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From: TSS ()
Subject: FDA mad cow nvCJD 'only' blood recalls 2ND WEEK JULY 2006
Date: July 16, 2006 at 6:57 am PST

PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6;
b) Fresh Frozen Plasma, Recall # B-1551-6
CODE
a) and b) Unit 2395371
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax on August 20, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1552-6;
b) Platelets, Recall # B-1553-6;
c) Fresh Frozen Plasma, Recall # B-1554-6
CODE
a), b) and c) Unit 2438702
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax on May 29, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units
DISTRIBUTION
TX

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1555-6;
b) Fresh Frozen Plasma, Recall # B-1556-6
CODE
a) and b) Unit 2454970
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax on July 23 and December 11. 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX

______________________________
PRODUCT
a) Red Blood Cells, Recall # B-1494-6
b) Cryoprecipitated AHF, Recall # B-1495-6
CODE
a) and b) Unit 5013100
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on May 17, 2005. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
GA

______________________________
PRODUCT
Source Plasma, Recall # B-1450-6
CODE
Unit numbers ST0824313 and ST0824764
RECALLING FIRM/MANUFACTURER
Stillwater Plasma Center LLC, Stillwater, OK, by fax on November 21, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor whose suitability pertaining to risk factors for Creutzfeldt-Jakob Disease (vCJD) was not adequately determined, were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
UK

______________________________
PRODUCT
Plasma Frozen, Recall # B-1422-6;
Recovered Plasma, Recall # B-1423-6
CODE
a) Unit 03E42218;
b) Unit 03E38153
RECALLING FIRM/MANUFACTURER
American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail or letter on February 20 or 21, 2004. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
GA and Switzerland

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1374-6;
b) Recovered Plasma, Recall # B-1375-6
CODE
a) and b) unit 2453906
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax on October 31 and November 5, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX and Austria

______________________________
PRODUCT
Source Plasma. Recall # B-1295-6
CODE
Units: NG0046551, NG0045950
RECALLING FIRM/MANUFACTURER
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 20, 2002, Firm initiated recall is complete.
REASON
Blood products, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire appropriately, were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
KY

______________________________
PRODUCT
Source Plasma. Recall # B-1296-6
CODE
Unit: NG 0044520
RECALLING FIRM/MANUFACTURER
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 12, 2002. Firm initiated recall is complete.
REASON
Blood product, collected from a donor who did not answer the questions on the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY

______________________________
PRODUCT
Source Plasma. Recall # B-1297-6
CODE
Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797, NG0044020, NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412, NG0045555
RECALLING FIRM/MANUFACTURER
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 20, 2002. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
13 units
DISTRIBUTION
KY

______________________________
PRODUCT
Source Plasma, Recall # B-1298-6
CODE
Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095, NG 0042525, NG 0042341
RECALLING FIRM/MANUFACTURER
DCI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax on December 20, 2002. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who answered questions on the variant Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were distributed.
VOLUME OF PRODUCT IN COMMERCE
7 units
DISTRIBUTION
KY

______________________________
PRODUCT
Recovered Plasma, Recall # B-1299-6
CODE
Unit: 4357117
RECALLING FIRM/MANUFACTURER
Department of the Navy, Naval Medical Center, San Diego, CA, by fax and letter on September 25, 2003. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at risk of exposure to Creutzfeldt-Jacob Disease (CJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
Germany

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html


CJD WATCH MESSAGE BOARD
TSS
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY
Fri Jul 7, 2006 09:37
70.110.83.160


FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY

PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1379-6;
b) Platelets, Recall # B-1380-6;
c) Fresh Frozen Plasma, Recall # 1381-6;
d) Recovered Plasma, Recall # B-1382-6
CODE
a) Unit numbers: 2343106, 2377779, and 2403533;
b) and c) Unit numbers: 2377779;
d) Unit numbers: 2343106 and 2403533
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June 12, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
7 units
DISTRIBUTION
TX and Austria
______________________________


PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1467-6;
b) Recovered Plasma, Recall # B-1468-6
CODE
a) and b) Unit numbers: 2329380
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on May 8, 2003. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX and Switzerland

______________________________

PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1479-6;
b) Cryoprecipitated AHF, Recall # B-1480-6;
c) Recovered Plasma, Recall # B-1481-6
CODE
a), b), and c) Unit numbers: 2383280
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on July 23 and 29, 2004. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units
DISTRIBUTION
TX and Switzerland

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1482-6;
b) Fresh Frozen Plasma, Recall # B-1483-6
CODE
a) and b) Unit number: 2501452
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on October 5, 2004. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX and NY

