CPE has landed in Manchester…officially

A really important point prevalence survey of CPE carriage in inpatients in a hospital in Manchester has just been published in the Journal of Hospital Infection. Important because of the high rate of carriage (11% of 662 patients included). Important because for every 1.6 known cases of CPE, there was an undetected case lurking, despite an extensive screening programme. Important because the lack of significant risk factors associated with CPE carriage suggests that it is distributed homogeneously, endemic in the population. And important because this is the first citable publication suggesting that Manchester has a problem with CPE, despite us having known about it for years via professional networks.

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Preventing carbapenem-resistant Salmonella or E.coli in foods

AMS test

We welcome another guest post from Prof Peter Collignon (bio below) on the risk of antibiotic resistance in the food chain…

Codex has recently announced they are doing more work on antimicrobial resistance.  This is an opportunity get Codex to have a couple of standards to better protect public health from one of the worst types of antibiotic resistance that might develop in the next few years or decade. Specifically to help prevent carbapenem-resistant bacteria transferring to people via the food chain including via imported foods into countries (some useful background on this issue from European Food Safety Authority (EFSA) here).

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Transmissible colistin resistance – made in China

colistin made in china

The emergence of CPE (and carbapenem-resistance in other Gram-negative bacteria) has forced us to reach to the dusty old antibiotic shelf to revive the clinical use of older agents with activity against Gram-negative bacteria, principally colistin. Colistin isn’t perfect by any means – it has poor tissue penetration compared with the carbapenems, and is associated with nephrotoxicity (although the high levels of nephrotoxicity in the older medical literature has not been reported due to better management of the drug). Furthermore, resistance has already been reported. To date – this has been mutational resistance, which does not have the capacity to spread horizontally. It was only a matter of time before a colistin resistance gene mobilised.

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What drives carbapenem resistance? Carbapenem use, stupid!

An outstanding study from colleagues at Imperial shows that if you use a bucket-load of meropenem (a carbapenem antibiotic) one year, you see an uptick in carbapenem-resistant Enterobacteriaceae (CRE) the next. The figure below plots meropenem use in the previous year with the incidence rate of OXA-48 producing K. pneumoniae CRE.

mero usage correlation

Figure: The use of meropenem in the previous year plotted against the incidence rate of OXA-48 producing K. pneumoniae

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CRE: coming to a hospital near you

carbapenemase

I thought for quite some time about whether the title to this post ought to be a statement or a question. I decided on a statement: pretty much wherever you are in the world, I am certain that CRE is now one (hospital) degree of separation from you.

I gave this talk yesterday at the imaginatively named “Darling Bugs of May” IPS conference, and you can download my slides here. I’ve given similar talks before, but the whole thing took on greater significance now I have had some first hand experience of making decisions around the management of CRE patients.

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Do you know your CRE from your CRAB?

I gave a talk today at a meeting on combating carbapenem-resistant organisms. My angle was to clearly differentiate the epidemiology of the Enterobacteriaceae (i.e. CRE) from the non-fermenters (most importantly carbapenem-resistant A. baumannii – CRAB), and you can download my slides here.

I’ve blogged before about how confusing the terminology surrounding multidrug-resistant Gram-negative rods has become. Non-expert healthcare workers have little chance in distinguishing CRE from CPE from CRO from CPO. So we need to help them by developing some clear terminology, given the gulf in epidemiology between CRE and CRAB (see below).

CRE and CRAB are like apples and pears: they share some basic microbiology but that’s about where the comparison ends!CRE CRAB

So, I think we should talk in terms of CRE (and CPE for confirmed carbapenemase carriers), and CRNF (or CRAB for A. baumannii and CRPA for P. aeruginosa). I don’t think that CRO is a useful term – in fact, I find it rather confusing. Carbapenem resistance in Enterobacteriaceae (CRE) and A. baumannii (CRAB) are both emerging problems, but they are not the same problem.

Filling the gaps in the guidelines to control resistant Gram-negative bacteria

I gave the third and final installment of a 3-part webinar series on multidrug-resistant Gram-negative rods for 3M recently. You can download my slides here, and access the recording here.

During the webinar, I provided an overview of the available guidelines to control CRE and other resistant Gram-negative bacteria. I then identified gaps in the guidelines, in terms of definitions of standard precautions, outbreak epidemiology and who should be on the guidelines writing dream team. Finally, I discussed some controversial areas in terms of effective interventions: patient isolation, staff cohorting and selective digestive decontamination.

One of the most important points when considering infection prevention and control guidelines is the issue of ‘standard precautions’. What do we apply to every patient, every time? As you can see from Figure 1 below, ‘standard precautions’ is far from standardized. This is problematic when developing and implementing prevention and control guidelines.

Figure 1: differences in the definition of ‘standard precautions’.

filling gaps std precautions

I had the opportunity to ask the webinar audience a few questions throughout the webinar, which are outlined in Figure 2.

Figure 2: response to the questions from the 120 or so participants.

filling the gaps1 filling the gaps2 filling the gaps3

I was somewhat concerned but not that surprised that more than a quarter of the audience did not know where to access control guidelines for MDR-GNR. I suppose this means that we need to do a better job of signposting the location of the various guidelines available. Here’s a non-exhaustive list for starters:

There was a fairly even split between active and passive surveillance to detect outbreaks. The problem with relying on passive surveillance (i.e. clinical cultures) is that there’s a good chance that the ‘horse will have bolted’, and you have a large outbreak on your hands, before a problem is detected. For this reason, I favour active surveillance.

But who to screen? In the case of CRE, I was pleased to see that virtually nobody said nobody. There was a pretty even split between everybody, high-risk individuals or all individuals in high-risk specialties. Accurately identifying individuals who meet screening triggers is operationally challenging, as outlined by the “backlash” to the UK toolkit, so I think screening all patients in high-risk specialties (e.g. ICU) makes most sense.

So, what works to control MDR-GNR transmission? We don’t really know, so are left with a “kitchen sink” (aka bundle approach) (more on this in my recent talk at HIS). We need higher quality studies providing some evidence as to what actually works to control MDR-GNR. Until then, we need to apply a healthy dose of pragmatism!