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From: TSS ()
Date: July 31, 2005 at 7:24 am PST

----- Original Message -----
From: "Terry S. Singeltary Sr."
Sent: Sunday, July 31, 2005 8:50 AM

##################### Bovine Spongiform Encephalopathy #####################

Posted on Sun, Jul. 31, 2005



The beef about mad cow

Texas case demonstrates weaknesses in testing of food supply for disease

By Barry Shlachter

Star-Telegram Staff Writer

Although meat from a 12-year-old Texas beef cow with mad cow disease never entered the food supply, critics of the Agriculture Department said the twisted, seven-month-long tale of this animal highlighted bureaucratic missteps and weaknesses in the food safety system.

Public confidence wasn't enhanced last week when the USDA announced that a private veterinarian had "forgotten" about a brain tissue sample he took in April. It came from another cow now suspected of having had the brain-wasting disease bovine spongiform encephalopathy. Definitive tests are under way.

Watchdog groups awarded barely passing marks to the department for its handling of the Texas cow, which turned up dead at a Waco packing plant Nov. 15. The USDA finally confirmed the mad cow case June 10 after multiple tests.

"USDA gets a D or D minus," said Caroline Smith Dewaal of the Washington-based advocacy group, Center for Science in the Public Interest. "The best thing that came out of this is the work of the inspector general."

It was the department's in-house watchdog, Inspector General Phyllis Fong, who skirted the USDA hierarchy by ordering retesting with a different method more than six months after a routine second-round test, known as the immunohistochemistry (IHC) test, proved negative for BSE.

Agriculture Secretary Mike Johanns, who assumed office in January, has said he neither knew about nor authorized the retesting by the National Veterinary Services Laboratories in Ames, Iowa.

Just why Fong, a lawyer who grew up in Hawaii, acted in such a forthright, hierarchy-dodging manner has puzzled many involved in the industry.

In a statement, her office said the retesting was prompted by a review of "voluminous records" showing an unusual pattern of conflicting test results in the case. Industry sources say there is speculation that she responded to concern expressed in scientific circles.

Two early tests, one reportedly conducted at Texas A&M University and a second in Ames, produced conflicting results -- one inconclusive, one negative.

Unbeknownst to Fong and the public, Ames researchers had also used an experimental rapid version of the IHC test on brain tissue from the Texas cow. That proved positive for BSE, but staff members thought the result was technically flawed and the USDA didn't disclose until just recently that the Ames lab had conducted the experimental test.

Months later, Fong stepped in and ordered more tests. A "Western blot" test proved positive, as did later tests at a lab in Weybridge, England.

Finally in June, two days after the Weybridge lab confirmed the mad cow case, a chastened USDA announced that in addition to the routine IHC test, it was adopting the Western blot procedure whenever an initial "BioRad" screening test points to possible BSE. In addition, backup tests will now be conducted at Britain's national veterinary laboratory in Weybridge when earlier test results conflict or are inconclusive.

All this sounded familiar to Consumers Union.

In February, the nonprofit public interest group that publishes Consumer Reports urged the USDA to take those same steps in regard to the Texas cow, noted Michael Hansen, a senior researcher with the organization.

In hindsight, the March 18 response to Consumers Union by Jere Dick, associate deputy administrator of USDA's animal health policy and programs, smeared egg clearly across the department's collective face.

Referring to the Texas cow, Dick wrote:

"We are confident in the expertise of USDA's laboratory technicians conducting BSE testing and do not feel that such confirmatory testing by the Weybridge laboratory is generally necessary, nor would the use of the Western blot test have enhanced the result of our November 2004 testing."

The opposite turned out to be true.

Sen. Tom Harkin, D-Iowa, noted the obvious in a July 7 letter to Johanns:

"Without the prompting of the [inspector general's office] , we still would not know that the brain sample in question tests BSE-positive."

While Americans should have no misgivings about eating steaks and hamburgers, Harkin said, "there is a limit to how much of its own errors, inconsistencies and lack of transparency USDA can reasonably expect consumers to abide and still have confidence in the safety of beef."

Food supply kept safe

All the criticism might obscure the fact that meat from diseased livestock has been kept out of the food supply. BSE is carried by hard-to-destroy protein prions, which scientists believe can cause a rare human disease -- variant Creutzfeldt-Jakob -- if found in beef.

