Respectful Insolence

It’s been a while since I’ve visited the cesspool that is Uncommon Descent, a.k.a. Bill Dembski’s home for wandering sycophants, toadies, and lackeys. There’s a good reason for this; I just get tired of the sheer stupidity that routinely assaults my brain every time I make the mistake of taking a look at UD’s latest attempt to try to refute evolution. Worse, there’s lots of other pseudoscience there these days, from the promotion of the use of cancer therapies that haven’t been subjected to clinical trials yet to anthropomorphic global warming “skepticism.” Yes, every time I peruse the posts at UD, I feel brain cells dying. Now that I’m middle-aged, I’m no longer as blasé about causing the premature death of so many neurons as I may have been as a younger man.

Sometimes, though, a skeptical doc’s gotta do what a skeptical doc’s gotta do, and this is one of those times. Once again, one of the lower-powered intellects in the “intelligent design” (ID) movement (and that’s really saying something) named Gil Dodgen has decided to propose a “practical medical application” for ID in a post entitled, ludicrously enough, A Practical Medical Application of ID Theory (or, Darwinism as a Science-Stopper). It’s proof positive that a little knowledge (and I do mean a little) is a dangerous thing:

Here’s a prediction and a potential medical application from ID theory: Design a chemical or protein which would require a triple CCC to defeat its toxic effects on a bacterium, and it will exhaust the probabilistic resources of blind-watchmaker mechanisms to counteract the toxic effects.

Such a success could and will only come from engineering and reverse-engineering efforts, not from Darwinian theory.

First, I wondered what Gil meant by a “triple CCC.” I assume he means, as Burt Humburg thinks, the Chloroquine Complexity Cluster proposed by Michael Behe in his latest book, The Edge of Evolution, as an example that supposedly shows that there is an “edge of evolution,” beyond which mutation and natural selection cannot produce novelty fast enough to account for the diversity of life. This example has been demolished in detail by Arthur Hunt; so I don’t feel compelled to rehash all of that. It’s also possible that, as Larry Moran thinks, Gil is referring to the more general idea of a selective pressure that requires three mutations simultaneously in order for an organism to survive it. It doesn’t really matter what Gil means; it’s all equally stupid and ignorant, because in reality it is standard evolutionary theory that makes the prediction that using multiple antibiotics would be more likely to prevent the emergence of resistance. Nor is it any challenge to evolutionary theory to postulate that there is a limit to useful mutations; it’s in using bad math and grossly miscalculating what that limit is that Behe and other ID creationists dive into pseudoscience. (Behe’s thesis is so bad that it doesn’t even take a Ph.D. to refute it, as Abbie Smith has so ably demonstrated again and again.)

As a brief aside, I ask: Do you find it irritating how ID creationists appropriate perfectly acceptable predictions made by evolutionary theory and try to convince the ignorant that they are really predictions made by ID? I do.

In fact, evolutionary theory, in concert with other aspects of biology, even suggests to us to large extent how antibiotics should be combined. For example, combining antibiotics with identical or very similar molecular mechanisms of action would be highly unlikely to suppress resistance, because any bacterial mutation that defeats one of these related antibiotics would be highly likely defeat all of them given their shared mechanism. No, what evolution would predict is that, to minimize the possibility of resistance, combination therapy should consist of multiple drugs with very different molecular actions. Such drug combinations are also clinically useful because they often interact synergistically to kill bacteria more effectively, even aside from evolutionary considerations. For example, penicillins work by inhibiting the formation of molecular crosslinks necessary for bacterial wall strength, thus weakening the wall and causing the osmotic swelling and death of the bacteria. (Cephalosporins have a very similar mechanism of action.) Aminoglycosides (example: Gentamycin), on the other hand, bind to the bacterial ribosome and cause the misreading of mRNA, so that the bacteria cannot synthesize vital proteins, while quinolones and fluoroquinolones (example: Ciprofloxacin) inhibit the bacterial enzyme gyrase or topoisomerase, thus inhibiting DNA replication and transcription. These drugs are often paired so that drugs with different mechanisms of action are used, one classic combination being a penicillin or cephalosporin paired with an aminoglycoside.

