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.
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.
Related post: One Random Scientist has a good post about this idiocy too.
Article cited: Sophie Maisnier-Patin, Otto G. Berg, Lars Liljas, Dan I. Andersson (2002). Compensatory adaptation to the deleterious effect of antibiotic resistance in Salmonella typhimurium. Molecular Microbiology 46 (2), 355-366. doi:10.1046/j.1365-2958.2002.03173.x
It can be argued that the majority of genetic mutations lead to some disadvantage in the organism with these mutations. However, in an environment where the benefit outweighs the cost, it becomes a benefit.
A good example for this is sickle cell anemia. It is obviously a bad thing right? But it also confers resistance to malaria. Also, the ill effects of sickle cell anemia are felt mostly when the temperatures are lower (where malaria is not likely to exist). There is some loss of function, but the malaria resistance is certainly a gain of function.
Now, it is also possible that such losses in function then constitute another stress that the organism can adapt to. For instance human muscles are less protein dense than that of most apes. This implies that there is some advantage to having less dense muscles. Or at least that some advantage in one area (such as connective tissue in the brain) may have led to decreased muscle mass but the benefits outweighed the losses. It is then possible that other benefits arose (such as brain capacity) to compensate for such a loss of function. It does not mean that we are any less off, but rather that we adapted to a different environmental stresses… or adapted differently to the same environmental stresses.
Evolution sure is some fun stuff.
Re: sickle cell, it’s not only the homozygous form that causes resistence to malaria (as well the severe heath effects of sickle cell disease). The heterozygous form (sicle cell trait) also produces resistence to malaria without any significant health problems to the carrier. This is also the case with the thalassemias, where homozygous thalassemia produces Cooley’s anemia and heterozygous thalassemia produces an asymptomatic microcytic anemia.
Heterozygoyes have the survival advantage. Homozygotes suffer “collateral damage” as a result.
Mutation and natural selection, thought to be the driving forces of evolution, only lead to a loss of functional systems.
This is the dumbest thing I’ve heard from a Ph.D. since Condoleeza Rice claimed that Iraq wouldn’t need sustained aid.
‘Purdom’ should not try to tell other people what mutations do and not do, but ask someone who knows how it works. … But all I can think at this point is ‘yet another creationist claim that will be parroted all over the place again’. At least we’re warned.
I recently got done debunking Answers in Genesis on this very issue.
Thank you very much