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 realized 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.306

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.307

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.308

Bacteria quickly become immune to antibiotics by transferring their resistance genes to one another. The picture above shows a colony of E. coli bacteria.

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.309

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."310 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!311

306 Dr. Lee Spetner, "Lee Spetner/Edward Max Dialogue: Continuing an exchange with Dr. Edward E. Max," 2001, http://www.trueorigin.org/spetner2.asp
307 Dr. Lee Spetner, "Lee Spetner/Edward Max Dialogue: Continuing an exchange with Dr. Edward E. Max," 2001, http://www.trueorigin.org/spetner2.asp
308 Dr. Lee Spetner, "Lee Spetner/Edward Max Dialogue: Continuing an exchange with Dr. Edward E. Max," 2001, http://www.trueorigin.org/spetner2.asp
309 Dr. Lee Spetner, "Lee Spetner/Edward Max Dialogue: Continuing an exchange with Dr. Edward E. Max," 2001, http://www.trueorigin.org/spetner2.asp
310 Francisco J. Ayala, "The Mechanisms of Evolution," Scientific American, Vol. 239, September 1978, p. 64.
311 Dr. Lee Spetner, "Lee Spetner/Edward Max Dialogue: Continuing an exchange with Dr. Edward E. Max," 2001, http://www.trueorigin.org/spetner2.asp