Antibiotic Resistance and Similar Phenomena
Eric Blievernicht
One claim that is becoming more common among apologists for evolution in the media is that toxin-resistant creatures are evidence of "evolution." This paper examines a number of those claims in some detail to reveal just what seems to be going on, and whether it makes more sense in the creation model or the evolutionary worldview.
The general claim put forth goes something like this: bacteria, insects, rodents and other undesirables (as far as we're concerned) are encountering manmade toxins such as antibiotics, and toxic chemicals such as DDT and warfarin, designed to kill off the offending nasties. In response, some of these creatures are adapting, changing and achieving capabilities that enable them to resist the toxins threatening to destroy them. These drug-resistant strains, we are told, are evolving. According to some doomsayers we are now faced with plagues of untreatable "supergerms" that will wreak havoc among Western civilization, striking down innumerable people as doctors watch helplessly, unable to prescribe an effective cure.
According to standard (monophyletic) evolutionary theory, all life on earth is descended from an original population of very simple single-celled organisms, perhaps something like algae. One of the inescapable conclusions of evolution, therefore, is that organisms have attained additional capabilities, additional functional structures, and greater complexity over time. This is unavoidable. No matter how one fudges, somewhere between algae and man all of the structures, systems, and abilities we see in the human body must have developed through the interplay of non-sentient natural processes.
This is where creationists draw the line and demand evidence. The argument is not over "change" as evolutionists sometimes try to argue, but rather the kind of change. Do we see new structures developing today? New systems and new features arising from mutations and natural selection? Or do we see only examples of neutral or degenerative change, such as vestigial organs or shifts in skin color where nothing new is gained?
Creationists believe in an original, perfected created world (Genesis 1:31), a Curse (Genesis 3:17-19), and subsequent degeneration in the arena of life as well as everything else. It is therefore absolutely incorrect to say that creationists do not believe in change, or believe that what we see today is identical to the original creation. The difference between the creation model and evolution model is over the direction things are headed - towards greater complexity, new features, additional genetic information (evolution) - or loss of features, genetic impoverishment, and steady or gradual degeneration (a fallen Creation).
So what kinds of change do we see when we examine drug and toxin resistance in detail? Are new abilities being gained by resistant specimens? Or are there other explanations?
Drug and Antibiotic Resistance is Pre-Existent
The first point to make is that there is no evidence of any organism gaining additional features or abilities as a result of introduction to antibiotics. When a given population is introduced to an antibiotic, one of two things will happen. In the first case none of them are resistant, in which case they are all dead, kaput. End of story.
On the other hand, different individuals of virtually any population of living things contain different genetic information. If, by chance, some of the organisms in the population turn out to be resistant to the toxin they will survive while all their little relatives drop dead. In this case, obviously only the surviving, antibiotic-resistant creatures will live to reproduce. Over time antibiotic strains will predominate (as long as the antibiotics are present).
Update (1/6/97): The following quotation expounds on this issue:
Some drugs do appear to promote genetic crossover, but no positive
effects have been observed from these recombinations. A more plausible
explanation for bacterial drug resistance is that the gene responsible for the
resistance was there from the beginning but just wasn't expressed...
But why
would a bacteria have a drug-resistant gene in the first place? After all,
aren't antibiotics recent human creations? ...Many of today's antibiotics are
derived from natural sources: molds, plants and - someday - even frogs.
...Many
synthetic drugs mimic naturally occuring compounds. There is an unbelievably
wide array of compounds found in plants that have very interesting and useful
biological properties.... The point is that it is not too difficult to imagine
that for every man-made antibiotic, somewhere on this earth is a plant that
makes a similar compound to protect itself from the decaying action of bacteria
and molds.
(Clark, Don, "Genetics and Creation," Bible-Science News 34:8 (Nov. 96), p. 5.
