More Evidence That Antibiotic Resistance Existed LONG BEFORE Antibiotics Were Developed

This is a drawing of a bacteriophage, a virus that attacks bacteria.  (click for credit)
This is a drawing of a bacteriophage, a virus that attacks bacteria. (click for credit)
Many people know that bacteria have developed resistance to popular antibiotics. Indeed, it is a big problem in medicine, and it has caused many health-care providers to call for doctors to prescribe antibiotics only when they are necessary. The Centers for Disease Control calls this “antibiotic stewardship” and thinks it will improve medical care throughout the country.1 I have written about antibiotic resistance before (see here and here), because some evolutionists try to cite it in support of the idea that novel, useful genes can be produced by evolutionary processes. Of course, the more we have studied the phenomenon, the more we have seen that this is just not the case.

There are essentially two ways that a bacterium develops resistance to an antibiotic. One way is to have a mutation that confers the resistance. For example, a bacterium can become resistant to streptomycin if a mutation causes a defect in the bacterium’s protein-making factory, which is called the ribosome. That defect keeps streptomycin from binding to the ribosome, which makes streptomycin ineffective against the bacterium. However, it also makes the ribosome significantly less efficient at its job.2 So in the end, rather than producing something novel (like a new gene that fights the antibiotic), the mutation just deteriorates a gene that already existed. While this is good for a bacterium in streptomycin, it doesn’t provide any evidence that novel, useful genes can be produced by evolutionary processes.

There is, however, a second way that a bacterium can develop resistance to an antibiotic: It can get genes that fight the antibiotic from another bacterium. Bacteria hold many genes on tiny, circular portions of their DNA called plasmids. Two bacteria can come together in a process called conjugation and exchange those plasmids, which allows bacteria to “swap” DNA. If a bacterium has a gene (or a set of genes) that allows it to resist an antibiotic, it can pass those genes to others in the population, ensuring their survival.

Of course, the natural question one must ask is, “Where did those antibiotic-resistance genes come from in the first place?” Many evolutionists want you to believe that evolution produced those genes in response to the development of antibiotics. After all, antibiotics didn’t exist until 1941, when penicillin was tested in animals and then people. Why would antibiotic-resistance genes exist before the antibiotics?

Well, it turns out that they did exist long before the development of antibiotics. As I wrote previously, some antibiotic-resistance genes were found in soil alongside mammoths! The mammoths died out quite some time before antibiotics existed, so it is very clear that these genes were not produced in response to antibiotics. A new study brings this fact closer to home.

In Namur, Belgium, a construction project uncovered latrines from the Middle Ages. Christelle Desnues and her colleagues studied the fossilized feces (some people are really committed to their science!), which is called coprolite to make it sound a little less disgusting. They drilled into the center of the coprolite and examined a sample under an electron microscope. They found several structures that were clearly viruses, so they sequenced the viral DNA that they could extract from the sample.3

They found two very interesting things. First, the viruses had all sorts of antibiotic-resistance genes in them. It turns out that bacteriophages are another means by which DNA gets transferred among bacteria. So the fact that these viruses had antibiotic-resistance genes indicates that the bacteria they were infecting back in the Middle Ages had those genes as well! While this doesn’t show that antibiotic-resistance genes have been around since the time of the mammoths, it does show that bacteria which are associated with people had them several hundred years before antibiotics were invented. Indeed, the authors state:

Here, we demonstrate that bacteriophages are an ancient reservoir of resistance genes associated with human samples that date back as far as the Middle Ages.

Since this isn’t news (except to students who have been taught incorrectly), it’s not the most interesting finding of the study. The most interesting finding is that the antibiotic-resistance genes in the viruses from the Middle Ages were more diverse than the antibiotic-resistance genes we see in modern-day viruses. In other words, based on this study, it seems that bacteria from the Middle Ages had more antibiotic-resistance genes than modern bacteria do! So far from producing such genes, it seems that evolution might have destroyed some of them over the past 700 years! This, of course, is consistent with Dr. John C. Sanford’s view that genomes deteriorate over time, despite the work of natural selection.


1. “Antibiotic Resistance Threats in the United States, 2013,” U.S. Department of Health and Human Services publication, p. 41 (available online).
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2. Gartner, T. and Orias, E., “Effects of mutations to streptomycin resistance on the rate of translation of mutant genetic information,” Journal of Bacteriology 91:1021–1028, 1966.
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3. Sandra Appelt, Laura Fancello, Matthieu Le Bailly, Didier Raoult, Michel Drancourt, and Christelle Desnues, “Viruses in a 14th-century coprolite,” Applied and Environmental Microbiology, 2014, doi:10.1128/AEM.03242-13
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11 thoughts on “More Evidence That Antibiotic Resistance Existed LONG BEFORE Antibiotics Were Developed”

  1. I am not sure if the following applies to microorganisms, but I had always heard that a certain percentage of the population is resistant to the pesticide or antibiotic. The common example was insects and DDT. When DDT was overused, it would kill out the non-resistant population and leave only the population that had immunity. Those with immunity would be the only ones to reproduce. Thus, in a few generations, the population would be back to its full strength and the DDT was no longer effective. The insects never actually developed any new genes or a special resistance in response to an outside catalyst, but rather something inherent in the population (or perhaps a genetic fluke that had left some receptor damaged, but that was not in response to the pesticide.)

