Superbugs not super after all
Dr Graham Beards en.wikipedia
Antibiotic resistance tests: Bacteria are streaked on the dish on which antibiotic impregnated white disks are placed. Bacteria in the culture on the left are susceptible to the antibiotic in each disk, as shown by the dark, clear rings where bacteria have not grown. Those on the right are fully susceptible to only three of the seven antibiotics tested.
After over 12 years as a medical practitioner, I suddenly found myself an avid consumer, rather than a provider, of medical care. Involved in a serious road accident in 1986, I spent many months in hospital, including weeks in an intensive care unit.
While in intensive care, I became infected with one of the varieties of so-called ‘supergerms’, which are the scourge of modern hospitals. These are strains of bacteria which are resistant to almost every (and in some cases every) type of antibiotic known to man.
Several others in the same unit with me died as a result of infection by the same bacterial strain. The germs overwhelmed their immune systems and invaded their bloodstream, untouched by the most expensive and sophisticated antibiotics available.
This ‘supergerm’ problem1 is an increasingly serious concern in Western countries. It strikes precisely those hospitals which are more ‘high-tech’, and handle more serious illnesses. Applying more disinfectant is not the answer; some strains of germs have actually been found thriving in bottles of hospital disinfectant! The more antibacterial chemical ‘weapons’ are being used, the more bacteria are becoming resistant to them.
The reality of increasing bacterial resistance seems at first to be an obvious example of onwards and upwards evolution. But the facts, when carefully examined, show otherwise.
Natural selection, but not evolution
Evolution is basically the belief that everything has made itself—that natural processes (over millions of years, without miraculous, divine input of intelligence) have created an increasingly complex array of creatures. According to evolution, there was once a time when none of the creatures in the world had lungs. This means that there was no genetic information (the ‘blueprint’ for living things, carried on the molecule DNA) for lungs—anywhere. Then, at a later time, ‘lung information’ arose and was added to the world, but no ‘feather information’ as yet—feathers evolved later.
In other words, for every feature which arises by evolution, there would need to be new genetic information added to the total information in the biosphere (i.e., all the information in all creatures on earth). Some features could be lost subsequently, of course, so there will not always be a gain, but if microbes turned into magpies, maple trees and musicians, there must have been a massive net increase in information. This is not just any jumble of chemical sequences, but meaningful information, since it codes for complex structures which have purposeful functions.
So if new information, new functional complexity, can be shown to be arising by itself where previously there was none, this would give some credibility to the idea of molecules-to-man evolution, although it would not strictly prove that it had occurred. However, it can be shown that in every situation where populations of living things change, they do so without increase (and often with a decrease) of information. Thus, it is completely illegitimate for anyone to claim that such changes show ‘evolution happening’. Let’s look at what is known about how the ‘superbugs’ became resistant, and ask—did any new structures or functions arise in the process (which is another way of asking whether there was any evidence of evolution)?
There are a number of different ways in which germs can become resistant to these poisons. A ‘superbug’ is, by definition, resistant to many different antibiotics. It may have become resistant to antibiotic A in one way, to antibiotic B in a completely different way, and to antibiotic C in another way again. So if we look at all the known ways of resistance arising in a population of germs, we will see if any of them are uphill, information-adding processes.
1. Some germs already had the resistance.
If out of a million bacteria, five already have a feature which makes them resistant (however that arose) to, say, penicillin, then soaking them in penicillin will kill all of them except for the five. Now the body’s natural defences will often ‘mop up’ such a small population before it can multiply and cause harm, so resistance will not become a problem. However, if that doesn’t happen, then those five germs can multiply, and their offspring will obviously also be resistant. So within a short time, there will be millions of germs resistant to penicillin. Notice that:
(i) This is why multiple resistance to major antibiotics is more common in hospitals which treat more serious conditions—these are the hospitals which will frequently be using the sophisticated, expensive ‘heavy artillery’ antibiotics, so this sort of ‘natural selection’ will happen more often.
(ii) In this kind of instance, the information to resist the antibiotic was already there in the bacterial population—it did not arise by itself, or in response to the antibiotic. That some germs were already resistant to man-made antibiotics before these were invented is common knowledge to microbiologists. Soil samples from villages where modern antibiotics had never been used show that some of the germs are already resistant to drugs like methicillin which have never existed in nature. Bacteria revived from the frozen intestines of explorers who died in polar expeditions carried resistance to several modern antibiotics, which had not been invented when the explorers died.2
2. Some germs directly transfer their resistance to others.
In an amazing process, the closest thing to sex in bacteria, one germ inserts a tiny tube into another, and a little loop of DNA called a ‘plasmid’ transfers from one to another. This sort of gene transfer, which can obviously pass on information for resistance to a drug, can even happen between different species of bacteria.
Notice, again, that the information for the resistance must already exist in nature before it can be passed on. There is no evidence of anything totally new arising which was not there before. This is information transfer, not information creation.
So far, we have dealt with situations in which resistance was obviously already there. Evolutionists would claim, of course, that such resistance evolved originally in the (unobservable) past. However, if observed changes in the present do not show us new information, what support is there for the idea that such information arose in the past? The mechanism that is put forward for this past evolution is invariably mutation—a copying mistake, an accidental change in the DNA code passed on to the offspring. So that brings us to the final way in which bacteria can become resistant.
