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Fitness and compensation
A selection of talks on Infectious Diseases
An introduction to the world of microbes
- Dr. David Westenberg
- Missouri University of Science and Technology, USA
Vaccines and the fight against antimicrobial resistance 1
- Dr. Annaliesa S. Anderson
- Pfizer Vaccine Research and Development, USA
Neglected tropical diseases caused by tapeworm infections
- Dr. Wendy Harrison
- Chief Executive Officer, SCI Foundation, UK
Dengue, Zika and Chickungunya viruses
- Prof. Ana Fernandez-Sesma
- Icahn School of Medicine at Mount Sinai, USA
Hello. My name is Sebastien Gagneux and I am a group leader at the MRC National Institute for Medical Research in London. I'm going to talk about the role of Darwinian fitness and compensation in the evolution of drug resistance in bacteria.
I would like to start this presentation by introducing the concept of Darwinian fitness in the context of antibiotic resistance. I will then outline why we should care about the role of Darwinian fitness in drug resistance and present several ways fitness can be measured. I will discuss how the fitness of drug-resistant bacteria can vary depending on the particular drug resistance mutation, the environment, or strain genetic background. And we'll review various aspects of compensatory evolution and end with a few suggestions for future research.
Darwinian fitness can broadly be defined as the ability of an organism to survive and reproduce in a given environment. In addition to measuring the total or absolute number of viable offsprings, Darwinian fitness is often expressed as a relative measure. For example, as the relative fitness of a drug-resistant organism compared to the corresponding drug-susceptible form.
There are at least four main reasons why we should care about the effects of drug resistance in bacterial fitness. First, we would like to be able to make predictions about the future trajectory of the global epidemic of drug resistance, and I will show you an example of that. Second, we need to be able to evaluate interventions aimed at reducing the spread of drug-resistant organisms. For example, will the withdrawal of a particular antibiotic result in the reduction of resistance? Third, a better knowledge of the fitness impact of drug resistance could help us design better antimicrobials. For example, by focusing on compounds to which developing resistance to, will be particularly costly to the pathogen. And four, studying fitness in the context of drug resistance allows us to address fundamental evolutionary questions.