• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

Experts: Mad cow cases could be spontaneous

Manitoba_Rancher

Well-known member
Experts: Mad cow cases could be spontaneous
Infections in Texas and Alabama may have come from mysterious strain


Updated: 12:19 a.m. CT June 11, 2006
WASHINGTON - Two cases of mad cow disease in Texas and Alabama seem to have resulted from a mysterious strain that could appear spontaneously in cattle, researchers say.

Government officials are trying to play down differences between the two U.S. cases and the mad cow epidemic that has led to the slaughter of thousands of cattle in Britain since the 1980s.

It is precisely these differences that are complicating efforts to understand the brain-wasting disorder, known medically as bovine spongiform encephalopathy, or BSE for short.

“It’s most important right now, till the science tells us otherwise, that we treat this as BSE regardless,” the Agriculture Department’s chief veterinarian, John Clifford, said in an interview.

The Texas and Alabama cases—confirmed last year and this one, respectively—are drawing international attention.

At a meeting in London last month, experts presented research on the U.S. cases and on similar ones in Europe.

These cows appear to have had an “atypical” strain that scientists are only now starting to identify. Such cases have been described in about a dozen cows in France, Italy and other European countries, as well as in Japan.

In the two U.S. cases, researchers did not detect the telltale spongy lesions caused by prions, the misfolded proteins that deposit plaque on the brain and kill brain cells. In addition, the prions in brain tissue samples from the Texas and Alabama cows seemed to be distributed differently from what would be expected to be found in cows with the classic form.

Laboratory studies on mice in France showed that both the classic and atypical strains could be spread from one animal to another. But scientists theorize the atypical strain might have infected cattle through an unusual way.

Mad cow disease is not transmitted from cow to cow like a cold or the flu. It is believed to spread through feed, when cows eat the contaminated tissue of other cattle. That happens when crushed cattle remains are added to feed as a protein source. This once-common practice ended in the United States in 1997.

Humans can get a related disease, variant Creutzfeldt-Jakob Disease, in similar fashion—by eating meat contaminated with mad cow. Mad cow in humans afflicts younger people; the average age at death is 28 years.

A more common form of CJD—not linked to mad cow—can happen spontaneously and is reported in nearly 300 people in the U.S. each year. This form occurs mostly in older people; the average age at death is 68.

Some scientists are raising the possibility that the atypical strain also might happen spontaneously in cattle. The Texas and Alabama cows were older animals, as were some of the other animals in Europe with seemingly atypical cases.

Linda Detwiler, a former Agriculture Department veterinarian who consults for major food companies, cautioned against making that assumption. “I think it’s kind of early to say that would be the case,” Detwiler said.

Other theories, she said, suggest the atypical strain might come from a mutation of mad cow disease or even from a related disease in sheep.

Mad cow disease has turned up three times in the United States:

in native-born animals in Texas and Alabama and in a Canadian import in Washington state.

In the Texas and Alabama cows, tests found patterns distinct from what turned up in an infected cow in Washington state and a cluster of Canadian cases, researchers say. The Washington and Canadian cases resemble the classic British cases.

No matter what the origins might be of an atypical strain, the government says there is no reason to change federal testing or measures that safeguard animals and people from the disease.

“We still feel confident in the safeguards that we have,” Clifford said. “We have to base our assumptions on what is scientifically known and understood.”

Meanwhile, mad cow research has been halted at the Agriculture Department’s lab in Ames, Iowa, because of employee allegations that the lab improperly was disposing of animal waste.

The department asked a group of international experts to review the lab’s disposal practices. The city of Ames also is investigating.
 

Silver

Well-known member
:lol: :lol: :lol: Well, it was really only a matter of time before it was pointed out that their strain of bse was better than our strain!!!! :lol: :lol: :lol: :lol:
 

Tam

Well-known member
What I wonder is does their spontaneous strain affect organically grown cattle or does it just affect those that have been fed ruminant laced feed? :?
 

Mike

Well-known member
Tam said:
What I wonder is does their spontaneous strain affect organically grown cattle or does it just affect those that have been fed ruminant laced feed? :?

All "Spontaneous" means is that they do not know the source of infection.

The "Atypical" is different in that the vacuoles (holes) in the brain caused by the prions are not visible. (The method employed by IHC, the old style tests.)

The rapid tests and the Western Blot pick up these cases because they are actually finding the mis-folded prions.

Wonder how many others we have had that were undetected with IHC?

The Japs know this full well. They are hesitant because of the incompetency of the USDA.
 

flounder

Well-known member
##################### Bovine Spongiform Encephalopathy #####################

Subject: USDA, SPONTANEOUS MAD COW DISEASE, THE TOOTH FAIRY AND SANTA CLAUS
Date: June 12, 2006 at 5:18 am PST

IF we all believe the BSe that the USDA is trying to put out now about atypical BSE in USA cattle just arising spontaneously,
then we all should believe in the tooth fairy and santa clause as well.

