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From: Terry S. Singeltary Sr. (216-119-144-9.ipset24.wt.net)
Subject: Research Project: Study of Atypical Bse Project Number: 3625-32000-073-07
Date: January 1, 2005 at 2:41 pm PST

-------- Original Message --------
Subject: Research Project: Study of Atypical Bse Project Number: 3625-32000-073-07
Date: Sat, 1 Jan 2005 16:27:35 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


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

Research Project: Study of Atypical Bse

Location:


Virus
and Prion Diseases of Livestock


Project Number: 3625-32000-073-07
Project Type: Specific C/A

Start Date: Sep 15, 2004
End Date: Sep 14, 2007

Objective:
The objective of this cooperative research project with Dr. Maria
Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is
to conduct comparative studies with the U.S. bovine spongiform
encephalopathy (BSE) isolate and the atypical BSE isolates identified in
Italy. The studies will cover the following areas: 1. Evaluation of
present diagnostics tools used in the U.S. for the detection of atypical
BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other
typical BSE isolates with atypical BSE cases. 3. Studies on
transmissibility and tissue distribution of atypical BSE isolates in
cattle and other species.

Approach:
This project will be done as a Specific Cooperative Agreement with the
Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale
del Piemonte, in Turin, Italy. It is essential for the U.S. BSE
surveillance program to analyze the effectiveness of the U.S diagnostic
tools for detection of atypical cases of BSE. Molecular comparisons of
the U.S. BSE isolate with atypical BSE isolates will provide further
characterization of the U.S. BSE isolate. Transmission studies are
already underway using brain homogenates from atypical BSE cases into
mice, cattle and sheep. It will be critical to see whether the atypical
BSE isolates behave similarly to typical BSE isolates in terms of
transmissibility and disease pathogenesis. If transmission occurs,
tissue distribution comparisons will be made between cattle infected
with the atypical BSE isolate and the U.S. BSE isolate. Differences in
tissue distribution could require new regulations regarding specific
risk material (SRM) removal.

http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490

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

yep, that's what i been talking about.
least i know they know now, and are concerned.
too bad they did not finish decades ago what they started
at Mission, TEXAS ;

WHEN in fact, the findings from Marsh and the findings at
MISSION, TEXAS support even further evidence that there
are furthers strains of TSE in the USA besides that one
accidently documented BSE case in Washington on
Dec. 23, 2003;

In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - Report of a visit to the USA - April-May 1989 - G A
H Wells [head of England's main veterinary lab]

2. Meeting with USDA, BSE Task Force

This group comprises Alex Thierman (USDA-APHIS, International Programs)
(Chairman), Roger Breeze (USDA-ARS Director, Plum Island), Bill Hadlow
(Neuropathologist - retired, formerly of NIH Rocky Mountain Laboratory,
Hamilton, Montana), John Gorhan and Mark Robinson (USDA-ARS, Pullman,
Washington) and Dick Marsh (Dept. Vet. Science, Univ Wisconsin - Madison).
The objectives of the group are to assess the implications of the
occurrence of BSE for US cattle particularly the risk of BSE occurrence
in the US in relation to endemic scrapie agent.
The purpose of my invitation to this meeting was to discuss aspects of
research which are of common interest and to identify a tentative USDA
research programme including any potential collaborative projects. The
discussions were informal and there was no agenda.
The general opinion
of those present was that BSE, as an overt disease phenomenon, could
exist in the USA but if it did it was very rare. The need for improved
and specific surveillance methods to detect it was recognised. Clinical
similarities between BSE and rabies suggested one means of sampling the
cattle population which might increase the probability of detection of
BSE. It was clear that the bovine rabies negative rate would vary
greatly between States but initially this should be determined and as it
would inevitably be high relative to positive cases, some differential
diagnosis carried out.

The work of Wilbur Clarke at Mission, Texas was discussed briefly. the
results of this study in which 10 calves were inoculated with scrapie
has not been published and perhaps would not be published. USDA are
sensitive regarding publicity of the results of the study which remain
far from conclusive. Apparently only 3 of the inoculated animals
developed neurological signs. The neuropathology of the affected cattle
has not been examined in any depth but Hadlow has the material. Marsh
indicated the requirement to obtain the fresh brain material from this
study in order to perform PrP extractions.

Because of the successful transmission of the Brecke (Stetsonville)
isolate of TME to cattle and the subsequent passage history in mink it
was generally considered important that comparisons be made with BSE
isolates in mink. Is BSE like scrapie in mink? Is BSE like the Brecke
isolate of TME?

