CPE contamination of hospital wastewater: smoking gun or innocent bystander?

A recent US study has investigated CPE contamination of sinks, drains, and wastewater. Carbapenemase-producing bacteria were identified throughout the drainage and water system, from drains in patient rooms, right through to wastewater sampled through manholes adjacent to the hospital. My main question in all of this is whether this huge reservoir of carbapenemases in hospital wastewater is a risk for patients. The lack of genetic similarity between isolates in hospital wastewater and isolates from patients suggest not, but I suspect there’s an indirect link and these carbapenemases find their way into isolates affecting humans, which is supported by genetic links between the plasmids carrying the carbapenemases.

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HIS Spring Meeting: ‘Contaminated surfaces: the missing link’

HIS_Spring_Meeting_2016

Thought I’d share some key points from the 2016 HIS Spring Meeting.

Outlining the problem(s)

Prof Gary French kicked off the meeting with a (sic) historical perspective, describing how the perceived importance of the environment in transmission has oscillated from important (in the 40s and 40s) to unimportant in the 70s and 80s to important again in the 2000s. Gary cited a report from the American Hospital Association Committee on Infections Within Hospitals from 1974 to prove the point: ‘The occurrence of nosocomial infection has not been related to levels of microbial contamination of air, surfaces and fomites … meaningful standards for permissible levels of such contamination do not exist.’ Gary covered compelling data that contaminated environmental surfaces make an important contribution to the transmission of Gram-positive bacteria and spores, highlighting that C. difficile in particular is a tricky customer, not helped by the fact that many ‘sporicides’ are not sporicidal!

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Up-date on M. chimaera

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More and more reports and guidance (Ref) appear with regard to Mycobacterial infections associated with heater cooler units used during thoracic surgery. As mentioned in this blog before, the infections are attributed to aerosol generated by the contaminated heater cooler units that are located in or adjacent to the operating room (Ref).

Just now, researchers published 10 patients with disseminated Mycobacterium chimaera infections subsequent to open-heart surgery at three (CH, GER, NL) European Hospitals (Eur Heart J. 2015 Jul 17).

What makes this infections special, is the fact that the time to infection may takes months to years and that the micro-organism in question is easily missed by routine bacterial diagnostics.

The word is out, that other, difficult to diagnose micro-organisms e.g. Legionella are possibly causing post-operative infections, too. Thus, I believe that we can expect more cases with different pathogens in the near future.

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CRE – too weak to spread!?

superbug

(Photo: thinkprogress.org)

In the May issue of ICHE, Weber et al. published their findings of a study looking at the environmental contamination of rooms occupied  by patients colonized or infected with CRE. In addition to their observations they actively inoculated test surfaces with 102 CRE (which I find rather low). They found that the contamination in the patients’ room was infrequent (8.4%) and at low levels (5.1 CFU/120cm2). With the single exception of K. pneumoniae on formica, alle CRE had a less than 15% survival at 24 hours and a 0% survival after 72 hours.

Should we just conclude that the chance of CRE transmission from the environment is very low?

I believe that this conclusion would be too early and probably wrong. The survival of micro-organisms in the environment is clearly strain dependent and while the authors used clinical isolates they did not mention if they included a strain that has proven its ability to spread (eg. outbreak isolates). In general multi-resistant bacteria may loose some of their fitness – including the ability to survive in the environment – but survival studies like those of Kramer et al. show survival of multiple weeks for E. coli and Klebsiella spp.

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Mycobacterium chimaera & Open-Chest Heart Surgery

20_det_heater_C_v1_Outbreak of Mycobacterium chimaera Infection After Open-Chest Heart Surgery

Reported by Andreas Widmer in Basel and now published by Hugo Sax and colleagues (CID April 15th, 2015), the amazing story of open-cheat heart surgery, Mycobacterium chimaera infections (years after the operation!), and contaminated heater-coolers in your operating room.

While the Swiss were first, we know by now that this problem is unfortunately not limited to the Alp region, but furthermore present e.g. in the Netherlands.   If your hospital has a program for open-chest heart surgery, now is the time to check your heater-coolers, to avoid further airborne transmission of M. chimaera from contaminated heater-cooler units.

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CRE “trafficking” plasmids through hospital surfaces

A team from the NIH Clinical Center in the US present a fascinating study, exploring the transmission of carbapenemase-encoding plasmids in unprecedented detail. The intro does a good job of introducing the ‘triple threat’ from CRE: pan-drug resistance, sharply increasing prevalence, and the potential for the horizontal transfer of carbapenemase genes between Enterobacteriaceae species. They introduce the idea of “plasmid trafficking”, which evokes images of shady bacteria dealing in antibiotic resistance genes (a la the infamous cartoon below):

File written by Adobe Photoshop? 4.0

NIH is a hospital that takes CRE seriously, after being stung by an outbreak in 2011. A quick look at who they screen for CRE illustrates just how seriously they take the threat:

  • ICU / high-risk patients screened twice weekly.
  • All patients screened monthly.
  • Admissions from other hospitals screened for CRE…twice (and given pre-emptive contact precautions until negative cultures are confirmed, for good measure).

