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Possible Antibiotic for MRSA Superbug 210

Posted by CowboyNeal
from the supersquishing-the-superbug dept.
darkmeridian writes "Merck has discovered a possible treatment for methicillin-resistant staphylococcus aureus, or MRSA, a virulent superbug resistant to many current antibiotics. The new compound, platensimycin, was found in a sample of South African soil and works by preventing the bacteria from assembling fatty acids into its cell membrane. This mechanism of action is novel among antibiotics, most of which currently block DNA assembly or protein assembly. Of course, this product still has to undergo human testing, but apparently looks promising."
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Possible Antibiotic for MRSA Superbug

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  • Re:No need. (Score:5, Interesting)

    by MagicDude (727944) on Friday May 19, 2006 @12:56AM (#15363369)
    Viagara was an accident. They were testing phosphodiesterase inhibitors as a therapy for keeping heart vessels open. It didn't work so well, but they discovered the unexpected side effect of opening vessels in the penis when the subjects were reluctant to return their unused pills.
  • by Bushwuly (585191) on Friday May 19, 2006 @01:06AM (#15363408)
    I used to work in a residential facility for disabled children with severe/profound mental retardation, and those who had the hardest time were the ones that contracted MRSA. Because these kids had such significant physical problems, they were often in and out of hospitals and would contract the virus while admitted there. Besides the scary fact that this bug is prevalent in hospitals of all places, it is so dangerous and contageous to children that those who contract it have to be kept in isolation.

    Every day I would walk by the isolation ward and look in, just to let the kids know that someone was concerned for them. These children already had the odds stacked against them, and to top it off with the fact those who attended to them had to avoid all physical contact cut me to the heart. How sad is it to be a kid who can never be hugged, having to live without anyone touching them?

    If someone can isolate and develop an antibiotic that can cure MRSA, I'll be one of the first in line to shake their hand.
  • by NitsujTPU (19263) on Friday May 19, 2006 @01:56AM (#15363550)
    I've heard mixed reviews on that one, but I'm inclined to agree. It doesn't sound like a good long-term strategy for anything.
  • Doing research on a fruit, called mangosteen, out of southeast Asia I came across this article on PubMed (via NIH.gov) [nih.gov] entitled Antibacterial activity of alpha-mangostin against vancomycin resistant Enterococci (VRE) and synergism with antibiotics [nih.gov]. A natural fruit tree fights the toughest bacteria mankind faces; amazing.


    After learning about this fruit and its many documented benefits, I bought into the company [goxan.net] that brought it to the market in the US.

  • by jeff4747 (256583) on Friday May 19, 2006 @02:46AM (#15363698)
    When will Washington ban the feeding of antibiotics to cattle? I am referring to the use of antibiotics as a food supplement. It is insane.

    Well, at this point the antibiotics they are feeding animals is already resisted by a great many bacteria, such as the original penicillin. You won't be getting that from your doctor because so many things are already resistant to it. Instead, you'll get something like amoxicillin, which is quite different despite the similar name.

    Since resistance to these antibiotics is so prevalent, feeding them to cattle really doesn't matter. Resistance to one antibiotic does not trigger resistance to another.

  • by Cyberax (705495) on Friday May 19, 2006 @02:49AM (#15363714)
    There's "bacteriophage therapy" ( http://en.wikipedia.org/wiki/Bacteriophage_therapy [wikipedia.org] ) which really works (it was successfully used BEFORE the invention of antibiotics) and doesn't produce resistant bacteria.

    Sadly, there's almost no research on this topic.
  • by Baldrson (78598) * on Friday May 19, 2006 @03:32AM (#15363817) Homepage Journal
    The book Plague Time : How Stealth Infections Cause Cancer, Heart Disease, and Other Deadly Ailments by Paul W. Ewald [amazon.ca] outlines a number of interesting strategies for dealing more effectively with the battle against antibiotic resistance. Basically, if you insist on having a world where international transporters (jets, ships, cars, busses, etc) act like mosquitoes to facilitate human-to-human transmission of disease, you have to resort to some other public health measures so that viruses and bacteria (and parasites) are least capable of winning the evolutionary arms race.

    Among these measures is to target virulence rather than the pathogen itself. The reason is that a species of pathogen can have varying virulence and you want the last virulent to win the competition for the ecological niche (human body). Ewald gives an example of a particular protein used by a bacteria to convert human lung tissue to useful food -- a protein that costs the bacteria about 5% of its budget but has huge returns. Vaccinating against this protein can let the more benign variants beat out the virulent variants for the lungs of humans, and give the human immune system the kick it needs to construct antibodies to suppress further infection.