The food supply has been protected by a ban for human consumption of tissue most prone to prion contamination, including beef brain, scrapings from the spinal column, and a small section of the intestine.

USDA's animal health officials were dealing with a highly unusual situation, said Keith Belk, a Colorado State University animal science professor who closely follows the BSE issue.

"There clearly were some mistakes made, but this was a pretty unique cow," Belk said. "She had the disease, and it incubated for a long time. But it apparently received a light dose of prions that were very sporadically spread" in the brain tissue.

The tissue sample, a pie-slice-shaped sliver taken from the obex, a slight bulge in the brain stem, had so few BSE prions at some points that a British expert, Dr. Danny Matthews of Weybridge, said tests easily could have missed them.

Matthews has said BSE is becoming rarer and more difficult to detect because of effective bans on tainted cattle feeds, which are believed to spread the disease.

Some of the missteps, ironically, were caused by USDA staff doing exactly what they were supposed to do -- faithfully following measures that go far beyond international standards, Belk said in a call from Fort Collins, Colo.

"They appeared to have made some significant errors, which unfortunately made them appear foolish," Belk said. "Most scientists around the world would have argued that they should have run both the Western blot and IHC tests. I think they would have liked to have done so; but because of policy in place, their hands were tied."

Under lab rules in effect in November, the USDA staff in Ames was not permitted to carry out any other type of test after it received a negative result from the second round of testing, using the IHC method.

Communication miscues haven't helped the USDA's image in its handling of the Texas case.

In June, the USDA finally confirmed that the yellow to cream-colored cow had arrived dead at a meatpacking plant, not a dog food plant as originally reported.

And it had not been a downer -- a live but nonwalking animal -- as described by officials for nearly seven months. Making matters worse, the initial description of the cow as an Angus was wrong, and some of its high-risk body parts were tossed in a bin with those of other cattle, creating the need to run a number of DNA tests.

Dewaal also criticized the successful effort to keep the name and location of the ranch that produced the Brahman cross-bred cow secret. The ranch has been speculated to be somewhere in Southeast Texas.

"Who are they protecting?" she asked. "The only person it protects is the rancher."

But officials like Carla Everett, a spokeswoman with the Texas Animal Health Commission, say that maintaining confidentiality is necessary to prevent such operations from being needlessly stigmatized and to ensure future cooperation from ranches to which other diseased animals might be traced.

Owning up

Although chastened, the USDA said it had no choice but to treat the Texas cow case as it had.

"It was handled within our protocol with few exceptions," said Jim Rogers, a spokesman for the department's Animal and Plant Health Inspection Service.

But the department is owning up to some mistakes.

Johanns has acknowledged that some things should have been done differently, Rogers said. Among them: Animal parts from different cattle should not have been commingled as they were at the Waco pet food plant; the Ames laboratory should not have run an experimental test while running the official test; and the lab made a verbal disclosure, but it should have presented a written report.

Whatever steps the USDA takes, it could find itself in a no-win situation, Rogers said.

In November, Western blot was not part of the testing protocol because it was not deemed appropriate in that situation.

"Let's go back in time and say we had conducted Western blot," Rogers said. "We would have critics saying we had stepped outside our protocol."

In fact, the National Cattlemen's Beef Association publicly criticized the inspector general for stepping out of the testing routine -- just before it became clear that her irregular action had turned up the positive BSE finding.

Reinforcing experts' description of the Texas cow as an unusual case, Rogers noted that after Fong requested that Western blot be used on the brain sample, "they tested it 10 times -- five of which were negative and five positive."

The results could be far different depending on what part of the sample was examined because of the erratic spread of BSE prions. Scientists believe that these submicroscopic flecks of protein spread BSE, a rare but always fatal disease discovered in 1986, through feed contaminated with rendered cattle parts.

The infected Texas cow was born before such tainted feed was banned in the United States in 1997. Ninety-seven percent of beef now consumed by Americans comes from cattle born after the ban, according to the National Cattlemen's Beef Association.

