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flounder
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Joined: 03 Sep 2005
Posts: 1700
Location: TEXAS
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 Posted: Sat Mar 08, 2008 9:33 am Post subject: Calif. meat worker: I was following orders |
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Calif. meat worker: I was following orders
ADELANTO, Calif. (AP) — A former slaughterhouse worker who was videotaped abusing ailing cattle in a case that led to the largest beef recall in U.S. history said in a jailhouse interview that he was only following orders.
Luis Sanchez said he felt bad when he saw how the cows were treated at Chino-based Westland/Hallmark Meat Co., and insisted his boss taught him to use a forklift to move so-called downer cows along the slaughter line.
HISTORIC RECALL: Meat plant concerns raised for years
LEGAL LOOPHOLE: Government sued over ailing cattle
"That's how I was taught. He taught me to do the work. I didn't know it was a serious crime," Sanchez told the San Bernardino Sun in an interview published Friday.
Sanchez, an illegal immigrant from Mexico, was being held at the Adelanto Detention Center on immigration charges. He was charged with animal cruelty in the slaughterhouse case, but he also faced charges in two unrelated drug cases.
Sanchez's ex-boss, Daniel Ugarte Navarro, 49, has pleaded not guilty to five felony counts of animal abuse and three misdemeanor counts of illegal movement of a non-ambulatory animal. The counts carry a maximum prison sentence of 5 years, 8 months, prosecutors have said.
Navarro will be assigned an attorney by the county public defender's office at his March 24 arraignment.
Last month, the Agriculture Department issued the recall after the Humane Society of the United States released undercover video of workers forcing sick and crippled cows to stand with electric prods and forklifts.
Sanchez appeared in the video using an electric prod.
Sanchez said he learned the company was handling the cows differently than other slaughterhouses from truck drivers who brought the animals to the plant. He said his supervisor told the workers to use care when federal inspectors were around.
Sanchez, who first came to the slaughterhouse about 10 years ago, said he doesn't understand why he's in jail.
"I think it's unjust that I'm here. Where are the people in charge?" he told the newspaper.
Copyright 2008 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
http://www.usatoday.com/money/industries/food/2008-03-08-slaughterhouse-abuse_N.htm
> Calif. meat worker: I was following orders
no doubt! i believe the guy, and i believe this practice of allowing downers into the food supply is wide spread.
here is just one more example $$$
Originally posted by worried about the industry
If the sick cattle don't get into the cooler how can anybody make a profit?
It is people like you that will cause the beef industry to colapse with your attitude. Get real.
And if you believe as you say I hope you get the first bite of that sick animal.
--------------------------------------------------------------------------------
3/6/2008 1:46 PM Posted By: GW
=====================================================snip...end...TSS
YOU REALLY DON'T THINK that all these downers are just buried $$$
Animal Mortality Figures
The U.S. Department of Agriculture (USDA) estimates 1.7103 million cattle
and 2.3656 million calves died prior to slaughter in 2002, for a total of
just under 4.1 million deaths.
snip...
Cattle, however, with their heavier body weights, comprise approximately 67
percent of the total weight of all mammalian livestock mortalities. In 2002,
the total weight for cattle was 2.7 billion pounds. Beef cattle account for
the largest proportion of farm, ranch, and feedlot mortality, in respect to
weight.
snip...
Focus on Non-Ambulatory Cattle
Non-ambulatory cattle have been estimated by USDA to be approximately
200,000 head per year based on a 1999 American Association of Bovine
Practitioners survey.(2) It is proposed that this estimate understates the
condition by not fully accounting for feedlot cattle of younger ages
commonly affected with metabolic and or respiratory disorders that often
present neurological-like clinical symptoms and thus described as
non-ambulatory. It is impossible to give accurate figures on incidence
because of variations in nomenclature and the accuracy of diagnosis. Because
it is a syndrome until an accurate diagnosis is confirmed, the exact
incidence is speculative.
http://www.rendermagazine.com/October2004/TechTopics.html
MARCH 2002
Livestock Mortalities:
Methods of Disposal and Their
Potential Costs
USDA/National Agricultural Statistics Service (NASS) estimates that in the
year 2000,
approximately 4.1 million cattle died before they could be sent to slaughter
(Table 2). Of these, 2.4 million were calves (under 500 lbs), with the
balance of 1.7 million over 6 months of age (or, as reported, in excess of
500 lbs). ....END...TSS
NASS
Non-Ambulatory
Cattle and Calves
Released May 5, 2005, by the National Agricultural Statistics Service
(NASS), Agricultural Statistics Board, U.S. Department
of Agriculture. For information on Non-ambulatory Cattle and Calves call
Mike Miller at 720-3040, office hours 7:30 a.m. to
4:30 p.m. ET.
Cattle and Calves: Non-Ambulatory Number,
by Region and United States, 2003-2004
ALL CATTLE 2003 = 465,000
ALL CATTLE 2004 = 450,000
SNIP...END...TSS
Non-Ambulatory
Cattle and Calves
Released May 5, 2005, by the National Agricultural Statistics Service
(NASS), Agricultural Statistics Board, U.S. Department
of Agriculture. For information on Non-ambulatory Cattle and Calves call
Mike Miller at 720-3040, office hours 7:30 a.m. to
4:30 p.m. ET.
Non-Ambulatory Cattle and Calves
Non-ambulatory cattle and calves in the United States totaled 465,000 head
during 2003 and
450,000 head during 2004. The number of non-ambulatory cattle 500 pounds or
greater totaled
280,000 head in 2003 and 270,000 head in 2004. The number of calves under
500 pounds reported
as non-ambulatory totaled 185,000 head in 2003 and 180,000 head in 2004.
...SNIP...END...TSS
Friday, March 7, 2008
USDA QUESTIONS AND ANSWERS HALLMARK/WESTLAND MEAT PACKING CO. March 6, 2008
QUESTIONS AND ANSWERS HALLMARK/WESTLAND MEAT PACKING CO.
March 6, 2008
Consumer Concerns
Q. My child/school recently consumed Hallmark/Westland products. What is the
risk to children's health?
SEE FULL TEXT ;
http://downercattle.blogspot.com/2008/03/usda-questions-and-answers.html
Wednesday, February 27, 2008
BEEF RECALL NATIONWIDE - SCHOOL LUNCH PROGRAM UPDATE
http://downercattle.blogspot.com/2008/02/beef-recall-nationwide-school-lunch.html
Thursday, March 6, 2008
California lists possible recipients of recalled non-ambulatory 'DOWNER'
(high potential for TSE) Hallmark beef
http://downercattle.blogspot.com/2008/03/california-lists-possible-recipients-of.html
Thursday, March 6, 2008
House committee subpoenas Hallmark/Westland CEO - i call for an
investigation of the investigators
http://downercattle.blogspot.com/2008/03/house-committee-subpoenas.html
Thursday, March 6, 2008
USDA to Hallmark: We want our plaque back
Legal/Regulatory News
http://downercattle.blogspot.com/2008/03/usda-to-hallmark-we-want-our-plaque.html
Thursday, March 6, 2008
To the hard working employees of USDA and their untiring efforts to protect
our childrens food supply
http://downercattle.blogspot.com/2008/03/to-hard-working-employees-of-usda-and.html
In this context, a word is in order about the US testing program. After the
discovery of the first (imported) cow in 2003, the magnitude of testing was
much increased, reaching a level of >400,000 tests in 2005 (Figure 4).
