National and international surveillance of antibiotic resistance 1

Published on December 31, 2009 Updated on August 31, 2016   38 min

Other Talks in the Series: Antibiotic Resistance

0:00
Hello, my name is David Livermore, I'm Professor of Medical Microbiology for the University of East Anglia in Norwich. I'm also Public Health England's lead on Antibiotic Resistance. And for 14 years, I headed Public Health England's National Reference Laboratory examining antibiotic resistant bacteria in the United Kingdom. What I want to do in this two-part presentation is to look at national and international surveillance of antibiotic resistance.
0:38
In this first part, I want to look at how data can be collected for surveillance of resistance. Why we seek to do surveillance, and some of the pitfalls and challenges with the data. In the second part, we'll look more at some of the data that have been collected and their interpretation, and how that can be used to assess the success or failure of interventions.
1:14
The reasons to do surveillance of resistance are really pretty obvious. Firstly, to identify changes in prevalence and trend, to detect new types of resistance as they emerge. Is the MRSA rate going up? Is it going down? Have we started to see something new appear? Resistance to Carbapenems in Gram-negative bacteria, for example, or new emerging Colistin resistance. Surveillance is also important to assess the coverage of empirical therapy. Now this always comes as a surprise to the non-medics, but usually you start treating an infection without knowing what the pathogen is. You've got a sick patient there. You've clinically diagnosed them as having urinary tract infection or being potentially septic. They need antibiotics now! Not after the two days or so that is going to take you to grow the bacteria into test which antibiotics are susceptible to. So, you need an idea of what are the most likely bacteria in urinary tract infections or sepsis or whatever and what the local prevalence of resistance is, so you can choose what antibiotics to give that patient upfront here and now before you've got the susceptibility results for the particular organism from the lab. Hopefully, after two days, once you do have those results, then you're going to be fine with the treatment. You'll step down from a broad spectrum antibiotic, one that's covering all the likely types of pathogen locally in that clinical setting, to something narrow spectrum that's tailored against the particular bug that's been growing from the patient. Lastly, we need surveillance to assess the impact of interventions. We take steps, improvements in infection control, better hand hygiene, whatever to try to combat our problems, well, let's say MRSA or Clostridium difficile. We need surveillance to know if our interventions have succeeded or if they failed.
3:33
Behind all this, it's axiomatic that use selects resistance. If we think back to the pre-antibiotic era, resistance was extremely uncommon. It was really confined to bacteria that were inherently resistant. Pseudomonas, for example, always has been, always will be a relatively impermeable bacterium with a lot of efflux activity. But as we've come to use antibiotics, we've selected for those strains which have acquired resistance, they survive, whereas more susceptible strains are killed. And if you doubt this, look at bacteria for example from the Murray collection just put together in the 1930's, they divide. They completely lack acquired plasmid-mediated antibiotic resistance genes often above the occasional mercury gene. Whereas nowadays, 60% of E. coli have got plasmid-mediated beta-lactamases of one sort or another. And 90% of Staph. aureus have got staphylococcal penicillinase. So, there's been a vast change in bacteria under the selection pressure of antibiotic use. Now, we see a repeated pattern whereby we introduce a new antibiotic to begin with, we have a virgin bacterial population all susceptible to that antibiotic. But, gradually resistance emerges with bio-mutation or gene transfer. It emerges in successful strains which then spread among multiple patients and countries. Thirdly, there is a relationship, we'll look at a few examples of this later on. There's good evidence that resistance prevalence tends to be highest where antibiotic use is greatest. The selection pressure is most, so this is the most accumulation of resistance. And lastly, we see a few instances where resistance is very directly selected during therapy. If you treat tuberculosis, for example, with any one of anti-tuberculosis agents, you're pretty well guaranteed to select resistance during therapy. And if you treat, say Enterobacter bacteremia with a third-generation cephalosporin there's about a one-in-five chance that during that treatment, you will select a mutant that makes a large amount of its chromosomal beta-lactamase and is resistant. So overtime, resistance has accumulated underscoring that need for good surveillance.
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National and international surveillance of antibiotic resistance 1

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