Evolutionists Couldn’t Have Been More Wrong About Antibiotic Resistance

A colony of bacteria similar to the one analyzed in the study being discussed.  (click for credit)
A colony of bacteria similar to the one analyzed in the study being discussed. (click for credit)
Back when I went to university, I was taught (as definitive fact) that bacteria evolved resistance to antibiotics as a result of the production of antibiotics. This was, of course, undeniable evidence for the fact that new genes can arise through a process of mutation and natural selection. Like most evolution-inspired ideas, however, the more we learned about antibiotic resistance in bacteria, the more we learned that there was a problem. It turns out that some cases of antibiotic resistance in bacteria were not caused by antibiotic-resistant genes. Instead, they were caused by the deterioration of genes that exist for other purposes. For example, the Anthrax bacterium can develop resistance to a class of antibiotics called quinolones, but it is the result of a mutation that degrades the gene that produces gyrase, the enzyme that those antibiotics attack. This allows the bacterium to survive the antibiotic, but the degraded gyrase gene causes the bacterium to reproduce much more slowly.

There are, however, specific genes found in bacteria that do produce proteins which fight antibiotics. It was generally thought that these genes arose through mutation and natural selection in response to our development of antibiotics. However, we now know that this just isn’t true. Antibiotic-resistant genes existed long before people developed antibiotics. I first wrote about this more than five years ago, when researchers found bacterial, antibiotic-resistant genes in permafrost alongside mammoth genes. Obviously, people weren’t making antibiotics when mammoths were alive. Thus, those genes existed long before human-made antibiotics. Later, I wrote about researchers who found bacterial, antibiotic-resistant genes in fossilized feces from the Middle Ages. Once again, this shows that antibiotic-resistant genes have been around long before our development of antibiotics.

Now an even more impressive study has been released. In it, researchers analyzed the DNA of a bacterium from the genus Paenibacillus. These bacteria form colonies, such as the one shown in the image above. The colors in the image indicate the density of bacteria – the brighter the yellow color, the higher the density of bacteria. While this genus of bacteria has been found in many, many environments, the specific species analyzed in the study was special: it has been living in a cave that has been isolated from the modern world. In fact, the cave is so isolated that no animals had ever ventured into it. When the researchers analyzed the DNA of this bacterium, they found all sorts of antibiotic-resistant genes.

In fact, they found that this bacterium was already resistant to most modern antibiotics, and they get this resistance from the same genes as pathogenic bacteria that have already been studied. In other words, the resistance to these antibiotics isn’t anything new. It didn’t come about as a result of the production of antibiotics. It has been in bacteria all along. The only thing antibiotics did was expose the fact that such genes already existed.

Now if this was the only conclusion in the paper, I probably wouldn’t have written about it. After all, we already know that the evolution-inspired explanation for antibiotic resistance isn’t correct. We know that bacteria possessed antibiotic-resistant genes long before the development of antibiotics, and when “new” antibiotic resistance arises, it is from mutations that deteriorate genes which already exist.

However, the thorough analysis done by the authors of this paper showed something else: potential antibiotic-resistant genes that had not yet been identified! In this bacterium, which had never been exposed to antibiotics, the researchers actually found five new families of genes that could potentially be used by bacteria to fight antibiotics! They say that these families of genes are widespread in the environment and can have clinical significance if they end up being transported into pathogenic bacteria. In other words, there are “stockpiles” of antibiotic resistant genes residing in bacteria that are not disease-causing. Since we know bacteria are adept at gaining genes from other bacteria, these stockpiles will probably find their way into disease-causing bacteria, producing even more antibiotic resistance.

Far from being evidence for flagellate-to-philosopher evolution, then, antibiotic resistance is evidence against it! After all, it shows that from a genetic point of view, there is nothing new being developed. There are only antibiotic-resistant genes that existed long before antibiotics, and there are mutations that degrade genes which also have existed long before antibiotics. This is precisely what you would expect in a creationist framework.

24 thoughts on “Evolutionists Couldn’t Have Been More Wrong About Antibiotic Resistance”

  1. If this is true, is there any reason to try to minimize the use of antibiotics in healthcare and in food animals? My understanding is that people want to minimize the use of antibiotics to slow down the development of antibiotic resistance in bacteria. Does the use of antibiotics make it more likely for the bacteria to gain those antibiotic resistant genes from other bacteria (so the resistance still spreads because of antibiotics, but from horizontal transfer rather than from the development of new genes)?

