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Test EVERY Cow in the Food Chain

Test EVERY Cow in the Food Chain
Like Other Countries Do

Monday, December 27, 2010

Mad Deer / Virginia

A ProMED-mail post

ProMED-mail is a program of the
International Society for Infectious Diseases

Date: 22 Dec 2010
Source: NV Daily [edited]

Chronic wasting disease likely could threaten the region's deer
population for years, according to the state agency studying the illness.

A 4-point buck killed in western Frederick County in late November
2010 tested positive for the disease, according to a news release
from the Department of Game and Inland Fisheries.

The positive test marked only the 2nd time the disease has appeared
in a deer specimen in Virginia, according to the release. A hunter
shot the buck near the West Virginia line, less than 2 miles from
where Virginia's 1st case of CWD appeared last year [2009], the
agency reported.

"The one thing this does is it confirms that last year's [2009] was
not a fluke," said Nelson Lafon, deer project coordinator for the
department. "We know the disease is in the area, and it means we're
in this for the long haul, and we've kinda told hunters and folks at
those public meetings we held that we see ourselves doing this
[testing] for years."

The agency foresees collecting 500 samples or more from the
containment area during each hunting season and monitoring the
disease in the hopes it doesn't spread, Lafon said.

The state's counterparts in West Virginia continue to find cases of
CWD in neighboring Hampshire County, WV, according to Lafon. The
agencies remain in contact almost weekly, he said, sharing sample
data and other information to model the prevalence of the disease.

"It is, realistically, all part of the same outbreak," Lafon said.
"Having the presence of that disease and then continuing to find it
right on our border is what concerns us. Even if we somehow knock it
out in Virginia, we still have that source, if you will, on the other
side of the border. It makes it more challenging to combat. You know,
the deer don't know the boundary, and the landscape's pretty much the
same on either side."

The project coordinator said he doesn't think the latest case will
spur more action because the deer was found close to the previous
year's [2009] discovery. The department after last season banned
feeding and rehabilitating deer, moving their waste, carcasses and
parts from the containment area, and put a bag limit in effect for
private lands, according to the press release. "We kind of opened the
tool box, and we're already using pretty much every tool in there,"
Lafon said. "But it does mean that we're gonna continue looking for
the disease."

The department also awaits test results on about 100 more samples.
The agency cannot determine whether to change its strategies until
after the season ends 1 Jan 2011 and the department has received all
test results, according to the release.

The agency lauded hunters for their cooperation in helping with the
study, which covers Shenandoah and Frederick counties west of
Interstate 81 and north of Va. 675 near Edinburg. Hunters submitted
the head and necks of the deer they bagged, and the department tested
the samples for the disease, along with carcasses of those killed on the road.

"Hunters have done just about everything they can," he said.

More than a week remains in this deer-hunting season, and the
department continues to urge successful hunters to submit samples in
the refrigerated stations set up at designated locations. Collection
centers likely will be open 2 Jan 2011 for hunters to drop off
samples, Lafon said.

CWD, which affects the nervous system, has been detected in 18 states
and 2 Canadian provinces. The disease [eventually] kills the infected
deer, elk or moose, but no evidence exists to show the animals can
naturally transmit the illness to humans, livestock or pets,
according to the release.

Visit for more

[Byline: Alex Bridges]

Communicated by:

[This does not seem to represent an expansion of the disease beyond
last year's 2009 containment zone. Although the state has referenced
last year, it refers to the last hunting season, which ended in January 2010.

The specimen referred to in the article above may lead us to believe
that either the animal was early in its infection and not showing
clinical signs, or the hunter saw an affected deer and gave it a
rapid death. We are not told the condition of the animal, but most
hunters are looking for healthy animals, so likely this deer was not
showing clinical signs.