IF USA scrapie transmitted to USA cattle long ago in experiments in a lab in Mission Texas did not produce UK BSE,
but something very different, then why would USA TSE cattle produce the UK human version of mad cow i.e. nvCJD?
IT wouldn't. USA sporadic cjd is increasing, the USA also has atypical human cases of unknown origin as well?

THERE are over 20 strains of scrapie, plus the atypical in sheep, and these strains are increasing in numbers.

SCRAPIE, CWD, AND TSE IN CATTLE i.e. ANIMAL TSE RAMPANT IN USA FOR DECADES, and amplified via rendering and
feeding practices, where USDA triple firewalls against BSE were nothing more than a mere smoke screen.

NO test tube TSE by either Prusiner or Soto, to date, have ever produced a TSE identical to the sporadic CJD. IN fact,
no test tube TSE has ever been produced that resembles _any_ natural field TSE.

IF you feed BSE tainted materials to cattle and primate, you have BSE and nvCJD.
IF you feed USA sheep strain to USA cattle, you get USA TSE.
IF you feed USA tainted cattle to humans, you get USA mad cow disease.
IF you feed sporadic CJD to primate you get a CJD infected primate.
NOTHING spontaneous about it at all.

USA is in a very unique situation. there are more documented TSE in different species than any other country,
all of which have been rendered and fed back to animals for human and animal consumption, for decades. Millions exposed,
and of these Millions, how many surgical and dental procedures have been done on these exposed, to pass on to others,
via the 'friendly fire' mode of transmission?

IF, the spontaneous TSE was true, then this would be Prusiner and everyone else that is trying to cash in on this agent with
there TSE rapid test, this would be there dream come true. IT would require mandatory BSE/TSE testing of all species,
due to the fact you could not ever eradicate it through any intervention. BUT, then again, the spontaneous TSE is like believing
in the tooth fairy or santa clause will be arriving at your house this year.


How long can this sharade continue $

How many more will become exposed and have to die $


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, Italy


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: [email protected]
www.pnas.org/cgi/doi/10.1073/pnas.0305777101


http://www.pnas.org/cgi/content/abstract/0305777101v1





: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

PMID: 6997404


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract




Atypical cases of TSE in cases of TSE in
cattle and sheep cattle and sheep
H. De H. De Bosschere Bosschere
CODA/CERVA CODA/CERVA
Nat. Ref. Lab. Vet. Nat. Ref. Lab. Vet. TSEs TSEs
Belgium


http://www.var.fgov.be/pdf/1100_TSEDAY.pdf




USDA 2004 ENHANCED BSE SURVEILLANCE PROGRAM AND HOW NOT TO FIND BSE CASES (OFFICIAL DRAFT OIG REPORT)

snip...


CATTLE With CNS Symptoms Were NOT Always Tested


snip...


Between FYs 2002 and 2004, FSIS condemned 680 cattle of all ages due to CNS symptoms. About 357 of these could be classified as adult. We could validate that ONLY 162 were tested for BSE (per APHIS records. ...

snip...

WE interviewed officials at five laboratories that test for rabies. Those officials CONFIRMED THEY ARE NOT REQUIRED TO SUBMIT RABIES-NEGATIVE SAMPLES TO APHIS FOR BSE TESTING. A South Dakota laboratory official said they were not aware they could submit rabies-negative samples to APHIS for BSE testing. A laboratory official in another State said all rabies-negative cases were not submitted to APHIS because BSE was ''NOT ON THEIR RADAR SCREEN." Officials from New York, Wisconsin, TEXAS, and Iowa advised they would NOT submit samples from animals they consider too young. Four of the five States contacted defined this age as 24 months; Wisconsin defined it as 30 months. TEXAS officials also advised that they do not always have sufficient tissue remaining to submit a BSE sample. ...

snip...


FULL TEXT 54 PAGES OF HOW NOT TO FIND BSE IN USA ;


http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf





HUMAN TSE USA 2005


Animal Prion Diseases Relevant to Humans (unknown types?)
Thu Oct 27, 2005 12:05
71.248.128.109


About Human Prion Diseases /
Animal Prion Diseases Relevant to Humans

Bovine Spongiform Encephalopathy (BSE) is a prion
disease of cattle. Since 1986, when BSE was recognized,
over 180,000 cattle in the UK have developed the
disease, and approximately one to three million are
likely to have been infected with the BSE agent, most
of which were slaughtered for human consumption before
developing signs of the disease. The origin of the
first case of BSE is unknown, but the epidemic was
caused by the recycling of processed waste parts of
cattle, some of which were infected with the BSE agent
and given to other cattle in feed. Control measures
have resulted in the consistent decline of the epidemic
in the UK since 1992. Infected cattle and feed exported
from the UK have resulted in smaller epidemics in other
European countries, where control measures were applied
later.

