A
Anonymous
What is your opinions of BSE? What is going to happen to us as producers when a confirmed case is discovered somewhere in the U.S. Because I feel that it is just a matter of time!
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frenchie
Well-known member
I hope you never get to find out......... When B.S.E hit here every auction barn closed down from May till Sept.. within 500 miles of us.
A lot depends on how its handled by the USDA.....
A lot depends on how its handled by the USDA.....
Texan
Well-known member
frenchie":1kwu9mdv said:
Now there's a scary thought, Frenchie.
There is one thing that I think they're doing right, however. And here again, just like with mandatory COOL and some other issues, I expect that I'm on the opposite side of the fence from most of my peers. I like the fact that they are announcing the presumptive positives, even though I realize that the first couple involved some pretty good market hits. But I agree with CM that its probably just a matter of time until we get to the "real deal" confirmed case, the case that we can't blame on our neighbors to the North. And I'm hoping that by then the consumer will be so de-sensitized to the BSE positive news that it will barely have an impact on domestic demand.
Jake
Well-known member
I'm definately not worried about eating a BSE cow because my grandpa always said that you could eat the cancer off of a CancerEyed Cow if you got it up to 180 degrees. The market effect is what worries me.
TheBullLady
Well-known member
Ewwwwww.. I'm glad I had dinner BEFORE I read that post!
Frankly I wouldn't be surprised if a BSE positive cow came up in the US. It would be a disaster, but like mentioned previously, hopefully consumers are pretty immune to it now, and realize the small risk it would pose.
Frankly I wouldn't be surprised if a BSE positive cow came up in the US. It would be a disaster, but like mentioned previously, hopefully consumers are pretty immune to it now, and realize the small risk it would pose.
heiferhoney
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It scares me. Just think if your herd was condemned. The genetics lost, the years of selective breeding. I've gotten real careful about who comes on the farm. And I've kept 18 embryos back from various flushes in case I would ever have to start over.
branxchar&charx
Well-known member
BSE is an incurable disease (no vaccines either) that affects the brain and possible the spinal cord. it can stay dormant for a number of years before it really starts to affect the cow or whatever. cooking the meat to a certain temperature will not kill it. that is IF it has been in contact with the brain or spinal cord. on a side note, cooking meat to a certain temperature from an infected hoof and mouth animal will kill it in the meat but is very devasting to many herds.
if another case did ever occur (God forbid) it will effect the market. and you can sure bet all the organic farmers and animal rights groups, etc. will be on their toes waiting for it this time. i hope we are just as prepared maybe even more prepared to deal with the situation if it ever happens again.
if another case did ever occur (God forbid) it will effect the market. and you can sure bet all the organic farmers and animal rights groups, etc. will be on their toes waiting for it this time. i hope we are just as prepared maybe even more prepared to deal with the situation if it ever happens again.
OP
OP
Anonymous
I don't feel that anyone has addressed the issue. We all know that if there was a case it would be horrible. But do you think that our government is adequately prepared? I feel that what goes around comes around. So if we enforce the seven year time period are we prepared to have our border closed for seven years? Because it is only a matter of time! So we should think about the consequences of our actions.
To the people that are not worried about getting (CJD) the equivalent of BSE. It is not a pleasant disease.
To the people that are not worried about getting (CJD) the equivalent of BSE. It is not a pleasant disease.
Texan
Well-known member
CM":o8uzlkt5 said:
Nobody's denying that new variant CJD is an unpleasant disease. Some of us might question the science that some of you rely on to link it with BSE, however. Here is a different point of view with a corrected link:
BSE
And by the way CM, I guess I'm one of those you're talking about that's just not gonna worry about it. I take a Hell of a lot more chances than that just going to the pasture everday! So give me one of those nice, big, thick T-bones or Porterhouses right straight out of Canada. And I'll take your's for my wife! That'll give you more time to worry!
frenchie
Well-known member
I agree with you Texan 100%.
No point in worrying.
No point in worrying.
Texan
Well-known member
Texan":dpzrvx5t said:
Texan
Well-known member
Another outlook on the same subject. Credit goes to Livestock Weekly from January 22, 2004. This issue is important enough that I decided to paste it here since I was having trouble linking it for everybody.