Very little was said about CWD but some present considered that its
occurrence may indicate a sylvatic origin of agent. It was also agreed
that the role of possible subclinical infection in the
epidemiology of transmissible spongiform encephalopathies could well
be important but was unknown.
Marsh remarked on the possibility that
BSE was due to an extremely thermostable strain of agent. His
experience in the past with one particular Wisconsin isolate of TME
(Hayward strain) suggested that i/c biopsy needles could not be
effectively "scrapie sterilised", even employing an experimental
autoclave system capable of 60 psi and 300"C+ for 5 hours. This
experience led him to the policy that in scrapie or TME transmission
studies re-use of instruments or glassware that had contained agent was
an unacceptable protocol.

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) show 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
inoculated 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 feature. The material requires detailed neuropathological
assessment but whether or not this will be done remains in question.

Appendix I

VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE

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 SAF were given.

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 emhryos 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 fetus.

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.

CONFIDENTIAL TRANSMISSION (Day 4)

6.1 BSE to pigs

snip...end

full text ;

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

3.57 The experiment which might have determined whether BSE and scrapie
were caused by the same agent (ie, the feeding of natural scrapie to
cattle) was never undertaken in the UK. 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.

http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm

Visit to USA ... info on BSE and Scrapie

http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf

Journal of Infectious Diseases 1994; 169:814-20 by The University of
Chicago

Intracerebral Transmission of Scrapie to Cattle

R.C. Cutlip, J.M. Miller, R.E. Race, A.L. Jenny, J.B. Katz, H.D.
Lehmkuhl, B.M. DeBey, and M.M. Robinson

To determine if sheep scrapie agent(s) in the United States would induce
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 euthanized 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.

> I advised the APHIS pathologists that I thought they should be very
> careful about trying make such an assessment. So, what are their
> options? They would need fresh brain specimesns for a good western
> blot analysis and that would be difficult since they don't control the
> laboratories submitting material; furthermore, western blots are
> extremely expensive to run and I'm pretty sure they don't have the
> resources to do many of those anyway.
>

Dateline: US at risk for BSE and CJD

Webmaster's recollections from the Dateline TV show of March 14, 1997 --
transcript to be posted. Friday's broadcast was actually Dateline's
second: in April 1996, a show discussed Dr. Marsh's mink findings and
questions about USDA's BSE surveillance program.

The show was well-done, carefully researched, and quite current:
... historic video clips of kuru; first transmission and symptoms of chimp;
... first showing of video clip of results of 1979 first scrapie-to-cow
transmission in US;
... transmission was by intra-cerebral injection and second passaging
(cattle-to-cattle) was seen.

Tape of Gibbs and quote from Gajdushek, each suggesting that home
gardeners in US are getting CJD from MBM used in their rose gardens,
from the dust. Gibbs stated that in every single case of sporadic CJD
where he personally knew the individual, intensive rose gardening with
bone meal was in the picture.

Stone Phillips stated point-blank on the show that the American Red
Cross has secretly sequestered 2 million units of various blood
products, because of uncertain provenance with regard to donors and CJD.

There is a new book out, Deadly Feast. The American author, Richard
Rhodes, is making the round of talk shows such as this and has a direct
pipeline to Gujdushek, even in prison. He reiterated Gibbs' warnings
about pigs (but see below
).

Steve Eckert , the producer of NBC Dateline, has
provided some helpful corrections and additions to our initial account
of the program. (The Dateline show caused a quadrupling of Mad Cow
Disease daily Web
visitation -- more so than after Oprah.) An exact transcript of the
broadcast concerning bone meal and rose gardening:

STONE PHILLIPS NARRATION: Rhodes ends his book with the question: could
breathing the dust from that bone meal transmit the disease? With
millions of gardeners using it with no apparent problem, to even pose
the question seems outlandish. But the government's chief researcher on
these brain diseases, the cautious Dr. Gibbs, told Dateline that the few
people he's known personally who've died of CJD had one unusual thing in
common.

DR. GIBBS: They all used bone meal. But I can't say that there's a
relationship between the bone meal and the disease in humans.

STONE PHILLIPS: But it's kind of spooky to hear that.

DR. GIBBS: Kind of spooky, yeah.

