patient’s room is pretty much the same thing as applying the soup directly to their skin. Personally, I’d like to choose whether or not I’m admitted to a room deliberately seeded with Bacillus spores!
  • The authors insist on calling the “live” cleaning agents ‘probiotics’, which seems misplaced. To me, ‘xxx-biotics’ implies something that is administered to a patient.

The use of “live” cleaning agents provides an interesting alternative approach to antimicrobial surfaces, or chemicals with residual biocidal activity. However, I am not sure I accept the authors stark choice as their final conclusion: ‘When it comes down to risk management, one has to decide whether a patient should stay in an environment dominated by food grade microorganisms or in an environment harboring an elevated level of increasingly resistant pathogens.’ Personally, I’d prefer to be cared for in an environment with minimal levels of bacterial contamination, and free from contamination with pathogens. Is that too much to ask?

Article citation: Vandini et al. Hard Surface Biocontrol in Hospitals Using Microbial-Based Cleaning Products. PLoS One 2014;9:e108598.

Reflections from HIS 2014, Part II: Dealing with the contaminated environment

Jon Otter (@jonotter) Conferences , , , , , , ,

HIS_Web_Banner_Jpeg

Welcome to Part II of my reflections from HIS. For the box-set, see the list at the beginning of Part I here.

Dr Karen Vickery – Multispecies biofilms on dry hospital surfaces – harbouring and protecting multiantibiotic resistant organisms

Probably the most important update from the entire conference was more data from the Vickery lab on biofilms on dry hospital surfaces. She excised 44 dry surface samples from the ICU, put them under the electron microscope and, lo and behold, 41 of them (93%) had fully-fledged (if somewhat unusual) EPS-producing biofilms on! The implications are huge: this could explain extended surface survival, poor success rate of surface sampling, and result in reduced biocide susceptibility up to the tune of 1000x (see my review just published in JHI with Karen as a co-author for more on biocides and biofilm susceptibility).

Dr Silvia Munoz-Price – Controlling multidrug resistant Gram-negative bacilli in your hospital: We can do it so can you!

Dr Munoz-Price described her hospital’s impressive reductions on carbapenem-resistant A. baumannii – from 12 new isolates per week to virtually none today. So what worked? It’s difficult to be sure since it was a bundled intervention. Dr Munoz-Price described the rationale behind some elements of the bundle: environmental surface and staff hand sampling to visualize the invisible, environmental cleaning and disinfection to deal with the ‘fecal [sic] patina’ [a stooly veneer emanating from the rectum] (see Dr Munoz-Price and Dr Rosa’s guest blog for more details), and chlorhexidine bathing. Perhaps the most interesting aspect was the various implementation challenges that were overcome. It was amazing how far removed practice ‘in the trenches’ was from the policy set by the epidemiologist’s office, exemplified by environmental staff buying their own UV lamps to for “spot cleaning” removal of fluorescent markers of cleaning thoroughness. Overcoming these challenges required more that the stick (citations for non-compliance, which failed); culture change takes understanding, time and a very large carrot (and some sticks too, sometimes).

Jim Gauthier – faeces management

A number of key pathogens are associated with faecal colonization and shedding: C. difficile, VRE, ESBL and CRE. Jim didn’t mention MRSA, but this can also cause gastrointestinal colonization and, more controversially, infection. Enterobacteriaceae can survive on dry surfaces for longer than you’d expect, too. We traditionally worry about surface contamination of high-touch sites in inpatient settings. Floor contamination isn’t important (unless you happen to be a wheel chair user, a toddler, or drop your pen). Contamination in outpatient settings isn’t a problem either (unless you happen to have a fairly short consultation for a patient with VRE). So, what to do? Jim introduced the idea of a ‘hierarchy of control’; put another way, prevention is better than cure, so do we have the right systems in place to manage faeces which is teeming with hospital pathogens? For example, should we be enforcing mandatory contact precautions for all contact with faeces (standard precautions – which aren’t very standard anyway – are probably not adequate)? Finally, Jim mentioned the growing importance of faecal microbiota transplantation (and hearing a Canadian speak about this reminded me of a hilarious spoof video).

No-touch automated room decontamination (NTD)

medical equipment in a hospital roomFigure: Hospital bed rails are frequently contaminated, and often not easy to clean and disinfect using conventional methods. 

Paul Dickens – establishing Ebola surge isolation capacity in the UK

Paul Dickens gave a whistle-stop overview of the detailed plans for Ebola surge capacity in the UK (perish the thought). He began by describing the replacement of formaldehyde with hydrogen peroxide vapour for the decontamination of the patient isolators at the Royal Free High Level Isolation Unit (HLIU). They now have a tried and tested process and protocols in place to get the HLIU back online within days using hydrogen peroxide vapour decontamination, where the previous protocol using formaldehyde put it out of action for 6 weeks! (I was involved in writing the protocols for this tricky decontamination assignment, which were reported on a poster published at HIS.) Other challenges in establishing surge capacity include staff expertise, and PPE recommendations, supply & training. Surge capacity is now established. Let’s just hope we won’t need it!

