A little while ago I blogged about the excellent study from Nottingham that demonstrated significant VRE and MRSA contamination on socks used to prevent falls in the hospitalised elderly. This has been followed by another paper suggesting that shoe coverings undurprisingly become contaminated. So, what? How does this really impact on transmission? A new study from Curtis Donskey’s group has looked at hand contamination in patients directly relating to floor contamination. Continue reading
Disinfection
Diluting the efficacy of hydrogen peroxide room decontamination?
A somewhat perplexing new study has just been published in the Journal of Hospital Infection comparing the effectiveness of two hydrogen peroxide based automated room decontamination systems: a low-concentration (5%) hydrogen peroxide system (Deprox) and a high-concentration (30%) hydrogen peroxide system (Bioquell).
The study evaluated the impact of the two systems each run in 10 single rooms containing seeded metal discs placed in five locations, with a 6-log load of MRSA, K. pneumoniae, and C. difficile spores. The MRSA and K. pneumoniae were either low soiling (0.03% BSA) or heavy soiling (10% BSA), and the C. difficile spores was either low soiling (0.03% BSA) or in body fluid. In addition, surface samples were taken from 22 surfaces in each room before and after decon using contact plates. The bottom line is that both systems achieved a >5-log reduction on all of the discs (including those with heavy soiling), and there were no real differences in the levels of surface contamination remaining. All this understandably moved the authors to conclude that ‘The starting concentration and mode of delivery of hydrogen peroxide may not improve the efficacy of decontamination in practice.’
What are we doing to improve hospital room cleaning and disinfection?
I gave a webinar last week for 3M (you can download my slides here) on “Your hospital room can make you sick: How improved cleaning and disinfection can help”. I asked the audience what they were doing to improve cleaning and disinfection, and thought I would share the findings. I don’t know the exact size of the audience (but it’s usually a couple of hundred mainly US based IPC folks), and the audience were allowed to choose any answers that applied to them for the second two questions.
Endoscope Reprocessing Survey
Recent reports of multidrug-resistant infections related to contaminated endoscopes, which have intricate mechanisms and channels that are especially difficult to clean, have raised awareness about the necessity for meticulous reprocessing of all types of endoscopes to prevent the transmission of pathogens to patients.
In response to concerns from various countries about inadequately reprocessed endoscopes and to prevent further transmittal of infections by endoscopes, the ISC Infection Prevention & Control Working Group prioritized this issue in a meeting earlier this year and created a survey on current Endoscope Reprocessing Practices that could be used to compare such practices of institutions around the globe.
We would ask you to share the link to the on-line survey and encourage as many of your colleagues from various health care facilities to complete this. To complete this survey you need to be involved in Endoscope reprocessing activities or know the guidelines and structure of your institutions with regard to Endoscope reprocessing.
Thank you for your participation and for sharing the link!
Link to survey: https://www.surveymonkey.com/r/6ZSGF5L
This checklist was created by the following members of ISC IPC working group. Andreas Voss, Alex Friedrich, Peter Collignon, Moi Lin Ling, Brenda Ang, Wing Hong Seto, Paul Tambyah, Eli Perencevich, Marin Schweizer, Leanne Frazer, Achilleas Gikas, Tom Gottlieb, Joost Hopman, Nikki Kenters, Inge Huijskens, Kalisvar Marimuthu, Rehab El-Sokkary, Yogandree Ramsamy, Margaret Vos, Ermira Tartari, Debkishore Gupta.
Probiotics for environmental cleaning – can’t B. cereus
Vandini et al. (1) evaluate the effect of a microbial cleaner, containing spores of food grade Bacillus subtilis, Bacillus pumilus and Bacillus megaterium in two Italian and one Belgium hospital.
According to the abstract 20,000 microbiological samples were taken from surfaces, during the 24-week investigation, which would equal approximately 120 samples per day!
While nothing about blinding or block-randomization (or any possible approach that would eliminate bias) was mentioned, it is stated that the cleaning staff was not aware which cleaning product they used. Seen the fact that chlorine based-cleaners were the standard products in the two Italian hospitals, this seems hard to believe. The study period started at different times in the hospitals (but not by design) and in opposite to the abstract for different periods of time, namely 6, 24, and 66 weeks, respectively.
Asthma and the "Hygiene Hypothesis": Does cleanliness matter? New study says “No”
Guest Blogger Prof Sally Bloomfield (bio below) writes…In proposing the hygiene hypothesis in 1989, Dr David Strachan suggested that lower incidence of early childhood infections could explain the 20th century rise in allergic diseases. This was based on data showing that larger family size appears to protect against hay fever. Strachan suggested that smaller families provided insufficient infection exposure because of less person to person spread of infections – but also because of “improved household amenities and higher standards of personal cleanliness”. From this the notion that “we have become too clean for our own good” has arisen.
