Author: Jon Otter (@jonotter)

Filling the gaps in the guidelines to control resistant Gram-negative bacteria

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

I gave the third and final installment of a 3-part webinar series on multidrug-resistant Gram-negative rods for 3M recently. You can download my slides here, and access the recording here.

During the webinar, I provided an overview of the available guidelines to control CRE and other resistant Gram-negative bacteria. I then identified gaps in the guidelines, in terms of definitions of standard precautions, outbreak epidemiology and who should be on the guidelines writing dream team. Finally, I discussed some controversial areas in terms of effective interventions: patient isolation, staff cohorting and selective digestive decontamination.

One of the most important points when considering infection prevention and control guidelines is the issue of ‘standard precautions’. What do we apply to every patient, every time? As you can see from Figure 1 below, ‘standard precautions’ is far from standardized. This is problematic when developing and implementing prevention and control guidelines.

Figure 1: differences in the definition of ‘standard precautions’.

filling gaps std precautions

I had the opportunity to ask the webinar audience a few questions throughout the webinar, which are outlined in Figure 2.

Figure 2: response to the questions from the 120 or so participants.

filling the gaps1 filling the gaps2 filling the gaps3

I was somewhat concerned but not that surprised that more than a quarter of the audience did not know where to access control guidelines for MDR-GNR. I suppose this means that we need to do a better job of signposting the location of the various guidelines available. Here’s a non-exhaustive list for starters:

There was a fairly even split between active and passive surveillance to detect outbreaks. The problem with relying on passive surveillance (i.e. clinical cultures) is that there’s a good chance that the ‘horse will have bolted’, and you have a large outbreak on your hands, before a problem is detected. For this reason, I favour active surveillance.

But who to screen? In the case of CRE, I was pleased to see that virtually nobody said nobody. There was a pretty even split between everybody, high-risk individuals or all individuals in high-risk specialties. Accurately identifying individuals who meet screening triggers is operationally challenging, as outlined by the “backlash” to the UK toolkit, so I think screening all patients in high-risk specialties (e.g. ICU) makes most sense.

So, what works to control MDR-GNR transmission? We don’t really know, so are left with a “kitchen sink” (aka bundle approach) (more on this in my recent talk at HIS). We need higher quality studies providing some evidence as to what actually works to control MDR-GNR. Until then, we need to apply a healthy dose of pragmatism!

Journal Roundup November 2014: Journal Roundup: Ebola (again), The rise (and rise) and fall of MRDOs & Infection Prevention 2014

Jon Otter (@jonotter) Roundup , ,

This month’s Roundup, as ever freely available on the Journal of Hospital Infection website, showcases some of the useful data emerging from the field of the ongoing outbreak of Ebola in West Africa. For example, emerging data suggests that the R0 (basic reproductive number) of Ebola is around 2, meaning that two transmissions will occur from every case. This means that Ebola is not massively transmissible compared with other infectious diseases – but this hasn’t stopped it increasing more or less exponentially in parts of West Africa!

Some interesting studies on the increasing or decreasing prevalence of MDROs are also covered in the Roundup. For example, one study reported a worrying doubling of the rate of CDI in the USA, whereas another study reports impressive reductions in S. aureus bacteraemia in Australia.

The Roundup includes a brief overview of the Infection Prevention 2014 conference, covered in more detail in a previous post in this blog, and finally, features Catherine Makison-Booth’s brilliant Vomiting Larry (pictured below)!

vomiting_larry

As ever, I’d be delighted to receive your feedback as to how the Roundup should evolve.

The inanimate environment doesn’t contribute to pathogen transmission in the operating room…OR does it?

Jon Otter (@jonotter) Contamination , , , ,

OR

Nosocomial or hospital-acquired infections are a worldwide problem affecting millions of patients yearly and increasing morbidity and mortality. The role of the hospital inanimate environment (environmental surfaces and surfaces of medical equipment) in the transmission of certain nosocomial pathogens such as C. difficile, norovirus, MRSA, VRE and Acinetobacter is now well established supported by various studies and publications. Most, if not all of these studies, investigated the transmission process in patient rooms or ICUs. Although the role of air in the transmission of pathogens has been extensively studies in the operating room (OR) setting, do contaminated surfaces play a role in pathogen transmission in the OR?

A recent review article published in the journal “Surgical Infection” questioned whether the OR inanimate environment contributed to the transmission of pathogens, hence possibly causing infections including surgical site infections (SSIs). Few studies have investigated surface contamination in the OR and even fewer have investigated possible pathogen transmission from the environment in this setting. While the inanimate environment in the OR has been considered a potential source for pathogens that may cause SSIs for more than 100 years, the role of this environment in the patient acquisition process within this setting is still debatable. Before revealing the conclusions of the review paper, I would like to look at both sides of the argument.

