Epidemiology

Spread the word, not the MDROs!

Guest Blogger Epidemiology , ,

xdro registry

Guest blogger, Rita Bos (bio below) writes:

This month, while randomly searching Pubmed with the subject MDRO (I know, a rather bizarre hobby), I came across a French study on MDRO information in patient transfer letters. In this paper, which was published in the French journal “Médecine et maladies infectieuses” Lefebvre et al (of the Infection Control Unit of the Dijon University Hospital, Dijon, France) investigated the proportion of transfer letters that contained information of infection or colonization with MDR bacteria.

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You wait for ages, and then two come at once..

Martin Kiernan (@emrsa15) Epidemiology, General, Infection Prevention and Control , , ,

NH

Sometimes waiting for research highlighting an issue that you know is a problem is like waiting for a bus..  Following on from my colleague @jonotter who last week posted about MRSA spread in nursing home settings, I was interested to read this new paper from the USA, published in the Journal of the American Geriatric Society. The study notes the high prevalence of Multi-Drug Resistant Organism (MDRO) carriage in nursing homes that was in excess of that in hospital settings and sought to determine any associations. The findings are interesting, if not surprising.

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Just passing through

Martin Kiernan (@emrsa15) Antibiotic resistance, Epidemiology, MDR-GNR , ,
Picture courtesy of Shanna Trim
Picture courtesy of Shanna Trim

Travel is easy, cheap (well, depending on your desire for luxury) and you get to meet some interesting characters on your way. Unfortunately, as this recent study from France just published in Clinical Infectious Diseases shows, some of the species that you interact with may have escaped your attention (unless you’re carrying agar plates or some fancy molecular kit with you).

The authors studied travellers attending five vaccination clinics in France prior to and post-travel looking for acquisition of MDR Enterobacteriaeceae. Over 50% came home with more than they bargained for, smuggling MDROs into France in their colons.

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Not all resistant Gram-negative bacteria are created equal: Enterobacteriaceae vs. non-fermenters

Jon Otter (@jonotter) Acinetobacter, CRE, Epidemiology , , , , ,

apples and oranges

Apples and oranges. They’re both more or less spherical and classified as fruits, and that’s about whether the similarity ends. It’s the same for antibiotic-resistant Enterobacteriaceae (e.g. Klebsiella pneumoniae) and non-fermenters (e.g. Acinetobacter baumannii): they both share the same basic shape (more or less) and classification (Gram-negative), and that’s about where the similarity ends (see the Table below):

Table: Comparing the epidemiology of resistant Enterobacteriaceae and non-fermenters.3M webinar QA Not all created equal_table

I gave a webinar yesterday as part of a three part series on resistant Gram-negatives. You can download the slides here, and access the recording here (although you’ll have to register to do so). I am increasingly hearing people talking about ‘carbapenem-resistant organisms’ (CRO), used as a catch-all term to encompass both the Enterobacteriaceae and the non-fermenters. As you can see from the comparison table able, this doesn’t make a lot of sense given the key differences in their epidemiology. Indeed, MRSA is a CRO, so why don’t we lump that together with the Enterobacteriaceae and non-fermenters? Carbapenem-resistant Enterobacteriaceae and carbapenem-resistant non-fermenters are both emerging problems, but they are not the same problem.

I asked a few questions of the audience, which I’ve summarised below:

Figures: Questions asked of around 150 webinar participants, mainly from the USA.3M webinar QA Not all created equal Q13M webinar QA Not all created equal q23M webinar QA Not all created equal q3

I was not surprised that so few people felt comfortable explaining the difference between the Enterobacteriaceae and non-fermenters – and this rather justified the whole thrust of the webinar! I was a little surprised that the ‘prevalence’ of the two groups of resistant bacteria were so similar; I was expecting the Enterobacteriaceae to be more common (although I admit this wasn’t a brilliantly worded question). In terms of control interventions, it’s true that we still don’t really know what works to control resistant Gram-negative bacteria. But it does seem likely that the control interventions will be different for Enterobacteriaceae and non-fermenters, and this did come across in the responses. Hand hygiene was selected by most people (which makes sense), with screening & isolation, and stewardship more commonly selected for Enterobacteriaceae, and cleaning / disinfection for the non-fermenters.

