
To further comment on my first statement: I have done a lot of reading on P. aeruginosa. This is the actual name of the Psuedomonas bacteria that inhabit the lungs of CF patients. One thing that interested me is how they have adapted to survive in the lung. The big thing that really affects the lungs is the production of a toxin called CFTR inhibitory factor (cif). This toxin is created and it induces the degradation of the CFTR. Like I said in the medical history, CF is caused because there is a mutation in the CFTR gene causing none or little CFTR to be made in the first place. Knowing this you can you can see the problem that cif causes the lung. If someone is only able to make small amounts of CFTR in the first place and then they get P. aeruginosa, it makes the initial problem worse and makes it harder to get the bacteria out. So in this case the bug is winning. Stopping the production of CFTR makes the environment for the bacteria that much better. Another thing I read is that when Psuedomonas are in a good environment they all cooperate with each other and "help" each other with survival. When antibiotics are introduced and the environment turns hostile, those little suckers turn hostile on each other. For every bug their own! Like I said though, they multiply so quickly I have to come in so often. If they would slow down they would live on a little longer. Then again evolution has "taught" them, the most important thing is to pass on its DNA....
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