    1. The use of antibiotics causes a stress to bacterial populations. That stress increases the rate of horizontal gene transfer, so it can lead to pathogenic bacteria acquiring the genes necessary for resistance. Thus, antibiotics should be used wisely. However, unlike many want you to believe, antibiotics don’t cause the evolution of new resistance genes. They just create the selective pressure that can cause the already-existing genes to be transferred to pathogenic bacteria.

  2. Wow. I guess I never really thought about what was meant by “evolution of antibiotic resistance,” though naturally I figured it was just microevolution. And maybe this was just me being naive, but I figured that if scientists were willing to say that bacteria evolved antibiotic resistance, they at least had to have already observed new genes being created in bacteria in response to the presence of antibiotics. If they haven’t, what they’ve been saying is incredibly misleading.

    Will the scientific community stop saying that bacteria evolved antibiotic resistance now, or are they willing to talk as if picking up already-existing genes is evolution?

    1. Evolutionary evangelists will often give an example of selection and call it evolution. Thus, those who are less interested in education and more interested in indoctrination will continue to say that bacteria evolved antibiotic resistance.

  3. To play Devil’s advocate a little bit, an evolutionist might argue that antibiotic resistance has been evolving since before antibiotic use became ubiquitous by humans. Since some of the most used and successful antibiotics are derived from compounds naturally produced by some organisms, e.g. the penicillins, it could be argued that there has been long-standing selection for the production of mechanisms to counteract them. While the common example I’ve heard in medical contexts is what you describe, comparing development of antibiotic resistance to a war in which germs and medicine respond to “maneuvers” by the other, that analogy might be extended to a larger war in nature between organisms synthesizing antibiotics and those developing ways to resist them. My undergraduate Microbiology textbook (Prescott’s Microbiology, 8th ed.) even posited that organisms producing antibiotic compounds would need to have resistance genes in order to avoid self-destruction. These then could at some point be horizontally transferred to other organisms that acquire resistance. In the mind of an evolutionist then, human use of antibiotics just intensified a process that had been ongoing in nature.

    I’m sure ideas have been modified over the years, but my sense is that would be the general line of thinking today.

    1. You are correct about the current line of thinking, John, but that’s not the original line of thinking. The original evolutionary explanation for antibiotic resistance was that bacteria produced new genes for resistance in response to antibiotics being developed. Consider, for example, how one paper that reported ancient antibiotic-resistant bacteria summarized the situation:

      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. (Vanessa M. D’Costa, et. al., “Antibiotic Resistance is Ancient,” Nature, doi:10.1038/nature10388, 2011)

      The current line of thinking (which you describe) was adopted after the original line of thinking was falsified.

  4. Im a bit confused. When we say “antibiotic resistance” I understood that to mean the bacteria had damaged some of their genes to inhibit the antibiotic from working on it. But you are saying there is an inherent resistance – a non-broken gene resistance that some bacteria have? And what would the functional purpose of these genes be if there were no antibiotics around for them to resist, according to evo bio?

    1. As I state in the article, Tim, damaging an already existing gene is one way that antibiotic resistance is produced. However, that’s not the most common way. The most common way a bacterium becomes resistant to an antibiotic is to acquire a gene (by transfer from another live bacterium or by absorption from a dead bacterium) that directly fights the antibiotic. Initially, evolutionists thought there would be no reason for ancient bacteria to be resistant to antibiotics, so they interpreted antibiotic resistant genes to have been produced by evolution after the use of modern antibiotics. Once that interpretation had been falsified, evolutionists moved to another interpretation: Some organisms (like fungi) naturally produce antibiotics (like penicillin), so some bacteria must have evolved the genes to fight antibiotics in response to those organisms, and modern antibiotic resistance mostly comes from those genes.

  5. I’m a fellow believer who wants to make sure that we argue from truth and understanding, rather than ideological motivations. So …

    Microbes have been “developing” antibiotic strategies almost from the beginning of time. Humans discovered antibiotics accidentally when an astute microbiologist noticed some old, unwashed Petri dishes accumulating in the lab’s sink were resisting the growth of new bacterial cultures. So to say that “antibiotic-resistance genes have been present in the genomes of bugs long before antibiotics were invented” is misinformed and misleading.

