https://apologeticspress.org/APContent.aspx?category=9&article=572
Bacterial Antibiotic Resistance--Proof of Evolution?
On November 24, 1859, Charles Darwin’s book,
The Origin of Species,
was published. As a result, the concept of organic evolution was
popularized. The science of genetics, of course, was completely unknown
at that time, and would not come into its own until approximately
forty-one years later. Since around 1900, evolutionists have advocated
“neo-Darwinism,” as opposed to “classical Darwinism.” In classical
Darwinian thought, natural selection alone served as the mechanism of
evolution. In neo-Darwinian thought, natural selection and genetic
mutations work together as evolution’s mechanism.
Genetics has played an increasingly important role in evolution,
especially in regard to mutations that alter the genetic code within
each organism. That code is expressed biochemically in deoxyribonucleic
acid (DNA). Mutations are “errors” in DNA
replication (Ayala, 1978, pp. 56-69). It is those errors that cause the
genetic change necessary for evolution to occur. In 1957, George
Gaylord Simpson wrote: “Mutations are the ultimate raw materials for
evolution” (1957, p. 430). Twenty-six years later, nothing had changed
when Douglas J. Futuyma remarked:
By far the most important way in which chance influences evolution is
the process of mutation. Mutation is, ultimately, the source of new
genetic variations, and without genetic variation there cannot be
genetic change. Mutation is therefore necessary for evolution (1983, p.
136).
Mutations can occur in several different ways, and can affect
individual genes or entire chromosomes (see Futuyma, 1983, p. 136).
Further, mutations can be placed, theoretically, into at least three
categories: (a) bad; (b) neutral; and (c) good.
Some mutations, therefore, can have profound effects. They can alter
the structure of a critical protein so much that the organism becomes
severely distorted and may not survive. Other mutations may cause
changes in the protein that do not affect its function at all. Such
mutations are adaptively neutral—they are neither better nor worse than
the original form of the gene. Still other mutations are decidedly
advantageous (Futuyma, 1983, p. 136).
Neither bad nor neutral mutations aid evolution, since the bad ones
produce effects that are deleterious (and often lethal), and the neutral
ones neither help nor hurt an organism. Neo-Darwinian evolution relies
entirely on
good mutations, since they not only alter the genetic
material, but are, to use Futuyma’s words, “decidedly advantageous.”
Evolutionary progress, then, is dependent upon nature “selecting” the
good mutations, resulting in genetic change that ultimately produces new
organisms.
BACTERIA AND RESISTANCE TO ANTIBIOTICS
What does all of this have to do with the resistance of bacteria to
antibiotics? Over the past several years, the medical community has
become increasingly concerned over the ability of certain bacteria to
develop resistance to antibiotics. Undoubtedly this concern is
justified. Antibiotics, which usually are substances naturally produced
by certain microorganisms, inhibit the growth of other microorganisms.
One of the first antibiotics to be discovered (in 1928) was penicillin,
produced by the mold
Penicillium chrysogenum. Since then, more
than a thousand similar substances have been isolated. Most people
recognize the tremendous impact antibiotics have had in the battle with
pathogenic (disease-causing) organisms. Without antibiotics, the death
toll from infections and diseases would be much higher than it is.
Today, however, there is compelling evidence that we are in danger of
losing our battle against certain pathogens. Bacteria sometimes develop
resistance to even powerful antibiotics. As a result, the number of
antibiotics that can be used against certain diseases is dwindling
rapidly. Both scientific and popular publications have addressed the
seriousness of this issue. The cover story of the March 28, 1994 issue
of
Newsweek was titled, “Antibiotics: The End of Miracle Drugs?” (Begley, 1994). Articles in
Scientific American (Beardsley, 1994),
Science (Travis, 1994; Davies, 1994),
Discover (Caldwell, 1994), and
Natural History (Smith, 1994), have all called attention to the impact on our lives that bacterial resistance to antibiotics is causing
.