By comparison, Japan did not ban such feed until 2001, possibly contributing to the 20 BSE cases there -- and a heightened popular distrust of its food security program, Belk said. That lack of public confidence prompted testing of every animal going to slaughter and a continued reluctance to end a 19-month ban on U.S. beef imports.

While such feed is banned for cattle, it can still be fed to pigs and chickens, which cannot contract BSE.

But some scientists and consumer groups, fearing mislabeling of sacks or other human errors, have urged the Food and Drug Administration, which regulates the feed industry, to act on its own January 2004 recommendation and ban it for poultry and pigs, too.

One U.S. case

Of the 153 worldwide cases of a fatal human ailment believed caused by BSE-contaminated beef products, the only victim of variant Creutzfeldt-Jakob disease in the United States was a Florida woman who had lived in Britain when such tainted food was available.

Six months after the first U.S. case in a Canadian-born dairy cow was discovered in December 2003, scientists said BSE was probably present at low levels in the U.S. herd, and the USDA launched a widespread surveillance effort. The beef industry notes that the Texas animal was the only cow found with BSE after 419,113 high-risk animals have been tested.

In the most recent case, involving a cow that was euthanized after severe calving problems whose test samples were forgotten about, the carcass was incinerated. The Texas and Washington state cows were discovered before they entered the food chain, reinforcing the government and industry's insistence that world-class firewalls have kept U.S. consumers protected.

After the Texas cow arrived dead at a Waco packinghouse, it was trucked across town to a dog food plant, where test samples were taken. The animal's body, kept segregated, was incinerated at Texas A&M University.

Unfortunately, by then its parts were commingled with three other cattle, making the difficult task of tracing a suspect cow without a mandatory national animal identification program even harder. This was seen as another blunder by authorities.

Hansen of Consumers Union complained that little is known publicly about the 419,113 tested cattle -- or many others with central nervous system problems that were never examined.

He cited an August 2004 audit by the inspector general's office as saying that only a fraction of the highest-risk cattle -- erratic-acting animals that tested negative for rabies -- were not given the rapid BioRad test for BSE.

In fiscal 2003, for example, 108 Texas cattle were tested and found clean for rabies, but only 29 of this high-risk group were checked for BSE. In South Dakota, 81 tested cattle were negative for rabies, but none were given BSE tests.

Rogers conceded that there was a "mix-up" in states where testing guidelines were not clearly understood. The confusion has been remedied, and by late September, all animal inspectors understood that such high-risk cattle must be tested for BSE, he said.

Call for tracking

Chief among complaints by watchdog groups like Consumers Union and the Center for Science in the Public Interest is that the United States -- unlike the European Union, Japan, Canada, Australia and New Zealand -- still has no mandatory national identification program for tracking cattle. An ID program would help quickly trace the origins of a contaminated cow.

As the mad-cow story developed this summer, the National Cattlemen's Beef Association got a head start on Johanns by saying it was starting its own animal ID system and hoped to have it operational in January 2007.

The association is seeking to have a system that would eventually be taken over as the national program. It envisions one that would ensure confidentiality of certain proprietary data that cattle operations and others want withheld for competitive reasons.

"For example, Cargill doesn't want Tyson to know where they purchase cattle," said Belk of Colorado State, referring to major beef processing companies.

And ranchers, some of whom have run cattle for generations, are worried about consumer lawsuits, he said.

"If you can determine where something comes from, it opens the door to liability," Belk said.

Johanns had announced that the government's mandatory ID system won't be up and running until 2009.

"I think the system is flawed as long as we don't have a national mandatory system for tracking cows," said Dewaal, who noted that Canada went from a voluntary to a mandatory system in one year. "We may be better at finding the one infected animal but not others similarly exposed to the disease.

"And we are surprised by the extraordinary delay."

Consumers, ever more concerned about food safety, are putting money where their mouths are and demanding beef traceability.

In Texas, chains such as United Market Street, Whole Foods and Central Market are offering source-verified beef -- meat whose herd or ranch origin is spelled out to consumers.

In doing so, the market will push for an animal ID system to be implemented before 2009, Belk predicted. And source verifiability might be needed to re-establish lost export markets, he said.

And such traceability carries plenty of benefits.

Some systems could go beyond a mandatory animal ID system, Belk said, providing useful information: Is the animal free of antibiotics? Was it given vitamin E for a certain antioxidant level?