Most experts now agree that the “hygiene hypothesis” is a misnomer. Although the basic concept is still seen as correct, the link to infectious disease and hygiene is now largely discounted. A number of refinements to the hypothesis offer a more plausible explanation. The Old Friends (OF) Mechanism was proposed by Graham Rook in 2003. He proposed that the required exposures are not childhood diseases such as colds, flu, measles, norovirus, which have evolved only over the last 10,000 years, but the microbes we co-evolved with in hunter-gatherer times when the human immune system was developing. These Old Friends include largely non-harmful organisms such as helminths, commensal microbiota and environmental saprophytes.
Although these microbes are still there, through lifestyle changes we have gradually lost our exposure to them. Improved water, sanitation and food quality, although protective against infections, have also inadvertently reduced exposure to Old Friends which occupy the same habitats. The decline in natural childbirth in favour of caesarean section, and bottle instead of breast feeding is another likely factor. Reduced exposure to our outdoor environment has also occurred – we now spend up to 80% of our time indoors. Also, antibiotics may alter our interaction with microbes leading to reduced diversity of human gut microbiota.
Despite a shift in scientific thinking, the so-called “hygiene hypothesis” is still widely accepted in the public domain and still discussed in terms of concepts such as ‘eat dirt’, ‘too clean is bad’, or ‘sterile homes’. The lay audience, and even the U.S. FDA attribute the problem to ‘the extremely clean household environments often found in the developed world’.” (See headlines below!)
What is overlooked is the fact that the relationship between household or personal cleanliness and development of allergies has never been properly investigated. At last – just this week, we have seen publication of the first study to directly evaluate this issue. From the study, Erika von Mutius, a highly respected researcher in this field, concludes – No. “Development of allergies and asthma was not related to cleaning activities”.
Methods: The study involved a birth cohort of 399 participant families recruited in urban and suburban regions of Munich, Germany, between Oct 1999 and Dec 2001. A telephone questionnaire interview comprising 31 questions was carried out to assess cleaning habits and cleaning frequencies in the homes, the use of detergents and the personal cleanliness of the child. In addition, 13 lifestyle factors and home characteristics were obtained from a self-administered questionnaire. Questions about the child’s health focused on respiratory and allergic problems. Bacterial markers of home cleanliness were assessed in samples of floor and mattress dust.
Results and conclusions: As found by other workers, bacterial exposure in house dust was found to be associated with reduced risk of childhood allergies. In turn, personal cleanliness, such as washing hands, and home cleanliness were objectively reflected by dust parameters. However, neither personal nor home cleanliness were associated with protection from asthma and allergies (see flow chart, below).
Note: In this study, cleanliness was substantiated by rather unspecific dust measurements. The findings however suggest that allergy protection operates through as yet unknown exposures, not assessed by unspecific markers. Future studies will require more detailed microbial analysis. Whether these microbes are affected by cleaning remains to be elucidated, but findings with unspecific markers suggest that normal cleaning does not affect permanent microbial colonization of indoor environments.
If, as now seems, allergies are not the price we have to pay for protection from infection, two fundamental questions need to be addressed:
- “How can we develop an approach to hygiene, which helps to reconnect us with the necessary microbial exposures, whilst also protecting us against infectious diseases? “
- How do we change public understanding about the difference between “cleanliness” (absence of visible dirt) and “hygiene” (protecting against infectious diseases)?
The answer to the first question is a return to basics, which means promoting “targeted hygiene”. This means identifying the critical points in the chain of infection transmission and applying effective hygiene procedures at the appropriate times to prevent further spread. Appropriate times are those associated with activities such as food and water hygiene, respiratory hygiene, toilet hygiene, laundry hygiene and so on.
Dispelling the misconceptions is a real challenge, made more difficult by the fact that people tend to think that hygiene and cleanliness is the same thing (i.e “if it looks clean it must be germ free”). It is possible that this is best done by promoting a more constructive approach i.e . stressing that getting dirty is healthy, but hygiene is vital in the times and places that matter.
Further Reading: Bloomfield SF, Stanwell-Smith R, Rook GA. 2013. The hygiene hypothesis and its implications for home hygiene, lifestyle and public health: summary.
The study can be found at: Am J Respir Crit Care Med. 2015 Jan 13. [Epub ahead of print] Asthma and the Hygiene Hypothesis – Does Cleanliness Matter? Weber J, Illi S, Nowak D, Schierl R, Holst O, von Mutius E, Ege MJ.
Guest blogger bio:
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.