    1. Thanks for your comment, Luke. Since I am also a believer who wants to make sure that we argue from the truth, I must correct you. To say, “antibiotic-resistance genes have been present in the genomes of bugs long before antibiotics were invented” is precisely correct, except for the fact that bacteria are not bugs. They are prokaryotes. In fact, that’s exactly what this study demonstrates. If you actually read the study, you will find that the researchers believe this species of bacterium has been isolated from the outside world for millions of years. Yet it has genes that make it resistant to most modern antibiotics. Thus, the genes for antibiotic resistance have been the in genome of that bacterium long before antibiotics were invented. In addition, the other two studies discussed in the post (of bacterial genes in permafrost and bacterial genes in fossilized feces from the Middle Ages) demonstrate that this is true for many bacteria, not just the species from the cave. Not only does the study demonstrate this, but it also demonstrates that there are stockpiles of antibiotic resistant genes in bacteria that haven’t even been used by pathogenic bacteria yet.

      In addition, you might want to believe that bacteria have been “developing” antibiotic strategies almost from the beginning of time, but the evidence doesn’t say that. There is no evidence of antibiotic-resistant genes developing. That evidence might come to light at some point, but the evidence doesn’t say that right now. Right now the evidence only says that antibiotic-resistance genes have been present in the genomes of bacteria long before antibiotics were invented.

      1. I’m a molecular biologist (though not a microbiologist; and yes, I’m an evolutionist.) We says “bugs” all the time as slang for bacteria.

        Luke makes a good point that this entire post glosses over, but which fortunately was raised here in the comments: nature “invented” antibiotics, not humans. While the cave bacteria are not exposed to antimicrobial compounds they bear resistance to, they are thought to have come from a surface strain that certainly was exposed to all sorts of these things. (Likewise, bacteria in permafrost and in fossilized feces certainly have a history of having been in a hostile environment.)

        Also, I don’t think any evolutionary microbiologist would claim that the development of antibiotics by humans (i.e. surverying the natural world to identify new such compounds, and/or engineering new compounds based on those occurring in nature) caused bacteria to create resistance genes “de novo”. As I said, I’m not a microbiologist, but as far as I know all of these “resistance genes” are really genes that had other functions in the cell and became repurposed (through evolution). The gyrA and gyrB genes in your example, for instance, don’t exist for the purpose of providing resistance to quinolones, they exist to help the bacterium manage this huge molecule (DNA), and the mutations confer resistance by making the enzyme bind the quinolone less well while still being able to do what it needs to do with DNA (albeit perhaps less well.) This is a great example of the “arms race” that goes on during evolution.

        1. Thanks for your comment, Jimbo. I understand that “bug” is typically used as slang for “bacteria.” I was simply pointing out that it is the only part of that statement that is not precisely correct.

          I certainly agree that antibiotics are a part of nature. Indeed, most of the antibiotics we use are natural compounds or based on natural compounds. However, that doesn’t change the fact that the generally-accepted idea of antibiotic resistance was that it evolved rapidly as a result of modern antibiotics. I doubt that anyone thought the genes appeared de novo, because the supposed evolution had to happen so quickly. I am sure it was thought that they appeared as a result of mutation of existing genes and their resulting selection. Nevertheless, the original idea was that this evolution was recent, as a result of selective pressure from the use of modern antibiotics. We now know that is simply false.

          I would point out that the gyrase genes are not antibiotic resistant genes, at least not using the language of the studies discussed. Antibiotic resistant genes produce proteins that fight antibiotics. The gyrase protein doesn’t do that. As you point out, it is attacked by quinolones. The mutations of the gyrase genes that give rise to quinolone resistance degrade the gyrases so that the quinolones can’t attack as well anymore. Whatever process produced antibiotic resistant genes must be radically different from the process by which gyrase mutation confers antibiotic resistance.