BSE, “Variant” CJD Statistics Showing Less Fearsome Picture
Hard on the heals of the first U.S. “mad cow” discovery comes a reassuring British report that cases of the human version appear to have peaked and may fall dramatically short of early projections. Tucked away in the verbiage is a tantalizing fact that suggests the whole issue may prove to have been wildly overblown.
Initial projections from British scientists when the first human cases surfaced in the mid-1990s indicated that literally thousands of Brits would be dying of “variant” Creutzfeldt-Jakob disease by now and that as many as half a million cases would eventually develop, all because of widespread exposure to tainted tissues from cattle with bovine spongiform encephalitis, so-called “mad cow” disease.
Statistics published recently by the U.K. Department of Health, however, show that only 139 deaths have occurred so far and that new cases are on the decline. Deaths last year totaled 18, down from 28 as recently as 2000, and the most current figures project no more than 40 additional cases over the next three-quarters of a century.
As tragic as any death is, far more people die each year of peanut allergies.
The new numbers represent quite a statistical correction in such a short timespan, especially given that the first researcher to propose a link between vCJD and “mad cow” was still warning as recently as 2000 that “thousands of people” soon would be “going slowly and painfully mad before dying.”
What happened?
The British government took quick steps to counter what was assumed to be the mode of transmission, for one thing. The U.K. slaughtered tens of thousands of cattle infected by or thought to have been exposed to BSE. It also imposed a ban on all bovine brain and spinal cord material in the human food chain, as well as any part of cattle more than 30 months of age. In addition, in an effort to stem further bovine infections, the U.K. banned ruminant-derived products from feed, the suspected vector between diseased animals and healthy ones.
Other factors may have been at work as well, however. The Department of Health report notes — almost in passing — that every human victim of vCJD so far shares a pre-existing, inherited genetic trait common to only a little more than a third of the general population.
The trait is a mutation of a gene relating to “prions,” one form of which is the infectious agent for BSE and other “spongiform encephalopathies.” All vCJD victims to date have been found to possess dual copies of the gene, meaning they inherited the mutation from both parents.
Scientists by nature and training are loathe to issue statements without equivocating baggage, so most studies and analyses of the vCJD-gene link include a caveat warning that the trait in question may only hasten incubation and that victims without the mutated gene may appear in future years. That, of course, is pure speculation, whereas the positive link is documented.
The mutation in question is also associated with the “sporadic” or pre-BSE version of CJD, as well as similar rare prion-based diseases such as kuru, and has even been linked to Alzheimers. No other condition, however, has been found to occur exclusively among patients with dual copies of the gene. Such exclusivity, in fact, is almost unheard-of in any medical condition aside, perhaps, from the fact that no man has ever contracted ovarian cancer or woman prostate cancer.
Studies in recent years have also shown that the overall infectivity of BSE is much less than originally feared. Simply stated, it takes much more infected material than originally assumed to transmit the infection to another victim — “the dose makes the poison.” That means a few stray prions lurking in a packing plant or tucked away in the bowels of a feed mill that processed ruminant-derived meal at some point pose a negligible threat.
And some researchers are even questioning the core assumption that “mad cow” disease has anything whatsoever to do with vCJD.
A paper published in the British Medical Journal edition of October 2001 evaluates the assumption based on long-respected epidemiological criteria for establishing cause and effect. It finds the BSE-vCJD “connection” lacking — or nonexistent — in virtually every specific.
The paper is the work of Scottish surgeon Dr. George A. Venters, former Chairman of the British Medical Association's Public Health Committee. Venters outlines the criteria that epidemiologists use to evaluate evidence linking a given disease to its supposed cause, then applies each of those criteria to the case of BSE and vCJD.
In some instances, he finds the evidence entirely lacking or notes that it may not be available for years. “Strength of association” is one example; there is no way to measure “details of individuals’ exposures” to infectious prions, for instance. Likewise, the “dose-response relation” for humans is unknown. “Reversibility” is another criterion, and Venters points out that the assumed BSE-vCJD link “will be falsified” only “as and when the disease occurs in people born after the bovine spongiform encephalopathy prion has been eliminated from the human food chain…”
In other words, if people continue to contract the disease after the supposed cause no longer exists, the link will definitely be broken — but that will take time.
