A study from Australia (click here for article) has found biofilms pretty much everywhere on an Australian ICU. The research team cut out 44 surfaces from the ICU and identified biofilms on 41 (93%) of them. This finding will be surprising for some, since biofilms are traditionally associated with hard surface – liquid interfaces (teeth, ship hulls, implanted medical devices). But this is not the first report of biofilms on dry hospital surfaces (click here for article), so isn’t out of the blue.
The existence of biofilms on dry surfaces is perplexing. How do they develop in the first place? And how do they survive in the absence of an obvious nutrient or water source (aside from ambient humidity)? Perhaps the very action of cleaning provides some measure of nutrients – put another way, is our daily cleaning only serving to feed the biofilms?
Now that we know biofilms are there on dry surfaces, we need to make some changes to how we approach hospital cleaning and disinfection. Biofilms will not be removed by a cursory wipe with a detergent. We need to develop new agents and new approaches to tackle biofilms. GAMA is on the forefront of this new frontier having recently commenced a KTP partnership with Cardiff University (click here for article) to investigate new approaches to biofilm management. Watch this space for some solutions to the challenge of biofilms on dry hospital surfaces as they emerge!
A study from New York reports a reduction in C. difficile infection associated with the introduction of a pulsed-xenon UV (PX-UV) device. The authors performed a before-after study of the impact of adding PX-UV to the terminal disinfection protocol of rooms housing patients requiring contact precautions, with 12 months before and 12 months after implementation. Overall, there was a non-significant 22% reduction in the rate of CDI (from 1.06 to 0.83 cases per 1000 patient days), and a significant 70% reduction in the ICU (from 1.83 to 0.55 cases per 1000 patient days).
The authors note a change in cleaning contractor towards the end of the pre-intervention period, which could be a confounding factor. And a change in paediatric case mix, which may explain the marginal increase in CDI rates in paediatrics. More importantly, there is a comment in the discussion intimating that PCR testing may have been implemented during the study period, which would be a much more important confounder – but it is not clear whether PCR testing was implemented in the study hospitals or surrounding hospitals.
The authors introduce an unfortunate new term into the literature: “UVD” (ultraviolet light for room decontamination). This is used by the authors as a “catch-all” term to encompass both ultraviolet-C (UVC) and pulsed-xenon UV (PX-UV) devices. This is unfortunate because a recent study shows that a UVC device was, photon for photon, more effective than a PX-UV device.
In the discussion, the authors comment that “Mercury bulbs emit a continuous low pressure light at a single range of 254 nm, and the effect of this UV light is cumulative requiring a longer cycle time of approximately 45 minutes for spore reduction.” Whilst the recommended cycle times for UVC devices are indeed longer than for PX-UV to address contamination with spores, the head-to-head study showed that UVC is more effective than PX-UV when run for the same length of time from the same point in the room. Put another way, a short blast of UVC would do more damage to spores than the same short blast of PX-UV. In the case of this study, if a UVC device had been run as per the PX-UV device, you’d expect to see more of an impact on the spores – and possibly more of an impact on CDI transmission.
The authors also comment that “Pulsed xenon devices also are somewhat safer because mercury-based devices can release toxic gases if they break accidentally.” This issue has been stirred up by manufacturers of PX-UV devices. The amount of mercury in the bulbs is tiny, and there are fail-safe systems in place to ensure that no mercury is released in the event of breakage. The truth is that a fluorescent bulb that you would see in an office block is more hazardous than the bulbs in UVC devices!
So, it seems that in line with other studies, augmenting terminal disinfection with a UV device does reduce C. difficile transmission. But there does not seem to be a good reason to choose PX-UV over a UVC device!
An oral abstract presented1 (click here for the full report) at APIC 2015 in Nashville in the last week has added to the burgeoning pile of evidence supporting the use of 2% Chlorhexidine wipes in reducing healthcare-associated infections. The paper reported that there was a 59% reduction in Paediatric Central Line-Associated Bloodstream Infection (CLABSI) during the study period. What is interesting about this study is that compliance with the intervention over the course of the study was reported, something that is rarely done. Compliance increased from 45% to 81% during the six-month study period. Significantly, the intervention was demonstrated to be effective even though by the end of the study one in five patients did not receive it. This brings into question our understanding of compliance with research protocols, so poorly reported when study results are published. The researchers estimated potential cost savings of $297,999 over the six-month implementation period. Are staff made aware of the financial aspect of what they are doing in addition to a human one?
If the intervention was significantly effective even when not universally applied, what would the results have been if there had been 100% compliance. How many studies do not reach significance and are deemed to be ineffective because of a low level of compliance with the planned intervention? It would also be interesting to know what the reasons were for the level of compliance with the intervention. Was this poor staff engagement, a lack of understanding of the rationales for the study, practical issues like product unavailability or staff shortage so that the replacements were unaware of the study or patient-specific issues?
It would be very interesting to see a lack of ‘success’ in a planned intervention examined in this way so that lessons can be learnt and shared to optimise the outputs of research. It is difficult enough to plan and implement a research study. To see it fail because of a lack of compliance with the research protocol is something that should be avoided at all costs.
There is currently a lot of interest in a group of bacteria collectively called “multidrug-resistant Gram-negative rods (MDR-GNR)”. This is a mixed group of various bacterial species and genera, with resistance to a variety of antibiotics. The flow-chart below illustrates the key groups. (Click image to enlarge.)
Enterobacteriaceae and non-fermenters
There are two families of Gram-negative bacteria that
are resistant to key antibiotics: the Enterobacteriaceae
and non-fermenters. The Enterobacteriaceae
(If you want to know how to pronounce ‘Enterobacteriaceae’, this should help), including Klebsiella pneumoniae and E. coli, are the big concerns:
– Enterobacteriaceae can be highly resistant to antibiotics
– Enterobacteriaceae are able to spread rapidly
within a healthcare environment
– Enterobacteriaceae have the potential to
establish a community reservoir
– Enterobacteriaceae invasive infections
have a high mortality.
