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From: TSS ()
Subject: California lists possible recipients of recalled non-ambulatory DOWNER Hallmark beef list nearly 3,000 restaurants and other businesses
Date: March 5, 2008 at 2:13 pm PST

Food Safety
California lists possible recipients of recalled Hallmark beef

By Janie Gabbett on 3/5/2008 for

It took the California Department of Public Health 120 pages to list nearly 3,000 restaurants and other businesses in the state that may have received some of the two years' worth of beef that Hallmark/Westland Meat Co. recalled last month.

The list, viewable on, could be over the top, however. Some food distributors told Nation's Restaurant News they gave California officials their entire customer list rather than a roster of the restaurants that purchased the recalled beef.

The agency has also posted a list of products recalled by companies including ConAgra Foods, Kirkland, General Mills, Nestle and Richwood Meat because they could have contained meat involved in the recall.

No illnesses have been linked to the Class II recall that USDA prompted after videos shot by the Humane Society of the United States revealed animal handling of downer cows that were out of compliance with USDA's animal welfare rules.

Under current federal rules, retailers of recalled products are not revealed. California law, however, allows the state to reveal the names of businesses that may be selling the food in question. Some consumer groups and U.S. legislators have been calling for federal rule changes to allow such listings nationwide.

>>>No illnesses have been linked to the Class II recall that USDA prompted after videos shot by the Humane Society of the United States revealed animal handling of downer cows that were out of compliance with USDA's animal welfare rules. <<<

THESE people writing this nonsense and making these false sense of security know perfectly well the incubation period for mad cow disease in humans and animals is a very long process. you can eat it now and not go clinical for years, even a decade or more, BUT, once clinical, it's 100% fatal.

PLEASE SEE LONG LIST OF RESTAURANTS AND EATERIES IN CALIFORNIA THAT WERE FEEDING DOWNER CATTLE TO THE PUBLIC, WITH JACK-IN-THE-BOX BEING AT THE TOP OF THE LIST. 120 PAGES OF THEM. seems they would have learned the first time after all that potentially tainted beef from the mad cow cohorts from the Washington mad cow. ...

Hallmark / Westland Meat Recall - Retail Distribution

Additional Products Containing Westland Recalled Beef

IF the USDA and the FDA et al were not in bed with the industry so much, they would come clean with the rest of the states, and produce a list for the public from each state as was done in California.

THAT'S just one state folks. nope, all the BSe about how No illnesses have been linked to the Class II recall that USDA prompted from BSE and or h-BASE or any other strain, is just that BS. the USDA knows PERFECTLY WELL that no one would get sick right off the bat from mad cow disease. Every parent out there should be demanding answers, not these same lies. THE USDA should follow every single child that consumed any of these products for the rest of there lives. there is no way out of it now. the product is gone, consumed, and these kids, the elderly, and most everybody in between have been exposed. non-ambulatory i.e. DOWNERS are the most likely to have a Transmissible Spongiform Encephalopathy. WE know it's here, we know why the USDA et al shut down the testing, they did not want to document any more. ...TSS

Science 23 November 2001:
Vol. 294. no. 5547, pp. 1726 - 1728
DOI: 10.1126/science.1066838


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

The size of the variant Creutzfeldt-Jakob Disease (vCJD) epidemic in the United Kingdom is a major public health concern and a subject of speculation. The cases are young (mean age = 28). Assuming that the risk of developing the disease in susceptible exposed subjects decreases exponentially with age after age 15, that all infections occurred between 1980 and 1989, and that the distribution of the incubation period is lognormal, we estimate that the mean duration of the incubation period is 16.7 years [95% confidence interval (CI): 12.4 to 23.2] and that the total number of cases will be 205 (upper limit of the 95% CI: 403).

1 Epidemiology and Information Sciences, INSERM U444, CHU Saint-Antoine, Université Pierre et Marie Curie et Assistance Publique-Hôpitaux de Paris, 27 rue Chaligny, 75012 Paris, France.
2 National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Edinburgh EH4 2XU, UK.
3 Immunité Anti-Infectieuse JE 2236, UFR de Médecine de Grenoble, Université Joseph Fourier, Domaine de la Merci, 38706 La Tronche, France.


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).