As a positive animal, does the department issue a hunting tag to
allow this hunter to try for another animal? While there is no
evidence that this disease affects people, most people dispose of the
meat as an exercise in an abundance of caution. This disease has been
in the United States since the 1960's and possibly farther back than
that without evidence of it affecting humans or other predators. - Mod.TG]

[see also:
Chronic wasting disease, cervid - USA (02): (VA) 20100124.0261]

More about CWD;

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Saturday, December 25, 2010

Big-Meat Beg Senators for Analysis of Rule

Sen. Mike Johanns (R-Neb.), this week sent a letter signed by 11 of his colleagues to USDA Secretary Tom Vilsack, urging him to follow through on his pledge to conduct a cost-benefit analysis of changes to livestock marketing regulations proposed by the Grain Inspection Packers and Stockyards Administration. Vilsack pledged in a recent meeting with meat industry officials that USDA would conduct "a far more rigorous cost-benefit analysis" of the proposed GIPSA livestock rule.

It is estimated that the rule would cost the pork industry, alone, $333 million annually after an initial $69 million expense. The National Pork Producers Council, in comments filed last month, asked that GIPSA withdraw all portions of the proposed rule that went beyond the five issues Congress asked it to address.

Full article;

Friday, December 17, 2010

Scripps Research Scientists Show Prions Mutate and Adapt to Host Environment

17/12/2010 05:18:00

Findings Point to Normal Prion Protein as Most Effective Therapeutic Target for "Mad Cow" and Related Diseases

JUPITER, FL – Scientists from the Florida campus of The Scripps Research Institute have shown that prions, bits of infectious protein that can cause fatal neurodegenerative disease such as bovine spongiform encephalopathy (BSE) or "mad cow disease," have the ability to adapt to survive in a new host environment.

In this regard, although they lack DNA and RNA, they behave much like viruses, producing distinct self-perpetuating structural mutations that provide a clear evolutionary advantage.

The study was published this week in the online Early Edition the journal Proceedings of the National Academy of Sciences.

"We found that when a particular prion strain is transferred from brain cells to a different cell line, its properties gradually change, giving rise to a variant strain that is better adapted to this new cellular environment," said Charles Weissmann, M.D., Ph.D., the head of Scripps Florida's Department of Infectology, who led the study. "If those same prions are subsequently transferred to another cell line, they change again, adapting to these new host cells. And if returned to the brain, the prions gradually regain their original properties. We found physical evidence that, at least in one case, the fold of the prion changed when its properties changed."

Darwinian Evolution Without DNA

These new findings come approximately one year after Weissmann and colleagues published a study in the January 1, 2010 edition of the journal Science that showed that prions were capable of Darwinian evolution.

That earlier study also showed that prions can develop large numbers of mutations and that these mutations can bring about such evolutionary adaptations as drug resistance, a phenomenon previously known to occur only in bacteria and viruses. This study also suggested that the normal prion protein – which occurs naturally in mammalian cells – may prove to be a more effective therapeutic target than its abnormal toxic relation.

"Because prions can adapt to changing environments, it now becomes clear that it will be more difficult than originally thought to find drugs that will work against them," Weissmann said. "But if you could develop a drug that inhibits formation of the normal prion protein, you could, in essence, starve the infectious prions and prevent them from reproducing. This approach to treatment, although technically demanding, can be envisaged because, as we have shown earlier, deprivation of PrP is not detrimental to health – at least to the health of mice."

Folding and Misfolding

Prions, which are composed solely of protein, are classified by distinct strains, characterized by their incubation time and the disease they cause. In addition to BSE/mad cow disease in cattle, diseases caused by prions include scrapie in sheep, chronic wasting disease in deer, and variant Creutzfeldt-Jakob disease in humans. Prions have the ability to reproduce, despite the fact that they contain no nucleic acid genome.

Mammalian cells normally produce cellular prion protein or PrPC. During infection, abnormal or misfolded protein – known as PrPSc – converts the normal host prion protein into its toxic form by changing its conformation or shape. The end-stage consists of large sheets (polymers) of these misfolded proteins, which causes massive tissue and cell damage.