3. Some germs become resistant through mutation.
Interestingly, where this happens, there is no clearcut evidence of information arising. All such mutations appear to be losses of information, degenerative changes. For example, loss of a control gene may enhance resistance to penicillin.3
Some antibiotics need to be taken into the bacterium to do their work. There are sophisticated chemical pumps in bacteria which can actively pump nutrients from the outside through the cell wall into the germ’s interior. Those germs which do this efficiently, when in the presence of one of these antibiotics, will therefore efficiently pump into themselves their own executioner.
However, what if one of these bacteria inherits a defective gene, by way of a DNA copying mistake (mutation) which will interfere with the efficiency of this chemical pumping mechanism? Although this bacterium will not be as good at surviving in normal circumstances, this defect actually gives it a survival advantage in the presence of the man-made poison.4 Once again, we see that information has been lost/corrupted, not gained.
It is precisely because the mutations which give rise to resistance are in some form or another defects, that so-called supergerms are not really ‘super’ at all—they are actually rather ‘wimpy’ compared to their close cousins. When I was finally discharged from hospital, I still had a strain of supergerm colonizing my body. Nothing had been able to get rid of it, after months in hospital. However, I was told that all I had to do on going home was to ‘get outdoors a lot, occasionally even roll in the dirt, and wait.’ In less than two weeks of this advice, the supergerms were gone. Why? The reason is that supergerms are actually defective in other ways, as explained. Therefore, when they are forced to compete with the ordinary bacteria which normally thrive on our skin, they do not have a chance. They thrive in hospital because all the antibiotics and antiseptics being used there keep wiping out the ordinary bacteria which would normally outcompete, wipe out and otherwise keep in check these ‘superwimps’.5
If they are ‘weaker’, then why do they cause so much death and misery in hospitals? These bacteria are not more aggressive than their colleagues, it is only that doctors have less power to stop them. Also, those environments which will tend to ‘select’ such resistant germs, like intensive care units, are precisely the places where there will be critically injured people, physically weakened and often with open wounds.
This is why more than one microbiologist concerned about these super-infections has mused (only partly tongue in cheek) that the best thing to happen in major hospitals might be to dump truckloads of germ-laden dirt into the corridors, rather than keep on applying more and more chemicals in a never-ending ‘arms race’ against the bacteria. In other words, stop using the antibiotics (which of course is hardly feasible), and all this ‘evolution’ will reverse itself, as the bacterial populations shift back again to favour the more hardy, less resistant varieties.
Summary and Conclusion
1. ‘Supergerms’ are actually not ‘super’ at all. They are generally less hardy, and less fit to survive outside of the special conditions in hospitals.
2. There are many instances in which germs become resistant by simple selection of resistance which already existed (including that ‘imported’ from other bacteria).
3. Where a mutational defect causes resistance, the survival advantage is almost always caused by a loss of information. In no case is there any evidence of an information-adding, ‘uphill’ change.
4. ‘Supergerms’ give no evidence to sustain the claim that living things evolved from simple to complex, by adding information progressively over millions of years.
Death, suffering and disease (including infection) are part of the curse which came upon a once-perfect world through the rebellion of our original ancestor, Adam, against his Maker.
Bacteria actually provide evidence against evolution. Bacterial populations multiply at incredibly high rates. In only a matter of a few years, bacteria can go through a massive number of generations, equivalent to millions of years in human terms. Therefore, since we see mutation and natural selection in bacterial populations happening all the time, we should see tremendous amounts of real evolution happening. However, the bacteria we have with us today are essentially the same as those described by Robert Koch a century ago. In fact, there are bacteria found fossilised in rock layers, claimed by evolutionists to be millions of years old, which as far as one can tell are the same as bacteria living today.
The famous French biologist Pièrre Grassé, who held the chair of evolution at the Sorbonne for many years, admitted that mutations in bacteria simply showed shifts back and forth around a mean, but no net effect. Overall, he said, ‘mutations do not produce any kind of evolution.’6
When next you read about ‘supergerms’, remember that everything known about them is consistent with the Genesis creation of an originally good, complex world ruined by sin.
References and Notes
- Common types of bacteria to become resistant to many different types of antibiotics at once (called multiple drug resistance) are Klebsiella, Pneumococcus, and Staphylococcus. The term ‘golden staph’ has become a lay expression for these superbugs, but it is actually a correct lay term for the most common type of staph, otherwise known as S. aureus, which applies even if the bug is not multiply resistant. Return to text
- McGuire, R., Eerie: Human Arctic fossils yield resistant bacteria, Medical Tribune December 1988, pp. 1, 23. Return to text
- The enzyme penicillinase, produced by some bacteria, destroys penicillin. If a member of a bacterial strain producing a modest amount of this substance were to inherit a mutational defect which damaged or deleted the gene controlling production of this enzyme, the organism would invest a lot of resources into producing copious amounts of penicillinase. Thus, this defect would be an advantage in an environment containing penicillin, but would be a disadvantage otherwise. Once again, a loss is involved. There is no evidence that the complex information coding for penicillinase production arose by mutation. Return to text
- For a somewhat more detailed and technical treatment of the whole matter of antibiotic resistance, with further references, see also Wieland, C., Antibiotic Resistance in Bacteria J. Creation 8(1):5–6, 1994. Return to text
- This of course is a real dilemma facing the medical profession, especially when faced with patient demand for antibiotics for illnesses which would probably get better without them. The more that antibiotics are used, the less effective they become for some of these life-threatening conditions. Return to text
- Grassé, P-P., Evolution of Living Organisms, Academic Press, New York, 1977, p. 88. Return to text
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