Evolution cannot anticipate. If one nest of rats is being killed off by application of warfarin, the rats over in the next nest cannot say, "Gee, look at that. Start concentrating guys, we really need to develop warfarin resistance fast!" Either the drug-resistant features are present in a population when the drug is applied, or they aren't. Drug resistance doesn't "evolve." As prominent evolutionist and geneticist Francisco Ayala has acknowledged,
The genetic variants required for resistance to the most diverse kinds
of pesticides were apparently present in every one of the populations exposed to
these man-made compounds.
Scientific
American, 239 (September 1978), p. 65.
In an environment where populations are exposed to toxins in which some individuals are resistant, natural selection will occur and favor the resistant strain. The more intense the application of toxin, the more rigorous the selection. In an extreme case, only the resistant strains will survive, such as in a patient being treated with anti-biotics in a hospital. But remember, this is only natural selection. Nothing new has been created that was not present in part of the population before the toxins were introduced.
Toxin Resistance Results from Neutral or Crippling Mutations - Not "Evolution"
But what about the specific means by which such resistance to pesticides, antibiotics, etc. is achieved? Surely resistant strains show the appearance and development of new features, even if they preceded the actual introduction of the toxin?
As it turns out, we have some understanding of the mechanisms that allow resistant organisms to survive. Several examples are described below.
Beginning in the 1950's the poison warfarin has been used to kill off rats in England. Within a few years populations resistant to the poison were noticed. Eventually the biochemistry of the process was elucidated.
Warfarin kills rats by inhibiting an enzyme involved in the metabolism of Vitamin K. Since Vitamin K is vital for life, normal rats who lost the ability to synthesize Vitamin K in their cells faced certain death. And the resistant rats?
Warfarin-resistant rats were found to have a mutated form of the enzyme that warfarin inhibited. The different shape and structure of the enzyme prevented warfarin from binding and blocking Vitamin K synthesis.
Eureka! Evolution, right? Not quite. If it weren't for the presence of
warfarin, this mutation is clearly degenerative in nature. The mutant enzyme is
not nearly as efficient in production of Vitamin K. It requires more than
10 times as much energy to synthesize a given amount of Vitamin K. Under
normal conditions a rat with this mutation will tend to be eliminated by natural
selection. The rat is a biochemical cripple.
(Ewan More, "Rats!
Another Case of Sickle-Cell Anaemia,"
Creation Ex Nihilo,
17:2 (March-May 1995), pp. 44-45.)
Nor is resistance confined to manmade compounds. Consider the following example. A population of aquatic worms from a cadmium-free environment was exposed to cadmium, a naturally occuring but toxic element. After three generations only cadmium-resistant worms were alive. The scientist reporting this described it as "rapid evolutionary change"! (J. Levinton, "The Big Bang of Animal Evolution," Scientific American, November 1992, pp. 52-59.)
Was there any evidence of a mutation? No. Was there any evidence of new structures or features enabling cadmium-resistance? No. Was there evolution? No. Was there natural (or unnatural) selection? Yes.
Some of the worms were cadmium resistant right from the beginning - otherwise they all would have died. Obviously, once all the non-cadmium resistant worms were dead only the cadmium-resistant worms were reproducing, producing a population heavily weighted towards cadmium-resistance. Population gene frequencies changed, but nothing new was added to the gene pool. If evolution happened as easily as the scientist apparently believed, it would be happening right in front of our faces all the time.
Creationist geneticist and forestry expert Dr. Maceirj Giertych (Ph.D., D.Sc.), a leading Polish researcher, offers another example, this one of a neutral mutation (so far as complexity, genetic information and structure is concerned).
A useful mutation (e.g., an orange without seeds) is not the equivalent
of a positive mutation. I felt uneasy [as an evolutionist] lecturing
about positive mutations when I could not give an example...
Much
evolutionary publicity is attached to forms that develop resistance to man-made
chemicals. Usually they are variants that exist in nature but were selected out
by the chemical reagent.
