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Biotech Science

Using Old Medications to Defeat Tuberculosis 70

TastesLikeCoughSyrup writes "Antibiotic resistant tuberculosis is spreading like wildfire in the developing world. While many researchers are looking for new drugs to combat the disease, those efforts could take years to bear fruit. Meanwhile, two scientists at the Albert Einstein College of Medicine have learned how the drug clavulanate can destroy the defenses of tuberculosis, making it vulnerable to medications in the penicillin family. The best part: it has already been approved by the FDA so doctors can start using it immediately."
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Using Old Medications to Defeat Tuberculosis

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  • by xmas2003 ( 739875 ) * on Saturday October 27, 2007 @01:33AM (#21137701) Homepage
    Research page at Blanchard Lab [] (part of the AE college of medicine) and the ACS paper [] about their research.

    Can't say I understand this stuff, but for those who do, these probably should have been in the story snippet.
  • by wizardforce ( 1005805 ) on Saturday October 27, 2007 @01:35AM (#21137719) Journal
    It's a beta-lactamase inhibitor, it stops beta-lactamase from cleaving the 4 atom ring of penicillin-like drugs. This ring is very important in the function of Penicillin which actually prevents the building of cell walls in gram-positive bacteria. these bacteria need a thick cell wall to keep from bursting. this drug in of its self does little, only combined with penicillins does it revive the drug's germ killing power.
  • by wizardforce ( 1005805 ) on Saturday October 27, 2007 @01:47AM (#21137771) Journal
    their research works on similar principles to the slashdot article although they work by very different pathways. The slashdot article is about a [penicillin degrading enzyme] inhibitor; penicillin inhibits cell wall synthesis which kills gram-positive bacteria. The research page you linked is about developing inhibitors to several amino acid/nutrient pathways that are common in these kind of bacteria but are very different than the pathway(s) penicillin acts on.
  • by wizardforce ( 1005805 ) on Saturday October 27, 2007 @02:25AM (#21137903) Journal
    bacteria can be fought nearly indefinitely by bacteriophages which evolve along side the bacteria in a never ending arms race, viruses are far trickier than that. Viruses evolve on very short timespans exceeding bacteria's rate of evolution in many cases so if there's something to fear it's them. Although even HIV has a weakness, one significant one has already been found in populations in Africa. It's an altered gene to be precise, one that alters a cell receptor on the outside of our cells that is a key site for HIV to bind to and gain access to the cell.
  • by darekana ( 205478 ) on Saturday October 27, 2007 @02:26AM (#21137909) Homepage
    Amoxicillin-Potassium Clavulanate Combination

    A fixed-ratio combination of amoxicillin trihydrate, an aminopenicillin, and potassium clavulanate, a beta-lactamase inhibitor, used to treat a broad-spectrum of bacterial infections, especially resistant strains.
    from CureHunter []
  • by penguin king ( 673171 ) on Saturday October 27, 2007 @05:12AM (#21138503)
    The FA mentions use of clavulanate, if you read the abstract for the ACS article linked to by the FA you will see there are three beta lactamase inhibitors - sulbactam, tazobactam, and clavulanate - trialled.

    Apparently nobody really has tried beta-lactam antibiotics in this indication, but it seems suprising that any medical professional would consider this a "one-two punch strategy". Realistically this would be one combo of a multi hit process. Modern day TB therapy always includes a specifically chosen 3-4 drug combination. This combination depends on where the infection was contracted along with any characterisation of the strain that is possible. This is simply because if you feed a drug that's not killing it, you're selecting for resistance to that drug. If physicians start using beta-lactamase inhibitors they'd better be careful because there are already several examples of other infections resistant to clavulanic acid (just google search).

    Whilst the article reports this as if it is a major breakthrough, this is purely sensationalism. It is a minor breakthrough in a major problem.
  • Re:In other news... (Score:2, Informative)

    by penguin king ( 673171 ) on Saturday October 27, 2007 @05:16AM (#21138529)
    Or the antibacterial agent had no antifungal activity? Keep in mind bacteria are prokaryotic, and yeast eukaryotic...
  • by TheMohel ( 143568 ) on Saturday October 27, 2007 @12:17PM (#21140529) Homepage
    It's an interesting study, and they're doing it right, but there's no particular breakthrough yet. This is an in vitro study with no clinical implications yet. TB is a significant problem where I work (I'm a doctor in the Western US), but there are some hurdles to get over before I can start using clavulanate.

    Clinical utility is the Holy Grail here - the biochemical activity of a drug is critical, but the effect of the drug on the infection in an infected person is a lot more complicated. You have to get an effective concentration of the antibiotic into the area of the organism, get the bug to take up appropriate quantities of it, and not injure the patient in the process. Every step of this can kill an otherwise promising use of the drug.

    In the case of clavulanate, we know that it causes significant side effects. I use it a LOT in kids (Augmentin is your friend for a variety of conditions, and clavulanate is what makes Augmentin Augmentin), and it causes pretty impressive diarrhea at fairly low doses. Diarrhea, especially if it involves altered intestinal flora, is a set-up for C. difficile colitis, which can be deadly. If we need high concentrations of clavulanate, we may not be able to give enough of it to patients. Or there may be other toxicities, although it's been quite benign in widespread use to date.

    Another problem is that the bacterium can mutate proteins to avoid drugs, and TB is pretty good at this. MDR TB didn't happen by accident, and mutation of beta-lactamases to avoid clavulanate is not unheard of. Overproduction of the enzyme is also possible, and would then increase the required dose of the drug (and see above).

    A final problem is the physical defenses of the bug. The cell wall for TB is quite effective and strong, and the bacterium has a variety of transport mechanisms to get antibiotics out of the cell. Again, we may not be able to get enough clavulanate into the cell long enough to kill it.

    Having said all of that, I'm delighted both that the work is being done and that these initial results are promising. It will be fun to see what happens clinically.

The other line moves faster.