Potential Cure For Antibiotic Resistant Infections 127
kpw10 writes to let us know about research to be published this week that offers hope in the battle against multi-drug-resistant bacteria. "Researchers at the University of North Carolina at Chapel Hill have discovered that two drugs used to treat bone loss in old folks can both kill and short-circuit the 'sex life' of antibiotic-resistant bacteria blamed for nearly 100,000 hospital deaths across the country each year."
Re:short term solution (Score:5, Informative)
Bacteria != viruses (Score:5, Informative)
Go ahead - laugh it up (Score:4, Informative)
Starts out like an ingrown hair or pimple. Might even be a spider bite. Then it gets angry. Take a large marble...light it on fire and have it surgically planted underneath, say, two layers of skin. Day three and the redness is now inches in diameter and the bump is still growing and...damn! It hurts! Burns like hell! Pimple my ass! Get that thing out of there! You can't sleep from the pain and you find yourself wondering which would be the better method to dig it out: kitchen cutlery or claw-hammer. In any case, if you don't have a doctor lance it, you're going to have to do it yourself.
Day four and it is open, draining and talk about cheese!! The stuff draining from the now open wound is so toxic, it blisters the surrounding skin. Makes it a bit difficult to remember to trash your clothes, bedsheets, etc., but at least the burning has lessened...a bit.
Ten or twelve days later, after finally getting on an anti-biotic (tetracycline?) that can put up a fight, the fluid draining out is almost stopped, the redness is almost gone and a bit of scar tissue is starting to form. Good news is, now that you know the routine, you can put up a slightly better fight next time - and there will be a next time...unless you died from this incident, of course. You did wash your hands before you helped your kids get dressed this morning, right...?
Re:Bacteria != viruses (Score:1, Informative)
Of course, antibiotics also kill useful bacteria (e.g. those that help you to digest milk and salad), so antibiotics are not really a good idea against a common cold.
Re:Unnatural Selection (Score:3, Informative)
Re:Bacteria != viruses (Score:5, Informative)
Huh? That's not even wrong. There is no reason to use antibiotics in a viral infection. Period. Now, there are a couple of real life caveats to this: Firstly, viral infections can alter host defenses (usually by trashing the lining of the respiratory system - essentially making holes in it - which allow bacteria to invade. The classic case is Haemophilus Influenza pneumonia that occurs after an influenza infection. Secondly and more commonly, a doctor may not know if the infection is viral or bacterial and antibiotics are often (likely too often) added empirically.
But bacteria "don't keep the immune system busy".
Re:For a change, this is actually interesting. (Score:4, Informative)
Re:Unnatural Selection (Score:3, Informative)
Before even penicillin, there were the miraculous sulfa drugs, which block a bacteria's ability to make folic acid: bacteria learned to uptake folate just as we do.
Beta-lactams like penicillin prevent bacteria from making peptidoglycan, the material of their cell walls: bacteria came up with beta-lactamase to break it down.
Better beta-lactams like oxacillin and methicillin were developed to be more effective at killing bacteria before lactamase neutralized them: mutant forms of proteins involved in making peptidoglycan (and were resistant to binding lactam drugs) began to proliferate, and now we of course have Methicillin Resistant Staphylococcus Aureus to deal with. (And studies have shown that MRSA bacteremia is just as deadly as regular SA, even correcting for the fact that MRSA tends to hit hospital patients. The rise in community-associated MRSA suggests it can fend for itself in the wild as well.)
Quinolones attack bacterial topoisomerases, the enzymes they use to wind and unwind DNA: mutant topoisomerases beat these.
Macrolides (most of the -mycin family) and oxazolidones bind to bacterial ribosomes to stop protein translation: modified ribosomal subunits beat these.
Vancomycin prevents peptidoglycan formation in by preventing incorporation of the monomers that make it up: modified monomers, and now we see VRSA.
We keep finding new targets for antibiotics, but as the Red Queen said, "It takes all the running you can do, to keep in the same place."
Re:short term solution (Score:3, Informative)
Anyway, I know there are multiple paths for drug resistance.
Generally speaking, antibiotics target a specific enzyme or pathway. Take penicillin: it inhibits an enzyme used in linking sugars used in building the cell wall. To evade this, some bacteria make beta-lactamases, enzymes that specifically attack and break down penicillin, while other bacteria just massively overproduce the enzyme that the penicillin targets, so that even under high penicillin dosages, there is enough enzyme activity left that the bacterium can build strong cell walls. Those are completely different forms of resistance, and one drug is unlikely to manage to stop both (unless it just kills the cell, which will of course stop both mechanisms, but that's not what we're talking about.)
If you're interested, here's an interesting article [postgradmed.com] that discussses a bunch of issues related to developing antibiotic-resistance, including quick takes on how it's not really related to massive widespread antibiotic use, to length of time using the antibiotic, and some other widely-held misunderstandings.