Reason &
Revelation, August 1994, 14[8]:61-63

Copyright © 1994 Apologetics Press, Inc., All
Rights Reserved

BACTERIAL ANTIBIOTIC RESISTANCE¾
PROOF OF
EVOLUTION?

by

Bert Thompson, Ph.D.

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
²neo-Darwinism,² as opposed to ²classical Darwinism.² 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 ²errors² 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:
²Mutations are the ultimate raw materials for evolution²
(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
neutral¾they 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, ²decidedly
advantageous.² Evolutionary progress, then, is dependent upon
nature ²selecting² 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, ²Antibiotics: The
End of Miracle Drugs?² (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, ²good,² and thus offer significant
proof of evolution. Their point is that the bacteria have
adapted so as to ²live to fight another day²¾an example of
²decidedly advantageous² mutations. Evolutionist Colin
Patterson of Great Britain has commented: ²The 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 ²need² of the
organisms. Futumya has noted: ²...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 them² (1983, pp.
137,138). What does this mean? Simply put, bacteria did not
²mutate² 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: ²What 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
bacteria² (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, ²the 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)²
(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 ²carriers² 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 ²evolution² is not vertical macroevolution
but horizontal microevolution (i.e., adaptation). In other
words, these bacteria ²...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 produced² (Bowden, 1991, p. 56). In commenting on
the changing, or sharing, of genetic material, ReMine has
suggested: ²It 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
life² (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 ²stabilized²
in its ²nested pattern.² 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 ²proves²
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), ²The
Mechanisms of Evolution,² Scientific American,
239[3]:56-69, September.

Beardsley, Tim (1994), ²La Ronde,² Scientific
American, 270[6]:26,29, June.

Begley, Sharon (1994), ²The End of Antibiotics,²
Newsweek, 123[13]:47-51, March 28.

Bowden, M. (1991), Science vs. Evolution (Bromley,
Kent, England: Sovereign Publications).

Caldwell, Mark (1994), ²Prokaryotes at the Gate,²
Discover, 15[8]:45-50, August.

Davies, Julian (1994), ²Inactivation of Antibiotics and the
Dissemination of Resistance Genes,² 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), ²Breaking the Antibiotic Bank,²
Natural History, 103[6]:39-40, June.

Travis, John (1994), ²Reviving the Antibiotic Miracle?,²
Science, 264:360-362, April 15.

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