A person with carbapenem resistance who is infected with Enterobacteriaceae has a 50% change of dying. The non-fermenters include Acinetobacter and
Pseudomonas. Although these bacteria typically have a high level of antibiotic resistance they are not that pathogenic and are rarely fatal. Therefore, the resistant Enterobacteriaceae
are the real concern.
Resistant Enterobacteriaceae: CRE and ESBL
Both carbapenemases and extended-spectrum beta-lactamases (ESBL) are enzymes produced by bacteria to break down (“hydrolyse”) beta-lactam antibiotics. These enzymes occur within the Enterobacteriaceae bacterial family, which includes E. coli and Klebsiella. They can cause infections such as UTIs, SSIs and BSIs, and can also colonise the gut without causing symptoms. Enterobacteriaceae that are resistant to carbapenems by any mechanism are called carbapenem-resistant Enterobacteriaceae (CRE) (those that produce carbapenemases are called ‘carbapenemase-producing Enterobacteriaceae’ (CPE)) and Enterobacteriaceae that produce ESBL enzymes are called ‘ESBLs’.
ESBLs produce an extended spectrum enzyme than breaks down and destroys most of the beta-lactams antibiotics such as penicillin and cephalosporins. But ESBLs have no effect on carbapenems (e.g., meropenem), the remaining beta-lactam antibiotic, so carbapenems are used to treat ESBLs.
Now we are seeing the bacteria product stronger beta-lactamases (carbapenemases) and these break down and destroy the remaining beta-lactam, carbapenem. So CREs are much stronger and more serious because few, if any, antibiotics are left to treat these.
Acronyms – CRO, CPO, CRE, CPE
All the acronyms start with C
This is based on a type of very strong antibiotic called carbapenem. It is delivered intravenously and has always had a very effective broad spectrum of activity against all bacteria. Now we are starting to see Gram-negative bacteria (also Gram-positive but the worry is around the Gram-negatives) becoming resistant to the carbapenem antibiotics which often means they are resistant to all other types of antibiotics. In the acronyms below, C refers to either the ‘carbapenem’ antibiotic itself, or the ‘carbapenemase’ enzyme that breaks it down.
P or R
P = producing and R = resistant
P is always twinned with carbapenemase (i.e. carbapenemase-producing) and R is always twinned with carbapenem (i.e. carbapenem-resistant). Put another way, you can’t have ‘carbapenemase-resistant’ or ‘carbapenem-producin.
O or E
O = organism and E = Enterobacteriaceae
If you wish to refer to the Enterobacteriaceae use ‘E’. If you wish to refer to a wider group of bacteria encompassing both the Enterobacteriaceae and non-fermenters, use ‘O’.
Putting it all together
Carbapenem-resistant organism (CRO)
These are all organisms (non-fermenters and Enterobacteriaceae) resistant to carbapenems by a variety of ways – some by mutation, some inherent and some by producing a carbapenemase enzyme that breaks down the antibiotic.
Carbapenemase-producing organism (CPO)
These are all organisms (non-fermenters and Enterobacteriaceae) resistant to carbapenems by producing carbapenemase enzymes that break down the antibiotic. CPO are a subset of CRO.
Carbapenem-resistant Enterobacteriaceae (CRE)
Enterobacteriaceae that are resistant to carbapenems by a variety of ways – some by mutation, some inherent and some by producing a carbapenemase enzyme that breaks down the antibiotic.
Carbapenemase-producing Enterobacteriaceae (CPE)
Enterobacteriaceae that are resistant to carbapenems by producing carbapenemase enzymes that break down the antibiotic. CPE are a subset of CRE. The PHE Toolkit uses the term ‘carbapenemase-producing Enterobacteriaceae’.
Risk of CRE infections
(click the image to enlarge)
How CRE take over
A study from China has evaluated the impact of a daily spray of a QAC polymer as an adjunct to wiping with bleach. The study was performed on a ward with some MRSA-positive and MRSA-negative. The study design was neat, with bed spaces sampled at 0800 and 1200, with or without the application of the QAC polymer (although it’s a shame they didn’t randomise the intervention). It’s fair to say the paper is “data rich”, so pulling out the key findings is challenging, but here goes:
â€“ 56% of bed spaces were contaminated with MRSA, at a concentration of 1-276 cfu/cm^2
â€“ No MRSA was identified on surfaces in the QAC polymer spray arm
â€“ The proportion of sites yielding staphylococci was 78% in the control arm, and 11% in the QAC polymer spray arm.
This study is impressive in terms of the reduction of bacterial contamination. Clearly, there is no clinical outcome, which would require a much more extensive study. But I would expect this degree of reduction in environmental contamination to make some impact on ongoing transmission.
There are a few practical challenges to consider though when using this sort of product.
– Is it safe to apply? The authors cite that the product is 98% water so should generate no dangerous aerosols. But surely a dangerous aerosol could be created from the 2% active ingredients, mindful of the fact that aerosolisation of QAC disinfectants was outlawed by the US CDC in the 1970s on safety grounds.
â€“ Would this be applied around an inpatient? How wet does it make the surfaces, and how long does it take to dry?
– How labour-intensive is the application, and how much do you rely on the operator to assure complete coverage?
â€“ How much does it cost?
– Is it really feasible to spray every surface in every ward once per day?
â€“ How would this approach (spraying a quat and using bleach) compare with using a disinfectant that already has a quat in it?
Leaving practical questions aside, there is some promise in this sort of approach. And we need to continue to explore the potential of antimicrobial surfaces to augment hospital hygiene.