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.
The Journal of Infectious Diseases has just published a special issue on norovirus, which is well worth reading. When norovirus strikes, there is an inclination to close the ward to new admissions at the earliest available opportunity in order to protect incoming patients. But when should the ward closure trigger be pulled? Not at all, as recommended by latest UK guidelines (risking continuation of the outbreak, fed by a steady stream of new victims…I mean admissions), when you get a single case of vomiting or diarrhoea (lots of unnecessary ward closure) or only when you have a lab confirmed outbreak on your hands (by which time the horse has already bolted and galloped through your hospital). The special issue included a useful modelling study providing some idea of the impact of various approaches to ward closure in response to noro outbreaks.
It’s the most Chunderful time of the year (or maybe not). The Norovirus ‘season’ will still be on us and a few points are well worth reflecting on. A recent systematic review of Norovirus risk in high and middle-income countries asserts that there may be as many as 12.5 million infections annually these countries alone, with possibly as many as 2.2 million outpatient visits related to the illness. Personally I have always liked having a bit of norovirus around. Keeps the staff on their toes and gives a good indicator of how IPC is really being performed rather than another set of 99% compliant hand hygiene audits.
Caffy et al. identified man’s best friend, dogs (sorry for all those cat lovers), as a possible source of human norovirus. The UK-based-researcher showed that different genotypes of human norovirus-like particles can bind to canine gastrointestinal tissue, suggesting that infection is (theoretically) possible. In addition, some of the dogs mounted an immune response to human norovirus.
How much of a problem do we actually have? Time to let Bella & Buster go?
In my opinion this seems still to be unclear. Neither do we know whether dogs could shed human norovirus in quantities necessary to cause infections in humans, nor (and most importantly) did the researchers succeed to detected human norovirus in the canine feces samples. Thus, so far no reason to switch your best friend with a gold fish – which, by the way, might carry the risk of atypical mycobacteria!
A new paper in Clinical Infectious Diseases suggests that aerosols and the airborne/inhalation route could transmit Norovirus, demonstrating that Norovirus genomes could be detected in air samples inside and outside of rooms during outbreaks. The authors suggest that a healthcare worker could inhale up to 60 copies of virus during a 5-minute stay in a ‘symptomatic’ patient’s room. These particles, it is suggested, are available then to be swallowed.
So, given the fact that I still have some staff left in the hospital when Norovirus comes to call I’m thinking either this virus has a larger infectious dose than we think or the assumptions are not quite right. There was no linkage with the time lapse from the symptomatic ‘event’ apart from this was within 24 hr. of the sampling or with the type of event, or putting it bluntly, which end of the body the virus was ejected from the body from. Presumably the top end is a more effective disperser of viral particles than the lower end (depending on how sharply the sheets are pulled back..) and it would be interesting to see the effect of frequency of symptoms. Continue reading
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…
Earlier this year, I wrote about an outbreak of norovirus in a US car dealership. There, the outbreak was traced to a toddler “spraying” norovirus around a public restroom and baby-changing station. Regrettably, I now have my own experience to relate.
Last Wednesday (let’s call it outbreak day 1), our 18-month old toddler “sprayed” projective vomit around our porch. My wife cleaned up the mess (not with dry paper towels, as in the US car dealership outbreak but with detergent and water). On outbreak day 3, 36 hours later, my wife presented (grumpily) with acute gastroenteritis. We made every effort to limit domestic horizontal transmission (including regular bleach disinfection of contact surfaces in the bathroom and cohorting of personal effects) but to no avail; a little over 24 hours later on outbreak day 4, I endured acute gastroenteritis.
What do we learn from this?
- Transmission routes for viral gastroenteritis are very difficult to disentangle. It seems likely that my wife acquired norovirus whilst cleaning up the vomit, and I acquired norovirus from my wife somehow. Of course, this may not have been the case. My wife could have acquired the infective agent in a number of ways from our toddler. Also, I could have acquired it directly from our toddler and not my wife. Finally, a common source seems unlikely due to the ‘domino’ type progression, but cannot be discounted. If I can’t be sure of transmission routes amongst three people in a single household, how can we hope to understand transmission routes on a hospital ward or aboard a cruise ship
- We are not sure what caused the outbreak. None of us were in the mood to submit a specimen during the outbreak and, even if we had bothered to collect one, how would we have got it analysed? Take it to the GP (bad idea) or hospital lab (even worse) or post it (unhappy mail carrier). Thus, our understanding of the prevalence and aetiology of gastroenteritis in the community is woefully lacking.
- It’s been expensive. I was unable to travel to mainland Europe for an important meeting last week due to this outbreak, which has meant re-booking the trip at expensive short notice. Plus, I am still unable to go to work today (since I’m still within 48 hours of my symptoms). Whilst I am fortunate in that my work can be conducted from home, others are not so lucky. I suspect that the economic impact of viral gastroenteritis is hugely underestimated. In fact, I am not sure anybody has really tried to estimate it, let alone underestimate it, due to the lack of meaningful prevalence data.
- Horizontal transmission is difficult to block. We took every precaution that we could think of to prevent horizontal transmission, without success. Part of the problem was that we did not recognise the outbreak immediately. This principle translates to preventing horizontal transmission in hospitals: the pre-diagnosis management of patients with diarrhoea and vomiting is crucial.
- It’s very, very unpleasant. We are a young, (fairly) healthy family and each of us were laid out for 12 hours, and pretty useless for at least 24 hours. I can see how somebody who is already unwell and in hospital would be affected very badly indeed. I recommend that anybody who cares for patients in hospitals with acute gastroenteritis should be sure to try it themselves, in the interests of empathy.
Could we have done a better job of preventing the spread of this acute bout of gastroenteritis through the Otter household? Probably, through better outbreak identification and more stringent cohorting (perhaps with universal gowns and gloves, and liberal use of masks). But really, I’m just counting our blessings that we didn’t all get it at the same time.