Egnor: Don’t Know Much about Antibiotic Resistance

OK, last post about this bozo, and then I’m done (famous last words…). In the previous post, I dealt with Egnor’s claim that the evolution of antibiotic resistance by selection of resistant genotypes is obvious, and not germane (namely, that it wasn’t obvious at one point in time). What bothered me with not just Egnor’s claim (which I’ll get to a minute) and ScienceBlogling Mike’s response is that evolutionary biology does have a significant role to play in combating the evolution and spread of antibiotic resistance.

First, what Egnor said:

The important medical research on antibiotic resistance in bacteria deals with how the mutations that give rise to resistance arise, exactly what those mutations are and how they work, and what can be done to counteract them. The important medical research involves genetics, molecular biology, and pharmacology. Darwin’s theory is of no substantive value to the research because, as Mr. Dunford admits, there is no difference between antibiotic resistant bacteria that emerge through artificial intelligent selection and antibiotic resistant bacteria that emerge through natural selection. Antibiotic resistance is a phenomenon that occurs because there are often a few bacteria in a large population of bacteria that have a mutation that renders them less sensitive to the antibiotic. These bacteria that aren’t killed by the antibiotic eventually outnumber bacteria that are killed by the antibiotic. Survivors survive. Does this mundane observation really help Mr. Dunford understand things he may not have otherwise understood? It certainly doesn’t advance medical research in any meaningful way. New insights into genetics, molecular biology, and pharmacology do advance medical research.

As I noted, when the problem of antibiotic resistance first became apparent several decades ago, the ‘Darwinist’ explanation was novel. Since then, as I noted, it is obvious–today. However, evolutionary biology does have several roles to play…but I’m getting ahead of myself. Now, ScienceBlogling Mike (italics mine):

I realize that I’m just begging for Dr. Egnor to take what I say out of context again, but he is not entirely wrong. If I was working on ways to fight antibiotic resistance, I would certainly want to focus more on the molecular mechanisms that are involved in the development of resistance than on the question of how resistance spreads through a population of bacteria after it appears.
The fact of the matter is that we already have a very good idea of how antibiotic resistance spreads through a population of bacteria.

So, I want to lay out how evolutionary biology can and is used to combat antibiotic resistance. (an aside: If someone claims that population genetics and phylogenetics are simply part of “genetics”, then we Evil ‘evolutionists’ have just had our point proven–tools and methods developed by evolutionary biologists are so integral to modern biological research such that you can’t do one without the other).
First, I disagree with Mike about understanding “how antibiotic resistance spreads through a population of bacteria.” Or more accurately, how resistance spreads through populations plural. We do know what happens when a local population is exposed to high levels of antibiotics, namely resistance increases in frequency locally for at least a short time–Stuart Levy and colleagues demonstrated this over three decades ago, so, as I said, this isn’t revolutionary at this point.
But what we don’t know is to what extent resistance genes or resistant strains move from high use environments, such as industrial agriculture, into the clinical setting. To do this will require tools from population genetics and phylogenetics. For instance, to determine transfer, you not only have to show that a gene is found in two different genotypes, but that these genotypes aren’t related, otherwise this could be a case of inheritance*. In other words, you have to construct ancestor-descendant relationships–you know, that evolutionary stuff.
Then there’s the issue of drug development. Without a doubt, it is vital. But the window of effectiveness of new antibiotics is shrinking, to the point where resistance in clinical isolates is observed in roughly six months, and the lifespan of a ‘silver bullet’ has decreased to only a few years at best**. But equally important is preserving the power of the antibiotics that we already have. To do that we have to understand the biology of resistant bacteria, most of which are not strict pathogens, but opportunistic pathogens. As I’ve said many times on this blog, the problem of antibiotic resistance does not start at the hospital door (as is the case with the ‘pig’ MRSA clone). To track the evolution of resistance, we need good, reliable genetic markers. To get those markers, we need a good sample of diversity–in other words, we need to understand the population genetics of the species of interest.
In a related vein, another point I’ve raised many times here is that the best way to avoid getting a resistant infection is not to get any infection (so wash your damn hands!). One potential way to reduce the need for antibiotics is to identify genes that could be potential therapeutic targets for vaccination or other therapies using tests of positive and negative selection on genes. Yes, these have to be followed experimentally, but evolutionary biology gives us a good starting point (colleagues are using this approach to develop malaria and TB vaccines).
This is just a small sample of how evolutionary biology is used to combat antibiotic resistance. I could also go into detail about how colleagues and I are using evolutionary genomics to identify genes and regions of genes that are important in the bacterial production of antibiotics, but this is a blog and you get what you pay for (or you can come hear me speak Mar. 24).
After writing three posts about this idiocy, it still is remarkable that the intelligent design creationists are fighting battles that became irrelevant decades ago. And while we’re at it, how is intelligent design going to solve any of these problems?
First post: The Intellectual Cowardice of Michael Egnor
Second post: Egnor and the Creationists: Partying Like It’s 1859
*In most cases, the genes were acquired via horizontal transfer (although some beta-lactamases appear to be a very ancient part of several bacterial groups, including E. coli and friends). The issue is when. We also want to know other things, such as are lineages that are able to cause disease more likely to acquire resistance, or is the acquisition of resistance more likely to occur in lineages that are associated with certain ecologies.
**The one exception to this is vancomycin, which, while widely used, is used under very controlled settings and usually for short durations (it’s expensive ad administered through an IV drip).

