There has been much coverage in the media this week for a new paper in the American Journal of Infection Control from the Cardiff group under the leadership of Prof Jean-Yves Maillard. We blogged on the detail of this paper last week, but in summary the paper demonstrated variability in the ability of a range of detergent wipes to remove bacteria and spores from surfaces. NHS Choices has a more balanced view of this paper than the rather sensationalist reporting elsewhere.
Most headlines have suggested that nurses are spreading superbugs around the ward by using wet wipes. The study shows that detergent wipes do not remove pathogens from surfaces in significant numbers. This is not a new finding and hardly surprising as a detergent wipe aims to be the first step in the cleaning process and is not a disinfection stage on its own. Also, it’s worth noting that the risk of spreading germs using detergent is not restricted to wipes – this has been reported for “mop and bucket” type application of detergent also. So, would you see the same results with a disinfectant wipe? The answer is no, since disinfectant wipes are formulated to remove dirt and kill microbes in a single step.
The key difference between a detergent and a disinfectant wipe is that pathogens not removed by the wiping action will be destroyed by the action of the disinfectants contained within the wipe. It is also important to use combined disinfectant and detergent wipes as Disinfectant Wipes that do not contain any form of detergent will have only limited cleaning properties and so the disinfectants may not be effective.
We worry often about asymptomatic colonisation (aka ‘silent carriage’) of a range of hospital pathogens â€“ MRSA, VRE, CRE â€“ but not C. diff. Screening for C. diff colonisation in the absence of diarrhoea is rarely performed. One of the interesting nuances of C. diff ecology is the high rate of colonisation in babies.
A US study surveyed the rate of asymptomatic C. diff carriage and environmental contamination in a neonatal intensive care unit (NICU). 9 (26%) of the 35 babies sampled were asymptomatic carriers, which is no surprise and in line with other studies. The levels of environmental contamination identified were actually pretty low. Only 2 (1.7%) of 120 sites sampled yielded C. diff in samples collected from the NICU, paediatric units and a haematology / oncology unit. More focussed sampling in the NICU did identify a higher rate environmental contamination â€“ with half of the ‘diaper’ (aka nappy) scales contaminated.
It’s not clear why the levels of environmental C. diff identified in this study were lower than in others. Perhaps the hospital had C. diff pretty much under control? Perhaps the lab methods were not optimal? Either way, the levels of contamination identified in the NICU are consistent with the levels of asymptomatic colonisation, and a potential risk for onward transmission.
So, should we start routinely sampling patients without diarrhoea for C. diff carriage? Should we start routinely sampling their environment? The jury is out on these questions, but asymptomatic carriers of C. diff can certainly be a source of environmental contamination.
An excellent study from the Maillard group has put a range of detergent wipes through their paces. The keys findings are that there was a surprising degree of difference in performance between the wipes. But all of them had a nasty tendency to spread contamination rather than remove it!
The study team put 7 different wipes through their paces, and tested their effectiveness in removing S. aureus, A. baumannii and C. difficile from surfaces. The imaginatively-named “Wiperator” was used, a specially-designed machine for testing wipes. There was a marked difference in performance in removing the organisms from metal discs, ranging from virtually 0 to more than 4-logs, depending on the wipe and organism. A. baumannii seemed to be easiest to remove, even more so than C. difficile spores that you may have expected to be more hardy. Leaving organism-specific differences aside, there was a marked difference in performance between the 7 wipes, probably explained by their specific formulation.
The authors also evaluated onward transfer onto three surfaces following the “Wiperator” test. Some wipes were better than others: Wipe C (the Sani Cloth Detergent Wipe, PDI) seemed particularly efficient at transferring the organisms, whereas Wipe G (Clinell Detergent Wipe) performed best, transferring no A. baumannii or S. aureus. But the bottom line is that all wipes transferred at least some of one of the organisms to the next surface.