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1484-6;
b) Plasma Cryoprecipitated Reduced, Recall # B-1485-6;
c) Recovered Plasma, Recall # B-1486-6
CODE
a) and c) Unit number: 2554077;
b) Unit number: 2415708
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on August 13, 2004. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units
DISTRIBUTION
TX and Austria

_____________________________________

END OF ENFORCEMENT REPORT FOR July 5, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00959.html

with new atypical TSE in the bovine, in the sheep, goat, and humans, and the fact that the new BASE TSE in cattle being very very similar to sporadic CJD, rather than the nvCJD, the fact that now science showing the TSE agent of the atypical cattle in Japan showing infectivity other than CNS tissue, the fact that the latest Texas mad cow and the recent Alabama mad cow both being of the atypical strain, it would seem prudent to include all human TSE in the blood ban, in my opinion. ...

TSS

CJD WATCH MESSAGE BOARD
TSS
Prion infections, blood and transfusions Aguzzi and Glatzel
Sat Jul 8, 2006 12:18
68.238.108.213


Prion infections, blood and transfusions

Adriano Aguzzi* and Markus Glatzel

Prion infections lead to invariably fatal diseases of the CNS, including

Creutzfeldt–Jakob disease (CJD) in humans, bovine spongiform

encephalopathy (BSE), and scrapie in sheep. There have been hundreds

of instances in which prions have been transmitted iatrogenically among

humans, usually through neurosurgical procedures or administration of

pituitary tissue extracts. Prions have not generally been regarded as bloodborne

infectious agents, and case–control studies have failed to identify

CJD in transfusion recipients. Previous understanding was, however,

questioned by reports of prion infections in three recipients of blood

donated by individuals who subsequently developed variant CJD. On

reflection, hematogenic prion transmission does not come as a surprise, as

involvement of extracerebral compartments such as lymphoid organs and

skeletal muscle is common in most prion infections, and prions have been

recovered from the blood of rodents and sheep. Novel diagnostic strategies,

which might include the use of surrogate markers of prion infection, along

with prion removal strategies, might help to control the risk of iatrogenic

prion spread through blood transfusions. ...

snip...

INTRODUCTION

Prion diseases, also termed transmissible

SPONGIFORM ENCEPHALOPATHIES, constitute

a group of neurodegenerative conditions that

are transmissible within and between mammalian

species. A characteristic of these diseases is

the accumulation of a misfolded prion protein,

PrPSc, which is a post-translationally modified

form of the host-encoded prion protein (PrPC).

The processes underlying PrPSc formation

remain enigmatic, but there is little doubt that

a conformer of PrPC, which might exist in an

oligomeric form,1 is identical to the infectious

entity.2 Prions damage the brain by transmitting

toxic signals to cells expressing PrPC.3

Although genetic evidence has been taken

to indicate that human prion diseases have

been with us since prehistoric times,4 the first

documented cases of Creutzfeldt–Jakob disease

(CJD) date back only 85 years.5–7 Since then, it

has become obvious that human prion diseases

have three distinct etiologies: they can arise in the

absence of any documented exposure to infectious

prions as sporadic CJD (sCJD), as an autosomal

dominantly inherited disease in the case

of genetic, or familial, CJD (gCJD/fCJD), or as

an acquired condition in the case of IATROGENIC

and variant CJD (iCJD, vCJD), or kuru, which

resulted from cannibalism.8

Some prion diseases that occur in animals

might have been recognized several centuries

ago, as suggested by early descriptions of sheep

diseases that seem to correspond to scrapie.

Most prion diseases affecting animals, however,

were discovered relatively recently.6 A transmissible

spongiform encephalopathy affecting

cattle (bovine spongiform encephalopathy,

or BSE) has caused a massive epidemic in

European countries, affecting around 2 million

animals.9 Epidemiological, biochemical, neuropathological

and transmission studies have

substantiated the concern that BSE prions might

have crossed the species barrier between cattle

and humans, resulting in a novel form of human

prion disease, vCJD.10–13 During 1996–2001, the

incidence of vCJD in the UK rose year upon year,

evoking fears of a large upcoming epidemic.

Since 2001, however, the incidence of vCJD in

the UK appears to have been stabilizing, indicating

that the extent of the epidemic might be

limited.14 As might be expected for in frequent

stochastic events, the numbers of new cases of

vCJD fluctuate from year to year. For example,

data available on the web page of the National

CJD Surveillance Unit15 show that the number

of onsets of vCJD was higher in 2004 than it was

in 2003, but this is not necessarily indicative of

an upward trend.