Compelling evidence indicates that BSE can be
transmitted to humans through the consumption of prion
contaminated meat. BSE-infected individuals eventually
develop vCJD with an incubation time believed to be on
average 10 years. As of November 2004, three cases of
BSE have been reported in North America. One had been
imported to Canada from the UK, one was grown in
Canada, and one discovered in the USA but of Canadian
origin. There has been only one case of vCJD reported
in the USA, but the patient most likely acquired the
disease in the United Kingdom. If current control
measures intended to protect public and animal health
are well enforced, the cattle epidemic should be
largely under control and any remaining risk to humans
through beef consumption should be very small. (For
more details see Smith et al. British Medical Bulletin,
66: 185. 2003.)

Chronic Wasting Disease (CWD) is a prion disease of elk
and deer, both free range and in captivity. CWD is
endemic in areas of Colorado, Wyoming, and Nebraska,
but new foci of this disease have been detected in
Nebraska, South Dakota, New Mexico, Wisconsin,
Mississippi Kansas, Oklahoma, Minnesota, Montana, and
Canada. Since there are an estimated 22 million elk and
deer in the USA and a large number of hunters who
consume elk and deer meat, there is the possibility
that CWD can be transmitted from elk and deer to
humans. As of November 2004, the NPDPSC has examined 26
hunters with a suspected prion disease. However, all of
them appeared to have either typical sporadic or
familial forms of the disease. The NPDPSC coordinates
with the Centers for Disease Control and state health
departments to monitor cases from CWD-endemic areas.
Furthermore, it is doing experimental research on CWD
transmissibility using animal models. (For details see
Sigurdson et al. British Medical Bulletin. 66: 199.
2003 and Belay et al. Emerging Infectious Diseases.
10(6): 977. 2004.)


http://www.cjdsurveillance.com/abouthpd-animal.html




SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is
with a human TSE surveillance system that is terrible
flawed. in 1997 cases of the _reported_ cases of cjd
were at 54, to 163 _reported_ cases in 2004. see stats
here;

p.s. please note the 47 PENDING CASES to Sept. 2005

p.s. please note the 2005 Prion D. total 120(8)
8=includes 51 type pending, 1 TYPE UNKNOWN ???

p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???

p.s. please note 2004 prion disease (6) 6=7 TYPE
UNKNOWN???


http://www.cjdsurveillance.com/resources-casereport.html




CWD TO HUMANS = sCJD ???


AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



snip...end
full text ;

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


VERY VERY IMPORTANT THING TO REMEMBER


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


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






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#820543




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


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

http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546




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.

3.58 There are several possible reasons why the experiment was not performed
in the UK. It had been recommended by Sir Richard Southwood (Chairman of the
Working Party on Bovine Spongiform Encephalopathy) in his letter to the
Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988, 35
though it was not specifically recommended in the Working Party Report or
indeed in the Tyrrell Committee Report (details of the Southwood Working
Party and the Tyrell Committee can be found in vol. 4: The Southwood Working
Party, 1988-89 and vol. 11: Scientists after Southwood respectively). The
direct inoculation of scrapie into calves was given low priority, because of
its high cost and because it was known that it had already taken place in
the USA. 36 It was also felt that the results of such an experiment would be
hard to interpret. While a negative result would be informative, a positive
result would need to demonstrate that when scrapie was transmitted to
cattle, the disease which developed in cattle was the same as BSE. 37 Given
the large number of strains of scrapie and the possibility that BSE was one
of them, it would be necessary to transmit every scrapie strain to cattle
separately, to test the hypothesis properly. Such an experiment would be
expensive. Secondly, as measures to control the epidemic took hold, the need
for the experiment from the policy viewpoint was not considered so urgent.
It was felt that the results would be mainly of academic interest. 38


http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550




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




REPORT OF THE COMMITTEE ON SCRAPIE

Chair: Dr. Jim Logan, Cheyenne, WY

Vice Chair: Dr. Joe D. Ross, Sonora, TX

Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.

The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.

The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.

Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.

For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.

snip...

Infected and Source Flocks

As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.

Regulatory Scrapie Slaughter Surveillance (RSSS)

RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm . RSSS started April 1,

2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.

Scrapie Testing

In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).

Animal ID

As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.

*This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.


http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf




Date: April 30, 2006 at 4:49 pm PST
SCRAPIE USA UPDATE AS of March 31, 2006


2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE
FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL


http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html




Published online before print October 20, 2005

Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
Medical Sciences

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

( sheep prion | transgenic mice )

Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||, Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude *
*Virologie Immunologie Moléculaires and ||Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway


Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)

Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.


--------------------------------------------------------------------------------

Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.

A.L.D. and V.B. contributed equally to this work.

To whom correspondence should be addressed.