Neither of the 2 more recently indigenously infected older animals with
nonspecific clinical features would have been detected without such testing,
and neither would have been identified as atypical without confirmatory
Western blots. Despite these facts, surveillance has now been decimated to
40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and
invites the accusation that the United States will never know the true
status of its involvement with BSE.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy
detailed critiques and recommendations to both the USDA and the Canadian
Food
Agency."
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125
3/6/2008
i call for an investigation of the investigators
>>>House committee subpoenas Hallmark/Westland CEO The subpoena orders him
to testify at a March 12 hearing titled "Regulatory Failure: Must America
Live With Unsafe Food?"<<<
what a hoot. the ones that should be subpoenad and held accountable are the
very ones on the committee. they have failed the public for years about BSE
risk and regulations. the very people that are going to investigate this
thing are the very folks responsible for all the children and elderly that
were exposed to the potential of mad cow via non-ambulatory i.e. DOWNERS,
the most likely to have a TSE. waxman et al have been claiming to be
concerned about BSE aka mad cow disease's and one issue was the
non-ambulatory 'downer' cattle, and i quote waxman;
Failure To Test Staggering Cow May Reflect Wider Problems Rep. Waxman raises
concerns that the recent failure of USDA to test an impaired cow for BSE may
not be an isolated incident, citing the failure of USDA to monitor whether
cows condemned for central nervous system symptoms are actually tested for
mad cow disease.
http://reform.democrats.house.gov/documents/20040607142914-86912.pdf
http://oversight.house.gov/documents/20040607142914-86912.pdf
folks, that was in 2004. why, in 2008, why are we still discussing the same failures$$$
THE PEOPLE BELOW SHOULD ALL BE SUBPOENAED AS WELL FOR THEIR CONTINUED
FAILURES TO PROTECT THE CONSUMER FROM MAD COW DISEASE. and i call for an
investigation of the investigators below. why in 2008 are we still floundering$$$
Committee on Energy and Commerce Subcommittee on Oversight and Investigations
http://energycommerce.house.gov/Subcommittees/ovin.shtml
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
Specified Risk Material SRM
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
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Oldtimer
Rancher
Joined: 10 Feb 2005
Posts: 15895
Location: Northeast Montana
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| Posted: Tue Mar 11, 2008 1:01 pm Post subject: |
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Oversight 'Flaw' Led to Meat Recall
Lax Monitoring Seen
At Plant's Cattle Pens
Before Closure
By DAVID KESMODEL
March 11, 2008; Page B1
Chino, Calif.
Steve Mendell poured millions of dollars into stainless-steel paneling and state-of-the art cleaning systems to upgrade the decades-old meatpacking plant he has run since the late 1990s. But while Mr. Mendell focused his attention on the inside of the five-acre plant, he and other top executives at Hallmark/Westland Meat Packing Co. spent little time monitoring the facility's outdoor cattle pens, plant employees say.
---------------------
The recall also has pointed a spotlight at the Department of Agriculture, which assigns full-time government inspectors to monitor safety at meat-packing plants. Lawmakers and consumer groups have criticized the department for failing to catch problems at the slaughterhouse. The USDA has suspended three employees pending the outcome of an agency investigation. One of them was the plant's supervising veterinarian, Gabriel Gurango, who worked on site for 20 years.
Dr. Gurango "did not spend a great deal of time" in the cattle pens because he was responsible for so many other duties, many of them inside the plant, says William G. Hughes, general counsel for the National Association of Federal Veterinarians, who is advising Dr. Gurango. Mr. Hughes contends the USDA didn't have enough inspectors on hand to monitor food safety at the plant. A USDA spokeswoman says the plant was "fully staffed" with five inspectors.
Dr. Gurango, a 68-year-old USDA veterinarian who oversaw four inspectors at the plant, was in the cattle pens twice daily, at 6:30 a.m. and 12:30 p.m., the undercover Humane Society worker told police. When a government inspector was present, Mr. Navarro would tone down his methods for trying to get cows to stand up, the Humane Society worker told police.
Full story:
http://online.wsj.com/article/SB120520382464126297.html?mod=googlenews_wsj |
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flounder
Rancher
Joined: 03 Sep 2005
Posts: 1700
Location: TEXAS
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| Posted: Tue Mar 11, 2008 2:14 pm Post subject: President of disgraced slaughterhouse taps high-profile advi |
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President of disgraced slaughterhouse taps high-profile adviser
Tuesday, March 11, 2008 1:48 PM CDT
GOP Rep. Asa Hutchinson of Arkansas, who has headed the Drug Enforcement Agency and served as the Homeland Security Department’s undersecretary for border and transportation security.
http://www.dailyamericannews.com/articles/2008/03/11/news/news10.txt
Asa Hutchinson (born December 3, 1950) is a former U.S. Attorney for the Fort Smith-based Western District of Arkansas, U.S. Congressman from the Third District of Arkansas, Director of the U.S. Drug Enforcement Administration and the first-ever Under Secretary for Border & Transportation Security at the U.S. Department of Homeland Security. In 2006, Hutchinson ran as Republican candidate for governor of Arkansas and lost to Democratic candidate Mike Beebe.
Contents [hide]
1 Legal career
2 Political career
2.1 U.S. Congress
2.2 Executive branch
2.3 2006 Governor's race
3 Business career
4 External links
Business career
In early 2005, Hutchinson founded a consulting firm, Hutchinson Group, LLC with partners Betty Guhman and Kirk Tompkins, in Little Rock and accepted a contract for a one-year position with the Venable Law Firm in Washington, D.C., as the chair of its Homeland Security practice. Hutchinson ended his contract with Venable in March 2006 to focus on his gubernatorial campaign and his consulting firm in Little Rock.
In June 2006, the Arkansas Democrat Gazette reported that Hutchinson's $2,800 investment in Fortress America Acquisition Corporation, a company that Hutchinson advises, was worth over a million dollars after the initial public offering. The Arkansas Democrat Gazette story noted that Hutchinson is unable to touch his stock for another two years. The six founding shareholders in Fortress America besides Hutchinson include: former U.S. Representative Tom McMillen of Maryland, former U.S. Senator Don Nickles of Oklahoma, and a private-equity firm that has former CIA Director James Woolsey among its partners.
On May 4, 2006, Hutchinson filed a financial disclosure form, which he was required to submit as candidate for governor, that did not include the Fortress American holdings. On the form, Hutchinson listed his stock and options in two other companies, and even disclosed bank and credit-union accounts with balances under $1,000. He did not list his 200,000 shares in Fortress America, which were trading at about $5 per share. "Just totally an oversight," Hutchinson said when questioned by the media. [6]. Hutchinson filed an amended report the next day to correct the error. [7]
http://en.wikipedia.org/wiki/Asa_Hutchinson
TSS
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flounder
Rancher
Joined: 03 Sep 2005
Posts: 1700
Location: TEXAS
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| Posted: Tue Mar 11, 2008 2:19 pm Post subject: |
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| Oldtimer wrote: |
| Quote: |
Oversight 'Flaw' Led to Meat Recall
Lax Monitoring Seen
At Plant's Cattle Pens
Before Closure
By DAVID KESMODEL
March 11, 2008; Page B1
Chino, Calif.