THE OR INANIMATE ENVIRONMENT DOES NOT PLAY A ROLE IN PATHOGEN TRANSMISSION AND INFECTION

The patient population and length of stay

In a hospital, patients colonised or infected may spend days or even months in ward rooms or ICUs increasing the chance that these patients will contaminate their environment or acquire pathogens from that environment. The likelihood of environmental contamination or pathogen acquisition increases with the length of hospital stay as well as other factors such as gross contamination and soiling.

In the OR setting however most patients spend only few hours under full or partial anaesthesia. This makes it less likely that these patients will contaminate their environment or acquire pathogens from the environment (by self inoculation at least). In addition, although gross contamination via blood for example is common, other type of gross environmental contamination linked to transmission such as diarrhoea and vomiting are less likely to occur in an OR.

The OR environment (surfaces and air)

Unlike most patient rooms, OR air quality is well regulated to prevent contamination via the air. This not only reduces the risk of infection via airborne pathogens but also reduces the amount of pathogens settling on and contaminating environmental surfaces in ORs. In addition, the OR inanimate environment is routinely cleaned/disinfected. Most ORs are cleaned at the end of the working day and many surfaces and areas are cleaned before and between surgeries with strict policies on how to deal with gross contamination (e.g. blood and tissue).

Minimising infection risk

As most SSIs are thought to originate from patients’ or healthcare personnel’s own flora, many interventions are in place in ORs to minimise the risk of contamination and infection. These include policies for hand scrubbing and disinfection, gloving, masks, and the proper preparation of patients’ skin before incision. The instruments used in surgery are also routinely sterilised before surgery to minimise the risk of infection.

Organisms involved in SSIs

The hospital environment has been implicated in the transmission of a number of pathogens including norovirus, C. difficile, MRSA, VRE and Acinetobacter. These pathogens are able to contaminate the environment at a high load and survive for long period of time facilitating transmission and acquisition.  While infections with these organisms can be acquired in the OR, with the exception of Staphylococcus species, these pathogens are not the major causes of SSIs. The environmental resilience of other organisms involved in SSIs is not well characterised and it is unclear whether they can survive long enough in the environment to be transmitted.

THE OR INANIMATE ENVIRONMENT IS A SOURCE OF PATHOGENS THAT CAUSE INFECTION

The OR environment

ORs are busy, with many personnel involved during a surgical procedure, some of whom come and go in and out of the OR during the process. It is also an environment with multiple and frequent contact between personnel, patients and the environment including medical equipment. It is difficult if not impossible to observe the WHO’s 5 moments for hand hygiene in such an environment, or to clean and disinfect the environmental surfaces effectively during a surgical procedure. Organisms originating from the floor of the OR can also be disturbed by walking and are taken into the air which may increase the risk of infection.

The OR inanimate environment is contaminated

Many people in the general public think of ORs as ultra clean, even sterile, environments. For anyone working in ORs, it is clear that this view is far from the truth. Although modern ORs have strict measures to reduce contamination, the OR inanimate environment becomes contaminated with various organisms including those involved in SSIs. Studies have reported contamination of various OR areas such as anaesthesia equipment, beds, intravenous pumps and poles, computer keyboards, telephones and OR floors.  A variety of pathogens capable of causing infections have been identified including Gram-negative bacilli such as Acinetobacter and Pseudomonas species, Staphylococcus including (MRSA) and Enterococcus. These results may be in part due to the fact that suboptimal cleaning in ORs is a widespread issue in hospitals.

Pathogen transmission occurs in ORs

A number of studies in ORs focusing on the role of anaesthesia equipment and providers in the contamination and transmission of pathogens in ORs have concluded that the hands of anaesthesia providers, patient IV tubing and the immediate patient environment were contaminated immediately before or during patient care with a wide range of bacterial pathogens leading to transmission. Transmission of pathogens from and to the hands of the anaesthesia providers involving the inanimate environment occurs frequently given the frequent contact with the environment in ORs.

Human behaviour in ORs contributes to environmental contamination and transmission

We are all familiar with the view that surgeons tend to be the worst healthcare workers as far as hand hygiene compliance is concerned. However, this is only the tip of the iceberg regarding lapses in infection prevention in ORs. For instance, anaesthesia provider’s behaviour and attitude including confusion on when and how often to perform hand hygiene during a procedure is a common cause of pathogen transmission. In one study, anaesthesia providers touched 1,132 objects during 8 hours of observations in OR, but only performed a total of 13 hand disinfections. No hand disinfections were witnessed at any time during 3 (43%) of the procedures observed. Furthermore, hand hygiene failed to precede or follow procedures, blood exposure or contact with the floor. Alarmingly, it has been reported that objects that fall onto the OR floors during surgery were frequently placed back either on to horizontal work surfaces or even on to the patients themselves during operations.

