Finally, after years of mostly bad news in the competition between antibiotics developed by medical researchers and drug-resistance developed by bacteria, we have some good news. A class of drugs currently used to treat osteoporosis appears to stop conjugation, or the sharing of DNA between bacteria. It is conjugation that enables one bacteria that has developed drug resistance (say, XDR tuberculosis) to share the portions of its DNA that confer the drug resistance with another bacteria that hasn’t (say, e. coli). Not only that, but conjugation is disrupted in a way that tends to directly scramble the bacteria involved, killing them directly. (Scientific American story)
Obviously, if we can kill off drug-resistant bacteria, then this means we can turn back the bacterial evolutionary clock and use good-old-fashioned penicillin and it’s many derivatives again instead of dramatically more toxic drugs like Keflex. And because the osteoporosis drugs are already FDA approved, they could be used tomorrow “off label” to aid in the treatment of a drug-resistant bacterial infection. All in all, excellent news for medicine.
But I want to insert a note of caution into this discussion that I just haven’t seen in the media yet – bacteria have been evolving ways to survive for a very, very, very long time now, and it’s hardly inconceivable to think that they will eventually become resistant to this new class of drugs. After all, people evolved from something not too dissimilar to a bacterium long ago, ancient viral DNA is scattered throughout our own DNA, and even our mitochondria (the part of our cells that metabolizes our food with oxygen) may be an ancestral bacteria that developed a symbiotic relationship with the cell it invaded. And given that most of the biodiversity of the Earth is bacterial, not multicellular (like us, seals, even coral, insects, and algae), it’s safe to say that bacteria have been survived and prospered even in the face of radiation, heat, freezing, acids, etc. So, while we should certainly rejoice in this rare good news in the race to save lives from infections, we shouldn’t use this news as a justification for reducing medical research into new antibiotics or new methods to stop conjugation. It’s not a question of if we’ll need more new drugs, but a question of when.
But at least now we have an opportunity to catch up.
Not an area of expertise for me, but when I saw the article yesterday this was the first thing I wondered about. Good news with a large dish of “but” on the side.
Ditto. I want to know more about that “but …”
knowing what i know about the impact of conjugation, it’s not really the sort of thing bacteria will just be able to circumvent. it would be like asking the human race to figure out how to survive without sex. *shudders*
i’ve read some interesting stuff on conjugation and replication of viruses. indeed, a strong case can be made that the very invention of sexual reproduction came about from this rudimentary gene sharing. if there’s a drug that can stop conjugation, my concern would be that, if used without restraint, we could conceivably destroy large cultures of bacteria throughout the world.
Note that the SciAm story says “Many drug resistant bacteria rely on relaxase… (emphasis mine)”. So these drugs aren’t going to be a silver bullet. And if other types of drug resistant bacteria use a different enzyme, there’s every reason to believe that the bacteria currently using relaxase could evolve to use something else as well.
And this doesn’t stop one culture from becoming drug resistant – that is inherent to the use of antibiotics. It just stops bacteria from sharing that drug resistance.
This is an interesting finding and may turn out to be a Nobel Prize worthy finding sometime in the future, but I doubt it. As Brian points out, bacteria evolve very quickly; one the order of days rather than centuries that it takes for us multicellular organisms. First, this does not help with drug resistance that develops from mutations occurring within the bacteria themselves that allows for propagation in the presences of antibiotics, which is how most drug resistance develops. Second, by the process just mentioned, bacteria would likely evolve ways to block the effectiveness of DNA relaxase. If I read the article correctly, it requires binding at two enzyme site to work; thus a single mutation at either site could block the action of the drug. Lastly, this would only help in for conjugation transferring drug resistance occurring in patients while receiving treatment. I don’t know this for a fact, but I suspect that a lot of conjugation occurs in wound dressing, bed sheets, table tops, and other places where these drugs will have no effect.
One editorial comment; I won’t say that Keflex is a dramatically more toxic drug than penicillin. They are both the same class of drug and have essentially the same side effect profile.
Willie – I just did a little more research into Keflex here, and what I thought were nastier side effects and toxicity were actually things that occur with straight ‘cillins too. My error, and thanks for correcting me.