Dr Frédéric Barbut – How to eradicate Clostridium difficile spores from the environment

There’s now plenty of evidence that contaminated surfaces contribute to the transmission of C. difficile. These environmental intervention studies show a 50-80% reduction in the rate of CDI; does this mean that 50-80% of CDI acquisition is environmentally-associated? This seems too high, but it’s difficult to think of another explanation. Furthermore, there is emerging but compelling evidence of a proportional relationship between the degree of C. difficile surface contamination and transmission risk? I really don’t think that the public have yet ‘got’ that the previous occupant can influence acquisition risk. And when they do, I think there will be increasing demand for properly decontamination rooms. So, is it time to turn to NTD systems? Sometimes, yes. And do you go for hydrogen peroxide or UV? Well, that depends on what you’re trying to achieve! If you’re trying to eliminate pathogens, which sometimes you will be, then hydrogen peroxide vapour is the best choice. But if you’re trying to reduce contamination levels without necessarily eliminating all pathogens, then UV is the best choice due to its speed and ease of use.

The debate: “Hospitals that do not use high-tech decontamination of the environment are doing their patients a disservice.”

This debate pitted Profs Hilary Humphreys and Phil Carling (pro) against Peter Hoffman and Martin Kiernan (con). It was lively, entertaining and engaging…

Prof Humphreys argued that it is not acceptable to admit patients to rooms with inherent additional risk for transmission. We can address this by ‘walking like the Egyptians’ and copperising our surfaces, for which there is now some data with a clinical outcome. Another approach is NTD systems, for which data (including some clinical outcomes) are emerging. Prof Carling’s presentation was somewhat unusual, with his arguments seemingly an appeal to common sense rather than drawn from the published literature.

Martin Kiernan began by acknowledging the role of the environment, but that hand contamination is almost always the final vector (and there’s some evidence for this). The cornerstone of Martin’s argument was that whether NTD systems work is the wrong question. We should be focusing our time, money and attention on improving conventional methods which have been shown to reduce transmission. Peter Hoffman complemented Martin’s pragmatic viewpoint with thorough, thoughtful critiques of the studies on HPV decontamination with a clinical outcome. The 2008 Boyce study has more holes than the 2013 Passaretti study, which itself is far from watertight!

The key argument for turning to NTD systems is that admission to a room previously occupied by a patient with an MDRO increases the risk of acquisition due to residual contamination, and NTD decontamination mitigates this increased risk. So, my own conclusion is that hospitals that do not use high-tech decontamination of the environment are indeed doing their patients a disservice. Sometimes!

Look out for the third and final installment of my reflections from HIS 2014 at some point tomorrow!

Image: Medical equipment in a hospital room.

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!

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.

CRE can survive on dry surfaces for longer than you may expect

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

If I was to perform a straw-poll of microbiologist on how long Enterobacteriaceae could survive on dry surfaces, I suspect that most answers would be measured in hours and days rather than weeks and months. However, a lab study that I performed in collaboration with Nancy Havill and John Boyce at Yale New Haven Hospital demonstrated that CRE are able to survive on dry surfaces for over a month.

For the study, which is published in the recent ICHE special edition on CRE and MDROs, we took two clinical isolates of CRE (Klebsiella pneumoniae and Citrobacter freundii) and dried them onto metal discs either in a water or TSB suspension. Discs were then enumerated every few days over a 19 day period. Both K. pneumoniae and C. freundii were able to survive for more than two weeks, and all but C. freundii dried in water survived to the end of the testing period (day 19) (Figure 1). In addition, K. pneumoniae and C. freundii dried in TSB survived for more than 40 days in an additional set of experiments.

CRE survival 1Figure 1. Survival of K. pneumoniae and C. freundii on dry surfaces dried on metals discs in either water or TSB; error bars represent +1 standard deviation on a mean of three replicates at each time point.

We shouldn’t be surprised by these findings. Previous drying studies of Enterobacteriaceae have demonstrated a range of survival times, from hours to months depending on the species, strain and testing conditions. Whist it is plausible that carbapenem-resistance imposes a fitness burden on Enterobacteriaceae that may curtail their survival time, the CRE that we studied seemed to exhibit survival times in the same range as carbapenem-susceptible Enterobacteriaceae. Furthermore, a previous study from my lab identified a stark difference in the survival times of three different K. pneumoniae strains (Figure 2). One of the three strains tested was dead by three weeks, whilst another survived for more than 6 weeks with a minimal log reduction.

CRE survival 2Figure 2. Survival of three different strains of K. pneumoniae dried on metal discs; error bars represent +1 standard deviation on a mean of three discs at each time point.

It seems that CRE can survive for long enough on surfaces to be potentially involved in transmission. However, recent studies by Nseir et al, and Ajao et al. have failed to identify an increased risk associated with admission to a room occupied by a patient infected or colonized with resistant Enterobacteriaceae, in contrast with other bacteria including Acinetobacter baumannii. I suspect part of this is due to the fact that the Enterobacteriaceae are such a diverse family. A number of studies have identified large differences in the rate of contamination when comparing ESBL-producing E. coli vs. K. pneumoniae. If the prior room occupancy studies had been stratified and powered according to species within the Enterobacteriaceae family, I’d expect to see the increased risk from the prior room occupant for K. pneumoniae but not for E. coli. Also, the substantial variation in survival times amongst K. pneumoniae strains has clear implications for outbreaks of K. pneumoniae: are you dealing with a strain that is a “survivor” on surfaces? If so, more attention to cleaning and disinfection may be required.

In summary, CRE are able to survive on dry surfaces for weeks to months, which is long enough to be potentially involved in transmission; this justifies the advice for enhanced cleaning and disinfection to control the spread of CRE.

