Colistin resistance genes found lurking on hospital surfaces

The emergence of colistin resistance in antibiotic resistant Gram-negative bacteria like CPE is a real concern. An Italian study just published has discovered colistin-resistance genes (mcr-1) on hospital surfaces. This raises the worrying possibility that hospital surfaces could be an important reservoir from which colistin resistance genes could spread to bacteria that cause healthcare-associated infection, making infections even more difficult to treat.

The study reanalysed a library of 300 Enterobacteriaceae isolates from environmental samples collected from floors, bedrails, and sinks in eight Italian hospitals during 2016-17. Amazingly, 8.3% (25/300) of the Enterobacteriaceae harboured the mcr-1 colistin resistance gene. A wide range of bacterial species were represented among those harbouring mcr-1, including a mixture of environmental bacteria, and those that are a common cause of human infection. The discovery of mcr1 in K. pneumoniae was most concerning, given the potential for this organism to spread rapidly in healthcare settings.

These findings have probable and important clinical implications. It seems likely that some of the species with mcr-1 identified on hospital surfaces could be transferred to patients – either directly or via the hands of healthcare workers ?? and establish colonisation and/or cause infection. Also, it seems likely that the mcr-1 gene will spread horizontally between bacteria in the environment, providing an active reservoir for the creation of colistin-resistant bacteria that could go on to cause human infection. This issue is made worse by the presence of dry surface biofilms, which provide a protected environment for the sharing of resistance genes.

The presence of the mcr-1 colistin resistance gene on hospital surfaces presents a risk of enhancing the development and spread of colisin-resistant bacteria in hospitals. In the light of these findings, we need to continue to focus on the best ways to reduce the risk associated with the contamination of surfaces with pathogens in the healthcare setting.

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Are surfaces a hidden reservoir for Mycobacterium contamination of heater-cooler units?

There’s an emerging global epidemic of Mycobacterium chimaera infections following cardiothoracic surgery associated with contaminated heater-cooler units (machines that are used in theatre during some procedures). It has been established that water within the machines can become contaminated with Mycobacterium species, and that this can create a bio-aerosol that finds its way into the surgical field and causes an infection. However, a recent study from Hong Kong highlights the potential for surfaces on the heater-cooler units to be reservoirs for Mycobacterium.

The study was performed as part of an investigation into a string of cases of Mycobacterium chimaera surgical infections following cardiac valve replacement. The investigation discovered, as with many others around the world, that the water reservoir within the machines was contaminated with M. chimaera before and after disinfection of the water, providing a plausible source for the surgical infections.

However, the authors went further, and performed sampling of the surfaces on the inside and the outside of the heater-cooler units. No contamination of the outside surfaces of the units, which were effectively disinfected using Clinell Universal Wipes, was identified. However, 4/8 (50%) of the inner surfaces of the units were contaminated with M. chimaera. It’s possible that this surface contamination could be involved, either directly or indirectly, in seeding the airflow exiting the units that then enters the surgical field and causes a surgical infection. For example, M. chimaera is eliminated successfully from the water reservoir within a unit, contamination of the internal surfaces of the unit could then decontaminate the water reservoir!

This is the first study (that we’ve come across) exploring surface contamination with M. chimaera in the context of heater-cooler units used for cardiothoracic surgery. The findings certainly raise some important questions and warrant further investigation. It was reassuring that no contamination was identified on the outer surfaces of the units. However, how much of a clinical risk does contamination of the internal surfaces of these units present? How can this be reduced or eliminated? Could vapour-phase decontamination methods such as hydrogen peroxide vapour could play a role? As the global community strives to mitigate the risk of M. chimaera infections associated with heater-cooler units, contamination of surfaces could be a new frontier!

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Dry surface biofilms: it’s time for action


We blogged last week about a lab study illustrating the potential for dry surface biofilms to harbour bacteria that can then be transferred via the hands of healthcare workers. This week, a new study in the Journal of Hospital Infection illustrates dramatically the scale of the problem of dry surface biofilms in hospitals: a whopping 95% of 61 surfaces tested from three UK hospital groups had dry surface biofilms, and 58% of these samples grew MRSA! We need to think of ways to tackle dry surface biofilms in hospitals.