  • The problem with bacteriophages is that they are extremely specific - for the most part you need to determine the precise strain of a disease, which requires more expensive tests. You then need to fine a bacteriophage that fits that specific strain of bacteria.

    So until we start seeing much more significant resistance to antibiotics they're not likely to be cost effective.

  • Since resistance to these antibiotics is so prevalent, feeding them to cattle really doesn't matter. Resistance to one antibiotic does not trigger resistance to another.

    I beg to differ. Many families of antibiotics share the same core mode of action, with only a few side-chains different. E.g. the original Penicillin and modern Methicillin are both beta-lactam antibiotics, which attack bacterial cell walls (more specifically, the enzyme that assembles them). Penicillin resistance is due to the bacteria producing a new enzyme (beta-lactamase) which safely inactivates the antibiotic. Current Methicillin resistance has developed gradually, as each new variant of Penicillin is introduced, the enzyme mutates to accomodate it.

    If two antibiotics are similar enough, resistance developed against one can confer resistance against the other. Agricultural use of Avoparcin is widely believed to have led to the development of Vancomycin Resistant Enterrococcus (VRE),

  • by CrankyOldBastard (945508) on Friday May 19, 2006 @05:42AM (#15364163)
    I have to stress how lucky you are. I got a MRSA infection in 1997, following a Bankart Repair (shoulder surgery). Initial tests indicated that Ciproxin would work - but it didnt, as we found after trying it for a few weeks. I can't remember what the final antibiotic was - but it wasnt Vancomycin.

    A lot of ignorant people are saying "MRSA is no big deal, vancomycin cures it". Well in my case there was no way that a dose of vancomycin strong enough to get MRSA out of my clavicle, scapula and humerus wasn't going to do some pretty major damage to me. There was a shortage of beds in Intensive Care as well, so it was decided to treat me with some other drug - I was so sick by that time that it's kinda patchy (such as my not remembering exactly what antibiotic cured me), but I recall being told that they were going to treat me with this stuff for 10 days, and hopefully it would work, as it was the ONLY antiobiotic besides vancomycin that my strain would respond to. I was told that if I took this medicine for 14 days it would kill me by shutting down my liver.

    After 10 days I was a delightful dayglo yellow colour, but the bug had died. Meanwhile I have to live with the aftermath of septic arthritis, osteomyelitis and periperal neuritis. In practical terms this means my shoulder had the cartlidges (sp?) eaten away and the bone surfaces have an interesting "finish" where they grind together when I move my arm. The nerves that pass through my shoulder were damaged by both the infection and the antibiotic, and I have constant pain which feels kinda like a permanantly dislocating shoulder. I take a lot of oxycodone, and as a result dont crap real well. Every 6 weeks I get a nerve block which gives me a few days (typically 3 to 5) with much lower pain. Getting these injections into the brachial plexus so often carries a real risk of further infection or nerve damage though.

    It's the only time I've ever got a letter from a pathologist, as when they did the tests that finally found what antibiotics would work I got a letter in red ink from them saying "See your doctor NOW as you have a LETHAL INFECTION". By that time I had acquired the delightful aroma of rotting meat - leave a raw shoulder roast out in the sun for a few weeks - that was the smell 8 inches from my nose.

    I was having the wound scraped clean twice a day, with it being packed with all sorts of things to try to help the wound drain. There was a hole through my shoulder - it was possible to slide a 5mm diameter glass rod from the top of my shoulder, through the center of what used to be a synovial capsule and out the other hole in my armpit.

    So don't trivialise MRSA - it's really impacted on my life, apart from nearly killing me. And don't trivialise vancomycin, unless you consider potential organ failure as trivial. MRSA and vancomycin are both very nasty stuff.

  • by drgonzo59 (747139) on Friday May 19, 2006 @05:50AM (#15364190)
    MRSA is already here and is bad enough, but there is already fear of the vancomycin resistant staph. Vancomycin, as it is clear from your story, is a last resort antibiotic, when all others have failed. There is evidence that there could be a super-super-bug that would be resistant to vancomycin as well. The common mechanism of action of these antibiotics is to provent the assembly of the cell wall. It so happens that only prokariotic cells (which staph. aureus is) have this external cell wall structure to prevent them from "exploding" due to high internal osmotic pressure. So this cell wall has been and is a good target for antiobiotics.