THE CONCLUSION

It is clear that the inanimate environment of the OR, including medical equipment, can become contaminated with pathogens that cause infections including SSIs. These pathogens can then be transmitted to the hands of healthcare workers and have the potential to cause infection. Further studies are necessary to quantify the role of contaminated surfaces in the transmission of pathogens and to inform the most effective environmental interventions in the ORs. Given the serious consequences of SSIs, special attention should be given to the proper cleaning and disinfection of the inanimate environment in ORs in addition to the other established measures to reduce the burden of SSIs. These include addressing the human behaviour that contributes to environmental contamination and transport of surface pathogens into the vulnerable sites of patients during surgery. Such measures include reducing human traffic in ORs, stricter adherence to the standard operating protocols during procedures, and compliance with proper hand hygiene and gloving. Specific hand hygiene guidelines tailored to OR personnel may be needed given the large number of hand contact events per hour in these settings.

Image: NIH Library.

Being bitten by antibiotic resistant CRAB hurts! (Acinetobacter that is.)

Jon Otter (@jonotter) Acinetobacter , , ,

Acinetobacter pink

Guest bloggers Dr. Rossana Rosa and Dr. Silvia Munoz-Price (bios below) write…

In everyday practice of those of us who work in intensive care units, a scenario frequently arises: a patient has a surveillance culture growing carbapenem-resistant Acinetobacter baumannii (CRAB). While the ultimate course of action we take will be dictated by the patient’s clinical status, that surveillance culture, in the appropriate context, can provide us with valuable information.

For this study1, we looked at a cohort of patients admitted to a trauma intensive care unit, and sought to identify the risk factors for CRAB infections. We found that patients who had surveillance cultures positive for CRAB had a hazard ratio of 16.3 for the development of clinical infections with this organism, compared to patient’s who remained negative on surveillance, even after adjusting for co-morbidities and antibiotic exposures. Since our results were obtained as part of a well-structured surveillance program, we know that colonization preceded infection.  Unfortunately for some of our patients, the time from detection of colonization to development of clinical infections was a matter of days. With therapeutic options for the effective treatment of infections with CRAB limited to tigecycline and polymixins, the consequences of delaying therapy are often fatal. As described by Lee et al, a delay of 48 hour in the administration of adequate therapy for CRAB bacteremia can result in a 50% difference in mortality rate2.

Surveillance cultures are not perfect, and may not detect all colonized patients, but they can be valuable tools in the implementation of infection control strategies3, and as we found in our study, can also potentially serve to guide clinical decision that impact patient care and even survival.

Bio:

TICU_photo1_031914

Dr. Silvia Munoz-Price (centre left) is an Associate Professor of Clinical Medicine at the Institute for Health and Society, Medical College of Wisconsin, currently serving as the Enterprise Epidemiologist for Froedert & the Medical College of Wisconsin. Dr. Rossana Rosa (centre right) is currently an Infectious Diseases fellow at Jackson Memorial Hospital-University of Miami Miller School of Medicine. She hopes to continue developing her career in Hospital Epidemiology and Infection Control.

References

  1. Latibeaudiere R, Rosa R, Laowansiri P, Arheart K, Namias N, Munoz-Price LS. Surveillance cultures growing Carbapenem-Resistant Acinetobacter baumannii Predict the Development of Clinical Infections: a Cohort Study. Clin Infect Dis. Oct 28 2014.
  2. Lee HY, Chen CL, Wu SR, Huang CW, Chiu CH. Risk factors and outcome analysis of Acinetobacter baumannii complex bacteremia in critical patients. Crit Care Med. May 2014;42(5):1081-1088.
  3. Munoz-Price LS, Quinn JP. Deconstructing the infection control bundles for the containment of carbapenem-resistant Enterobacteriaceae. Curr Opin Infect Dis. Aug 2013;26(4):378-387.

Image: Acinetobacter.

Reflections from HIS 2014, Part III: Education, communication, and antibiotic resistance

Jon Otter (@jonotter) Conferences , , ,

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Welcome to the third and final installment of my reflections from HIS 2014. You can access the ‘box set’ via the list at the start of Part I.

Prof Alison Holmes – Impact of organisations on healthcare-associated infection

Self-professed pragmatist Prof Holmes reminded us that the perceived and actual priorities of society, politicians and healthcare systems mean that it’s not all about infection control. We must harness macro (inter-hospital) and meso (inter-departmental) and micro (inter-team) relationships to successfully control transmission. This requires shared beliefs, reinforcement systems, role models, and the right staff skills. Plus, we need to get HCAI on the metric dashboard of CEOs. Indeed, HCAI outcomes are a sensitive surrogate marker of organisation performance, so this should be attractive to the hospital CEO once understood. We also need to embrace the public to tackle antibiotic resistance. Government messages about reducing antibiotic resistance have helped our day job (and proved popular on Twitter)! Involving patients and the public in our research makes everybody happy; patients and the public like it, and it improves our research (and helps to win grants). We need to embrace ‘mHealth’ in all its forms – games, apps and more – remembering that dinosaurs became extinct. The bottom line? Organisational, structural and managerial issues are crucial for the prevention of healthcare-associated infection (and the Lancet ID agrees).

