Re: Why is it that bacterial resistance to antibiotics is not an example of evolution ?
- From: "Robert" <RobertsSong@xxxxxxxxxxx>
- Date: Wed, 14 Sep 2005 17:13:53 -0700
<harunyahya2011@xxxxxxxxx> wrote in message
> Why is it that bacterial resistance to antibiotics is not an example of
> evolution ?
> HARUN YAHYA
> 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.
They already exist in nature because they were exposed in nature through
genetic mutation and selection. In order for bacteria to multiply they must
be alive and not killed off by antibiotics. Their survival results in the
transfer of this resistance to other bacteria that are not yet resistant. A
bacertia can not evolve if it is dead. This constitutes direct evidence that
evolution is pivitol in selective survival of mutated genes.
> 2) The building of resistance as a result of losing genetic data
> because of mutation.
There are many ways of which genetic resistance to antibiotics are
transfered. Plasmid genetic material transfer of one resistant bacteria to
another is direct transfer of this resistance.
> 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.
There are shotgun mutations many of which are not very helpful. These random
mutations can florish or not dependending on environment. They may die or
provide an advantage for survival.
Those that confer advantages make survival more likely and thus evolve to
survive another day. There are many dead ends in evolution.
> 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.
Evolution implies concsitutional difference over time to the organism and
not simply genetic mutations.
It is a process and can't be answered in terms of single mutations.
Resistance is a mode of survival in order to give the bacteria a mode of
replication in which evolution can take place.
> 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.
Only time will tell. There are other ways in which bacteria incorporate
genetic foreign material and thus increase information.
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