Why is it that bacterial resistance to antibiotics is not an example of
evolution ?

HARUN YAHYA
www.harunyahya.com

ONE of the biological concepts that evolutionists try to present as
evidence for their theory is the resistance of bacteria to antibiotics.
Many evolutionist sources mention antibiotic resistance as an example
of the development of living things by advantageous mutations. A
similar claim is also made for the insects which build immunity to
insecticides such as DDT.
However, evolutionists are mistaken on this subject too.

Antibiotics are "killer molecules" that are produced by microorganisms
to fight other microorganisms. The first antibiotic was penicillin,
discovered by Alexander Fleming in 1928. Fleming realised that mould
produced a molecule that killed the Staphylococcus bacterium, and this
discovery marked a turning point in the world of medicine. Antibiotics
derived from microorganisms were used against bacteria and the results
were successful.
Soon, something new was discovered. Bacteria build immunity to
antibiotics over time. The mechanism works like this: A large
proportion of the bacteria that are subjected to antibiotics die, but
some others, which are not affected by that antibiotic, replicate
rapidly and soon make up the whole population. Thus, the entire
population becomes immune to antibiotics.

Evolutionists try to present this as "the evolution of bacteria by
adapting to conditions."
The truth, however, is very different from this superficial
interpretation. One of the scientists who has done the most detailed
research into this subject is the Israeli biophysicist Lee Spetner, who
is also known for his book Not by Chance published in 1997. Spetner
maintains that the immunity of bacteria comes about by two different
mechanisms, but neither of them constitutes evidence for the theory of
evolution. These two mechanisms are:
1) The transfer of resistance genes already extant in bacteria.
2) The building of resistance as a result of losing genetic data
because of mutation.

Professor Spetner explains the first mechanism in an article published
in 2001:
Some microorganisms are endowed with genes that grant resistance to
these antibiotics. This resistance can take the form of degrading the
antibiotic molecule or of ejecting it from the cell... [T]he organisms
having these genes can transfer them to other bacteria making them
resistant as well. Although the resistance mechanisms are specific to a
particular antibiotic, most pathogenic bacteria have... succeeded in
accumulating several sets of genes granting them resistance to a
variety of antibiotics.

Spetner then goes on to say that this is not "evidence for evolution":
The acquisition of antibiotic resistance in this manner... is not the
kind that can serve as a prototype for the mutations needed to account
for Evolution... The genetic changes that could illustrate the theory
must not only add information to the bacterium's genome, they must add
new information to the biocosm. The horizontal transfer of genes only
spreads around genes that are already in some species.

So, we cannot talk of any evolution here, because no new genetic
information is produced: genetic information that already exists is
simply transferred between bacteria.
The second type of immunity, which comes about as a result of mutation,
is not an example of evolution either. Spetner writes:
... [A] microorganism can sometimes acquire resistance to an antibiotic
through a random substitution of a single nucleotide... Streptomycin,
which was discovered by Selman Waksman and Albert Schatz and first
reported in 1944, is an antibiotic against which bacteria can acquire
resistance in this way. But although the mutation they undergo in the
process is beneficial to the microorganism in the presence of
streptomycin, it cannot serve as a prototype for the kind of mutations
needed by NDT [Neo-Darwinian Theory]. The type of mutation that grants
resistance to streptomycin is manifest in the ribosome and degrades its
molecular match with the antibiotic molecule.

In his book Not by Chance, Spetner likens this situation to the
disturbance of the key-lock relationship. Streptomycin, just like a key
that perfectly fits in a lock, clutches on to the ribosome of a
bacterium and inactivates it. Mutation, on the other hand, decomposes
the ribosome, thus preventing streptomycin from holding on to the
ribosome. Although this is interpreted as "bacteria developing immunity
against streptomycin," this is not a benefit for the bacteria but
rather a loss for it. Spetner writes:
This change in the surface of the microorganism's ribosome prevents the
streptomycin molecule from attaching and carrying out its antibiotic
function. It turns out that this degradation is a loss of specificity
and therefore a loss of information. The main point is that
Evolution... cannot be achieved by mutations of this sort, no matter
how many of them there are. Evolution cannot be built by accumulating
mutations that only degrade specificity.

To sum up, a mutation impinging on a bacterium's ribosome makes that
bacterium resistant to streptomycin. The reason for this is the
"decomposition" of the ribosome by mutation. That is, no new genetic
information is added to the bacterium. On the contrary, the structure
of the ribosome is decomposed, that is to say, the bacterium becomes
"disabled." (Also, it has been discovered that the ribosome of the
mutated bacterium is less functional than that of a normal bacterium.)
Since this "disability" prevents the antibiotic from attaching onto the
ribosome, "antibiotic resistance" develops.

Finally, there is no example of mutation that "develops the genetic
information." Evolutionists, who want to present antibiotic resistance
as evidence for evolution, treat the issue in a very superficial way
and are thus mistaken.

The same situation holds true for the immunity that insects develop to
DDT and similar insecticides. In most of these instances, immunity
genes that already exist are used. The evolutionary biologist Francisco
Ayala admits this fact, saying, "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." Some other examples explained by mutation, just as with the
ribosome mutation mentioned above, are phenomena that cause "genetic
information deficit" in insects.

In this case, it cannot be claimed that the immunity mechanisms in
bacteria and insects constitute evidence for the theory of evolution.
That is because the theory of evolution is based on the assertion that
living things develop through mutations. However, Spetner explains that
neither antibiotic immunity nor any other biological phenomena indicate
such an example of mutation:
The mutations needed for macroevolution have never been observed. No
random mutations that could represent the mutations required by
Neo-Darwinian Theory that have been examined on the molecular level
have added any information. The question I address is: Are the
mutations that have been observed the kind the theory needs for
support? The answer turns out to be NO!