Steve Mendell poured millions of dollars into stainless-steel paneling and state-of-the art cleaning systems to upgrade the decades-old meatpacking plant he has run since the late 1990s. But while Mr. Mendell focused his attention on the inside of the five-acre plant, he and other top executives at Hallmark/Westland Meat Packing Co. spent little time monitoring the facility's outdoor cattle pens, plant employees say.
---------------------
The recall also has pointed a spotlight at the Department of Agriculture, which assigns full-time government inspectors to monitor safety at meat-packing plants. Lawmakers and consumer groups have criticized the department for failing to catch problems at the slaughterhouse. The USDA has suspended three employees pending the outcome of an agency investigation. One of them was the plant's supervising veterinarian, Gabriel Gurango, who worked on site for 20 years.
Dr. Gurango "did not spend a great deal of time" in the cattle pens because he was responsible for so many other duties, many of them inside the plant, says William G. Hughes, general counsel for the National Association of Federal Veterinarians, who is advising Dr. Gurango. Mr. Hughes contends the USDA didn't have enough inspectors on hand to monitor food safety at the plant. A USDA spokeswoman says the plant was "fully staffed" with five inspectors.
Dr. Gurango, a 68-year-old USDA veterinarian who oversaw four inspectors at the plant, was in the cattle pens twice daily, at 6:30 a.m. and 12:30 p.m., the undercover Humane Society worker told police. When a government inspector was present, Mr. Navarro would tone down his methods for trying to get cows to stand up, the Humane Society worker told police.
Full story:
http://online.wsj.com/article/SB120520382464126297.html?mod=googlenews_wsj |
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----- Original Message -----
From: "Terry S. Singeltary Sr." <flounder9@verizon.net>
To: <david.kesmodel@wsj.com>
Sent: Tuesday, March 11, 2008 1:04 PM
Subject: re-Oversight 'Flaw' Led to Meat Recall
re-Oversight 'Flaw' Led to Meat Recall
http://online.wsj.com/article/SB120520382464126297.html?mod=googlenews_wsj
for your info david. it was more than just 'oversight flaw'.
it's what i call corporate and political homicide, i.e. 'for profit',
due to incubation period for TSE, officials have decided we are ALL,
expendable.
for what it's worth, i have followed this nightmare for over a decade,
daily. for various reasons, i am vested in nothing but the truth.
and the truth my friend, none of us have been told. but here is what
i have come to know. i hope you take the time to read all of it.
the chino plant is but the tip of the iceberg.............
thank you.......
kind regards,
terry
FSIS NOTICE
17-08
3/10/08
DISTRIBUTION: Electronic
NOTICE EXPIRES: 4/1/09 OPI: OPPD
INCREASED VERIFICATION OF HUMANE HANDLING REQUIREMENTS IN LIVESTOCK
SLAUGHTER ESTABLISHMENTS
http://www.fsis.usda.gov/OPPDE/rdad/FSISNotices/17-08.pdf
FSIS NOTICE
16-08
3/10/08
DISTRIBUTION: Electronic
NOTICE EXPIRES: 4/1/09 OPI: OPPD
HUMANE HANDLING ACTIVITIES AND DOCUMENTATION IN LIVESTOCK SLAUGHTER
ESTABLISHMENTS
http://www.fsis.usda.gov/OPPDE/rdad/FSISNotices/16-08.pdf
not a word about all the children exposed to the most high risk animal for
mad cow disease i.e. non-ambulatory downers. not a word.
TO THE CHILDREN OF THE USDA CERTIFIED NON-AMBULATORY DOWNER COW SCHOOL LUNCH PROGRAM.
out of sight, out of mind. possibly literally in anywhere from 16 years to
22 years i.e. incubation period for nvCJD in children.
God bless America, and all the industries that control it now. ...TSS
Science 23 November 2001:
Vol. 294. no. 5547, pp. 1726 - 1728
DOI: 10.1126/science.1066838
Reports
Estimation of Epidemic Size and Incubation Time Based on Age Characteristics
of vCJD in the United Kingdom
Alain-Jacques Valleron,1 Pierre-Yves Boelle,1 Robert Will,2 Jean-Yves
Cesbron3
SNIP...
The distribution of the vCJD incubation period that best fits the data
within the framework of our model has a mean of 16.7 years, with a standard deviation of 2.6 years. The 95% upper percentile of this distribution is 21.4 years. The 95% confidence interval (CI) of the estimates of the mean and standard deviation is relatively narrow: The 95% CI for the estimate of the mean incubation period is 12.4 to 23.2 years, and the 95% CI of the standard deviation is 0.9 to 8 years (10). The decrease in susceptibility to infection in exposed subjects older than 15 years, as estimated from the parameter , was found to be very sharp: 16% per year of age (CI: 12 to 23%). This means that, under the best fitting hypothesis, an individual aged 20 years in 1981 had 55% less risk of becoming infected than a child aged 15 years (99.9% for an individual aged 70).
http://www.sciencemag.org/
NOW, the price of poker in the USA may be shorter, due to the fact the
strain of mad cow disease in the USA (h-BASE) is more virulent to humans,
thus, the incubation period, for the same titre log of infectivity, via same
route and source, might be faster. ...TSS
Audit Report
Animal and Plant Health Inspection Service
Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II
and
Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
Our prior report identified a number of inherent problems in identifying and
testing high-risk cattle. We reported that the challenges in identifying the
universe of high-risk cattle, as well as the need to design procedures to
obtain an appropriate representation of samples, was critical to the success
of the BSE surveillance program. The surveillance program was designed to
target nonambulatory cattle, cattle showing signs of CNS disease (including
cattle testing negative for rabies), cattle showing signs not inconsistent
with BSE, and dead cattle. Although APHIS designed procedures to ensure FSIS
condemned cattle were sampled and made a concerted effort for outreach to
obtain targeted samples, industry practices not considered in the design of
the surveillance program reduced assurance that targeted animals were tested
for BSE.
USDA/OIG-A/50601-10-KC Page 27
observe these animals ante mortem when possible to assure the animals from
the target population are ultimately sampled and the clinical signs
evaluated.
snip...
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
GAO-05-51 October 2004 FOOD SAFETY
over 500 customers receiving potentially BSE contaminated beef .....
* GAO-05-51 October 2004 FOOD SAFETY (over 500 customers receiving
potentially BSE contaminated beef) - TSS 10/20/04
October 2004 FOOD SAFETY
USDA and FDA Need
to Better Ensure
Prompt and Complete
Recalls of Potentially
Unsafe Food
snip...