    It is interesting how most of the antibiotics -- this new one and including the first one -- penicillin, are sythesized and produced by fungi. There is a constant battle for nutrition and space between the bacteria and the fungi -- some kind of an evolutionary yin and yang. One will always try to overtake the other and will develop new mechanisms for resistance or attack.

  • Re:Coming Soon (Score:4, Interesting)

    by arivanov (12034) on Friday May 19, 2006 @06:38AM (#15364311) Homepage
    I would not bet on that.

    Most Staph strains with antibiotic immunity gain it from a phague infection. While bacteriophagues are very large and complex there is not that much spare room for carry an extra resistance gene on top of what they drag around at the moment. It will most likely have to lose either the penicillin resistance gene or the tissue necrosis toxin gene to accommodate an extra antibiotic group resistance.

    In the first case it can be smacked on the head using conventional penicillin derivatives.

    In the second case the normal immunity mechanisms will take care of it. By the way, it is the necrosis toxins produced by MRSA which make it so dangerous, not the antibiotic resistance as such. They kill tissue around the infected zone before it actually gets infected creating the environment in which staph can trhive. In addition to that none of the immune system cells can traverse this dead zone and get to the staph either.

    This is all IIRC of course, as it has been very long time since I have done something with mol biol and microbiol.
  • by wizardofodd (762187) on Friday May 19, 2006 @08:05AM (#15364522)
    Talk about timing... 4 weeks ago I was diagnosed with MRSA. They kept me in the hospital in isolation for the first week. The MRSA was located in my right foot. It was so severe that the had to amputate it to in order to save my life. The worst part of the ordeal was spending 2 weeks without Slashdot. The best part was the spongebath with 3 of the nurses. :-)

    Now I'm at home taking a antobiotic called cefazolin every 8 hours until the remainder of the infection clears up. But now I get to spend all day reading Slashdot. I guess somepeople would give their right foot to be able to do that. ;-)

    Hey, what do you expect me to do, cry about it? Just keeping my spirits up.

  • I can't stand it. (Score:3, Interesting)

    by Fantastic Lad (198284) on Friday May 19, 2006 @02:20PM (#15367430)
    I've met people who have held up bottles of pills and said stuff like, "Wow! These are great anti-biotics. They made me better so fast! I'm going to save the rest of these because they're so good. I want to have them around for when I get sick again. --Which I probably will in a few weeks. I hate the cold season."

    And similar.

    In that particular case, I sat the individual down and explained how anti-biotics work and the importance of finishing ALL the medication. He nodded and seemed to understand, and then said, "Yeah, well, I'm going to save the rest of these pills for when I get sick again in a few weeks. I hate the cold season."

    It's at times like those when I feel strongly compelled to get on a rocket ship and nuke the planet from orbit.


    -FL

  • by NilesDonegan (136760) on Saturday May 20, 2006 @02:36AM (#15370977)
    I do research on Staph. It's frustrating to everyone doing this work that in 50 years, we have really just a handful of targets in bacteria to attack. Here are our targets and some examples of the antibiotics we use

    1) DNA replication/Gyrase (cipro)
    2) RNA synthesis (rifampin)
    3) folate metabolism (sulfa drugs)
    4) Protein synthesis (erythromycin, chloramphenicol, linezolid)
    5) cell wall (penicillin, vancomycin)

    What's great about this this new drug from Merck is that it's target isn't on the list above. It's a new target (fatty acid metabolism) and it's well tolerated by mammals.

    But it's not the only new one out there. Check out these papers on:

    a) targeting the proteolytic machinery of bacteria, i.e. clp proteases
    Brötz-Oesterhelt, H. et al. Dysregulation of bacterial proteolytic machinery by a new class of antibiotics. Nature Med. 11, 1082-1087 (2005)
    http://www.nature.com/nm/journal/v11/n10/abs/nm130 6.html [nature.com]

    and

    b) targeting Holliday junctions, i.e. how DNA recombines
    Gunderson Carl and Segall Anca, 2006. DNA repair, a novel antibacterial target: Holliday junction-trapping peptides induce DNA damage and chromosome segregation defects. Mol. Micro. 59 (4), 1129-1148.
    http://segall-lab.com/PDF/Gunderson2006.pdf [segall-lab.com]

    And don't forget to wash your hands! Make a researcher happy and save the drugs for another day!

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