This concept of combining drugs with different mechanisms of action to minimize the likelihood of the evolution of resistance is not limited to bacterial resistance. Indeed, antiretroviral therapy for HIV is a classic example of how successful this strategy can be. Before the mid-1990s, HIV evolved rapid resistance to single drug therapy with, for example, AZT. However, with the advent of protease inhibitors, it was discovered that it was possible to produce “cocktails” of at least three drugs, which must contain at least two different classes of antiretroviral drugs, usually two nucleoside analogue reverse transcriptase inhibitors plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor. As evolutionary theory would predict, these cocktails are far less likely to select for resistant strains of HIV than monotherapy and have led to the enormously increased length of survival in HIV-positive patients, in many cases allowing HIV to be managed as a chronic disease. Unfortunately, as is frequently the case when multiple powerful drugs are taken concurrently, there are side effects; worse, these regimens are often inflexible, requiring carefully timed dosing. HIV is so prone to developing resistance that it doesn’t take missing many doses to give the retrovirus the opening it needs.

Finally, the concept of using multiple drugs to minimize resistance isn’t even limited to infectious disease, such as viral, bacterial, or parasitic diseases. Indeed, it’s a cornerstone of chemotherapy for cancer. One of the most commonly used regimens for breast cancer includes three drugs: doxorubicin, which intercalates itself between DNA helices and inhibits DNA replication; cyclophosphamide results in DNA crosslinking; and taxol interferes with microtubules. GilDodgen preens as though ID creationists were the first ones to have thought of this concept, but in reality it was medical scientists, making real practical use of evolutionary theory and, admittedly, a fair amount of trial-and-error, who put the concept of polydrug therapy to good use. Moreover, this is not a new strategy by any means. Combination therapies, such as the ones I discussed, have been in use for several decades. Even so, it’s hard not to point out to Gil that we still see resistance evolving in bacteria, viruses, and cancer even to combination therapy, contrary to what he apparently thinks that ID would predict.

There are probably several reasons for this, depending upon the specific situation. At the base of it all, though, is probably, as Larry puts it, the fact that scientists don’t yet know every mechanism by which bacteria (or viruses or cancer cells) can develop resistance. Evolution also has a way of bypassing the simplistic sort of thinking that Michael Behe and his sycophant Gil Dodgen invoke when they claim that it is impossible for evolution to produce a CCC-type simultaneous mutation to overcome the selection pressure of multiple simultaneously administered drugs. The reason is that biology tends to be very redundant and thus often not so easily defeated. To demonstrate my point, I’ll start by asking Gil just one question:

Have you ever heard of multidrug resistance?

You haven’t? I’ll forgive you if you haven’t (although if you had done even the most rudimentary Googling of mechanisms of multidrug resistance in bacteria or cancer cells, you would have discovered this mechanism fairly rapidly). It’s a fascinating topic and, among cancer biologists and infectious disease experts, a deadly enemy. Indeed, in cancer, multidrug resistance (MDR) is the primary means by which cancer cells evolve resistance to chemotherapeutic agents. This resistance is due usually to one or both of two molecular “pumps” on the cell surface with broad specificity that are able to actively expel a wide variety of chemotherapy drugs from the cell. The two pumps commonly found to confer chemoresistance in cancer are P-glycoprotein and the so-called multidrug resistance−associated protein (MRP), and mutations in these transporters can allow cancer cells to become resistant to multiple chemotherapeutic agents at once. No “CCC”-like event is required. It turns out that these pumps belong to a family of ATP-binding cassette (ABC) transporters that share sequence and structural homology. As of 2002, 48 human ABC genes had been identified and characterized, divided into seven distinct subfamilies (ABCA-ABCG) on the basis of their sequence homology and domain organization. Drugs that are affected by this method of multidrug resistance include the a drugs with a wide variety of different mechanisms of action, including vinca alkaloids (vinblastine and vincristine), the anthracyclines (doxorubicin and daunorubicin), the RNA transcription inhibitor actinomycin-D, and the microtubule-stabilizing drug paclitaxel, among others.

That’s not the only molecular mechanism by which cancer cells can develop resistance to multiple drugs at the same time. It’s just one of several. But what about bacterial resistance to antibiotics? Unfortunately, bacteria have MDR-like proteins as well, and can also develop multidrug resistance without necessarily having to undergo a CCC-like simultaneous mutation. Indeed, targeting these proteins is an active area of drug development. Once again, it’s a case of evolution being more complex and “clever” than we think. It’s also a case of ID creationists simply being ignorant of basic mechanisms of drug resistance and and the relationship between them in different cells. Indeed, the very fact that MDR-like efflux proteins are conserved between bacteria and mammals would tend to favor evolution, not ID. Finally, using evolutionary theory, it is possible to design clever drug combinations that select against resistance alleles. No ID “theorist” can say the same.

