Friday, April 19, 2013

"Conspiracy theories: How bacteria collude to harm us, and how small molecules might protect"

I attended the seminar this afternoon which featured Dr. Michael Federie from the University of Illinois at Chicago.  His presentation was great and really interesting.  As some of you may realize, there is a huge demand for the development of drugs to combat bacterial infections.  While there are many antibiotic medications already out there, the issue is that bacteria tends to become resistant fairly quickly to these drugs.  This resistance causes huge issues in the treatment of different infections.  Infections like MRSA are very common and can be tough to treat.  While it used to be that these types of infections where typically hospital acquired, they are now found in most environments.  Some can even live on surfaces for several weeks in the right conditions.  Dr. Federie has set out to take a different approach to combat bacteria.  Instead of developing another antibiotic, he is looking to develop a drug which has the ability to block or stop the communication between bacteria in the development of the toxins which are harmful to the body.  He has identified the fact that bacteria communicate through pheromones, and has identified 4 Rgg regulators and three short peptide pheromones.  He has figured out a way to use this information to turn off and on the bioluminescence of a certain strain of bacteria and is hoping to apply this idea to the bacteria's ability to produce different toxins.  He stated that they are currently asking three questions in his lab:
1) What are the mechanisms that sustain communication?
2) What do bacteria do with this info?
3) How does communication contribute to disease?

 I find this idea pretty fascinating and it is an interesting approach to the battle against dangerous bacteria.  His presentation implied that each individual bacterial strain has it's own pheromones and regulators for communication.  By pinpointing the strain, treatment could be very exact.  However, it left me wondering on the practicality of this approach in the current world of medicine. 

One question I proposed to him was if a drug of this type was to be used to treat a patient with a serious infection, would we first have to wait for the lab results of the exact bacterial strain before initiating treatment?  This could run into problems as not all lab tests are able to be turned around very quickly.  Some could take a week or more, so would that patient have to wait for the lab results while the infection spread in the meantime.  He stated that he wasn't sure how this would work and it would likely mean that we would have to develop a faster lab test in the identification of the exact bacteria.

My next question was, how would this drug or treatment affect the "good" bacteria in our body?  While we generally think of bacteria as being bad, there are many that we can't live without and serve and important role in maintaining our health.  An example of the issue of destroying the "good" bacteria can be seen with the issue of the infection of c-difficile.  With the over use of antibiotics, many have destroyed the "good" bacteria in the gut, leaving them at risk of developing this infection.  C-diff is becoming more and more common and it can be directly linked to over use of antibiotics.  Something to think about next time you have a cold or bug and you run to your Dr to ask for antibiotics.  C-diff is a very unpleasant and can be potentially life threatening infection to have and is not easily treated.  Although a somewhat newer treatment for it is actually a fecal transplant which is to help restore the "good" bacteria to the colon.  His response to this question was that they were not sure yet how this may affect other bacteria in the body.

The third question I proposed was if one was to be treated with this type of drug, would they be required to continue this treatment for the rest of their life if we are not destroying the bacteria, but simply stopping their communication?  Would this shut down communication permanently even if the drug was discontinued and the bacteria continued to live and reproduce?  He stated that this was something that would have to be investigated further.

Another question that came to my mind was the fact that bacteria mutates and evolves, so I wonder how easily a drug like this would be able to keep up with this. 

Overall, it was a very interesting talk and it is definitely and interesting approach to treating bacterial infections. 

4 comments:

  1. Just happened to run across this and thought this would be interesting to add. Here's another approach being researched to battle bacteria

    http://www.the-scientist.com/?articles.view/articleNo/34784/title/The-Upside-of-Suicide/

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  2. Seems like a very interesting seminar. When reading your synopsis of the findings, I, too, had the same question! What would happen to the bacteria if it's never destroyed, but simply stops communicating? The idea seems unprecedented, but there seems to be a lot of unanswered questions. Nonetheless, I'd love to see the future of this mechanism.

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  3. Good questions. I was also wondering about adaptive resistance to pheromone blockers. I wonder how effective his blockers are currently? Do they prevent the reproduction of all bacteria? I wonder how many pathways control pheromone communication in bacteria, and how complicated it would be to regulate that versus antibiotic treatment.

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  4. After leaving the talk I had several questions on my mind similar to the ones you brought up. Perhaps this line of research is a dead end if all these problems can't be solved, but if they somehow can be overcome, the payoff would be immense (obviously).

    I didn't quite catch all of the communication pathways Dr. Federie discussed, but it seemed like he talked mostly about the bacterial communication system involved in biofilm formation. Since bacteria secrete toxins after forming a biofilm, I don't know how harshly his treatment methods would affect our natural, good bacteria. It seems like they may be unaffected if they don't have active Rgg genes. (This is just my mind spewed out on paper, I don't know if 'good' bacteria have inactive Rgg genes...).

    Another thing I'm very uncertain about but feel like sharing in this comment is that maybe the patient wouldn't have to get continual treatment because the immune system would eventually identify the infectious bacterial cells and ingest/destroy them. Perhaps the treatment proposed in the study would leave the infectious cells solitary, helpless, and easy to gobble up by WBCs? Again, just my thoughts.

    Great talk, I'm glad I attended.

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