A very enjoyable few days in Edinburgh this week for the Federation of Infection Societies / Healthcare Infections Society (FIS/HIS) meeting. Some reflections follow…
outbreak
Norovirus – The organisation’s IPC ‘Canary’
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.
Mycobacterium chimaera & Open-Chest Heart Surgery
Outbreak of Mycobacterium chimaera Infection After Open-Chest Heart Surgery
Reported by Andreas Widmer in Basel and now published by Hugo Sax and colleagues (CID April 15th, 2015), the amazing story of open-cheat heart surgery, Mycobacterium chimaera infections (years after the operation!), and contaminated heater-coolers in your operating room.
While the Swiss were first, we know by now that this problem is unfortunately not limited to the Alp region, but furthermore present e.g. in the Netherlands. If your hospital has a program for open-chest heart surgery, now is the time to check your heater-coolers, to avoid further airborne transmission of M. chimaera from contaminated heater-cooler units.
Journal Roundup August 2014: seeking your input
The August edition of the Journal of Hosptial Infection Journal Roundup is now available, featuring:
- A whopping five-fold increase in the detection of CRE in 25 US community hospitals.
- MALDI-TOF as a new frontier for rapid detection of carbapenemase activity.
- More on fist bumping instead of hand shaking. (Would you like a fist bump greeting from your doctor? No thanks!)
- Triclosan-impregnated stitches would be cost-effective if they were only a little bit effective, but turns out they’re not effective at all.
- The new ‘crAssphage bacteriophage’, C. difficile biofilms, and increasing rates of antibiotic resistance – all in the human gut microbiome.
- Some hope for Ebola drug and vaccine targets.
- How to reduce the number of sickies that children take from school (through effective school-based immunization programmes).
- Thoughtful analysis on S. aureus outbreaks of old with lessons for now.
- Reviews of CRE mortality, global antibiotic use, microbial hitchhikers, overdiagnosis & overtreatment, useless reporting of science in the mainstream media, and whether biocide use drives biocide resistance.
I’ve written three editions of the Journal of Hosptial Infection Roundup now (June, July and August), so there’s a few examples to review. You can read about my methods for producing the Roundup in the blog accompanying the June edition. I thought that now would be a good time to get some feedback, specifically:
- Is the title right? A few people have expected it to be an overview of articles in the Journal of Hospital Infection only.
- Is the length about right? (Do you fall asleep reading it or find yourself begging for more?)
- Is the depth right? Or would you like to read more about less articles, or less about more articles?
Any feedback that you have would be most appreciated. Please either submit a comment below or email me.
Photo credit: ‘Fist bump’.
What can outbreaks of Salmonella from the 1950s tell us about CRE?
I recently came across a fascinating review article published in 1963 mainly about outbreaks of Salmonellosis during the 1950s. The review focuses on epidemics that were traced to contaminated surfaces, including ingested, contact and inhaled transmission routes. A number of interesting epidemics stand out:
- An outbreak linked to contaminated neonatal respirators.
- An outbreak linked to a contaminated chopping board (see Figure). In this outbreak, one of the investigators apparently contracted Salmonellosis after touching the chopping board during sampling and then having a cigarette before washing his hands.
- An outbreak (of microbial endotoxin syndrome) linked to a contaminated mouthpiece of SCUBA equipment. Here, the outbreak occurred in naval diving academy and the pattern of lessons and cases was so regular, that the epidemiologist could predict precisely when to visit to see the next case.
Figure: A chopping board at risk of persistent microbial contamination due to surface damage.
Although most outbreaks covered in the review relate to ancient catering-related outbreaks of Salmonella, there may be some useful learning for hospital epidemiology today, specifically CRE. It’s rare although not unheard of to find Salmonella carrying a carbapeneamase (i.e. Salmonella CRE). However, Salmonella is a member of the Enterobacteriaceae, so the involvement of contaminated surfaces during outbreaks of Salmonella suggests that contaminated surfaces may also be important during outbreaks of CRE.
It’s interesting that even back in the 1960s contaminated surfaces were recognized as potentially important in epidemics, whereas by the 1980s, the role of contaminated surfaces in endemic transmission was considered negligible. It’s difficult to know whether experts of the 1960s (perhaps there are some reading this?) would have considered contaminated surfaces important in both epidemic and endemic transmission? I suspect so, and we just lost sight of that in the 1980s and 90s.
Article citation: Sanborn WR. The relation of surface contamination to the transmission of disease. Am J Public Health Nations Health 1963;53:1278-1283.
Image: Ben Hosking.
A domestic outbreak of gastroenteritis
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.
CRE outbreak control: a view from the trenches
Drs Tara Palmore and David Henderson have written an engaging ‘view from the trenches’ in CID reflecting on their efforts to control an ongoing outbreak of CRE at the NIH Clinical Center, beginning in 2011.
The review outlines their interventions, including:
- aggressive active surveillance (including regular house-wide surveys);
- rapid identification and characterization of resistant organisms and resistance mechanisms (a mixture of conventional culture-based microbiology, mass-spec and mass spec);
- whole-genome sequencing of outbreak isolates (which allowed the identified of counterintuitive transmission patterns);
- enhanced contact precautions for all infected or colonized patients (patients only to leave room for medical reasons, visitors to wear gloves and gowns, staff not to touch personal electronic devices, preferable use of single-use equipment and enhanced terminal disinfection);
- geographic and personnel cohorting;
- daily chlorhexidine gluconate baths;
- dedicating equipment for cohorted patients and aggressive decontamination of equipment that had to be reused on uncohorted patients;
- monitoring adherence to infection control precautions, including unwavering attention to adherence to appropriate hand hygiene procedures (included the use of observing ‘enforcers’ to make sure staff complied with the basics);
- enhanced environmental decontamination (including double bleach wipe daily disinfection, hydrogen peroxide vapor for terminal disinfection and careful management of drains);
- engagement of all stakeholders involved in care of at-risk patients;
- and detailed, frequent communication with hospital staff about issues relating to the outbreak.