It must be assumed that a number of asymptomatic

carriers of vCJD exist in human populations

that have been exposed to BSE. The

existence of such a chronic carrier state is a

logical and unavoidable consequence of the

long incubation time of prion diseases, which

is typically in the order of several years and—

in the case of oral exposure to prions—can

reach several decades. Consequently, anybody

who has contracted the infection but has not

developed clinical signs and symptoms might

be consider ed a carrier. Some of these carriers

are likely be ‘preclinical’, and will proceed,

in due course, to the development of disease.

Alternatively, it is conceivable that the carrier

state can persist for an indefinite period of

time, in which case infected individuals could

be regarded as ‘permanent asymptomatic

(sub clinical) carriers’. Studies performed in

rodents indicate that the permanent subclinical

carrier state might be a common phenomenon,

such as occurs when immune deficient mice

are exposed to prions.16 Unlinked anonymous

screens for hallmarks of prion infection in

archival tissues have suggested that the prevalence

of individuals with sub clinical vCJD might

be higher than previously antici pated, and could

reach 237 cases per million individuals.17

The recent discovery of transmission of vCJD

via blood in three individuals indicates with

near certainty that blood-borne prion transmission,

in conjunction with an unknown

prevalence of vCJD-infected carriers, leads

to secondary transmission of host-adapted

prions.18 Consequently, the vCJD epidemic

might be prolonged, or, in the worst-case

scenario, vCJD be rendered endemic and selfsustained.

In this article, we review how prions

could act as blood-borne infectious agents, and

consider strategies aimed at minimizing the risk

of secondary trans mission of prion diseases.

TRANSMISSION OF PRION DISEASES

IN HUMANS

The cause of most human prion diseases is

unknown. In the case of sCJD, the term ‘sporadic’

is used as a euphemism, meaning that we have

no idea about the origin of this form of CJD. By

contrast, gCJD always segregates within families

with mutations in the gene encoding the prion

protein (PRNP), suggesting that these mutations

are causally involved in disease pathogenesis. As

no families have been described in which gCJD

segregates with mutations in genes other than

PRNP, it has been difficult to use human genetics

to understand the pathogenesis of prion diseases.

The discovery of PRNP mutations in gCJD has

led to the proposal that at least some cases of

sCJD might be due to somatic PRNP mutations

analogous to those found in the germline of

gCJD patients. It is equally possible, however,

that some of the cases of alleged sCJD derive

from hitherto unrecognized infectious causes.

In apparent agreement with the ‘intrinsic’

origin of sCJD, which accounts for more than

90% of all human prion diseases, epidemiological

studies were not able to identify a

conclusive link between this form of CJD and

external risk factors.19 This fact is reflected in

the pathological and biochemical features of

these diseases. Although low levels of PrPSc and

prion infectivity can be demonstrated in peripheral

sites such as lymphoid organs or skeletal

muscle,20,21 the highest levels of PrPSc and prion

infectivity appear to occur in the CNS. These

facts might account, at least in part, for the lack

of evidence of sCJD transmission by labile or

stable blood products.22 Indeed, several retrospective

studies have failed to identify blood

transfusion or exposure to plasma products as

risk factors for the development of sCJD,19 and

prion diseases appear to be exceedingly rare

in hemophiliacs, a group of patients that is at

particularly high risk of contracting emerging

blood-borne infectious diseases. Although these

studies cannot exclude the possibility that transmission

of sCJD might have occurred through

blood transfusions in rare cases, and despite

the fact that the etiology of sCJD is unclear,

it would appear that transmission of sCJD by

trans fusion of blood or blood products does

not play a major role in the pathogenesis of this

disease entity.

In the case of acquired prion diseases, however,

the situation is very different. For vCJD, high

levels of prion infectivity and of PrPSc have

been detected in lymphoid organs such as the

appendix and tonsils (Figure 1).23,24 For this

reason, it has been speculated for almost a decade

that vCJD might be associated with a higher risk

of blood-borne transmission than sCJD. It is

important to be cautious, however, as the differences

in the organ tropism of sCJD and vCJD

might be quantitative rather than qualitative, and

PrPSc has been detected in the lymphoid organs

of both vCJD and sCJD patients.21 Initial studies

have failed to detect PrPSc and prion infectivity

in the blood of patients with vCJD, but these

negative data are likely to be attributable to

the lack of sensitivity of the assays available at

the time.23

The recent identification of three indiv iduals

with probable transmission of vCJD via blood

transfusion has provided tragic evidence that vCJD

prions can indeed be transmitted through blood

(Figure 2). On the basis of the epi demiological

and pathogenetic considerations discussed above,

it can only be a matter of time before further

cases of blood-transfusion-associated cases of

vCJD will ensue (Figure 3).