Hubert Laude, E-mail: [email protected]

www.pnas.org/cgi/doi/10.1073/pnas.0502296102


http://www.pnas.org/cgi/content/abstract/0502296102v1




12/10/76
AGRICULTURAL RESEARCH COUNCIL
REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note
CHAIRMAN: PROFESSOR PETER WILDY

snip...

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
countries.

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
dementias"

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
grievously.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf




Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284
What if you can catch old-fashioned CJD by eating meat from a sheep infected
with scrapie?
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but
Singeltary was suspicious. The diagnosis didn't fit her violent symptoms,
and he demanded an autopsy. It showed she had died of sporadic
Creutzfeldt-Jakob disease.

Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number
of campaigners who say that some sCJD, like the variant CJD related to BSE,
is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.

Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in ...

The complete article is 889 words long.

full text;

http://www.newscientist.com/article.ns?id=mg16922840.300




Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*,
Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James
Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Département de Recherche Medicale, Centre de
Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc,
BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre
Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de
Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital,
75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western
General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and
Institute for Animal Health, Neuropathogenesis Unit, West Mains Road,
Edinburgh EH9 3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)


Abstract

There is substantial scientific evidence to support the notion that bovine
spongiform encephalopathy (BSE) has contaminated human beings, causing
variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns
about the possibility of an iatrogenic secondary transmission to humans,
because the biological properties of the primate-adapted BSE agent are
unknown. We show that (i) BSE can be transmitted from primate to primate by
intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD
to humans could be readily recognized pathologically, whether it occurs by
the central or peripheral route. Strain typing in mice demonstrates that the
BSE agent adapts to macaques in the same way as it does to humans and
confirms that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. 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. These data will be key in identifying the origin of human cases of
prion disease, including accidental vCJD transmission, and could provide
bases for vCJD risk assessment.


http://www.pnas.org/cgi/content/full/041490898v1




USDA CWD PROGRAM

http://www.aphis.usda.gov/vs/nahps/cwd/



USDA CWD MAP (slow to update)

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html




DRAFT

WYOMING GAME AND FISH DEPARTMENT

CHRONIC WASTING DISEASE MANAGEMENT PLAN

February 17, 2006


snip...


5. Predicted population effects on free-ranging elk based on captive elk chronically exposed to the CWD prion.
Forty-three female elk calves were trapped at the National Elk Refuge and transported to Sybille in February 2002. Elk were housed in pens, assumed to be environmentally contaminated with the CWD prion. Elk will be held throughout their lifetimes. Elk dying will be examined and cause of death determined. From these data, it will should be possible to model free-ranging elk mortality and population dynamics under extreme circumstances of CWD prion exposure and transmission. As of December 2005 (46 months post capture), 11 of 43 elk have died due to CWD. This compares to 100% mortality in less than 25 months in elk orally inoculated with different dosages of the CWD prion.



REVISED DRAFT


http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf




Prions in Skeletal Muscles of Deer with Chronic Wasting Disease


Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J.
Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§

1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders
Brown Center on Aging, 3Department of Neurology, University of Kentucky,
Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and
Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado
Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA.

*These authors contributed equally to this work.

†Present address: Department of Infectology, Scripps Research Institute,
5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA.

‡Present address: Institute of Neuropathology, University of Zurich,
Schmelzbergstrasse 12, 8091 Zurich, Switzerland.

§To whom correspondence should be addressed: E-mail: [email protected]

Prions are transmissible proteinaceous agents of mammals that cause fatal
neurodegenerative diseases of the central nervous system (CNS). The presence
of infectivity in skeletal muscle of experimentally infected mice raised the
possibility that dietary exposure to prions might occur through meat
consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious
prion disease of North American cervids, is of particular concern. The
emergence of CWD in an increasingly wide geographic area and the
interspecies transmission of bovine spongiform encephalopathy (BSE) to
humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns
about zoonotic transmission of CWD.

To test whether skeletal muscle of diseased cervids contained prion
infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein
(CerPrP), were inoculated intracerebrally with extracts prepared from the
semitendinosus/semimembranosus muscle group of CWD-affected mule deer or
from CWD-negative deer. The availability of CNS materials also afforded
direct comparisons of prion infectivity in skeletal muscle and brain. All
skeletal muscle extracts from CWD-affected deer induced progressive
neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times
ranging between 360 and ~490 d, whereas the incubation times of prions from
the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the
diagnosis of prion disease was confirmed by the presence of PrPSc in the
brains of multiple infected Tg(CerPrP)1536 mice (see supporting online
material for examples). In contrast, skeletal muscle and brain material from
CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1)
and PrPSc was not detected in the brains of sacrificed asymptomatic mice as
late as 523 d after inoculation (supporting online material).