Article citation: Havill NL, Boyce JM, Otter JA. Extended survival of carbapenem-resistant Enterobacteriaceae on dry surfaces. Infect Control Hosp Epidemiol 2014;35:445-447.

What can outbreaks of Salmonella from the 1950s tell us about CRE?

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

I recently came across a fascinating review article published in 1963 mainly about outbreaks of Salmonellosis during the 1950s. The review focuses on epidemics that were traced to contaminated surfaces, including ingested, contact and inhaled transmission routes. A number of interesting epidemics stand out:

  • An outbreak linked to contaminated neonatal respirators.
  • An outbreak linked to a contaminated chopping board (see Figure). In this outbreak, one of the investigators apparently contracted Salmonellosis after touching the chopping board during sampling and then having a cigarette before washing his hands.
  • An outbreak (of microbial endotoxin syndrome) linked to a contaminated mouthpiece of SCUBA equipment. Here, the outbreak occurred in naval diving academy and the pattern of lessons and cases was so regular, that the epidemiologist could predict precisely when to visit to see the next case.

chopping board 2

Figure: A chopping board at risk of persistent microbial contamination due to surface damage. 

Although most outbreaks covered in the review relate to ancient catering-related outbreaks of Salmonella, there may be some useful learning for hospital epidemiology today, specifically CRE. It’s rare although not unheard of to find Salmonella carrying a carbapeneamase (i.e. Salmonella CRE). However, Salmonella is a member of the Enterobacteriaceae, so the involvement of contaminated surfaces during outbreaks of Salmonella suggests that contaminated surfaces may also be important during outbreaks of CRE.

It’s interesting that even back in the 1960s contaminated surfaces were recognized as potentially important in epidemics, whereas by the 1980s, the role of contaminated surfaces in endemic transmission was considered negligible. It’s difficult to know whether experts of the 1960s (perhaps there are some reading this?) would have considered contaminated surfaces important in both epidemic and endemic transmission? I suspect so, and we just lost sight of that in the 1980s and 90s.

Article citation: Sanborn WR. The relation of surface contamination to the transmission of disease. Am J Public Health Nations Health 1963;53:1278-1283.

Image: Ben Hosking.

What do we mean by ‘cleaning’ and ‘disinfection’?

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

clean definition 2

We urgently need to decide what we mean when we use the terms “clean” and “cleaning”.

In the last few years, the accumulated microbiological and epidemiological data (and prolonged heated debate) has lead us to conclude that  environmental surfaces need to be considered alongside hands, laundry etc so on, as part of a multibarrier approach to infection prevention and control in healthcare settings, and hygiene at home. Set against this however, our current approach of “what do we do to these surfaces to break the chain of infection transmission?” is both unscientific, and also highly misleading to the people we need to communicate with.  This part of the equation is fast becoming the weak link, preventing us from maximising health benefits from infection prevention and control measures.  This really hit home on reading the different contributions to the excellent 2013 AJIC supplement by Rutala and Webber which, on one hand showed just how much our thinking about environmental surface risks  has developed, but in many papers “environmental cleaning” was used interchangeably with “environmental disinfection” which made it confusing to know what the writer really meant.

From our IFH experience of home hygiene, we know what happens when advising consumers (or equally, hospital cleaning staff) to “clean” a surface e.g. after preparing raw poultry. They will clean until the visible dirt is gone – and we know that this is not necessarily enough.  For the home, we have data showing that after cleaning kitchen surfaces with soap and water following preparation of a chicken (in the UK 60% are contaminated with Campylobacter),  surfaces may LOOK squeaky clean, but the Salmonella or Campylobacter is now spread everywhere (and in numbers up to 103 or more).   We have similar data for surfaces contaminated with norovirus-containing faecal matter from an infected person (for which the infectious dose may be very small).

As a start, we need a term to advise/communicate “this surface needs to be cleaned to a level that breaks the chain of infection” and we currently have NO way to do this.   If we accept that the term “clean” means absence of visible dirt/soil, we need a term to describe “microbiologically safe clean”, not just for consumers or hospital cleaning professionals, but also for communicating with each other as scientists.

There is also another common misconception. Some people work on the basis that “clean” means visibly clean, and “microbiologically safe clean” means a chemical or thermal disinfectant has been used.  But then how can we communicate that hand washing can make hand surfaces microbiologically safe” without need for a disinfectant.  There is a notion that “cleaning” is hygienically inferior to disinfection – but data now shows that the log reduction by handwashing with soap can be equivalent to that achieved by alcohol handrubs if done properly, and you have access to running water.  We put much effort into hand hygiene compliance, but relatively little into stressing that handwashing technique to deliver hands which are “fit for purpose” is equally important.

We need to go back to the simple principles of what we are trying to achieve – namely to break the chain of onwards transmission of pathogens by treating surfaces (hands or environmental) to reduce germs to an “acceptable level” i.e. make a surface “fit for purpose”.  This can be done in 2/3 ways – removing them, inactivation, or a combination of both. For the last 14 years, IFH has successfully used the word “hygienically clean” to mean “microbiolgically safe”, and “hygienic cleaning”  to describe the process to achieve this – which could be soap and water with rinsing – or cleaning disinfection, or a combination of both.