In one instance, it was demonstrated that a single
nucleotide substitution in the genome was responsible for resistance to a
weed-specific herbicide. The herbicide is 'custom-made' for attachment and
deactivation of a vital protein specific for the weed plant. A single change in
the genetic code for this protein, in the sector used for defining the herbicide
attachment, deprives the herbicide of attachability and therefore of its
herbicidal properties. Such a change has no selective value except in the
context of the man-made herbicide. Even if originating from mutation (it could
be a rare neutral allele always present in the population but springing
into prominence because of the use of herbicide) this would be no more than a
neutral mutation; not depriving the protein of its function but neither
creating a new function for it. So where is the evolution?
(Maceirj
Giertych, "Professor of Genetics Says "No!" to Evolution,"
Creation Ex Nihilo,
17:3 (June-August 1995), pp. 47-48.)
Dr. Carl Wieland, an Australian medical doctor, tackled the issue of antibiotic resistance in bacteria head-on. His article is worth quoting at some length.
This misconception [about antibiotic resistance and evolution] may be
partly due to the fact that even many science graduates believe that the
mechanism of antibiotic resistance involves the acquisition of new DNA
information by accidental mutations... But resistance does not normally arise
like this.
Loss of control over an enzyme's production can engender
antibiotic resistance. Take for instance penicillin resistance in Staphylococcus
bacteria. This requires the bacterium to have DNA information coding for
production of a complicated enzyme (penicillinase) which specifically destroys
penicillin. It is extremely unlikely that such complex information could arise
in a single mutation step, and in fact it does not. Mutation can cause the loss
of control of its production, so much greater amounts are produced, and a
bacterium producing large quantitites of penicillinase will survive when placed
in a solution containing penicillin, whereas those producing lesser amounts will
not. The information for producing this complicated chemical was, however,
already present.
(Carl Wieland, "Antibiotic Resistance in Bacteria,"
Creation Ex Nihilo Technical
Journal, 8:1 (1994), p. 5.)
More examples:
A mutational loss or defect can cause resistance. For instance, Mycobacterium
tuberculosis, the cause of TB, has an enzyme which (as well as its other
useful functions) changes the antibiotic isoniazid into a form which destroys
the bacterium. A mutation causes the loss of that enzyme and helps the pathogen
withstand isoniazid. To give another example: the 4-quinolone antibiotics
attack the enzyme DNA gyrase inside various bacteria. An informationally
insignificant mutation which results in the substitution of one amino acid by
another destroys the enzyme/antibiotic interaction.
(Ibid.)
In other words, a number of these cases result from a mutation in the shape of an enzyme. Recall from your high-school biology class that enzymes have a specific shape that allows them to "lock" onto other molecules - or vice-versa. A simple change in shape can throw off a toxin that is trying to latch onto the enzyme, while the functional binding site of the enzyme (on another part of the enzymes' surface) may be unaffected.
Wieland continues:
More commonly, resistance arises through mutational defects that cause
the inactivation of genes which control transport through the cell membrane. If
the antibiotic is less efficiently taken up, it does not accumulate as readily
to toxic levels.
Antibiotic resistance commonly arises in ways that have
nothing to do with mutation. For instance, in some microbes the antibacterial
chemical, sulphonamide, works by blocking the ability to synthesize the vitamin
folic acid. If the bacterium acquires new DNA which bypasses the block to
produce this vitamin, then sulphonamide will not work as well. This pathogen is
therefore resistant.
(Ibid.)
Wieland goes on to explain the discovery of plasmid DNA, rings of DNA that can almost literally be tossed from one cell to another like a frisbee, sharing the information they contain without actually needing to reproduce. I direct the reader to any recent text on cell biology for further information. (For example, Lewis Kleinsmith and Valerie Kish, Principles of Cell and Molecular Biology (New York: HarperCollins College Publishers, 1995), pp. 100-104.)
Finally, I should note in passing the nature of sickle-cell anaemia, which has also been described as proof of evolution. Sickle-cell anaemia is a sort of human equivalent to antibiotic resistance. Only in this case, it is not a disease which is resistant to an antibiotic but rather a human who is resistant to a disease!
