Reposted from Mad Mike's Blog.

While the most recent misrepresentation of antibiotic resistance at Answers in Genesis by Georgia Purdom is not of the two usual varieties (either resistance evolves through gene transfer, and therefore mutation does not cause antibiotic resistance, or resistance arises through mutations only, and so mutations can't lead to novel 'kinds'--yes, creationists are that stupid), it's still pretty bad, and it shows a profound ignorance of recent work in the field of antibiotic resistance.

Purdom writes:

The mechanisms of mutation and natural selection aid bacteria populations in becoming resistant to antibiotics. However, mutation and natural selection also result in bacteria with defective proteins that have lost their normal functions.

Evolution requires a gain of functional systems for bacteria to evolve into man--functioning arms, eyeballs, and a brain, to name a few.

Mutation and natural selection, thought to be the driving forces of evolution, only lead to a loss of functional systems. Therefore, antibiotic resistance of bacteria is not an example of evolution in action but rather variation within a bacterial kind. It is also a testimony to the wonderful design God gave bacteria, master adapters and survivors in a sin-cursed world.

Well, I'm not sure how one quantifies "a sin-cursed world"*, but let's deal with the claim that mutation leads to "a loss of functional systems."

The short version: that claim is utter bullshit.

Now the long version. Research by Dan Andersson and colleagues has demonstrated that following mutations that confer resistance, and that lower growth rates in the absence of antibiotics (the supposed "loss of functional system"), compensatory mutations evolve.

What's a compensatory mutation? A compensatory mutation reduces or eliminates the fitness cost of a mutation (often lower growth rate)--in this case, the original mutation that confers resistance. For instance, compensatory mutations in the rpsL gene reduced or eliminate the costs of streptomycin resistance in Salmonella typhimurium. More recent work has demonstrated this in other bacteria, and in mouse models**.

In other words, mutation has expanded function. A ribosomal protein now functions in an environment with antibiotics, where, before the mutation, it did not. This isn't a loss of functional systems, but an increase in the range of function due to point mutation.

I take back what I said earlier: this creationist argument is just as lousy as all of the others.

*And are sins parametrically distributed?

**Interestingly, the types ('spectrum') of mutations observed are different in laboratory culture versus mice.

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