Correction

Last week, I (and Kathy) posted about the Department of Agriculture trying to prevent meatpackers from testing their own animals for mad cow disease. In that post, I quoted an AP article that said:

“The Agriculture Department regulates the test and argued that widespread testing could lead to a false positive that would harm the meat industry.”

This was not accurate.

Hilzoy at Obsidian Wings, who had posted about the same article, looked up the brief and decisions on the case at the prompting of one of her commenters, and found “that the government had in fact made a completely different and much more defensible argument.”

[I]n short: the government argues that since tests for BSE only pick up the disease a few months before an animal becomes symptomatic, a point which is usually well after most US cattle are slaughtered, testing would miss most infected animals. It would, essentially, be a marketing gimmick designed to produce unfounded confidence. … I have no idea whether the government’s argument is right or not, but it’s important to be accurate about what, exactly, that argument was. And it’s completely different from the argument the AP story claims that the government made.

So, for the record, the Bush administration was arguing that the test “offers no animal health or food safety value” because of issues with the test that was to be used, and they appear to have been more concerned with false negatives than false positives. (In fact, the term “false positive” doesn’t show up anywhere in their 62-page brief.)

Perhaps there’s a Shaker who knows more about BSE testing and can provide some context to the actual argument being made here by the Dept. of Agriculture, or speak to its veracity.

Thanks to Hilzoy for the heads-up. Here ends this Public Service Announcement from the Reality-Based Community. Carry on.

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15 Comments

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15 responses to “Correction

  1. It’s true that tests currently available only show positive results shortly before symptoms appear and years after the initial infection. However, in the early (asymptomatic) stages of infection, infectivity is low. (Low in science-speak. I.e. astronomically low. You’d be likelier to die of a lightning strike kind of low.) In the later (still asymptomatic) stages, BSE tests come up positive *and* the animal is infective.

    In other words, the tests are a pretty good indicator of how infective the animal is.

    Large-scale testing in Germany uncovered two animals — which means two herds, in effect — with unsuspected infections.

    Yes, you can get false positives and negatives. There’s a way to deal with that. You re-test.

    Yes, this is all an expense for the industry. Something tells me that’s the real issue, because the tests are not useless if done the right way and at the right time.

  2. Dee

    It is my understanding that the mechanism of BSE-infection of humans is not yet completely understood. As I understand it, it might be possible that humans are infected due to a cumulative effect of eating infected beef over time.

    Additionally, it is my understanding that the test is considered ineffective by some because cows are rushed to slaughter at a young age before symptoms manifest. But that does not mean that the cow(s) are not infected.

    So, I guess what I’m asking at this point is that the reason we rush beef to slaughter in the United States so that the growers/processors can cover themselves in the mantle of plausible deniability?

    If a rancher wishes to take on the expense of testing the herd, why should they not be allowed to do so and to label the product as tested?

    This strikes me very similar to the outcry against organic dairy farmers labeling their products hormone-free. Or allowing produce farmers to note that their products are free from genetic engineering and pesticides. The corporate farmers do not want the public to have this information.

    Why do we not insist that all food chain animals be raised to the point where diseases can be discovered before they enter our food supply?

    It seems to me that we as consumers should have all pertinent information available to us and that we decide what we wish to consume.

  3. Pingback: Blanton's and Ashton's: In the interest of accuracy: testing meat for BSE

  4. oddjob

    So, I guess what I’m asking at this point is that the reason we rush beef to slaughter in the United States so that the growers/processors can cover themselves in the mantle of plausible deniability?

    I doubt this is the answer for that practice. Unless that practice has arisen since BSE became an issue, it seems far more likely to me that the reason to rush to market has to do with profitability. In any given regime there will be a balance between how long one takes to slaughter an animal and how much money one gets from the sale of the meat & byproducts. That’s determined by market conditions (in commodities markets for such things as pork bellies), and my guess is the answer to your question lies in an examination of the circumstances governing return on investment more generally than in the specific impact of BSE on those circumstances.