Guest Blogger Bio

SBPHOTO

Dr Sally Bloomfield is an Honorary Professor at the London School of Hygiene and Tropical Medicine. She is also is the Chairman and Member of the Scientific Advisory Board of the International Scientific Forum on Home Hygiene (IFH).  Through these roles Professor Bloomfield continues to develop her work in raising awareness of the importance of home hygiene in preventing the transmission of infectious disease, and developing and promoting home hygiene practice based on sound scientific principles. She is also working to develop understanding of “hygiene issues” such as the “hygiene hypothesis” and “antimicrobial resistance”.

Professor Bloomfield’s background is in healthcare and infectious disease. She has a degree in Pharmacy, and PhD in Pharmaceutical Microbiology from the University of Nottingham. Sally was previously a Senior Lecturer in Pharmaceutical Microbiology at Kings College London (1995 – 1997) and a Hygiene Liaison manager at Unilever Research Port Sunlight UK (1997 – 2001).  She has published 100 research and review papers on the subject of home hygiene and the action and mode of action role of antimicrobial agents.

Contaminated surfaces contribute to transmission; the question is, how much?

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

mop

I’ve been asked to write a chapter on the role of the environment in transmission in an Springer book (on the potential role for antimicrobial surfaces in healthcare). So, I’ve been busy updating my 2011 ICHE literature review on a similar topic, drawing on an excellent recent AJIC review by Dr Donskey.

There are some epidemiological associations that suggest an important role for contaminated surfaces in transmission. Most compelling are the studies showing that admission to a room previously occupied by a patient with certain environmentally-associated pathogens increases the risk of acquisition for incoming patients, presumably due to residual contamination. However, in order to really nail a scientific association, an intervention is required. Hence, the environmental intervention studies provide the highest quality evidence evaluating the role of the environment in transmission (see the Table below).

These studies have shown that switching to more effective agents, improving the cleaning / disinfection process or turning to automated “no-touch” room disinfection systems (NTD) can reduce transmission in endemic settings. It’s important to note that some studies report an ineffective environmental intervention. These are important to publish to avoid publication bias. Looking under the bonnet of these studies usually offers an explanation as to why they did not show a significant reduction in transmission. For example:

  • Wilcox 2003. There was virtually no impact on the frequency of C. difficile environmental contamination on the wards using bleach, so it’s surprising that they saw any reduction in CDI!
  • Valiquette 2007. The bundle of interventions, some of which were environmental, was only given a few months to be effective.
  • Wilson 2011. This one is more difficult to explain. Perhaps it was underpowered to detect a clinical impact in the declining prevalence of MRSA in the UK?
  • Dharan 1999. The intervention was focused mainly on improving the cleaning and disinfection floors, which are not exactly a high-touch, high-risk sites.

Believe it or not, I still occasionally meet people who tell me that contaminated surfaces do not contribute to transmission. That rather dated viewpoint is becoming increasingly untenable as the volume and quality of data evaluating the role of the environment in transmission continues to increase. For me, the question has now moved on to how much contaminated surfaces contribute to transmission, and how best to address contamination of the hospital environment.

Table. Intervention studies evaluating the role of contaminated surfaces in the endemic transmission of nosocomial pathogens.

