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Madrid case not Mad Cow
By h.b. - Jun 5, 2006 - 5:23 PM

Javier Monge was found to have died from the classic version of Creutzfeldt Jakob's disease

The full autopsy carried out on Madrid resident, Javier Monge, who died in the city on April 27th this year, has revealed that death was not caused by Mad Cow’s disease, but was instead from the classic version of Creutzfeldt Jakob’s disease.

This means that the illness has arisen without any link to the exposure or ingestion of infected beef. Javier Monge had lived in the U.K, at the end of the 90’s which had led his family to believe that he was suffering from Mad Cow’s disease. They say they still do not believe today’s findings.
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ALSO SEE :
Two deaths in Castilla y León confirmed to be from Mad Cow disease
- Apr 7, 2008 - 3:25 PM
Madrid youngster thought to have died from Mad Cow disease
- Apr 27, 2006 - 3:54 PM
Possible Mad Cow case in Elba
- Nov 3, 2005 - 8:18 AM

Comments

Terry S. Singeltary Sr.
05 Jun 2006, 22:58
HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory

TSEs have been rampant in the USA for decades in many
species, and they all have been rendered and fed back
to animals for human/animal consumption. I propose that
the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the
continued belief of the UKBSEnvCJD only theory in 2005.
With all the science to date refuting it, to continue
to validate this myth, will only spread this TSE agent
through a multitude of potential routes and sources
i.e. consumption, surgical, blood, medical, cosmetics
etc. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE
Tranmissible Spongiform Encephalopathy is far from an
exact science, but there is enough proven science to
date that this myth should be put to rest once and for
all, and that we move forward with a new classification
for human and animal TSE that would properly identify
the infected species, the source species, and then the
route. This would further have to be broken down to
strain of species and then the route of transmission
would further have to be broken down. Accumulation and
Transmission are key to the threshold from subclinical
to clinical disease, and of that, I even believe that
physical and or blunt trauma may play a role of onset
of clinical symptoms in some cases, but key to all
this, is to stop the amplification and transmission of
this agent, the spreading of, no matter what strain.
BUT, to continue with this myth that the U.K. strain of
BSE one strain in cows, and the nv/v CJD, one strain in
humans, and that all the rest of human TSE is one
single strain i.e. sporadic CJD (when to date there are
6 different phenotypes of sCJD), and that no other
animal TSE transmits to humans, to continue with this
masquerade will only continue to spread, expose, and
kill, who knows how many more in the years and decades
to come. ONE was enough for me, My Mom, hvCJD, DOD
12/14/97 confirmed, which is nothing more than another
mans name added to CJD, like CJD itself, Jakob and
Creutzfeldt, or Gerstmann-Straussler-Scheinker
syndrome, just another CJD or human TSE, named after
another human. WE are only kidding ourselves with the
current diagnostic criteria for human and animal TSE,
especially differentiating between the nvCJD vs the
sporadic CJD strains and then the GSS strains and also
the FFI fatal familial insomnia strains or the ones
that mimics one or the other of those TSE? Tissue
infectivity and strain typing of the many variants of
the human and animal TSEs are paramount in all variants
of all TSE. There must be a proper classification that
will differentiate between all these human TSE in order
to do this. With the CDI and other more sensitive
testing coming about, I only hope that my proposal will
some day be taken seriously.


My name is Terry S. Singeltary Sr. and I am no
scientist, no doctor and have no PhDs, but have been
independently researching human and animal TSEs since
the death of my Mother to the Heidenhain Variant of
Creutzfeldt Jakob Disease on December 14, 1997
'confirmed'. ...TSS




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



SOURCES

snip...FULL TEXT


Singeltary et al 2006


http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13
Edd
06 Jun 2006, 11:25
I am no expert either, and have not been as unfortunate as yourself. I have been facinated with TSE'S for several years now. I have seen hints that TSE'S are a form of Bio weapon, in some media circles. I have even strayed into some casual interest in genetics. Have you come across any sources, that pertain to an RNA virus that is encapsulated in a Calcium shell, recentley discovered in prostate cancers(also a form of shell virus), being involved in transmission? Two fields of research that cross over into the field of unexplained illness are those of Epigenetics, and a process called DNA Methylation. These research fields also relate to cellular NANO technology. I think some form of "codet" attachment(through Methylation) to the PRP gene is responsible for the breakdown(folding). If you have not crossed into the topics of Epigenetics, DNA Methylation, and cellular NANOtechnology; you might well find some food for thought. I think before we define its origin(natural selection, accidental man made, or bio weapon), we must determine what it is, and what causes it. I pretty much agree with your assesment. I think this illness will open a pandoras box in science. It is much more than a savage illness.
Terry S. Singeltary Sr.
22 Aug 2007, 17:59
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...



64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...



http://www.seac.gov.uk/minutes/95.pdf




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




SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


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



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
collection.

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


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf



From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Sent: Tuesday, August 21, 2007 9:50 AM
Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing
total to 3 cases to date


Infected and Source Flocks

As of June 30, 2007, there were .....

snip...

One field case and one validation case were consistent with Nor-98 scrapie.

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/m onthly_scrapie_rpt.pps


IN the February 2007 Scrapie report it only mentions ;

''One case was consistent with Nor98 scrapie.''

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/


(please note flocks of origin were in WY, CO, AND CA. PERSONAL COMMUNCATIONS
USDA, APHIS, VS ET AL. ...TSS)



NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=14553


An evaluation of scrapie surveillance in the United States


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3427



FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=10451


SEAC New forms of Bovine Spongiform Encephalopathy 1 August 2007
From: Terry S. Singeltary Sr.
Date: Sun, 5 Aug 2007 13:09:38 -0500


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3573


POTENTIAL MAD CAT ESCAPES LAB IN USA

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=7062




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