Prof Herman Goossens – European Antibiotic Awareness Day

eaad 2014

Since it was the occasion of European Antibiotic Awareness Day (EAAD) 2014, the talk from the impressive Prof Goossens was well timed! EAAD is a campaign aimed at the public and professionals to highlight the issues around antibiotic use and resistance. Many of the campaign materials are useful, including a toolkit for self-medication without antibiotics and various infographics. Prof Goossens spent some time discussing how to measure the impact of EAAD. A lot of questionnaire type surveys have been performed, and it does seem that EAAD has prompted a swing towards a better understanding of antibiotics, so well done to all involved.

What’s hot and what’s not in infection prevention and control?

Dr Jenny Child (JHI Editor) presented a view of the literature through the eyes of a journal editor! Bad research can do much damage:  look no further than the MMR & autism debacle. Worth remembering that indifferent, uncitable papers will not get published; it’s just not in the journal’s interest. Also, clever, ‘pseudo-scientific’ language is a barrier to good science. The bigger the journal, the plainer the language. Finally, whilst JHI has traditionally been a quantitative medicine journal (with p values and 95% confidence intervals!), like it or not, social science is coming!

I gave a talk on ‘What’s trending in the infection prevention and control literature’. You can access the slides and recording on a separate blog, here. Finally, Dr Jim Gray (JHI Deputy Editor) scanned the horizon of the infection control literature, seeing studies with specific interventions and real clinical outcomes (not proxy measures), SSIs, antibiotic resistance (especially CRE), obesity, design & technology, diagnostics and decontamination!

Antibiotic stewardship: persuasion or restriction?

Esmita Charani began by explaining the need to achieve behaviour change, not education in isolation, in order to effectively moderate antibiotic prescribing behaviour. The local prescribing culture is likely to influence prescribing policy more than the national guidelines. Junior doctors often don’t have a clue what to prescribe, so it’s a case of follow-my-leader (i.e. consultant). But targeting hospital consults alone won’t get us out of the mess of antibiotic resistance. We need to engage a wider audience, including the public.

Meanwhile, Prof Inge Gyssens outlined the impact of antimicrobial restriction: contribute to MRSA reductions, prevent the emergence of MDR-GNR, and may help to bring outbreaks under control. The only downside is that switching to another antibiotic may cause more problems than it solves – a ‘squeezing of the balloon’ type effect. In a way, doctors are “addicted” to antibiotics. Put simply, antibiotic stewardship through restriction is a ‘cold turkey’ approach that works.

Although not a formal debate, Esmita Charani and Prof Gyssens did a good job of presenting both viewpoints. I was left concluding that both persuasion and restriction are important but when it comes down to it, restriction is more important than persuasion. Left to their own devices, antibiotic prescribers will sometimes make poor choices; restriction takes away that choice!

Summary

I really enjoyed HIS 2014 – especially the opportunity to contribute to the conference via my talk (on trends in the IPC literature) and poster round. The conclusion of my talk was to look into my crystal ball and highlight what will be trending by the time HIS 2016 comes around:

  • I’m pretty certain that Ebola and MERS will not be trending (at least I hope not). However, the scars of Ebola in West Africa will take a generation to heal. There’s a chance that we could be experiencing the next Influenza pandemic, but it’s more likely we’ll be talking pandemic preparedness.
  • Whilst I personally favour targeted interventions, I fear there will be a general move towards universal interventions. I also fear that the confusing ‘vertical’ (aka targeted) vs. ‘horizontal’ (aka universal) terminology will be widely adopted, despite the fact that it’s confusing!
  • Faecal microbiota transplantation is only going to get bigger. It will be the standard of care for recurrent CDI by the time the next HIS conference comes around – perhaps even via oral ‘crapsules’.
  • Whole genome sequencing will not be as trendy as it is right now – it will just be a standard tool that we all use.
  • The trend of CRE (and other multidrug-resistant Gram-negatives) is only going to go one way – upwards!
  • I’m hoping to see some high-quality studies (ideally cluster RCTs) of environmental interventions with clinical outcomes.
  • Finally, as we all deal with increasing cost constraints, studies evaluating the cost-effeteness of infection prevention and control interventions are going to become increasingly important.

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

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

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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.