The producer could also receive feedback on whether livestock management techniques led to more tender cuts, for example.

"It's not all related to safety," Belk said.

BSE timeline

• Nov. 11, 2004

A no longer productive 12-year-old beef cow is sold at a Texas auction.

• Nov. 15, 2004

A cattle buyer ships the cow and others to H&B Packing Co. in Waco, where it arrives dead. The animal is transported across town to Champion Pet Food Co., where its head is severed and shipped to a laboratory at Texas A&M University in College Station.

• Nov. 18, 2004

Results of two Bio Rad rapid tests are announced by the U.S. Department of Agriculture as "inconclusive," meaning positive for this error-prone, sensitive method of determining bovine spongiform encephalopthy, or BSE. This prompts rounds of confirmatory tests.

• Nov. 23, 2004

Results are negative on brain tissue sent to the National Veterinary Services Laboratories in Ames, Iowa, for two immunohistochemistry (IHC) tests. A positive result four days earlier from an experimental rapid IHC test is not released because researchers believe that it was technically flawed.

• June 10, 2005

The USDA announces that a Western blot test ordered by the department's inspector general without Agriculture Secretary Mike Johann's knowledge is positive for BSE.

• June 24, 2005

Britain's national veterinary laboratory gets positive results using both IHC and Western blot tests. Johanns also discloses British confirmation that the Ames' experimental IHC test was positive for BSE.

• July 11, 2005

Sixty-seven cattle from the infected cow's herd test negative for BSE with the Bio-Rad method. Investigators are still trying to track down the infected cow's last two calves.


Barry Shlachter, (817) 390-7718

Subject: MAD COW USA STRAIN MISSION TEXAS and the infamous USA sporadic
CJDs, something to ponder

Date: July 29, 2005 at 11:16 am PST


DR. CLIFFORD: "Basically the IHC test, besides looking at location of the
brain stem you're also doing a staining technique to identify abnormal prion
proteins. In this case they had some staining, but the staining did not
match up with what they would typically see in a BSE case. It didn't have
the normal distribution it would see within the samples. So basically that's
why the request for doing additional testing, and that's why we're sending
it to Weybridge as well."

DR. CLIFFORD: "There was some staining present. But it did not match a
normal pattern, and we're taking through that to do additional tests in
additional parts of the brain stem to try to see if we can find a normal
staining pattern as well as sending that sample to Weybridge to run against
their IHC."



1985 The Stetsonville outbreak (farmer's name: Brecke). In addition to the
downer cows and horses Brecke's mink recieved a cereal supplement.
Hartsough's view was that this would contain bone meal and would be from a
commercial source. If this were so and it was contaminated with a TME agent
why were no other ranches affected?

Many mink ranches now feed a commerical pelleted diet. Brecke was equipped


Dead mink go for rendering but are used only in poultry feed.

A commercial mink ranch was visited. This was Johny Werth's, Capitol Fur
Farm comprising 1400 breeding females. The feed is bought in from a
commercial supplier in the form of frozen packs of ''poultry'', ''fish'',
''dried egg'' or ''tripe''. A commercial mink cereal supplement is used and
contains ''animal meat meal'' which was said to contain material mainly from
poultry or fish origin but OCCASIONALLY FROM BEEF SOURCES. the partially
thawed packs were tipped into an augur mixer which has a fully loaded
capacity of 6000lb and this would be approximately 15000 mink per day.

In the fall at pelting time the skinned carcasses of the mink are placed in
large barrels which are left in the open to freeze. When full, a renderer
collects ''for use in poultry feeds''.

Sections from the brains of the two Brecke TME inoculated cattle were
examined and Marsh provided all the blocks from the 2nd steer for study at
CVL and comparison with BSE. In general the vacuolar changes were more
severe than in most cases of BSE but very similar in distribution.
Unfortunately material aken fro histopathology from those anials omitted
representaion of most of the brain stem. ...........

Wilbur Clarke (reference the Mission, Texas scrapie transmission
transmission to cattle study) is now the State Veterinarian for Montana
based at Helena.

