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From: TSS ()
Subject: Two deaths in Castilla y León Spain confirmed to be from Mad Cow disease
Date: April 9, 2008 at 2:39 pm PST

Two deaths in Castilla y León confirmed to be from Mad Cow disease

By h.b. - Apr 7, 2008 - 3:25 PM

The two youngsters have not been named and they are thought to have eaten
infected meat some eight years ago

The death of two youngsters in Castilla y León has been confirmed today to
have been caused by Creutzfeld-Jakob, Mad Cow disease. Experts in Spain now
consider that more cases are likely to be detected here over the next few

Juan José Badiola director of the centre which investigates the disease in
Spain has called for calm. He said that both the victim probably ate the
infected meat more than eight years ago.
The deaths follow that of a 26 year old woman in Madrid back in 2005.

The exact localities of the new deaths has not been revealed, but the
Castilla y León health department say that one death was a month ago and the
other some time earlier. Neither of those to die was a farmer.

April 7, 2008 - 1:35 PM Two die in Spain from human form of mad cow
MADRID (Reuters) - Two people have died in Spain from variant
Creutzfeldt-Jakob Disease, the human form of mad cow disease, the health
department at the regional Castilla-Leon government said on Monday.

Mad cow disease, bovine spongiform encephalopathy, first emerged in Britain
in the 1980s and has been found in herds in several European and other
countries. Scientists believe it is transmitted through infected meat and
bone meal fed to cattle and may cause vCJD in humans.

The health department said these were not the first vCJD deaths in Spain but
did not give details.

Spanish gov't urges calm after deaths from mad-cow disease

Monday, April 07, 2008; Posted: 01:32 PM 7

Lanzarote, Spain, Apr 7, 2008 (EFE via COMTEX) -- -- Spain's agriculture
minister on Monday sent a message of "categorical calm and guarantees" to
the public regarding the consumption of beef after confirmation of the
deaths of two people from mad-cow disease.

Elena Espinosa made the announcement during a recess at the agricultural
sector conference being held Monday on the island of Lanzarote, in the
Canary Islands, after receiving confirmation by telephone of the two deaths.

The government of the Spanish region of Castile-Leon confirmed to Efe that
the deaths had occurred on Dec. 28, 2007, and Feb. 7, 2008.

A spokesman for the Health Ministry said that both cases were detected prior
to 2001.

Espinosa also said that, although there was a lack of information on the two
deaths, everything was pointing to the conclusion that both cases arose
after the victims ate infected beef before 2001.

She insisted that in 1996 the European Union and Spain adopted all known
control measures to avoid, prevent and control bovine spongiform
encephalopathy, better known as mad-cow disease, which was detected in Spain
for the first time in November 2000.

Espinosa transmitted to the public her full guarantee of food safety for
Spanish beef, noting that for more than 10 years quality and tracing
controls had been in place. EFE


> "categorical calm and guarantees" to the public regarding the consumption

> of beef after confirmation of the deaths of two people from mad-cow

CACHING $$$ what they call, political science. let me see, have we not
heard that a time or two ;

John Gummer tried to feed his daughter a beefburger to try to convince the

Prime Minister Jean Chretien shows that Canadian beef is
safe by having it for lunch at a Ottawa restaurant.

BUSH: LET THEM EAT BEEF, and a lot of it.

"One area where I've been disappointed is beef,'' Bush said of the Chinese.
"They need to be eating U.S. beef. It's good for them. They'll like it.''

The president had told an interviewer from Japanese television in 2005:
"U.S. beef if safe. Of course, our cattlemen here believe the beef is safe.
I'm more than willing to eat U.S. beef, and do -- eat a lot of it.''

The president, appearing at a convention of the National Beef Cattlemen's
Association this spring, said: "In the last three years, we've conducted
over 800,000 tests to assess the health of our cattle herds. And today,
because of our collaborative efforts and a strong scientific approach to
deal with BSE (mad cow), we can say to global consumers with complete
assurance, American beef is safe and it is good to eat.''

The cattlemen applauded that line in March.

BSE in America

This article, written by Prof John
Collinge QBE, appeared in The Times
newspaper 3 January 2004.