Reflections from HIS 2014, Part I: Updates on C. difficile, norovirus and other HCAI pathogens

Jon Otter (@jonotter) C. difficile, Conferences, Norovirus , , , ,

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The 2014 Healthcare Infection Society (HIS) Conference was in Lyon, France, and combined with SFH2 (The French Society for Hospital Hygiene). Congratulations to all involved (especially Martin Kiernan and Prof Hilary Humphreys) for such a stimulating programme, and enjoyable conference. The abstracts from the oral presentations can be downloaded here, and the posters here. I plan to share some of my reflections on key conference themes over the next few days:

Prof Wing-Hong Seto – Airborne transmission and precautions – facts and myths

Prof Seto’s energy and enthusiasm lit up the stage, just like a few years ago in Geneva for ICPIC. Prof Seto spent his lecture convincingly debunking the idea that airborne transmission of respiratory viruses is common, notwithstanding some data that, prima facie, suggests this. Only very few pathogens require obligate airborne transmission (e.g. TB); some have preferential airborne transmission (e.g. measles); and some have potential airborne transmission (respiratory viruses). There is some evidence that respiratory viruses such as influenza can be transmitted via the airborne route, but the most important route of transmission will depend on context. One important point is that studies demonstrating airborne “transmission” using PCR rather than viral culture as an endpoint, or using artificial aerosol generation should not be taken as definitive evidence of airborne transmission. Prof Seto’s view is that medical masks are sufficient to prevent the transmission of respiratory viruses, as demonstrated by his own work during SARS. Finally, we can forget the requirement for negative pressure isolation rooms: open doors and windows yields a whopping 45 air changes per hour!

Prof Mark Wilcox – Is Clostridium difficile infection (CDI) underestimated due to inappropriate testing algorithms?

Prof Wilcox began by reporting an unusual epidemic: “PCRitis”, which can cloud rather than clarify accurate diagnosis of CDI. Perhaps the most important point made by Prof Wilcox is that the ultimate “gold standard” for CDI should be clinical, and not laboratory based. Prof Wilcox spent most of his time reflecting on the recent multicentre European study of CDI underdiagnosis in Europe. There are some real shockers in here: the reported rate of CDI in Romania was 4 cases per 1000 patient days vs. closer to 100 per 1000 patient days when samples from the same patients were tested in the reference lab. This is no surprise in a sense because only 2/5 local laboratories were using optimal methods. However, even in the UK where around 80% of local labs are using optimal methods, around 2-fold more cases were identified in the reference vs. the local laboratory. Clearly, if we’re going to have a hope of controlling the spread of C. difficile in Europe, laboratory diagnosis needs to improve.

Norovirus

norovirus

Norovirus is especially topical in the UK given the recent PHE announcement about unusually high rates of norovirus in the NHS. The prolific Dr Ben Lopman (CDC) began by explaining the ‘image problem’ that norovirus has in US hospitals, where it is considered an uncommon cause of gastroenteritis. In fact, a systematic review found that norovirus cases around 20% of acute gastroenteritis. However, I would say it’s just not possible to get an accurate assessment of how common norovirus is on a population level due to chronic under-reporting. When we had an outbreak of ”norovirus” in the Otter household, the last thing we felt like doing was submitting a specimen, and I suspect we are not alone in this! Although norovirus is usually mild and self-limiting, it is by no means benign: one Lopman study suggested that it is responsible for 20% of deaths due to gastroenteritis not caused by C. difficile in those ages >65. And then there’s the infection control challenges. Due to the exquisitely low infectious dose, 2g of stool from an infected individual is enough to infect the entire human population! Plus, it is shed in high titre, stable in the environment, and resistant to many disinfectants. Rather depressingly, it seems that effective interventions to control norovirus teeter around the cost-effectiveness threshold. More optimistically though, prospects for vaccines look promising.

Prof Marion Koopmans then described the huge diversity within the “norovirus” family, spanning more phylogenic space than many single species occupy. For chapter and verse on nomenclature, see Norovirus Net. It’s difficult to know what works to control norovirus due to dynamic outbreak settings combined with multiple interventions. One key aspect for control is understanding shedding profiles of infected, recovered and asymptomatic individuals. Whilst all can shed norovirus, much like Ebola, those who are symptomatic are by far the highest risk for transmission. Finally, our inability to culture norovirus in the lab has been an important barrier to understanding the virus; a recent study (in Science no less) suggests that a working lab model for culturing norovirus may be just around the corner.

Dr Lennie Derde – Rapid diagnostics to control spread of MDR bacteria at ICU

Given the turnaround times of conventional culture (24 hours to preliminary results – at best), rapid PCR-based diagnostics make sense in principle. But do they work in practice? There is some evidence that rapid diagnostics may work to reduce MRSA transmission, although other studies suggest that they don’t make a difference. In order to put rapid diagnostics to the test Dr Derde et al. ran the impressive MOSAR study. This study suggest that screening and isolation by conventional or rapid methods does not help to prevent the transmission of MDROs in the ICU, but I don’t think we should take that away from this study, not least due to the fact that many units were already doing screening and isolation during the baseline period!

