There are pros and cons of increasing the proportion of single rooms. One of the commonly-cited pros is a reduction in HCAI. A recent UK study provides some evidence that C. difficlie infection, and MSSA / E. coli BSIs are not reduced by a move to a hospital with more single rooms, but that norovirus control is more effective when you have more single rooms.
I am heading home from an outstanding Infection Prevention 2017. There was a fair bit of discussion about hospital-associated pneumonia (HAP). HAP does not get the attention it deserves and there is more that we can and should be doing to prevent it. Although, we need to keep an eye out for unintended consequences in tackling HAP.
A very enjoyable few days in Edinburgh this week for the Federation of Infection Societies / Healthcare Infections Society (FIS/HIS) meeting. Some reflections follow…
How do you like your crap? Fresh or frozen?
Since Jon’s post on crapsules is one of the most favorite on the blog, I assumed that many of you might enjoy a sequel.
Clostridium difficile infections (CDI), most certainly after the emergence of hypervirulent strains at the beginning of this millennium, have become a major cause of morbidity and mortality in hospital and (to a lesser degree) community patients. One in four patients will suffer from recurrent CDI and treatment options are limited. Consequently, fecal microbiota transplantation (FMT) has become a valuable alternative, but is not readily available. Using frozen FMT would make the logistics far easier and finally something frozen seems to be as good as fresh, according to this JAMA study!
To be honest I’m a bit fed up with quoting the £4000 per CDI case that was calculated by Mark Wilcox and colleagues back in 19 0 plonk (1996 to be exact) and so I was quite excited to stumble across a new estimate from Merseyside whilst browsing ‘Value in Health‘, one of my usual reads. Well, possibly not.. although perhaps it should be – and it does support open access.
Nakamura and colleagues presented an abstract at the 18th International Society for Pharmacoeconomics and Outcomes Research (ISPOR) meeting and have calculated the mean extra cost of a patient with CDI to be £10,956.82, although as the authors point out, how much of this is attributable to the extra cost of CDI rather than the multiple co-morbidities that likely contributed to the infection leading to the antibiotic treatment, which led to the CDI continues to elude us. The authors are continuing to work on this and I await their final findings with interest, however for now I’ll settle for £11,000 per case as opposed to the 1996 figure of £4000 (data collected in 1995) and is probably more realistic than just allowing for inflation that has averaged at 2.8% pa, which would have made it £6868. As we know (well all of us apart from the Treasury), health inflation is way ahead of normal financial indicators.
It is well-established that fidaxomicin reduces the recurrence rate of C. difficile infection (CDI), but this study from my old research group at GSTT / KCL is the first to evaluate the impact of treatment with fidaxomicin on environmental contamination. The bottom line is that patients treated with fidaxomicin had less C. difficile contamination than patients treated with vancomycin / metronidazole.
In total, the rooms of 38 / 66 (57.6%) patients treated with metronidazole / vancomycin had one or more positive environmental cultures compared with 25 / 68 (36.8%) patients treated with fidaxomicin (P = 0.02). Similarly, when considering all of the sampled environmental sites (four per room), 68 / 264 (25.8%) were positive in patients treated with metronidazole / vancomycin compared with 47 / 272 (17.3%) in patients treated with fidaxomicin (P = 0.02) (see Figure below).
Figure: Environmental contamination with C. difficile in the rooms of patients treated with fidaxomicin vs. vancomycin / metronidazole.
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:
- Part I: Updates on C. difficile, norovirus and other HCAI pathogens
- Part II: Dealing with the contaminated environment
- Part III: Education, communication, and antibiotic resistance
- ‘What’s trending in the infection prevention and control literature?
HIS 2012 -> HIS 2014’
- ‘HIS Poster Round: Dealing with contaminated hands, surfaces, water and medical devices.’
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 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…