Our results show that skeletal muscle as well as CNS tissue of deer with CWD
contains infectious prions. Similar analyses of skeletal muscle BSE-affected
cattle did not reveal high levels of prion infectivity (3). It will be
important to assess the cellular location of PrPSc in muscle. Notably, while
PrPSc has been detected in muscles of scrapie-affected sheep (4), previous
studies failed to detect PrPSc by immunohistochemical analysis of skeletal
muscle from deer with natural or experimental CWD (5, 6). Since the time of
disease onset is inversely proportional to prion dose (7), the longer
incubation times of prions from skeletal muscle extracts compared to matched
brain samples indicated that prion titers were lower in muscle than in CNS
where infectivity titers are known to reach high levels. Although possible
effects of CWD strains or strain mixtures on these incubation times cannot
be excluded, the variable 360 to ~490 d incubation times suggested a range
of prion titers in skeletal muscles of CWD-affected deer. Muscle prion
titers at the high end of the range produced the fastest incubation times
that were ~30% longer than the incubation times of prions from the CNS of
the same animal. Since all mice in each inoculation group developed disease,
prion titers in muscle samples producing the longest incubation times were
higher than the end point of the bioassay, defined as the infectious dose at
which half the inoculated mice develop disease. Studies are in progress to
accurately assess prion titers.

While the risk of exposure to CWD infectivity following consumption of
prions in muscle is mitigated by relatively inefficient prion transmission
via the oral route (8), these


results show that semitendinosus/semimembranosus muscle, which is likely to
be consumed by humans, is a significant source of prion infectivity. Humans
consuming or handling meat from CWD-infected deer are therefore at risk to
prion exposure.

References and Notes

1. P. J. Bosque et al., Proc. Natl. Acad. Sci. U.S.A. 99, 3812 (2002).

2. S. R. Browning et al., J. Virol. 78, 13345 (2004).

3. A. Buschmann, M. H. Groschup, J. Infect. Dis. 192, 934 (2005).

4. O. Andreoletti et al., Nat. Med. 10, 591 (2004).

5. T. R. Spraker et al., Vet. Pathol. 39, 110 (2002).

6. A. N. Hamir, J. M. Miller, R. C. Cutlip, Vet. Pathol. 41, 78 (2004).

7. S. B. Prusiner et al., Biochemistry 21, 4883 (1980).

8. M. Prinz et al., Am. J. Pathol. 162, 1103 (2003).

9. This work was supported by grants from the U.S. Public Health Service
2RO1 NS040334-04 from the National Institute of Neurological Disorders and
Stroke and N01-AI-25491 from the National Institute of Allergy and
Infectious Diseases.

Supporting Online Material

www.sciencemag.org/

Materials and Methods

Fig. S1

21 November 2005; accepted 13 January 2006 Published online 26 January 2006;
10.1126/science.1122864 Include this information when citing this paper.


Table 1. Incubation times following inoculation of Tg(CerPrP)1536 mice with
prions from skeletal muscle and brain samples of CWD-affected deer.

Inocula Incubation time, mean d ± SEM (n/n0)*

Skeletal muscle Brain

CWD-affected deer

H92 360 ± 2 d (6/6) 283 ± 7 d (6/6)

33968 367 ± 9 d (8/8) 278 ± 11 d (6/6)

5941 427 ± 18 d (7/7)

D10 483 ± 8 d (8/8) 231 ± 17 d (7/7)

D08 492 ± 4 d (7/7)

Averages 426 d 264 d

Non-diseased deer

FPS 6.98 >523 d (0/6)

FPS 9.98 >454 d (0/7) >454 d (0/6)

None >490 d (0/6)

PBS >589 d (0/5)

*The number of mice developing prion disease divided by the original number
of inoculated mice is shown in parentheses. Mice dying of intercurrent
illnesses were excluded.


http://www.sciencemag.org/


www.sciencemag.org/




Supporting Online Material for

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease

Rachel C. Angers, Shawn R. Browning, Tanya S. Seward, Christina J.
Sigurdson,

Michael W. Miller, Edward A. Hoover, Glenn C. Telling§

§To whom correspondence should be addressed: E-mail: [email protected]

Published 26 January 2006 on Science Express

DOI: 10.1126/science.1122864

This PDF file includes:

Materials and Methods

Fig. S1

Supporting Online Materials

Materials and Methods

Homogenates of semitendinosus/semimembranosus muscle (10% w/v in phosphate

buffered saline) were prepared from five emaciated and somnolent mule deer,
naturally

infected with CWD at the Colorado Division of Wildlife, Wildlife Research
Center.