New insights from whole geneome sequencing (WGS)

WGS is trendy and trending in the infection prevention and control sphere. Prof Derrick Crook gave an engaging overview of the impact that WGS has made. It’s analogous to the manual compilation and drawing of maps to GPS; you wouldn’t dream of drawing a map by hand now that GPS is available! Desktop 15 minute WGS technology will be a reality in a few years, and it will turn our little world upside down. The major limiting step, however, is that mathematics, computer science and computational biology are foreign to most of us. And we are foreign to most of them! But, these issues are worth solving because the WGS carrot is huge, offering to add new insight into our understanding of the epidemiology of pathogens associated with HCAI. For example, Prof Crook WGS study on C. difficile suggests that transmission from symptomatic cases is much less common than you’d expect. So if the C. difficile is not coming from symptomatic cases, where is it coming from? Contact with animals and neonates in the community are plausible sources However, I was surprised that Prof Crook didn’t mention the large burden of asymptomatic carriage of toxigenic C. difficile, which must be a substantial source for cross-transmission in hospitals.

WGS has yielded similar insight into the epidemiology of TB and MRSA, outlined by Drs Timothy Walker and Ewan Harrison, respectively. One challenging idea from Dr Harrison is how much of the “diversity cloud” that exists within an individual is transferred during a transmission event? Finally, WGS can turn a ‘plate of spaghetti’ of epidemiological links to a clear transmission map, as was the case during a CRE outbreak at NIH in the USA.

Look out for some more reflections from HIS posted over the next few days…

What’s trending in the infection prevention and control literature? HIS 2012 -> HIS 2014

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

I was privileged to speak at the Healthcare Infection Society meeting in France today on ‘What’s trending in the infection prevention and control literature? HIS 2012 -> HIS 2014’. You can download my slides here, and view the recording below:

I have always enjoyed attending these light-hearted summary sessions at other conferences, so I hope I struck the right tone. In order to track some of the trends in the infection prevention and control literature since the last HIS conference (in late 2012), I plugged some search terms into Google trends (Figure).

Figure: Google Trends for all search terms (excluding viruses) (2004 to present). Logos and arrows represent the time of the HIS 2012 and HIS 2014 conferences. Search terms: hospital cleaning; carbapenem resistant Enterobacteriaceae, whole genome sequencing, fecal microbiota transplantation. [Note, I had to spell it ‘wrong’ (fecal v faecal) to detect a trend. Blasted Americans.]what's trending google trends

Based on my search terms, there was one infection control trend that trumped all others: Ebola. If I include in with the other Google search terms, it eclipses all others! Whilst trends in Google searches may not necessarily correlate with trends in the infection prevention and control literature, in this case, it is true that the outbreak of Ebola in West Africa has prompted a lot of publications in the literature – and consumed an awful lot of professional time for all who are connected with hospital infection prevention and control! Aside from Ebola, other trends in the infection prevention and control literature that I covered include MERS-CoV, universal vs. targeted interventions, faecal microbiota transplantation, whole genome sequencing, carbapenem-resistant Enterobacteriaceae (CRE), and some aspects of environmental science. Finally, I looked into my crystal ball and predict some of the trends in the infection prevention and control literature by the time HIS 2016 comes around.

HIS Poster Round: Dealing with contaminated hands, surfaces, water and medical devices

Jon Otter (@jonotter) Conferences , , ,

poster round

I was delighted to be asked to lead a poster round at the Healthcare Infection Society (HIS) conference. I was a bit disappointed to see that the poster sessions are tacked on to the end of the day (when everybody’s had enough and really just wants to retreat to their hotel room for an hour before the evening’s activities). My view is that posters are the lifeblood of conferences (and I am not alone in this view); they should have much more prominence, with a “ringfenced” session integrated into the main program.

Anyway, whinge over, I thought I’d share which posters I chose, why I chose them, and what I want to know about them.

You can access the abstracts here.

GENERAL CATEGORY

#3200 Longhurst et al. Hand drying methods in NHS England Trusts, September 2013.

I chose this poster because it’s becoming increasingly clear that the choice of hand drying method can influence the degree of bacterial contamination. Also, whilst I accept the economic and environmental benefits of jet and warm air dryers, they always seem to leave my hands a bit damp. (Perhaps I just have sweaty palms.) Anyway, this is what I want to know about this poster:

  • Why did you feel the need to ‘enforce’ a response by using the Freedom of Information act?
  • Why do you think jet / warm air dryers were rare in clinical areas?
  • Do you think that jet and to a lesser extent warm air dryers result in dangerous dispersal of microbes?

