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Anthrax and antibiotics: Is evolution relevant?

by Dr Jonathan Sarfati

15 November 2001; updated 8 April 2005

After the terrorist attack on 11 September, many people fear a new danger—biological warfare in the form of anthrax. Perhaps understandably, many Americans are taking antibiotics such as Cipro (ciprofloxacin) as a preventative measure. Data from the pharmaceutical tracking company NDCHealth of Atlanta, Georgia, show that almost 63,000 more Cipro prescriptions have been issued in the third week of October alone than for the entire previous year. However, this has caused some concern in the medical profession that antibiotic overuse could result in antibiotic resistance in many types of bacteria. Not surprisingly, the humanist-dominated secular media has used phrases such as ‘Bacteria evolve drug resistance very quickly’. Fortunately, in the current round of articles, I haven’t seen repeated the hysterical outburst of one particular evolutionary propagandist who claimed that people will die because of creationists, because they will allegedly fail to understand this vital fact of evolution of drug resistance.

We have covered antibiotic resistance in many articles on this website. So here it will suffice to summarize the main issues to enable people to assess critically any articles on this current scare. First some principles:

  • Watch for equivocation, i.e. using the same term in different ways in the same article. It’s very common for evolutionary propagandists to define evolution as (1) simply ‘change in a population over time’, as well as (2) the idea that all life came from a single cell, which itself came from a chemical soup. Then they produce examples of ‘evolution’ (1) and use this to prove evolution (2), and then claim that Biblical creation is wrong! However the Biblical creation model does imply that organisms change over time—but these changes would always involve sorting or loss of already existing (created) genetic information, never the gain of new information. But evolution (2) requires the gain of new information. Even if information losing (or neutral) processes could continue for billions of years, they would never add up to a gain of information. Rather, to support evolution (2), evolutionists must demonstrate changes that increase information. If this theory were true, there should be plenty of examples, but we have yet to observe even one. Since evolution (2) is the only issue at stake in the creation/evolution controversy, we advise against referring to any mere change as ‘evolution’—not even ‘micro-evolution’—and reserving the term ‘evolution’ for (2).
  • Natural selection is not evolution. This merely weeds out organisms and the information they contain; it doesn’t generate new information. The creationist Edward Blyth discussed natural selection 25 years before Darwin, but recognized that it was a conservative, not a creative, force.
  • Mutations are not evolution. They are copying mistakes in the genes. No mutation is known to increase information content; every known mutation has either decreased information content or was informationally neutral. This applies even to the rare examples of beneficial mutations.

To apply these principles to antibiotic resistance, there are several ways that germs can acquire resistance to drugs, none of which have anything to do with evolution from goo to you via the zoo:

  • Natural selection: the drugs wipe out all the non-resistant germs, so the most resistant germs survive and multiply. This leads to a whole population that’s resistant to antibiotics. This is not evolution because the resistance already existed in the population. Despite this, the PBS Evolution propaganda series used selection of pre-existing antibiotic resistance in tuberculosis germs as a major ‘proof’. In fact, some bacteria revived from corpses frozen before the development of antibiotics have shown resistance.

Selection for resistant bacteria is a real danger when a patient fails to complete a prescribed course of antibiotics (60 days for Cipro)—i.e. stops taking the drug when the symptoms ease, which just means that most germs have been destroyed. The remnants require the final doses of antibiotic to finish them off, but if the treatment stops, they are free to multiply. This time the drug is far less effective, since the remnant population will tend to be the more resistant ones.

This problem of selection of resistant varieties applies not only to the targeted germ, but all the other types affected by the same antibiotic. This is the main reason that the medical profession is concerned with people taking Cipro for a few days because of the anthrax scare. Indeed the over-use of Cipro could result in many germs that are resistant to this drug, so the concern is very well founded. Antibiotics as a preventative measure are warranted only where there’s evidence that people were in a ‘breathing zone’ of the deadly airborne anthrax spores, not for the milder skin form of anthrax.

  • Sometimes bacteria can pass on information to other bacteria, via loops of DNA called plasmids. Sometimes plasmids contain information for antibiotic resistance. But here too, the information already existed, so this is not evolution.
  • Information-losing mutations can confer resistance. Such mutations are often harmful in an ‘ordinary’ environment without antibiotics. It is well documented that many ‘superbugs’ are really ‘superwimps’ for this reason—see Superbugs not super after all . Also, some sorts of information-losing mutations evidently cause HIV resistance to antivirals, because the ‘wild’ types easily out-compete the resistant types when the drugs are removed. Despite this, this was promoted as another ‘proof’ of evolution by the PBS series.

    So, how can an information loss confer resistance? Here are some observed mechanisms:

    • A pump in the cell wall takes in the antibiotic. A mutation disabling this pump will prevent the bacterium pumping in its own executioner. But in the wild, a bacterium with a disabled pump will be less fit than other bacteria because the pump also brings nutrients, etc., into the cell.
    • A control gene regulates the production of an enzyme that destroys the antibiotic, e.g. penicillinase which destroys penicillin. A mutation disabling this gene destroys the regulation of the production, so far more enzyme is produced. Such a bacterium can cope with more antibiotic than others can, but in the wild, it would be less fit than normal because it’s wasting valuable resources producing more enzyme than is needed.
    • An enzyme is highly specialized to break down one specific type of chemical very well, and hardly affect other chemicals. A mutation could reduce its specificity, i.e. it no longer does its main job so well, and affects other chemicals to some extent too. Normally, a biological system with such a mutation would not function as well, and reduced specificity is reduced information by definition. But sometimes the other affected chemicals happen to be antibiotics, so this type of mutation confers resistance. See further discussion in this refutation of a critic and Not By Chance (top right), ch. 5.
    • The antibiotic streptomycin works by attaching onto a precisely matching site on the surface of a bacterium’s ribosome, where decoding of DNA information to proteins occurs. When the streptomycin attaches, it stops this machinery from producing the right proteins, and the bacterium dies. Resistance to the drug can be caused by an information-losing mutation that degrades the surface of a bacterium’s ribosome, which reduces the binding ability of the drug to the ribosome, preventing it from ruining the protein manufacturing machinery.
    • More detail on information-losing resistance-increasing mutations can be found in the article Is bacterial resistance to antibiotics an appropriate example of evolutionary change?

These principles should be enough to demonstrate that these latest claims about bacteria ‘evolving’ resistance are not a threat to Biblical creation. Despite all this, many evolutionists crow about antibiotic resistance as an amazing ‘prediction’ of evolution. Even aside from the above points, this is revisionist history. Historically, antibiotic resistance first took the medical profession by surprise—even as late as 1969, experts stated that ‘infectious diseases were a thing of the past’. I.e. antibiotic resistance was hardly a ‘prediction’ of evolution, but is really a phenomenon explained ‘after the fact’ by evolutionary language. But as shown, the Biblical Creation/Fall model explains it better.

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