What do we mean by ‘cleaning’ and ‘disinfection’?
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
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?
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.
Is it time to turn to ‘no-touch’ automated room disinfection?
I gave a webinar for 3M yesterday entitled ‘Is it time to turn to ‘no-touch’ automated room disinfection (NTD)?’ It was based broadly on a recent Journal of Hospital Infection review article, and you can access the slides here.
The webinar covered:
- The key data supporting the need for improved hospital disinfection, particularly ‘terminal disinfection’ when patients are discharged.
- The strengths and limitations of conventional disinfection methods, particularly in terms of reliance on the operator to ensure adequate formulation, distribution and contact time of the active agent.
- The potential benefits of introducing automation into the room disinfection process.
- Coverage of the advantages and disadvantages of the various “no-touch” automated room disinfection systems currently available.
- Scenarios in which NTD systems may be warranted.
To summarize the rationale for using an NTD system: enhanced conventional methods are able to eliminate pathogens from surfaces, but the inherent reliance on a human operator to ensure adequate formulation, distribution and contact time of the active agent introduces variability into the process. NTD systems remove or reduce reliance on the operator for delivering hospital disinfection. However, they do not obviate the need for cleaning, so they are designed to augment rather than replace conventional methods.
So when to consider an NTD system? The flow chart below (Figure 1) shows a decision tree for which cleaning and disinfection approach to take. Given their practical limitations, NTD systems are best suited to disinfection of a room after a patient colonized or infected with a pathogen has been discharged to protect the incoming patient from acquiring the pathogen left behind by the prior room occupant. A recent study of a hydrogen peroxide vapor (HPV) NTD system shows that patients admitted to rooms disinfected using HPV were 64% less likely to acquire any multidrug-resistant organism (MDRO) than patients admitted to rooms disinfected using standard methods when the prior room occupant had an MDRO.
Figure 1. A disinfection decision diagram for when to consider an NTD system. a) Key pathogens associated with contamination of the environment include C. difficile, VRE, MRSA, A. baumannii, P. aeruginosa and norovirus. b) All NTD systems are applied after a cleaning step to ensure that surfaces are free from visible contamination, which is unacceptable to subsequent patients and will reduce the efficacy of the NTD disinfection. c) There is limited equivocal evidence that enhanced cleaning / disinfection in a low-risk general ward setting can reduce the spread of pathogens.
Ok, so you’ve decided that you want to use an NTD system. Which one to choose? Every conference I go too seems to have more and more NTD systems on show, all with bold and often conflicting claims. There are essentially four classes of NTD system that are commonly used in hospitals:
- Hydrogen peroxide vapor (HPV)
- Aerosolized hydrogen peroxide (aHP)
- Ultraviolet C (UVC)
- Pulsed-xenon UV (PX-UV)
I asked the audience which, if any, NTD system had been used in their hospital (Figure 2). 90% of the predominantly US based audience had not used an NTD system at all, which was a surprise. In the hospitals that had used an NTD system, there was a fairly even split between HPV and the UV systems.
Figure 2. Has your hospital used an NTD system and if so, which one?
Each of these systems have advantages and disadvantages, which I have tried to summarize in the following table by ranking the systems in the key categories. The hydrogen peroxide systems tend to have higher efficacy and better distribution than the UV systems. But the UV systems are faster and easier to use. Thus, there is a trade-off between efficacy / distribution and cycle time / ease of use when deciding which NTD system would be more appropriate.
Table: Comparing the key features of the four commonly used NTD systems.
In order to illustrate the challenges in choosing a) whether to use and NTD system and b) which to use, I presented the audience with three scenarios. In scenario 1, below, I was expecting most people to select ‘conventional methods’ or one of the UV systems, which have both been shown to reduce the burden of contamination without reliably eliminating pathogens. The sheer number of patients with MRSA colonization transferred or discharged from general medical wards means that the additional time for HPV may not be warranted.
Scenario 1. What do you do when a patient who was colonized with MRSA has been discharged from a room on a general medical ward?
Scenario 2 is an occasion where you want to be sure that residual contamination has been dealt with so that the incoming susceptible ICU patient will not acquire the virtually untreatable carbapenem-resistant A. baumannii. Therefore, HPV, which is associated with the elimination of pathogens from surfaces, is a rational choice. 
Scenario 2: What do you do when a patient who had an infection with carbapenem-resistant A. baumannii has been discharged from an ICU room?
Scenario 3 is more tricky. While the likelihood of C. difficile spore contamination argues for the higher efficacy of the hydrogen peroxide systems, the number of transfers or discharges of patients with C. difficile on a surgical unit may be high, which argues for the lesser efficacy but faster cycles from the UV systems. The majority of the audience selected HPV in this scenario, considering that the combined risk of the pathogen and specialty required the elimination of C. difficile spores from the room prior to the admission of the next patient. 