"The infectious prion protein can fold in different ways, and depending on the fold, a different prion strain results," Weissmann said. "As long as prions are maintained in the same host, they retain their characteristic fold, so that strains breed true."

When prions multiply, however, that fold is not always reproduced correctly, so a prion population contains many variants, albeit at low levels.

The new study found that when a prion population is transferred to a different host, one of the variants may replicate faster – an evolutionary advantage – and become the dominant strain. This new population also contains variants, one of which may be selected over others when transferred to a different host.

"The result is that prions, although devoid of genetic material, behave similarly to viruses and other pathogens, in that they can mutate and undergo evolutionary selection," Weissmann said. "They do it by changing their fold, while viruses incur changes in their nucleic acid sequence."

Diverse Yet Related

The new study suggests that prion populations constitute a "quasi-species" similar in nature to RNA viruses and retroviruses, such as flu viruses and HIV.

The idea of a quasi-species was first conceived by Manfred Eigen, a German biophysicist who won the Nobel Prize in Chemistry in 1967. Basically, a quasi-species is a complex, self-perpetuating population of diverse and related entities that act as a whole. It was Weissmann, however, who in 1978 provided the first confirmation of the theory through the study of a particular bacteriophage – a virus that infects bacteria – while he was director of the Institut für Molekularbiologie in Zürich, Switzerland.

But that's where the comparison ends, Weissmann said.

"The fact that they behave like viruses doesn't mean they're anything like a virus," he said. "A bicycle is like a car in that it gets you from one place to the other, but they're not the same. The end effect is the same, however. Prions and viruses are both able to change their structure to survive."

The first author of the study, "Transfer of a Prion Strain to Different Hosts Leads to Emergence of Strain Variants," is Sukhvir P. Mahal of Scripps Research. Other authors include Shawn Browning, Jiali Li, and Irena Suponitsky-Kroyter, also of Scripps Research. For more information, see .

The study was supported by the National Institutes of Health and the Alafi Family Foundation.

About The Scripps Research Institute

The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations, at the forefront of basic biomedical science that seeks to comprehend the most fundamental processes of life. Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neurosciences, autoimmune, cardiovascular, and infectious diseases, and synthetic vaccine development. Established in its current configuration in 1961, it employs approximately 3,000 scientists, postdoctoral fellows, scientific and other technicians, doctoral degree graduate students, and administrative and technical support personnel. Scripps Research is headquartered in La Jolla, California. It also includes Scripps Florida, whose researchers focus on basic biomedical science, drug discovery, and technology development. Scripps Florida is located in Jupiter, Florida. For more information, see .


Mika Ono
10550 North Torrey Pines Road
La Jolla, California 92037
Tel: 858-784-2052
Fax: 858.784.8136

Wednesday, December 8, 2010

First Case of Death from Human Mad-Cow Disease Reported in Tiawan

A Taiwanese man, who spent eight years in the United Kingdom before returning home, died earlier this year from what appeared to be mad-cow disease, the Centers for Disease Control reports.

Full Article;

Saturday, December 4, 2010

Rapid Test for Mad-Cow Disease Coming Soon

No doubt in my mind, this is NOT good news for the USDA and the "Meat-Growers" of the world. Once this test is in production, the REAL gravity and prevalence of the matter will become known;

"Meat-Growers" Ask: Wheres the Beef in S. Korea's Free Trade Agreement

Apparently, the issue of American Beef Imports to S. Korea was left out of the Free Trade Agreement;

Wednesday, December 1, 2010

New Prion Discovery Reveals Drug-Target for Mad Cow Disease & Related Illnesses

Counsil Conclusions on TSE / USA the Worst

The U.S. has lower sanitary and phyto-sanitary standards (SPS) for imports than many other countries, especially those concerning bovine spongiform encephalopathy (BSE). These low standards have made the U.S. a dumping ground for beef from the countries that have experienced BSE problems.

Full article;