Exercise 5

How realistic do you think the simulator is?

Answer –

Ways in which the simulator is realistic-

The simulator does display bacterial division; the random nature of mutation is also highlighted in the simulation. Genes do have different functions that can interact and contribute to bacteria causing disease.

Ways in which the simulator is unrealistic-

There is no selection pressure such as the role of the immune system. There are many more phase variable genes in real bacteria and their interactions are often more complex. The mutation rates in the simulator are too high and the bacterial populations are too small. There is no simulation of environmental factors which in real life would affect the speed of cell division.


What advantages do you think using a simulation can have over real experiments?

Answer - There are several advantages to a simulation. The simplest is cost: once the simulator is written, it costs nothing to run. There is also time: in silico experiments can take seconds, so thousands of repeats can be performed. This makes simulations particularly useful for teaching because you can explore the behaviour of the model is a visual and accessible fashion without ever needing to enter a lab.

But simulations are also useful in research, although this particular example probably isn't research grade small modifications of the underlying simulation might be. Simulation can produce more precise results, for example, there is no way for a real experiment to precisely determine the state of every cell in a colony.


Do you think phage therapy is a suitable treatment option for Campylobacter infection? What further research may be required?

Answer – With the problem of antimicrobial resistance becoming ever more a problem, the need for novel antimicrobial treatments has never been greater. Phage therapy has successfully been used for the treatment of bacterial infections in some countries and its future use is becoming more and more likely. As a result, they may be useful for treating Campylobacter.

Firstly we need a better understanding of the relationship between phase varying each of the above genes and sensitivity to phage infection. We need to also understand how each phasotype may be met be the immune system. Finally, these principles need to be tested in live infection models.

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