Last Friday the results of the ESBL Attribution study (ESBLAT) were presented. After considerable media attention for ESBL-producing bacteria on our meat (especially retail chicken meat) and a 84-year old woman being “the first deadly victim of the new chicken-ESBL bacterium” a research consortium was asked to quantify the role of ESBL in animal industry for human health. The “research lab” was the Netherlands: one of the most densely populated countries in the world for both humans and animals, with the highest antibiotic use in the world for animals and the lowest for humans. If anywhere, zoonotic transmission should happen there! Continue reading
A new paper by Hopman and colleagues (Andreas is also another author but is being modest) has evaluated the effect of removing sinks from the ICU. The trigger for this intervention was an outbreak caused by an ESBL-Enterobacter that could be related to contaminated sinks. The study looked at what happens if you remove all water sources from the ICU, and all water-related activities were migrated to a tap water-free solution. Continue reading
I blogged on mcr-1 (colistin resistance) in China last week, to share the latest reassuring data. Well, the paper on which todays’ blog is printed will be used to wrap tomorrows’ market fish (typical Dutch expression). Nicolle Stoesser (Oxford) send me the latest news, coming from a Nature Microbiology study providing evidence for the potential of spread of carbapenamases by flies and birds. Not reassuring at all, and potentially with major consequences. Continue reading
In this era of increasing patient choice, let’s imagine you were offered the choice between two identical looking hospital rooms. Your chances of picking up a multidrug-resistant organism (MDRO) are approximately doubled if you choose the wrong room. But you have no way of knowing which room is safest.
So what explains this lottery? The key information you have not been told is the MDRO status of the previous room occupants. One of the rooms was previously occupied by a patient with C. difficile, and if you choose this room, your risk of developing C. difficile infection doubles. And it’s not just C. difficile – this same association has been demonstrated for MRSA, VRE, Acinetobacter baumannii and Pseudomonas aeruginosa. Underpinning this association is the uncomfortable fact that cleaning and disinfection applied at the time of patient discharge is simply not good enough to protect the incoming patient.
It is well-established that fidaxomicin reduces the recurrence rate of C. difficile infection (CDI), but this study from my old research group at GSTT / KCL is the first to evaluate the impact of treatment with fidaxomicin on environmental contamination. The bottom line is that patients treated with fidaxomicin had less C. difficile contamination than patients treated with vancomycin / metronidazole.
In total, the rooms of 38 / 66 (57.6%) patients treated with metronidazole / vancomycin had one or more positive environmental cultures compared with 25 / 68 (36.8%) patients treated with fidaxomicin (P = 0.02). Similarly, when considering all of the sampled environmental sites (four per room), 68 / 264 (25.8%) were positive in patients treated with metronidazole / vancomycin compared with 47 / 272 (17.3%) in patients treated with fidaxomicin (P = 0.02) (see Figure below).
Figure: Environmental contamination with C. difficile in the rooms of patients treated with fidaxomicin vs. vancomycin / metronidazole.
I was asked to speak to a group of link nurses at Southampton Hospital earlier in the week, and thought I’d share my slides, here.
I am passionate about the importance of surface contamination in transmission: I still think it’s really under-rated. I am pretty sure that most healthcare workers would have no idea that your chances of acquiring C. difficile infection (and others) is influenced by who used the room or bed space before you. And who would believe that VRE could survive on a dry surface for 4 years? Or that touching a surface is as important as touching the patient in terms of acquiring contamination on your hands?
So I’m really quite interested in seasonality of infections. I first became interested in it when looking at increases in E. coli bacteraemia for ARHAI (report here) because of Jennie Wilson’s excellent paper showing seasonality of gram negative bacteraemia, echoed by similar observations and conjecture on warmer weather, more infection. This is true in hospitals as well as the community. Why would this be? We have tussled with increasing E. coli bacteraemia in the UK for a few years now. Goes up every summer, does not return to the baseline, goes up again next summer etc., etc.. Other countries have also reported this. I have heard some suggest this is due to longer hours of daylight leading to more barbeques and more sexual activity. Given that the majority of infections in the UK are >70 years of age, my senior years have no fears for me then.