And don’t even get me started on how bacteria can exchange DNA through the process of bacterial conjugation, thus allowing the spread of resistance alleles rapidly through a population.

I was tempted to stop here, having subjected myself to enough stupid for one night and being in a rather merciful mood, but unfortunately GilDodgen couldn’t stop while he was behind. He had to bury himself even deeper:

In the meantime, medical doctors should prescribe multiple antibiotics for all infections, since this will decrease the likelihood that infectious agents can develop resistance through stochastic processes. Had the nature of the limits of Darwinian processes been understood at the outset, the medical community would not have replaced one antibiotic with another in a serial fashion, but would have prescribed them in parallel.

The stupid, it burns. Indeed, the above paragraph is such a hunk a’ hunk a’ burnin’ stupid that I had to step back from my computer screen, lest it scorch my face. Burt‘s done a fine job of describing why the medical community replaced one antibiotic with another over time; I’ll restrict myself to other aspects of this statement.

I would hope that any physician, even an ID proponent like Dr. Michael Egnor, should know that treating all infections with multiple antibiotics “in parallel” is a really, really dumb and wasteful thing to do (and that’s an evidence-based statement). For one thing just adding another antibiotic or two (or three) is not a benign thing; blasting away with antibiotics shotgun-style is likely to do far more harm than good. Indeed, broadening the spectrum of antibiotics used by using multiple antibiotics with different mechanisms of action “in parallel” has a nasty tendency to kill off the beneficial bacteria along with the pathogens, leading to antibiotic-associated diarrhea or even C. difficile colitis, which in extreme cases can progress to the life-threatening toxic megacolon. That’s just one example. There are also the toxicities of the antibiotics themselves (for example the damage to kidneys and hearing that can be caused by aminoglycosides) and the allergic reactions to penicillins. I could go on, but you get the idea.

Worse, using multiple antibiotics can actually lead to more drug resistance. How is this possible, given that I just said that combining antibiotics is a good way to minimize the possibility of resistance? Actually, there is no contradiction. It is true that combining antibiotics minimizes the possibility of resistance evolving–in the bacteria that are sensitive to the antibiotics in the combination, that is. However, whenever physicians combine antibiotics, they also increase the spectrum of bacteria that the combination will kill, leading to “collateral damage” among many other species of bacteria. Given that different drugs kill different species of bacteria with different levels of efficacy, broadening the spectrum of antibiotics will subject species of bacteria other than the one(s) being targeted to antibiotics to which they are not as sensitive as the bacteria being targeted. These other non-targeted bacteria will thus be put under selective pressure to evolve resistance, even as the organisms causing the infection are killed off. Thus, while the targeted organism(s) might not be able to evolve resistance, other non-targeted organisms can. In the case of serious polymicrobial infections, we can’t afford to worry all that much about this consequence if combination antibiotic therapy is what it takes to save the patient’s life, but using, say, triple antibiotics to treat a case of strep throat or an uncomplicated pneumonia, as Gil seems to think we should do all the time, would enormously exacerbate the problem of emerging bacterial resistance to antibiotics.

This is the sort of stuff medical students are taught in the second year of medical school in our basic pharmacology class.

Perhaps you think I’m being too hard on Gil. After all, he clearly never went to medical school, appears never to have taken a basic pharmacology or microbiology course, and clearly knows jack squat about antibiotics, infectious disease, or bacterial resistance. He clearly has no clue that multidrug therapies have been used in medicine to try to prevent antibiotic resistance at least since the 1940s or that combination antibiotic therapy has been a mainstay in the treatment of diseases like tuberculosis and leprosy for decades, just as combination chemotherapy has been for various cancers. (Indeed, some drug regimens for TB utilize three or four different drugs to overcome resistance.) Unfortunately, Gil’s proudly trumpeted arrogant ignorance wasn’t finished at this point. He couldn’t resist adding to it by concluding:

This represents yet another catastrophic failure of Darwinian presumption, which is based on hopelessly out-of-date 19th century scientific naïveté.