RICHARD RHODES: I was sitting with Dr. Gajdusek, and he finally leaned
forward and said: "Do you use bone meal on your roses?" I was startled.
And I said, yes I do use bone meal on my roses. And he said: "I wouldn't
if I were you."

The producer continues:
"In fairness, these important qualifiers:
-- from the start Dr. Gibbs said he was only talking about a few cases,
not a full study .
-- Dr. Gibbs clearly stated that, in spite of his personal observation,
he could NOT claim there was a relationship between bone meal fertilizer
and human cases of CJD.
Dr. Gibbs comments were worth reporting not ot because they proved a
connection, but because they made Rhodes' question to Gajdusek -- which,
at first glance, had seemed so outlandish -- was that far-fetched after
all." --------

The 1979 video clip of sheep-to-cow was from an exeriment in Mission,
Texas. It apparently has never been made public before and was obtained
under Freedom of Information Act but the results were no 'secret.' The
program made clear that transmission was from [intra-cerebral] injection
and not from feed. Brain tissue from the infected Mission cattle were
later injected into other cattle to determine if second passage was
possible, with positive results. The 1979 experiment is discussed in
later publications by the Cutlip-Robinson group, relevent abstracts below.

You can order a Dateline videotape
containing the
clips by visiting or see what they posted on the show


Transcripts: $6 each, payable by check only:
Burrelle's at (800) 777-TEXT. Or write to:
Burrelle's
Box 7
Livingston, NJ 07039

The simple history of scrapie-to-cattle research in the U,S. seems to be:
Dr. Wilbur Clark at the USDA's scrapie research station in Texas
injected cattle, starting in 1979. Several fell ill, but because the
brain lesions were subtle, researchers apparently weren't sure what they
had. Several years later, Joe Gibbs tested the cattle brains chemically,
found PrP-res in the symptomatic cattle (but not others), and thus
confirmed transmission.

At that point, Hourrigan wrote up the original Clark results, and Gibbs
reported finding the marker protein. Cutlip followed up in Iowa with a
new sheep-to-cattle experiment; and Robinson & others used the Texas
cattle brains for a second passage experiment in Pullman.


How hard is USDA really looking for US BSE?

19 Mar 1997 Dr. Janice Miller

We work very closely with the pathologists at the National Veterinary
Services Laboratories Pathobiology Laboratory [APHIS] and they were
aware of our results long before they were published. The problem APHIS
has is that most of the specimens they receive from cattle with CNS
signs have been collected by non-USDA people (state veterinay diagnostic
or public health laboratories) and they have been fixed in formalin, as
is standard practice for tissues to be examined by histopathology.

Unfortunately, that is not a good fixation method for detecting the
intraneuronal PrP staining that we found in cattle inoculated with sheep
scrapie. If you read the Materials and Methods section of that paper you
will see that the brains we examined by immunohistochemistry were fixed
in PLP with an extremely low percentage of paraformaldehyde, 0.25%.
Using this fixative, as we described in our 1993 paper, the PrP which
appears in the neuron cell bodies of normal brains is destroyed by
formic acid treatment, whereas the abnormal PrP in neurons of affected
cattle remains immunoreactive.

The problem with tissue fixed in formalin (we collected tissues in that
fixative also) is that the hydrated autoclaving procedure used to
"unmask" PrP in formalin-fixed tissue reveals some PrP staining in
neuron cell bodies of normal (control) brains. Therefore, the question
then becomes quantitative and highly subjective. At which point does the
pathologist think he is seeing more than a normal amount? I believe a
person would have to look at an awful lot of normal brains before
feeling very comfortable about saying a brain had "more than normal"
amounts of intraneuronal PrP.

I advised the APHIS pathologists that I thought they should be very
careful about trying make such an assessment. So, what are their
options? They would need fresh brain specimesns for a good western blot
analysis and that would be difficult since they don't control the
laboratories submitting material; furthermore, western blots are
extremely expensive to run and I'm pretty sure they don't have the
resources to do many of those anyway.

The option they chose was to use the immunohistochemical test that we
used for our experimental cattle, but applying it only to brains that
were collected in the special PLP fixative by APHIS personnel. The
brains that fit this category are those collected from selected
slaughter plants that kill lots of "downer cows".

They felt the history of those cows most closely fit the kind of
syndrome that we saw in the cattle inoculated with U.S. sheep scrapie. I
can't tell you how many of them have been examined in that way but if
you want that information you could contact Dr. Arthur Davis
, Chief, Pathobiology Laboratory, National
Veterinary Services Laboratories, APHIS, Ames, Iowa 50010. His phone
number is 515-239-8521 and the fax number is 515-239-8527.

