The cost of antivaccinationism

We seem to have an infestation of a couple of very persistent anti-vaccinationist trolls. (It happens; every so often someone new thinks they can take me and my readers on. They’re usually pretty quickly disabused of that notion.) That infestation is why I thought now would be an opportune time to refer my readers to a post that shows the world to which we could return if the anti-vaccine contingent gets its way. Written by the always irascibly sarcastic Dr. Mark Crislip of Quackcast, it’s entitled Amanda Peet is My Hero (1).

Remember, Dr. Crislip is an infectious disease specialist. As he tells us, he doesn’t “make dime one if people do not get infected.” So he’s hoping that Jenny McCarthy and her brain dead ilk are successful. Well, not really. Dr. Crislip is very good at sarcasm, so much so that I can’t always tell when he is being sarcastic. This time I’m pretty sure he doesn’t really mean it.

I think.

Oh, wait, he left a footnote to let us know it was sarcasm. All is well.

Comments

  1. #1 franklin
    August 20, 2008

    Undergraduate gal,

    You say it is up to me to find disqualifying weaknesses in the Cook et al. study.

    What? Are you afraid to risk thinking about the methodological flaws in a study that, in your deluded state, you imagine supports HIV denialism?

    Most undergraduates I know are happy to critique the methodologic flaws of scientific papers because they are interested in learning how to think critically.

    You seem more like a sock puppet than an undergraduate.

  2. #2 Undergraduate-gal
    August 21, 2008

    Dr. Trrll,

    You state you find something “highly amusing”. You know very well you’re stretching the truth now. You don’t have a sense of humour.

    You’re finding inconsistencies in the strangest of places.
    I have all along been reporting what the study authors conclude. You’re asking me a specific question about mortality, but I am not even allowed to mention what the authors themselves have addressed that point? Life sure ain’t easy for us denialists.

    But, dear Dr. Trrll, your mirth seems to have made you overlook that I did offer a couple of comfounders that would blur the line between intermittent and persistent drug users: The unreliability of self-reporting and earlier history. I definitely didn’t say anything about what I find persuasive, so it seems your great joke is entirely self-fabricated.

    Dr. Trrll, a scientist ought to always attempt to critcize herself. Merely reporting the fact that such an attempt has taken place in this case is not an argument in itself. Do you understand that? If anything, it makes the final results even more persuasive when you know the researchers have done their damned best to fit them into the obligatory drug adherence-resistant strain model. Do you understand that? I was passing over these point lightly, because I don’t trade in taking cheap shots at your basic understanding of the way such a study would be worded. Do you understand that, my friend? The opportunistic “gotcha” strategy is all yours, and it’s only blog bimbos of the sort who hang out here that are impressed with it.

    Dr. Trrll, I hate to break this to you – again. This study didn’t last 40 years, ok? It went on for eight years. In fact HIV was only invented about 25 years ago. There was a very clear baseline difference in molecular markers between persistent crack users and intermittent and non-users. As one would expect, both on your drug adherence theory and my cocaine = AIDS theory, the gradation became clearer as the study progressed. As one would also expect, AIDS events were more frequent among the intermittent users than non-users regardless what the molecular markers might have indicated at baseline. It is not possible to say definitively what the primary cause is that goes without saying, Mr. Black&White. But after controlling and explaining away all they could, the authors still felt they had to conclude as they did. What do you and franklin want me to do about it?

    Come to think of it, maybe I was being unkind saying you have no sense of humour, because this was actually quite funny.

    Clearly, you would very much like to believe that the high mutation rate of HIV is just an ad hoc hypothesis–a “tall tale.” But in reality it has been repeatedly confirmed experimentally and at this point is well understood.

    But I suspect it was all straight-faced. I guess the repeated experimental confirmations you are referring to are those routinely conducted on african women sucah as this one reported in Washingtn Post in their 2007 overview of spectacular medical failures:

    Hospitals routinely use antiretroviral drugs, for example, to prevent infections in doctors and nurses stuck by HIV-infected needles. But when researchers asked healthy West African women to take such medicine every day, the difference in infection rates was so small that scientists could not determine whether the medicine worked.

    Of course the medicine worked! It just made the women select resistant strains, right?

    Or maybe it’s those Nevirapine experiments (also carried out on African women, because Nevirapine is too toxic for domestic use) which concluded that a single dose confers drug resistant mutations in 41% of the cases.

    I guess we needed to confirm and reconfirm this well understood fact on 875,000 pregnant African women, although every schoolgirl in Dr. Trrll’s class considers it quite elementary, according to even better understood neo-darwinian principles of selection, that if you withhold further Nevirapine for 6 months after delivery the drug resistant strains will disappear themselves, thus decreasing the risk of treatment failure to a measly 12%.

  3. #3 Militant Agnostic
    August 21, 2008

    Like Laser Potato I am also getting flashbacks to Cooler and like Cooler, UGG and Dawn are unable to use Occam’s Razor because they are not allowed to have sharp objects.

  4. #4 trrll
    August 23, 2008

    Dr. Trrll, I hate to break this to you – again. This study didn’t last 40 years, ok? It went on for eight years. In fact HIV was only invented about 25 years ago. There was a very clear baseline difference in molecular markers between persistent crack users and intermittent and non-users. As one would expect, both on your drug adherence theory and my cocaine = AIDS theory, the gradation became clearer as the study progressed.

    What “drug adherence theory?” I offered 3 hypotheses:

    1) The deleterious effect of drug abuse has been unmasked as HIV patients live longer. This increases the statistical sensitivity of studies and makes it easier to detect a deleterious effect.

