US "Atypical" Mad Cow Threat Was Predicted
By John Stauber
Created 06/14/2006 - 09:33
The small scientific world of prion researchers -- the scientists who investigate "transmissible spongiform encephalopathies" (TSE) such as mad cow disease in cattle and Creutzfeldt-Jakob Disease (CJD) in humans -- is abuzz. That's because the two confirmed cases of US mad cow disease in Texas and Alabama are an "atypical" strain different from the British strain but identical to an atypical strain found so far in a small number of cattle in France, Germany, Poland and Sweden.
The discovery of "atypical" mad cow disease in the US should not be surprising. Sheldon Rampton and I reported way back in 1997 that very strong evidence of an "atypical" TSE disease infecting US cattle was established by the work of Dr. Richard Marsh, the researcher to whom we dedicated our book Mad Cow USA [1].
Even before Britain confirmed its first case of mad cow, Dr. Marsh of the University of Wisconsin was investigating a similar disease in Stetsonville, Wisconsin,
a 1985 outbreak in mink that he traced to Wisconsin dairy cattle. Marsh's published research confirmed suspicions among US scientists since the mid 1960s that the rare but deadly TSE disease in US mink -- transmissible mink encephalopathy or TME --
resulted from their having eaten TSE-infected US cattle.
DID THE US INFECT EUROPE WITH ATYPICAL MAD COW DISEASE?
The discovery that the Texas and Alabama BSE cases are a variant strain identical to EU cases begs the question of whether the atypical EU cases resulted from European cattle being fed infected US feed made from rendered by-products and sold in Europe. After all,
the US has been the biggest creator, user and exporter of by-product feed made from slaughterhouse waste. Also, scientists need to examine the TSE isolated by Richard Marsh in mink and traced to Wisconsin cattle, and compare it to the atypical BSE strain found in Texas, Alabama, France, Poland, Germany and Sweden. Is the Stetsonville TSE strain discovered by Richard Marsh the same strain as the US and EU atypical BSE cases, or is it another atypical strain?
Here below is our report on
Marsh's discovery in 1985 of an atypical strain of BSE in US cattle from our 1997 book Mad Cow USA [2]. (You can order the book for free from your favorite library and it is for sale in the usual places.)
###
MAD COW USA
(The following excerpt is from Mad Cow USA [3], by Sheldon Rampton and John Stauber, pages 154-156
The common denominator in all of these [transmissible mink encephalopathy - TME] outbreaks was either "cattle" or "unknown." It was possible, of course, to imagine other scenarios, but Marsh believed he had at least strong circumstantial evidence that a TSE similar to mad cow disease already existed in U.S. cattle. "You can trace it back to feed real easy in mink," Marsh said. "And then you're left with the question, what was it in the feed that affected them? And what we find is it's these downer cows that are the common link. You don't have to be a genius to figure it out."
Within the field of veterinary medicine, "downer cow syndrome" was a
"garbage can" category, used indiscriminately as the official diagnosis for any
animal that died or had to be put down after failing to stand on its own legs
for 24 hours or more. These included cows suffering from paralysis, arthritis,
grass tetany, ketosis, bone fractures, and a form of calcium deficiency known
as "milk fever." Most downer cows died from causes unrelated to the spongi-
form encephalopathies, but it was possible that the generic nature of the clas-
sification enabled some TSE-infected cows to slip into the mix.
It was impossible in practice to absolutely prove the link between downer
cows and transmissible mink encephalopathy. By the time the disease appeared
in mink, any cow that might have been the source would be long gone, its
tissues unavailable for testing. To test his theory, therefore, Marsh did the next
best thing—a series of experiments using brain matter from one of the mink
that had died in the Stetsonville outbreak. He puréed the brain in a blender
and used hypodermic syringes to inject the homogenized liquid into test animals: fourteen healthy mink, eight ferrets, two squirrel monkeys, twelve hamsters, forty-five mice and two Holstein bull calves.