Q&A

Following the webinar, the audience asked a few interesting questions:

  1. Can you get chlorhexidine resistant organisms? A number of studies have hinted that reduced susceptibility to chlorhexidine may be an emerging problem, (for example Batra, Otter, Lee and Suwantarat). But increases in bacterial MICs (for Gram-positive bacteria at least) appear to be a long way below the applied concentration. However, it’s worth noting that the measured CHG skin concentration in one study (15-312 mg/L before the daily bath and 78-1250 mg/L after the daily bath) was much lower than the applied CHG concentration (10,000 mg/L). This is around the CHG MIC for some Gram-negatives and potentially brings the subtly reduced susceptibility to CHG reported in MRSA into play. On balance though, the rationale and data on reduced susceptibility are cautionary but not enough to recommend against universal use in the ICU given the clinical upside.
  2. Do you think we should be doing universal chlorhexidine bathing? On our ICU in London, we have been using universal chlorhexidine decolonization for a decade combined with targeted screening and isolation, and have seen a dramatic reduction in the spread of MRSA. So yes, I think we should be doing universal chlorhexidine bathing, but the need to monitor carefully for the emergence of clinically-relevant reduced susceptibility.
  3. Can we discontinue contact precautions for CRE? The short answer is no. Quite a few studies have found that gut colonization with CRE typically lasts for at least 6 months to >1 year. And those that become spontaneously ‘decolonised’ sometimes revert to colonized, suggesting that they weren’t really decolonized at all – it’s just that their load of CRE at the time of sampling had fallen below the limit of detection. So I favour a “once positive, always positive” approach to CRE colonization.
  4. Which disinfectant would you recommend for resistant Gram–negatives? It does seem that the non-fermenters (and in particular A. baumannii) are “more environmental” than the Enterobacteriaceae. However, the Enterobacteriaceae (including CRE – especially K. pneumoniae) can survive on dry surfaces for extended periods. Therefore, I think enhanced disinfection – especially at the time of patient discharge – is prudent for both groups. Consider using bleach or hydrogen peroxide-based liquid disinfectants, and terminal disinfection may be a job for automated room disinfection systems, such as hydrogen peroxide vapour.
  5. Should we use objective tools to monitor cleaning? Effective tools are available to objectively monitor cleaning (e.g. ATP and fluorescent dyes), and these have been shown to improve surface hygiene. Therefore, we should all now be using these tools to performance manage our cleaning processes.

Image credit: ‘Apples and oranges’.

Preventing HCAI: go long or go wide?

Jon Otter (@jonotter) Epidemiology , , , , , ,

quarterbackThere seems to be a general movement away from targeted, pathogen-based precautions (principally screening and isolation) in the USA. This changing professional opinion was clear from the recent SHEA conference, where several leading experts gave what amounted to a collective justification for abandoning contact precautions for MRSA.

The update of the SHEA Compendium of Strategies to Prevent Healthcare-Associated Infections in Acute Care Hospitals is accompanied by a commentary from a group of leading US figures titled ‘Approaches for preventing HCAI: Go long or go wide’. In the commentary, the authors weigh the evidence and opinion for so-called ‘vertical’ (aka targeted) vs. ‘horizontal’ (aka universal) interventions (Table).

go wide or longTable: Go long or go wide? Examples of targeted and universal interventions (adapted from Wenzel & Edmond, via Septimus et al.).

The commentary outlines the potential drawbacks of targeted approaches (such as fewer visits from healthcare workers and feelings of isolation), but doesn’t spend a lot of time discussing the potential drawbacks of universal approaches. For example, “isolation fatigue”, where a procedure loses its impact if it has to be applied to every patient. And then there’s the possibility of resistance when performing universal decolonization. This is particularly worrysome when using antibiotics, but could also be a problem when using biocides such as chlorhexidine.

