Chlorhexidine resistance: a remote risk?

CHGA helpful US study tracked the non-emergence of phenotypic or genotypic chlorhexidine resistance associated with hospital-wide use of chlorhexidine gluconate (CHG) antisepsis.

The 700 bed hospital introduced hospital wide CHG bathing in 2010, removed it in 2011, and reinstated it in 2015. They evaluated a collection of S. aureus isolates that were considered hospital-acquired and found that there was no reduction in CHG susceptibility during the two periods of CHG use, and found no evidence of qacA or qacB genes, which have been linked with reduced susceptibility to CHG. The study is one of the few that evaluated hospital-wide use of CHG, so there was certainly a pretty strong selective pressure for reduced susceptibility to emerge!

Whilst this study does not prove that CHG is somehow ‘resistance-resistant’ – indeed, other studies have found evidence of reduced susceptibility associated with CHG use – it does reinforce that CHG is a well-tolerated antiseptic that does not readily promote reduced susceptibility.

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Updates on chlorhexidine from ECCMID 2017

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A number of key studies were published at ECCMID 2017, providing further evidence of the utility of chlorhexidine for reducing the risk of HCAI.

A study from South Korea evaluated the impact of universal skin antisepsis using 2% chlorhexidine gluconate (CHG) washcloths in reducing MRSA acquisitions and bloodstream infections. Following a 12 month baseline period, a 2 year intervention using CHG was following by a 1 year intervention using CHG plus mupirocin. The study showed a significant impact of CHG bathing in reducing MRSA acquisition, and also an incremental benefit of adding nasal mupirocin to the decolonisatoin regieme. Whilst it is useful to have more data that mupirocin and CHG combined reduces the risk of MRSA, it may be that a ‘screen and treat’ approach is the most balanced way forward for mupirocin treatment, because of the risk of resistance, which seems to be less of a risk for CHG.

A bundle of interventions was tested in reducing the spread of CRE and ESBL Gram-negative bacteria in an Italian organ transplant unit. The bundle included screening, isolation, CHG bathing for known carriers, hand hygiene, and staff education. Screening and isolation was performed for CRE and ESBL, whereas the other interventions were implemented for CRE only. A sharply increasing rate of CRE was reversed, and returned below baseline levels following the intervention. The ESBL rate was static before the intervention, but decreased significantly in response. This shows that a intervention bundle aimed primarily at CRE also had some impact on ESBL, which was a bonus!

Finally, a large randomised controlled trial of 2% CHG / alcohol vs. 5% povidone-iodine / alcohol showed that there was no significant difference in the blood culture contamination rate following blood culture collection. This reinforces findings from other studies.

So, some evidence that chlorhexidine represents a versatile and effective antiseptic biocide!

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Watch out: C. difficile about (and you may not know it)

c-diff1
There has been some recent discussion on whether we should implement screening for asymptomatic carriage of C. difficile. Whilst there is some evidence that cross-transmission of C. difficile from symptomatic cases is rare (in English hospitals, at least), a recent study shows that asymptomatic carriers are an important source of in-hospital transmission of C. difficile.

The study was performed over 4 months in a Danish ICU. All admissions were screened for asymptomatic carriage of C. difficile. The key outcome was that exposure to a C. difficile asymptomatic carrier resulted in an increased risk of C. difficile infection: C difficile infection was detected in 2.6% of patients not exposed to carriers and in 4.6% of patients exposed to asymptomatic carriers (odds ratio 1.8, 95% confidence interval 1.2-2.8). Put another way, patients exposed to asymptomatic carriers were approximately twice as likely to develop C. difficile infection!

One unique aspect of the study was that hospital staff were blinded to the C. difficile carriage status of the patients on the unit. This means that no attempts were made to reduce the risk of C. difficile transmission from known carriers. So, the study provides some tantalising evidence that improving the management of known C. difficile carriers (perhaps through isolation and enhanced disinfection) could reduce the incidence of C. difficile infection.

Patients with C. difficile diarrhoea will shed a lot more spores and need to remain the key focus of prevention and control initiatives. However, this study suggests that asymptomatic carriers should be a separate focus of prevention and control interventions.

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Look behind you: Acinetobacter!

hospital-room

We recently posted a blog on a review and meta-analysis on the increased risk of acquiring key hospital pathogens from the prior room occupant. A similar review and meta-analysis has just been published focussing on the ICU environment. The new study highlights the 5-fold increase in risk of acquiring Acinetobacter when the previous room occupant had this pathogen!

The main result is the same from both meta-analyses: the risk of acquiring MRSA, VRE, C. difficile, Acinetobacter, Pseudomonas, and Klebsiella or E. coli is approximately doubled when patients were admitted into rooms where the previous occupant had these pathogens. The presentation of the data grouped by organism in the most recent review draws attention to a greater increase in risk from one pathogen in particular: Acinetobacter. There was a
5-fold increase in risk for this pathogen, which was itself double the increase in risk for all pathogens combined, suggesting that Acinetobacter is somehow "more environmental" than the others*. Whilst differences in study design and setting may go some way to explain this, this is plausible:
we know that Acinetobacter is shed in high quantities and has
exceptional survival properties.

In the previous post, we reiterated the need to redouble our efforts to tackle contamination of the hospital environment based on these findings, especially at the time of patient discharge, in order to mitigate or even eliminate this increased risk through:

  • Improving the cleaning / disinfection process
  • Developing new modalities to make cleaning / disinfection easier
  • Producing novel disinfectants
  • Improved design
  • Reduced patient shedding
  • Considering antimicrobial surfaces
  • Implementing automated room decontamination (ARD)

We now know that being admitted to a room where the previous room occupant had a pathogen is a risk factor for the incoming occupant in acquiring these pathogens, and that improving the quality of terminal cleaning and disinfection mitigates or removes completely this increased risk. So, let's get out there and ensure that all rooms are clean, safe, and ready to deliver the highest quality of care to our patients.

*Only one of the studies included C. difficile, which was performed in an outbreak setting - we would expect future studies to show a higher increased risk for acquiring C. difficile from the prior room occupant!

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Dismiss hospital floors as a potential source of HCAI pathogens at your peril!

floor1

A multicentre US study has shown that hospital floors can be a source of pathogens that can cause HCAI. Floors were heavily contaminated, high-touch items were in frequent contact with floors, and hands became contaminated with hospital pathogens as a result of contact with these items. Anybody who dismissed hospital floors as a potential transmission risk are missing a trick!

Historically, floors have been considered a minor risk in terms of transmitting hospital pathogens, and the focus has been on the disinfection of high-touch surfaces. In order to assess the potential for cross-transmission, a group of five hospitals collaborated to study the frequency of contamination of hospital floors and whether high-risk objects could be a contaminated as a result of contact. Around half of the 318 floors sampled in 159 patient rooms were contaminated with C. difficile (regardless of if the patient had C. difficile infection or not, and whether or not the patient had been discharged and terminal disinfection performed), and between 10 and 30% of floors were contaminated with MRSA and VRE. Amazingly, a point prevalence survey found that 41% of the rooms had one or more high-touch surface in contact with the floor. These objects transferred C. difficile to 3%, VRE to 6%, and MRSA to 18% of researcher hands following contact.

What we need now is a good quality intervention study to show that enhanced disinfection of floors (perhaps using our Sporicidal Granules) reduces the transmission of hospital pathogens. Any takers?

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