These deer were identified as D10, D08, 33968, H92, and 5941. CWD infection
was

confirmed in all cases by the presence of histologic lesions in the brain
including

spongiform degeneration of the perikaryon, the immunohistochemical detection
of

disease-associated PrP in brain and tonsil, or by immunoblotting of
protease-resistant,

disease associated PrP (CerPrPSc). Semitendinosus/semimembranosus muscle was
also

obtained from two asymptomatic, mock inoculated deer, referred to as FPS
6.68 and 9.98,

that originated from a CWD non-endemic area and which were held indoors at
Colorado

State University from ten days of age. These control deer were confirmed
negative for

CWD by histopathological and immunohistochemical analysis of brain tissue at
autopsy.

The utmost care was taken to avoid inclusion of obvious nervous tissue when
muscle

biopsies were prepared and to ensure that contamination of skeletal muscle
samples with

CNS tissue did not occur. Fresh, single-use instruments were used to collect
each sample

biopsy and a central piece from each sample was prepared with fresh,
disposable

instruments to further isolate muscle tissue for inoculum preparation. Brain
samples for

transmission were prepared separately from muscle as additional insurance
against cross

contamination.

1

Groups of anesthetized Tg(CerPrP)1536 mice were inoculated intracerebrally
with 30 µl

of 1 % skeletal muscle or brain extracts prepared in phosphate buffered
saline (PBS).

Inoculated Tg(CerPrP) mice were diagnosed with prion disease following the
progressive

development of at least three neurologic symptoms including truncal ataxia,
‘plastic’ tail,

loss of extensor reflex, difficultly righting, and slowed movement. The time
from

inoculation to the onset of clinical signs is referred to as the incubation
time.

For PrP analysis in brain extracts of Tg(CerPrP)1536 mice, 10 % homogenates
prepared

in PBS were either untreated (-) or treated (+) with 40 µg/ml proteinase K
(PK) for one

hour at 37oC in the presence of 2% sarkosyl. Proteins were separated by
sodium dodecyl

sulfate polyacrylamide gel electrophoresis, analyzed by immunoblotting using
anti PrP

monoclonal antibody 6H4 (Prionics AG, Switzerland), incubated with
appropriate

secondary antibody, developed using ECL-plus detection (Amersham), and
analyzed

using a FLA-5000 scanner (Fuji).

2

Fig. S1

PrP in brain extracts from representative Tg(CerPrP)1536 mice receiving
muscle or CNS

tissue inocula from CWD-affected or CWD-negative deer. Extracts were either
treated

(+) or untreated (-) with proteinase K (PK) as indicated. The positions of
protein

molecular weight markers at 21.3, 28.7, 33.5 kDa (from bottom to top) are
shown to the

left of the immunoblot.

3


http://www.sciencemag.org/



Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †University of Wyoming, Laramie, Wyoming, USA; ‡Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


Research

Environmental Sources of Prion Transmission in Mule Deer
Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort Collins, Colorado, USA

Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm


http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm




ATYPICAL TSEs in USA CATTLE AND SHEEP ?


http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf







UKBSEnvCJD only theory Singeltary et al 2006
(please note, et al in this term means all victims and familes of the sporadic CJD
that are still looking for answers. ...TSS)


http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13


http://www.microbes.info/forums/index.php?showtopic=306




NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING???


http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf




CJD WATCH

http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm



CJD WATCH MESSAGE BOARD

http://disc.server.com/Indices/167318.html




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

#################### https://lists.aegee.org/bse-l.html ####################
 

Econ101

Well-known member
flounder, the USDA (and current administration) is promoting loyalty over competency. Look at the new undersecretary at GIPSA.

It is a short term strategy of self interest over being able to competently run the government and it hurts us all.
 
A

Anonymous

Guest
Mike said:
All "Spontaneous" means is that they do not know the source of infection.

I agree Mike-- Its the scientific way to say they don't know their arse from a hole in the ground as to why? :roll: :wink:
 

Kathy

Well-known member
Flounder stated:

BUT, then again, the spontaneous TSE is like believing
in the tooth fairy or santa clause will be arriving at your house this year.

Spoken like a true researcher looking to find answers. NOT!!!!!

Very sad, flounder, that you refuse to believe in cases of BSE which were not the result of ingestion of the so-called "infectious" prions.

Nothing is spontaneous! Everything has a cause!

And by the way, Prusiner has said for years, that "spontaneous" cases can occur. I am actually quite amazed at some of the research he has been involved with.

Finding the causal agent, the ellusive Factor X, may not be in his best interest though. As you stated, 'spontaneous' causes could lead to the testing of all animals; but, if the causal agent were revealed - they wouldn't be looking for the prion protein; but the rogue metals floating around in our blood or urine.

Strains are the result of different metal contaminants and different glycosylation patterns, (and probably due to the bodies ability to remove them - stated by Prusiner). Contamination is not infection!

I am surprised nobody is talking about the fact that the Ames, Iowa facility has halted further BSE research.

research has been halted at the Agriculture Department’s lab in Ames, Iowa

reasons given may indeed be valid (appearing); but, I suspect there are other factors which have lead to their chilling on the BSE research.