I’m not ready to abandon pathogen-based targeted interventions just yet. Conceptually, it just does not make sense. If you have a patient with MRSA and a respiratory virus, chances are they will become a ‘super-spreader’. Those who favour universal approaches do make some provision for exceptional cases that really should be identified and isolated via a ‘syndromic’ approach to isolation: crudely, only isolate patients when they’re oozing. However, this syndromic approach would likely miss our ‘super-spreading’ patient, which may well result in an MRSA outbreak – that we could all do without.

Furthermore, if you have a patient who is colonized with CRE, are you brave enough to take no special precautions, as would be the case for a ‘universal only’ approach? The success of this strategy would depend on a high level of compliance with standard precautions such as hand hygiene and environmental cleaning and disinfection. Whilst sound in theory, this just doesn’t happen in the trenches; your facility is above average if your hand hygiene compliance rate is the right side of 40%. Whilst still not 100%, hand hygiene compliance is higher when patients are placed in isolation, most likely because there’s a stronger psychological trigger to comply with hand hygiene.

It’s important to note that targeted and universal approaches are by no means mutually exclusive. For example, on our ICU in London, we have been using universal chlorhexidine decolonization for a decade combined with targeted screening and isolation, and have seen a dramatic reduction in the spread of MRSA.

So, should we go long or go wide in the prevention of HCAI? The answer is both. We should optimize case for all patients, which means careful standard precations with liberal application of chlorhexidine and tight restriction of antibiotics. But we should also identify those with communicable pathogens and segregate them from others. In this regard, we have the weight of history on our side.

Image: Jeff Weese.

What works to control antibiotic-resistant bacteria in the ICU? A two-for-the-price-of-one study

Jon Otter (@jonotter) Antibiotic resistance, Epidemiology , , , , , , , , , , ,

Not content with a single well-planned study to provide information on what works to control multidrug-resistant organisms (MDROs) in the ICU, the MOSAR study group published an interrupted time series and a cluster randomized trial of various interventions in the Lancet ID. This makes the study rather complex to read and follow, but there are a number of important findings.

Interrupted time series – ‘hygiene’ intervention (chlorhexidine and hand hygiene)

Following a 6-month pre-intervention period, a 6-month interrupted time series of a ‘hygiene’ intervention (universal chlorhexidine bathing combined with hand-hygiene improvement) was performed. The key outcomes were twofold: whether there was a change in trend during each phase, and whether there was a step-change between the phases. The hygiene intervention effected a trend change reduction in all MDROs combined and MRSA individually, but not in VRE or ESBLs (Table). However, there was no step-change compared with the baseline period.

Table: Summary of reduced acquisition of all MDROs combined, or MRSA, VRE and ESBLs individually.

Derde table

Cluster RCT – screening and isolation

In the 12-month cluster RCT of screening and isolation, the 13 ICUs in 8 European countries were randomized to either rapid screening (PCR for MRSA and VRE plus chromogenic media for ESBL-Enterobacteriaceae) or conventional screening (chromogenic media for MRSA and VRE only). When analysed together, the introduction of rapid or conventional screening was not associated with a trend or step-change reduction in the acquisition of MDROs (Table).  In fact, there was an increase in the trend of MRSA acquisition. When comparing rapid with conventional screening, rapid screening was associated with a step-change increase in all MDROs and ESBLs.

