The evolution of antibiotic resistance has been for some time the Darwinists’ favorite example for “demonstrating” evolution (Common Descent). Superficially their case looks good. Antibiotics date only from about 1930 with the discovery of penicillin (Fleming 1929), followed by the development of a method to produce it with high yield (Chain et al. 1940). Antibiotics were first introduced to the public in 1942 to cure bacterial infection (Levy 1992, 4), and by the mid 1940s the first strains appeared of Staphylococcus resistant to penicillin (Fisher 1994, 15). Just a few years after antibiotics were introduced, resistant strains of the pathogens were found to have already evolved. As each new antibiotic was discovered and put into use against pathogenic bacteria, resistant strains soon followed. The argument then goes, with a wave of the hand, like this: If a small but significant evolutionary change like antibiotic resistance can evolve in only a few years, then surely in a million years huge evolutionary changes must occur. Darwinists expect this argument to support Common Descent.
An examination of the phenomenon of antibiotic resistance, however, shows it lends no support at all to Common Descent (Spetner 1997, 138143). Antibiotics are natural molecules produced by some microorganisms for the purpose of killing other hostile microorganisms. A microorganism that makes an antibiotic must, itself, be resistant to the antibiotic it makes. For this purpose it is typically endowed with a battery of genes that code for a resistance mechanism. Most useful antibiotics have come from soil bacteria (D’Costa et al. 2006). How bacteria have acquired this resistance initially is not known, nor can neo-Darwinian theory shed any light on it. Antibiotic resistance genes have been found to predate the use of antibiotics by at least many thousands of years (D’Costa et al. 2011). Moreover, bacteria are known to be able to transfer genetic material to other bacteria through HGT (see above). On occasion, copies of the genes for resistance can find their way from a type of bacterium that is normally resistant to a type that is not normally resistant. When that happens, the recipient bacterium becomes resistant. This is indeed evolution, but it is a limited evolution of the population-change type. It is not the Common-Descent type of evolution.
The resistance genes already exist in the biosphere. No new information has appeared in the biosphere through this type of evolution of antibiotic resistance. Common-Descent evolution cannot be achieved by this procedure even if it were repeated innumerable times in succession, because no new information would be built up. This method of evolving antibiotic resistance therefore lends no support for Common Descent.
Sometimes, however, antibiotic resistance can indeed appear through a random mutation — a DNA copying error, which would bring something new to the biosphere. This kind of change looks like it might satisfy the requirements for Common Descent, so I shall give a brief description of it here, although I have already dealt with it in my previous book.
As an example, let us look at how a bacterium acquires resistance to streptomycin through a random mutation. All cells, whether of bacteria or of plants or animals, contain organelles called ribosomes, whose function it is to make protein according to instructions from the DNA of a gene. Proteins are large molecules, consisting of long chains of small molecules called amino acids, and are essential to all living things. They function as enzymes, which catalyze all the chemical reactions in a cell — each chemical reaction catalyzed by a specific enzyme. Proteins can also serve as structural elements. Often, and maybe even always, a structural protein functions also as an enzyme. For an enzyme to perform its function, it must have a specific sequence of amino acids.
A ribosome is an organelle within a cell that manufactures protein. It makes a protein by putting together a chain of amino acids according to the instructions in the DNA. A segment of the DNA is transcribed into an RNA molecule that matches the DNA nucleotide by nucleotide. This RNA is called messenger RNA because it carries the DNA message to the ribosome. The ribosome translates the message in the DNA into amino acids according to the genetic code. Three nucleotides translate into one amino acid. Accordingly, the ribosome constructs a chain of amino acids to form a protein.
The antibiotic streptomycin, for example, acts on a bacterial cell by attaching to a ribosome at a site to which it matches, the way a key fits into a lock. When the streptomycin molecule attaches to this site, it interferes with the ribosome function and causes it to make mistakes leading to incorrect, dysfunctional or nonfunctional, protein. The errors it causes prevent the cell from growing, reproducing, and eventually from living. The important feature of streptomycin, and indeed of all other antibiotics, is that it kills bacteria but does not harm the mammalian host. Streptomycin kills the bacterial cells that are infecting you without killing your own cells. It discriminates between the cells of the bacteria and the cells of the host by its specific attachment to a matching site on the bacterial ribosome, a site not found on the host’s ribosomes.
A bacterium will gain resistance to streptomycin if a point mutation occurs in the gene coding for the protein in the ribosome, ruining the matching site, destroying the specificity of the protein, and preventing a streptomycin molecule from attaching. If the streptomycin cannot attach to the matching site, the bacterium is resistant. Just one mutation in the portion of the DNA coding for the matching site can mess up the site so the streptomycin cannot attach. It turns out that any one of several mutations in that portion of the DNA will grant the bacterium resistance (Gartner and Orias 1966). Note that this type of resistance is caused by a single random point mutation, but it cannot serve as an example of mutations that can support Common Descent. One cannot expect mutations destroying specificity, no matter how many of them there are, to build information and lead to Common Descent. Destruction of specificity does not add information — it destroys it. One cannot add information by destroying it, no matter how many times one repeats the process. I have previously (Spetner 1997) compared trying to build up information in this manner to the merchant who was losing a little money on each sale but thought he could make it up on volume. The acquisition of antibiotic resistance is indeed evolution, but only a limited form of it. It cannot lead to Common Descent.
No example of antibiotic resistance in bacteria adds information to the biosphere. To become resistant, the bacteria either pick up ready-made resistance genes from other bacteria or they undergo a mutation that destroys information. Antibiotic resistance cannot therefore be an evolutionary example that could support Common Descent because a chain of such mutations, no matter how long, does not add information and thus cannot lead to Common Descent. The Darwinists’ favorite example of evolution fails to pass muster.
Chain, E. et al. (1940) Penicillin as a Chemotherapeutic Agent. Lancet 239: 226-228.
D’Costa, Vanessa M., Katherine M. McGrann, Donald W. Hughes, and Gerard D. Wright. (2006) Sampling the antibiotic resistome. Science 311: 374-377.
D’Costa, Vanessa M. et. al. (2011) Antibiotic Resistance is Ancient. Nature 477:457-461.
Fisher, Jeffrey A. (1994) The Plague Makers: How we are creating catastrophic new epidemics — and what we must do to avert them. New York: Simon & Schuster.
Fleming, A. (1929) On the antibacterial action of cultures of a Penicillium, with special reference to their use in the isolation of B. influenzae. British Journal of Experimental Pathology 10: 226-238.
Gartner, T. K. and E. Orias, (1966) Effects of mutations to streptomycin resistance on the rate of translation of mutant genetic information. Journal of Bacteriology 91: 1021-1028.
Levy, Stuart B. (1992) The Antibiotic paradox: How Miracle Drugs are Destroying the Miracle. New York: Plenum Press.
Spetner. L. M. (1997) Not by chance! Shattering the Modern Theory of Evolution. Brooklyn: Judaica Press.
Lee Spetner, The Evolution Revolution: Why Thinking People Are Rethinking the Theory of Evolution (Brooklyn, NY: Judaica Press, 2014), 119-120.