In the first of the cases reported, a patient

received a single unit of non-leukodepleted

erythrocyte concentrate from an individual who

went on to develop vCJD 3.5 years later, and

was therefore likely to have been subclinically

prion-infected at the time of the donation. The

recipient developed vCJD 6.5 years following

the transfusion.25

In the second case, transmission of prion

disease occurred again via a single unit of nonleukodepleted

red-blood-cell concentrate.

The donor developed vCJD 2 years following

blood donation, again raising the possibility

of pre clinical infection at the time of the donation.

18 The recipient died of causes unrelated

to the prion infection 5 years after the transfusion.

Although this individual did not display

overt signs of vCJD, PrPSc could be detected

in lymphoid organs, enforcing the concept of

subclinical prion disease in this individual.

Recently, a third case of blood-borne prion

transmission has been reported.26 In this case,

the incubation time in the recipient was 8 years,

whereas the donor showed vCJD symptoms

20 months following his blood donation.

Until now, sequencing of the PRNP gene

in all individuals who succumbed to vCJD

revealed homozygosity for the sequence ‘ATG’,

which encodes methionine, at codon 129. In

the general population, only 33% of people are

homozygous for ATG at this codon of PRNP, so

this particular genetic trait, known as the MM

genotype, has been regarded as a risk factor for

vCJD.8 The second identified recipient of prioninfected

blood, however, was heterozygous for

methionine/valine at codon 129 (MV genotype).

The MV genotype is underrepresented in

sporadic and acquired CJD, and has therefore

been considered a protective genetic trait. The

fact that this individual died of a cause unrelated

to prion disease raises the question of whether

MV heterozygotes might develop a permanent

carrier status, in which the prion replicates

within their body but clinical signs are absent

for an indeterminate period of time.

Of course, it would be imprudent to draw

far-reaching conclusions on the basis of three

cases of blood-borne prion infection. We deem

it justified, however, to highlight a number of

surprising details that have become clear on

analysis of these cases.

First, vCJD prions can indeed propagate using

blood as a vector. In the past, this idea has often

been regarded as ‘worst-case scenario’, ‘highly

specula tive’, and ‘barely a theoretical possibility’.

The wishful thinking of many physicians

involved in blood transfusion has often conjured

up a sense of safety, which, as we regrettably now

know, is unwarranted.

Second, a single unit of vCJD-prion-infected

blood is sufficient to cause transmission of the

disease. This fact is particularly unsettling, as it

can only be taken to signify that the concentration

of ID50 units in blood is relatively high.

One ID50 unit is defined as the infectious

dose sufficient to establish infection in 50% of

recipients; animal experiments indicate that the

amount of prion infectivity needed to reach

one ID50 unit is much higher when prions are

administered intravenously than when they

are inoculated intracerebrally.

Third, blood from preclinically vCJD-infected

patients can be infectious. Although not

un expected, this aspect is particularly worrisome,

as it suggests that preclinical donors

might subjectively not consider themselves at

risk. Consequently, the only way to identify such

donors would be to subject the donation to a

prion screen of satisfactory sensitivity, which is

currently unavailable.

Last, despite all epidemiological evidence to

the contrary, patients who are methionine/valine

heterozygous at codon 129 of the PRNP gene are

susceptible to infection with vCJD prions, which

raises several important questions. Is the virulence

of BSE prions enhanced when passaged

from human to human, as opposed to the

original bovine to human situation? Passaging

experiments of scrapie infectivity between mice

and hamsters indicate that this scenario is highly

plausible.6 Even more importantly, can vCJD

infection of heterozygous individuals establish

a permanent subclinical carrier state? Although

this situation might constitute a best-case

scenario for the infected individuals, it could be

disastrous from an epidemiological viewpoint,

as it might lead to an unrecognized and possibly

self-sustaining epidemic. ...

snip... full text ;

JUNE 2006 VOL 2 NO 6 AGUZZI AND GLATZEL NATURE CLINICAL PRACTICE NEUROLOGY 329

www.nature.com/clinicalpractice/neuro


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is
with a human TSE surveillance system that is terrible
flawed. in 1997 cases of the _reported_ cases of cjd
were at 54, to 163 _reported_ cases in 2004. see stats
here;

p.s. please note the 47 PENDING CASES to Sept. 2005

p.s. please note the 2005 Prion D. total 120(8)
8=includes 51 type pending, 1 TYPE UNKNOWN ???

p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???

p.s. please note 2004 prion disease (6) 6=7 TYPE
UNKNOWN???


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

CWD TO HUMANS = sCJD ???


