Answer by Diane Eager
Antibiotic resistance is regularly presented as proof of evolution in school courses and to the general public, and hardly a week goes by without some health experts warning us about “superbugs” evolving resistance to antibiotics. Scientists have also carried out experiments where they expose bacteria to gradually increasing amounts of antibiotics and found bacteria that survived the highest doses with multiple genes that resist antibiotics. So yes, the rise of multi-resistant bacteria is a real observation, but how do we check whether is or is not evolution?
What is missed by most researchers and the educators in all experiments used to demonstrate the rise of antibiotic resistance within a population of bacteria, is the bacteria at the end of the experiment without exception prove to be the same species as the bacteria used at the beginning. Therefore, there has been no ‘origin of any species’ at all, since bacteria have not evolved into anything else. The same applies to the multi-resistant superbugs found in hospital infections – they all turn out to be the same species as non-resistant varieties.
So what is the origin of this resistance? Did any new genes evolve, even if no new species have appeared?
To find the answer to this scientists have studied bacteria from old soil samples kept in sealed containers in museums, or from isolated wilderness areas not exposed to human activity. As a result of testing these microbes for resistance, we now know that bacteria with genes for antibiotic resistance existed before antibiotics were used in human medicine, and antibiotic resistance did not arise by evolution from non-resistant bacteria after humans started using antibiotics. Here are some examples.
The Lechuguilla cave is a vast deep cave in Carlsbad Caverns National Park, New Mexico, discovered in 1986. Since its discovery, entry to the cave has been strictly limited to a few researchers. In 2008 the National Park authorities permitted microbiologists to take samples of biofilms (mats of bacteria) from regions in the cave that had not been exposed to humans. They tested 93 kinds of bacteria with a barrage of modern-day antibiotics and found most of them could resist three or four classes of antibiotics. Three of them could fight off 14 different antibiotics, including semi-synthetic compounds. Gerald Wright of McMaster University commented: “Our study shows that antibiotic resistance is hard-wired into bacteria. It could be billions of years old, but we have only been trying to understand it for the last 70 years.” (Ref. PLoS ONE, 2012; 7 (4): e34953 DOI: 10.1371/journal.pone.0034953. Also see ScienceDaily and National Geographic News 11 April 2012)
Scientists have also extracted bacteria from soil that has been frozen for thousands of years in high arctic regions of Canada and tested them for antibiotic resistance. They found resistance to multiple antibiotics, including some modern semi-synthetic compounds. One research team found bacteria that could resist Vancomycin, a modern antibiotic usually reserved for treating infections with multi-resistant “superbugs”. The scientists were able to insert the gene for Vancomycin resistance from the permafrost bacteria into modern-day laboratory grown strains to see if it produced the same effect as modern day superbugs. They found it “showed the same activity and had almost the same structure as its modern counterpart”. The scientists concluded: “These results show conclusively that antibiotic resistance is a natural phenomenon that predates the modern selective pressure of clinical antibiotic use”. (Ref. Nature doi:10.1038/nature10388. Also see ScienceNOW 31 August 2011, and ABC News in Science 1 September 2011.)
The two studies described above of extremely isolated or dormant frozen bacteria fit with studies of living functioning soils that indicate antibiotics and antibiotic resistance are part of normal soil microbial life. The McMaster University scientists who studied the cave bacteria, had also studied 480 strains of a bacterium named Streptomyces, isolated from soil samples collected from numerous different urban and forest sites in Canada. They then tested the bacteria with 21 different antibiotics. Most of the bacteria were resistant to seven or eight antibiotics, but two particularly tough specimens were resistant to 15. (Ref. Science, vol 311, p374, 20 January 2006.)
Most of the antibiotic resistant microbes found in soil or on other natural places in the environment are not associated with causing disease in humans, but they can pass on their resistance genes to other bacteria that do cause disease. They do this through process called conjugation, a type of bacterial sex, where pieces of DNA containing the resistance genes can be passed from one bacterium to another, even to other species of bacteria. This means there was a pool of naturally occurring resistance genes out in the environment that could be passed onto microbes that can infect people, way before we discovered modern antibiotics. This process is the key to understanding the rapid rise of antibiotic resistance in the modern era.