REPORTS
1. Food Safety: USDA and FDA Need to Better Ensure Prompt and Complete
Recalls of Potentially Unsafe Food. GAO-05-51, October 7.tss
http://www.gao.gov/new.items/d0551.pdf
Highlights -
http://www.gao.gov/highlights/d0551high.pdf
SADLY, DEC 2005 SHOWS THAT WE STILL HAVE A SERIOUS PROBLEM WITH BSE/TSE MAD
COW DISEASE FEED
GAO
GAO-06-157R FDA Feed Testing Program
October 11, 2005
SNIP...FULL TEXT 29 PAGES ;
http://www.gao.gov/new.items/d06157r.pdf
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/
MAD COW FEED IN COMMERCE USA
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
snip...end...TSS
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Shaft
Member
Joined: 14 Feb 2008
Posts: 100
Location: The Big Smoke
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| Posted: Tue Mar 11, 2008 5:54 pm Post subject: |
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| Quote: |
| NOW, the price of poker in the USA may be shorter, due to the fact the strain of mad cow disease in the USA (h-BASE) is more virulent to humans, thus, the incubation period, for the same titre log of infectivity, via same route and source, might be faster. ...TSS |
Terry,
You keep saying that H type BSE is more virulent to humans, but the only articles I have seen that indicate increased virulence in apes and/or mice refer very specifically to L type BSE (BASE).
Do you have any references for your assertion that H type BSE is more virulent to humans?
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flounder
Rancher
Joined: 03 Sep 2005
Posts: 1700
Location: TEXAS
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| Posted: Tue Mar 11, 2008 8:00 pm Post subject: |
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| Shaft wrote: |
| Quote: |
| NOW, the price of poker in the USA may be shorter, due to the fact the strain of mad cow disease in the USA (h-BASE) is more virulent to humans, thus, the incubation period, for the same titre log of infectivity, via same route and source, might be faster. ...TSS |
Terry,
You keep saying that H type BSE is more virulent to humans, but the only articles I have seen that indicate increased virulence in apes and/or mice refer very specifically to L type BSE (BASE).
Do you have any references for your assertion that H type BSE is more virulent to humans? |
howdy shaft,
now this gets complicated friend, and i thhhink you are more educated on
the TSE issues than you put out to be. and i ttthink that is a good thing?
not sure what kind of player your are? and i dont know where the big
smoke is. course, i dont goes anywhere either. doesn't matter though.
but it really gets complicated, so ppplease pay close attention.
seems to be a conflict of interest........OOOOPS, i mean 'science'
between most scientists around the world and Gambetti et al at case western
on classification differential on the sporadic CJDs. so please read carefully.
then read what deepthroat told me many moons ago, now this was in 2000-2001ish.
you just can't have your cake, and eat your ice cream too ;-) and i think you will
get the picture i have painted. also, as you know, i have never been one to keep
things short, but i have tried lately. anyway, to answer your question, here goes...
i first became aware here ;
3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit
Hall
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse
Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University
Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years. ***These results indicate that BASE is
transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.
6:30 Close of Day One
http://www.healthtech.com/2007/tse/day1.asp
then, seems everyone was writing that the BASE was very similar to some subtypes
of sporadic CJD, and GSS, pathologically. you have seen those studies i have posted
here. and then Gambetti comes out with this just last month. well, actually it came out
today, but i had it a month or so ago. but theres a twist. there always is, but confusious
may be on to something. ... kind regards, terry
J. Virol. doi:10.1128/JVI.02561-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed
Authors/Institutions. All Rights Reserved.
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform
Encephalopathy Prion Strain
These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic.
http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc
see full text ;
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html
i am reminded of a few things deep throat told me years ago. these are snips from several emails,
but i had to take some stuff out. ...terry
============================================================
2000 - 2001
The most frightening thing I have read all day is the report of Gambetti's
finding of a new strain of sporadic cjd in young people......... Dear God,
what in the name of all that is holy is that!!! If the US has different
strains of scrapie.....why???? than the UK... then would the same mechanisms
that make different strains of scrapie here make different strains of BSE...
if the patterns are different in sheep and mice for scrapie..... could not
the BSE be different in the cattle, in the mink, in the humans....... I
really think the slides or tissues and everything from these young people
with the new strain of sporadic cjd should be put up to be analyzed by many,
many experts in cjd........ bse..... scrapie Scrape the damn slide and put
it into mice..... wait..... chop up the mouse brain and and spinal
cord........ put into some more mice..... dammit amplify the thing and start
the damned research..... This is NOT rocket science... we need to use what
we know and get off our butts and move.... the whining about how long
everything takes..... well it takes a whole lot longer if you whine for a
year and then start the research!!! Not sure where I read this but it was a
recent press release or something like that: I thought I would fall out of
my chair when I read about how there was no worry about infectivity from a
histopath slide or tissues because they are preserved in formic acid, or
formalin or formaldehyde..... for God's sake........ Ask any pathologist in
the UK what the brain tissues in the formalin looks like after a year.......
it is a big fat sponge... the agent continues to eat the brain ...... you
can't make slides anymore because the agent has never stopped........ and
the old slides that are stained with Hemolysin and Eosin...... they get
holier and holier and degenerate and continue... what you looked at 6 months
ago is not there........ Gambetti better be photographing every damned thing
he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come of
it and there is not a damned thing anyone can do about it. Don't even hint
at it as it will be denied and laughed at.......... USDA is gonna do as
little as possible until there is actually a human case in the USA of the
nvcjd........ if you want to move this thing along and shake the earth....
then we gotta get the victims families to make sure whoever is doing the
autopsy is credible, trustworthy, and a saint with the courage of Joan of
Arc........ I am not kidding!!!! so, unless we get a human death from
EXACTLY the same form with EXACTLY the same histopath lesions as seen in the
UK nvcjd........ forget any action........ it is ALL gonna be sporadic!!!
And, if there is a case....... there is gonna be every effort to link it to
international travel, international food, etc. etc. etc. etc. etc. They will
go so far as to find out if a sex partner had ever traveled to the
UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted
journey to the truth. They have all the cards, all the money, and are
willing to threaten and carry out those threats.... and this may be their
biggest downfall...
Thanks as always for your help. (Recently had a very startling revelation
from a rather senior person in government here.......... knocked me out of
my chair........ you must keep pushing. If I was a power person.... I would
be demanding that there be a least a million bovine tested as soon as
possible and agressively seeking this disease. The big players are coming
out of the woodwork as there is money to be made!!! In short: "FIRE AT
WILL"!!! for the very dumb.... who's "will"! " Will be the burden to bare if
there is any coverup!"
again it was said years ago and it should be taken seriously.... BSE will
NEVER be found in theUS! As for the BSE conference call... I think you did
agreat service to freedom of information and making some people feign
integrity... I find it scary to see that most of the "experts" are employed
by the federal government or are supported on the "teat" of federal funds. A
scary picture! I hope there is a confidential panel organized by the new
government to really investigate this thing.
You need to watch your back........ but keep picking at them....... like a
buzzard to the bone... you just may get to the truth!!! (You probably have
more support than you know. Too many people are afraid to show you or let
anyone else know. I have heard a few things myself... you ask the questions
that everyone else is too afraid to ask.)