The authors discuss the problem of determining which of these interventions worked, since they were implemented more or less simultaneously; the so-called “kitchen sink” approach (Figure). A recent systematic review performed by ECDC identified this problem in virtually all studies evaluating control interventions for CRE.
Figure. Perceived relative importance of outbreak control interventions at NIH.
There’s an interesting section on the ‘unintended consequences’ of publishing in report, including the inevitable scaremongering in some parts of the lay-press. It wasn’t all bad though; this is an unusually detailed article based on the original NIH outbreak report in the Washingtonian.
Some reflections from me:
- This all started with the transfer of a colonized patient from New York. Recognizing and containing colonized patients that are transferred from other hospitals is going one of the most important fronts in the battle against CRE. Worth noting that ECDC are recommending a rectal screen of all cross-border transfers of hospital patients in Europe.
- Mortality was especially high in the NIH outbreak (albeit in patients with serious underlying illness), illustrating the clinical ‘teeth’ that this issue bares.
- The outbreak reignited from an unidentified reservoir after apparently being brought under control; we have a limited understanding of the challenging epidemiology of these organisms.
- It’s sad, though not surprising, that the high hand hygiene compliance achieved during the outbreak could not be sustained following the outbreak.
- As you would expect, relying on clinical cultures only is looking at the tip of the iceberg. Active surveillance is a must.
- One unique aspect of their enhanced contact precautions was an instruction for staff to avoid touching personal electronic items. This makes a lot of sense, and should be considered for inclusion in regular contact precautions.
- There are some telling insights on the practical challenges of cohorting staff, not least the fact that there were not enough physicians to feasibly cohort!
- The initial isolation measures failed, and NIH (commendably) went to extraordinary lengths to bring the outbreak under control. ‘Aggressive’ is used to describe several aspect of their strategy, which seems apt. Israel is another success story of extraordinary CRE control measures. Greece and Italy are examples of where extraordinary measures have not been undertaken and CRE have quickly become endemic.
Article citation: Palmore TN, Henderson DK. Managing Transmission of Carbapenem-Resistant Enterobacteriaceae in Healthcare Settings: A View From the Trenches. Clin Infect Dis 2013 in press.
This is what happens when norovirus “sprays” from a toddler
An outbreak report in the Journal of Infectious Diseases tells the fascinating story of a norovirus outbreak in a car (auto*) dealership in Oregon that was initially thought to be foodborne, but was eventually traced to contaminated surfaces on a baby changing table (diaper changing station*) in a public toilet (restroom*). The outbreak had a startlingly high attack rate, affecting 75% of 16 employees who attended a team meeting. A thorough investigation of the restaurant that provided the sandwiches for lunch turned out to be a blind alley following the recollection of a staff member of a toddler with “spraying” diarrhoea using the baby changing table in the public toilet of the dealership. The (generous) mother left the mess for the staff member to clean up, which was accomplished using, wait for it, dry paper towels.
The environmental investigation included samples from the baby changing table in the dealership and some ‘control’ samples from 14 baby changing tables in public toilets throughout the state. Norovirus of the same genotype as the outbreak strain was identified from the baby changing table in the car dealership, but norovirus was not identified from the control baby changing tables.
Some limitations of the outbreak include the fact that it is difficult to disentangle the relative importance of the environmental reservoir and secondary transmission via contaminated food. The PCR method used for environmental sampling does not assure that the norovirus RNA identified on the baby changing table was viable. Also, the environmental norovirus isolates could not be sequenced meaning that they could not be sequence-matched with the patient isolates.
Perhaps the most shocking part of the story is that the image of visible soiling on the baby changing table (after two rounds of cleaning) was consistently viewed on baby changing tables in public toilets. Or perhaps it’s even more shocking that only 3 of the 12 affected individuals actually took time off work. As a “survivor” of a norovirus outbreak that swept through the Otter household in 2012, I can vouch for the fact that a) you need to take time off work and b) you ought to take time off work!
One important discussion point was the finding of Dr Carling’s group that baby changing tables were least likely to be cleaned on cruise ships, a setting in which persistent norovirus outbreaks are common. This outbreak report and Dr Carling’s earlier work highlight an important deficiency in how to clean and disinfect baby changing tables in public toilets. As a frequent user over the past 14 months, I can vouch for the fact that, much like a hospital bed, turnover is high which pressurizes effective terminal disinfection! I agree with the authors that disinfection with a chlorine-containing disinfectant would be ideal, but question whether this is feasible in practice.
There’s surprisingly little data supporting the role of environmental contamination in the transmission of norovirus. I’m persuaded by the various outbreaks affecting separate cohorts of patients / staff on cruise ships or aeroplanes, but this outbreak is even more compelling due to the environmental findings. Quantifying the role of the environment in the transmission of norovirus is difficult to study because it always occurs in outbreaks (hence difficult to perform a controlled study). But I’d be interested to see whether the “prior room occupancy” concept that has been established for other environmentally-associated pathogens holds true for norovirus.
Article citation: Repp KK, Hostetler TP, Keene WE. A norovirus outbreak related to contaminated surfaces. J Infect Dis 2013;208:295-298.
Also, take a look at Dr Repp’s blog.
* = for my American readers! Current data indicates that around 40% of the readers of this blog are US based, 40% are UK based and 20% are rest of world!
Reflections on Infection Prevention and Control 