Reference Setting, location Organism Study design Key findings
Mayfield 2000 1 Three units, USA C. difficile 18-month before-after study of a switch from QAC to bleach disinfection. Significant reduction in CDI incidence on the highest risk unit from 8.6 to 3.3 cases per 1000 patient-days.
Wilcox 2003 2 Two units, UK C. difficile 2-year ward cross-over study of a switch from detergent to bleach disinfection. Significant reduction in CDI incidence on one of the units (from 8.9 to 5.3 cases per 100 admissions), but not on the other.
McMullen 2007 3 MICU and SICU, USA C. difficile 2-month before-after evaluation of bleach disinfection of CDI rooms on SICU and 4-month evaluation of bleach disinfection of all rooms on MICU in a hyper-endemic setting. Significant reduction in CDI incidence on both units (10.4 to 3.9 cases per 1000 patient days on SICU; 16.6 to 3.7 cases per 1000 patient days on MICU).
Valiquette 2007 4 Hospital-wide, Canada C. difficile 5-month evaluation of enhanced infection control and disinfection, including a switch to bleach, and a subsequent switch to ‘accelerated’ hydrogen peroxide. Neither environment intervention made a significant impact on the incidence of CDI; a reduction in the use of high-risk antibiotics significantly reduced the incidence of CDI.
Boyce 2008 5 Hospital-wide, USA C. difficile 20-month before-after study on the use of HPV disinfection for terminal disinfection of CDI rooms. Significant reduction in CDI incidence on five high incidence units (from 2.3 to 1.3 cases per 1000 patient-days). Lesser reduction in CDI incidence hospital wide.
Hacek 2010 6 Three hospitals, USA C. difficile 3-year before-after study on switching from QAC to bleach for terminal disinfection of CDI rooms. Significant reduction in the incidence of CDI (from 0.85 to 0.45 per 1000 patient days).
Orenstein 2011 7 Two medical units, USA C. difficile 2-year before-after study on switching to bleach wipes for daily and terminal disinfection of all rooms. Significant reduction in the incidence of CDI (from 24.2 to 3.6 per 1000 patient days).
Manian 2013 8 Hospital-wide, USA C. difficile 3-year before-after study on enhanced terminal disinfection of CDI rooms using HPV and bleach. Significant reduction in the incidence of CDI (from 0.88 to 0.55 cases per 1000 patient days).
Hayden 2006 9 ICU, USA VRE 9-month before-after study on educational improvement of cleaning and hand hygiene. The frequency of environmental contamination and patient acquisition of VRE were reduced  from 33 to 17 acquisitions per 1000 patient-days during the improved cleaning phase.
Datta 2011 10 ICU, USA VRE / MRSA 3-year before-after study of an intervention (fluorescent markers, “bucket method” and education) to enhance daily and terminal cleaning. Significant reduction of MRSA (3.0% to 1.5% of admissions) and VRE (3.0% to 2.2% of admissions) acquisitions; intervention significantly reduced the increased risk from the prior occupant for MRSA but not VRE.
Perugini 2011 11 Hospital-wide, Brazil VRE 4-year before-after study of an educational and observational intervention for cleaners. Significant reduction in VRE infection (from 7.7 to 1.9 per 1000 patient days) and environmental contamination.
Grabsch 2012 12 Hospital-wide, Australia VRE 18-month before-after study of a multimodal intervention (switch to bleach, improved monitoring of cleaners, modification of VRE contact isolation, periodic ‘super-clean-disinfection’ of high-risk wards). Significant reduction of VRE colonization (from 10.7% to 8.0% of patients) and VRE environmental contamination.
Passaretti 2013 13 ICU, USA VRE / all MDROs 30-month cohort study on the impact of HPV decontamination. Patient admitted to rooms disinfected using HPV significantly less likely to acquire an MDRO (15.7 to 6.2 per 1000 patient days) and VRE (11.6 to 2.4 per 1000 patient days).
Mahamat 2007 14 Hospital-wide, UK MRSA 8-year interrupted time series analysis of multiple infection control interventions. Introduction of bleach disinfection, environmental sampling, alcohol gels and admission screening all reduced the prevalence of MRSA.
Dancer 2009 15 Two wards, UK MRSA 12-month cross over-study on the impact of one extra cleaner. Enhanced cleaning was associated with significant reductions surface contamination, hygiene fails and MRSA acquisition.
Wilson 2011 16 ICU, UK MRSA 12-month randomized crossover study on the impact of additional twice daily cleaning of hand contact surfaces. Significant reduction in the detection of MRSA on surfaces and hands, but no significant change in MRSA acquisition was detected.
Dharan 1999 17 5 medical wards, Switzerland – 4-month controlled study where 3-wards received an intervention (including an active oxygen based compound) and 2 wards continued current practice. Intervention associated with reduced contamination but not reduced nosocomial infection or MRSA infection / colonization.

HPV = hydrogen peroxide vapour.

 

References

1.       Mayfield JL, Leet T, Miller J, Mundy LM. Environmental control to reduce transmission of Clostridium difficile. Clin Infect Dis 2000; 31: 995-1000.

2.       Wilcox MH, Fawley WN, Wigglesworth N, Parnell P, Verity P, Freeman J. Comparison of the effect of detergent versus hypochlorite cleaning on environmental contamination and incidence of Clostridium difficile infection. J Hosp Infect 2003; 54: 109-114.

3.       McMullen KM, Zack J, Coopersmith CM, Kollef M, Dubberke E, Warren DK. Use of hypochlorite solution to decrease rates of Clostridium difficile-associated diarrhea. Infect Control Hospital Epidemiol 2007; 28: 205-207.

4.       Valiquette L, Cossette B, Garant MP, Diab H, Pepin J. Impact of a reduction in the use of high-risk antibiotics on the course of an epidemic of Clostridium difficile-associated disease caused by the hypervirulent NAP1/027 strain. Clin Infect Dis 2007; 45 Suppl 2: S112-121.

5.       Boyce JM, Havill NL, Otter JA et al. Impact of hydrogen peroxide vapor room decontamination on Clostridium difficile environmental contamination and transmission in a healthcare setting. Infect Control Hosp Epidemiol 2008; 29: 723-729.

6.       Hacek DM, Ogle AM, Fisher A, Robicsek A, Peterson LR. Significant impact of terminal room cleaning with bleach on reducing nosocomial Clostridium difficile. Am J Infect Control 2010; 38: 350-353.

7.       Orenstein R, Aronhalt KC, McManus JE, Jr., Fedraw LA. A targeted strategy to wipe out Clostridium difficile. Infect Control Hosp Epidemiol 2011; 32: 1137-1139.

8.       Manian FA, Griesnauer S, Bryant A. Implementation of hospital-wide enhanced terminal cleaning of targeted patient rooms and its impact on endemic Clostridium difficile infection rates. Am J Infect Control 2013; 41: 537-541.

9.       Hayden MK, Bonten MJ, Blom DW, Lyle EA, van de Vijver DA, Weinstein RA. Reduction in acquisition of vancomycin-resistant enterococcus after enforcement of routine environmental cleaning measures. Clin Infect Dis 2006; 42: 1552-1560.

10.     Datta R, Platt R, Yokoe DS, Huang SS. Environmental cleaning intervention and risk of acquiring multidrug-resistant organisms from prior room occupants. Arch Intern Med 2011; 171: 491-494.

11.     Perugini MR, Nomi SM, Lopes GK et al. Impact of the reduction of environmental and equipment contamination on vancomycin-resistant enterococcus rates. Infection 2011; 39: 587-593.