Meanwhile, he assesses the other criteria, beginning with “biological plausibility.” Venters points out that there is “no direct evidence” that the BSE prion is infectious to humans, whereas “there is evidence for a robust species barrier between humans and prions from ungulate species.” For one thing, he notes, “Prions produced in ungulates and humans have different sequences of amino acids.” He adds that ingestion, the assumed mode of transmission, is “an inefficient route” for prions aside from cannibalism — where there is, obviously, no species barrier to overcome.
Venter thus concludes that “Infection of humans from eating the (BSE) prion is therefore unlikely.”
Another criterion is “specificity.” Venter explains that “prion infection differs from the conventional understanding of the infectious process” in that “cells can only produce prion specific to the species they belong to.”
A human E.coli infection, for instance, can be traced to contaminated food because the same bacteria can be found in both the victim and the tainted source. However, Venter points out, the BSE prion itself “can never be detected in human brains or in any species other than cattle.”
Researchers instead have attempted to link the bovine and human diseases through similar damage to brain tissues, though that, too, is of limited value because brain tissues themselves differ between species. Venter says those who argue the connection are reduced at best to pointing out “similarities” in “physico-chemical properties and strain typing in laboratory experiments.”
For that reason, he concludes, “the specificity of the link between the prion and the disease can only be inferred and remains an open question.
“Given that it is impossible to prove that the (BSE) prion is infectious to humans,” Venter continues, “evidence for the case has to be indirect,” and this is where proponents of the theory may have fallen victim from the beginning to wishful thinking or vested interests.
“The evidence that has been amassed” so far, Venter chides, “is directed towards confirming the hypothesis rather than testing it.” In other words, those who promote the idea of such a link concentrate their efforts on shoring up their position rather than challenging it to see if it can stand on its own.
Most damning from an objective scientific perspective is Venter’s flat assertion that “salient contrary information has been either played down or ignored.”
What supposedly sets “new variant” CJD apart from the traditional disease, for example, is the fact that it tends to strike young victims whereas the conventional wisdom holds that the original version strikes only in middle age or later. Venter points out, however, that the first case of “traditional” CJD, described by German researcher Creutzfeldt himself more than 80 years ago, was in a 23 year-old victim. So much for a “new” variant.
The idea that CJD is limited to older patients, in fact, didn’t become popular until proposed decades later by the disease’s second namesake, Jakob. To support his position, Jakob had to virtually ignore Creutzfeldt’s pioneer case.
Venter adds — pointedly — that the paper claiming the existence of a “new” disease and linking it to BSE also ignored Creutzfeldt’s case and likewise ignored similarities between the “new variant” of CJD and the South Pacific disease kuru, spread within a primitive tribe by cannibalism. It cited kuru as a prion disease spread by ingestion, Venter notes, but only as a way to support the idea that “variant” CJD could be spread through food.
Kuru was thus cited where it was useful to the hypothesis, but “the possibility of them being the same disease was not raised,” he says, one example of “contrary information” being “either played down or ignored.”
He cites several other examples in which “quality of evidence,” a key criterion, is suspect, and concludes that evidence overall “is of variable quality” and “seems to have been selectively developed” along the lines of a fallacious “belief that multiple pieces of suspect or weak evidence provide strong evidence when bundled together.”
So why is BSE linked to vCJD?
For that, Venter turns to the “temporality” criterion, which essentially ties the two diseases together by virtue of their timing.
The “new variant” was discovered shortly after the epidemic of BSE in British cattle, Venter explains, so researchers attempted to link them.
Unfortunately, he continues, “To prove that a disease is new, it is necessary to review and legitimately reject other possibilities,” and this the linkage proponents failed to do.
Specifically, he charges, they failed to rule out kuru and/or Creutzfeldt’s original encephalopathy case. Venter notes “clinical and neuropathological features” common to vCJD and kuru as well as to the Creutzfeldt case. There are differences as well, he concedes, but these “may be more of degree than of kind, in that survival of patients with new variant Creutzfeldt-Jakob disease is likely to be longer because they will generally have received better health care than was available to people with kuru.”
A second element of “temporality” is what Venter terms the “pattern of infection relative to exposure,” and he finds the link weak here, as well.