    2) The risk does not apply generally to drug users but only to a subpopulation extremely heavy drug users–possibly only heavy female users of cocaine. Previous studies did not isolate this population, so the effect was not large enough to detect the adverse effect on survival

    3) Heavy female cocaine use is associated with some other factors that increase the risk of HAART failure, with plausible candidates being female prostitution, poor nutrition, or a pharmacological effect of cocaine that interferes with the efficacy of HAART drugs.

    Now I suppose that you could come up with a drug adherence hypothesis, if you really insist on doing so. Cook et al. tried to control for this, but they used self-reports of drug use, and perhaps people who are sicker are subject to selective recall and report more drug use, but it didn’t strike me as one of the leading hypotheses.

    As for your cocaine = AIDS notion, it has multiple problems: AIDS is observed in non-cocaine users, AIDS is not observed in cocaine users who are HIV-negative, and heavy cocaine users in the US was around long before AIDS emerged. Discovering that HAART does not work as well in warding off AIDS for heavy drug abusers as for people without habits that damage health (but do not produce AIDS) even in people without HIV does not rescue the drug abuse hypothesis of AIDS.

    But I suspect it was all straight-faced. I guess the repeated experimental confirmations you are referring to are those routinely conducted on african women sucah as this one reported in Washingtn Post in their 2007 overview of spectacular medical failures

    No, I am talking about the many, many laboratory studies that have examined the replication fidelity and the mutation and recombination rate of the HIV virus, as well as the studies documenting the association between the emergence of drug-resistant HIV strains and HAART treatment failure.

  5. #5 Undergraduate-gal
    August 23, 2008

    Dr. Trrl,

    Most studies assume that evidence of drug resistance (increasing viral replication) IS treatment failure. No further “association” is needed, although CD4 count may be taken into consideration and sought correlated with the viral load.

    Buffalo hump, for example, is not considered treatment failure if the viral load is low.

    In this study there is no talk of HAART or ART “treatment failure” or “resistant strains”:

    “Abstract

    Background: Studies of antiretroviral therapy (ART) programs in Africa have shown high initial mortality.
    Factors contributing to this high mortality are poorly described. The aim of the present study was to assess mortality and to identify predictors of mortality in HIV-infected patients starting ART in a rural hospital in Tanzania.

    Methods: This was a cohort study of 320 treatment-naïve adults who started ART between October 2003 and November 2006. Reliable CD4 cell counts were not available, thus ART
    initiation was based on clinical criteria in accordance with WHO and Tanzanian guidelines. Kaplan- Meier models were used to estimate mortality and Cox proportional hazards models to identify predictors of mortality.

    Results: Patients were followed for a median of 10.9 months (IQR 2.9-19.5). Overall, 95 patients died, among whom 59 died within 3 months of starting ART. Estimated mortality was 19.2, 29.0 and 40.7% at 3, 12 and 36 months, respectively. Independent predictors of mortality were severe anemia (hemoglobin <8 g/dL; adjusted hazard ratio [AHR] 9.20; 95% CI 2.05-41.3), moderate anemia (hemoglobin 8-9.9 g/dL; AHR 7.50; 95% CI 1.77-31.9), thrombocytopenia (platelet count <150 × 109/L; AHR 2.30; 95% CI 1.33-3.99) and severe malnutrition (body mass index <16 kg/m2;
    AHR 2.12; 95% CI 1.06-4.24). Estimated one year mortality was 55.2% in patients with severe anemia, compared to 3.7% in patients without anemia (P < 0.001). Conclusion: Mortality was found to be high, with the majority of deaths occurring within 3 months of starting ART. Anemia, thrombocytopenia and severe malnutrition were strong independent predictors of mortality. A prognostic model based on hemoglobin level appears to be a useful tool for initial risk assessment in resource-limited settings." Predictors of mortality in HIV-infected patients starting antiretroviral therapy in a rural hospital in Tanzania Asgeir Johannessen*1, Ezra Naman2, Bernard J Ngowi2,3, Leiv Sandvik4, Mecky I Matee5, Henry E Aglen6, Svein G Gundersen6,7 and Johan N Bruun1

  6. #6 Dr Von Frankenmundt
    August 25, 2008

    Dear Dr Trrll:

    The high mutation rate of HIV is an assumption based on Eigen’s quasispecies model for RNA viruses.

    Maybe you flunk and maybe you don’t have a clue why retroviruses can’t fit this model.

    Can their complete dimeric RNAs ever be in sufficient quantity (without amplification) to be visible on those gels after extraction and fractionation ex vivo? Are we talking about femtograms here?

    Can you state Eigen’s model for us in terms of a typical RNA picornavirus? What exactly is the hypercycle? Please include the significance of synonomous codon substitutions and RNA secondary structures.

  7. #7 Undergraduate-gal
    August 25, 2008

    There! And that goes double for me Dr. Trrl, cuz I think you can’t, you being a biologist an’ all. I bet you don’t even believe in the concept of quasispecies.

    Where are all those virions, defect or not?

    And only one of the all diferent critters can infect the next person. That’s right, only one out of the Eigenous multitudes is fit to penetrate the mucosa of the sexual partner. They said so at the XVIIth, so you like can’t argue with it. Ain’t that something?

    Eigen sure is sexy, but that’s just cuz he’s abstracted the “competing sperm” theory of conception and made it into a viral theory. Just like the early virologists observed a parasitic infection in larvae or some such, and thought to themselves “As above so below (the level of the filterable)”.

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