    I learned this quite a few years ago and our professor had informed us that the book we were using was out of date on some topics. I do not know if this is one of them, if this idea has since been disproven, or is indeed correct.

    1. That’s the way it actually happens, D. Perrine, so you were taught correctly. However, when you ask most evolutionists where the genes in those few resistant organisms came from, they will suggest that the genes evolved in response to the antibiotics.

  2. I am currently trying to broaden my understanding and knowledge of evolution. In pursuit of that, I have started “The Greatest Show on Earth.” From my current knowledge of evolution, it seems to me that there is only reaction, never innovation.

    What I mean is that, animals only seem to change in reaction to something. Whether it be the opportunity to claim a niche in the ecosystem that has opened up, develop something to become a better killer or survivor. There never seems to be any change for the sake of change. Perhaps, it is just the way I am looking at it, that any change is a matter of survival. So, no matter what a change would have an impact on how successful the species is. As it seems to me, if things only react, then there would be a limited amount of diversity. I was curious as to what you thought and if there were any misconceptions or errors.

    1. It’s good that you are reading Dawkins, D. Perrine. He is pretty sloppy these days, but he still gives a reasonable view of what evolution is. I think his earlier books were better, but unfortunately, they are more out-of-date as well.

      I think most evolutionists would agree with you that evolution doesn’t produce change for the sake of change. Change is going on all the time, but without any selection pressure, it doesn’t get preserved, at least not as the predominant version of the organism. Thus, the evolutionary changes that occur are the result of a reaction to new selection pressures.

  3. Hi Dr Wile,

    I ve been reading creationist literature at CMI and AIG to see if science affirms the Bible. So far Im still unconvinced of the veracity of creation science, although I have a lot to learn.

    For example, it was discovered that ancient Nubians and even some South Europeans drank antibiotic-laced beer.

    Furthermore, it is known that certain bacteria have been known to secrete antibiotics themselves to kill competing micro-organisms. Perhaps this could be the cause of increased antibiotic-resistant gene expression in early bacteria?

    Check out this article :

    Id like to know whats your take on nylon-eating bacteria as well, it seems more likely to be a product of evolution than evidence of innate design in plasmids. But then again, Im no expert in genetics (except for UK A levels, so what the heck)

    1. Thanks for your comment, Daren. I am sorry it took so long for me to reply. I have been on a speaking tour, and it kept me rather busy. I am glad that you are looking at the creationist literature. That’s more than most people do!

      I am not surprised that people drank antibiotic-laced beer in the past. However, as the previous article I linked to shows, antibiotic-resistant genes seem to go back to at least the time of the mammoths. Indeed, as the authors of that study indicate:

      These results show conclusively that antibiotic resistance is a natural phenomenon that predates the modern selective pressure of clinical antibiotic use.

      You are probably correct that it is related to the “warfare” that is known to go on between bacteria. We know for a fact, however, that unlike most unsuspecting students are taught by zealous evolutionists, it has nothing to do with modern antibiotics.

      I think the ability for certain bacteria to adapt to feed on nylon is a result of the design of plasmids. Indeed, follow-up studies in the lab consistently produced nylon-feeding bacteria from non-nylon feeding bacteria. You wouldn’t expect this if random mutations were the only mechanism producing the new enzymes. In addition, the plasmid that contains the enzyme genes in the nylon-digesting bacteria (pOAD2) has five transposable elements, which creationist speculate are one of the design features that produce rapid adaptation. That’s always the plasmid the genes developed on. Given the repeatability of the results, this indicates something that the plasmid is designed to do.

      In reference to genomic decay, you seem to be confusing length with information. Certainly there are many processes that can add to the length of a genome. However, that tells us nothing about the information content of the genome. Dr. Sanford’s hypothesis of genomic decay has a lot of support, and his most recent study of the H1N1 virus seems to indicate that genomic decay continues to occur even under strong selection conditions.

      You ask how science can detect evidence of the supernatural when it involves study of only the natural world. The answer is rather simple. When a model is built that depends on supernatural events and that model makes predictions about the natural world that are different from other models, and those predictions are confirmed by studying the natural world, science has given us evidence that the supernatural events occurred. For example, Dr. Russell Humphreys built a model of planetary magnetic fields assuming a supernatural mechanism by which planets were formed, and that model was able to make many successful predictions about data that had not yet been measured (see here, here, and here). In addition, the competing model made predictions that were quite different, and those predictions were falsified by the same data. This lends scientific support to Dr. Humphreys’s supernatural-based model.