  6. I still don’t think this is evidence against evolution and for creationism. It is evidence against a certain simplified interpretation of the phrase “antibiotic resistance evolved rapidly as a result of modern antibiotics”, which more accurately might be stated “antibiotic resistance in a clinical setting arose quickly through micro-evolutionary mechanisms (mutation and/or horizontal gene transfer, and selection) as a result of modern antibiotics (hastened by their overuse/misuse, by the way.)” The genomes of the bacteria are changing in response to their environment, even if it’s just a single nucleotide change at a time. That’s still evolution, not a static creation.

    On the other point, yes, so a bacterium can become resistant by changing the gene that the antibiotic is targeting (as with gyrase) or by producing a protein that directly fights the antibiotic. But just as the gyrase has its own job to do, I would bet that if you were to look at the proteins that fight antibiotics, they would still themselves be related to pre-existing proteins that serve other functions in the cell, e.g. an enzyme that breaks particular chemical bonds for everyday metabolic purposes, mutating to allow the resulting protein to now also see the antibiotic compound as a substrate. Not such a “radically different” process after all. I’m unclear what you think a “creationist” result would be here — finding genes that in fact had never been used and had never been under any selective pressure, that were just waiting for humans to discover them for our benefit? I really don’t think that’s what this is.

    I think it’s disingenuous to say that the cave bacterium “had never been exposed to antibiotics” when its ancestors (the surface version) certainly had been — the only question in my mind is why the cave version might not have lost those genes if they didn’t need them, in the intervening time. But that’s a question for microbiologists to try to answer. In any case, the authors of the paper certainly didn’t seem to think (or realize?) they’d found the smoking gun of creationism.

    1. It is most definitely evidence for creation and against evolution. When a scientific theory makes accurate predictions about the data, it is more reliable. When a scientific theory makes incorrect predictions about the data, it is less reliable. The cause of resistance to modern antibiotics was predicted correctly by the creationists (who said it is not the result of new, novel genes) and incorrectly by the evolutionists (who thought it was the result of new, novel genes). Creationists don’t think creation is static. They understand what the data indicate: creatures change based on selective pressures and within the limits of the information content of the genes that are available to them.

      The process by which antibiotic resistant genes arose would have to be radically different from the way in which gyrase mutations confer antibiotic resistance. In the latter case, the gene isn’t doing anything new. It is doing the same thing, much less effectively. The fact that it confers antibiotics resistance is because the mutation degraded the protein produced by the gene. For antibiotic resistant genes to be developed, the genes would have to mutate and be selected to do something different from what they were doing before. That is radically different from a gene mutating to do the same thing it did before, but much less effectively.

      The creationist result is exactly the result we see. In the creationist view, organisms can’t evolve beyond the information content of the existing genome possibilities. Thus, if a bacterium becomes resistant to an antibiotic, it’s not because a new gene has arisen. It’s because an old gene has been degraded (as in the gyrase case) or because a gene that carried the necessary information to fight the antibiotic already existed in the genome of the bacterium or was available to be incorporated into the bacterium’s genome (as is the case in this study).

      It is certainly not disingenuous to say that the cave bacterium had never been exposed to antibiotics. In fact, it is disingenuous to say otherwise. You may want to believe that its ancestors were exposed to antibiotics, but there is no evidence for that. The only evidence we have is that the bacterium has been isolated from the surface. The best you can say, then, is that its ancestors may have been exposed to antibiotics in the past. However, as you point out, the problem then becomes why they haven’t lost those genes (or at minimum, the genes became silenced) in the time between this hypothetical exposure and now.

      I never called this finding the “smoking gun of creationism.” There is rarely a “smoking gun” for any scientific theory. There is simply evidence that can be cited in favor of the theory and evidence that can be cited against a competing theory. This is clearly evidence for creation and against evolution, as discussed above.

  7. These bacteria are indeed amazing but maybe not for the reasons listed here. I just sat down with one of the authors of the paper who is a colleague of mine at UA and was the one who collected the bacteria and has been studying this cave for many years. She pointed out a few things that are important to know about these bacteria that may not have been clear in the paper or have been published in other papers on these bacteria and cave system.

    First, the resistance to antibiotics has indeed been considered increased in many pathogenic bacteria since the production and application of many antibiotics. The fierce selection this imposes has caused bacterial which can share resistance or have mutations that adapt genes for better resistance to be selected for creating large suites of resistance genes in many strains. However, human production of antibiotics did not create resistance genes.

    Resistance genes have been common among bacteria, in part because many produce chemicals to defend themselves but if they produce a chemical they must also have a defense for it in their own genome. So antibiotic resistance genes are a product of natural chemical warfare and have always been around and no one ever thought that our use of antibiotics created resistance de-novo but we have created a greater resistance and new combinations of genomes.
    Consider that most bacteria only deal with a few competitors at a time and thus only produce a few chemicals and only need a small suit of resistance genes. So before massive doses of antibiotics (requiring more efficient or duplicate versions of resistance genes) and many different kinds used bacteria didn’t need the long stretches of multiple resistance genes. With selection they have accumulated more and more of them but these are mostly accumulated from pre-existing genes.

    Second, The bacteria in this cave have been isolated from their common ancestors for a long time. One might wonder why they have resistance genes. Part of this is due to the fact that there above ground common ancestors have large numbers of the same resistance genes albeit with some sequence differences but the genes are in the same places in the genomes. So they inherited them but one might also wonder why they have kept these resistance genes and even come up with some new ones. What I found out is that even deep down in this isolated cave there is high diversity of bacterial species/phyla but in this environment there is an extreme lack of nitrogen. This is a critical resource for the growth and survival of any bacteria. As a result there is extremely high competition for resources in this cave. They have documented very high levels of chemical warfare among bacterial lineages even within strains as the bacteria directly compete for limited resources. As such these bacteria are all producing antibiotics and must also express resistance genes to protect from their own antibiotic and try to ward off other toxins in their environments. This severe pressure on bacteria which favors any new version of a defense chemical then selects for any new mutations of other genes to be transformed into new chemical toxins. The “novel” antibiotics in the cave are adaptations of other genes to produce new antibiotics and new resistance genes to those have then also been selected as changed to resistance genes giving them the capacity to resist the new antibiotics.

    Regarding information loss or gain, these are relative terms not ones one can define irrespective of the organism in its environment. From the organisms perspective what is best is what combination of sequences make the bacteria most fit in that environment. If losing one gene product to make a different gene product improves fitness then the new gene product is an upgrade on the old gene product.

    In many ways the cave is creating conditions for bacteria much like we have by placing them under severe duress and thus creating the conditions under which high selection results in fast paced adaption. This could result in the loss of genes, the change of one gene product into another or the duplication and adaption of genes for additional functions. Calling it information loss or gain doesn’t have much meaning.

    Third, interestingly, when synthetic antibiotics created by man are introduced none of the bacteria survive. They are only resistant to many natural antibiotics because that is what they are used to (co-evolved with) and they have no capacity to resist new antibiotics. Given high selection and billions of bacteria with mutations in each we have “created” resistance to these new antibiotics because resistance genes have had mutations which have been selected for.

    1. Thanks for the extra information, Joel. I do have to correct a couple of your points, however. You say, “…no one ever thought that our use of antibiotics created resistance de-novo but we have created a greater resistance and new combinations of genomes.” However, that is quite false. As the paper that reported resistance in bacteria in permafrost says explicitly:

      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. (Vanessa M. D’Costa, et. al., “Antibiotic Resistance is Ancient,” Nature, doi:10.1038/nature10388, 2011, emphasis mine)

      As that study, this study, and other studies demonstrate, that evolution-inspired idea is quite false.

      Also, the process of producing antibiotic resistant genes from one or more genes that have a different function definitely requires addition of information into the genome. If a gene does one job and then mutates to do a very different job, that requires a new set of information. Thus, information is a very important consideration. This can certainly be defined irrespective of the organism or environment. Any novel gene is a source of novel information. Thus, adding a novel gene to a genome is an addition of information, regardless of the environment.

      1. Hello Dr. Wile.

        As a biochemist from background I might not be the most qualified person to talk about evolutionary microbiology. But please let me try to correct you in a thing or two if I can.

        Your comments are very much interesting and generally well fundamented, I’ve hunderstood you seem to be a believer of God, thus creationism and all that involves Genesis and etc.

        In this particular matter, there are 2 things.

        First, what the statement you quoted and the paper overall tell us, is that the antibiotic resistance process isn’t a product of modern clinical use of antibiotics (as it is widely expressed as an oversimplification) but rather an old process that already existed. Yet, none of this proves that this old antibiotic resistance phenomenon isn’t derived from an evolution-based mechanism. Once again, it just says that it was already happening before.

        And this means, that there is a misinterpretation nowadays about antibiotic resistance mechanism. Most common people think that ‘de novo’ antibiotic resistance genes are popping up here and here everytime someone wrongly misuses antibiotic prescriptions. This may not be true as it is, but evolutionary steps are still happening, but at a much slower pace than people picture or imagine it.

        And this is where it leads me to my 2nd point. Where I think your apparently reasonable denial of evolution falls apart. Evolution does not has to happen for a reason, evolution is simply a process where the fittest survive. But this ‘fitness’ does not have to come due any specific reason. Mutations occur most of the times due to the lack of 100% accuracy of DNA error-correcting machinery in all the several steps that involve DNA itself, from replication to strand formation or nucleotide conjugation, nucleotides can be wrongly positioned and the repairing machinery fail to notice it. This all bound to stochasticity in of itself.
        This nucleotide exchange that happened due to a random mistake, can create a change in the aminoacid coded, the 3D structure of the protein might be altered, which might lead to an increased range of molecules degradaded which can include an antibiotic that was not being metabolized by the bacteria prior to this mutated protein appear.

        This is all to say that, mutations and thus newer fitness and adaptability that ultimately lead to evolution, do not need an the input of any new information that drives this process. Evolution most of the times just happens due to stochasticity, that’s why strains with the most diverse gene pool have an ‘a priori’ more probability of adapting and surviving new environment changes.

        So using your words, if a gene does one job and then mutates to do a very different job, that DOES NOT require a new set of information. Just sometimes it happens due to a series of events based on chance itself.

        1. Thanks for your comment, João. I agree that this paper and the others mentioned don’t show that antibiotic resistance couldn’t have come about by some unspecified evolutionary mechanism. It simply shows that the initial evolution-inspired interpretation of antibiotic resistance is completely false. This is, of course, precisely what I said in the article.

          However, I will have to correct you on your second point. If a gene mutates so that a protein with a very different function is produced, it most certainly does require new information. The vast, vast, vast majority of combinations of nucleotide bases will produce proteins that have no function whatsoever. Thus, the function of a protein does, indeed, represent information. You can think of this in terms of letters and words. The vast, vast, vast majority of series that can be made with letters have no function, but the correct combination of letters that results in a recognizable word represents information.

          Now, you are correct that evolution doesn’t have any reason. However, to produce a functional protein, it must be able to produce information. The evolutionist believes (incorrectly) that such information can come about as a result of random mutation. The creationist understands that this simply isn’t possible to any meaningful degree. Thus, while random mutations can alter information, it is generally to deteriorate it, not to enhance it. This, of course, is precisely what we see when evolution is tested in the laboratory (see here and here, for example). The evolution of antibiotic-resistant genes requires that random mutations regularly enhance information, and all the evidence indicates this simply doesn’t happen.

  8. “Creationists don’t think creation is static.” They don’t any more (I suppose because the evidence became too overwhelming) but they certainly used to think that, not only with regard to life on earth but its geology, although I’ll grant you that was over 100 years ago. You say that creationists understand that the data indicate that “creatures change based on selective pressures and within the limits of the information content of the genes that are available to them.” I don’t disagree with that, though I think describing it in terms of “information content” leads to conceptual pitfalls, and I think we certainly differ in what we consider those limits to be.

    “For antibiotic resistant genes to be developed, the genes would have to mutate and be selected to do something different from what they were doing before.” Well, no, for the reason I gave before: bacteria and other cells have enzymes that break down all sorts of natural compounds already, so say they get a mutation that tweaks an enzyme’s substrate specificity so it’s now able to break down an antimicrobial compound that resembles the original substrate. Not so hard to imagine, certainly not radical.

    You say that according to creation theory the organism can’t “evolve beyond the information content of the existing genome possibilities.” But then you would agree that those possibilities must include other bacteria (via horizontal gene transfer)? And with regard to theorized mechanisms of evolution more generally, you wouldn’t dispute that genes can become duplicated, by a variety of mechanisms? I think you are building a classic straw man when you claim that evolutionists believe that “new genes” can arise during evolution. No evolutionist I know thinks that antibiotic resistance arose when humans began their widespread use in the clinic because bacteria evolved totally novel, dedicated resistance genes out of thin air.

    I guess you’re right that you’re not being disingenuous if you don’t believe that the ancestors of the cave bacterium had at one time been exposed to antibiotics; I think it’s overwhelmingly likely that the cave bacterium arose from the surface version, and that the surface version almost certainly was exposed to antimicrobial compounds. This is apparently not what you believe, but I was making the assumption that you did. I would nonetheless agree with Luke’s earlier assertion that this and your related posts on the subject are misleading with regard to the origin of antibiotics, suggesting they are human inventions (you even used the word yourself in your reply to him) rather than natural products generated by relatively simple organisms (and as such, have probably been around for eons.)

    1. Thanks for your reply, Jimbo. I agree that your proposed scenario (tweaking a gene that already produced a decomposition enzyme) isn’t hard to image. However, that is still radically different from the way the gyrase mutations confer resistance. Once again, gyrase mutations confer resistance by deteriorating the protein, and the protein continues to do the same thing it did before, but much less effectively. Your scenario is radically different, since the protein is now doing another job as a result of being tweaked. Of course, the issue is how far this tweaking can go. The evidence suggests that the tweaking is very limited, which is precisely what creationists suggest.

      You say, “No evolutionist I know thinks that antibiotic resistance arose when humans began their widespread use in the clinic because bacteria evolved totally novel, dedicated resistance genes out of thin air.” Once again, I agree that no one thought they came out of thin air, because the supposed evolution happened too quickly. However, they did think they came as a result of modern antibiotic use, as demonstrated by the quote I shared with both John and Joel. Once again, as the original post indicates, this evolution-inspired idea has been falsified by these kinds of studies.

    2. “Creationists don’t think creation is static.” They don’t any more (I suppose because the evidence became too overwhelming) but they certainly used to think that


    3. From evolution mill, NCSE:

      The idea that species were universally thought to be fixed prior to Darwin is simply wrong — many creationist thinkers of the classical period through to the 19th century thought that species could change. Linnaeus, the father of modern taxonomy, began his career committed to the fixity of species, but began accepting the evidence against such fixity approximately a century before Darwin’s ideas were published. Nor was fixism widely accepted within the scientific community…

      What is more, nothing in the biblical or theological traditions requires that species are fixed, only that kinds exist, which neither evolutionists nor traditional creationists ever denied.

      Your claim is in the same bag with the “but creationists, er, flatearth… something, er…” myth.

      1. Addressing your two comments together: I guess you mean “evidence” that they used to think that, versus the evidence that changed their viewpoint? In either case, I admit I wasn’t at all clear here what I meant. “Static” may have been an overstatement in the absolute sense when I first used it, but not in the relative sense. From the same NCSE article you quote from, “Initially, creationism did require fixity of species.” Thinking that all life on earth arose from a handful of “kinds” that could fit on an ark, over a few thousand years, I would describe as “static” relative to an alternative theory that it arose over millions of years from a common ancestor. (I was also thinking of geological uniformitarianism vs. catastrophism, the latter of which might be described as “a mostly static creation with a big flood now and then.”)

        The creationists I suppose I was thinking of when I said “they don’t (think that way) any more” are actually the theistic evolutionists, ID proponents, even OEC’s (though I realize there are clear differences in those groups) as opposed to YEC’s.

        1. Come off it—‘Jimbo’ clearly meant to tie creationists with the straw man of ‘fixity of species’. Certainly, a major founder of uniformitarian geology and mentor of Darwin, Charles Lyell, taught this false and antibiblical doctrine.

          Much of Darwin’s “Origin of Species” was devoted to knocking down this straw man. As demonstrated above, nothing much has changed with modern evolutionary agitprop—and that of their churchian allies.

          In reality, creationists have long pointed out that the created kinds were broader than ‘species’, regardless of how they are defined. This is true of Whitcomb’ and Morris’ classic “The Genesis Flood” which is older than I am. Frank Marsh coined the term ‘baramin’ 20 years before that, in 1941.

          The biblical creationist view has long been likened to an ‘orchard’ in contrast to the single evolutionary ‘tree’ or the straw man of a creationist ‘lawn’ of fixed species.

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