They also performed some environmental sampling and recovered several CRE from the hospital environment. This will surprise some, but Enterobacteriaceae do have the potential to survive on surfaces for longer than you may expect.

Surveillance cultures identified 10 patients with KPC-producing Enterobacteriaceae and environmental surveillance identified 6 KPC-producing Enterobacteriaceae. They combined these with several historic isolates from the 2011 outbreak, and a couple of imported isolates to give a sample size of 20 isolates. They wanted to dig deeper into these isolates to explore whether or not they shared any plasmids. And here’s where it gets rather complicated. Conventional whole genome sequencing produces many short reads (100-500 bp) but these cannot distinguish between plasmids and chromosome-encoded genes. Therefore, the authors used a technique called single-molecule, real-time (SMRT) to generate longer reads (around 1000 bp) that make it possible to distinguish between plasmids and chromosome-encoded genes. [I know that I’ve over-simplified this clever genomics massively – but I’ll quickly get out of my depth otherwise!]

The report presents a picture of rare patient-to-patient nosocomial transmission (only 1 of 10 patients were thought to be in-hospital acquisitions), continual importation of diverse CRE, and a complex network of even more diverse plasmids. To illustrate the diversity, one strain of CRE contained no fewer than three distinct KPC-encoding plasmids!

The authors find some evidence of environmental spread of carbapenemase-encoding plasmids, with the carbapenemase-encoding plasmid from a patient matching plasmids recovered from different species of Enterobacteriaceae found in the patient’s environment. What the authors did not demonstrate is transmission of carbapenemase-encoding plasmids from the environment to patients – but I wouldn’t want to be admitted to a room with CRE lurking in the hospital environment!

There’s quite a bit of science around the horizontal transmission of plasmids within biofilms. Combine this with the recent finding of biofilms on dry hospital surfaces, and you have a concerning new angle on how CRE may be transmitted in hospitals.

Image credit. Nick Kim, with permission.

Article citation: Conlan S, Thomas PJ, Deming C et al. Single-molecule sequencing to track plasmid diversity of hospital-associated carbapenemase-producing Enterobacteriaceae. Sci Transl Med 2014; 6: 254ra126.

APIC New England 2014 Conference Report: ‘The how, when, & where of C. diff – can you “C” the difference?’

apic new england logo

I was privileged to be asked to speak at the APIC New England Conference today in Springfield, Massachusetts. It was a vibrant day, and congratulations to the organizing committee for putting on such an enjoyable event.

Marie-Louise Landry MD – Continuing conundrums and controversies in the laboratory diagnosis of Clostridium difficile.

Dr Landy, a virologist by trade, began by reflecting on the fact that CDI is relatively new phenomenon, discovered in the late 1970s and initially thought to be viral! Having briefly presented the clinical problem and pathogenesis of CDI, Dr Landry got to the nitty gritty of how to test for CDI. You can choose to target the toxin, bacteria or bacteria capable of producing toxin:

  • Toxin: cytotoxicity cell culture assay (complex and requires overnight incubation) or enzyme immuno assay (terrible sensitivity).
  • Bacteria: culture (slow and doesn’t tell you much) or rapid GDH antigen assay (sensitive, but requires a confirmatory test of toxigenicity).
  • Bacteria capable of producing toxin: toxigenic culture (requires incubation) or Nucleic Acid Amplification Test (NAAT) such as PCR or LAMP (rapid, expensive).

To be honest, before Dr Landry’s talk, I thought that testing for CDI was pretty much sorted: GDH as a sensitive screening test following by PCR to detect the toxin gene for GDH positives. However, Dr Landry presented a compelling case that whilst GDH makes sense as a screening test, detecting the toxin gene via PCR is only half the story: the real gold-standard test is a cytotoxicity cell culture assay to confirm that the disease-causing toxin is present. Cost & clinical association makes compelling case for cell culture cytotoxicity assays; convenience for PCR! Indeed is the initial enthusiasm for PCR CDI testing waning as reality sets in (like the famous ‘Going and Coming’ by Rockwell)?

A final point for discussion: you can have the best laboratory diagnostics in the world, but if you’re testing inappropriate specimens, you’ll end up with false positives. We need a firm “no diarrhea, no CDI diagnostics” rule!