======================================
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/creutzfeldt-jakob-disease-delaware.html
Subject: U.S.A. - 50 STATE BSE CONFERENCE CALL JAN. 9, 2001 (my notes)
Date: January 10, 2001 at 1:36 pm PST
Subject:
BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date:
Tue, 9 Jan 2001 16:49:00 -0800
From:
"Terry S. Singeltary Sr."
Reply-To:
Bovine Spongiform Encephalopathy
To:
BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Greetings List Members,
I was lucky enough to sit in on this BSE conference
call today and even managed to ask a question.
that is when the trouble started.
I submitted a version of my notes to
Sandra Blakeslee of the New York Times,
whom seemed very upset, and rightly
so.
"They tell me it is a closed meeting and
they will release whatever information
they deem fit. Rather infuriating."
and i would have been doing just fine,
until i asked my question. i was surprised
my time to ask a question so quick.
(understand, these are taken from my notes for now.
the spelling of names and such could be off.)
[host Richard Barns]
and now a question from Terry S. Singeltary of
CJD Watch.
[TSS]
yes, thank you,
U.S. cattle, what kind of guarantee can you
give for serum or tissue donor herds?
[no answer, you could hear in the back ground,
mumbling and 'we can't. have him ask the question
again.]
[host Richard]
could you repeat the question?
[TSS]
U.S. cattle, what kind of guarantee can you
give for serum or tissue donor herds?
[not sure whom ask this]
what group are you with?
[TSS]
CJD Watch, my Mom died from hvCJD and we are
tracking CJD world-wide.
[not sure who is speaking]
could you please disconnect Mr. Singeltary
[TSS]
you are not going to answer my question?
[not sure whom speaking]
NO
from this point, i was still connected, got to listen
and tape the whole conference. at one point someone
came on, a woman, and ask again;
[unknown woman]
what group are you with?
[TSS]
CJD Watch and my Mom died from hvCJD
we are trying to tract down CJD and other
human TSE's world wide. i was invited to
sit in on this from someone inside the USDA/APHIS
and that is why i am here. do you intend on banning
me from this conference now?
at this point the conference was turned back up,
and i got to finish listening. They never answered
or even addressed my one question, or even addressed
the issue. BUT, i will try and give you a run-down
for now, of the conference.
IF i were another Country, I would take heed to my
notes, BUT PLEASE do not depend on them. ask for
transcript from;
RBARNS@ORA.FDA.GOV
301-827-6906
he would be glad to give you one ;-)
Rockville Maryland,
Richard Barns Host
BSE issues in the U.S.,
How they were labelling ruminant feed?
Revising issues.
The conference opened up with the explaining of
the U.K. BSE epidemic winding down with about 30
cases a week.
although new cases in other countries were now
appearing.
Look at Germany whom said NO BSE and now have BSE.
BSE increasing across Europe.
Because of Temporary Ban on certain rendered product,
heightened interest in U.S.
A recent statement in Washington Post, said the
New Administration (old GW) has a list of issues.
BSE is one of the issues.
BSE Risk is still low, minimal in U.S. with a greater
interest in MBM not to enter U.S.
HOWEVER, if BSE were to enter the U.S.
it would be economically disastrous
to the render, feed, cattle, industries,
and for human health.
(human health-they just threw that in cause i was listening. I will now
jot down some figures in
which they told you, 'no need to write them down'.
just hope i have them correct. hmmm, maybe i hope
i don't ???)
80% inspection of rendering
*Problem-Complete coverage of rendering HAS NOT
occurred.
sizeable number of 1st time FAILED INITIAL INSPECTION,
have not been reinspected (70% to 80%).
Compliance critical, Compliance poor in U.K.
and other European Firms.
Gloria Dunason
Major Assignment 1998 goal TOTAL compliance.
This _did not_ occur. Mixed level of compliance,
depending on firm.
Rendering FDA license and NON FDA license
system in place for home rendering & feed
76% in compliance
79% cross contamination
21% DID NOT have system
92% record keeping
less than 60% total compliance
279 inspectors
185 handling prohibited materials
Renderer at top of pyramid, significant
part of compliance.
84% compliance
failed to have caution statement render
72% compliance & cross contamination
caution statement on feed, 'DO NOT FEED TO CATTLE'
56 FIRMS NEVER INSPECTED
1240 FDA license feed mills
846 inspected
"close to 400 feed mills have not been inspected"
80% compliance for feed.
10% don't have system.
NON-FDA licensed mills
There is NO inventory on non licensed mills.
approximately 6000 to 8000 Firms ???
4,344 ever inspected.
"FDA does not have a lot of experience with"
40% do NOT have caution statement 'DO NOT FEED'.
74% Commingling compliance
"This industry needs a lot of work and only half
gotten to"
"700 Firms that were falitive, and need to be
re-inspected, in addition to the 8,000 Firms."
Quote to do BSE inspection in 19 states by end
of January or 30 days, and other states 60 days.
to change feed status??? Contract check and ask
questions and pass info.
At this time, we will take questions.
[I was about the third or fourth to ask question.
then all B.S.eee broke loose, and i lost my train
of thought for a few minutes. picked back up here]
someone asking about nutritional supplements and
sourcing, did not get name. something about inspectors
not knowing of BSE risk??? the conference person assuring that Steve
Follum? and the TSE advisory Committee were
handling that.
Some other Dr. Vet, whom were asking questions
that did not know what to do???
[Dennis Wilson]
California Food Agr.
Imports, are they looking at imports?
[Conference person]
they are looking at imports,
FDA issued imports Bulletin.
[Linda Singeltary ??? this was a another phone in
question, not related i don't think]
Why do we have non-licensed facilities?
(conference person)
other feed mills do not handle as potent drugs???
Dennis Blank, Ken Jackson
licensed 400
non FDA 4400 inspected of a total of 6000 to 8000,
(they really don't know how many non licensed Firms
in U.S. they guess 6000 to 8000??? TSS)
Linda Detwiler
asking everyone (me) not to use emergency BSE number,
unless last resort.
(i thought of calling them today, and reporting the
whole damn U.S. cattle herd ;-) 'not'
Warren-Maryland Dept. Agr.
Prudent to re-inspect after 3 years.
concerned of Firms that have changed
owners.
THE END
TSS
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
http://www.microbes.info/forums/index.php?showtopic=377
FROM New York TIMES
Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...
Date: Thu, 11 Jan 2001 22:02:47 -0700
From: "Sandy Blakeslee"
To: "Terry S. Singeltary Sr."
References: 1
Hi terry -- thanks for all your help. I know it made a difference with the FDA getting out that release.
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: Sent: Thursday, January 11, 2001 2:06 PM
Subject: BSE 50 STATE CONFERENCE CALL thread
from BSE List and FDA Posting of cut version...