Discussion

  • The study suggests, prima facie, not to bother with screening and isolation. Indeed, the authors conclude: “In the context of a sustained high level of compliance to hand hygiene and chlorhexidine bathing, screening and isolation of carriers do not reduce acquisition rates of multidrug-resistant bacteria, whether or not screening is done with rapid testing or conventional testing”. However, the major limitation here is that many of the ICUs were already doing screening and isolation during the baseline and hygiene intervention phases! I checked the manuscript carefully (including the supplemental material) to determine exactly how many units were, but it is not disclosed. To make this conclusion, surely the cluster RCT should have been ‘no screening and isolation’ vs. ‘screening and isolation’.
  • The increasing trend of MRSA associated with screening and isolation by either method, and step-change increases in all MDROs and ESBLs associated with rapid screening are difficult to interpret. Is an increase in acquisition due to screening and isolation plausible? Can more rapid detection of carriers really increase transmission (the turnaround time was 24 hours for rapid screening, and 48 hours for chromogenic screening)? The rapid screening arm also included chromogenic screening for ESBLs, whereas the conventional screening arm did not, so perhaps this apparent increase in acquisition is due to improved case ascertainment somehow?
  • Looking at the supplemental material, a single hospital seemed to contribute the majority of MRSA, with an increasing trend in the baseline period, and a sharp decrease during the hygiene intervention. There’s a suspicion, therefore, that an outbreak in a single ICU influenced the whole study in terms of MRSA. Similarly, a single hospital had a sharp increase in the ESBL rate throughout the screening intervention period, which may explain, to a degree, the increasing trend of ESBL in the rapid screening arm.
  • There was an evaluation of length of stay throughout the study phases, with a significant decrease during the hygiene intervention (26%), a significant increase during the rapid screening intervention, and no significant change during the conventional screening intervention. It seems likely that improved sensitivity of rapid screening identified more colonized patients who are more difficult to step down, resulting in an overall increase in length of stay.
  • The carriage of qacA and qacB was compared in the baseline and hygiene intervention phase, finding no difference in carriage rate (around 10% for both). This does not match our experience in London, where carriage rates of qacA increased when we introduced universal chlorhexidine bathing. However, this was restricted to a single clone; the acquisition of genes associated with reduced susceptibility to chlorhexidine seems to be clone-specific.
  • ICUs varied from open plan to 100% single rooms. Whilst the average proportion of patients in single rooms (15-22%) exceeded the average requirement of patients requiring isolation (around 10%), there was no measure of unit-level variation of single room usage. Since the study was analysed by cluster, the lack of single rooms on some units could have been more important than would appear from looking at the overall average. Put another way, a 100% open plan unit would have been forced to isolate all carriers on the open bay, and vice versa for a 100% single room unit.
  • The impact of the various interventions was moderate, even though a ‘high’ MRDO rate was necessary for enrollment (MRSA bacteraemia rate >10%, VRE bacteraemia rate >5%, or ESBL bacteraemia rate >10%). Would the impact of screening and isolation be different on a unit with a lower rate of MDROs? It’s difficult to tell.
  • Some of the microbiology is quite interesting: 8% of MRSA were not MRSA and 49% of VRE were not VRE! Also, 29% of the ESBLs were resistant to carbapenems (although it’s not clear how many of these were carbapenemase producers).

In summary, this is an excellent and ambitious study. The lack of impact on ESBL transmission in particular is disappointing, and may lead towards more frequent endogenous transmission for this group. The results do indicate screening and isolation did little to control MDRO transmission in units with improved hand hygiene combined with universal chlorhexidine. However, we need a ‘no screening and isolation’ vs. ‘screening and isolation’ cluster RCT before we ditch screening and isolation.

Article citation: Derde LP, Cooper BS, Goossens H et al. Interventions to reduce colonisation and transmission of antimicrobial-resistant bacteria in intensive care units: an interrupted time series study and cluster randomised trial. Lancet Infect Dis 2014; 14: 31-39.

How much patient-to-patient spread of S. aureus occurs? Apparently, not much

Jon Otter (@jonotter) Epidemiology, MRSA , , , , , ,

I recently posted an article on surprising finds of a study suggesting that horizontal transmission of C. difficile from known symptomatic cases may be less common that we thought. A group of researchers from Oxford, Brighton and London in the UK applied similar methodology to Staphylococcus aureus transmission with similar findings: only a fifth of S. aureus acquisitions could be attributed to patient-to-patient transmission.

All patients admitted to a 16 bed ICU in Brighton were screened on admission and weekly to detect S. aureus colonization and acquisition. Each isolate was typed by spa and whole genome sequencing (WGS). The number of acquisitions that could be linked using conventional methods (spa typing combined with an analysis of overlapping stays) vs. WGS was evaluated.

Overall, 185 (16.7%) of 1109 admissions carried S. aureus; 59 carried MRSA (5.3%). 680 patients were on the unit for long enough to have a weekly screen and hence were eligible for assessing acquisition. Of these, 44 S. aureus (22 MRSA) acquisitions were detected in 41 patients. 35 of these acquisitions were in patients who were screen-negative on admission and 9 were acquisitions of different strains in patients who were already colonized on admission.

