Bless their hearts. The Creationists over at Answers in Genesis are working their perfectly designed fingers to the bone. Blowing the Discovery Institute out of the water by not only publishing a for-realsies science journal (well, at least once), but also performing ‘semi-technical’ research!
While its just adorable to see them working so hard, their crippled understanding of basic science leaves this semi-technical article completely worthless.
Problem #1– Comparing Chihuahuas to Great Danes If *I* were designing a similar experiment, I would have used two types of bacteria.
- Bacteria A- susceptible to ampicillin
- Bacteria B- genetically identical to Bacteria A in every way, except resistant to ampicillin
Thus if there is a fitness difference between the two bacteria, I could be 100% sure it was because of the ampicillin resistance, not anything in the genetic background muddling things up.
This is not crazy magic work.
I am not making unreasonable demands.
That is exactly what I do in my experiments. I take a ‘white mouse’ version of HIV-1, called NL4-3. I chop out a bit of it, and paste in regions from patient samples. All of my viruses are 100% identical, except for the bit I pasted in, so if there are fitness differences between my viruses, I know it has to be genetic differences in the bit I pasted in causing the effect.
Yeah. They didnt do that.
They took two kinds of bacteria with the same species name and compared them. The ‘wild type’ strain they got from a friggen pond. While that is the cutest thing ever, you cant do that. They have no idea what its genome looks like. They dont know if phenotypic differences between the bacteria are because of antibiotic resistance or because of other genetic differences.
Problem #2– ‘Fitness’ doesnt mean what they think it means. What does it mean to be a ‘less fit’ variant? When Im competing various viruses against one another, I define ‘fitness’ as who infects the most cells in a certain environment. Virus A might be a wussy loser on dendritic cells, but a deadly monster on macrophages. Virus B might tear up every cell you feed it, but is easily neutralized by antibodies. ‘Fitness’ changes depending on the environment, and how you define it, and how you measure it.
This paper defines ‘fitness’ as ‘growth rate and colony “robustness” in minimal media’. Considering Problem #1, we have no idea whether the ‘smaller colonies’ or a delayed log phase in the antibiotic resistant bacteria are because of the antibiotic resistance… or something else.
Additionally, their ‘growth curve’ (Figure 2) is useless. A growth curve with no error bars. A growth curve that shows two types of bacteria reaching an identical stationary phase at the same time. Which leads me to believe that if they had performed this experiment more than once, the error bars of these two bacteria would overlap, ie, there is no significant difference between the growth kinetics of these two bacteria. Just like there is not a growth difference between the bacteria in rich media.
But lets grant their premise. The antibiotic resistant Serratia marcescens is ‘less fit’ than ‘wild type’.
Then why does antibiotic resistant Serratia marcescens makes up 92% of the Serratia marcescens infections in hospitals (according to their paper)?
Because while antibiotic resistant Serratia marcescens might be ‘less fit’ in ‘minimal media’, they use ANTIBIOTICS in hospitals. And in the presence of ANTIBIOTICS the ANTIBIOTIC RESISTANT bacteria has a clear reproductive advantage: IT DOESNT DIE.
You have to use an appropriate definition for ‘fitness’.
Problem #3– ‘Comparison’ does not mean the same thing as ‘competition’. I compare viruses every day. I infect a set number of cells with a set number of viruses, and I count how many cells get infected. Lets say in these mono-infections, Virus A infects 90% of the cells, and Virus B infects 90% of the cells. Are these two viruses equally fit?
Hmm. The key to this game is ‘competition’. Throw two kids in a room full of Cheetos, and youre going to have two very obese, very orange children. BUT! Throw two kids in a room with a snack sized bag of Cheetos… one of those kids is going to eat, and one of those kids is going to get a black eye.
To compete viruses, I put the same amount of Virus A and Virus B onto a set number of cells, and I scream ‘FIGHT! FIGHT FIGHT! FIGHT!’ Virus A and Virus B have equal ‘odds’ of infecting cells at that point, so if theyre about the same, they will infect the same number of cells (50/50). However, if Virus A is better in that particular environment, it might infect 90% of the cells, while B dawdles around and can only claim 10%. Its a head-to-head battle for limited resources.
Despite the fact the word ‘compete’ is uses multiple times in this article, nothing is ‘competed’ in this article. Two different bacteria are ‘compared’. There is a difference.
Look, I know relatively little about bacteria. They arent the ‘micro’ in microbiology Im most interested in. But I can do a basic PubMed search to find a paper that analyzed the fitness cost of antibacterial resistance in Serratia marcescens the hard way (ie, the right way): A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β-Lactamase Its a little more than ‘semi-technical’, but they do things right. From their discussion:
Antibiotic resistance that occurs via mutation of an antibiotic target often results in a fitness cost to the bacteria under permissive conditions. This suggests that the removal of antibiotic pressure will reduce the prevalence of resistant bacteria. However, the effectiveness of this strategy is dependent upon a fitness cost that can be overcome or reduced in several ways. First, antibiotic resistance genes are often genetically linked in the form of multi-resistant mobile DNA elements and selection of one resistant determinate can result in the maintenance of other resistance genes by linkage. Second, fitness costs are typically negated by the appearance of compensatory mutations that alleviate the fitness cost while preserving the resistance phenotype. Without a significant fitness cost, there is no selective pressure to drive a loss of the resistance determinant. Finally, multiple routes of resistance can exist and be highly variable with regard to the fitness costs they engender. Therefore, a spectrum of resistant clones can exist; some with no fitness costs or even enhanced fitness under permissive conditions. (references removed for ease of reading– ERV)
*sigh* Its really, really cute that Creationists are trying to do big-kid research. But ‘Darwin at the Drugstore?’ is just a friggen mess.