“Scientific naïveté“? Gil owes me a new irony meter to replace my old one, which just fried itself into a molten blob of metal and rubber, thanks to the above statement. (He also owes me a new computer keyboard, as I can’t get the Coke his statement led me to spew up out of my keyboard.) The phrase “pot, kettle, black” comes to mind.

ADDENDUM: OK, OK, it’s too easy, but just get a load of this comment by Gil in the comment thread to the question:

Malaria was designed not to be totally cured?

Replies Gil:

No, malaria was not designed to be capable of evolving to become resistant to anything.

Gee, that “intelligent designer” was one nasty bastard, then, wasn’t he? He/she/it must have “designed” malarial drug resistance from the beginning, then.

ADDENDUM #2: The Panda’s Thumb has a less–shall we say?–insolent response to Gil’s cluelessness that nonetheless utterly demolishes every point he’s tried to make.

Comments

  1. #1 Jason Failes
    December 11, 2007

    “Perhaps you think I’m being too hard on Gil. After all, he clearly never went to medical school, appears never to have taken a basic pharmacology or microbiology course, and clearly knows jack squat about antibiotics, infectious disease, or bacterial resistance.”

    I don’t feel sorry for him at all.

    These people feel absolutely no hesitation at commenting on/ trying to discredit science they not only do not understand but have not even tried to understand. They don’t talk to a biology professor before they post. They don’t even wiki the subject matter.

    I’m interested in quantum physics, but I’ve never been interested enough to sit down for a few years and really deeply understand it. Right now, it seems a little bit counterintuative to me. Well, who’s fault is that? Do I bone up on quantum physics, or do I start blogging about the “quantum physics conspiracy” based on false premises, just because I personally don’t understand it?

    you got it right in one: the stupid, it burns.

  2. #2 Warren
    December 11, 2007

    No, malaria was not designed to be capable of evolving to become resistant to anything.

    Isn’t presuming to “know” the “mind” of the “creator” hubris, at best — and blasphemy at worst?

    (At the very least, it’s an odious form of arrogant stupidity.)

  3. #3 Hermagoras
    December 11, 2007

    I had been operating at UD under the name “getawitness” for a month or so, having been banned as “Hermagoras” back in the day. They tolerated getawitness for a while, but Gil’s stupidity was the last straw.

  4. #4 hrun
    December 11, 2007

    Well, I had been sporadically posting there as well. Unfortunately, most of my comments never make it past DaveScot. In Gil’s post I pointed out the a) combination treatment has already been used b) is perfectly consistent with evolution c) is not easy to achieve d) poses moral dilemmas (must hold back perfectly working drug while waiting for development of further drugs targeting the same bug) e) that MDR genes give rise to resistance against combination treatments and f) that ID gives no help whatsoever for this ‘reverse engineering’ of drugs that go ‘beyond the edge of evolution’.

    I wonder why Dave didn’t approve of this post. I was being very cordial in my tone, too. :)

  5. #5 Blake Stacey
    December 11, 2007

    Random aside:

    and taxol interferes with microtubules.

    According to Stuart Hameroff, that means taxol must interfere with consciousness, because microtubules are where the quantum consciousness resides!

  6. #6 daedalus2u
    December 11, 2007

    Orac, regarding your loss of brain cells when reading crap. That is not a bug, it is a feature. You are actively pruning the (few) defective brain cells that can get a glimmer of activation from such nonsense. You are better off without them. Losing them makes you smarter.

    Pity the IDiots who come to Science Blogs. They prune the brain cells than activate when exposed to reality. That is readily apparent. When ever they come here and post, or even when they read posts made by non-IDiots at the IDiot blogs, their responses show increased stupidity.

    If stupidity really did burn, soon we would be able to replace fossil fuels with the stupidity of the IDiots.

  7. #7 viggen
    December 11, 2007

    No, what evolution would predict is that, to minimize the possibility of resistance, combination therapy should consist of multiple drugs with very different molecular actions.

    I would also suggest that the drugs would optimally have very different chemical structures so that they be subject to as different of bacterial remediation pathways as possible. It is possible that the chemical functionalities that cause a drug to operate (say an aptly placed Fluorine atom or carboxy-group) can be remediated by a particular general enzyme which attacks a chemical feature in foreign compounds as opposed to protecting a specific cellular pathway. As I recall, Pseudomonas have enormous resistance to antibiotics based on general remediation capabilities rather than small mutations in pathways rendering those pathways inaccessible to a particular antibiotic attack. A small mutation in some remediator enzyme might give it a broader spectrum activity and make it sufficient to break down relatively closely related compounds that might have vastly different antibiotic targets.

