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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CPE and plasmid transfer in hospitals – what can we do? A rapid reflection from ICPIC 2023

I’ve had the pleasure of a few days in Geneva enjoying some fine Swiss hospitality, and fine science at ICPIC 2023. Here’s rapid reflection on scaling the risks attached to plasmid-mediated transmission of CPE, and what we can do about it (or not…!).

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CPE showing its teeth: mortality associated with carbapenem-resistant Gram-negative BSI

Now is a really good time to focus on carbapenem-resistant bacteria. We have spent much of the past 3 years focusing on one particular virus. But now that the clinical issues linked to SARS-CoV-2 are waning for our hospital patients, the threat of carbapenem-resistance in Gram-negative bacteria comes to the fore. An excellent study with far-reaching consequences has been published from Italy. Carbapenem resistance is bad news if you have a BSI: patients with carbapenem-resistant BSI were roughly twice as likely to die as patients with carbepenem-susceptible BSI.

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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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CPE: seek and ye shall find

We recently published a study in the Journal of Antimicrobial Chemotherapy relating the impact of introducing an enhanced testing* programme for CPE in London. (And yes, this is the first post for a while that isn’t on COVID-19!) Following an outbreak of NDM-producing Klebsiella pneumoniae affecting 40 patients in 2015 (published elsewhere, here and here), we ramped up our CPE testing programme. The number of patients carrying CPE increased substantially, from around 10 patients per month in June 2015 to around 50 per month in March 2018. However, the proportion of tests that were positive for CPE remained constant at around 0.4%, suggesting this was more effective carrier identification rather than a swelling pool of carriers per se; seek and ye shall find! Curiously, the majority of CPE identified were not linked in time and space with other CPE, suggested they represented a ground-swell of CPE coming into the hospital, rather than frequent in-hospital transmission. Also, the number of patients with CPE infections during the study period did not increase, which was reassuring.

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Can you GES which carbapenemase caused this CPE outbreak?

An unusual and interesting outbreak of CPE was published recently in Clinical Infectious Diseases. Several key points: don’t rely solely on a PCR detecting the “Big 5” carbapenemases (NDM, KPC, OXA-48, IMP, VIM) – at some point you need to test for phenotypic carbapenemase activity; WGS can really help us in unravelling complex transmission routes; and covert plasmid propagation within and between species is a reality.

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CPE has landed in East London

The team at Barts Health, one of the largest NHS hospital groups in the country, has published the findings of a point prevalence screen of all inpatients for carbapenemase-producing organism (CPO) carriage. Overall, 30 (3.1%) of the 977 patient tested were carrying 35 different CPOs (all but one of which were CPE). Risk factors for CPO carriage included hospitalisation abroad, any hospitalisation, and overseas travel (especially to India, Pakistan, and Bangladesh). These findings help us to understand an emerging picture of CPO in the UK.

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Navigating guidelines for MDR-GNR

There’s a plethora of guidelines for MDR-GNR. But how do we choose between them? And how do we implement them effectively in our hospitals? I did a talk on this recently in London, here:

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