  5. RayCeeYa

    “As I understand it, it might be possible that humans are infected due to a cumulative effect of eating infected beef over time.”

    That’s the mechanism I learned in my Food Microbiology course a couple of years ago. One common misconception is that BSE is a disease like the flu or a bacterial infection. BSE is caused by prions, rogue protein molecules. They have no genetic material and are incapable of replicating themselves.

    Instead they infect the neural tissue of the consumer and cause other proteins with a similar amino acid sequence to reshape into a dangerous conformation. Specifically the prions responsible for BSE cause an alpha helix to reform into a beta sheet. Beta sheets are more stable in teh environment and make the prion harder to break down. This reshaping also the once beneficial protein to turn into a prion.

    While one the surface this makes it sound like all you need is need prion to cause an out of control chain reaction corrupting all the proteins and causing the disease, this is not the case. While the beta sheet conformation makes them harder to break down, it doesn’t make it impossible to break down. Your body makes enzymes that spend all day breaking down unnecessary proteins. Because the beta sheet is more stable than the alpha helix, some proteins will naturally reform on their own.

    As far as BSE is concerned, there seems to be a level at which a consumer has ingested enough of the BSE prions to trigger the disease. Unfortunately we don’t know what this level is. However, we do know how they originally started building up in our food supply. BSE prions were allowed to build up in the food supply because cattle feed manufacturers were using waste from the meat packers, i.e. brain, spinal cord, and other neural tissue as a cheap protein source in their products. This practice has since been banned. Because of the ban the levels of BSE prions have begun to fall.

    We don’t know how far they have to fall to reach safe levels again. Also the level of consumption varies from person to person and this the level of risk as well. In conclusion if you really want to avoid BSE eat grass or grain fed cattle, or buffalo. It’s disgusting to think that this all happened because a few feedlot owners wanted to save a buck by feeding leftover bits of cows to other cows.

  6. Arkades

    Mad cow disease (bovine spongiform encephalopathy, or BSE) can induce a degenerative brain condition in humans known as Creutzfeldt-Jakob disease (CJD). Some cases of CJD arise sporadically in the adult human population as a result of an inherited genetic abnormality. Cases of CJD believed to have been acquired environmentally (from eating BSE-tainted material, for instance) are termed ‘new variant Creutzfeldt-Jakob disease’ (nvCJD) to distinguish them from the classic, inherited-bad-gene version of CJD.

    It’s believed that tissues from the brain and spine of affected individuals are potentially highly infective, whereas other proteins (such as muscle tissue) remain low-risk as long as they are not also contaminated with tissue from the central nervous system. Unfortunately, ‘mechanically recovered’ meat from around the spine can easily be contaminated with spinal tissues. Generally speaking, whole cuts of meat are safer than ground meats, and meats grounds from specific parts (chuck, sirloin) are safer than generic ‘ground beef’ (because the latter can also contain meat mechanically recovered from around the spine).

    None of which makes me very confident that we know exactly how to dodge the bullet with respect to BSE. It does make me a lot choosier about the grade of meat I’m willing to purchase at the store, though.

    It is my understanding that the mechanism of BSE-infection of humans is not yet completely understood. As I understand it, it might be possible that humans are infected due to a cumulative effect of eating infected beef over time.

    Hmm. Whereas my understanding is that even very small amounts of highly infective material are sufficient to induce the infection, which would seem to favor a pattern of acute exposure rather than a cumulative effect.

    The most dramatic example of single-source exposure comes from patients who contract iatrogenic (ie, medically induced) Creutzfeldt-Jakob disease, usually from contaminated surgical equipment or probes that had previously been used on other CJD victims (some of who may not have been known to be suffering from CJD at the time, since a diagnoses of CJD can only be confirmed and distinguished from other dementias by autopsy of the brain). Some sterilization procedures used on the equipment to eliminate bacteria and viruses didn’t work on prions, which maintained their power to directly infect the new patients’ brains. Certain transplants, such as dura matter, can also transmit CJD in this way.