This is a very complex problem and seems to get more so every day.


Encephalopathy in cattle experimentally infected with the
scrapie agent.

Am J Vet Res 56: 606-612 (1995)
Clark WW, Hourrigan JL, Hadlow WJ
USDA, Animal and Plant Health Inspection Service, Veterinary Services, Mission, TX 78572, USA.

Ten 8- to 10-month-old cattle were each inoculated intramuscularly,
subcutaneously, intracerebrally, and orally with the scrapie agent to
determine whether cattle are susceptible to it. Two inocula, both 10%
homogenates of cerebrum, were used. One inoculum was from a sheep used
for the second experimental ovine passage of the agent from 4 naturally
affected Suffolk sheep. The other inoculum was from a goat used for the
first experimental caprine passage of the agent from 2 naturally
affected dairy goats living with the Suffolk sheep, the source of their
infection. Between 27 and 48 months after inoculation, neurologic
disease was observed in 1 of 5 cattle given the sheep brain homogenate
and in 2 of 5 given the goat brain homogenate. In all 3 affected cattle,
the disease was expressed clinically as increasing difficulty in rising
from recumbency, stilted gait of the pelvic limbs, disorientation, and
terminal recumbency during a 6- to 10-week course. Neurohistologic
changes, though consistent with those of scrapie, were slight and
subtle: moderate astrocytosis with sparse rod cells, some neuronal
degeneration, a few vacuolated neurons, and scant spongiform change.
Clinically and neurohistologically, the experimentally induced disease
differed from bovine spongiform encephalopathy. The differences
emphasize that such infections in cattle induce diverse responses,
presumably depending largely on the strain of the agent. Pathologists
should keep this variability in mind when looking for microscopic
evidence of a scrapie-like encephalopathy in cattle.

1)Hourrigan JL Experimentally induced bovine spongiform encephalopathy
in cattle in Mission, Tex., and the control of scrapie. J Am Vet Med
Assoc 1990;196;1678-9
2) Gibbs CJ Jr. Experimental transmission of scrapie to cattle. Lancet,
1990; 335;1275


Intracerebral transmission of scrapie to cattle.

J Infect Dis 169: 814-820 (1994)
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 50010.

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.


Experimental infection of cattle with the agents of
transmissible mink encephalopathy and scrapie.

J Comp Pathol 113: 241-251 (1995)
Robinson MM, Hadlow WJ, Knowles DP, Huff TP, Lacy PA, Marsh RF, Gorham JR
USDA-ARS Animal Disease Research Unit, Washington State University, Pullman 99164-7030, USA.

Cattle are susceptible to experimental infection with the Stetsonville
isolate of the transmissible mink encephalopathy (TME) agent. To
determine if they are susceptible to other TME isolates, two groups of
calves were inoculated intracerebrally with homogenate of mink brain
containing the Hayward isolate or the Blackfoot isolate. For comparison,
a third group was inoculated with a brain homogenate from a steer
infected with the Stetsonville isolate in its primary cattle passage and
a fourth group was inoculated with a pool of brain homogenate from three
cattle experimentally infected with a sheep and goat scrapie agent in
its primary cattle passage. Clinical signs of neurological disease
appeared in each steer of every group between 15 and 25 months after
inoculation. An encephalopathy characterized by severe spongiform change
and pronounced astrocytosis occurred in the three groups inoculated with
the TME agent. In contrast, the neurohistological changes in the steers
inoculated with the cattle-passaged scrapie agent were slight and
subtle. Analysis of the octapeptide repeat region of the bovine
protease-resistant protein (PrP) gene showed that variations in
incubation period, clinical signs, and neurohistological changes were
unrelated to the homozygous or heterozygous condition of six or six/five
octapeptide repeats.


Experimental infection of mink with bovine spongiform
encephalopathy.

J Gen Virol 75: 2151-2155 (1994)
Robinson MM, Hadlow WJ, Huff TP, Wells GA, Dawson M, Marsh RF, Gorham JR
USDA-ARS Animal Disease Research Unit, Pullman, Washington 99164-7030.

