Does Emergence of Antibiotic-Resistant Bacteria Prove Evolution?

By Jon A. Covey, BA, MT(ASCP)
Edited by Anita K. Millen, MD, MPH, MA

Evolutionists say that mutations are the source of new genetic material, and they point to development of antibiotic resistant bacteria from a population of nonresistant bacteria as evidence. This does not support their claim, because the resistance is already present in a small number of the bacteria except for the occasional point mutation examined below. The nonresistant bacteria die, while the resistant bacteria survive and begin to multiply just about the time the patient thinks he is getting better. Maybe this has happened to you. Your doctor does another culture and sensitivity test, discovers that you are now infected with a resistant strain of the same bacteria, and orders a new antibiotic. This time, if there are no bacteria carrying a gene for resistance, you get better. You were lucky; many people die from hospital-acquired infections--over 300,000/year. Some had other problems, which made them more susceptible to deadly infections, but many of these people had a normal immune system.

How Do Bacteria Develop Resistance?

Resistance to an antibiotic develops in several ways, all of which relate to the bacteria's gene pool, which is the sum total of genetic material available to a specific strain or species of bacteria (You cannot swim in a gene pool, a secretary pool, or a car pool). Resistance does not come about by haphazard mutations developing genetic material to code for one or another means of resistance, but from genetic material that has always existed in the bacteria's gene pool ever since its Divine creation. From a reference text, Principles and Practice of Infectious Diseases, p. 219, 1990, Drs. Kenneth Mayer, Steven Opal, and Antone Medeiros write:

"Genetic variability is essential in order for microbial evolution to occur. Antimicrobial agents exert strong selective pressures upon bacterial populations and favor those organisms that are capable of resisting them, Genetic variability may occur by a variety of mechanisms. A Point mutation may occur at a nucleotide base pair, a process referred to as microevolutionary change. Point mutations may alter the target site of an antimicrobial agent, thereby interfering with its activity."

While they give a passing nod to evolution by mentioning microbial evolution, they are careful not to state that new genetic material evolves. They do say that some individuals in a bacterial population are already "capable of resisting." Mayer, Opal, and Medeiros' article deals with the types of genetic variability available to bacterial populations and how they transfer resistance and other traits to one another.

Point mutations, e.g., Tautomeric Shifts

Changing the DNA code for one amino acid to code for another amino acid causes the point mutation called a substitution. Often this is a copying mistake. Other errors can cause the addition or subtraction of one or more amino acids. A point mutation can cause the production of a resistance mechanism to be turned on, e.g., an enzyme able to attack the antibiotic. A point mutation could also cause a structural change, so that the antibiotic’s target site on or in the bacterium is modified.

Biochemistry professor Kenneth Devore gave an example of an enol-keto tautomeric shift in a DNA base. This takes place during replication of a reproducing bacterium's genetic material. Such a point mutation can cause subsequent generations to be resistant [see Lehninger's Principles of Biochemistry and Gardner's Principles of Genetics on tautomerism]. When this kind of shift takes place in one of the two strands of DNA and is replicated with the enol form, the complementary strand will reflect this change. The wrong base will be selected and a different amino acid coded. This change can cause the activated form of enzyme to be produced or change the antibiotic target site, so that the bacteria are resistant to the antibiotic. Stability favors reversion of such a mutation to the nonresistant form because the keto form is usually more stable.

Transposons, Genetic Rearrangements

Mayer, Opal, and Medeiros further say,

"A second level of genomic variability in bacteria is referred to as a macroevolutionary change and results in whole-scale rearrangements of large segments of DNA as a single event. Such rearrangements may include inversions, duplications, insertions, deletions, or transpositions of large sequences of DNA from one location of the bacterial chromosome to another. These whole-scale rearrangements of large segments of the bacterial chromosome are frequently created by specialized genetic elements known as transposons, or insertion sequences that have the capacity to move independently of the rest of the bacterial chromosome."

These independently moving portions of DNA cannot be considered new genetic material, because they do not add anything new to the genetic capacity of the organism, and may actually be harmful. Similar things take place in human DNA and there are many heartbreaking examples of deleterious effects in children related to these kinds of mutations, some of which Dr. Anita Millen showed in her presentation at our September 1992 meeting, such as Fragile X Syndrome, Cri du Chat Syndrome, and the various trisomies, e.g., Downs Syndrome.