    Why do we not insist that all food chain animals be raised to the point where diseases can be discovered before they enter our food supply?

    It’s believed that eating animals slaughtered younger than the age of onset is protective inasmuch as the long incubation period makes it less likely that the animal is infective. Or so the theory goes.

    Personally, I generally agree with the premise that we should be testing every animal. I’m just not sure it makes much sense to wait until the animal is older (and thus potentially *more* infective) before doing so.

  7. Arkades

    As far as BSE is concerned, there seems to be a level at which a consumer has ingested enough of the BSE prions to trigger the disease.

    Fascinating. I had assumed, based on learning about the iatrogenic CJD cases, than a point source exposure was likely, rather than a cumulative/threshhold exposure model. But one could certainly make the case that iatrogenic infection is an extreme example, given that a single dose of highly infective material is directly introduced into the brain or dura matter, which admittedly is a very different situation than long-term environmental exposure.

  8. oddjob

    There are also other animals known to suffer from this syndrome. In sheep and goats it’s known as scrapie. There are also elk (&/or deer?) in North American that suffer from it. Squirrels are known to get it, too.

  9. Yes, you can get false positives and negatives. There’s a way to deal with that. You re-test.

    It’s amazing that the Bush administration is insisting that there is no way to invent a round object that might make cart travel easier.

    Consider – can you think of a First World sub-continent which has implemented stringent BSE testing after a major scandal from one of the countries there? Think carefully – starts with an “E”, ends with a “urope”…

  10. It’s amazing that the Bush administration is insisting that there is no way to invent a round object that might make cart travel easier.

    Phydeaux say: “(W) heel” 🙂

  11. christine

    “So, I guess what I’m asking at this point is that the reason we rush beef to slaughter in the United States so that the growers/processors can cover themselves in the mantle of plausible deniability?”

    Beef cattle farmers send to market as soon as the cow reaches ideal weight. Because the cost of maintaining that weight is much more expensive and reduces the profitablity of the cow in question. Farmers get around 100 – 150 dollars per hundred weight (that’s up to $1.50 per pound of the animal) and we’re paying as much as $10 per pound in the supermarket. The cost of grain is going through the roof now due to ethenol production. Corn is going for something like $4 a bushel and cows eat lots and lots of food.

    Around 10 years ago the cost to raise pork was almost a losing proposition to the market price. Many farmers were talking with ‘town’ folk that if the town folk would pay x, they’d get a personally raised hunk of good pork for cost. Meat farming can be a tricky business.

  12. christine

    Oh, to add to Oddjob – yes there is a wasting disease going around the white tail deer population. If the ‘animal lovers’ would just ‘let’ culling occur, much of the problem could go away. The deer herds are in desperate need of culling.

  13. Deanna

    Why do we not insist that all food chain animals be raised to the point where diseases can be discovered before they enter our food supply?

    For the most part, no one wants to eat the tougher older animals. Also, the farmer or feedlot owner makes very little profit per animal already. If they have to keep and feed the animal for an additional year so that the tests will work properly (plus pay the cost of the testing), the farmer will be working at a loss per animal.

    From the producer’s point of view, it’s better to do four things:

    1. Develop and follow feeding best practices at the farm level.
    2. Ensure that feed producers are regulated and follow regulations. (For example, don’t allow feed mills that produce dog food to also produce cattle supplements.)
    3. Develop a test that can detect BSE at an earlier age.
    4. Track cattle so that when BSE is detected, you can track an animal’s history.

  14. Thank you for the correction.

  15. Arkady: re single vs repeated doses causing infection. I remember hearing an interesting theory when I lived in England. There was some evidence that maybe the infected meat had to be eaten when the consumer had any kind of mouth or throat lesions, eg a sore throat. That would allow prions to enter the blood stream without dealing with digestive enzymes. It would also explain both the apparent need for a “repeated dose” and direct-to-blood single dose infection. It’s not really a repeated dose, but rather that the chances of eating infected meat *and* having throat problems can take time to occur together.

    I never heard about any follow-up to this interesting and plausible theory.

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