      In answer to your question about why I support creationism, I do so because the scientific evidence strongly supports it. This idea that creationists believe in the supernatural because we can’t explain certain aspects of nature comes from non-creationists. Creationists believe in creation because of what they see as evidence. Some believe based mostly (or solely) on Biblical evidence. Others use a mix of Biblical and scientific evidence. Some (like myself) agree that the Bible is silent on the details of creation, and we use mostly the scientific evidence to come to our conclusion. I don’t know a single creationist who relies on the supernatural because he or she can’t explain the natural.

  4. Sorry for double posting!

    I think when you say that genomes deteriorate over time, it may be too broad and encompassing. For example, evidence has been shown that DNA telomeres could lengthen when leading a healthy lifestyle. There are other mutations, like frame shift additions or chromosome duplication that could add extra material our genome.

    The reason why Im bringing this up is because I ve been debating with a Christian friend of mine (we respectfully disagree on evolution and the age of the Earth, instead of hurling ad hominems at each other) who recommended I investigate creation science. So far its still difficult to accept their theories, how can science detect evidence of the supernatural when science purely involves the study of the natural world?

    As an agnostic and a supporter of evolution, I am curious why you would support creationism, since many phenomena once thought to be supernatural have had scientific explanations. (It doesnt mean that ALL supernatural phenomena are explainable of course, abiogenesis seems bizzarely unimaginable given our knowledge of chemistry).

  5. Dr Wile…I apologise in advance for being off-topic, but I dont think I will ever believe in young earth creationism. Probably never, in fact.

    This concerns the RATE teams geological findings. I thought it would be a good way to improve radiometric dating, then a friend sent me these to read

    The last one really killed it for me….how are we supposed to trust RATE “scientists” if they are being so callously deceitful about their findings….really….

    1. Daren, I find it interesting that of the three links you give, only one discusses data. The other two are simply composed of ad hominem attacks. As far as the first link is concerned, the author contradicts himself. For example, he claims that isotopes such as Rb, Sr, Sm, and Nd are not related to the age of the eruption but instead are the result of the “…history of subduction, composition of the mantle, and how oceanic sediments and crust are incorporated back into the mantle.” Then he turns around and tries to claim that the isochron plots of both Rb-Sr and Sm-Nd show a zero age, which they should only show if those isotope ratios are related to the age of the eruption. The problem, of course, is that the author shows the data on a ridiculously insensitive scale. Of course the slopes of the isochrons look like zero when the scale of the vertical axis is huge. Compare his plots to those of Snelling (Figure 4 in Snelling’s report). Snelling uses a vertical scale that is reasonable for showing trends in the data. When you use that scale, you find that when you include all the data, you don’t get a valid isochron – the ratios are all over the map. The reason Snelling chooses only 5 points is because they are the only ones that form a valid isochron. You can’t see it in the link you gave me because the author is using a vertical scale that is insensitive to variations in the data. When the proper scale is used, the problem is readily apparent.

      The author also quotes Dr. Snelling out of context. He says that when Snelling writes, “These outcomes would thus seem to have some validity and meaning to them, implying some significance to these trends in the Pb isotopic data,” he is somehow admitting that there might be some truth to the data. No. Read the whole paragraph. What he is saying is that some isotopes give significant results (like the Pb isotopes), and some don’t (like the Rb-Sr and Sm-Nd isotopes). If such dating were accurate, they should all give consistent results. Since they don’t, that means there is a problem with using isotope dates.

      Regarding the two ad hominem attacks, I think you need to be made aware of how scientific publications work. The papers that the “noanswersingenesis” article quotes to imply that sometimes, Snelling is an old-earther are all based on Snelling’s PhD thesis (note that there are no dates beyond 1990). Having written a PhD thesis myself, I can tell you that the contents of that thesis are not always determined by the PhD candidate. They are significantly influenced by the PhD adviser. Thus, a PhD thesis does not necessarily reflect all the views of the PhD candidate. So far from there being “two Snellings” doing geology, there is only one. His PhD thesis necessarily had to contain some views from his thesis adviser, while his own work contains solely his own views. The author of this ad hominem attack complains that Snelling won’t debate him. Well, Snelling does debate other geologists. I suspect that he chooses to debate those who concentrate on the evidence, not on ad hominem attacks.

      The third link contains an ad hominem attack against Dr. Baumgardner. Once again, the person doesn’t seem to realize that when you write a paper with other authors, the views of the other authors must be taken into account. The paper represents the work of a group, and it should not be expected to represent all the views of all the members of the group. Where the members’ views are divergent, compromise has to be reached. Having written several such scientific papers, I can tell you that this is sometimes a difficult process that leaves some members of the group very disappointed.