12.     Grabsch EA, Mahony AA, Cameron DR et al. Significant reduction in vancomycin-resistant enterococcus colonization and bacteraemia after introduction of a bleach-based cleaning-disinfection programme. J Hosp Infect 2012; 82: 234-242.

13.     Passaretti CL, Otter JA, Reich NG et al. An evaluation of environmental decontamination with hydrogen peroxide vapor for reducing the risk of patient acquisition of multidrug-resistant organisms. Clin Infect Dis 2013; 56: 27-35.

14.     Mahamat A, MacKenzie FM, Brooker K, Monnet DL, Daures JP, Gould IM. Impact of infection control interventions and antibiotic use on hospital MRSA: a multivariate interrupted time-series analysis. Int J Antimicrob Agents 2007; 30: 169-176.

15.     Dancer SJ, White LF, Lamb J, Girvan EK, Robertson C. Measuring the effect of enhanced cleaning in a UK hospital: a prospective cross-over study. BMC Med 2009; 7: 28.

16.     Wilson AP, Smyth D, Moore G et al. The impact of enhanced cleaning within the intensive care unit on contamination of the near-patient environment with hospital pathogens: a randomized crossover study in critical care units in two hospitals. Crit Care Med 2011; 39: 651-658.

17.     Dharan S, Mourouga P, Copin P, Bessmer G, Tschanz B, Pittet D. Routine disinfection of patients’ environmental surfaces. Myth or reality? J Hosp Infect 1999; 42: 113-117.

Key themes from ID Week 2013

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

idweek

Having somewhat dipped in towards the end of ID Week 2013 due to the overlapping Infection Prevention 2013 Conference in London, I can’t begin to provide a comprehensive overview of such a large event. Instead, I’ve tried to summarize new data on two important areas: the epidemiology and control of multidrug-resistant Gram-negative rods (MDR-GNR) and the role of the environment in transmission. You can access all of the abstracts free online here. Also, the poster abstracts that I cite below are either individually hyperlinked or can be downloaded here.

MDR-GNR

Dr Kavita Trivedi (California Department of Public Health) gave an overview of CRE in the USA, which has now been reported in virtually every state. Whilst surveillance sites, methods and definitions are problematic, CDC are coordinating some useful emerging data. For example, an NNIS prevalence survey indicates an increase in CRKP from 1% in 2001 to 10% in 2011. Also, the Multi-Site Resistant Gram-Negative Bacilli Surveillance Initiative (MuGSI) is beginning to yield some data. Early results from four states indicate that CRE is 10x less common than MRSA in the population, predominantly from urine cultures (85%) from patients with co-morbitities (93%) with a low mortality rate (4%). The CDC CRE toolkit provides a practical overview of recommended interventions. Finally, the challenges outlined by Dr Trivedi included: long-term care; variable prevalence; unknown epidemiological associations of different strains and genes; and colonization duration.

Oral presentations

A featured oral abstract by Bamburg et al. described an outbreak of NDM-producing K. pneumoniae affecting eight patients. The complex transmission map was dissected using whole genome sequencing, reminiscent of the NIH experience.

There was a useful oral session on ‘Identifying and Overcoming Challenges in Preventing Transmission of MDRO GNR’:

  • 1207, Haverkate. A Dutch group found that Klebsiella carrying OXA-48 can appear susceptible in vitro, risking ‘silent transmission’ of both the gene and the organism. The mean duration of colonization was almost one year and modeling indicated that readmission of CRE colonized patients needs to be carefully accounted for.
  • 1208, Mody. A cluster RCT in nursing home residents with urinary catheters or feeding tubes found that enhanced and preemptive isolation; ASC; and education led to a significant reduction in MDROs and CAUTI.
  • 1209, Hayden. A bundled intervention (ASC and isolation; daily CHG bathing; education; and adherence monitoring) significantly reduced CR Klebsiella in three of four LTACs included in the study. The prevalence of CR Klebsiella was remarkably high: 45% of patients at baseline. Environmental contamination was not identified, so no enhanced cleaning and disinfection was implemented, which is different to the experience of NIH.
  • 1210, Lewis. Varying the definition of ‘MDR’ made a profound impact on the proportion of patients requiring contact isolation, from 8-30%. Subsequent discussion with the authors indicated that the proposed MDR definitions developed by ECDC and CDC to be too sensitive for bacteria with less intrinsic resistance, such as E. coli. Perhaps a separate definition for the Enterobacteriaceae and non-fermenters is the way forward here?
  • 1211, Apisarnthanarak. The implementation of chlorhexidine bathing plus a switch to bleach for environmental disinfection brought an outbreak of A. bauamannii in Thailand under control. But which worked?
  • 1212, Barnes. A mathematical model indicated that hand hygiene is twice as important as environmental hygiene for interrupting A. baumannii, MRSA and VRE transmission. Whilst an awful lot of assumptions are required in this model, I can believe this 2:1 ratio in light of the following: “healthcare personnel are like small children: they touch everything and don’t always wash their hands” (Curtis Donskey) and “healthcare personnel hands are like very mobile shared surfaces” (Eric Lofgren).

