Toilets as a reservoir for CPE transmission?

Picked up this interesting article in Infection Prevention in Practice suggesting that contaminated toilet fixtures could be a reservoir for CPE transmission. It’s always difficult to disentangle cause and effect when it comes to surface contamination, but the study makes a compelling case that toilets were a reservoir for transmission. The solution? More cleaning and disinfection is required – but also a look at some newer approaches to bathroom disinfection, along the lines of continuous disinfection.

Intro:

Hospital environments are well-documented reservoirs for multidrug-resistant organisms. While sinks and drains have long been implicated in outbreaks, toilets have received less attention despite their potential for aerosolization during flushing. This Danish study focused on the Gastric Surgery Unit, where two ongoing CPE outbreaks were linked to Citrobacter freundii ST18 and Klebsiella oxytoca ST2, both carrying the blaNDM-1 gene. The study asked whether toilets serve as the primary source of transmission, and how genetically related are environmental and patient isolates?

Methods:

This was a longitudinal study without an intervention, tracking patient and environmental contamination on the unit. Over 450 days, the following were undertaken:

  • Weekly rectal swabs for all patients on the unit.
  • Environmental sampling of toilets, drains, and dry surfaces at multiple time points.
  • Whole-genome sequencing (WGS) and plasmid profiling using Illumina and Oxford Nanopore platforms.
  • Core genome MLST (cgMLST) for phylogenetic analysis.

Key findings:

  • Three toilets consistently harbored NDM-1-producing K. oxytoca ST2, each forming distinct genomic sub-clades.
  • Four patients later tested positive for isolates genetically related to those found in toilets.
  • No evidence of direct patient-to-patient transmission was detected.
  • Additional sampling of dry surfaces yielded no CPE, reinforcing toilets as the primary reservoir.
  • Interestingly, one toilet lacked a lid—a factor that may have facilitated aerosol spread during flushing, as suggested by prior studies on pathogen dispersal.
  • Environmental isolates carried either a novel IncR plasmid (pKo2) or the pT1 plasmid previously associated with C. freundii outbreaks.
  • cgMLST revealed tight clustering of isolates from the same toilet across time points, confirming persistence.

Limitations:

  • The main limitation of the study is the design itself. Whilst there is compelling evidence from the individual patient timelines that the contaminated toilets were the source of acquisition, we don’t know this for sure. Environmental sampling is always hit and miss, staff were not screened, and patients were ‘only’ screened weekly. Plus, we don’t know whether there was a lag between the point of actual acquisition and when the patients became culture positive.
  • The lack of control or an intervention reinforces the challenges in drawing something definitive from this study.

Implications for practice:

Despite the limitations, the study provides compelling evidence for the role of the inanimate environmental in the spread of CPE. So, we to:

  • Clean and disinfect more frequently and more thoroughly.
  • Use a disinfectant with a good chance of inactivating CPE, even in the presence of soiling (such as peracetic acid or chlorine dioxide).
  • Consider approaches for ‘continuous disinfection’. The big challenge here is that people use toilets all the time! And clearly with an organism that colonises the gut, high levels of contamination will ensue. So, some sort of continuous disinfection approach would help here, be it antimicrobial surfaces, far UV, UVC (when the toilet is vacant), or some other approach.
  • Improved design of our bathrooms to reduce contamination risks.
  • Implement continuous genomic surveillance to ensure we are identifying and rapidly acting on clusters as they emerge.

Summary

This study underscores the potential role of toilets in the transmission dynamics of CPE. While ‘traditional’ cleaning and disinfection protocols remain essential, they may be insufficient when faced with continuous contamination in high-use areas. This feels like an area that would benefit a lot from ‘continuous disinfection’ approaches, improved bathroom design, and genomic surveillance.

CP-CRE in the USA – up, up, and away?

A concise but powerful study has just been published in Archives of Internal Medicine, showing that the incidence of CP-CRE in clinical cultures has increased a whopping 69% between 2019 and 2023 in the USA, from 2.0 to 3.1 per 100,000 people.

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Where is CPE in the UK?

The prevalence of CP-CRE can be eye-wateringly high in some parts of the world. In Greece, for example, the rate of carbapenem-resistance in invasive K. pneumoniae isolates was 70% in the latest EARS-Net data. In the USA, one study from a long-term acute care facility in California found that almost 50% of patients were colonised. The picture is very different in the UK, with a very low prevalence of CPE reported in most studies as illustrated by the systematic review and meta-analysis that we’re going to look at today.

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Establishing the transmission rate of CPE in hospitalised patients

A helpful new study has combined shoe-leather epi and WGS to establish a transmission rate of CPE in hospitalised patients. Overall, 3 (2%) of 152 exposed patients ended up colonised with the same CPE from 47 index patient exposures. None of the 54 exposed staff ended up colonised with CPE. This transmission rate is a bit lower than I would have expected, but it’s also not zero!

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How often does colonization precede infection with MDR-GNB and VRE?

Ever found yourself wondering how often colonization precedes infection with MDR-GNB and VRE? A new systematic review and meta-regression in Lancet ID gives us a pretty solid answer: about 14% of MDR-GNB and 8% for VRE. This information is helpful for us to qualify the significance of acquiring these organisms in healthcare settings.

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CPE infection prevention and control guidelines: an update

Since writing this 2015 review on gaps and controversies in the guidelines for the prevention and control of CPE (and other MDR-GNR) I’ve tried to keep it fairly up to date. So, here’s the latest iteration, including the 2015 CDC guidelines.

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Cheap and slow (culture) is usually better than fast and expensive (PCR) for CPE screening: Bertha says so!

BMC Medicine has published some research from our group reporting the findings of a mathematical model comparing various approaches to screening for CPE carriage. The model compared how several operational metrics varied with different approaches to screening (‘slow and cheap’ laboratory culture vs. ‘fast and expensive’ PCR) and in various specialties with variable levels of compliance with CPE admission screening and at various levels of admission prevalence of CPE. The main conclusion was that culture proved to be the best approach in most scenarios, balancing risk and resource.

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