#3349 Tang et al. A 3 year hand hygiene program to increase compliance rate for heatlhcare providers in the A&E Department of Tuen Mun Hospital in Hong Kong.

There’s not a lot of data on hand hygiene compliance in A&E. A 2005 study examined compliance with hand-washing in the TV show ER, reporting a hand hygiene compliance rate of 0.2%. Yep, that’s ZERO POINT TWO PERCENT! Although reality is marginally better (according to this review), there’s work to be done, so I chose this poster mainly because of the impressive impact in improving hand hygiene compliance. My questions are:

  • Which of the barriers to hand hygiene that you mention do you think is most important?
  • Who was on your task-force to decide what to do?
  • How many people completed the questionnaires?
  • How many observations were done in each time period?
  • How do you measure that the awareness of hand hygiene increased?

#3174 Khanafer et al. Hospital management of Clostridium difficile infection: a literature synthesis

This is a novel review of the literature: using the ORION checklist to capture variables that help us to determine what works to control CDI from outbreak reports and intervention studies. Here’s what I want to know:

  • Can we really derive anything useful about which intervention works when you have more than one variable, even if studies are reported in a structured way? (High school science is pretty clear: change one variable at a time!)
  • How can these % reductions be so high when (apparently) only 30% of CDI is hospital-acquired (according to some people’s interpretation of the Oxford WGS difficile study)?
  • Which is the single most important intervention to prevent CDI transmission?

ENVIRONMENT CATEGORY

#3285 Cunningham et al. VRE Outbreak Control – the Need for Speed (Use of Molecular Technology)

Two of my favourite subjects: VRE and rapid diagnostics! Here are my questions:

  • Why bother trying to control VRE? Some pretty persuasive voices are arging that it’s not worth it!
  • Are you sure that rapid diagnostics made the difference? You also introduced enhanced cleaning / disinfection, extra screening, pre-emptive isolation, and extra staff and equipment.
  • How do you explain the four clusters?
  • Did you culture in parallel? If so, what was the sensitivity and specifity of the PCR test?

#3312 Whiteley et al. The problem of rapid ATP systems may be scaling using Relative Light Units (RLU)

This poster wins the prize for the most detailed poster in conference history; I think they’ve squeezed enough words in for a full length article. But the findings are important. All ATP bioluminescence systems are not equal: a way to standardize RELATIVE light unit (RLU) output would be extremely useful.

  • What is ‘coeffecient of variance (CoV)’, and what does it mean?
  • Does lower CoV = a better ATP bioluminescence system?
  • Clearly, hand held luminometers will not match HPLC in terms of accuracy, but what should our ‘CoV’ tolerance be?
  • Do you have a way to distinguish variaibilty of sampling (i.e. pickup of ATP on the swab) from variability in ATP detection by the device?
  • Would ATP correlate better with microbial concentration if device variability were removed (e.g. through HPLC analysis)?

#3393 Maynard et al. The use of Pseudalert® for the routine analysis of water samples by engineers

I like technology and I like innovation, so this is right up my steet. Here’s my questions:

  • How does the limit of detection for Pseudalert (1 cfu / 100 mL) compare with conventional culture, in theory?
  • How much training is required to use it?
  • Why 100 mL for Pseudalert, and 500 mL for culture?
  • Is culture the gold standard method? If so, the specificity of Pseudalert in Hospital 1 is terrible!

DEVICE-RELATED INFECTION CATEGORY

#3197 Farrugia et al. Reducing methicillin resistant Staphylococcus aureus (MRSA) bacteraemia in haemodialysis patients within a high incidence setting

I chose this poster purely for the dramatic reduction in MRSA bacteraemia in a specialist setting. I would like to know:

  • Is the high initial rate explained by haemodyalisis cathethers being left in for too long?
  • ‘Prevalence of CA-MRSA 8.8%’? What does this mean? 8.8% of healthy individuals carrying CA-MRSA, or 8.8% of hospital MRSA is community-associated clones?
  • Lots of interventions – do you have a feel for which was most important?

#3277 Stenger et al. A hydrogel interpenetrating polymer network in vascular catheters loaded with thioridazine and dicloxacillin facilitates slow surface release and inhibits staphylococcal biofilm formation in vitro and in vivo

I am interested in approaches that replace the traditional use of antibiotics with biocides (which have a much lower risk of promoting bacterial resistance). Whilst this catheter was dosed with an antibiotic, I think the technology could theoretically be dosed with any biocide. Also, I’m fascinated by the application of an anti-psychotic drug in infection control:

  • Please explain the principle of ‘interpenetrating polymer network’ (IPN).
  • Could this same technology be used to dose the catheters with any drug or biocide?
  • Can you modify the rate of release?
  • Who on earth decided to see whether an anti-psychotic drug (thioridazine) has antibacterial properties?