  8. #8 daedalus2u
    December 11, 2007

    Actually, what one would predict by using evolutionary theory would be treatments that prevent disease without killing (and so inducing organisms to evolve resistance) the disease causing organism. That is a major strategy of many eukaryotes. They prevent surface infections by suppressing quorum sensing by disease sensing organisms.

    Virtually all bacterial pathogens express quorum sensing compounds which switch them from a free-living planktonic phenotype to a biofilm phenotype. They only express virulence factors when activated by quorum sensing.

    A large part of the natural defenses of the body is having the “right” comensal bacteria, which suppress the bad bacteria which can cause disease. That is what I am working on, ammonia oxidizing bacteria which live on the external skin and generate NO and nitrite from sweat. This NO is a quorum sensing compound for Pseudomonas.

    http://jb.asm.org/cgi/content/abstract/188/21/7344

    At high NO levels Pseudomonas is planktonic and doesn’t form a biofilm, and doesn’t express the virulence factors it expresses when not planktonic.

    I suspect that this is why the immune system generates so much NO so quickly when exposed to bacteria. The NO is to suppress the formation of biofilms in the vasculature for example.

  9. #9 Rev. BigDumbChimp
    December 11, 2007

    No, malaria was not designed to be capable of evolving to become resistant to anything.

    I must speak to this Gil who obviously has a direct line to God… I mean the the Designer.

  10. #10 Magainin
    December 11, 2007

    Thank you lord for our daily d-alanine:d-lactate ligase. Resistance is futile.

  11. #11 Prometheus
    December 11, 2007

    No, malaria was not designed to be capable of evolving to become resistant to anything.

    I can defeat that in one phrase – one that’s heard all too often in Southeast Asia: “chloroquine-resistant malaria.”

    Maybe I missed something, but is Gil really so far gone that he didn’t notice that malaria has become resistant to not only quinine but also chloroquine? And all of that within a few human lifetimes.

    Another mechanism of multi-drug resistance that is just now coming into focus is what are known as “persisters”. These bacteria go through prolonged periods when they don’t divide and exist at a very low metabolic state.

    If this happens when there are antibiotics around, they live while their “cousins” die. They “wake up” after a while and, if the antibiotics are gone, they replicate in the nice empty niche.

    These “persisters” don’t need to evolve fancy drug-resistance cassettes, they have just evolved a ability to take prolonged “siestas”. They can resist almost any antibiotic, since almost all antibiotics (maybe all, but I may have missed one) need the cells to be metabolically active to work.

    “Persistence” may explain those infections that keep coming back even though they’ve been “blasted” with drugs that cultures show they are sensitive to. Interestingly, the way to increase the percentage of cells in the “persistent” state (and the duration of that state) is to bombard them with multiple antibiotics.

    Ain’t evolution a pain?

    Prometheus

  12. #12 Chris Noble
    December 11, 2007

    The one that gave me brain failure was the idea that it was a failure of evolution that the malaria parasites don’t become resistant to sickle-cell anemia.

    This is a classic “according to evolution” strawmen.

    Even in regions with a high incidence of malaria the majority of people do not carry this gene. There is very little if any selective pressure on the malaria parasites to evolve resistance.

  13. #13 Reynold Hall
    December 11, 2007

    I too, can’t get any of my comments past moderation. Usually, I post, my comment doesn’t show up, I post again, and I get an error message saying “Duplicate Comment detected: looks like you’ve already said that”!

    Only rarely will my comment even show up with the “Your comment is awaiting moderation” notice.

    Then, it disappears later on. And those are the people who complain about “Darwinists” censorship. Effing cowards. Fortunately, I’ve saved the HTML page from one time when my comment at least made it (albeit temporarily) to their board.

    Though I’m really ignorant of this topic, and thus my comment didn’t touch all the bases about the topic we’re all talking about, I still feel it refuted part of what they were saying.

    My comment was #32 over there before it disappeared.