When antibiotic resistance was first discovered it was assumed bacteria were evolving new genes by random mutations. However, as new antibiotics were introduced, and bacteria with resistance to more than one antibiotic were found, scientists realised this gain of resistance was happening too quickly to be explained by random mutations. Furthermore, patients were presenting with bacterial infections that were resistant to antibiotics they had not been treated with. So it was soon argued that there had to be another process besides random mutations newly evolving resistance in one microbe which was then being passed onto their progeny.
By the 1960’s it had been discovered that bacteria could transfer pieces of DNA to other bacteria, and further research has shown that this “horizontal gene transfer” is a major means by which antibiotic resistance can rapidly spread through the population of bacteria, even across species. Bacteria were not evolving new genes – they were redistributing existing ones. This gene transfer can involve whole clusters of genes, and enables bacteria to accumulate multiple resistance genes even for antibiotics they had not been exposed to. In spite being found some 50 yrs ago, the text books and popular media have still largely not caught up, and repeat the ignorance of the 1950 “evolving resistance” stories.
Some antibiotic resistance is however due to mutations, especially concerning antibiotics that work by using their shape to lock onto (binding) an enzyme in the bacterial cell. Enzymes are proteins that facilitate chemical reactions. Antibiotics that target such enzymes do so by fitting into the shape of the protein. This binding preventing the enzyme from carrying out its function. As a result anything that can change the shape of the enzyme, can prevent it doing its job, so sometimes a small mutational change in the DNA code for the enzyme, results in an enzyme with a slightly distorted shape. This may be enough to hinder the antibiotic from binding to it. Such enzymes are usually less efficient than un-mutated ones, and the bacteria carrying them are less viable than the norm in the everyday environment. But if the bacteria carrying them are placed in an artificially high-antibiotic environment (e.g. hospital) they do have a survival advantage. Slow versus dead is a real winner! However, there is a fine balance here. Since it doesn’t take much more change in the shape of an enzyme to move it from inefficient to useless, so any further mutations kill the bacteria rather than make it more resistant.
So key to understanding here is that these mutated bacteria, only survive and flourish in places where the un-mutated bacteria are killed off by antibiotics. This is selection, but it is not evolution. The bacteria are still the same species. They just have some slightly degenerate proteins. Furthermore, such mutations do not explain where the proteins, let alone the whole bacterial cell, came from in the first place, so despite the enthusiasm of text books and teachers, they are no evidence for life evolving from non-life, or for one life form evolving into another.
The rise of antibiotic resistant superbugs is not due to the bacteria evolving, but is the result of extreme selection of bacteria carrying pre-existing resistance genes when they find themselves in artificial environments such as vet clinics, farms, factories and hospitals. Large doses of antibiotics kill off the non-resistant forms, leaving already resistant forms with pre-existent genes to multiply and flourish. The resistant forms pass on the useful genes to their own progeny (a process labelled vertical gene transfer) and also to other bacteria in the same microbial community by horizontal gene transfer, and it doesn’t take long for multi-resistant superbugs to dominate the population as our antibiotic medicines kill off the non-resistant forms.
A Natural Phenomenon
This research showing antibiotic resistance is a part of normal microbial ecology leads to an obvious question: What was and is it for?
Julian Davies, a microbiologist at University of British Columbia has made an intriguing suggestion when describing his team’s research: “Our interest in antibiotics also includes studies of the roles of antibiotics in nature; are they used as weapons in inter-cellular warfare, or are they signalling agents that help to stabilize the interactions between bacterial communities in different environments? We believe the latter is more correct and have been accumulating evidence for years that resistance genes are primarily designed for communication between differing bacteria and other chemical messaging even with other organisms such as plants and even animals”. (Julian Davies UCB web page here)
Davies’ suggestion fits well with the Biblical view that bacteria were created as fully functioning organisms in a very good world. The original bacteria were part of fully functioning ecosystems where organisms had to interact with one another to keep the system going. Antibiotics and resistance were part of that system.
It was only after the system began breaking down that bacteria started causing disease. As a result of the degeneration of our immune systems and degeneration in the bacteria ended up in wrong places and caused disease.
When people started using large amounts of antibiotics to control disease the process of selection eliminated the non-resistant microbes, leaving the resistant ones to survive until superbugs became a self-made problem, which we can neither blame God for nor credit evolution with. Thus, a pre-existing natural phenomenon with a useful function in a very good world has been co-opted to enable bacteria to survive in a world that has been corrupted and is no longer very good. Again we need to emphasise the point that this is survival of the fittest, it is natural and artificial selection, but it is not evolution!
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