It is certainly true that no matter how tight the policy is in mandating that one wipe is used for one surface, in practice, this doesn’t always happen. Wipes are “stretched” to cover more surface area than they were designed for and this is bound to spread contamination and not deal with it effectively. Thus, the authors conclusion that combination disinfectant/detergent wipes (and possibly antimicrobial surfaces) are the way forward seems sound.
This year’s ECCMID meeting in Copenhagen was universally accepted to be the first one with a significant infection prevention and control component, although it would be fair so say that the sessions were not the best attended, meaning that levels of interest in infection control in the majority of the infectious disease physicians attending still need to be stimulated. There were a number of significant sessions, one of which entitled ‘The year in infection control’ was a whistle-stop tour through the most significant papers of 2014 as selected by Petra Gastmeier, Eli Perencevich and Stephanie Dancer. This was a rollercoaster of a session and the abstracts presented are available here. There was, as you would imagine an interest in Chlorhexidine bathing with a very interesting debate between Stephan Harbarth (in favour) and Andreas Voss (against). The main argument against seemed to be that compliance is poor and so why bother. This in fact was a major theme at the meeting, where many papers were presented, in some of which interventions had little effect however the implementation just did not take place.
There were a couple of interesting abstracts. Michelle Allen presented the pilot to her very interesting cleaning bundle study that has some positive initial results (poster here).
The second was a small study from Turkey, unfortunately not an e-poster, that used a Chlorhexidine wipe to cleanse the genital area prior to sending a urine specimen showed impressive results in reducing contaminants and the need for repeat specimens and possibly warrants further investigation in a well-designed study since most micro labs are submerged under the number of inclonclusive urine specimens that result in repeats being requested and possible treatment delays.
The third was from Prof Hilary Humphreys group in Dublin, which looked at the use of chlorine on mattress covers contaminated with Carbapenem resistant Klebsiella pneumoniae, demonstrating that they survive for longer on mattress fabric and are more resistant to hypochlorite than other carbapenem-resistant Enterobacteriaceae. The link to the abstract is here
Will there be as much attention on IPC at ECCMID 2016 in Instanbul? Watch this space
There’s an ever increasing wealth of data that contamination of hospital surfaces are important in the transmission of key hospital pathogens. However, the importance of contaminated air in the transmission of these pathogens is much less certain.
There are some pathogens – like measles – for which airborne spread is by far the most important route. But for the most common pathogens associated with healthcare-associated infection, including MRSA, VRE, C. difficile, A. baumannii and norovirus, contaminated air has not been considered to be an important reservoir, historically.
A recent study published in Clinical Infectious Diseases provides some data that contaminated air may be more common than previously thought. The authors collected 48 air samples from 8 hospitals during outbreaks. Samples were collected close to patients, outside their rooms and at nurses’ stations. The authors found norovirus nucleic acid in 6/8 hospitals from which samples were taken, and at a concentration of 101 to 103 per m3. Finally, they also did some lab work demonstrating that an aerosol of a norovirus surrogate (murine norovirus) preserved its infectivity.
A few key technical questions arise: how do you know whether the norovirus was viable? The authors did not actually attempt to grow the norovirus and could have detected nucleic acid from dead virus particles. If the norovirus is alive, is there enough of it there to cause an infection? (The minimum infective dose of norovirus can be as low as one virus particle, so the answer, in theory, is yes.) A follow-on question from this is: if there is so much viable norovirus floating around in the air, why doesn’t everybody get it?
A more fundamental question is whether the contaminated air detected in this study is a cause or effect of norovirus transmission. For many years, contaminated surfaces were considered to be an effect rather than a cause of transmission and it took detailed intervention studies to convince the scientific community that contaminated surfaces can be a cause of transmission. In the case of norovirus – and other pathogens associated with healthcare-associated infection – we don’t yet have those convincing intervention studies that contaminated air is a cause of transmission.
However, the theoretical risk is there and I’m sure that those of us who have experienced norovirus would prefer to err on the side of caution rather than acquire norovirus via an airborne route!