The sooner these researchers "characterize" the entire prion protein (the mal-formed versions), the sooner we will have clues as to why they misfold.
 

mrj

Well-known member
reader (the Second) said:
Linda Detweiler is the US expert on BSE and note what she said -- she cautioned people from jumping to conclusions based on the fact that the BSE was "atypical."

And yes, "spontaneous" or "sporadic" means that they have NO idea of the cause. These are still mystery diseases as diseases go. That's the reason for taking more precautions.

If the British Govt had taken more precautions, if the manufacturers of dura mater and human growth hormone had taken more precautions, if the regulators had erred on the side of precaution, thousands of lives would have been saved. It is only in the past several years that regulation, research into cleansing surgical instruments and blood and into better surveillance for BSE have had the focus necessary. The reason is that the danger is now apparent, which it was not until the late 1990s.


reader 2, please explain your statement that "thousands of lives would have been saved".

MRJ
 

Econ101

Well-known member
MRJ said:
reader (the Second) said:
Linda Detweiler is the US expert on BSE and note what she said -- she cautioned people from jumping to conclusions based on the fact that the BSE was "atypical."

And yes, "spontaneous" or "sporadic" means that they have NO idea of the cause. These are still mystery diseases as diseases go. That's the reason for taking more precautions.

If the British Govt had taken more precautions, if the manufacturers of dura mater and human growth hormone had taken more precautions, if the regulators had erred on the side of precaution, thousands of lives would have been saved. It is only in the past several years that regulation, research into cleansing surgical instruments and blood and into better surveillance for BSE have had the focus necessary. The reason is that the danger is now apparent, which it was not until the late 1990s.


reader 2, please explain your statement that "thousands of lives would have been saved".

MRJ

MRJ, why don't you read the OIG report first? We need to know that you can read a report like that and come back home with something other than the company line.
 

bse-tester

Well-known member
Kathy wrote:

Nothing is spontaneous! Everything has a cause!

Just like thunder - it is the result of something else that made it happen. The lack or abundance of metals does have an overwhelming affect on how the firing or neurons is maintained in the brain. Consider that a neuron is fired, then it has to travel along a neuro-pathway to energize a particular part of the brain in order for us to move that arm, lick that lip, or, for you romantics, kiss that favorite pig. But suddenly the pathway is interupted by a broken or interupted network. Just like a corrupted hard-drive, a pathway needs to be completely intact for the neuron to make it to its destination. Otherwise the arm will not move and the pig will be most lonely.

Science suggests that some metals will provide a basic insulation along the pathway and yet some metals will actually corrode the pathway and make the neron almost totally ineffective. Others will provide for rapid sequencing of the firing order that is often manifested in Parkinson's patients - the jerky movements and so on. Compare this to having a timing chain in your car's engine that has jumped out of timing and the firing order of the engine is altered to a point where it jerks and coughs and sputters, but still runs -somewhat anyway. The manner in which prions are altered or corrupted by metals is an amazing study and deserves to be looked into more seriously. The misfolded prion causes nothing but havok for the neuron trying to make it to the destination target.

I have some details on how this works and will search for that data and post it soon. Meanwhile folks, its off to the coast for a week to kill some fish. Have fun and hey, play nice in the pool kids and keep the blood inside your bodies.
 

flounder

Well-known member
BEEF NEWS Two U.S. BSE cases: New questions, no answers by Pete Hisey on 6/13/2006 for Meatingplace.com


The two cases of bovine spongiform encephalopathy discovered in the United States in the past year or so, one in Texas and the other more recently in Alabama, are distinct from the earlier case discovered in Washington state and from very similar cases discovered in Canada and the United Kingdom, as well as several other countries around the world.

These so-called atypical cases match results in seven cases discovered in France, says Dr. Jean-Philippe Deslys, project coordinator for NeuroPrion, the European Network of Excellence, but are dissimilar to three other French cases as well as a handful in Italy and Germany, among others. The U.S. cases are so-called "high-weight" on a molecular basis, while the other atypical cases are "low-weight." (Results of ongoing experiments on this topic are due to be presented at Prion2006 in Turin, Italy in October.)

What it means is anyone's guess. Deslys says it could mean one of three things: that the "classic" BSE infection has mutated, much like a virus; that these cases are linked to scrapie in sheep or are truly spontaneous like most CJD (Creutzfeldt-Jakob disease) cases in humans and present little or no infective risk; or most ominously, that a new pattern of infectivity has emerged and may not be identified for years.

Deslys points to the spread of chronic wasting disease (CWD), which has moved geographically from the western United States to the Midwest and from there into Canada and the Northeast. Along the way, it has jumped from elk and mule deer to white-tailed deer and perhaps to other species, creating a geographic spread that Deslys says is "now almost out of control. Theoretically, it could be a bovine disease previously unidentified that could spread through feed as BSE does, or by means yet to be identified.