Curtis Donskey MD – Controlling the spread of C. difficile: a multifaceted approach

Dr Donskey began by considering that no healthcare facility is an island, and that long-term care facilities are an integral part of CDI spread. Dr Donskey spent most of the talk considering the environmental considerations related to CDI. Why does cleaning fail? Due to poor implementation: a research team with a bucket of bleach can eliminate C. difficile from surfaces! Various tools are available to help us tackle C. difficile environmental contamination. However, fluorescent markers and UVC did not eliminate C. difficile contamination whereas carefully enhanced disinfection did; bleach goes round corners better than UV, apparently. A related (and under-reported) unintended consequence of introduction a “no-touch” room disinfection (NTD) system such as UVC is that cleaners stop cleaning, mistaking UVC for magical cleaning robots! Plus, you could find yourself spending more time screening than cleaning, to the extent that those tasked with monitoring the cleaning process would be better deployed by getting their hands dirty! Dr Donskey covered a number of other important environmental issues: who cleans what (“the nurses thought EVS were doing it; EVS thought the techs were doing it; nobody was doing it”), the need for daily disinfection, pre-emptive and extended isolation, the potential and under-recognized importance of proper daily bathing for CDI patients, and the potential contamination risk from asymptomatic carriers. The final word: “getting doctors to prescribe antibiotics appropriately is like getting EVS to clean properly: an ongoing challenge.” Oh, and he finished on a song.

Jon Otter PhD (who invited him?) – No-touch room disinfection (NTD) systems: when to use them and how to choose between them (Can you ‘C’ the difference?)

You can download my slides from the talk here.

The talk was loosely based around a review paper recently published in JHI. The increased risk from the prior room occupant argues for doing a better job of terminal disinfection. The goal of hospital disinfection is controversial: the ‘Pragmatist’ says a reduction in contamination is good enough, whereas the ‘Prior room occupantist’ says elimination of pathogens is required. I presented some data suggesting that transmission risk ∝ contamination level; ergo reduction in transmission ∝ decontamination level? The NTD scene is a four-horse race currently, with hydrogen peroxide vapour (HPV), aerosolized hydrogen peroxide (AHP), ultraviolet C (UVC), and the relatively new kid on the block, pulsed xenon UV (PX-UV). Each system has its pros and cons so which is best? My view is that will depend on the scenario: if you have a carbapenem-resistant Acinetobacter baumannii in your ICU, then the ‘belt and braces’ approach of HPV is warranted. However, if you have MRSA colonization on a medical ward, a ‘quick and easy’ UV treatment may the only feasible option.

To try to keep everybody awake after lunch, I polled the audience on a few questions (Figure). I was not surprised that most people had not used an NTD system. However, I was surprised that so few people selected UV in the scenarios!

APIC NE q1 APIC NE q2 APIC NE scenarios

Figure. Question 1: Should all acute hospitals be using a ‘no-touch’ automated room disinfection (NTD) system for terminal disinfection of some patient rooms? Question 2: Has your hospital has used the following NTD systems? Scenario 1: A patient with carbapenem-resistant A. baumannii is discharged from the ICU. Scenario 2: A patient with MRSA colonization is discharged a general medical unit. Scenario 3: A patient with recently resolved CDI is discharged from a general medical unit (‘Enhanced’ = enhanced conventional methods).

Mike McCarthy – Sustaining your gains in infection control initiatives

Mike McCarthy rounded off the day with an engaging overview of his experience from a number of industries of how to ‘sustain your gains’. There’s a temptation from administrators to dismantle the team once it has been shown to work; clearly, the results will disappear with the people! Mike gave useful advice on how to embed change in an individual and organization. Do not confuse respect for people with respect for their bad practices. We need to be good coaches of best practice – reinforce proper execution; correct improper execution. The typical number of audits is “once and done”, but this not enough to form good habits. Establishing a new habit takes 60-90 days of work to reach the happy state of ‘unconscious competence’. People like data-led feedback (we’re all nerds at heart), which results in tangible performance management and improvement.  So, implement a checklist, audit it, provide positive reinforcement and feedback and your gain will be sustained!

Points for discussion:

  • Laboratory diagnostics are only part of the story. We need to focus on making sure only appropriate specimens are tested. Dr Donskey mentioned that a shocking 12% of their stool specimens were not tested due to sample leaking or labeling errors. Unfortunately, the stools most likely to be from CDI are also most likely to be liquid! Conversely, testing formed stools doesn’t do anybody any favours.
  • Do we need to focus on asymptomatic toxigenic C. difficile carriers and, if so, how?
  • How far can conventional methods go in tacking environmental contamination with C. difficile and is it time to turn to NTD systems, at least some of the time?
  • How best to sustain our gains?