Venter notes that all food-borne illnesses follow a common pattern or “curve” in their distribution. “The shape of this curve holds true for foodborne infections no matter whether the incubation period is days,” as for E. coli, “or years, as is the case for prions,” he insists. That curve would have followed the BSE infection rate in cattle, he contends, if that were the source of vCJD.
But it doesn’t.
Venter notes that vCJD cases “have been appearing since 1994,” but that “their rate of increase since then falls far short of what would be expected if this was a foodborne infection.”
Given its weaknesses, he terms the “temporality” connection “at best uncertain.”
Venter concludes with the observation that scientists have been trying to draw boundaries around traditional or “sporadic” CJD ever since Creutzfeldt’s first report more than eight decades ago, and those boundaries have been repeatedly adjusted.
He accepts the idea that “variant” CJD is “a different disease” from “sporadic” CJD, but questions “whether it is different from kuru or from Creutzfeldt’s original case.” This, he says, remains to be determined and will only be “clarified with the passage of time.”
Meanwhile, Venter says, “I believe the evidence now casts serious doubt on the case for a causal link between bovine spongiform encephalopathy and ‘new’ variant Creutzfeldt-Jakob disease,” adding that “The medical profession should, at least, be publicly debating this as an issue.”
BSE, “Variant” CJD Statistics Showing Less Fearsome Picture
Hard on the heals of the first U.S. “mad cow” discovery comes a reassuring British report that cases of the human version appear to have peaked and may fall dramatically short of early projections. Tucked away in the verbiage is a tantalizing fact that suggests the whole issue may prove to have been wildly overblown.
Initial projections from British scientists when the first human cases surfaced in the mid-1990s indicated that literally thousands of Brits would be dying of “variant” Creutzfeldt-Jakob disease by now and that as many as half a million cases would eventually develop, all because of widespread exposure to tainted tissues from cattle with bovine spongiform encephalitis, so-called “mad cow” disease.
Statistics published recently by the U.K. Department of Health, however, show that only 139 deaths have occurred so far and that new cases are on the decline. Deaths last year totaled 18, down from 28 as recently as 2000, and the most current figures project no more than 40 additional cases over the next three-quarters of a century.
As tragic as any death is, far more people die each year of peanut allergies.
The new numbers represent quite a statistical correction in such a short timespan, especially given that the first researcher to propose a link between vCJD and “mad cow” was still warning as recently as 2000 that “thousands of people” soon would be “going slowly and painfully mad before dying.”
What happened?
The British government took quick steps to counter what was assumed to be the mode of transmission, for one thing. The U.K. slaughtered tens of thousands of cattle infected by or thought to have been exposed to BSE. It also imposed a ban on all bovine brain and spinal cord material in the human food chain, as well as any part of cattle more than 30 months of age. In addition, in an effort to stem further bovine infections, the U.K. banned ruminant-derived products from feed, the suspected vector between diseased animals and healthy ones.
Other factors may have been at work as well, however. The Department of Health report notes — almost in passing — that every human victim of vCJD so far shares a pre-existing, inherited genetic trait common to only a little more than a third of the general population.
The trait is a mutation of a gene relating to “prions,” one form of which is the infectious agent for BSE and other “spongiform encephalopathies.” All vCJD victims to date have been found to possess dual copies of the gene, meaning they inherited the mutation from both parents.
Scientists by nature and training are loathe to issue statements without equivocating baggage, so most studies and analyses of the vCJD-gene link include a caveat warning that the trait in question may only hasten incubation and that victims without the mutated gene may appear in future years. That, of course, is pure speculation, whereas the positive link is documented.
The mutation in question is also associated with the “sporadic” or pre-BSE version of CJD, as well as similar rare prion-based diseases such as kuru, and has even been linked to Alzheimers. No other condition, however, has been found to occur exclusively among patients with dual copies of the gene. Such exclusivity, in fact, is almost unheard-of in any medical condition aside, perhaps, from the fact that no man has ever contracted ovarian cancer or woman prostate cancer.
Studies in recent years have also shown that the overall infectivity of BSE is much less than originally feared. Simply stated, it takes much more infected material than originally assumed to transmit the infection to another victim — “the dose makes the poison.” That means a few stray prions lurking in a packing plant or tucked away in the bowels of a feed mill that processed ruminant-derived meal at some point pose a negligible threat.
