DOWNERS AND THE FACTS!!!!!!!!!!

[Guest guest]

The News coming out of the B.S.E. Inquiry, and the FACT that they

(cattle ranchers) have been burying their DOWNER CATTLE, FOR YEARS, to

hide the true count of B.S.E., so their herds would be spared from

slaughter, is just that FACT, THEY KNOW THIS IS HAPPENING. AND, IT'S

ALSO HAPPENING IN THE UNITED STATES. This policy happens in Texas all

the time. WE HAVE WITNESSED THIS, just after my mothers death from

nvCJD.....SO, this might be a good time to print another article from

MADCOW U.S.A. ABOUT DOWNERS AND TSE RESEARCH BY RICHARD MARSH, WHOM BY

FAR, WAS ONE OF THE LEADING RESEARCHERS IN THIS FIELD///DOWNER COWS --

The common denominator in all of these 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 MADCOW 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 IN THE FEED that affected them? And what we

find is IT'S THESE DOWNER COWS THAT ARE A 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

spongiform encephalopathies, BUT IT WAS POSSIBLE THAT THE GENERIC NATURE

OF THE CLASSIFICATION 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 pureed the brain in a blender and used

hypodermic syringes to inject the homogenized liquid into test animals:

fourteen healthy mink, eight fettets, two squirrel monkeys, twelve

hamsters, fourty-five mice and two Holstein bull calves.....The mice,

remarkable, 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 months. These species

barrier effects corresponded closely to the results from experiments

with previous mink ourbreaks.....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 MADCOW type of disease where the

animal would have behavioral changes, become aggressive and look very

much like a rabis 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 to suddenly

collapsed " .....Indeed, the test bulls behaved exactly like downer

cows--the type of animals 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 APPEARD

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. (MADSON NOTE: when differintiating between nvCJD AND CJD, this

is also the MAIN THEORY, kinda blows that theory all to h*ll, but with

BSE in sheep now, there probably REALLY CONFUSED)..... " Without the brain

lesions, the best way to diagnose the infectin 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 THIS

COUNTRY " .....Histopathology and immunohistochemistry test 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 MADCOWS, 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. 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, jusl 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 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 incidence rate 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 suggest 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. MADCOW DISEASE HAD ALSO BEEN RARE ONCE IN ENGLAND. The VERY

fact that is 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 SIMPLE FELL OVER, like the cows in Marsh's test--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 beef forced to adopt: BAN THE PRACTICE OF FEEDING RENDERED COWS

AND OTHER RUMINANT ANIMALS BACK TO MEMBERS OF THEIR OWN SPECIES. (MADSON

NOTE: TO LATE FOR MY MOM AND MANY OTHER LOVED ONES).....In England,

meanwhile, the consequences of FAILING TO TAKE ACTION SOONER WERE

BECOMING PAINFULLY EVIDENT. By the end of 1991, nearly 50,000 cases of

MADCOW DISEASE had been confirmed--more than TWICE the total predicted

by the Southwood Committee. And the end was NOWHERE in sight.....In

December 1991, the British Medical Research Council announced interim

results of an experiment in which MRC researchers had injected two

marmoset monkeys with SCRAPIE and two others with BSE. The ones injected

with SCRAPIE had died, but the ones injected with BSE remained healthy.

Given the closeness of monkeys to human beings, the result seemed

encouraging, prompting a story in the Meat Trades Journal headlined

" Meat Given Clean Bill of Health " .....BY THE SUMMER OF 1992, HOWEVER,

THE BSE MONKEYS HAD ALSO DIED OF SPONGIFORM BRAIN DISEASE. Dr. lind

Ridley, who had overseen the experiment, struggled to put a positive

spin on the result by pointing out that the BSE monkeys had lived longer

than monkeys exposed to SCRAPIE. " Everything we know tells us that

SCRAPIE is no risk to humans " , Ridley said. HER STATEMENT WAS ABSURD,

LACKING ANY SCIENTIFIC BASIS WHATSOEVER, BUT AT LEAST IS SOUNDED

REASSURING/////////// Terry/MADSON -- flounder@...>