    If anyone’s interested, this is what I tried to say:
    —–
    From the original article here:

    In the meantime, medical doctors should prescribe multiple antibiotics for all infections, since this will decrease the likelihood that infectious agents can develop resistance through stochastic processes. Had the nature of of the limits of Darwinian processes been understood at the outset, the medical community would not have replaced one antibiotic with another in a serial fashion, but would have prescribed them in parallel.
    Uh, are you sure that’s a good idea? What about the different ways that the multiple drugs can interact with each other and with the human body? Perhaps with a dangerous unknown bug that you don’t know what will kill, that may be acceptable, but not with a bug for which an antibiotic is known.

    This represents yet another catastrophic failure of Darwinian presumption, which is based on hopelessly out-of-date 19th century scientific naïveté.
    No, only your strawman of it. If you’re so certain that “Darwinism” is out-of-date, perhaps you’d care to explain how it’s so successful in it’s predictions. While you’re at it, you may want to provide a comparable list of successful ID predictions.
    http://www.talkorigins.org/faqs/comdesc/

    They couldn’t seem to do that at Dover….and at least one Conservative pundit has a negative view of ID’s scientific value:
    http://www.humanevents.com/article.php?id=23404

    So in light of the issue’s new prominence and with a desire to improve the mental hygiene of others, I would just like to say that Intelligent Design is a really, really bad idea –scientifically, politically, and theologically. I say this as a dedicated conservative, who has on many occasions defended and espoused religion and religious conservatism. I also say it as a professional molecular biologist, who has worked daily (or at least week-daily) for years with biological problems to which the theory of evolution has contributed significant understanding — and to which Intelligent Design is incapable of contributing any understanding at all.
    I’ve noticed in the sidebar here that you guys are complaining that Mac didn’t read any ID articles. When did you guys ever publish any evidence for ID? I’m talking about research and verified predictions done from experimentation. I should note that he’s worked in a relevant field for years!

    BTW: in response to #15, bornagain’s AIG linked article about how the “superbugs” are actually “wimps”, it turns out to not always be the case.
    Check out
    http://www.talkorigins.org/faqs/mutations.html

    and other such sites…

    In modern times antibiotics, drugs that target specific features of bacteria, have become very popular. Bacteria evolve very quickly so it is not surprising that they have evolved resistance to antibiotics. As a general thing this involves changing the features that antibiotics target.

    Commonly, but not always, these mutations decrease the fitness of the bacteria, i.e., in environments where there are not antibiotics present, they don’t reproduce as quickly as bacteria without the mutation. This is not always true; some of these mutations do not involve any loss of fitness. What is more, there are often secondary mutations that restore fitness
    —–
    If I can’t post there, I’ll post here. When “Darwinists” “suppress” ID, they go and publish detailed rebuttals, as opposed to the ID people’s just quietly deleting comments and pretending that they never existed!

  14. #14 Bad
    December 11, 2007

    Nor can things always develop resistance to everything. If there isn’t a nearby pathway to something, they’re sh** out of luck, and that’s that. Designers could overcome such things easily of course, but somehow we never see that happening.

    What we do find are organisms that, when faced with an impenetrable wall for some solution, develop in entirely different ways and expand into new functions and niches. Or they die off. And as it happens, that occurs quite a lot too… just as evolution suggests it would.

  15. #15 Freddy the Pig
    December 12, 2007

    Whats with the ID obsession with malaria? I have heard Behe going on about maria having th have been intelligently designed in Point of Inquiry interview and he seems to make the same argument about HIV (and got his head handed to him by ERV for it). The “Designer” must have really something against Africans. Maybe the “Designer” is punishing them for wandering out of their assigned continent and out evolving the “Designer’s” chosen people (the Neanderthals).

  16. #16 DLC
    December 12, 2007

    Thanks for taking this one on, Orac.
    By the way, does Dodgen explain how MRSA (for example) became resistant to multiple antibiotics in the first place ?
    Oh, right, it was Designed to make itself resistant, because the designer was prescient and knew what drugs would be used against it. I guess smiting people directly isn’t good enough, GodThe Designer needed a bacterium to infect people with and cause them misery.

  17. #17 Macnerdzcare
    December 17, 2007

    MRSA is sort of the bacterial version of HIV right?

  18. #18 J-Dog
    December 20, 2007

    Thanks for the psot Orac – I missed it the first time around. And BTW – Thanks to all the commentators also – they are to the point and extremely helpful.

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