NOW, the price of poker in the USA may be shorter, due to the fact the strain of mad cow disease in the USA 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

Communicated by:
Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to
the steady increase in the "type unknown" category, which, according
to their definition, comprises cases in which vCJD could be excluded.
The total of 26 cases for the current year (2007) is disturbing,
possibly symptomatic of the circulation of novel agents.
Characterization of these agents should be given a high priority. - Mod.CP]

[see also:


Become a ProMED-mail Premium Subscriber at

Visit ProMED-mail's web site at .

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.


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
*** 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)

************************************************** *****



USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW,both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS

************************************************** *****

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

Oral Abstracts 14



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


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.


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.


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).


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.


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 4
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).

Subject: Aspects of the Cerebellar Neuropathology in Nor98

Date: September 26, 2007 at 4:06 pm PST


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

full text ;


The flocks of origin are WY, CO, CA, IN, and MN.

personal communication USDA et al. ...TSS




Friday, February 8, 2008

Creutzfeldt Jakob Disease Delaware UPDATE


Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States

Creutzfeldt Jakob Disease

Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPSc
Type in a Young British Woman

Friday, January 11, 2008


Sunday, December 16, 2007

Risk factors for sporadic Creutzfeldt-Jakob disease

Published Online: 11 Dec 2007

Monday, December 31, 2007

Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in
Endodontic Practice in Absence of Adequate Prion Inactivation

Friday, January 25, 2008

January 2008 Update on Feed Enforcement Activities to Limit the Spread of


Sunday, February 17, 2008
Release No. 0046.08

Statement by Secretary of Agriculture Ed Schafer Regarding Hallmark/Westland
Meat Packing Company Two Year Product Recall

USDA Press Office (202) 720-4623


Wednesday, February 27, 2008


Specified Risk Material SRM

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified
Risk Materials for Human Food and Requirements for the Disposition of
Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS
Prohibition of the Use of Specified Risk Materials for Human Food and
Requirements for the Disposition of Non-Ambulatory Disabled Cattle


Non-Ambulatory Disabled Cattle Broken bones and such may be the first signs
of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;

SUB CLINICAL PRION INFECTION MRC-43-00 Issued: Monday, 28 August 2000


A team of researchers led by Professor John Collinge at the Medical Research
Council Prion Unit1 report today in the Proceedings of the National Academy
of Sciences, on new evidence for the existence of a ?sub-clinical? form of
BSE in mice which was unknown until now. The scientists took a closer look
at what is known as the ?species barrier? - the main protective factor which

limits the ability of prions2 to jump from one species to infect another.
They found the mice had a ?sub-clinical? form of disease where they carried
high levels of infectivity but did not develop the clinical disease during
their normal lifespan. The idea that individuals can carry a disease and
show no clinical symptoms is not new. It is commonly seen in conventional
infectious diseases. Researchers tried to infect laboratory mice with
hamster prions3 called Sc237 and found that the mice showed no apparent
signs of disease. However, on closer inspection they found that the mice had
high levels of mouse prions in their brains. This was surprising because it
has always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain. In addition the
researchers showed that this new sub-clinical infection could be easily
passed on when injected into healthy mice and hamsters. The height of the
species barrier varies widely between different combinations of animals and
also varies with the type or strain of prions. While some barriers are quite
small (for instance BSE easily infects mice), other combinations of strain
and species show a seemingly impenetrable barrier. Traditionally, the
particular barrier studied here was assumed to be robust. Professor John
Collinge said: "These results have a number of important implications. They
suggest that we should re-think how we measure species barriers in the
laboratory, and that we should not assume that just because one species
appears resistant to a strain of prions they have been exposed to, that they
do not silently carry the infection.

This research raises the possibility, which has been mentioned before, that
apparently healthy cattle could harbour, but never show signs of, BSE. "This
is a timely and unexpected result, increasing what we know about prion
disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best to
safeguard health and reduce the risk that theoretically, prion disease could
be contracted through medical and surgical procedures."



PNAS | August 29, 2000 | vol. 97 | no. 18 | 10248-10253 Neurobiology

Species-barrier-independent prion replication in apparentlyresistant species

Andrew F. Hill*, Susan Joiner*, Jackie Linehan*, Melanie Desbruslais*, Peter
L. Lantos , and John Collinge*,

SEE FULL TEXT 17 pages ;

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

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