Posters

  • 740, Jamal. CRE rate: 3% of 2000 Kuwaiti clinical isolate; 15.9% of CRE NDM-1 producers.
  • 746, Koper. A match made in hell between hypervirulent K2 Klebsiella and KPC; in vitro plasmid transfer demonstrated.
  • 1578, Madigan. No CRE detected in 69 international patients at Mayo Clinic; 22% carried ESBLs.
  • 1582, Johns. 50% of 66 MDR A. baumannii cases in Ohio in 2012 presented in first two days of admission, mostly admitted from extended care facilities, illustrating the ‘revolving door’ between acute and other healthcare facilities.
  • 1586, Carrilho. 26% of 157 Brazilian CRE polymyxin-resistant, though polymyxin resistance was not associated with increased mortality.
  • 1603, Drees. Remarkably, a survey from the SHEA Research Network indicates that 6% of hospitals do NOT isolate patients with CRE.
  • 1609. Decker. A study of CRE colonization patterns indicates median colonization of 216 days (range 134-376). One patient was colonized for >500.
  • 1611, Odom. CRE cultured from 12 (4.4%) of surfaces, predominantly sink drains.
  • 1612, Fitzpatrick. Selective broth enrichment added 10% sensitivity for detecting CRE. Is the resulting diagnostic delay worth the wait?
  • 1615, Lin. Chlorhexidine gluconate (CHG) daily bathing significantly reduces the number of body sites growing CRE, but several sites remain colonized.
  • 1618, Cheng. CRE identified in 1.2% of 6533 rectal screens and faecal specimens in Hong Kong, which is lower than I would expect.

Reflections from MDR-GNR research

  • We now have some intervention studies, but many include bundled interventions. We need more resolution on what works.
  • The duration of colonization with CRE seems to be long, probably around 1 year on average. Is this enough for a “once positive, always positive” approach?
  • Prevalence of CRE is variable around the USA, and in other parts of the world.
  • There is poor resolution between the epidemiology of Enterobacteriaceae and non-fermenters.
  • Most would agree that contaminated surface play an important role in the transmission of MDR non-fermenters such as A. baumannii. But is CRE an environmental issue? Some groups have found contamination and implemented enhanced disinfection, others have not.
  • Should chlorhexidine decolonization be part of the intervention for MDR-GNR?
  • Different research groups use different terminology and the meaning is sometimes obscured. International consensus is required.

Role of the environment in transmission

Dr Curtis Donskey (Cleveland) gave an excellent overview of ‘Environmental Controls for the Prevention of C. difficile Transmission’. Dr Donskey is one of the most active researchers anywhere in the world, focusing much of his attention on the role of the environment. Having established the importance of contaminated surfaces in the transmission of C. difficile, Dr Donskey explored emerging themes in addressing surfaces contaminated with spores covering conventional and automated terminal cleaning, and the impact of improving daily disinfection. The current challenges outlined included where to clean, how to validate “no-touch” automated room disinfection systems (NTD) to disentangle product claims from real-world performance, how best to engage environmental services and how to make disinfection easier in order to facilitate compliance.

Posters

  • 347, Livorsi. Patients with a higher nasal burden of MRSA are more likely to carry MRSA at other sites and contaminate their environment.
  • 348, Sitzlar. Useful stratification of MRSA/VRE room contamination rate by patient C. difficile status. Rooms of patients on precautions for CDI 3x more likely to be contaminated.
  • 1393, Deshpande. One hospital found more C. difficile contamination in the rooms of patients who were not on precautions for CDI than in rooms of patients on precautions for CDI!
  • 1394, Kundrapu. Suggests that the result would be better if those tasked with monitoring cleaning performance got their hands dirty and cleaned.
  • 1541, Sunkesula. Reduction in VRE in new unit; attributable to no shared rooms and bathrooms in the new unit?
  • 1685, Rose. A couple of carbapenem-resistant bacteria on public surfaces outside New York hospitals; I bet you it’d be higher in New Delhi!
  • 1685, Havill. Extended survival of CRE on dry surfaces; will surprise some.
  • 1690, Kirk. Almost no MRSA cultured from medication cabinets in isolation rooms. Direct plated swab lacks sensitivity?
  • 1691, Suwantarat. Quantitative assessment of HCP contact with equipment and fomites helps to define high touch (risk?) items; medication chart highest frequency of contact (1 per patient hour) yet possibly also the least cleaned item.
  • 1692, Hirsh. ipads (and other personal electronic devices) can become contaminated with pathogens; contact precautions should include an explicit instructions not to touch these items. (This was implemented at NIH during recent CRE outbreak there).
  • 1695, Williams. Pathogens identified on the clothing of HCP at the BEGINNING of their shift! (Reminds me of Hayden article where VRE commonly found on the hands of HCP BEFORE they entered patient rooms.)
  • 1697, Vassallo. Universal standard precautions didn’t stop impressive trend reductions. Time to abandon contact precautions?
  • 1698, Mann. Cleaning survey response rate of 100% (unprecedented). EVS staff have something to say, if only we’d listen.
  • 1700, Gerba. What’s for lunch in the hospital cafeteria? MRSA, enteric bacteria and spores, apparently.
  • 1701, Wiemken. Wipes are quicker and easier than bucket methods. Why wouldn’t you? (Perhaps only due to lack of wetting reducing efficacy.)
  • 1705, Boyce. The informal ‘standard’ for ‘clean’ is <2.5 cfu/cm2. This equates to 65 cfu/contact plate, which is almost 1/3 of the way to uncountable. Is this an acceptable standard for ‘clean’?
  • 1706, Power. Contaminated neonatal incubator? An hour of UVC should do the trick.
  • 1707, Horn. HPV for terminal room disinfection associated with significant reduction in CDI. Study design controlled for hand hygiene compliance, but time series analysis may have been more appropriate.
  • 1708, Anderson. Is variation in UVC cycle time for room disinfection explained entirely by variation in room size?
  • 1709, Uslan. Assessment of various Cu surfaces; I was unaware that you could apply Cu as a spray though have concerns over durability.