The mice, remarkably, all stayed healthy, but every other species proved
susceptible. The mink went down first, four months after inoculation. The two
monkeys were the next to show neurological signs, at months nine and thirteen
respectively. Two of the twelve hamsters survived, but the other ten succumbed
in the fifteenth and sixteenth months. The two calves went down in months
eighteen and nineteen. The ferrets lasted longest, but eventually the disease
emerged in all but one of them, with incubation periods ranging between
twenty-eight and thirty-eight months. These species barrier effects corresponded
closely to the results from experiments with previous mink outbreaks.
Cattle are expensive test animals, and Marsh's experiments marked the
first time that cattle had been tested for susceptibility to transmissible mink
encephalopathy. His results proved that cattle could get the mink disease, and
in turn led to unexpected new questions. "The real surprise of this experiment
is that the clinical signs were quite different from what we've seen in Great
Britain," he said. "This is what's changed our perspective on a surveillance of
BSE in the United States. We thought BSE in the U.S. would look like BSE in
Great Britain—a mad cow type of disease where the animal would have behav-
ioral changes, become aggressive and look very much like a rabies infection
does in cows."
Marsh's bull calves showed none of the unusual "mad" behavior that
emerged as early warning signs in British cattle. "Eighteen months after
inoculation, one animal simply collapsed in its holding room and could not
be returned to a standing position," he reported. "This animal had shown no
previous signs of behavioral change or loss of body condition. . . . The second
animal was normal until nineteen months after inoculation when it too sud-
denly collapsed."
Indeed, the test bulls behaved exactly like downer cows—the type of ani-
mals which the Stetsonville rancher had been feeding to his mink. "The most
disturbing finding of all is that they have very minimal spongiform lesions in
their brains," Marsh said. In previous experiments with mink, he had shown
that the spongy holes in brains were a secondary effect of the disease which
did not always appear in noticeable quantities. Some mink breeds infected with
TME would develop all of the usual clinical symptoms, but upon autopsy their
brains showed a marked lack of spongiform degeneration. Now it appeared
that cattle could also develop a form of TSE without the telltale lesions to aid
in diagnosis. Their symptoms would look like downer cow syndrome, and
even a brain autopsy might find nothing out of the ordinary.
"Without the brain lesions, the best way to diagnose the infection is a protein in the brain," Marsh said. "But there are only a few labs in the country that can look for this protein. This is not something that can be done by the local veterinarian or even most state diagnostic laboratories. You need to have pretty sophisticated means of testing. This is going to complicate our efforts at surveillance and testing for BSE in thiscountry."
Histopathology and immunohistochemistry tests confirmed that Marsh's
bulls had died of a spongiform encephalopathy, but it was a different strain of
spongiform encephalopathy than the one that was killing cows in England. Its
behavior in test animals showed significant differences also. In England, mice
succumbed when exposed to brain tissue from mad cows, but hamsters seemed
immune. In Marsh's experiments with the Stetsonville isolate of TME, the pattern
was exactly the opposite: mice lived, but hamsters died.
FROM MAD COWS TO MAD MINK AND BACK
To test whether passage through cattle altered the characteristics of the Stetsonville isolate, Marsh injected another 45 mice with brain tissue from his two test bulls. They also stayed healthy, just like the mice he had previously injected with mink brains. By itself, the fact that mink encephalopathy could infect cows was not terribly significant or surprising. After all, scientists had previously shown that TME could be transmitted to a wide variety of other test animals. What was significant was the result when Marsh took the brains of the dead bulls and used them on further tests with healthy mink. When backpassaged into mink, the bull brains behaved exactly the way mink brains behaved, causing symptoms of TME to emerge within four months after exposure by inoculation, or within seven months after oral exposure.
