As PZ mentioned, today would be Charles Darwin's 197th birthday. To celebrate, Mike over at The Questionable Authority is putting together a mini-carnival of posts on evolution. Specifically, he asked how those of us who are scientists use evolutionary theory in our work.
Personally, I'm a bit of a hybrid. I'm a microbiologist by training (my PhD is in microbial pathogenesis and gene regulation), but I loved epidemiology as an undergrad, and so did post-doctoral work in that area--and now am officially titled and "infectious disease epidemiologist". But, I'm still a lab rat rather than an epidemic-chaser, and so my bench work is actually pretty closely aligned with the work I did as a graduate student--trying to figure out what makes a specific pathogen cause disease.
Specifically, my central project involves about 200 isolates of the group B streptococcus (Streptococcus agalactiae, GBS). This is a bacterium that's one of the leading causes of death in newborns. It's also a frequent cause of disease in the elderly and people with diabetes, and has been increasingly found to cause severe disease in healthy young adults as well. In my collection, about half of these are from invasive disease (blood infections, meningitis, etc.) and half are strains that were just hangin' around in people's vaginas or rectum (we call these "colonizing" isolates). The idea is that, sometimes, there are factors present in the invasive isolates that are less frequently found in the colonizing isolates that give them the ability to invade and subvert the host's defenses--and one thing I work on is trying to identify these differences.
Why do we think that there might be differences in the first place?
Well, for one, because an "invasive" lineage of GBS has been found. About a decade ago, some researchers found that a majority of invasive neonatal isolates were practically identical. They did this by cutting up their DNA using restriction enzymes and running it on a gel--and all isolates gave the same banding pattern, suggesting a clonal lineage (that is, they all had a fairly recent common ancestor and therefore are very closely related).
From here, other studies were done to find out where this particular lineage came from--and it was found to be most closely related to isolates found in a cow. This may sound a bit strange, but GBS was first recognized as a cause of bovine mastitis (infection of the mammary glands) long before it was recognized to be a cause of human disease. This suggests a transmission event between the two species--potentially human-to-cow, but more likely cow-to-human.
I mentioned I'm not an outbreak-chaser, but similar methods are used for infectious disease outbreaks as well. Say, for instance, a local epidemiologist has received notice of a dozen suspected cases of food poisoning. The first thing she wants to do is collect isolates from the patients. When she does so, she'll do a test--similar to the one I described above--using restriction enzymes to cut apart the DNA, and then run it on a gel. If the poisoning is due to a common source--say, potato salad at a family gathering--you'll see identical band patterns on the gel. In many cases, one can even go back to the suspected food (if any is left) and isolate bacteria from that as well--which will also have the same band pattern. Closely related isolates, closely related patterns--and a critical component of modern infectious disease epidemiology.
Why is this of consequence? Because those conclusions only make sense if you assume common descent. Sure, we could say that the bacteria that have the same restriction enzyme digest patterns display them because "the designer" made them that way. Or we could say that those patterns have no relationship on ancestry at all--it's just a coincidence. However, a number of lines of evidence converge--notably the phenotype of these bacteria (how the bacteria look, and what proteins they produce) and genetic sequences (hypervariable genes whose DNA sequnces have been compared), that suggest they're very closely related.
Now, many creationists (and I'm including IDists here) say, "what does it matter--they're just bacteria!" (Or viruses, for that matter). But what they don't seem to understand is that we determine other organisms are related in the exact same way we determine bacteria are related. Sure, bacteria don't have bones to fossilize, but what is fossil comparison but a look at morphological similarities? Additionally, we can use molecular genetics--DNA and protein sequences, for example--to determine relationships among *living* organisms (such as chimps and humans), and from there, determine approximately how long it's been since we shared a common ancestor. (We do this for bacteria as well, using the same methods). So, it's a bit crazy to me that some people will accept "microevolution"--often using bacteria as an example--but deny "macroevolution," even though we can use the exact same techniques to examine ancestry!
So, happy birthday, Charles. I find it sad that so many people continue to question your theory, despite all the incredible advances that have been made in understanding it over the years.
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Very nice to know in more detail what you do.
BTW, I do not see any call for posts for a mini-carnival over on Questionable Authority - was that just e-mailed to a chosen few?
Tara-
You wrote:
The idea is that, sometimes, there are factors present in the invasive isolates that are less frequently found in the colonizing isolates that give them the ability to invade and subvert the host's defenses--and one thing I work on is trying to identify these differences.