Other highlights

  • Decolonization has been a hot topic since several high-profile articles have been published recently. It’s a shame that universal chlorhexidine was conflated with universal mupirocin in the Huang study; the two should be considered separately in my view. The potential for resistance to mupirocin is extremely high, whereas the risk for ‘resistance’ or continued reduced susceptibility to chlorhexidine is lower. However, an interesting finding from poster 1615 was that the measured CHG skin concentration (20-1200 mg/L) was MUCH lower than the applied CHG concentration (10,000 mg/L). This brings the subtly reduced susceptibility to CHG reported in MRSA into play. Both Dr Aaron Milsone (Hopkins) and Prof Mary-Claire Roghmann (University of Maryland) highlighted the importance of the need to ‘tend the human microbiome’ and to consider the ‘host-microbiome-pathogen’ interaction rather than the ‘host-pathogen’ interaction, remembering that decolonization can cause considerable collateral damage to the host microbiome.  
  • Dr Denise Cardo (CDC) delivered the SHEA Lectureship on HAI Science and Policy. CDC are streets ahead of any other government health agency in leading HAI science through the development of common, simple goals; accountability; transparency; efficiency and strategy. HAI science alone is not sufficient to influence policy; this requires congressional briefings, senate hearings and the use of the scientific and lay press. The recently published CDC threat report outlines how the (somewhat bleak) future may look. Most poignantly, Dr Cardo could not attend the conference and delivered her lecture remotely due to the government shutdown, which signals leaner times ahead for CDC.  
  • BUGG. Dr Anthony Harris (University of Maryland) presented the results of the ‘Benefits of Universal Glove and Gown’ (BUGG) study. This RCT with impressive compliance to screening, gloving and gowning showed a significant 40% reduction in MRSA but no significant reduction in VRE. The a priori primary outcome (a composite measure of MRSA and VRE acquisition) was non-significant. I’m generally not a fan of universal approaches, since compliance in the real world is likely to tail off when the spotlight of a large study fades. Indeed, poster 1696 showing a ‘dismal’ 20% compliance rate with gowning in the field sheds a shadow on the BUGG study.   
  • Dr Brad Spellberg (UCLA) gave a wake-up call on the future of antibiotics and resistance. Reflecting on the three things guaranteed in life (death, taxes and resistance), Dr Spellberg outlined the unfair fight between humans and bacteria: we’re outnumbered to begin with, and multiply much more slowly! Dr Spellberg’s recent papers in CID and NEJM outline the radical approach required to curb and reverse antibiotic resistance including embracing technology, rekindling R&D, preserving effective agents and exploring novel therapies. Dr Spellberg gave a fascinating insight from the 1960s revealing that it’s not the first time the antibiotic pipeline has dried. We need to learn from history and rekindle R&D before the pipeline dries completely. More importantly though, exploring non-antibiotic therapies, or novel applications of existing agents, has a more realistic chance of brightening the future of antimicrobial therapy.   

Three good reasons why not to “copperize” your hospital surfaces

Jon Otter (@jonotter) Antimicrobial surfaces , , ,

I recently received an email from the Copper Development Association entitled “Five Good Reasons to Install Antimicrobial Copper Touch Surfaces”. The five reasons are as follows:

  1. “Continuous and significant bioburden reduction, 24/7.
  2. Improved patient outcomes.
  3. A supplement to standard hygiene practices.
  4. Simple, cost-effective intervention.
  5. Payback in less than one year.”

I agree with all of these points in principle, and like the recently published copper study a lot, but I recently had two experiences that gave me three good reasons why not to “copperize” a hospital room.

Firstly, I was kindly given a copper pen at a conference. I’ve had it for a few months now and it’s beginning to look slightly the worse for wear (note the tarnishing where my grubby mits have been holding it, and the bright shiny part that has had less exposure to air underneath the swivel top). Is this how a bedrail would look after a few months of use?

copper pen annotated

Secondly, the pen works well but my hands smell of metal after using it. Would it be the same after touching my copper bedside table?

Thirdly, we had a new boiler installed last year resulting in a small pile of scrap copper pipes. I eventually got around to taking the copper pipes to the scrap metal merchant last weekend, expecting to get nothing for them and he gave me £50. So, exactly how much would it cost to “copperize” a hospital room, and would you really see ‘payback in less than one year’?

I appreciate that much of this may have to do with the composition of the copper alloy. I would imagine that reducing the amount of copper in the alloy would mean lower cost, less smell and less tarnishing. However, it would also reduce the ability to inactivate microbes deposited on the surfaces, so the research data really only applies to the composition of the copper alloy in the items that were tested. Also, there’s been some academic criticism of the copper study on the Controversies in Hospital Infection Prevention blog which is worth reading.

There are still a lot of questions around the implementation of copper surfaces in hospital rooms, and there are other options to consider. But I do think we should be thinking seriously about evaluating the clinical impact and cost-benefit of implementing antimicrobial surfaces.