Scenario 3: What would you do when a patient who had C. difficile infection has been discharged from a room on a surgical unit?
To summarize, the use of an NTD system to augment terminal disinfection is warranted in some circumstances. The choice of NTD system will depend on a number of factors, including efficacy, distribution, ease of use, cycle time and cost. The features of the various NTD systems make them best suited to different applications, dictated by the clinical setting and the environmental-pathogenic characteristic of the target pathogen. So, is it time to turn to NTD systems? 52% of the audience voted ‘yes’ at the start of the webinar; 74% voted ‘yes’ at the end!
Figure 3: Is it time to turn to ‘no-touch’ automated room disinfection? The audience were asked this question at the start and the end of the webinar, indicating a swing towards the affirmative!
The effect of closing and cleaning wards on infection rates
Not so long ago, the UK Government ordered a national ‘deep clean’. This prompted a fair amount of debate among experts and the public. If the NHS needed a spring clean, then does that mean that it was dirty in the first place? Perhaps. There does not seem to have been a formal evaluation of impact, but there is some rationale for closing and cleaning wards. For example, this paper from the early 1970s evaluated the impact of closing and cleaning five wards in London.
The five wards (four surgical and one medical) had an outbreak of MRSA (termed ‘cloxacillin-resistant S. aureus’). Rates of infection (termed ‘sepsis’) were monitored on the study wards before and after closing and cleaning. Wards were closed to admissions and emptied of patients. All fabrics were sent for laundering and all left over supplies were discarded. Cleaning comprised washing floors, walls and all other surfaces with hot water containing detergent; bed frames and furniture were also washed. The length of time that all this cleaning too is not specified, but I suspect it took place over several days. Crucially, staff and patients were screened for carriage of epidemic strains of S. aureus; colonised patients were not re-admitted after ward cleaning where possible.
The charts below show the impact on all infections (Figure 1), all S. aureus infection (Figure 2) and MRSA infection (Figure 3). Infection rates were compared 3 months before vs. 3 months after cleaning on Wards 1-3 and 6 months before vs. 6 months after on Wards 4 and 5. As you can see, the impact was pretty dramatic.
Figure 1. Total infection rate (proportion of admissions infected) on the five wards before vs. after ward closing and cleaning.
Figure 2. S. aureus infection rate (proportion of admissions infected) on the five wards before vs. after ward closing and cleaning.
Figure 3. MRSA infection rate (proportion of admissions infected) on the five wards before vs. after ward closing and cleaning.
The poor reduction in total infection rate on Ward 1, a gynecological ward, (Figure 1) is largely due to high Gram-negative infection rates before and after cleaning, most likely explained by endogenous urinary tract infections. Reductions in total infection rate and S. aureus infection rate appeared to be less on Wards 4 and 5, which could be influenced by the fact that rates were compared for 6 months pre and post ward closing and cleaning rather than 3 months on Wards 1-3. The impact of a one off environmental intervention is likely to diminish over time. It’s also interesting to note that the MRSA infections identified on Ward 5, a general surgical ward, after cleaning were due to a different strain of MRSA (determined by phage typing and antibiogram) than before cleaning. This new strain matched the outbreak strain from Ward 2. Two of the patients on Ward 5 who became infected with this strain were operated on in the same theatre as the infected patients from Ward 2 within two weeks of one another. Four other patients (on different wards) also appeared to acquire the strain in the same operating theatre.
The study has several important limitations. It is not possible to be certain whether active screening and isolation or ward closing and cleaning were responsible for the reduction in infection rates; it was probably combined impact. The study design lacked the rigor of more modern investigations: infection rates were not expressed in terms of patient-days and infection rates were compared for different time periods making direct comparison of the impact across the five wards difficult. Also, no environmental sampling was conducted to demonstrate the efficacy of the cleaning procedure (both initially and in terms of recontamination).
Notwithstanding these limitations, the study provides evidence that ward closing and cleaning combined with active screening and selective readmission resulted in a dramatic reduction in the rate of nosocomial infection on five study wards. The impact appeared to be most pronounced in the first three months, which is consistent with a reduction in environmental contamination. Outbreaks of MRSA were eradicated by closing and cleaning on all five study wards. However, there was evidence of new nosocomial transmission following the re-admission of infected patients. Finally there was some interesting circumstantial evidence of transmission within operating theatres.
Article citation: Noone P, Griffiths RJ. The effect of sepsis rates of closing and cleaning hospital wards. J Clin Pathol 1971;24:721-725.
Reflections on Infection Prevention and Control 