I was given confidential access to sections from the Clarke scrapie-cattle
transmission experiment. Details of the experimental design were as supplied
previously by Dr. Wrathall (copy of relevant information appended). Only 3
animals (2 inoculated with 2nd pass Suffolk scrapie and 1 inoculated with
Angora goat passaged scrapie) showed clinical signs. Clinical signs were
characterised by weakness, ''a stilted hindlimb gait'', disorientation,
ataxia and, terminally, lateral recumbency. The two cattle from which I
examined material were inocluated at 8 months of age and developed signs 36
months pi (goat scrapie inoculum) and 49 months pi (one of the Suffolk
scrapie inoculated) respectively. This latter animal was killed at 58 months
of age and so the clinical duration was only 1 month. The neuropathology was
somewhat different from BSE or the Stetsonville TME in cattle. Vacuolar
changes were minimal, to the extent that detection REQUIRED CAREFUL
SEARCHING. Conversely astrocyte hypertrophy was a widespread and prominent

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases

{the following was written but with a single line marked through it ''first
passage (by this route)}...TSS

resulted in a more rapidly progressive clinical disease with repeated
episodes of synocopy ending in coma. One control animal became affected, it
is believed through contamination of inoculum (?saline). Further CWD
transmissions were carried out by Dick Marsh into ferret, mink and squirrel
monkey. Transmission occurred in ALL of these species with the shortest
incubation period in the ferret.


Appendix 3


1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-

Expt A
6 Her x Jer calves born in 1978 were inoculated as follows with
a 2nd Suffolk scrapie passage:-

i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BSE-like disease.

Expt B
6 Her or Jer or HxJ calves were inoculated with angora Goat
virus 2/6 went down similarly after 36 months.

Expt C
Mice inoculated from brains of calves/cattle in expts A • B
were resistant, only 1/20 going down with scrapie and this was the
reason given for not publishing.

Diagnosis in A, B, C was by histopath. No reports on SAT were given.

2. Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally- (and naturally) infected sheep by ET.
He had found difficulty in obtaining embryos from naturally infected
sheep (cf SPA).

3. Prof. A Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr A Thiermann showed the
picture in the "Independent" with cattle being incinerated and thought
this was a fanatical incident to be avoided in the US at all costs.
BSE was not reported in USA.

4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started
there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.

5. Scrapie agent was reported to have been isolated from a solitary

6. A western blotting diagnostic technique (? on PrP) shows some promise.

7. Results of a questionnaire sent to 33 states on the subject of the
national sheep scrapie programme survey indicated

17/33 wished to drop it

6/33 wished to develop it

8/33 had few sheep and were neutral

Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.



>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.


full text 33 PAGES ;

It was, however, performed in the USA in 1979, when it was shown that cattle
inoculated with the scrapie agent endemic in the flock of Suffolk sheep at
the United States Department of Agriculture in Mission, Texas, developed a
TSE quite unlike BSE. 32 The findings of the initial transmission, though
not of the clinical or neurohistological examination, were communicated in
October 1988 to Dr Watson, Director of the CVL, following a visit by Dr
Wrathall, one of the project leaders in the Pathology Department of the CVL,
to the United States Department of Agriculture. 33 The results were not
published at this point, since the attempted transmission to mice from the
experimental cow brain had been inconclusive. The results of the clinical
and histological differences between scrapie-affected sheep and cattle were
published in 1995. Similar studies in which cattle were inoculated
intracerebrally with scrapie inocula derived from a number of
scrapie-affected sheep of different breeds and from different States, were
carried out at the US National Animal Disease Centre. 34 The results,
published in 1994, showed that this source of scrapie agent, though
pathogenic for cattle, did not produce the same clinical signs of brain
lesions characteristic of BSE.

1: J Infect Dis. 1994 Apr;169(4):814-20.

Intracerebral transmission of scrapie to cattle.

Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM,
Robinson MM.

USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA

To determine if sheep scrapie agent(s) in the United States would induce a
disease in cattle resembling bovine spongiform encephalopathy, 18 newborn
calves were inoculated intracerebrally with a pooled suspension of brain
from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after
inoculation. All calves kept longer than 1 year became severely lethargic
and demonstrated clinical signs of motor neuron dysfunction that were
manifest as progressive stiffness, posterior paresis, general weakness, and
permanent recumbency. The incubation period was 14-18 months, and the
clinical course was 1-5 months. The brain from each calf was examined for
lesions and for protease-resistant prion protein. Lesions were subtle, but a
disease-specific isoform of the prion protein was present in the brain of
all calves. Neither signs nor lesions were characteristic of those for
bovine spongiform encephalopathy.