> > hi sandy,
>From the New York Times
NYTimes.com,
January 11, 2001
Many Makers of Feed Fail to Heed Rules on Mad Cow Disease
By SANDRA BLAKESLEE
Large numbers of companies involved in manufacturing animal feed are not complying with regulations meant to prevent the emergence and spread of mad cow disease in the United States, the Food and Drug Administration said yesterday. The widespread failure of companies to follow the regulations, adopted in August 1997, does not mean that the American food supply is unsafe, Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at the F.D.A., said in an interview. But much more needs to be done to ensure that mad cow disease does not arise in this country, Dr. Sundlof said. The regulations state that feed manufacturers and companies that render slaughtered animals into useful products generally may not feed mammals to cud-chewing animals, or ruminants, which can carry mad cow disease. All products that contain rendered cattle or sheep must have a label that says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers must also have a system to prevent ruminant products from being commingled with other rendered material like that from chicken, fish or pork. Finally, all companies must keep records of where their products originated and where they were sold. Under the regulations, F.D.A. district offices and state veterinary offices were required to inspect all rendering plants and feed mills to make sure companies complied. But results issued yesterday demonstrate that more than three years later, different segments of the feed industry show varying levels of compliance. Among 180 large companies that render cattle and another ruminant, sheep, nearly a quarter were not properly labeling their products and did not have a system to prevent commingling, the F.D.A. said. And among 347 F.D.A.-licensed feed mills that handle ruminant materials - these tend to be large operators that mix drugs into their products - 20 percent were not using labels with the required caution statement, and 25 percent did not have a system to prevent commingling. Then there are some 6,000 to 8,000 feed mills so small they do not require F.D.A. licenses. They are nonetheless subject to the regulations, and of 1,593 small feed producers that handle ruminant material and have been inspected, 40 percent were not using approved labels and 25 percent had no system in place to prevent commingling. On the other hand, fewer than 10 percent of companies, big and small, were failing to comply with the record-keeping regulations. The American Feed Industry Association in Arlington, Va., did not return phone calls seeking comment.
http://www.nytimes.com/2001/01/11/science/11COW.html
Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL
Jan. 9, 2001
Date: Wed, 10 Jan 2001 14:04:21 -0500
From: "Gomez, Thomas M."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
USDA/APHIS would like to provide clarification on the following point from Mr. Singeltary's 9 Jan posting regarding the 50 state conference call. [Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not'] Dr. Detwiler was responding to an announcement made during the call to use the FDA emergency number if anyone wanted to report a cow with signs suspect for BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants to use the FDA emergency number as a last resort to report cattle suspect for BSE. What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement. Surveillance for BSE in the United States is a cooperative effort between states, producers, private veterinarians, veterinary hospitals and the USDA. The system has been in place for over 10 years. Each state has a system in place wherein cases are reported to either the State Veterinarian, the federal Veterinarian in Charge or through the veterinary diagnostic laboratory system. The states also have provisions with emergency numbers. Dr. Detwiler asked participants to use the systems currently in place to avoid the possibility of a BSE-suspect report falling through the cracks. Use of the FDA emergency number has not been established as a means to report diseased cattle of any nature.
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: Re: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan.9, 2001
Date: Wed, 10 Jan 2001 13:44:49 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de References: 1
######### Bovine Spongiform Encephalopathy #########
Hello Mr. Thomas,
> What Mr. Singeltary failed to do was provide
> the List with Dr. Detwiler's entire statement. would you and the USDA/APHIS be so kind as to supply this list with a full text version of the conference call and or post on your web-site? if so when, and thank you. if not, why not?
> The system has been in place for over 10 years. that seems to be a very long time for a system to be in place, and only test 10,700 cattle from some 1.5 BILLION head (including calf crop). Especially since French are testing some 20,000 weekly and the E.U. as a whole, are testing many many more than the U.S., with less cattle, same risk of BSE/TSEs. Why does the U.S. insist on not doing massive testing with the tests which the E.U. are using? Why is this, please explain? Please tell me why my question was not answered?
> U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds? It was a very simple question, a very important question, one that pertained to the topic of BSE/feed, and asked in a very diplomatic way. why was it not answered? If all these years, we have been hearing that pharmaceutical grade bovines were raised for pharmaceuticals vaccines etc. But yet the USA cannot comply with feed regulations of the ruminant feed ban, PLUS cannot even comply with the proper labelling of the feed, cross contamination etc. Then how in the world can you Guarantee the feed fed to pharmaceutical grade bovine, were actually non ruminant feed? Before i was ask to be 'disconnected', i did hear someone in the background say 'we can't'-- have him ask the question again. could you please be so kind, as to answer these questions?
thank you,
Terry S. Singeltary Sr.
Bacliff, Texas USA
P.S. if you will also notice, i did not post that emergency phone number and do not intend on passing it on to anyone. I was joking when i said i should call and report the whole damn U.S. Herd. So please pass that on to Dr. Detwiler, so she can rest easily. BUT, they should be reported, some are infected with TSE. The U.S. is just acting as stupid as Germany and other Countries that insist they are free of BSE. ...TSS
====================================================================
2008
confusious is confused again ;-)
omitting the hypothesis of a literal spontaneous happening for the BASE cases
there is absolutely no proof for a spontaneous TSE anywhere in the field.
some scientist are trying to claim now that the BASE cases arise spontaneously
like they claim the 85%+ of all cases of CJD are sporadic/spontaneous
without any cause. i prefer to believe in santa clause instead. there's more proof
for that.
aside from that myth ;
i keep hearing that these atypical BSE h-base and l-base, similar to
some subtypes of sporadic CJD and GSS pathologically, that these atypical
BSE BASE cases are just 'aged' BSE cases. SO, would it not be that what's
good for the goose is good for the gander i.e. sporadic CJDs are nothing more
than 'aged' nvCJD. i mean, if that hypothesis plays out with the 'aged' BSE=ing
BASEs in cows, why not humans. it's just all the same BSe. just 'aged' brains =
different pathology, different symptoms and such. it goes back to the old myth
with the first nvCJD 10 cases that only young kids with CJD have amyloid
kuru type plaques, until the elderly started showing up with them.
confusious just pondering out loud again. ...TSS
or these new phenotypes may be found, at least in part, to result from infections
at an older age by a typical BSE agent, rather than neonatal infections with new
"strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
SEAC unusual cases of BSE
http://www.seac.gov.uk/papers/96-2.pdf
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy
detailed critiques and recommendations to both the USDA and the Canadian
Food Agency."
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125
TSS
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Shaft
Member
Joined: 14 Feb 2008
Posts: 100
Location: The Big Smoke
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| Posted: Wed Mar 12, 2008 2:43 am Post subject: |
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Terry,
It appears that you are lumping H-type BSE in with L-type BSE. They are not the same. The term BASE refers only to L-type, not H-type.
"We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass."
"The two atypical BSE are identified as BASE (bovine amyloidotic spongiform encephalopathy) or L-type and H- type, respectively; the “L” and “H” identify the higher and lower electrophoretic positions of their protease-resistant PrPSc isoforms (7)."
"Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE... These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic."
"Two major patterns have been described, named L (resembling the original Italian case pattern with a lower molecular weight than typical BSE) and H (for a distinct pattern first seen in France with a higher molecular weight than typical BSE)."
"To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE."
So, while I agree that the data indicates that BASE may be more virulent in humans, I have yet to read any such allegation concerning H-type BSE. On the other hand, I also agree with Brown, Detwiler and Zanusso that the US testing program is wholly inadequate:
"In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE."
