Determining the Relationship between the carbon source for Escherichia coli and T1 Phage Growth Rate
Eric R I Chapman 1*, Aidan T Brown 1, Teuta Pilizota 2
- School of Physics and Astronomy, University of Edinburgh
- School of Biological Sciences, University of Edinburgh
Bacteria play a huge role in the human and natural world, for richer and for poorer, with their most well-known role being a pathogen. With the gradual reduction in antimicrobial efficacy, the promise of phage as a potential solution has gathered attention. For phage therapy to be successful it must be applicable in a wide range of environments.
In each of these environments, phage relies on bacterial ribosomes to takeover the bacterium. In exponential growth in environments with different quality of a carbon source to be metabolised, bacteria must find the optimal number of ribosomes to allow it to reproduce, and this number has been shown to alter linearly with the growth rate in each environment.
Here I have investigated how the bacteria-bacteriophage system dynamics depends on the carbon source being used by the bacteria. Escherichia coli, grown in a range of media with various carbon sources were exposed to T1 bacteriophage. In all cases the bacteria developed resistance to the phage at long time. However, the population dynamics of the system both post and during infection varied with both carbon source and the number of phage added. Through initial fitting of the phage dynamics by using a simple model, it appeared that the growth rate of phage was uncorrelated with the growth rate of the bacteria. Then, with a more sophisticated model we probe which factors are dominant in the growth of a phage population as well as whether there are multi-stage processes dominant within the dynamics.
These results show the relationship between carbon source and the progression of a bacterial populations response. These results contribute to the understanding of the dominance and structure of factors in the growth of phage which could result in significant differences between the rates of death and resistance development in vivo and in vitro due to differing environmental conditions.