MeSH Terms:
Cattle Diseases/etiology*
Cattle Diseases/pathology
Encephalopathy, Bovine Spongiform/etiology*
Encephalopathy, Bovine Spongiform/pathology
Motor Neurons/physiology
Sleep Stages
Time Factors


Intracerebral transmission of scrapie to cattle FULL TEXT PDF;



WE conclude that American sources of sheep scrapie are transmissible to
cattle by direct intracerebral inoculation but the disease induced is NOT
identical to BSE as seen in the United Kingdom. While there were
similarities in clinical signs between this experimental disease and BSE,
there was no evidence of aggressiveness, hyperexcitability, hyperesthesia
(tactile or auditory), or hyperemetria of limbs as has been reported for BSE
(9). Neither were there extensive neurologic lesions, which are primary for
BSE, such as severe vacuolation of neurons and neuropil or neuronal necrosis
and gliosis. Although some vacuolation of neuropil, chromotolysis in
neurons, and gliosis were seen in the brains of some affected calves, these
were industinguishable from those of controls. Vacuolated neurons in the red
nucleus of both challenged and normal calves were considered normal for the
bovines as previously described (50).

the amount of PrP-res positively related to the length of the incubation.


WE also conclude from these studies that scrapie in cattle MIGHT NOT BE
THAT DETECTION OF PrP-res by immunohistochemistry or immunoblotting is
necessary to make a definitive diagnosis. THUS, undiagnosed scrapie
infection could contribute to the ''DOWNER-COW'' syndrome and could be
responsible for some outbreaks of transmissible mink encephalopathy proposed
by Burger and Hartsough (8) and Marsh and harsough (52). ...


Multiple sources of sheep affected with scrapie and two breeds of cattle
from several sources were used inthe current study in an effort to avoid a
single strain of either agent or host. Preliminary results from mouse
inoculations indicate multiple strains of the agent were present in the
pooled inoculum (unpublished data). ...

Transmission of the sheep scrapie to cattle was attempted in 1979 by using
intracerebral, intramuscular, subcutaneous, and oral routes of inoculation
of 5, 8- to 11-month old cattlw with a homologous mixture of brain from 1
affected sheep (61, 62). ONE of the 5 cattle develped neurologic signs 48
months after inoculation. Signs were disorientation, incoordination, a
stiff-legged stilted gait, progressive difficulty in rising, and finally in
terminal recumbency. The clinical course was 2.5 months. TWO of the 5 cattle
similarly inoculated with brain tissue from a goat with scrapie exhibited
similar signs 27 and 36 months after incoluation. Clinical courses were 43
an 44 days. Brain lesions of mild gliosis and vacuolation and mouse
inoculation data were insufficient to confirm a diagnosis of scrapie. This
work remained controversial until recent examination of the brains detected
PrP-res in all 3 cattle with neurologic disease but in none of the
unaffected cattle (62). Results of these studies are similar to ours and
underscore the necessity of methods other than histopathology to diagnose
scrapie infection in cattle. We believe that immunologic techniques for
detecting PrP-res currently provide the most sensitive and reliable way to
make a definitive diagnosis...

Visit to USA ... info on BSE and Scrapie;f=12;t=0003

Office Note


A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer



FDA Statement
May 4, 2004
Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow
with central nervous system symptoms had been killed and shipped to a
processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the
animal came from, and the processor that initially received the cow from the

FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That
material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as
"mad cow disease," can exhibit such symptoms. In this case, there is no way
now to test for BSE. But even if the cow had BSE, FDA's animal feed rule
would prohibit the feeding of its rendered protein to other ruminant animals
(e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and informing
the firm that FDA will not object to use of this material in swine feed
only. If it is not used in swine feed, this material will be destroyed. Pigs
have been shown not to be susceptible to BSE. If the firm agrees to use the
material for swine feed only, FDA will track the material all the way
through the supply chain from the processor to the farm to ensure that the
feed is properly monitored and used only as feed for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian protein
out of animal feed for cattle and other ruminant animals. FDA established
its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that
the disease spreads by feeding infected ruminant protein to cattle.

Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action
specifying that the material go only into swine feed means also that it will
not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates closely
with the U.S. Department of Agriculture on all BSE issues. The animal feed
rule provides crucial protection against the spread of BSE, but it is only
one of several such firewalls. FDA will soon be improving the animal feed
rule, to make this strong system even stronger.


IN TEXAS, we feed our cattle ruminant protein, and lots of it. but remember
(the fda cannot seem to get this right)

.1 gram is lethal;


January 30, 2001
Print Media:
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Today the Food and Drug Administration announced the results of tests
taken on feed used at a Texas feedlot
that was suspected of containing meat and bone meal from other domestic
cattle -- a violation of FDA's 1997
prohibition on using ruminant material in feed for other ruminants.
Results indicate that a very low level of
prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams -
approximately a quarter ounce -- of prohibited material. These animals
weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in
origin (therefore not likely to contain infected
material because there is no evidence of BSE in U.S. cattle), fed at a
very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even
if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators
and industry is to keep this disease out of the United States. One
important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined
with other steps, like U.S. Department
of Agriculture's (USDA) ban on the importation of live ruminant animals
from affected countries, these steps
represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless
announcing that it is voluntarily purchasing all 1,222
of the animals held in Texas and mistakenly fed the animal feed
containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA
believes any cattle that did not consume
feed containing the prohibited material are unaffected by this incident,
and should be handled in the beef supply
clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first
reporting the human error that resulted in the
misformulation of the animal feed supplement and then by working closely
with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food
supply and that continued vigilance needs to be taken, by all concerned,
to ensure these rules are followed

FDA will continue working with USDA as well as State and local officials
to ensure that companies and
individuals comply with all laws and regulations designed to protect the
U.S. food supply.

From: TSS (
Date: January 27, 2005 at 7:03 am PST

Risk of oral infection with bovine spongiform encephalopathy agent in

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.

Published online January 27, 2005

It is clear that the designing scientists must

also have shared Mr Bradley’s surprise at the results because all the dose

levels right down to 1 gram triggered infection.


6. It also appears to me that Mr Bradley’s answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to

that the actual result was within both a lower and an upper limit within the

and the designing scientists would not have expected all the dose levels to

infection. The dose ranges chosen by the most informed scientists at that

ranged from 1 gram to three times one hundred grams. It is clear that the

scientists must have also shared Mr Bradley’s surprise at the results
because all the

dose levels right down to 1 gram triggered infection.

Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)


Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy:
Molecular similarities with sporadic Creutzfeldt-Jakob disease

Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari
, Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria
Caramelli *

*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto
Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via
Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual
Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale
L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale
della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and
¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan,

Edited by Stanley B. Prusiner, University of California, San Francisco, CA,
and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are
mammalian neurodegenerative disorders characterized by a posttranslational
conversion and brain accumulation of an insoluble, protease-resistant
isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and
animal TSE agents exist as different phenotypes that can be biochemically
differentiated on the basis of the molecular mass of the protease-resistant
PrPSc fragments and the degree of glycosylation. Epidemiological, molecular,
and transmission studies strongly suggest that the single strain of agent
responsible for bovine spongiform encephalopathy (BSE) has infected humans,
causing variant Creutzfeldt-Jakob disease. The unprecedented biological
properties of the BSE agent, which circumvents the so-called "species
barrier" between cattle and humans and adapts to different mammalian
species, has raised considerable concern for human health. To date, it is
unknown whether more than one strain might be responsible for cattle TSE or
whether the BSE agent undergoes phenotypic variation after natural
transmission. Here we provide evidence of a second cattle TSE. The disorder
was pathologically characterized by the presence of PrP-immunopositive
amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE
cases, and by a different pattern of regional distribution and topology of
brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc
type with predominance of the low molecular mass glycoform and a
protease-resistant fragment of lower molecular mass than BSE-PrPSc.
Strikingly, the molecular signature of this previously undescribed bovine
PrPSc was similar to that encountered in a distinct subtype of sporadic
Creutzfeldt-Jakob disease.