I have a question- again. Do you also do research that examines the differences in the HOST? I remember you writing back in regards to a question about differences in MS patients in regards to genetics. Is it prudent to think that there are probably a variety of factors present in both the host and the organism that will affect how a disease presents itself and the course it will take? How does one put those two factors together? In PANDAS which strep infection morphs into OCD, how did doctors figure out that a strep infection preceded sudden onset compulsions in children? Was it a case of many anecdotal cases finally being recognized as a possible syndrome of sorts? Was it a new strain of bug responsible for this behaviour, or is there a biological/genetic difference in these children that predisposes them to this illness?
What about back pain and Proprionibacterium Acnes? A small study out of England in the Lancet in 2001 showed this bactera present in almost half of patients presenting with disc pain? If this was a "good" study" and there was no contamination of the samples as one letter I read suggested, why would this not be a good area of research for insurance companies and those with vested interest in keeping people working? Could this be an explanation as to why not all bulging discs on MRI scans cause pain?
Again, I am going back to the psychological versus the biological causes of disease. I think that real science has a lot to offer the "people sciences" in regards to how small things can effect big change in an organism. When people try to discredit Pasteur with his so-called repudiation of his theory of bugs causing disease, by saying he meant it was the host- which people obviously took to be psychological indictment- maybe what can be countered is that yes- people's bodies are different, and even if Pasteur never said that, diseases can be overdetermined in ways that we still do not biologically understand, and do not have to be explained by bad mothers, stress, and how the moon hangs in the sky?
Tara,
ditto what coturnix said. Where's the announcement on Questionable Authority?
Tara,
Interesting stuff you do. Is "invasive" GBS defined based on ability to invade epithelial cells (ala invasive GAS ala Cleary's lab and others) or is it based on the epidemioligical data (i.e. these are the ones that are isolated from diseased patients). I spent a quarter doing those invasion assays, and it was no fun at all! It was and is a very interesting subject, though.
www.stnews.org/Research-1951.html
Spirituality soars among scientists, study says
Scientists, especially social scientists , identify as spiritual, recent research indicates.
Could this possibly be an explanation for bad science???
Taken from the Science and Theology News
Now I need to go to hockey
Tara said, "and half are strains that were just hangin' around in people's vaginas or rectum (we call these "colonizing" isolates)".
You really missed your true calling as a science writer. Anyone who can give me a visual like that is in a league with Zimmer! I gotta go take a shower now.
Impatientpatient
Although I'm not sure if this kind of research is a part of Taras focus, this is the sort of research I have been involved with. It does in fact turn out that there are a large number of mediating genetic factors that can render hosts susceptible to disease. In particular, the organism that is my pet interest, Mycobacterium tuberculosis tends to cause infections in people with certain mutations.
Some of the most common are found in Toll-like receptors (notably TLR2 and TLR4), which are involved in detecting microbial products to activate initial immune responses. Similarly, mutations that inhibit key cytokine pathways like IL-12 or INF-gamma have profound effects on susceptibility to mycobacterial infections.
For some more detail on how host genetic factors can affect pathogenicity, this review is quite approachable:
Casanova J.L. (2001). Mendelian susceptibility to mycobacterial infection in man. The swiss medical weekly, 131:445-454.
Re: carnival, it was kind of a, "hey, I'm putting this together" email. The collection is here.
impatient patient, my work only centers on the bacterium, and I don't have data on the host. That's definitely another factor that likely plays a role in the development of disease, but unfortunately, it takes a lot of money that I don't have to carry out studies on both. That's in my future plans...maybe 5-10 years from now.
As far as Strep and PANDAS, it was a few separate lines of evidence. One, as you mention, was a lot of antecdotal evidence that drove them to carry out a more controlled study. Two, there's a post-strep complication called Sydenham's chorea that was similar to some symptoms and affected the same part of the brain. Three, some early studies showed higher levels of anti-strep antibodies in those with tic disorders, Tourette's, etc. It's still a developing hypothesis, but there are a lot of factors that seem to fit.
Re: Proprionibacterium, never heard of that with disc pain. I'll have to check it out.
More to the rest of you later...heading to an appointment.
Paul,
The latter, though the isolates from the neonatal infections I mentioned also contain a protein that increases their invasion into cells when added to cells that normally don't invade.