This multicentre study involved three hospital groups in Scotland, Wales, and England. 61 surface samples were collected from various wards and other clinical areas, and tested for the presence of dry surface biofilms. Almost every single surface had dry surface biofilm present. Surprisingly, despite the variability in the types of sample included (from alcohol gel bottle tops to keyboards to note holders), the physical structure of the biofilm was similar. Oddly though, the microbial composition of the biofilms was very different in one of the hospitals, containing mainly Bacillus species DNA compared with Staphylococcus DNA predominating in the other two hospitals. Its not clear why this difference existed, but could be due to differences in cleaning and disinfection frequency, materials, or chemicals.

This helpful study guides us in moving forward to tackle dry surface biofilms on hospital surfaces. The extent of dry surface biofilms given the range in hospital and items sampled was surprising, and reinforces the need to consider biofilms when planning hospital cleaning and disinfection strategies. The finding that the structure of the biofilms was consistent across the hospitals is useful, and can feed into research and development activities to develop representative dry surface biofilm models. The heterogeneity in microbial composition of the biofilms warrants further investigation, but suggests that differences in local cleaning and disinfection strategy will influence the composition of dry surface biofilm, which could have clinical implications.

The fairly recent findings of dry surface biofilms on hospital surfaces may well prompt a new era in the discovery and development of novel hospital disinfectants and disinfection strategies configured to tackle dry surface biofilms.

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The role of dry surface biofilm in spreading hospital pathogens

We have discovered only in recent years that dry surface biofilms are commonplace on hard surfaces in hospital. A recent Australian study illustrates clearly (and alarmingly!) that bacteria can be transferred from dry surface biofilms to the hands of healthcare workers – and so probably have an important role in transmission.

This simple lab study evaluated the amount of Staphylococcus aureus that were transferred from dry surface biofilms grown on glass and plastic coupons. Volunteers pinched the coupons on which the dry surface biofilms were grown, and then touched agar plates. In order to test the possibility of sequential transfer from hands, the volunteers touched a series of 19 agar plates (without touching the coupons again).

Around 5% of the S. aureus on the coupons was transferred to volunteers hands, and 1% to the agar plates via contaminated volunteers hands. While this doesnt sound like much, when you start with a couple of million bacteria, even 1% is a significant amount of bacterial transfer (around 20,000 or 105 cells)! Worryingly, bacteria were transferred to agar plates for up to 19 sequential transfers.

The study also modelled whether detergent cleaning of the biofilms would help to mitigate the transfer of bacteria. However, in the case of the plastic coupons, wetting them with detergent actually made things worse, increasing the rate of bacterial transfer to the agar plates from 1% to 5%! Perhaps this is because the physical action of cleaning the coupons mobilised bacteria in the biofilms?

We have suspected since their discovery that dry surface biofilms in the hospital environment present a reservoir for the transmission of microbes that cause hospital infections. Although performed in a laboratory setting, this study provides compelling evidence that dry surface biofilms on hospital surfaces present a clinical risk.

 

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A “halo” effect of chlorhexidine patient bathing: reduced environmental contamination

CHG_bathing_alternative_pack1 An Irish study has examined whether daily bathing of patients using chlorhexidine results in a “halo” effect, in reducing environmental contamination. The study found that contamination of surfaces with VRE and ESBL Enterobacteriaceae (ESBL-E) in the near-patient environment was significantly lower when chlorhexidine bathing was in operation.

The study was performed in a 12-bed mixed speciality ICU over 20 months including 157 patients, during which daily chlorhexidine bathing was introduced. Each occupied bed was sampled twice weekly for a range of antibiotic-resistant bacteria. 9.4% of 745 surfaces sampled prior to the introduction of chlorhexidine were contaminated with VRE or ESBL-E vs. 5.0% of 958 surfaces samples after (p<0.001). There was a stark and significant reduction in contamination with VRE or ESBL-E from hand-wash basins: before the introduction of chlorhexidine, 10% of hand-wash basins were contaminated (!), which fell to <2% after chlorhexidine was introduced.

The study evaluated a number of potentially confounding variables: hand hygiene compliance remained more or less the same, and bed occupancy and antibiotic usage increased. It is impressive that a reduction in contamination was observed despite increases in bed occupancy and antibiotic consumption, which have been shown to increase the risk of HCAI. The team even evaluated whether the ambient mean temperature differed between the two periods (it did not).

Although the study was performed in a single centre and no randomisation was involved, it was extraordinarily well controlled for the impact of potentially confounding variables. This study illustrates the “halo” effect of chlorhexidine daily bathing in reducing environmental contamination. This reduction in environmental contamination is likely to be a contributing factor to the improvement in clinical outcomes associated with chlorhexidine daily bathing.

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