Antibiotic resistance is older than antibiotics

This came out while I was traveling, but I wanted to post it here in case you missed it. It is very cool, in that "maybe cool isn't the right word" sort of way. Our modern antibiotics are really just purified and pumped-up versions of naturally occurring compounds, right? So, it makes sense that, long before we started using them as antibiotics, bacteria had already started building defenses against the natural compounds. In other words: Antibiotic resistance is older than the use of antibiotics.



  1. That makes as much sense as the corollary (or actually, primary concept), “Antibiotic use is older than the use of antibiotics.”

  2. Your corollary is poorly formed–a more accurate version (which happens to be true) would be “The presence (and effects, including the development of resistances by bacteria) of antibiotic compounds predate the modern use of antibiotics by humans.”

  3. I’m not really sure on the logic behind anti-biotic resistance and “super-bugs.”  I mean, it’s not like resistance emerges differently than any other evolutionary trait.  Whether we treat with anti-biotics or not, there will be resistant strains out there.  There’ll just be non-resistant strains too.  Are the two strains in competition?  Does the resistant strain benefit at all from the destruction of the non-resistant?  It’s not like it’s impossible for a single individual to carry multiple strains at the same time any more than it’s impossible for someone to have a cut on their hand and a cut on their arm at the same time.

  4. Is this a discussion by non biologists?  Forgive me, but it just doesn’t make much sense. Better to deal with the facts. There are antibiotics that work, demonstrably. And those that don’t. In Vancomycin, we have an “antibiotic of last resort.” In between, there are a number of antibiotics that are sometimes useful with some bugs, and sometimes not. The pharmacological action of most antibiotics is understood, as is their lifecycle. Mutation & resistance are understood as well, though not entirely. What is important is to focus on proper medical dispensing of antibiotics (a huge problem); continuing research, hard these days because antibiotics are not used “every day for life” and thus not popular with drug companies; and, devoting the kind of academic resources necessary to stay ahead of the curve. Otherwise, MSRAs will become major killers just as epidemics of the past.

    1. How does the use of anti-biotics lead to the spread of MRSAs?  I understand that they don’t work against MRSAs and that they do work against non-resistant strains, but doesn’t that just mean we’re ending up with less disease overall, and the same people who get MRSA would have gotten it anyway?  It’s a bad situation to be surrounded by bears, but even if you kill all but one bear you’re still probably going to die.  One bear is all it takes.

      Can someone explain this to me?

  5. “Authoritative biology (including the ’emergent’ gang) are SO 19th century reductionist it makes me nauseous. Panpsychic-organicism or BUST.”
    — Love, Negentropy.

  6. I must be missing something in the NYT article because this does not seem like news.  As noted, bacterial and fungal organisms, like the mold that produces penicillin, often secrete nasty molecules like antibiotic compounds in order to reduce competition for nutrients.  That’s how we discovered antibiotics in the first place.  In response, many of those competing organisms have developed resistances.  That’s how a lot of molecular biology (by which I mean recombinant DNA in E. coli and other systems) is possible – by taking advantage of those resistance genes.  Heck, the ability to take up foreign genes coding for antibiotic resistance is an evolutionary advantage for bacteria in their native environment, forget hospitals.  And that SAME ability to take up foreign DNA, again, makes recombinent DNA cloning possible.

    In short
    a) This is kind of an unexciting conclusion unless I’ve missed something (I haven’t got the Nature article handy). Sorry to sound so dismissive, I really should read the Nature article.
    b) Bacteria are awesome and nature is awesome and therefore modern molecular biology is awesome.

  7. ^^ No case to rest (except anti-scientific claptrap)?

    I have to say I agree with mayryr — that this is an unsurprising finding.  It is very well understood that microorganisms use antibiotic resistance as part of their eternal arms-race with each other. It’d be startling if anti-antibiotic genes had *not* originated long before Homo sapiens started messing around with penicillin et al. I’m not sure we need to dig up organisms to see this: a little phylogenetic inference should tell us more or less how long these genes have been around. Probably a very long time indeed.

  8. Each antibiotic was effective at wiping out bugs to begin with because the bacteria that live in our bodies didn’t have to face it — at least until the 20th century came along, and the production of these chemicals in potent drug form became relatively straightforward to do (our bodies don’t manufacture penicillin etc, but antibiotics are also produced naturally in the soil by microbes there. Microbes often do this to fight each other for resources). Any bug in our bodies that gains a resistance gene against, say, penicillin, and is then challenged by a penicillin treatment, can duck its own death. It survives where it would have died (is ‘selected for’), and becomes immune to what is supposed to kill it. If we gradually challenge human-borne bacteria with different, multiple antibiotics, we inadvertently favour ones (‘select for’) bacteria that carry multiple resistance genes. So, these MRSA bacteria accumulate resistance genes in a way they wouldn’t otherwise have done while trying to live in our bodies, through the overuse and misuse of antibiotics.  So the bear gets ‘stronger’.

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