The phenomenon of bacterial drug resistance was first documented around
1952 (see Lederberg and Lederberg, 1952). Interest in the phenomenon
has increased as fewer antibiotics are effective against pathogens, and
as deaths from bacterial infections increase. Scientific interest in
this problem is both pragmatic and academic. In the pragmatic sense,
those working in medical fields (doctors, nurses, pharmacists,
researchers, etc.) are interested because lives are at stake. In an
academic sense, this issue is of importance to evolutionists because
they believe the mutations in bacteria responsible for drug resistance
are, from the standpoint of the bacterial population, “good,” and thus
offer significant proof of evolution. Their point is that the bacteria
have adapted so as to “live to fight another day”—an example of
“decidedly advantageous” mutations. Evolutionist Colin Patterson of
Great Britain has commented: “The development of antibiotic-resistant
strains of bacteria, and also of insects resistant to DDT and a host of
other recently discovered insecticides,
are genuine evolutionary changes (1978, p. 85, emp. added). But are these mutations sufficient to explain long-term, large-scale evolution (macroevolution)?
AN ALTERNATIVE EXPLANATION
Bacteria do not become resistant to antibiotics merely by experiencing
genetic mutations. In fact, there are at least three genetic mechanisms
by which resistance may be conferred. First, there are instances where
mutations produce antibiotic-resistant strains of microorganisms. Second, there is the process of
conjugation,
during which two bacterial cells join and an exchange of genetic
material occurs. Inside many bacteria there is a somewhat circular piece
of self-replicating DNA known as a plasmid,
which codes for enzymes necessary for the bacteria’s survival. Certain
of these enzymes, coincidentally, assist in the breakdown of
antibiotics, thus making the bacteria resistant to antibiotics. During
conjugation, plasmids in one organism that are responsible for
resistance to antibiotics may be transferred to an organism that
previously did not possess such resistance.
 |
GERM WARFARE: During conjugation, one bacterial cell (A) can transfer any tiny DNA
circle (plasmid) to another cell (B). This act can occur even between
cells of different species. The transfer gives bacterium B a resistance
to a drug that formerly was not present in its own DNA.
In this example, the plasmid contains a gene (shown in red) to
manufacture an enzyme that destroys the drug’s ability to interfere with
bacterial cell division (as in the case of penicillin). |
Third, bacteria can incorporate into their own genetic machinery foreign
pieces of DNA by either of two types of DNA transposition. In
transformation, DNA from the environment (perhaps from the death of another bacterium) is absorbed into the bacterial cell. In
transduction, a piece of DNA
is transported into the cell by a virus. As a result of incorporating
new genetic material, an organism can become resistant to antibiotics.
Commenting on these processes, Walter J. ReMine wrote:
Transformation and transduction occur extremely infrequently, but this
rarity can be offset somewhat by the enormous population sizes that
bacteria can achieve, especially under laboratory conditions. By those
three methods bacteria can acquire DNA that alters their survival.... For example, DNA
transposition can result in reduced permeability of the cell wall to
certain substances, sometimes providing an increased resistance to
antibiotics (1993, p. 404).
The issue is not whether bacteria develop resistance to antibiotics
through alterations in their genetic material. They do. The issue is
whether or not such resistance helps the evolutionists’ case. We suggest
that it does not, for the following reasons.
First, the mutations responsible for antibiotic resistance in bacteria
do not arise as a result of the “need” of the organisms. Futumya has
noted: “...the adaptive ‘needs’ of the species do not increase the
likelihood that an adaptive mutation will occur; mutations are not
directed toward the adaptive needs of the moment.... Mutations have
causes, but the species’ need to adapt isn’t one of them” (1983, pp.
137,138). What does this mean? Simply put, bacteria did not “mutate”
after being exposed to antibiotics; the mutations conferring the
resistance were present in the bacterial population even prior to the
discovery or use of the antibiotics. The Lederbergs’ experiments in 1952
on streptomycin-resistant bacteria showed that bacteria which had never
been exposed to the antibiotic already possessed the mutations
responsible for the resistance. Malcolm Bowden has observed: “What is
interesting is that bacterial cultures from bodies frozen 140 years ago
were found to be resistant to antibiotics that were developed 100 years
later. Thus the specific chemical needed for resistance was inherent in
the bacteria” (1991, p. 56). These bacteria did not mutate to become
resistant to antibiotics. Furthermore, the non-resistant varieties did
not become resistant due to mutations.