Plasmids, bacteriophages, acquisition of foreign DNA

Later, they say,

"A third level of genetic variability in bacteria is created by the acquisition of foreign DNA carried by plasmids, bacteriophages, or transposable genetic elements, Inheritance of these extrachromosomal elements further contributes to the organism's ability to cope with selection pressures imposed by antimicrobial agents. These mechanisms endow bacteria with the seemingly unlimited capacity to develop resistance to any antimicrobial agent, once an antibiotic resistance gene evolves, this resistance determinant may spread to other bacteria by transformation, transduction, conjugation, or transportation. Favored clones of bacteria may then proliferate in the flora of patients exposed to antibiotics,"

They imply that plasmids (DNA material transported into a bacterium from other bacteria and usually incorporated into the bacterium's chromosome) and the other types of extrachromosomal elements are created by the evolutionary process, generating new genetic material. They offer no evidence that new genetic material develops this way, and it has never been shown, only assumed. Concerning plasmids, however, they say:

"Extrachromosomal elements were present in bacteria before the advent of antibiotics. However, the introduction of antibiotics into clinical medicine over the past five decades has created selection pressures that favored the dissemination of antibiotic resistance genes via mobile genetic elements, i.e., plasmids and transposons."

What must not be overlooked, is not whether an organism can become resistant to an antibiotic, but whether an organism can develop new genetic material, independent of human intervention, that will give it new capabilities that will raise it to the status of a "higher" life form. This is what has never been demonstrated but must be if evolution is to be proven true.

L.A. McKeown wrote in Medical World News for Nov'92, p. 27:

"While researchers have always known of a genetic component to TB resistance [to isoniazid--an antibiotic used in patients with tuberculosis], investigators at Hammersmith Hospital in London took a major step forward this summer by identifying a probable cause for resistance. Dr. Ying Zhang and colleagues linked the loss of a gene on a plasmid to the development of isoniazid resistance."

In the Journal of the American Medical Association, 1/2/91, p. 14, Andrew Skolnick reports on work done by Alexander Tomasz, professor of microbiology at Rockefeller University:

"It is not surprising that bacterial pathogens have been able to develop resistance strategies in the escalating chemical arms race. What is surprising Tomasz says, is the complexity of some of the recently discovered biochemical defense mechanisms, and how quickly they have evolved."

Skolnick continues his report by saying that the changes bacteria are going through no longer involve just single mutations or the importation of plasmids, but that some of the changes involve complex multigene systems. According to Skolnick, some pneumococci show signs of redesigned enzymes that code for the penicillin binding protein required for their cell walls. "These enzymes [which make them resistant to penicillin]," says Tomasz, "were probably acquired as an entire block of genetic material from an unknown organism." He did not say they developed from a series of random mutations. Tomasz, Skolnick, Mayer et al, and many others have long seen how our use of antibiotics is selectively ridding the human population of non-resistant strains, leaving only the resistant strains. The rise of antibiotics, which has been so beneficial, may actually be setting the stage for the apocalyptic horrors of deadly, worldwide plagues as outlined in Revelation 16.

Bacterial Identification Depends on Their Genetic Stability

Bacteria are identified by their ability to use specific sugars and other biochemicals as energy sources. In the case of intestinal bacteria (the Enterobacteriaceae), it is often the ability of an organism to use a certain carbon source that identifies it. Classic Salmonella typhi cannot metabolize the milk sugar lactose, but Esherichia coli can. If S. typhi could evolve the enzyme lactase and give it the ability to use lactose, it probably would, because lactose is readily available in the environment and the ability to use this carbon source would enhance the survivability of the organism. When I began college in 1968, a suite of biochemical tests identified S. typhi. Today, after millions of generations, these bacteria have remained essentially unchanged and are still the agent of the deadly typhoid fever. The only way we know S. typhi has ever gained new characteristics has been through plasmids, bacteriophages, and transposable genetic elements, and that is rare. David Coppedge, author of How Big Is God?, remarked:

"220 Million Years ... and No Evolution! The oldest examples ever found of microorganisms, preserved in detail in amber, are virtually identical with modern species," reports Science News of Jan. 16, 1993, saying that these organisms have remained in a state of evolutionary suspended animation since the dawn of the age of the dinosaurs. This phenomenon is termed morphological stasis, which being interpreted means "no evolution, folks!"

This morphological stasis is true for dozens of living organisms that once had the honor of being identified as index fossils, such as the tuatara, the coelacanth, and the sea snail Neopilina galatheae.

If anything, one should realize that antibiotic resistance emerging in non-resistant bacteria is probably an inappropriate example for evolutionists to cite as evidence for evolution. There is no scientific evidence to show that resistance, regardless of how it is acquired, is the kind of activity that would eventually give rise to a whole new organism. Evolutionists assume that, given enough time, a series of mutations honed by natural selection would produce a new organism. It may be logical, but it is not scientific. The long time required for such change would make observation impossible. It is also logical that an intelligent designer could make a new organism, but this is outside the domain of the scientific method as well.