Some scientists believe that CWD may be transmitted through urine, which would indicate a level of infectivity never seen with BSE.

Ed Curlott, a spokesman for USDA's Animal and Plant Health Inspection Service, agrees that the major issue is the source of infectivity. "We have no data on transmission at all," he says. "Right now, we are just following the science."

That may take several years, says Deslys, one of the world's top researchers in prion diseases. In the meantime, he recommends, steps should be taken to increase testing of animals sent to slaughter, and feed bans and other means of controlling amplification of the disease should be maintained or strengthened. "Risk assessment of this development is going to take at least a few years," he says. He notes that, to date, all atypical cases have been found in relatively older cattle, most more than six years of age.

Rapid tests, he says, are getting more sensitive and far more affordable, and coupled with an SRM strategy that keeps the most infective animal parts out of all food supplies, could provide enough protection to keep the disease at bay while research continues.


http://www.meatingplace.com/MembersOnly/webNews/details.aspx?item=16071


TSS
 

Econ101

Well-known member
The globalization of trade has brought with it the globalization of disease. APHIS has not done its job well.

I like hunting and as a hunter, I know that wild animals use urine as a breeding signal. If tses can be spread this way, which is where this article goes, we might be in a lot more trouble. One of the things the cattle industry has going for it is the seperation of cattle herds into numerous seperate herds. Barbed wire and fences help control the spread of disease from what you might expect from one large herd. Wildlife are not so constrained. We can control bse through feed transission pretty easily but if it EVER goes from wildlife to cattle, we are in big, big trouble.
 

Murgen

Well-known member
With nothing known about these two cases and the manner in which they may be spread, what does this do to the confidence of the export market for American Beef?

This may just hold up the US border opening to trade for awhile yet!
 

Murgen

Well-known member
Reader, exactly, the USDA has not been totally honest in respects to BSE from the get go. Can this "new strain" be passed along by urine, that's kind of what the article implys might be a possibility!

How will the OIE regard risk now, with a strain, that nothing is known about? Time to rewrite the rules again.
 

Mike

Well-known member
This revelation throws the new report by the USDA on the estimated number of cases in the USA completely out the window.

Anybody wanna bet that they still use it as the "Gospel"? (Even after the "bought-off" peer review company approves it.)
 

Tam

Well-known member
Mike said:
Tam said:
What I wonder is does their spontaneous strain affect organically grown cattle or does it just affect those that have been fed ruminant laced feed? :?

All "Spontaneous" means is that they do not know the source of infection.

The "Atypical" is different in that the vacuoles (holes) in the brain caused by the prions are not visible. (The method employed by IHC, the old style tests.)

The rapid tests and the Western Blot pick up these cases because they are actually finding the mis-folded prions.

Wonder how many others we have had that were undetected with IHC?

The Japs know this full well. They are hesitant because of the incompetency of the USDA.

If Spontaneous means "they do not know the source of infection", then I will bet any and all US cases will be ruled "spontaneous". Since Atypical US investigation ends with no real results. :wink:
 

Econ101

Well-known member
Tam said:
Mike said:
Tam said:
What I wonder is does their spontaneous strain affect organically grown cattle or does it just affect those that have been fed ruminant laced feed? :?

All "Spontaneous" means is that they do not know the source of infection.

The "Atypical" is different in that the vacuoles (holes) in the brain caused by the prions are not visible. (The method employed by IHC, the old style tests.)

The rapid tests and the Western Blot pick up these cases because they are actually finding the mis-folded prions.

Wonder how many others we have had that were undetected with IHC?

The Japs know this full well. They are hesitant because of the incompetency of the USDA.

If Spontaneous means "they do not know the source of infection", then I will bet any and all US cases will be ruled "spontaneous". Since Atypical US investigation ends with no real results. :wink:

You are probably right about that one Tam.
 

Tam

Well-known member
Econ101 said:
Tam said:
Mike said:
All "Spontaneous" means is that they do not know the source of infection.

The "Atypical" is different in that the vacuoles (holes) in the brain caused by the prions are not visible. (The method employed by IHC, the old style tests.)

The rapid tests and the Western Blot pick up these cases because they are actually finding the mis-folded prions.

Wonder how many others we have had that were undetected with IHC?

The Japs know this full well. They are hesitant because of the incompetency of the USDA.

If Spontaneous means "they do not know the source of infection", then I will bet any and all US cases will be ruled "spontaneous". Since Atypical US investigation ends with no real results. :wink:

You are probably right about that one Tam.

Don't get me wrong eCON I don't think the USDA is fully to blame for the lack of answers. As if the US beef Industry would do their part and ID their cattle then just maybe the USDA would have half a chance in ending an investigation with some answers. But until then all the US cases will be SPONTANEOUS AS IN UNKNOWN SOURCE.
 
Top