Watching Ann Veneman, US
Agriculture Secretary, announce the
first case or BSE in the United
States at Christmas was profoundly
disappointing, not simply because
another country was blighted by
this degenerative brain disease, but
the presentation was all too
familiar. That agriculture rather
than health secretary sought to
reassure about risk to human
health, and that she said she would
be feeding her own children beef,
was as reminiscent of the early
stages of the outbreak in Britain as
it is scientifically inane. There are
many lessons the Americans could
learn from the British experience,
and the following months will
prove crucial.





MARCH 26, 2003

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

disease in the United States

Email Terry S. Singeltary:

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

should be drastic measures to safeguard the medical and surgical arena

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

CJDs in the USA are type 2 PrPSc?

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.

like i said before ;


(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries.
The OIE is not responsible for inaccurate publication of country disease
status based on inaccurate information or changes in epidemiological status
or other significant events that were not promptly reported to then Central

*** The different "strains" are now called atypical BSE. ***

full text, skroll down to page 6 ;

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or
Italian L-BASE

Association of a Bovine Prion Gene Haplotype with Atypical BSE

Received December 20, 2007; Accepted February 14, 2008.


Transmissible spongiform encephalopathies (TSEs), or prion diseases, are
infectious, invariably fatal neurodegenerative disorders that occur in
humans, ruminants, cats, and mink [1]. TSEs are unique in their ability to
manifest through acquired, inherited, and sporadic routes [1]. Classical
bovine spongiform encephalopathy (BSE) is an acquired cattle TSE of unknown
origin that spreads through the consumption of meat and bone meal
contaminated with the infectious prion agent [2]. Classical BSE is accepted
as the probable cause of the human TSE variant Creutzfeldt-Jakob Disease
(CJD) [3], [4]. Two BSEs distinct from classical BSE, so called "atypical
BSEs" (H-type and L-type) have recently been identified in Asian, North
American and European cattle [2]. Approximately, 30 atypical BSEs have been
identified worldwide and their etiology is unclear.

Variation in the prion gene (PRNP) correlates with TSE susceptibility in
some mammals including cattle [1], [5]-[7]. The deletion alleles of two
bovine PRNP insertion/deletion polymorphisms, one within the promoter region
and the other in intron 1, associate with classical BSE susceptibility
[5]-[7]. These same alleles do not correlate with atypical BSE
susceptibility [8]. In 2006, a United States atypical BSE case was
identified and subsequently found to have a PRNP nonsynonymous polymorphism
(E211K) that is homologous to the human PRNP E200K polymorphism (observation
by J.A.R). The human K200 allele is a highly-penetrant risk factor for
genetic CJD [9]. To date, the K211 allele has not been observed in other
atypical BSE cases or reported in healthy cattle [10], [11]. Thus, while the
K211 allele may have been a genetic cause for one case of atypical BSE, it
has not accounted for the majority of atypical cases. Consequently, any
association of PRNP alleles with atypical BSE was largely unknown prior to
this study.

see full text ;

Original Paper

Association between Deposition of Beta-Amyloid and Pathological Prion
Protein in Sporadic Creutzfeldt-Jakob Disease

Laura Debatina, Johannes Strefferb, Markus Geissenc, Jakob Matschkec,
Adriano Aguzzia, Markus Glatzela, c

aInstitute of Neuropathology, and
bDivision of Psychiatry Research, University Hospital Zurich, Zurich,
cInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf,
Hamburg, Germany

Address of Corresponding Author

Neurodegenerative Dis (DOI: 10.1159/000121389)


Key Words

Sporadic Creutzfeldt-Jakob disease
Alzheimer's disease
Deposition of -amyloid
Prion protein