      RATE scientists aren’t being “callously deceitful” about their findings. Unfortunately, their detractors do everything they can to put them in a bad light, because they aren’t happy with what the data say. If you want to come to a reasonable conclusion on the origins issue, you need to concentrate on the data, not the ad hominem attacks.

  6. Dr. Wile,

    I believe your article misrepresents evolutionists, and evolution in general. There are three ways in which I believe you do this.

    The first is in your fourth paragraph. In it you say that “[m]any evolutionists want you to believe that evolution produced those genes in response to the development of antibiotics.” You give no support for this statement. I have never, in my research on evolution, come across any evolutionist who would actually endorse that notion. You could have easily fabricated that statement. I would ask that you show me an example of one evolutionist in the past twenty-five years who actually believe(s/d) that antibiotic-resistance genes develop in response to antibiotics.

    The second is in the same statement that I quoted above. I believe that you are mischaracterizing the genes that you call “antibiotic-resistance” genes. The term you use implies that you think evolutionists believe that those genes have the designated purpose of antibiotic resistance. The evolutionist position is that those genes were created by random mutations; they were the product of chance. The genes simply happen to ALLOW resistance to a certain antibiotic or multiple antibiotics. Unless one invokes divine intervention, it is hard to say that these genes are purposed to resist antibiotics.

    Finally, you make a parenthetical statement in your final paragraph [“(except to students who have been taught incorrectly)”] that, once again, implies that there ARE students who have been taught that these magical “antibiotic-resistance” genes actually developed in response to the creation of antibiotics. Again, you offer no support for this idea. I would ask that you give me an example of a textbook from the past twenty-five years that teaches this.

    the Truth is a Lie,


    1. Thanks for your comment, MP. I am definitely not misrepresenting evolutionists or evolution in general. Here are quotes from two recent textbooks that make exactly this claim:

      Penicillin, an antibiotic produced by a fungus, was used for the first time in the 1940s and is still one of the most effective antibiotics known. However, penicillin has now been in use for more than 50 years, and more and more types of bacteria have evolved that are resistant to it. Bacteria that are resistant to penicillin produce an enzyme that breaks down this antibiotic. (emphasis mine)

      Glencoe Science Biology: The Dynamics of Life, McGraw Hill 2004, p. 1030

      Obviously, the book says that the bacteria evolved after the antibiotics, and it cites the mechanism as production of an enzyme, which (of course) is coded for by a gene. This college text makes it more explicit:

      In the 1950s, Japanese physicians began to notice that some hospital patients suffering from bacterial dysentery, which produces severe diarrhea, did not respond to antibiotics that had generally been effective in treating this type of infection. Apparently, resistance to these antibiotics had evolved in certain strains of Shigella, the pathogen. Eventually, researchers began to identify the specific genes that confer antibiotic resistance in Shigella and other pathogenic bacteria. Some of these genes, for example, code for enzymes that specifically destroy certain antibiotics, such as tetracycline or ampicillin. (emphasis mine)

      – Neil A. Campbell and Jane B. Reece, Biology, 6th Edition, Benjamin Cummings 2002, pp. 344-345

      Of course, you can also look at the evangelistic evolutionary literature to see the same thing. As Dawkins says in The Greatest Show on Earth: The Evidence for Evolution (p. 132):

      Many bacterial strains have evolved resistance to antibiotics in spectacularly short periods. After all, the first antibiotic, penicillin, was developed, heroically, by Florey and Chain as recently as the Second World War. New antibiotics have been coming out at frequent intervals since then, and bacteria have evolved resistance to just about every one of them.

      This, of course, is why the first paper that definitively showed antibiotic resistance to be an ancient phenomenon (published in 2011) said:

      The discovery of antibiotics more than 70 years ago initiated a period of drug innovation and implementation in human and animal health and agriculture. These discoveries were tempered in all cases by the emergence of resistant microbes. This history has been interpreted to mean that antibiotic resistance in pathogenic bacteria is a modern phenomenon; this view is reinforced by the fact that collections of microbes that predate the antibiotic era are highly susceptible to antibiotics. Here we report targeted metagenomic analyses of rigorously authenticated ancient DNA from 30,000-year-old Beringian permafrost sediments and the identification of a highly diverse collection of genes encoding resistance to Beta-lactam, tetracycline and glycopeptide antibiotics. Structure and function studies on the complete vancomycin resistance element VanA confirmed its similarity to modern variants. These results show conclusively that antibiotic resistance is a natural phenomenon that predates the modern selective pressure of clinical antibiotic use. (emphasis mine)

      When “the Truth” is evolution, it is most definitely a lie!

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