"There was no evidence for any deadaptation of the bovine agent for mink compared to . . . non-bovine-passaged mink brain," Marsh observed. "This suggests that there are no species barrier effects between mink and cattle in relation to the Stetsonville source of
TME" — more evidence pointing to cattle as the source of the infection. "If mink on the Stetsonville ranch were exposed to TME by feeding them infected cattle, there must be an unrecognized scrapie-like disease of cattle in the United States," Marsh concluded. "If this is true, the disease is rare. The low incidencerate of TME and the fact that the Stetsonville mink rancher had fed products from fallen or sick cattle to his animals for the past 35 years suggests a very low prevalence of this disease."
The rarity of the disease, however, did not mean that it posed no danger.
In fact, it could mean the very opposite. Mad cow disease had also been rare
once in England. The very fact that it was rare, combined with its slow incubation period, were the factors that prevented the British from recognizing its dangers until it had already infected tens of thousands of animals. Moreover, the British had an advantage that U.S. farmers might not enjoy. Their strain of bovine spongiform encephalopathy was picked up fairly soon once cattle started behaving strangely. If a different strain of BSE existed in U.S. cattle— a strain where the animals didn't act deranged but simply fell over, like thecows in Marsh's tests—the disease could conceivably go unrecognized for a long time, invisible within the larger population of U.S. downer cows.
Every year, some 100,000 U.S. cows get classified as downers. Marsh was
not suggesting that all 100,000 were carriers of a spongiform encephalopathy.
What concerned him was the possibility that downer cow syndrome could
mask the emergence of a TSE in the cattle population, allowing the disease to
invisibly spread until it reached dangerous levels. It could multiply the same
way it had multiplied in England, as rendering plants recycled the infection
by converting sick animals into meat and bone meal which was then fed back
to other cattle. The only certain way to prevent a cattle epidemic, therefore,
would be to adopt the same policy that the British had already been forced
to adopt: ban the practice of feeding rendered cows and other ruminant ani-
mals back to members of their own species.
### (End of excerpt)
HOW TO HIDE A MAD COW
Today the ability to test cattle for mad cow disease has greatly advanced, and so-called rapid tests are used on all cattle before they are allowed into the human food chain in Japan, for example.
I describe the situation in the United States as a cover-up of the extent of mad cow disease because the US needs to test millions of cattle a year, and in a transparent and verifiable way, before we can know with accuracy how much disease is present in the US herd. Currently the US is testing less than 1% of its cattle a year, and the procedures are shrouded in secrecy. The US forbids anyone but the government to conduct tests in the United States making it impossible for Americans to purchase meat that has been tested and found free of the disease.
In addition, despite the false PR assurances from government and the livestock industry,
there is no "firewall feed ban" in the United States to completely stop the spread of mad cow disease. Today it is legal and widespread to feed US cattle on cattle fat contaminated with cattle protein, on cattle blood, and on poultry shirt and litter contaminated with cattle protein. In addition, slaughterhouse waste from cattle is fed to pigs, and in turn the slaughterhouse waste from pigs is fed back to cattle.
We now know we have "atypical" mad cow disease in the US and even the USDA admits that it has probably been spreading for at least a decade through feeding cattle to cattle. Yet, the cannibal feeding practices continue and the US's mad cow testng program is a farce.
Dick Marsh died in 1997 before our book Mad Cow USA [4] was published. He was a careful scientist who undersood the precautionary principle and who worked tirelessly and was terribly and personally attacked for his prescient warnings that a unique strain of mad cow disease already existed in the US, and that unless the dangerous feeding practices of cow cannibalism were stopped, it would spread through cattle and threaten human health.
Perhaps if cancer had not silenced Dick Marsh a decade ago, his strong voice would have helped change the current dangerous policies of the United States Department of Agriculture (USDA) and the Food and Drug Administration (FDA). Currently these federal agencies are threatening animal and human safety in the US simply so the US government can protect and preserve the livestock industry's deadly but lucrative practice of animal cannibalism, turning slaughterhouse waste into cheap feed for cattle and other livestock.
that's OK, because the Interstate only handles trucks going north loaded and passenger cars coming south to shop. :wink: :wink: :wink: :wink:
