Tuesday, November 1, 2011

Cheatobiotics: how can we use them?

http://www.zoo.ox.ac.uk/group/gardner/media/NewScientist_Oct_2011.pdf


This article is SO interesting and provocative. It was found and contributed by one of your classmates (Danielle J., yes extra credit for being chosen for the blog!). By all means read it (you won't regret it), and think about the way that the article proposes we exploit these lazy, cheating, bacteria. Make a list of the vocabulary in the article that you have learned already in this course. Would you have understood this article in the same way last August as you hopefully do now? What do you think--about the social behavior aspects of the article, about potential benefits, what could be some of the problems with the proposed therapy (think horizontal gene transfer, among other things), microbial evolution, can you relate bacterial behavior to successful human behaviors? Oh, so many things to think about. Share what you are thinking!

11 comments:

  1. I don't think I would have really understood a great deal of the vocabulary, yes I would have been able to figure it out, but truly understand probably not. Some of the vocabulary that stands out is Biofilm; never heard of it before and now I see it in ads and hear others talking about it. Mutant bacteria, little rebels that fight themselves; MRSA, again I knew what it was but didn't understand the whole picture, which is really scary and finally quorum sensing, a very basic thought that is very involved at the same time. If we beat them at their own game, then maybe we can win. The way we have been doing it isn't working, bacteria are smart and are consistently a few steps ahead of us. Creating new antibiotics isn't the way, we need to block them and just as the human body can attack itself, we need to use cheaters to attack and self destruct themselves.

    The flaws are semi obvious in that it only takes 20 mins for a new generation of bacteria. Can we really get ahead of them? Their evolution is very fast forcing us to really think outside the box and try to figure out how we can cheat and exploit a bacteria's social habits.
    Maybe by doing this and seeing that our old ways although initially very successful are no longer viable. The odds are against you due to resistance and what's laying in wait at the hospital, bacteria have evolved very well, yet we have remained static.

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  2. The article highlighted many vocabulary terms such as: population, MRSA, mutant, evolution, strains, and antibiotic. I definately would not have understood the topics in the article as well as I did had I not taken this course. Originally, I assumed that all mutations and mutagens were bad, but now I understand that some mutaions actually provide the bacteria with advantageous new genes.
    Before reading the article, I had no idea the field of sociobiology existed or that there would be such productive cross-over between thier field and the medical field. Most people do not think of bacteria as living organisms that communicate amongst populations, but this article really highlights this characteristic.
    The biggest problem I can asses from the theory of adding cheating bacteria into a population is elimination of the noncheating strands. Although the cheaters are able to out-compete the noncheating strands there is still some competition that creates a biological balance. Completely eliminating an entire population will disrupt the balance, and may cause more unforseen issures in the furture.
    I do understand that there are many risks with innoculating an infected person with a cheating strain, but I believe that the benefits out weight the risks. Either way, the paitient is sick with virulent bacteria that are known to be semi-resistant to anitbiotics. Saving some lives is better than saving none.

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  3. Yes, I would have understood this article in the same way as I do now. I have had a lot of experience reading and analyzing scientific journal articles, and have a strong background in biology.
    They propose tackling superbug infections by deliberately encouraging the growth of cheater strains, perhaps by injecting them into people. Cheater bacteria survive because they outcompete virulent bacteria and do not produce virulence factors. This could be beneficial because we could inoculate those who are vulnerable with a dose of the cheater bacteria, thereby improving their conditions. But, this could be risky because of the reproductive capacities of bacteria. The non-virulent bacteria could receive a plasmid or part of a plasmid that encodes for the ability to produce virulence factors. This would allow the cheater bacteria to proliferate and be virulent. The bacteria could even spontaneously mutate on its own to become virulent. Also, the article stated that the organism that causes malaria alters its reproductive strategy depending on how many of its fellows are present in the same human and how closely related they are. This could be dangerous because the bacteria would constantly evade immune response.This treatment sounds very good in theory, mainly because of the rise in antibiotic resistance. But it is still to be seen if society would agree with inoculating people with cheater bacteria as a viable form of treatment.

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  4. Before taking Microbiology, these are the words I never heard or did not understand fully: biofilm, quorum sensing, virulent, fruiting bodies, spores, and MRSA.
    The article was written well for the lay person, so I would have understood, but I have a much better, fuller understanding now.
    Regarding antibiotic resistance, I think that it will be a work in progress from now on to stay one step ahead of infectious bacteria. As soon as we come up with a treatment to stop them, they will, through horizontal gene transfer, be able to get around that treatment with something new. I like the idea of using themselvs against each other. I also think that we are going to have to learn to be smarter about antibiotic drug use,and to go back and revisit basic hygiene.
    I think that everything in life is a mirror of everything else in life, and there is no better example than the cheater bacteria. We see this behavior all of the time in humans. If I can get something without having to expend the energy, then I will take advantage of that. You can also see that too much of one behavior leads to disaster, and that moderation is the name of the game.

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  5. The information from this article would not have been as clear to me as it is now if I had tried to read it back in August. Now that I have more insight on antimicrobial resistance and the use of antibiotics and the lifestyle and survival techniques of bacteria, I am able to obtain much more information from this article. The vocabulary that really stood out to m was quorum sensing, biofilm, fruiting body and antimicrobial resistance. We also would not be able to understand what pseudomonas was if we did not address it and work with it this semester in lecture and lab.
    I never really thought about the communicative side of bacteria I guess because I never really thought of bacteria as a living thing that is trying to survive, strategizing ways to evade death and harm us. I do think that we need to stop them from communicating and that is a pretty big step if we can do this because if they cannot communicate, then they cannot form protection such as endospores to survive. We could potentially save lives and improve a person’s situation if we can generate mechanisms that mitigate and prevent social interacting amongst bacteria ( such as injecting an ill person with a strain of cheater bacteria) then we have a chance to save our cells and live; however there are risks associated with these bacteria. In relation to what we learned in class about horizontal gene transfer can be applied to this situation. The non-virulent bacteria could potentially inherit plasmids that code for the ability to promote virulence factors and replicate spontaneously which enable the cheater bacteria to become harmful and virulent to the host.
    Energy conservation is the main thing that humans try to preserve everyday in order to mitigate any potential overuse. Any energy that we have preserved in the future will allow for better performance and quite possibly longevity which is the same idea we can apply when we relate our behaviors to that of cheating bacteria as far as the concept of them stealing protein to avoid making chemicals such as pyoverdin. It is very important to pay attention to what these bacteria are doing in their natural environment because we have to figure out ways to stop quorum sensing, chemical production etc. I think that this is an option, but not a great option. We probably should explore more opportunities to solve this growing problem.

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  6. The vocabulary used throughout the article: Spore-formers, virulence factors, biofilms, drug-resistance, MRSA etc. Most terminology in regards to bacteria discussed in this article I would not have been able to understand last August. However, I understand how bacteria actually work and how they are building up drug-resistance to the antibiotics used for treatment. I also learned that bacteria have mobile genetic elements, so these bacteria can pass from one bacteria to another via HGT. S. aureus for example is multi-drug resistance to every antibiotic now, and this could eventually be a problem to create drugs to combat the bacteria that gain R plasmids. I think that its interesting that the mouse infected with cheater strains is most likely to survive longer than the mouse just infected with the bacteria. It could be beneficial to give cheaters to people who are already infected with the normal strains of bacteria. This may help save lives in the future and could potentially be able to treat many other kinds of infection. However, the problems with this therapy is that the bacteria could get a strain that becomes virulent, mutates and evolves which would harm the host. Bacteria behaviors are similar to successful human behavior in the sense they can communicate and use up energy. But, bacteria sends chemical signals for communication for virulence factors to be produced. I think it is interesting and frightening at the same time that bacteria keep evolving until treatment is limited until no antibiotics are available. It is essential to stop the rapid growth of multi-drug resistance in bacteria by eliminating their ability to communicate and produce the chemicals that will harm the host.
    Amy W. M/W

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  8. No, I would not have understood this article in the same way last August as I do now. One of the few things I knew about bacteria was that it can give us diseases. Without this class I would not have understood virulence factors, biofilms, pathogens, and antibiotic resistance the same way I do now, to help me understand how cheating bacteria works and how some bacteria can be beneficial.

    I think there are many potential benefits. Antibiotic resistance seems to be becoming less effective because bacteria is continually changing. We could try to use these cheaters instead of antibiotics. I also think that because of the experiments done, cheater strains might be more beneficial. It is a good change to inspire more people to research cheater strains because of a potential profit from discovering and it might be more beneficial. However, with minimal research on cheater bacteria, people might be skeptical on how to test its effectivity and if they should use it on humans. Along with the benefits comes problems. One problem may be that since we do not know too much of the bacteria genome, if it mutates, we don’t know what will happen. Since cheaters take over a population, they can lead to extinction. Extinction may pose more problems in the future generations but we wouldn’t know until it might be too late.

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  9. Yes, I believe I would have understood this article the same way as I do now. I have read scientific and nursing journals, articles, because I had been an LVN for so many years now even though a lot has been forgotten because I specialized in Mental Health. But bacteria…cheating? Even BACTERIA are lousy little cheaters, doing anything they can to gain an edge. This “cheating” mechanism forces other bacteria do all the work while the lazy bacteria save their energy, grow faster and out-compete other cells. When bacteria invade a host, they exchange chemical signals that activate genes responsible for producing virulence factors — toxic molecules that break down connective tissue, stop cellular defenses and wreak cell-level havoc, creating an environment in which the bacteria can flourish. Bacteria are both good and bad. Without bacteria we would die, but some bacteria could easily kill us: depending which ones they are. Good bacteria are those we need to survive; they are there to digest our food (in our intestines) and to live on our skin and in our mouth. By doing so they provide a protection against bad bacteria, that make you sick, which are known as pathogenic bacteria. Those opportunistic bacteria jump at the chance if your immune system is weakened, or if they manage to get into your body via wound, bite, airborne, etc. Anyway, the simple question has a complicated never ending answer.

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  10. I believe I would have understood a good amount of information that is stated, however, I would not have understood this article in the same way I do now. I would be able to recognize some of the names and I knew what bacteria could do. If I had not taken this class I would not have understood virulence factors, biofilms,and antibiotic resistance the way I do now.

    I think that there are many benefits. Antibiotics seem to be becoming less effective because bacteria is is now able to change and become antibiotic resistant. This is where cheater strains might can potentially come into play.

    R.Davis
    T/Th

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  11. I believe I wouldnt have understood this article to its full potential. Terms like virulence factors, biofilms, pathogens, spore formers would have been a blur to me. Now that we are at the end of this class I have a much better understanding of the terminology used in this article.
    Cheater strains of bacteria are very beneficial. Like they stated in the article, it could save lives. In the hospital setting catching pneumonia is very common and a huge threat. I feel that instead of waiting for people to become infected and then treating them, introducing the cheater strains beforehand is much better. I does sound a little crazy, but in the case of potentially saving many, it does not.
    When those that are immunosupressed catch pneumonia, the last thing they need are the side effects. If a cheater strain is introduced to each patient, then there chances are much lower.
    Which antibiotic resistant bacteria on the rise, I feel cheater strain bacteria is a great opportunity to fight back against the pathogens.

    Oddly enough this article made me think of the unknowns. Thinking of the bacteria that benefit from other bacteria doing work, made me think of those in class walking around trying to figure out who had theres, and then copying what they were doing! Little cheating bacterias in class!!! LOL

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