Background: Alzheimer's disease (AD) and prion diseases such as sporadic
Creutzfeldt-Jakob disease (sCJD) share common features concerning their
molecular pathogenesis and neuropathological presentation and the
coexistence of AD and CJD in patients suggest an association between the
deposition of the proteolytically processed form of the amyloid precursor
protein, -amyloid (A), which deposits in AD, and the abnormal form of the
prion protein, PrPSc, which deposits in sCJD. Methods: We have characterized
sCJD patients (n = 14), AD patients (n = 5) and nondemented controls (n = 5)
with respect to the deposition of PrPSc and A morphologically, biochemically
and genetically and correlated these findings to clinical data. Results:
sCJD-diseased individuals with abundant deposits of A present with a
specific clinicopathological profile, defined by higher age at disease
onset, long disease duration, a genetic profile and only minimal amounts of
PrPSc in the cerebellum. Conclusion: The co-occurrence of pathological
changes typical for sCJD and AD in combination with the inverse association
between accumulation of A and PrPSc in a subgroup of sCJD patients is
indicative of common pathways involved in the generation or clearance of A
and PrPSc in a subgroup of sCJD patients.

Copyright © 2008 S. Karger AG, Basel


Author Contacts

Markus Glatzel
Institute of Neuropathology, University Medical Center Hamburg-Eppendorf
Martinistrasse 52, DE-20246 Hamburg (Germany)
Tel. +49 40 42 803 2218, Fax +49 40 42 803 4929

Saturday, March 22, 2008
10 Million Baby Boomers to have Alzheimer's in the coming decades
2008 Alzheimer's disease facts and figures

Alzheimer's Association*

Abstract Alzheimer's disease is the seventh leading cause of all deaths in
the United States and the fifth leading cause of death in Americans older
than the age of 65 years. More than 5 million Americans are estimated to
have Alzheimer's disease. Every 71 seconds someone in America develops
Alzheimer's disease; by 2050 it is expected to occur every 33 seconds.
During the coming decades, baby boomers are projected to add 10 million
people to these numbers. By 2050, the incidence of Alzheimer's disease is
expected to approach nearly a million people per year, with a total
estimated prevalence of 11 to 16 million persons. Significant cost
implications related to Alzheimer's disease and other dementias include an
estimated $148 billion annually in direct (Medicare/Medicaid) and indirect
(eg, caregiver lost wages and out-of-pocket expenses, decreased business
productivity) costs. Not included in these figures are the estimated 10
million caregivers who annually provide $89 billion in unpaid services to
individuals with Alzheimer's disease. This report provides information to
increase understanding of the public health impact of Alzheimer's disease,
including incidence and prevalence, mortality, lifetime risks, costs, and
impact on family caregivers.

snip... see full text 24 pages ;

© 2008 The Alzheimer's Association. All rights reserved.

Regarding Alzheimer's disease

(note the substantial increase on a yearly basis)


The pathogenesis of these diseases was compared to Alzheimer's disease at a
molecular level...


And NONE of this is relevant to BSE?

There is also the matter whether the spectrum of ''prion disease'' is wider
than that recognized at present.

Human BSE


These are not relevant to any possible human hazard from BSE nor to the much
more common dementia, Alzheimers.




Subject: Re: Hello Dr. Manuelidis Date: Fri, 22 Dec 2000 17:47:09 -0500
From: laura manuelidis Reply-To: Organization: Yale Medical School To: "Terry S.
Singeltary Sr."

References: <

Dear Terry,

One of our papers (in Alzheimer's Disease Related Disord. 3:100-109, 1989)
in text cites 6 of 46 (13%) of clinical AD as CJD. There may be a later
paper from another lab showing the same higher than expected incidence but I
can't put my hands on it right now. We also have a lot of papers from 1985
on stating that there are likely many silent (non-clinical) CJD infections,
i.e. much greater than the "tip of the iceberg" of long standing end-stage
cases with clinical symptoms. Hope this helps.

best wishes for the new year laura manuelidis


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

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Since this article does not have an abstract, we have provided the first 150
words of the full text and any section headings.

To the Editor:

In their Research Letter, Dr Gibbons and colleagues1 reported that the
annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable
since 1985. These estimates, however, are based only on reported cases, and
do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number
of persons with a diagnosis of Alzheimer disease in fact may have CJD,
although only a small number of these patients receive the postmortem
examination necessary to make this diagnosis. Furthermore, only a few states
have made CJD reportable. Human and animal transmissible spongiform
encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr
Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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

Thursday, March 6, 2008

House committee subpoenas Hallmark/Westland CEO - i call for an
investigation of the investigators



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