A scientific urban myth
An often-repeated claim is that disease organisms, such as tuberculosis, are ‘evolving’ to become resistant to antibiotics such as penicillin. There’s no doubt that antibiotic-resistant strains of disease organism are becoming prevalent - but is this Darwinian evolution or simply Darwinian myth making? The talk.origins “FAQ” makes repeated reference to the ‘evolution of antibiotic resistance.’ A representative example is the essay entitled ‘The Evolution of Improved Fitness By Random Mutation Plus Selection’, in which Dr Edward E. Max says:
However, the experiments necessary to demonstrate a beneficial mutation can be done with laboratory organisms that multiply rapidly, and indeed such experiments have shown that rare beneficial mutations can occur. For instance, from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance. In this case (in contrast to the situation with the peppered moth populations described above) origin of the population from a single bacterium allows comparisons of the mutated genes with the corresponding genes from the original bacterium, verifying that the variant sequences were not present before the culture with antibiotics and therefore arose as de novo beneficial mutations.
On the face of it, claims such as this seem to be strong evidence for Darwinian processes. There is a beneficial genetic mutation; the mutation makes the bacterium better adapted so enabling it to survive and flourish giving rise to offspring that also possess the beneficial mutation; natural selection is seen in action.
And because the appearance of resistance to antibiotics is essentially a modern phenomenon — antibiotics being a twentieth century discovery — it also seems on the face of it to be strong evidence of rapidly breeding organisms evolving a brand new characteristic within the space of a single human lifetime.
For the moment, let us accept that the facts as given by Dr Max are the truth, the whole truth and nothing but the truth (although I shall show later that this is far from the case). If the facts are as presented, then isn’t the case of acquired antibiotic resistance by bacteria strong evidence in favour of Darwinism?
The answer turns out to be ‘no’, even on the facts as given. Darwinism is a theory accounting for speciation — Darwin’s book is concerned with ‘The origin of species’ and it proposes that the species of plant and animal in the world today have arisen gradually from previous species by mutation and natural selection, a process also known as speciation.
Does the acquisition of antibiotic resistance shed any light on the process of speciation? No it does not, because a bacterium (such as E. coli, for example,) which acquires antibiotic resistance remains the same species, E coli.
Some humans have natural disease resistance, some don’t. The same is true for dogs, horses and plants, but this natural resistance hasn’t made them into new species. An aardvark that is tuberculosis-resistant is still an aardvark; a zebra still only a zebra. The acquisition of such resistance provides no evidence on speciation.
It can, of course, be argued that the acquisition of antibiotic resistance by spontaneous mutation is one step on the long road from one species to another. But such an argument is of no use here because whether speciation occurs at all is the very question that is to be proved, scientifically.
Darwinists believe that speciation can and does occur. But when pressed to provide examples of speciation they have signally failed to do so (for a detailed critique of the talk.origin “FAQ” on Speciation, click here).
This is more than mere semantics. It cannot legitimately be argued by Darwinists that the acquisition of antibiotic resistance by mutation is a step along the road to speciation, if they have failed to provide concrete evidence for the existence of such a road in the first place.
Perhaps, then, the acquisition of antibiotic resistance by spontaneous mutation helps Darwinists make the case that advantageous genetic mutations of the Darwinian kind occur? This is more promising for the Darwinist case, but again doesn’t entirely make the grade as evidence. Noone who is in possession of the facts — whether Darwinist or not — doubts that genetic mutations occur. Such mutations are merely DNA copying errors and it would be surprising if they did not occur — since all copying systems are fallible. Many diseases are known, all of which result from genetic mutation — including Down’s syndrome, Huntington’s Chorea and Achondroplasia or dwarfism.