Second, while pre-existing mutations may confer antibiotic resistance,
such mutations may also decrease an organism’s viability. For example,
“the surviving strains are usually less virulent, and have a reduced
metabolism and so grow more slowly. This is hardly a recommendation for
‘improving the species by competition’ (i.e., survival of the fittest)”
(Bowden, 1991, p. 56). Just because a mutation provides an organism with
a certain trait does not mean that the organism
as a whole has
been helped. For example, in the disease known as sickle-cell anemia
(caused by a mutation), people who are “carriers” of the disease do not
die from it and are resistant to malaria, which at first would seem to
be an excellent example of a good mutation. However, that is not the
entire story. While resistant to malaria, these people do not possess
the stamina of, and do not live as long as, their non-carrier
counterparts. Bacteria may be resistant to a certain antibiotic, but
that resistance comes at a price. Thus, in the grand scheme of things,
acquiring resistance does not lead necessarily to new species or types
of organisms.
Third, regardless of how bacteria acquired their antibiotic resistance
(i.e., by mutation, conjugation, or by transposition), they are still
exactly the same bacteria
after receiving that trait as they were
before
receiving it. The “evolution” is not vertical macroevolution but
horizontal microevolution (i.e., adaptation). In other words, these
bacteria “...are still the same bacteria and of the same type, being
only a variety that differs from the normal in its resistance to the
antibiotic. No new ‘species’ have been produced” (Bowden, 1991, p. 56).
In commenting on the changing, or sharing, of genetic material, ReMine
has suggested: “It has not allowed bacteria to arbitrarily swap major
innovations such as the use of chlorophyll or flagella. The major
features of microorganisms fall into well-defined groups that seem to
have a nested pattern like the rest of life” (1993, p. 404).
Microbiologists have studied extensively two genera of bacteria in their attempts to understand antibiotic resistance:
Escherichia and
Salmonella. In speaking about
Escherichia in an evolutionary context, France’s renowned zoologist, Pierre-Paul Grassé, observed:
...bacteria, despite their great production of intraspecific varieties,
exhibit a great fidelity to their species. The bacillus Escherichia coli,
whose mutants have been studied very carefully, is the best example.
The reader will agree that it is surprising, to say the least, to want
to prove evolution and to discover its mechanisms and then to choose as a
material for this study a being which practically stabilized a billion
years ago (1977, p. 87).
Although
E. coli allegedly has undergone a billion years’ worth
of mutations, it still has remained “stabilized” in its “nested
pattern.” While mutations and DNA transposition
have caused change within the bacterial population, those changes have
occurred within narrow limits. No long-term, large-scale evolution has
occurred.
CONCLUSION
The suggestion that the development in bacteria of resistance to antibiotics as a result of genetic mutations or DNA
transposition somehow “proves” organic evolution is flawed.
Macroevolution requires change across phylogenetic boundaries. In the
case of antibiotic-resistant bacteria, that has not occurred.
REFERENCES
Ayala, Francisco (1978), “The Mechanisms of Evolution,”
Scientific American, 239[3]:56-69, September.
Beardsley, Tim (1994), “La Ronde,”
Scientific American, 270[6]:26,29, June.
Begley, Sharon (1994), “The End of Antibiotics,”
Newsweek, 123[13]:47-51, March 28.
Bowden, M. (1991),
Science vs. Evolution (Bromley, Kent, England: Sovereign Publications).
Caldwell, Mark (1994), “Prokaryotes at the Gate,”
Discover, 15[8]:45-50, August.
Davies, Julian (1994), “Inactivation of Antibiotics and the Dissemination of Resistance Genes,”
Science, 264[5157]:375-382, April 15.
Futuyma, Douglas J. (1983),
Science on Trial (New York: Pantheon Books).
Grass‚, Pierre-Paul (1977),
The Evolution of Living Organisms (New York: Academic Press).
Lederberg, J. and E.M. Lederberg (1952),
Journal of Bacteriology, 63:399.
Patterson, Colin (1978),
Evolution (Ithaca, NY: Cornell University Press).
ReMine, Walter J. (1993),
The Biotic Message (St. Paul, MN: St. Paul Science).
Simpson, George Gaylord, C.S. Pittendrigh, and L.H. Tiffany (1957),
Life: An Introduction to Biology (New York: Harcourt, Brace and World).
Smith, John Maynard (1994), “Breaking the Antibiotic Bank,”
Natural History, 103[6]:39-40, June.
Travis, John (1994), “Reviving the Antibiotic Miracle?,”
Science, 264:360-362, April 15.
[NOTE: Auxiliary staff writer