And some researchers are even questioning the core assumption that “mad cow” disease has anything whatsoever to do with vCJD.
A paper published in the British Medical Journal edition of October 2001 evaluates the assumption based on long-respected epidemiological criteria for establishing cause and effect. It finds the BSE-vCJD “connection” lacking — or nonexistent — in virtually every specific.
The paper is the work of Scottish surgeon Dr. George A. Venters, former Chairman of the British Medical Association's Public Health Committee. Venters outlines the criteria that epidemiologists use to evaluate evidence linking a given disease to its supposed cause, then applies each of those criteria to the case of BSE and vCJD.
In some instances, he finds the evidence entirely lacking or notes that it may not be available for years. “Strength of association” is one example; there is no way to measure “details of individuals’ exposures” to infectious prions, for instance. Likewise, the “dose-response relation” for humans is unknown. “Reversibility” is another criterion, and Venters points out that the assumed BSE-vCJD link “will be falsified” only “as and when the disease occurs in people born after the bovine spongiform encephalopathy prion has been eliminated from the human food chain…”
In other words, if people continue to contract the disease after the supposed cause no longer exists, the link will definitely be broken — but that will take time.
Meanwhile, he assesses the other criteria, beginning with “biological plausibility.” Venters points out that there is “no direct evidence” that the BSE prion is infectious to humans, whereas “there is evidence for a robust species barrier between humans and prions from ungulate species.” For one thing, he notes, “Prions produced in ungulates and humans have different sequences of amino acids.” He adds that ingestion, the assumed mode of transmission, is “an inefficient route” for prions aside from cannibalism — where there is, obviously, no species barrier to overcome.
Venter thus concludes that “Infection of humans from eating the (BSE) prion is therefore unlikely.”
Another criterion is “specificity.” Venter explains that “prion infection differs from the conventional understanding of the infectious process” in that “cells can only produce prion specific to the species they belong to.”
A human E.coli infection, for instance, can be traced to contaminated food because the same bacteria can be found in both the victim and the tainted source. However, Venter points out, the BSE prion itself “can never be detected in human brains or in any species other than cattle.”
Researchers instead have attempted to link the bovine and human diseases through similar damage to brain tissues, though that, too, is of limited value because brain tissues themselves differ between species. Venter says those who argue the connection are reduced at best to pointing out “similarities” in “physico-chemical properties and strain typing in laboratory experiments.”
For that reason, he concludes, “the specificity of the link between the prion and the disease can only be inferred and remains an open question.
“Given that it is impossible to prove that the (BSE) prion is infectious to humans,” Venter continues, “evidence for the case has to be indirect,” and this is where proponents of the theory may have fallen victim from the beginning to wishful thinking or vested interests.
“The evidence that has been amassed” so far, Venter chides, “is directed towards confirming the hypothesis rather than testing it.” In other words, those who promote the idea of such a link concentrate their efforts on shoring up their position rather than challenging it to see if it can stand on its own.
Most damning from an objective scientific perspective is Venter’s flat assertion that “salient contrary information has been either played down or ignored.”
What supposedly sets “new variant” CJD apart from the traditional disease, for example, is the fact that it tends to strike young victims whereas the conventional wisdom holds that the original version strikes only in middle age or later. Venter points out, however, that the first case of “traditional” CJD, described by German researcher Creutzfeldt himself more than 80 years ago, was in a 23 year-old victim. So much for a “new” variant.
The idea that CJD is limited to older patients, in fact, didn’t become popular until proposed decades later by the disease’s second namesake, Jakob. To support his position, Jakob had to virtually ignore Creutzfeldt’s pioneer case.
Venter adds — pointedly — that the paper claiming the existence of a “new” disease and linking it to BSE also ignored Creutzfeldt’s case and likewise ignored similarities between the “new variant” of CJD and the South Pacific disease kuru, spread within a primitive tribe by cannibalism. It cited kuru as a prion disease spread by ingestion, Venter notes, but only as a way to support the idea that “variant” CJD could be spread through food.
Kuru was thus cited where it was useful to the hypothesis, but “the possibility of them being the same disease was not raised,” he says, one example of “contrary information” being “either played down or ignored.”