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flounder
Rancher
Joined: 03 Sep 2005
Posts: 1700
Location: TEXAS
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| Posted: Wed Mar 12, 2008 8:35 am Post subject: |
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| Shaft wrote: |
Terry,
It appears that you are lumping H-type BSE in with L-type BSE. They are not the same. The term BASE refers only to L-type, not H-type.
"We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass."
"The two atypical BSE are identified as BASE (bovine amyloidotic spongiform encephalopathy) or L-type and H- type, respectively; the “L” and “H” identify the higher and lower electrophoretic positions of their protease-resistant PrPSc isoforms (7)."
"Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE... These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic."
"Two major patterns have been described, named L (resembling the original Italian case pattern with a lower molecular weight than typical BSE) and H (for a distinct pattern first seen in France with a higher molecular weight than typical BSE)."
"To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE."
So, while I agree that the data indicates that BASE may be more virulent in humans, I have yet to read any such allegation concerning H-type BSE. On the other hand, I also agree with Brown, Detwiler and Zanusso that the US testing program is wholly inadequate:
"In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE." |
i disagree. base is base. then the break down to l and h. it plainly states you have typical bse, h-base, and l-base, 3 strains. why would they call it h-base if it was BSE ??? i disagree with you shaft. now, some of officials are trying to say that none of it is base, but just atypical bse. but if you read all the data, there are 3 seperate strains. call em what you like. ...tss
P02.35 Molecular Features of the Protease-resistant Prion Protein (PrPres)
in H- type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE- infected
cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres
molecular mass and decreased levels of the diglycosylated PrPres band, in
contrast to the classical type of BSE. This type is also distinct from
another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass.
Retrospective molecular studies in France of all available BSE cases older
than 8 years old and of part of the other cases identified since the
beginning of the exhaustive surveillance of the disease in 20001 allowed to
identify 7 H- type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1.
Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C- terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The
identification of these two additional PrPres fragments (PrPres #2 and 7kDa band)
*** reminds features reported respectively in sporadic Creutzfeldt-Jakob
disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
FC5.5.1 BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments
Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S3 1University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA
The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human prion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K- resistant prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1
of all genotypes,;
(ii) the second was found in M/M-2 (cortical form); (iii) the third in
amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) .
Recently, we showed that sCJD subtype M/V-2 shared molecular and
pathological features with an atypical form of BSE, named BASE, thus
suggesting a potential link between the two conditions. This connection was
further confirmed after 2D-PAGE analysis, which showed an identical PrPSc
signature, including the biochemical pattern of CTFs. To pursue this issue,
we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculated with brain homogenates from BASE. Samples were separated by using a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJD MV-2 subtype.
*** These data strongly support the link, or at least a common ancestry,
between a sCJD subtype and BASE.
This work was supported by Neuroprion (FOOD-CT-2004-506579)
FC5.5.2 Transmission of Italian BSE and BASE Isolates in Cattle Results into
a Typical BSE Phenotype and a Muscle Wasting Disease
Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2;
Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini,
M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1;
Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual
Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin,
Animal Pathology, Italy; 5Isituto Carlo Besta, Italy
The clinical phenotype of bovine spongiform encephalopathy has been
extensively reported in early accounts of the disorder. Following the
introduction of statutory active surveillance, almost all BSE cases have
been diagnosed on a pathological/molecular basis, in a pre-symptomatic
clinical stage. In recent years, the active surveillance system has
uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle
*** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob
disease.
Oral Abstracts 14
snip...
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie
Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute
for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was
titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this,
to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study,
animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
and i really think nor-98 is just bse in sheep. ...tss
Subject: Aspects of the Cerebellar Neuropathology in Nor98
Date: September 26, 2007 at 4:06 pm PST
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway
Nor98 is a prion disease of old sheep and goats. This atypical form of
scrapie was first described in Norway in 1998. Several features of Nor98
were shown to be different from classical scrapie including the distribution
of disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study
here presented aimed at adding information on the neuropathology in the
cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter.
*** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
full text ;
ATYPICAL NOR-98 SCRAPIE LOCATION UPDATE ON 5 DOCUMENTED CASES THIS YEAR ;
The flocks of origin are WY, CO, CA, IN, and MN.
personal communication USDA et al. ...TSS
http://nor-98.blogspot.com/
ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)
http://animalhealthreport2006.blogspot.com/
tss
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Shaft
Member
Joined: 14 Feb 2008
Posts: 100
Location: The Big Smoke
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| Posted: Wed Mar 12, 2008 10:16 am Post subject: |
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| Quote: |
| Western blot analyses of PrPres accumulating in the brain of BSE- infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. |
Terry,
The point of the piece is that BASE is indeed BASE, which refers strictly to L-type BSE not H-type BSE.
I think you may be confused by the anagram BASE itself which refers to Bovine Amyloid Spongiform Encephalopathy. It does not refer to (and never has) Bovine Atypical Spongiform Encephalopathy.
Why is this important, you may well ask? The answer is simple. In my experience the only way to foster change is to build a chorus of voices. While the lone voice crying from the wilderness may provide a level of self-satisfaction, it very rarely engenders change. To build that chorus you need credibility. Factual accuracy is critical in the credibility-building process.
If a USDA scientist, or anyone else for that matter, can say that Terry doesn't know what he is talking about, he can't even differentiate between H-type and BASE, it hurts your credibility.
So, I guess it comes down to what you are trying to accomplish.
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flounder
Rancher
Joined: 03 Sep 2005
Posts: 1700
Location: TEXAS
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| Posted: Wed Mar 12, 2008 1:53 pm Post subject: |
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| Shaft wrote: |
| Quote: |
| Western blot analyses of PrPres accumulating in the brain of BSE- infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. |
Terry,
The point of the piece is that BASE is indeed BASE, which refers strictly to L-type BSE not H-type BSE.
I think you may be confused by the anagram BASE itself which refers to Bovine Amyloid Spongiform Encephalopathy. It does not refer to (and never has) Bovine Atypical Spongiform Encephalopathy.
Why is this important, you may well ask? The answer is simple. In my experience the only way to foster change is to build a chorus of voices. While the lone voice crying from the wilderness may provide a level of self-satisfaction, it very rarely engenders change. To build that chorus you need credibility. Factual accuracy is critical in the credibility-building process.
If a USDA scientist, or anyone else for that matter, can say that Terry doesn't know what he is talking about, he can't even differentiate between H-type and BASE, it hurts your credibility.
So, I guess it comes down to what you are trying to accomplish. |
shaft, i understand your concern 
and i never pretended to be the sharpest knife in the drawer 
and i really don't think USDA et al are sitting around pondering what my credibility is. they know. 
there is and has been for a while a difference of opinion between scientists of the definition of atypical BSE and or BASE (also nvCJD and sporadic CJD's), a difference of opinions an or terminology of the science.
i don't agree with the diagnostic criteria's here between the h-bse l-bse and base (but that's besides the point). and, this old brain syndrome bse just does not compute. and if it does, then why not for sCJD as well?
i.e. atypical bse's = old BSE cases ...... nvCJD = old sporadic CJD cases.
i am reminded of what was said here ;
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
NOW, the studies i pointed out clearly speak of h-BASE, and l-BASE.