C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.

E-mail: .


AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure
3). There were 11 new infected and source flocks reported in March (Figure
4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total
infected and source flocks that have been released in FY 2005 are 39 (Figure
6), with 1 flock released in March. The ratio of infected and source flocks
released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN
addition, as of March 31, 2005, 225 scrapie cases have been confirmed and
reported by the National Veterinary Services Laboratories (NVSL), of which
53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in
March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported
since 1990 (Figure 9). The last goat cases was reported in January 2005. New
infected flocks, source flocks, and flocks released or put on clean-up plans
for FY 2005 are depicted in Figure 10. ...


WITH the MAY report, a scrapie case documented in a GOAT IN THE USA...TSS


SCRAPIE has increased drastically since the report i posted in March 2005,
with additional case in a goat;


AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure
3). There were 11 new infected and source flocks reported in March (Figure
4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total
infected and source flocks that have been released in FY 2005 are 39 (Figure
6), with 1 flock released in March. The ratio of infected and source flocks
released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN
addition, as of March 31, 2005, 225 scrapie cases have been confirmed and
reported by the National Veterinary Services Laboratories (NVSL), of which
53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in
March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported
since 1990 (Figure 9). The last goat cases was reported in January 2005. New
infected flocks, source flocks, and flocks released or put on clean-up plans
for FY 2005 are depicted in Figure 10. ...



Press Releases
5/13/2005: More Negatives for Chronic Wasting Disease in Captive Heards
Learn More

5/9/2005: Negative Results for Chronic Wasting Disease in Captive Herd Learn

5/4/2005: DEC Announces Sampling Results for Chronic Wasting Disease Learn

4/29/2005: DEC Issues Emergency Regulations in Response to Discovery of
Chronic Wasting Disease. Learn More

4/27/2005: Chronic Wasting Disease Found in Oneida County Deer. Learn More.

4/21/2005: DEC Releases Results of Tests for Chronic Wasting Disease. Learn

4/13/2005: DEC to Test For Chronic Wasting Disease in Hamilton County. Learn

4/8/2005: Chronic Wasting Disease Update: Test Results Reveal Three
Additional Positives From Index Herd. Learn More.

4/5/2005: Chronic Wasting Disease Update. Learn More.

4/2/2005: Second Case of CWD Found in Oneida County Deer. Learn More.

3/31/2005: Positive Case of CWD Found in Oneida County Deer. Learn More.

Transcript from March 31 Press Conference Regarding First Case of CWD in
NewYork State

If you have difficulty opening the PDF files, please contact the Department
of Agriculture & Markets.

THE infamous USA SPORADIC CJDs, something to ponder;

IF the USA TSE in cattle does not look like UK BSE, why would the USA human
TSE look like UK nvCJD???

i guess WE will never know due to the CJD Foundation INC. and there PHONE
CALL only cjd questionnaire.

THEY don't want the rest of the world knowing any potential route and source
of this agent.

JUST SAY NO TO ORAL CJD QUESTIONNAIRE, demand a written one with a copy
going to family...


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
281-559-3131 PRIVATE PLEASE
CJD Watch/CJD VOICE member
AAAS Member Professional/Regular

Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE
SAFEGUARDS (comment submission)


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2



File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [] Monday, January 08,200l 3:03 PM freas ...

Asante/Collinge et al, that BSE transmission to the 129-methionine

genotype can lead to an alternate phenotype that is indistinguishable

from type 2 PrPSc, the commonest _sporadic_ CJD;

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food
Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...

Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1

Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... - 05-20-2003
- Cached

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

Send Post-Publication Peer Review to journal:

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


Volume 3, Number 8 01 August 2003


Tracking spongiform encephalopathies in North America

Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.

49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD)the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.

Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.

Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.

Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very


he complained in a letter to the Journal of the American Medical

Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<

actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...

Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.






BY Philip Yam

Yam Philip Yam News Editor Scientific American

IN light of Asante/Collinge et al findings that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: (until 9/12/02)

New e-mail: (active from now)



full text ;

AND the new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic

Creutzfeldt-Jakob disease

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

ALL animals for human/animal consumption must be tested for TSE.

ALL human TSEs must be made reportable Nationally and Internationally, OF

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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