If we accept that the acquisition of antibiotic resistance does open the door to the possibility of beneficial genetic mutations, does this materially assist Darwinists? I do not think so. My reason for saying this is that the feature in question is almost trivial in comparison with the kind of beneficial genetic mutations that would have to happen for speciation to occur: mutations such as the feathered wing, the mammalian eye or even the human hand. At best, therefore, antibiotic resistance provides only weak circumstantial evidence for the kind of genetic mutation that is necessary to sustain Darwinian processes.
But, in any case, there is a far more serious objection to acquired antibiotic resistance than this. Darwinists do not have even this slim comfort, because there are a number of things scientifically wrong with Dr Max’s account — in fact, three things wrong with it.
First, there are objections to the idea of novelty, second, objections to the idea of Darwinian mutation being involved at all and, third, objections to the idea that the process can be demonstrated experimentally in the laboratory with any certainty.
The first objection is that antibiotic resistance is not new. Antibiotics such as penicillin, from the Penicillium spore, and similar organisms, have existed for millions of years in natural form. It is only their discovery by mankind in the twentieth century and their medical use to combat organisms harmful to humans that is new. So there is no question of disease organisms suddenly evolving natural resistance to antibiotics — there must be microorganisms that have been resistant to Penicillium for millions of years. This in turn means that antibiotic-resistant genes of various kinds must already be present in some, perhaps many strains of microorganism.
The second objection is that, although many common disease microorganisms, such as the tuberculosis bacterium, may be killed off by antibiotics, there are often a few individual organisms that are genetically resistant to the antibiotic — just as in any community of humans there will be a minority who possess natural resistance to tuberculosis and other disease organisms.
When such a colony of tuberculosis bacteria is exposed to an antibiotic, it will kill off all the bacteria except those who possess natural resistance, and it is these few who will remain and recolonise.
Despite Dr Max’s denials, the case of antibiotic resistance in microorganisms is exactly the same in principle as that of so called ‘industrial melanism’ in the peppered moth. It is simply a case of one variety of the species flourishing while another variety dies off, because of changed environmental conditions.
If Darwinists wish to claim that this is natural selection in action, they are free to do so. But they cannot claim this as a credible mechanism for evolution.
The third objection takes a little more explanation. Some scientists, such as Dr Max above, insist that laboratory experiments have been conducted which prove scientifically that antibiotic resistance was not genetically present in the microorganism used to culture the experimental colony, thus proving conclusively that it must have arisen by spontaneous genetic mutation, de novo — as an entirely new genetic feature.
This claim is scientifically flawed for two reasons.
As pointed out earlier, resistance to antibiotics is nothing new. It is perfectly possible that genes for such characteristics are present in all or many microorganisms but are merely ‘switched off’ or unexpressed. The genes can be ‘switched on’ by environmental pressure such as an antibiotic environment.
Dr Max also makes the claim, frequently repeated by Darwinists on the Internet, that (the emphasis is added by me);
from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance. In this case (in contrast to the situation with the peppered moth populations described above) origin of the population from a single bacterium allows comparisons of the mutated genes with the corresponding genes from the original bacterium, verifying that the variant sequences were not present before the culture with antibiotics and therefore arose as de novo beneficial mutations.
This claim can never be strictly true. In order to do what Dr Max describes here, the experimenter would necessarily have to both culture the new population from his single experimental bacterium AND fully sequence the DNA in that same single bacterium for later comparison. But, of course, analysing the DNA of the experimental bacterium must necessarily destroy it, making it impossible to culture from.
Instead the experimenters do the next best thing: they select a number of individuals from the same culture, which they assume to be genetically identical and they analyse the genes of one (or more) and use the others to culture the new colony. If the bacterium they select to analyse appears not to have any genes for antibiotic resistance then they assume that the same must be true for its close relative they are using to breed.
Now if the experiments always worked as Dr Max claims, if the new culture always exhibited antibiotic resistance, then one might be inclined to give some credence to their interpretation of the results. But that is not what happens. Sometimes the new culture develops antibiotic resistance; sometimes it doesn’t.
What happens to the experiments which do not develop antibiotic resistance? The experimenters put the failed experiments into the waste bin, while reporting the experiments that do work. So how do they know the true cause of experimental success and experimental failure? For it is possible that their experiments are succeeding when they choose a progenitor that already has antibiotic resistance and failing when they choose one that does not possess those genes — regardless of what their genetic analysis of the sacrificial bacterium shows.
Perhaps Dr Max and other convinced Darwinists might say that choosing one bacterium for genetic analysis and a very close relative for culturing is as close as one can get to experimental certainty, and is almost scientific proof. But the whole point of science is that ‘almost’ isn’t good enough. Either the lab proves what Dr Max claims, or it doesn’t prove it, in which case he cannot make the claim. There is already enough sloppy thinking and bad science in Darwinism without deliberately introducing more.
And as we have already seen, there are other possible explanations for their pattern of success and failure. Most importantly, antibiotic resistance is not a modern phenomenon, it may have been around for millions of years. So it is perfectly feasible that many bacteria possess genes that can provide resistance — whether or not those genes are currently expressed, and whether or not they have even been identified by geneticists as genes for providing antibiotic protection.
Such unexpressed genes are known to be sometimes ‘switched on’ by environmental pressures of just the life-threatening kind that are applied to bacteria in the lab. So, even if antibiotic resistance were genuinely arising during the experiment, it is not necessarily arising de novo, as Dr Max claims, but may merely be a genetic throwback.
It isn’t only Dr Max who perpetuates the scientific urban myth of the ‘evolution’ of antibiotic resistance. Other talk.origins “FAQs” make similar false claims.
For example, In the “FAQ” entitled ‘Are Mutations Harmful?’ Richard Harter says;
In modern times antibiotics, drugs that target specific features of bacteria, have become very popular. Bacteria evolve very quickly so it is not surprising that they have evolved resistance to antibiotics.
And in the “FAQ” entitled ‘Publish or Perish’ by John Catalano, he baldly asserts that ‘Drug resistance is biochemical evolution’ and cites an article in Scientific American entitled ‘The Challenge of Antibiotic Resistance.’
All of these “FAQs” are scientifically flawed and Messrs Max, Harter and Catalano should be asked to provide detailed concrete evidence in place of mere assertions.
If they fail to provide such detailed concrete evidence, then their “FAQs” should be amended to remove any reference to the ‘evolution’ of antibiotic resistance in microorganisms, or of the acquisition of such resistance providing supporting evidence of Darwinian evolution.
Update - 1st September 2006
A number of visitors to this site have pointed out to me a second important conclusion that can be drawn from the scientific facts reported above. The failure of Darwinists to demonstrate the evolution of acquired resistance to antibiotics actually casts considerable doubt over the entire theory. The reason is as follows.
Microorganisms multiply very rapidly. Under the right conditions of temperature and nutrients, a single bacterium can reproduce in minutes, giving rise to more than 4 million offspring in 8 hours. This rate of reproduction is more than fast enough to demonstrate the Darwinian process of mutation and natural selection happening in real time. In thousands of laboratories all over the world, literally billions and billions of reproductions take place under controlled conditions. The DNA of these microorganisms can be analysed as a matter of routine. Yet no microbiologist has so far announced observing the appearance of a new species of bacteria through the Darwinian process of the natural selection of genetic mutations (other than the bogus claims described above.)
If the natural selection of genetic mutations really were the primary driver of evolution, then there should be hundreds, or even thousands of new species appearing on an almost daily basis. Schoolkids should be able to breed new species on their classroom window sill. Yet far from such profligate innovation, what is actually found in the laboratory is stability and resistance to change - what Ernst Mayer called genetic homeostasis.
What is true for rapidly breeding microrganisms is likely also to be true of much slower breeding multi-celled creatures; that far from being the driver of evolution, the natural selection of genetic mutations has a neglible effect on inheritance.