To determine whether the aetiological agent of bovine spongiform
encephalopathy (BSE) is pathogenic for mink, standard dark mink were
inoculated with coded homogenates of bovine brain from the U.K. Two
homogenates were from cows affected with BSE. The third was from a cow
that came from a farm with no history of having had BSE or having been
fed ruminant-derived, rendered by-products, the proposed vehicle for
introduction of the BSE agent. Each homogenate was inoculated
intracerebrally into separate groups of mink and a pool of the three was
fed to a fourth group. Signs of neurological disease appeared in mink an
average of 12 months after intracerebral inoculation and 15 months after
feeding. Decreased appetite, lethargy and mild to moderate pelvic limb
ataxia were the predominant clinical signs, quite unlike the classic
clinical picture of transmissible mink encephalopathy (TME).

Microscopic changes in brain sections of most affected mink were those
of a scrapie-like spongiform encephalopathy. Vacuolar change in grey
matter neuropil was accompanied by prominent astrocytosis. Varying
greatly in severity from one mink to another, the degenerative changes
occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe,
corpus striatum, diencephalon and brainstem. Although resembling TME,
the encephalopathy was distinguishable from it by less extensive changes
in the cerebral cortex, by more severe changes in the caudal brainstem
and by sparing of the hippocampus. The results of this study extend the
experimental host range of the BSE agent and demonstrate for the first
time the experimental oral infection of mink with a transmissible
spongiform encephalopathy agent from a naturally infected ruminant species.

Veteran researcher Dr. Richard Marsh
at U. Wisconsin was
rumored to be, but in fact was not, suffering from CJD. \

Marsh had told friends that little or no safety precautions in handling
TSEmaterial were taken in the early days at NIH labs. He cannot speak to
the public without written clearance from the Attorney General of the
State of Wisconsin because of a lawsuit threatened on the University by
the rendering industry. Wisconsin is a big dairy state.


Richard Marsh, 58, Cow-Disease Researcher

By FORD BURKHART March 27, 1997 NY Times

Richard F. Marsh, whose research in veterinary science at the University
of Wisconsin at Madison led him to sound an alarm about the risks of mad
cow disease a decade before the outbreak of the disease in Britain last
year, died on Sunday at his home in Middleton, Wis. He was 58. The cause
was cancer, his family said.

Dr. Bert Mitchell, associate director of the Center for Veterinary
Medicine in the National Institutes of Health in Bethesda, Md., credited
Marsh with bringing up the possibility in 1985 that the disease could
pass from animal to animal through tissue used in feed.

In his research, Marsh observed diseases in minks and learned from a
mink rancher that the animals had been fed with a food supplement made
from cattle parts. He theorized there was a pathway for transmission of
cattle diseases that the industry was unaware of and urged a ban on such
feeding. The disease, mink spongiform encephalopathy, destroys brain
tissue in a manner similar to the way mad cow disease affects cattle.

He lived to see the first steps toward a federal ban on the feeding of
tissue from cud-chewing animals, or ruminants, like cattle and sheep, to
other ruminants. The ban is expected to become law by this summer,
federal officials said. The mad cow disease, or bovine spongiform
encephalopathy, has been tentatively linked to the fatal
Creutzfeldt-Jakob disease, a variant of which British experts have
confirmed in about a dozen cases. A colleague at Wisconsin, Dr. Judd
Aiken, said Marsh had alerted the veterinary field to the virtual
impossibility of killing, by sterilizing the tissue used in animal feed,
the agent that is believed to cause mad cow disease. "He showed these
things are iron-clad agents," Aiken said.

He said Marsh had shown that the symptoms of these cattle diseases were
slow in developing. An infected calf can look normal, perhaps for as
long as five to eight years without a signal of the dangerous agents,
until a mature cow begins to stagger or become aggressive. So Marsh
lobbied for a ban even in absence of symptoms in cattle.

Marsh received a doctorate in veterinary medicine from Washington State
University in 1963. He worked at the U.S. Public Health Service from
1968-70, then joined the University of Wisconsin, working there until
his death.

http://www.mad-cow.org/~tom/Dateline.html

WHY is USA insisting _now_ not to use WB, when on the 1st _confirmed_
case Dec. 23, 2003
USA mad cow, WB was used ???

maybe this is the reason ;

JAPAN BSE # 8 & 9 cow

8. 6/10/2003 Holstein Steer 13/10/2001 23 mths
No clinical signs WB+, IHC-, HP-


9. 4/11/2003 Holstein Steer 13/1/2002
21 mths No clinical signs WB+, IHC-, HP-

===========

it's gonna be a long year........

TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########





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