Carriers of the sickle-cell trait, whether expressed (dominant) or recessive, are resistant to malaria. This is not due to improvements however. As in the examples above, sickle-cell is a severely degenerative - in fact, fatal - mutation that destroys the structure of red blood cells. Rather than healthy disc-like cells, people with the sickle-cell trait expressed in their body develop blood cells distorted roughly into the shape of a crescent or sickle - hence the name. Such cells are more prone to get hung up or stuck and cause blockages in blood vessels than healthy cells.
Sickle-cell persists in some areas of Africa because malaria is such a severe threat that the benefits gained by recessive carriers of the sickle-cell gene outweigh the lethal effects it has on dominant carriers. But weighed in the balance this is a terribly destructive mutation.
A leading authority on sickle-cell, Dr. Felix Konotey-Ahulu, had this to say in his book (excerpted in Creation Ex Nihilo, 16:2, p. 40-41):
Sixth-graders I have lectured on genetic counselling invariably pop some
questions such as:
'Is it true that the sickle-cell phenomenon has
established Darwinian evolution as fact?'
Behind the question, of course,
lies the assumption that observing selection/adaptation involving a mutation (an
inherited random change or defect) somehow implies that the more complicated
forms seen today arose from simpler forms traced ultimately to one-cell
organisms.
The answer is of course 'no'. In the early 1950s I did a course
on evolution and metaphysics at the feet of Professor J.Z. Young, perhaps the
greatest evolutionist of recent years. Nothing has happened during the past 30
years in molecular biology in general, and the sickling phenomenon vis-a-vis
malaria in particular, to have raised evolution to established fact.
... For
people to state that because sickle-cell trait children are resistant to
cerebral malaria, therefore the whole neo-Darwinian scenario is fact, is like
saying that my black skin's ability to withstand the tropical sun establishes an
evolutionary process, starting perhaps with a 'big-bang', leading to
single-celled organisms, multi-celled organisms, invertebrates, vertebrates, and
on up to man....
The hypotheses of some anthropologists and theoretical
geneticists detract from more serious work. While natural selection is fact,
attention to selection hypotheses is frequently overdone and other factors
ignored...
I have indicated more than once that African anthropogenetics
would be much better served by thinking along factual lines rather than
theoretical evolutionary concepts. The same could certainly be said for science
and medicine in general.
(Felix Konotey-Ahulu, The Sickle Cell
Disease Patient (New York: Macmillan, 1991), p. 106-108.)
As mentioned earlier, antibiotic resistance existed before the introduction of antibiotics. Wieland cites the example of bacteria recovered from the frozen bodies of a party of early Arctic explorers who died in 1845. The bacteria were recovered from their colons in 1988, carefully cultured and exposed to modern antibiotics. Many were found to be resistant to the most powerful modern antibiotics, proving that such resistance was present ahead of time and has not "evolved" as a response to new selective pressures. (See R. McQuire, "Eerie: human Arctic fossils yield resistant bacteria," Medical Tribune, 12/29/1988, pp. 1, 23.)
So-called 'supergerms' in hospitals are not 'super' at all. What has
happened is that the use of antibiotics in modern hospitals has meant that the
only ones surviving are those which have all the resistance factors. If a
person gets a serious infection with one of these resistant types, the infection
is not therefore more aggressive than if it was a non-resistance form of the
same bug; it is simply that doctors are powerless to treat it. In fact, it is
generally a weaker form of the pathogen.
(Wieland, p. 6)
So far from being evidence for upwards evolution, for greater complexity and improvement, we see that drug and antibiotic resistance actually supports the creation paradigm of degeneration and decay within the conservative mechanism of natural selection. Toxin resistance offers no help to those who are seeking a mechanism by which new organs, new features, structures and useful information can be formed without intelligent input.
Update 3/2797: (From Sarfati, Jonathan D., "How did all the animals
fit on Noah's Ark,"
Creation
Ex Nihilo 19(2):19)
Viruses often become much more infectious by
random mutations causing changes in their protein coats. This makes it harder
for the antibodies to recognize them, but there is no increase in information
content, so no real evolution.
(In other words, these protein coat
mutations are sort of like random changes in the combination to a lock; they
throw off the antibodies that had the "key" and force the body to
begin trying to identify the new combination.)
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