A Canadian study reports the findings of a prospective survey of bacterial contamination of privacy curtains in hospitals. The curtains became contaminated with antibiotic resistant bacteria within weeks of being introduced into the clinical environment. The calls into question the management of privacy curtains in the healthcare setting.
Previous studies have found that privacy curtains can be contaminated with antibiotic-resistant bacteria when sampled at a point in time. The unique aspect of this study was that 8 newly hung test curtains in a ward were sampled regularly over 21 days, and compared to control curtains hung in non-clinical areas. This allows us to understand how rapidly the curtains became contaminated. Within 3 days, the curtains in the clinical areas were showing increased contamination compared with the control curtains, and by day 14, 5 of the 8 curtains were contaminated with MRSA.
Protocols for managing privacy curtains vary considerably from hospital to hospital. Some are changed regularly, others, once in a blue moon! Whilst it may be possible to partially disinfect curtains whilst they are hung in a clinical setting (e.g. by using a chemical spray), this will be challenging. Therefore, linen privacy curtains should be changed frequently, and immediately if visibly contaminated with blood or other body fluid and after moving a patient known to be infected or colonised with antibiotic resistant bacteria or other HCAI pathogens such as C. difficile or norovirus. Also, it’s worth considering other patient privacy options (such as non-linen curtains, disposable curtains, screens, or temporary single rooms).
A study from Singapore has highlighted extensive environmental contamination with carbapenem-resistant Acinetobacter baumannii in the ICU. This reinforces the need for enhanced environmental measures to reduce the transmission of carbapenem-resistant Acinetobacter baumannii in the ICU setting.
Carbapenem-resistant Acinetobacter baumannii is in many ways a scary organism: it’s highly resistant to antibiotics with few therapeutic options left in some cases, seems to spread readily in ICUs and burns units, and has an extraordinary ability to survive in the dry environment. One study reported that A. baumannii can survive for more than a year on dry surfaces – and that’s without a water or nutrient source!
During an outbreak of carbapenem-resistant Acinetobacter baumannii in an ICU in Singapore, the team performed a point prevalence survey of patient colonisation / infection and environmental contamination with carbapenem-resistant Acinetobacter baumannii. Environmental contamination was identified in 28% (5/18) of the rooms on the ICU. Whole genome sequencing found that environmental isolates were closely related to the patient in the room, but differed between rooms. This suggests that the environmental isolates originated from the patient in the room.
These findings reinforce the need for enhanced disinfection when dealing with carbapenem-resistant Acinetobacter baumannii, especially at the time of patient discharge. This will reduce the risk that contaminated surfaces become a reservoir for room-to-room transmission of carbapenem-resistant Acinetobacter baumannii.
A useful review published recently in an orthopaedic surgery journal (by Katarincic et al.) covers the various interventions that are often introduced to reduce the risk of surgical site infection (SSI). The evidence for some interventions is stronger than others, but there’s much we can do throughout the patient journey to reduce the risk of SSI, from pre-operative bathing, through antisepsis of the incision site, to effective post-operative wound care.
The evidence for the prevention of SSIs is reviewed thoroughly in the NICE guidelines on SSI prevention, which cover pre-operative, intra-operative, and post-operative measures. However, these guidelines were published in 2008, so a whole decade of SSI prevention research is missing! The review by Katarincic et al. is more pragmatic, spending more time on some of the more contentious issues. For example, whilst antisepsis of the incision site using either chlorhexidine or povidone-iodine is recommended, the NICE SSI guidelines are lukewarm on whether or not to implement chlorhexidine body washing prior to surgery, recommending bathing or showing using soap on the day before, or on the day of, surgery. The authors of the review by Katarincic et al. come to a different conclusion following their review of the evidence on chlorhexidine bathing before surgery: ‘Use chlorhexidine wipes both the night before and the morning of surgery, provide patients with written instructions, and institute a web-based alert for maximum compliance.’
Part of the reason for this difference is that much evidence around the use of chlorhexidine bathing has been published since the NICE recommendations were published. Also though, the review by Katarincic et al. is careful to consider compliance with the chlorhexidine bathing protocol when interpreting the evidence. A number of ‘negative’ studies, concluding that chlorhexidine bathing does not reduce SSIs have poor compliance with chlorhexidine bathing. For example, a prospective cohort study by Johnson et al. found that the infection rate in non-compliant patients in the chlorhexidine bathing arm of the study was 1.6% compared with 0% in the compliant patients in the chlorhexidine bathing arm of the study. And we know from other studies that the use of wipes (vs. solution) can help improve compliance with chlorhexidine bathing.
SSI prevention measures need to be supported by effective guidelines, which take into account compliance with interventions, when considering recommendations. To tackle SSI effectively requires the implementation of prevention measures throughout the patient journey. Based on the latest evidence, bathing with chlorhexidine before surgery makes sense as part of an SSI prevention programme.
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 mcr–1 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.
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!