This entry was posted in Antibiotics, Creationism, Evolution, Genetics, Genomics, Microbiology, Public Health, The War on Science. Bookmark the permalink.

6 Responses to Egnor: Don’t Know Much about Antibiotic Resistance

  1. killinchy says:

    First, I am not trolling. I am a retired chemist prof who would like some advice. I think I’m correct when I write that Egnor and his ilk say that resistance to antibiotics is present in some bacteria, and this type of bacteria will flourish when antibiotics are given to all the bacteria. There is no new dna produced. That’s what I think Egnor says.
    But, readers of this blog (except me) dismiss this because it’s been clearly shown that new dna has appeared.
    Please remember that I am a chemist…. would anybody care to point me to where I can learn how I can too can refute Egnor. I am prepared to spend some time over this. Thanks

  2. blue says:

    The paper that kicked off this whole debate is a nice example of a change in the DNA (or a mutation) leading to new types of antibiotic resistance. There’s a nice description here:

  3. _Arthur says:

    Killigchy, when one experioment tries to find and isolate bacteria resistant to antibiotics, by subjecting colonies of bacteria WITH NO PREVIOUS KNOWN RESISTANCE to antibiotic doses, in vitro, until resistance manifests itself, there are 2 possibilities.
    1) resistance was already present (in a tiny number of cateria) at the start of the experiment
    2) resistance appeared, thru mutations, during the course of experiment.
    From an ToE standpoint, both cases are pretty much equivalent. New genes appear (and as many as discarded) all the time. Mutation rates are high enough that resistance can be EXPECTED to manifests itself during the duration of the experiment, even without using, say, radiation, to increase the mutation rate.
    The explanation that the resistance gene was *necessarily* already present in the initial starting bacteria population can be disproved by:
    1) That gene hasn’t been observed before, the whole experiment setup was because that particular bacteria was not known to have resistance to that particular antibiotic.
    2) Similar experiments have been (with say, lactose assimilation) done with clonal initial colonies. The initital colonies all died (from inability to digest lactose), and, after a long while, one daughter colony finally survived, and found a way to eat lactose raw. The explanation is that one (or several) mutations, happening dyring the timeframe of the experiment) provided the necessary genes/enzymes to digest lactose.
    Nowadays, the fun part of the experiment is to track down wich precise proteins confer the resistance, map the genes that produce those proteins, and track which gene has been modified, and how, by comparing the new version gene to the original version in the initial population.
    That does establish that resistance is due to mutation, as filtered by selection (to die or not to die from the antibiotic).
    Now, what is Egnor’s counter-explanation ? What does he knows that true biologists don’t ?

  4. feromon says:

    thnaks blog very much good

  5. mirc says:


  6. The explanation that the resistance gene was *necessarily* already present in the initial starting bacteria population can be disproved by:

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