HOWEVER, what has happened shaft, is that the original BASE cases were not recognized by some, SO, goal posts were moved again. they have decided not to use that terminology, and it is now just atypical BSE h or l.
there is no BASE. its just h-BSE and or l-BSE. so, we are at what ever you want to call it, h-base or atypical h-BSE and l-base or atypical l-BSE. either way, h-base and or h-bse is MORE VIRULENT, which is what you original question was. ...tss
Atypical BSE: What is it and what is the significance
Linda A. Detwiler, Paul Brown, Lisa M. McShane, and Gianluigi Zanusso
For almost the entire two decades that BSE has been known in the world it was thought that there was only one “strain” that infected cattle and caused disease in some other species such as humans ( Bruce et al., 1997; Hill et al., 1997; Casalone et al., 2004). We now know that there are other manifestations of prion diseases in cattle which have been termed atypical BSE. Atypical BSE is a study in progress with more unknowns than knowns. One of the most important of the unknowns is the significance of atypical BSE in regard to human and animal health. Previous research in mice had suggested the existence of a number of scrapie strains. Historically, research involving the differentiation of Transmissible Spongiform Encephalopathy (TSE) strains was based on biological typing using panels of inbred mice inoculated with homogenates of infected tissues. If the mice developed a TSE it was characterized by length of incubation and lesion pattern in the brain. (Bruce et al. 1992; Bruce et al. 1994) More recently it has been determined that the human and animals variations may be biochemically differentiated on the basis of molecular mass of the protease resistant prion protein (PrPres) and the degree of glycosylation (Collinge et al., 1996) In 2004, cases of a bovine prion disease molecularly different than already documented as classical BSE were described by scientists in both Italy (Casalone et al., 2004) and France (Biacabe et al., 2004). In both countries the cattle were over 8 years of age. The Italian cases (11 and 15 years of age) originally named bovine amyloidotic spongiform encephalopathy (BASE) were characterized by an unglycosylated protein band with a lower molecular mass (thus named L cases) and the predominance of the monoglycosylated band. In addition, immunohistochemical detection of PrPres in these cases found greater deposits in the cerebral cortex and thalamus versus the brain stem. The French cases found a higher molecular mass associated with the unglycosylated protein band and were called H cases (see figure 1). The
different “strains” are now called atypical BSE. ...
full text, skroll down to page 6 ;
http://www.usaha.org/committees/reports/2006/report-fe-2006.pdf
SEAC
Position Statement
--------------------------------------------------------------------------------
New forms of Bovine Spongiform Encephalopathy
Issue
1. SEAC considered the implications of scientific research on recently identified novel forms of bovine spongiform encephalopathy (BSE).
Background
2. Very low numbers of cattle with abnormal prion proteins (PrPsc) with different biochemical properties from those normally associated with BSE have been detected in active surveillance programmes in a number of countries. SEAC considered (SEAC 97, May 2007) published and unpublished research relating to these putatively new forms of BSE.
Characterisation of cases
3. Different forms of BSE were initially identified and distinguished from classical BSE on the basis of their PrPsc profiles in biochemical tests. All BSE cases identified to date conform to one of three different PrPsc profiles on western blot tests. The European Union (EU) Community Reference Laboratory has suggested that cases be classified on the basis of these profiles as classical, L- or H-type BSE. The key distinguishing features in western blot tests are the lower concentration of the diglycosylated band and the slightly lower molecular mass of unglycosylated band of PrPsc in L-type BSE, and the higher molecular mass of the unglycosylated band in H-type BSE, compared with classical BSE. A western blot method to discriminate between the three types of BSE has been developed .
4. All the reported cases of L-4,5,6,7 and H-type7,9,8,9 BSE have been detected during active surveillance of healthy slaughtered animals or fallen stock. In the majority of cases, retrospective investigations indicated that these animals either showed no clinical signs of BSE or showed non-specific signs such as ataxia and recumbency. As these cases have been detected following active rather than passive surveillance, it has not been possible to observe the clinical signs associated with L- or H-type BSE in sufficient detail to assess whether there are differences in the clinical features between L-type, H-type and classical BSE. However, a significant distinction between classical BSE and L- and H-type BSEs is the age distribution of cases as L- and H-type BSE are found in older cattle with an age range of 5.5 to 19 years. One putative L-type BSE case was aged two years6, however the BSE typing of this case has not been verified. Around 85% of L- or H-type BSE cases have been found in animals more than 10 years old, which is much older than most cases of classical BSE.
5. Neuropathological investigations suggest that PrPsc may be more widely distributed, with a different brain distribution pattern for L- and H-type BSE, compared with classical BSE. However, these investigations are limited by the very low number of animals for which a complete brain has been available for analysis. There are no data on the peripheral distribution of PrPsc or infectivity of L- and H-type BSE or on the pathogenesis of these diseases. However, studies to assess the tissue distribution of infectivity and PrPsc in animals throughout the incubation period following intracerebral challenge are underway.
Prevalence
6. As there is no regulatory requirement to specify the type of BSE when notifying the EU or the World Organisation of Animal Health of BSE cases, it is not possible to accurately quantify the number of H- or L-type BSE cases that have occurred world-wide. Information presented to SEAC indicated that at least 37 cases of L- and H-type BSE have been identified world-wide to date. These cases are widely distributed geographically with L-type cases identified in a number of European countries and Japan, and H-type cases identified in a number of European countries and North America.
7. Due to the different approaches to surveillance between countries, proportions of animals tested and methods used, which do not necessarily include systematic molecular typing, these surveillance systems are not equally capable of detecting L- and H-type BSE. Furthermore, surveillance procedures, including the most appropriate brain region to sample, have not been optimised for the detection of L- and H-type BSE. Therefore, it is not possible to accurately assess and compare the prevalence of L- and H-type BSE in different countries. Origins and Causes
8. It is not known whether L- or H-type BSE are newly emerging forms of BSE or whether they have existed for some time and have only come to light following extensive active surveillance programmes in the EU and elsewhere, together with the introduction and development of new biochemical tests. Studies using historic frozen brain samples from cattle collected from passive surveillance during the early years of the UK BSE epidemic are underway to investigate whether L- and H-type BSE existed in the UK in the past. However, if the prevalence of these BSE types was low, these studies may not identify many, if any, cases.
9. Genetic analyses of a few L- and H-type BSE cases4,5,8,9 have not identified associations between the occurrence of such cases and known genetic polymorphisms in the prion protein gene. There are no mutations in the prion protein gene open reading frame in all, but one, sequenced case. However, the analyses conducted to date are limited by the small number of cases and controls analysed. Thus, a genetic cause of the disease cannot be ruled out.
10. No detailed epidemiological investigations have been conducted to investigate the possible causes for, or links between, L- and H-type BSE cases. No geographical clusters of L- and H-type BSE cases have been found to date. Therefore, it is not possible to rule out feed related, environmental or spontaneous causes for these types of cases.
Transmission studies
11. Transmission studies5,10,11 have demonstrated that both L- and H-type BSE are transmissible to other species by the intracerebral route. No studies have assessed the transmissibility by the oral route. Thus, the available information show | |