If anybody has any answers to my questions, please fire away!

Image: Andrea Wiggins.

Carbapenem-resistant Enterobacteriaceae (CRE): so what should an infection prevention and control team do now?

Jon Otter (@jonotter) CRE , ,

kleb pneumoGuest blogger Dr Evonne Curran (bio below) writes…

Jon asked me to write on his blog about our column (‘#15: Carbapenemase-producing Enterobacteriaceae’). As he kindly accepted my offer to co-write a column, I accept his to write this blog. I am calling this blog (which contains only my personal views): ‘Carbapenem-resistant Enterobacteriaceae (CRE): so what should an infection prevention and control team do now?’.

The problems with CRE are numerous, and the different actions needed to control or at least delay its endemnicity are likewise legion; the task can seem insurmountable. The approach being taken at national and international level covers much of what is needed. The question for individual infection prevention and control teams (IPCTs) is this: where do you begin to protect a healthcare system that has little capacity (and in some cases little will) to start to solve a problem that essentially has yet to arrive, that has at least 6 names (none of which can be spelt with confidence) and is absent from the CEO’s performance monitoring agenda? The additional challenge for IPCTs is this: it will be difficult for those working in clinical areas to believe that for all the improvement in infection prevention and control that reduced MRSA and C. difficile, still more is required for this new microbiological-kid on the block.

If I were still part of a hospital based IPCT this is where I would start…..

  1. Give it a name and stick to it in all correspondence / education / awareness sessions;
  2. Succinctly provide the reasons as to why this should be on everyone’s radar;
  3. Take a high-reliability approach to strengthening your healthcare system;
  4. Involve patient advocates.

1)      Give it a name and stick to it…

As mentioned in the column (and many times by Jon) there needs to be a name that we can a) all agree on and b) conveys to non-microbiology people the problem and its seriousness. We have to stop fighting about what it is: CPE, CRO, CPE etc, etc.  I don’t know who is on (or how you get on) the micro-organism naming committee, but I am beginning to think they need to make it more democratic and involve people who don’t understand microbiology. There is no perfect name that will keep all microbiologists happy, so let’s stop trying to find one. It’s important that IPCTs have a short name that denotes this big problem and makes this consistent in all documentation. (See this previous blog by Jon for more info on nomenclature surrounding this issue.)

2)      Succinctly provide the reasons as to why this should be on everyone’s radar

I offer the following as a succinct summary for why this should be on everyone’s radar:

  • These resistant organisms inactivate commonly used antibiotics. For any infected patient there are Few Treatment Options and there will eventually be No Treatment Options.
  • They are spread Person to Person by touch, splash or contaminated equipment / environments.
  • The resistance mechanisms are spread between different species of bacteria.
  • They are difficult to detect when people are screened.
  • They cause outbreaks, which are also difficult to detect and very costly to manage.
  • Spread across the world makes at least some transmission here inevitable.

3)      Take a ‘high-reliability’ approach to the problem in your area…

I am not going to regurgitate what is in existing guidelines but offer some high-reliability characteristics.

Sensitivity to operations: Given your patient/client population, consider how and why your healthcare system is vulnerable; share this information within your organisation.

Deference to expertise: Identify who you would go to for expert advice within and outwith your organisation should an incident arise. Keep contact details accessible.

Preoccupation with failure: Consider in which clinical areas you most likely to have an outbreak – visit these clinical areas and see if there can be changes to ways of working that would make outbreaks less likely.

Reluctance to simplify: Look for and don’t dismiss alert signals – this could be data that suggests you may have cases, cross-transmission, that you are insufficiently looking for possible cases or that your antibiotic prescribing data could make your healthcare system more vulnerable.

Commitment to resilience: Good as you and your team are – consider how you can make your systems better at preparedness, prevention and management of outbreaks.

High-reliability theory provides a framework to achieve mindfulness. Google ‘High-Reliability Theory’ and ‘Weick’ for some very useful information.

4)      Involve patient advocates

Patient advocates only really knew about MRSA and Clostridium difficile infection when the media told them. Letting patient advocates know that your team is alert to this emerging threat and that you are taking actions to prevent outbreaks may help. They can also lobby for leaders to take further action if required.

Here ends my first blog! Happy I think to receive comment, suggestions or improvements. Thanks for reading. Of note: Outbreak column 17 is on Cognitive Errors in Outbreak Prevention, Preparedness and Management.

Dr Evonne Curran bio:

curran cropped

Evonne is a practicing infection control nurse (since 1987) and a Doctor of Nursing (since 2010). She is the editor of the Outbreak column in the Journal of Infection Prevention (since 2011).