He cites several other examples in which “quality of evidence,” a key criterion, is suspect, and concludes that evidence overall “is of variable quality” and “seems to have been selectively developed” along the lines of a fallacious “belief that multiple pieces of suspect or weak evidence provide strong evidence when bundled together.”
So why is BSE linked to vCJD?
For that, Venter turns to the “temporality” criterion, which essentially ties the two diseases together by virtue of their timing.
The “new variant” was discovered shortly after the epidemic of BSE in British cattle, Venter explains, so researchers attempted to link them.
Unfortunately, he continues, “To prove that a disease is new, it is necessary to review and legitimately reject other possibilities,” and this the linkage proponents failed to do.
Specifically, he charges, they failed to rule out kuru and/or Creutzfeldt’s original encephalopathy case. Venter notes “clinical and neuropathological features” common to vCJD and kuru as well as to the Creutzfeldt case. There are differences as well, he concedes, but these “may be more of degree than of kind, in that survival of patients with new variant Creutzfeldt-Jakob disease is likely to be longer because they will generally have received better health care than was available to people with kuru.”
A second element of “temporality” is what Venter terms the “pattern of infection relative to exposure,” and he finds the link weak here, as well.
Venter notes that all food-borne illnesses follow a common pattern or “curve” in their distribution. “The shape of this curve holds true for foodborne infections no matter whether the incubation period is days,” as for E. coli, “or years, as is the case for prions,” he insists. That curve would have followed the BSE infection rate in cattle, he contends, if that were the source of vCJD.
But it doesn’t.
Venter notes that vCJD cases “have been appearing since 1994,” but that “their rate of increase since then falls far short of what would be expected if this was a foodborne infection.”
Given its weaknesses, he terms the “temporality” connection “at best uncertain.”
Venter concludes with the observation that scientists have been trying to draw boundaries around traditional or “sporadic” CJD ever since Creutzfeldt’s first report more than eight decades ago, and those boundaries have been repeatedly adjusted.
He accepts the idea that “variant” CJD is “a different disease” from “sporadic” CJD, but questions “whether it is different from kuru or from Creutzfeldt’s original case.” This, he says, remains to be determined and will only be “clarified with the passage of time.”
Meanwhile, Venter says, “I believe the evidence now casts serious doubt on the case for a causal link between bovine spongiform encephalopathy and ‘new’ variant Creutzfeldt-Jakob disease,” adding that “The medical profession should, at least, be publicly debating this as an issue.”
From what I have ever known about BSE, the danger is from eating the brains or meat connecting to the spinal cord or the juices out of the spinal cord. According to all the information that I have ever heard or read BSE is known to be only found in cattle over 30 mo. of age. If even the age limit was dropped to 20 mo. of age With this in mind most of the choice-select meat bought at the grocery store for steaks or roasts would be, according to the USDA and sound science information virtually impossible to contact BSE from the muscle cuts of these animals. The animals that are susceptible to BSE are the animals over 30 mo. old, most of which are mostly used in institutions and in processed meats, or ground beef. To my knowledge, according to Sound Science the muscles of these animals are absolutely safe to eat, as long as the meat that is stripped off the spinal cord and is trimmed far enough away from the spinal cord so as not have any spinal cord residue. Anyone that I know of or have heard that has eaten the brains, myself included is consuming the brains of calves. Well under the 20 or 30 month limit. As well as it is the muscle cuts being consumed and the meat is off animals under 30 mo. of age, or muscle cuts of animals over 30 mo. of age that has been trimmed far enough away from the spinal cord so as to not have any of the spinal cord residue contaminating the meat, there is virtually no chance of contacting BSE.Bez":2dpm6iw4 said:
So in a nutshell lets all go have a steak tonight and be don't worry about contacting BSE.
Personally I would like to have a Prime Dry Aged, New York Strip fed in one of our good Canadian Friends and Neighbors Feedyards.
Texan
Well-known member
la4angus":2drf09xy said:
LA, while you're at it, I'll take a box of those good Canadian T's and Porterhouses. Assuming you can smuggle them past the R-CALF border guards!
MULDOON
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If you could get the canadian cows to be registered democrap voters(not a big mental difference)They'd reopen the borders :lol: :lol: :roll: :cboy:
