A very enjoyable few days in Edinburgh this week for the Federation of Infection Societies / Healthcare Infections Society (FIS/HIS) meeting. Some reflections follow…
Firstly, I ought to explain the cauliflower reference in the title of this post. More than 15 years ago, a fascinating study was published illustrating the spectacular speed and distance of spread of some cauliflower DNA that was inoculated onto a phone receiver in a neonatal ICU. Whilst this certainly doesn’t prove the role of the contaminated environment in transmission, it’s a powerful conceptual model of rapid and widespread contamination spread, with a modern-day counterpart with similar findings! I gave a talk on the role of the environment in the transmission of gastrointestinal pathogens (like C. difficile, norovirus, and to a lesser extent, CPE, MRSA, and VRE) (slides here). These pathogens present some unique challenges in terms of sheer numbers involved, amount shed, and lack of decolonisation options. But how much does the environment contribute to their spread? It is difficult to scale and evidence is sketchy, but the sizable reductions suggested by improving the level of disinfection in the case of C. difficile (I calculated a crude mean reduction of 44%) suggests that the contaminated environment contributes to spread in a large minority or small majority of cases.
I mentioned the emerging data that biofilms are present on dry hospital surfaces, and offer a real challenge to cleaning and disinfection. The idea of dry surface biofilms turned out to be a bit of a theme throughout the conference (or at least in the parts of the conference that I frequented). Biofilms made an appearance in discussions around whether seeding the hospital environment with Bacillus cereus spore probiotics is a good idea, in discussing repeated (and I mean repeated to the extent of 17x) transfer of pathogens from dry surface biofilms to hands, in the lack of activity of sodium hypochlorite against S. aureus-containing biofilms, and in relation to Candida auris (see below).
Dr Sara Mumford told the story of the massive peak and then control of C. difficile at Maidstone. At its worst, 68 cases of CDI were reported in a calendar month, which is unthinkable around a decade later. One of the most striking aspects of the talk was frequent reference to extensive press coverage at the time. Although this brought challenges, I think that, on balance, it was a good thing, holding the hospital to account for some poor practices, and providing impetus for addressing them urgently.
Prof Mark Wilcox then gave a general update on CDI. As usual, this prompted much discussion on what exactly is “HA-CDI”. PHE definitions don’t include previous hospitalisation in attributing healthcare-association, which I think is a mistake. Indeed, our group presented some data at the conference suggesting that a high proportion of CDI cases presenting in the first 72 hours of hospitalisation have a history of recent overnight hospitalisation, suggesting they are, in fact, healthcare-associated (poster here). Also, certainly not new data, but a useful reminder that C. difficile really is all around us, so I have no doubt there always has been and always will be a background level of CA-CDI. In terms of treatment for CDI, a couple of key updates: there is now strong evidence that metronidazole is inferior to vancomycin, and bezlotoxumab (an anti-toxin monoclonal antibody) is firmly on the horizon as a therapeutic option.
Dr Andrew Dodgson gave the Manchester perceptive on CPE. CPE is a ‘broad street’, unlike MRSA and the other ‘usual suspects’. It is likely that KPC in Klebsiella sp. presents a different threat to KPC in E. coli, or NDM in Klebsiella sp. At one point, Andy said that “One would expect CPE would not survive well on dry surfaces”, although I think it’s fair to say that CPE will survive on dry surfaces for longer than you may expect. So, we need more epi data, and fast, to understand the basics of transmission and prevention for CPE. There are worrying signs that CPE is now homogeneously distributed in the Manchester region, but more positive reports that CPE outbreaks can be controlled with early, aggressive intervention. Whether controlled or not, CPE is expensive. In Manchester, board papers suggest a £5m price tag, and Andy reported a mean cost per CPE bacteraemia of £14k. In London, our group reported a cost of £1m over 10 months for a 40-case CPE outbreak. If these relatively small, short-term reports come up with such large costs, how much is CPE costing the NHS? Or the global healthcare economy? On the therapeutic front, it seems from Prof Hawkey’s lecture that beta-lactamase inhibitors (especially Avibactam) are promising (for example, ceftazidime-avibactam is now approved and non-inferior to carbapenem). However, beta-lactamase inhibitors will likely always have limited activity against some classes of carbapenemase enzyme. Related to this, co-production of different classes of carbapenemase is a real problem for beta-lactamase inhibitors, and I worry that their widespread use will drive co-production of carbapenemases in CPE.
It was fascinating to hear the anatomy of the emergence and management of the Candida auris outbreak at the Brompton, the report of which is now published. The conference coincided with the first reports of C. auris from the US, although as Andreas pointed out earlier in the week, this issue is hardly new! That said, there is very little data on how to control C. auris effectively, with key questions outstanding regarding transmission routes, reservoirs, clonal structure, cleaning and disinfection, patient decolonisation, and which IPC interventions are effective. It seems that the Brompton threw the kitchen sink of IPC measures at C. auris (including costly interventions such as ICU closure and HDU relocation), and yet transmission continued. It is unclear what is so special about this fungus at this stage, although it may be that biofilm production is a key virulence factor, promoting environmental survival, and explaining, to a degree, high levels of antifungal resistance. Could it be that antibiofilm strategies are required to prevent the transmission of C. auris effectively?
It’s always good at these conferences to push your comfort zone and go to some lectures outside your expertise. Behaviour change fits that bill for me! Behaviour change is a science, but it’s not a quantitative data-based science that I am comfortable in and around. So, it was news to me that there are NICE guidelines on behaviour change, and structured tools for effecting behaviour change (like the Behaviour Change Wheel). It was useful to consider cultural barriers and determinants of behaviour change, the relationship between knowledge and changed behaviours, and question whether we are trying to apply high-school methods to teach expert adults. I quite like the idea that it’s futile to rely on individual choice and decision making (we all make bad ones after-all); we need to change the environment and embedded behaviours. I am appreciative towards Carmen Lefevre, Michael Borg, and Jacqui Reilly for my lecture in behaviour change theory!
A big thanks to the conference organising committee and those involved in the delivery of the conference. I enjoyed it very much. Finally, great to see the abstracts published in full on the Journal of Hospital Infection website.