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


ATYPICAL TSEs in USA CATTLE AND SHEEP ?


http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf


Infected and Source Flocks

As of August 31, 2005, there were 115 scrapie infected
and source flocks (figure 3). There were 3 new infected
and source flocks reported in August (Figure 4) with a
total of 148 flocks reported for FY 2005 (Figure 5).
The total infected and source flocks that have been
released in FY 2005 are 102 (Figure 6), with 5 flocks
released in August. The ratio of infected and source
flocks released to newly infected and source flocks for
FY 2005 = 0.69 :
1. In addition, as of August 31, 2005, 574 scrapie
cases have been confirmed and reported by the National
Veterinary Services Laboratories (NVSL), of which 122
were RSSS cases (Figure 7). This includes 55 newly
confirmed cases in August 2005 (Figure 8). Fifteen
cases of scrapie in goats have been reported since 1990
(Figure 9). The last goat case was reported in May 2005.

snip...

full text ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html

Published online before print October 20, 2005

Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
Medical Sciences

A newly identified type of scrapie agent can naturally
infect sheep with resistant PrP genotypes

( sheep prion | transgenic mice )

Annick Le Dur *, Vincent Béringue *, Olivier
Andréoletti , Fabienne Reine *, Thanh Lan Laï *,
Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||,
Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert
Laude *
*Virologie Immunologie Moléculaires and ||Génétique
Biochimique et Cytogénétique, Institut National de la
Recherche Agronomique, 78350 Jouy-en-Josas, France;
Unité Mixte de Recherche, Institut National de la
Recherche Agronomique-Ecole Nationale Vétérinaire de
Toulouse, Interactions Hôte Agent Pathogène, 31066
Toulouse, France; Agence Française de Sécurité
Sanitaire des Aliments, Unité Agents Transmissibles Non
Conventionnels, 69364 Lyon, France; **Pathologie
Infectieuse et Immunologie, Institut National de la
Recherche Agronomique, 37380 Nouzilly, France; and
¶Department of Pathology, National Veterinary
Institute, 0033 Oslo, Norway


Edited by Stanley B. Prusiner, University of
California, San Francisco, CA, and approved September
12, 2005 (received for review March 21, 2005)

Scrapie in small ruminants belongs to transmissible
spongiform encephalopathies (TSEs), or prion diseases,
a family of fatal neurodegenerative disorders that
affect humans and animals and can transmit within and
between species by ingestion or inoculation. Conversion
of the host-encoded prion protein (PrP), normal
cellular PrP (PrPc), into a misfolded form, abnormal
PrP (PrPSc), plays a key role in TSE transmission and
pathogenesis. The intensified surveillance of scrapie
in the European Union, together with the improvement of
PrPSc detection techniques, has led to the discovery of
a growing number of so-called atypical scrapie cases.
These include clinical Nor98 cases first identified in
Norwegian sheep on the basis of unusual pathological
and PrPSc molecular features and "cases" that produced
discordant responses in the rapid tests currently
applied to the large-scale random screening of
slaughtered or fallen animals. Worryingly, a
substantial proportion of such cases involved sheep
with PrP genotypes known until now to confer natural
resistance to conventional scrapie. Here we report that
both Nor98 and discordant cases, including three sheep
homozygous for the resistant PrPARR allele
(A136R154R171), efficiently transmitted the disease to
transgenic mice expressing ovine PrP, and that they
shared unique biological and biochemical features upon
propagation in mice. These observations support the
view that a truly infectious TSE agent, unrecognized
until recently, infects sheep and goat flocks and may
have important implications in terms of scrapie control
and public health.


--------------------------------------------------------------------------------


Author contributions: H.L. designed research; A.L.D.,
V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed
research; T.B., B.B., P.S., and S.L.B. contributed new
reagents/analytic tools; V.B., O.A., and H.L. analyzed
data; and H.L. wrote the paper.

A.L.D. and V.B. contributed equally to this work.

To whom correspondence should be addressed.

Hubert Laude, E-mail: laude@jouy.inra.fr

www.pnas.org/cgi/doi/10.1073/pnas.0502296102


http://www.pnas.org/cgi/content/abstract/0502296102v1


BRITISH MEDICAL JOURNAL




SOMETHING TO CHEW ON



BMJ



http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2



BMJ



http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1



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

03-025IFA
03-025IFA-2
Terry S. Singeltary


Page 1 of 17

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Thursday, September 08, 2005 6:17 PM

To: fsis.regulationscomments@fsis.usda.gov

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

THE BSE/TSE SUB CLINICAL 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

NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT
RESEARCH

FINDINGS RELEVANT TO CJD AND BSE

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf






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