Only 14% (5/36) of the acquisitions available for typing were of the same spa type as another patient on the unit at the same time. All of these were MRSA. WGS discounted three of these apparent occurrences of patient-to-patient transmission, confirmed two and identified a further five (3 MRSA, 2 MSSA). So, in total, 7 / 36 (19%) of acquired isolates (5 MRSA and 2 MSSA) were linked to isolates from other patients (Figure).

Price MRSA WGSFigure: Source of S. aureus acquisitions identified through WGS.

The paper raises some interesting questions:

  • Principally, if almost 80% of patients did not acquire their S. aureus from other patients on the unit, where on earth did they acquire them from? In the C. difficile study, unrecognized importation of diverse strains from the community that would not be detected on admission since admission screening was not performed represents a plausible explanation for the surprisingly low incidence of horizontal transmission from known cases. This is not the case in this study, where all patients were screened on admission for S. aureus. So where were the diverse isolates acquired from? Staff carriers? Contaminated surfaces? S. aureus has the capacity to survive on surfaces for very long periods (more than 1 year), so an ancient environmental reservoir is possible. Furthermore, there was no ‘lead in’ period to the study, so it could be that S. aureus on the unit in the months before the study left an environmental reservoir that led to acquisition in some cases, which would not have been captured by this study. The fact that 4/7 patient-to-patient transmissions acquired the same strain of S. aureus without sharing time on the ICU together supports this, although could also be explained by staff carriers. It was a shame that 16% of the 329 S. aureus isolates (including 16% (7/44) of the acquired isolates) were not available for sequencing, which represents a substantial reservoir from which patient-to-patient transmission likely occurred in some cases.
  • It was interesting that some 20% (9/44) acquisitions that were detected occurred in patients who were already colonized on admission; these would have been missed altogether if molecular typing was not performed. I wonder how much ‘silent’ acquisition of this type occurs?
  • Assuming temporal relationship between strains assumes a constant mutation rate. The ‘speed of the mutation clock’ was assessed in this study through repeated sampling of the same patient. This exercise demonstrated minimal diversity, as was the case for C. difficile.
  • WGS is rapidly becoming the gold standard for transmission mapping. In this study, the conventional approach of evaluating spa typing with overlapping stays lacked both sensitivity and specificity for identifying transmitted isolates.

In summary, the major finding is that only 20% of patients who acquired S. aureus appeared to acquire it through horizontal spread from other patients. The next frontier of transmission mapping must be a more comprehensive evaluation of other potential sources: contaminated surfaces, contaminated air, nurses, doctors, cleaners, tea-tray deliverers and the list goes on…

Article citation: Price JR, Golubchik T, Cole K, Wilson DJ, Crook DW, Thwaites GE, Bowden R, Walker AS, Peto TE, Paul J, Llewelyn MJ. Whole-genome sequencing shows that patient-to-patient transmission rarely accounts for acquisition of Staphylococcus aureus in an intensive care unit. Clin Infect Dis 2014. Jan 9. [Epub ahead of print].

Meeting up with ‘old friends’ keeps you healthy – especially when they’re worms

Jon Otter (@jonotter) Epidemiology , , ,

hookwormHigh income countries are undergoing a massive increase in chronic inflammatory disorders, at least partly due to a failure of immunoregulation. A review in PNAS from Prof Graham Rook at UCLH explores how exposure to the “right” microorganisms (so called ‘old friends’) is crucial for the development of an effective immune system.

Early microbial exposures teach the body how to differentiate friend and foe, fundamentally affect the development of the crucial gut microbiome and prime the development of a functional immune system. Without these exposures, the immune system may attack self (leading to autoimmune diseases), attack harmless airborne particles (leading to allergic disorders such as hay fever), attack gut contents (leading to inflammatory bowel disease), or not be able to turn off background inflammation (leading to cardiovascular disease).

