Tuesday, 21 July 2015

Jan Kreft Intervention @ LeSpar AMR Workshop - The Nottingham Edition

Jan Kreft from the University of Birmingham shared with the audience at the MediCity a very interesting perspective (with loads of questions outside the box) on Antimicrobial resistance in the human gut. But before we move on to Jan's participation, if you haven't had the opportunity to read also Chris Dodd's contribution and Rachel Gomes' contribution, already posted in the blog, just click on the names to do so.

Now moving onto Jan's presentation, his most remarkable shared views and points are listed below:

  • There is diagnosed antimicrobial resistances present in people who have not taken any antibiotics ever or that for a long time never took them. How was such resistance acquired?
  • Resistances are found even in individuals from the Yanomani tribe in Brazil's 'Amazon' [1] that were never in contact with humans.
  • The prevalence of antimicrobial resistance will decline if the use of an antibiotic is discontinued because of a fitness cost of carrying the resistance. Resistance rises if an antibiotic is used because of positive selection for the resistance. So we have to ask ourselves if discontinuing works? And why does resistance persist?
  • Fitness costs, diversity, variation of costs and diversity of microbes, hitchhiking (when a gene is coupled to another gene that is positively selected, e.g., resistance to mercury). We have to consider an approach to the real world.
  • There is a huge bacterial diversity in gut also affecting the spread of plasmids. There are huge numbers of bacteria in the gut, ~ 5E13 individual cells. The heterogeneity  goes from small to large scale.
  • Will a more prudent use of existing antibiotics be enough? What can we do? Give a narrower spectrum of antibiotics, higher dose or lower dose? Should we give a combination of two drugs rather than one? Should we invest in new drugs, ideally new classes of drugs (new strategies)?
  • On the other hand should we start attacking directly the resistance genes and plasmids preventing a possible transfer? Should we prevent infections as they mean fewer treatments? What kind of research do we need? 
  • We need to consider consequences of diversity of strains, plasmids, resistance genes and quantitative models to optimise treatment at population level.
  • We cannot deal with complexity without models. Take for example the developed iDynoMics software, a free software available online.
Next post will have the final contribution taken from the Learned Society Partnership seminars on antimicrobial resistance - Nottingham Edition, that took place on the 7th of July this year. It will be about getting funding (by Lizzie Garratt) and some final notes on the most important questions that have emerged from the event. Hope to see you soon, have a nice time!

[1] The Yanomami: An isolated yet imperiled Amazon tribe, The Washington Post, [http://www.washingtonpost.com/wp-srv/special/world/yanomami/], last visited on the 21st of July 2015, last update on the 25th July 2014.

2nd image kindly taken from Natural selection, Wikipedia, [https://en.wikipedia.org/wiki/Natural_selection], last visited on the 21st of July 2015, last published on the 14th of July 2015.

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