**Standard disclaimer: these are my notes taken during the sessions, as accurate as I can make them, please let me know if any inaccuracies. I’m putting them here as others have said they found them useful. However worth re-checking anything before you re-quote it. If this continues to be useful, I’ll continue. If it’s clear i’m not reaching the standards of accuracy I’m aiming for, I’ll review future posting plans.**
More of the same – mainly a report back on the MDRO sessions again, especially some good looks at the wider picture and environmental/animal carriage. If you want to read two abstracts on MDROs I highly suggest two companion studies by the Tim Walsh group on `ESBLs and carbapenem-resistance in Karachi (90% faecal/site of infection swabs contain of CTX-M-15 ESBL beta-lactamase, approaching 50% NDM1 ). And the accompanying environmental study sampling bugs, bird droppings, water, basically showing that this is everywhere.
Same disclaimer – written in a hurry, may be numbers wrong, double checking recommended.
In the morning, Nick Loman gave a very, very useful talk for clinicians on what your bioinformatics department is really doing with their time, and all the questions that should be considered in whether you’re doing what you think you’re doing. In genomic analysis: rubbish in, rubbish out!
Honestly, any clinician who is starting out in genomics should review this and be aware of the issues.
Here are the slides he uploaded to slideshare (props!):
There was some discussion from Fournier about virulence, basically saying that virulence gene databases are similar to resistance gene databases (many, do different things, different info), and WGS currently not able to predict virulence. Some good reviews quoted with much more support for virulence genetics being much more about the loss of antivirulence genes. Frank Aarestrup spoke last and re-iterated that real-time pathogen surveillance in clinical practice will require real time data sharing.
The best studies of the day from me: from Tim Walsh’s group – two companion studies: one poster on faecal carriage of ESBL/CRE in a hospital in Karachi, and and oral session on the accompanying environmental study
here is the faecal carriage study :http://eccmid.meetingexpert.net/ECCMID_546/poster_124965/program.aspx
In a nutshell, when screening admitted patients for faecal carriage, 27% samples were NDM1 positive 90% (!!!!!) CTXM15 positive. Genes on diverse species and diverse strains. The normal E. coli is ESBL, and a fairly normal E.Coli is Carbapenem Resistant..
The evironmental study: http://eccmid.meetingexpert.net/ECCMID_546/poster_122365/program.aspx/anchor122365 Hassan presenting the environmental dissemination of MDRBs NDM and CTXM
In an analysis I’m highly glad I wasn’t doing the lab work for, birds droppings, insects, drinking water and surface/equipment (ICUs/oxygen masks…) around the hospital underwent screening for ESBL and CRE. Apparently to improve detection in flies and cockroaches you have to smash the bugs, and culture in LB broth. Take home message was that there was a diverse population of multidrug resistant bacteria – not just E.coli and Klebsiella, but Citrobacter, Enterobacter, you name it.. and it was detectable on all of the above.
As we already sort of knew, but hadn’t had shown quite this well before, this isn’t just a case of highly-hospital-adapted resistant strains spreading between patients. This is the demonstration of the fact that multi-drug resistance has become a widespread characteristic of the colonising micro-organisms on patients, animals, around the hospital environment and beyond. Unbelievably worrying, and the group should be applauded for measuring it. One can only speculate at the state of affairs at places where it isn’t being measured, or reported …
Many of the rest of the sessions were further demonstrations of this fact.
Marques-Saraiva: Companion animal UTIs – demonstrated to carry very similar resistant strains to humans. Abrahams talked about how Australia’s rigorous and rigid laws on imports, (and Island status) has probably helped protect it’s livestock against widespread colonisation with resistant strains. Bonnedhal talked about how there may be a significant avian reservoir of ESBL genes, showed some slightly miffed-looking gulls being sampled, and speculation about god only knows what is happening with the marine microbiome. Borjesson talked about some interesting data from the Swedish food monitoring program, with the aim of progressing knowledge on whether there is food to human transmission of resistance. Hard to say, but some nice comparisons of the plasmids found in ESBLS Enterobacteriaceae from food, colonisation strains and bloodstream isolates.
In the afternoon session, Trends in antimicrobial resistance (AKA I can’t believe it’s more MDROs)
The standout presentations were the Karachi group (already covered) and a presentation from the Glupczynski group in Belgium
Huang presented data from Belgium on carbapenemases. Pre2010 they saw sporadic cases, mainly from patients coming from abroad. Post 2010 – they saw rapid emergence and a completely different picture. In 2011 Belgian health authorities set up national detection guidelines. They’ve seen a diversification of the carbapenemases detected – OXA48 predominant, with KPC, NDM1 also common, and in diverse Enterobacteriaceae. There was a very nice demonstration of Meropenem diameters/MICs – suggesting EUCAST breakpoints miss 20% of their CRE . The Chair C.Giske (who said he helped set EUCAST breakpoints) said: CONVINCED, EUCAST need to change. Huang also said ERTAPENEM should be used as substrate for resistance screening. Chair said LESS CONVINCED.