So, what are the most useful early microbial exposures to prime the immune system? The “hygiene hypothesis” suggests that we are ‘too clean for our own good’. However, Dr Rook suggests that exposures to a diverse group of our microbiological ‘old friends’ is what the immune system needs to develop properly, not indiscriminate microbial exposure, which will result in unnecessary exposure to harmful pathogens. Exposure to some of our ‘old friends’ (such as the worm-like parasitic helmiths) has been lost altogether in developed countries, and exposure to other microorganisms has been changed fundamentally by our urban living. Put another way, we should not allow our children to lick the toilet bowl, but should not discourage them from eating a bit of soil occasionally!

Where could this lead? Perhaps we could develop synthetic ‘crapsules’ to augment microbially deficient youngsters (in the same way that vitamin D supplements can be useful)? Or maybe the careful administration of our worm-like parasite old friends (helminths) would help to halt the progression or even reverse the course of previously incurable diseases (such as multiple sclerosis)?

I love the description of a newborn human as a computer loaded with programs (genetics) but no data, and that the type of data entered will affect how the computer functions. Also, the idea that our limited understanding of the depth, breadth and complexity of the microbial world based on the microbes we can grow in the lab can be likened to ‘microbial dark matter’. Notwithstanding the substantial gaps in our understanding, it seems that exposure to our microbial ‘old friends’ early in life is the best way to reverse the worrying trend in chronic inflammatory disorders for future generations.

Photo credit: Jay Reimer.

This study has been BUGGing me for a while

Jon Otter (@jonotter) Epidemiology, MRSA, VRE , , , , , ,

bug glove

A fabulous study recently published in JAMA evaluates the ‘Benefits of Universal Glove and Gown’ (BUGG) in US ICUs. This is a model study design: one of the first cluster randomized controlled trials of a non-therapeutic infection control intervention. Twenty ICUs were paired and randomized to either universal glove and gowning, or to continue the current practice of placing patients known to be infected or colonized with MRSA and VRE on contact precautions. The hypothesis is that undetected colonization with MRSA and VRE is common, and the only real way to address this is to assume everybody is colonized!

Summary of findings:

  • Universal glove and gowning was not associated with a reduction in a composite measure of MRSA / VRE acquisition (the primary outcome).
  • VRE acquisition was not reduced by universal glove and gown use, whereas MRSA was.
  • CLABSI, CAUTI and VAP; ICU mortality; and adverse events did differ significantly between the two groups.
  • Hand hygiene compliance on room entry was not significantly different between the two arms, whereas hand hygiene compliance on room exit was significantly higher in the intervention arm.
  • Healthcare workers visited patients 20% less frequently in the intervention arm (4.2 vs. 5.2 visits per hour).

BUGGFigure: The change in acquisition rate, comparing the baseline period with the study period for the intervention and control units.

Here’s what’s BUGGing me about this study:

  • The acquisition rate in both intervention and control study arms reduced (Figure). The acquisition rate reduction in the control arms may be due to improved compliance with admission screening, resulting in more accurate ascertainment of who required contact precautions.
  • The significant reduction was achieved for MRSA but not for VRE. The authors suggest that VRE colonization may have been suppressed on admission and not detected, and flourished during antimicrobial therapy giving the impressive of acquisition. I wonder whether differences in the routes of transmission may also have contributed; for example, VRE seems to be substantially “more environmental” than MRSA. Another potential confounder is that, by chance, the prevalence of MRSA or VRE on admission to the intervention ICUs was more than double that in the control ICUs (22% vs. 9%). In actual fact, the raw rate of MRSA acquisition in the intervention ICUs was marginally higher than in the control ICUs during the intervention period (6.00 vs. 5.94 per 1000 patient days), even though the change in rate was significantly greater on the intervention ICU. Although adjustment was made for this difference in the analysis, it may have skewed the findings somewhat.
  • The authors achieved remarkably high compliance with admission screening (around 95%), discharge screening (around 85%) and glove and gowning (around 85%). Each site had the luxury of a study coordinator and a physician champion to lead implementation, plus weekly feedback on screening compliance and visits from study investigators. Most ICUs would not be afforded these luxuries so I suspect that real-world compliance outside of the somewhat artificial study environment would be considerably lower. Indeed, an ID Week poster suggests that compliance with gowning in one US ICU was a ‘dismal’ 20%!
  • Adverse events were not significantly higher in the universal glove and gowning arm, which may seem surprising prima facie. However, the reason why adverse events are more common for patients on contact precautions is that they are marginalized by being on contact precautions. If all patients are effectively on contact precautions, the time of healthcare workers would be spread evenly.
  • Universal gloving is likely to result in universally bad hand hygiene compliance within the room during patient care; when healthcare workers feel protected, they are less likely to comply with hand hygiene and gloves are a good way to make healthcare workers feel protected. The increase in hand hygiene compliance on room exit is probably also a symptom of inherent human factors, since healthcare workers feel more ‘dirty’ when exiting the room of a patient with a higher perceived risk of MDRO ‘contamination’ (the so-called “urgh” factor).
  • Healthcare workers had less time for patient care in the intervention arm because they were busy donning and doffing gloves and gowns. Interestingly, the authors suggest that fewer visits may be a good thing for patients, and may have contributed to their reduced chances of acquiring MRSA. This seems unlikely though, given the fact that VRE acquisition was not reduced. On balance, less contact with healthcare workers is likely to be bad for patients.
  • The increased cost of universal glove and gowning was not evaluated and, whilst incrementally small, would be a substantial sum.

In summary, this study sets the standard in terms of rigorous assessment of an infection prevention and control intervention. Universal application of gloves and gowns is unlikely to do as much harm as universal administration of mupirocin, but it will not make a profound reduction in the transmission of MDROs. Therefore, I shouldn’t think many ICUs will be rushing to implement universal gloves and gowns on the strength of these findings.

Article citation: Harris AD, Pineles L, Belton B et al. Universal glove and gown use and acquisition of antibiotic-resistant bacteria in the ICU: a randomized trial. JAMA 2013;310:1571-1580.

Is “community-acquired” CDI real?

Jon Otter (@jonotter) C. difficile, Epidemiology, MRSA , , , ,

A recent high profile US study delved into apparent community-associated CDI cases to evaluate healthcare exposures. The study was large, evaluating almost 1000 cases of community-associated CDI from 8 US states. Only 177 (18%) of the 984 cases had no recent healthcare exposure (Figure 1). Furthermore, healthcare exposure was only evaluated for the 12 weeks prior to the positive specimen, so I would wager that a portion of this 18% acquired their infecting C. difficile in a healthcare facility.  CA-CDIFigure 1. Data demonstrating that most MRSA and CDI presenting on admission to hospital are likely to have been acquired in a healthcare facility.  

So, it seems that the majority of these cases are more likely to be community-onset, healthcare-acquired CDI, rather than community-acquired CDI. I feel like we’ve been here before. In the 1990s before the emergence of distinct strains of CA-MRSA, MRSA presenting at hospital admission was commonly termed ‘community-associated’ or, worse, ‘community-acquired’ when really it was MRSA that had been acquired in hospital during a previous stay (Figure 1). The situation has now changed since distinct MRSA clones have emerged that have the capacity to cause infection outside the healthcare environment.

Turning our attention to the UK, the mandatory report scheme classifies cases of CDI as ‘Trust-apportioned’ if the specimens is collected from patients who have been in hospital for four or more days (Figure 2). It is tempting to speculate that the cases of CDI that are non Trust-apportioned are CA-CDI. However, the definition for ‘Trust-apportioned’ does not account for previous healthcare contact, and the rate of Trust-apportioned and non-Trust-apportioned cases tracks so closely that, once again, these are likely to be healthcare-acquired CDI presenting on admission.

Slide1Figure 2. Number of cases of CDI in England through the mandatory reporting scheme, 2004-2013.

The epidemiology of C. difficile is fundamentally different to MRSA, in that healthy neonates typically have a high rate of C. difficile colonization. Thus, there is a ready reservoir for a low rate of genuinely community-acquired CDI. However, it seems to me that most “CA-CDI” reported thus are likely to be acquired in a healthcare facility and I have not seen any data to convince me that community-acquired CDI is increasing.

Article citation: Chitnis et al. Epidemiology of Community-Associated Clostridium difficile Infection, 2009 Through 2011. JAMA Intern Med 2013;173:1359-67.