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SRM

flounder

Well-known member
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Diseases of Livestock

Title: BSE: description of typical and atypical cases


Author

Richt, Juergen


Submitted to: American College of Veterinary Internal Medicine
Publication Type: Proceedings/Symposium
Publication Acceptance Date: April 1, 2007
Publication Date: June 6, 2007
Citation: Richt, J. 2007. BSE: description of typical and atypical cases.
In: Proceedings of the American College of Veterinary Internal Medicine.
2007 ACVIM Forum, June 6-9, 2007, Seattle, Washington. Paper No. 159.

Technical Abstract: Introduction Transmissible spongiform encephalopathy
(TSE) agents or prions induce fatal neurodegenerative diseases in humans and
in other mammalian species. They are transmissible among their species of
origin, but they can also cross the species barrier and induce infection
and/or disease in other species. Human TSEs include Creutzfeldt¿Jakob
disease (CJD), Gerstmann¿Sträussler¿Scheinker syndrome (GSS), Kuru and fatal
familial insomnia (FFI) (1). In animals, four distinct TSE diseases are
recognized: scrapie in sheep and goats, transmissible mink encephalopathy
(TME) in mink, chronic wasting disease (CWD) in cervids, and bovine
spongiform encephalopathy (BSE) in cattle. Although considerable research
has been undertaken, the precise nature of the causative agent remains
controversial. A number of theories describe the etiology, however the
"protein only" theory has emerged to dominate the literature. Bovine
Spongiform Encephalopathy (BSE) Widely referred to as "mad cow disease", BSE
was first identified as a TSE of cattle in the mid 1980s in the U.K. and
more than 180,000 positive cases have been diagnosed in the U.K. to date.
BSE is also transmissible via BSE-contaminated feed to cats (feline
spongiform encephalopathy, FSE) and exotic ungulates (exotic ungulate
encephalopathy, EUE) (2, 3). BSE is a chronic degenerative disease affecting
the central nervous system of cattle. Affected animals display changes in
temperament, abnormal posture, incoordination and difficulty in rising,
decreased milk production, and/or loss of body weight despite continued
appetite (4). The average incubation period is about 4-6 years and all
affected animals succumb to the disease (5). Following the onset of clinical
signs, the animal's condition deteriorates until it either dies or is
destroyed. This process usually takes from 2 weeks to 6 months. Most cases
in the U.K. occurred in dairy cows between 3 and 6 years of age with the
highest susceptibility to infection being in the first 6 months of life;
adult cattle appear to be at relatively low risk of infection (6). Using
epidemiological surveillance programs, many European and non-European
countries have discovered BSE-positive animals within the last decade (7)
(8). BSE has been reported in native-born cattle in twenty-four countries
with a geographic distribution that includes Europe, the Middle East, North
America, and Asia. These outbreaks, caused by the consumption of infected
meat and bone meal containing a malformed prion protein, have resulted in
the destruction of thousands of cattle and have caused significant economic
losses. All currently validated diagnostic tests for BSE require brain
tissue. There are no validated ante mortem tests for BSE available at
present. "Typical" versus "Atypical" BSE cases Molecular characterization of
the abnormal form of the prion protein, called PrPres, has allowed the
identification of "atypical" cases of BSE cases in cattle. BSE in cattle was
considered to be a disease with unique features (9) and the majority of BSE
cases so far have been defined as "typical" BSE cases. However, unusual or
"atypical" cases of BSE have been reported in the past 3 years by
investigators from several countries. Most of these animals were greater
than 8 years of age and of various breeds. There have been two molecular
types of "atypical" BSE isolates described in the literature so far: (i) a
type with a lower molecular mass of the unglycosylated isoform also called
the L-type and (ii) a type with a higher molecular mass of the
unglycosylated isoform, also called the H-type. The L-type has been found in
cattle in Italy (10), Japan (11), Germany (12) and Belgium (13). So far, the
H-type has been described in cattle from France (14), Germany (12) and the
United States (15). The U.S. cases were animals born and raised in the U.S.
(Texas, Alabama). Unusual cases of BSE are an unexpected finding since it
was previously believed that BSE disease in cattle is caused by a single
strain of infectious agent, which has been shown to be very consistent and
uniform in appearance, even after transmission to other species. The reports
of unusual phenotypes of BSE in cattle suggest that different PrPSc
phenotypes exist in cattle with BSE. There are several hypotheses which can
explain these findings: (i) there are variants of the BSE agent with
different molecular features in cattle; (ii) cattle may have been infected
by another source of an infectious prion agent (e.g. scrapie or CWD); or
(iii) a rare sporadic or genetic form of TSE disease could exist in cattle
as described for humans.


http://arsserv0.tamu.edu/research/publications/publications.htm?seq_no_115=208195



Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Diseases of Livestock

Title: Experimental transmission of transmissible spongiform
encephalopathies (scrapie, chronic wasting disease, transmissible mink
encephalopathy) to cattle and their differentiation from bovine spongiform
encephalopathy


Authors

Hamir, Amirali
Cutlip, Randall - ARS RETIRED
Miller, Janice - ARS RETIRED
Kunkle, Robert
Richt, Juergen
Greenlee, Justin
Nicholson, Eric
Kehrli, Marcus


Submitted to: World Association of Veterinary Laboratory Diagnosticians
Publication Type: Proceedings/Symposium
Publication Acceptance Date: August 10, 2007
Publication Date: November 11, 2007
Citation: Hamir, A.N., Cutlip, R.C., Miller, J.M., Kunkle, R.A., Richt,
J.A., Greenlee, J.J., Nicholson, E.M., Kehrli, Jr., M.E. 2007. Experimental
transmission of transmissible spongiform encephalopathies (scrapie, chronic
wasting disease, transmissible mink encephalopathy) to cattle and their
differentiation from bovine spongiform encephalopathy. In: Proceedings of
the World Association of Veterinary Laboratory Diagnosticians 13th
International Symposium, November 11-14, 2007, Melbourne, Australia. p. 29.

Technical Abstract: Introduction: Experimental cross-species transmission of
TSE agents provides valuable information for identification of potential
host ranges of known TSEs. This report provides a synopsis of TSE (scrapie,
CWD, TME) transmission studies that have been conducted in cattle and
compares these findings to those seen in animals with BSE. Materials &
Methods: Generally 6-month-old bull calves were obtained and assigned to
inoculated and control groups. Inoculated calves were housed in a Biosafety
Level 2 isolation barn at the National Animal Disease Center (NADC), Ames,
Iowa. Calves were inoculated intracerebrally with 1 ml of a 10% TSE brain
inoculum. Results: Results of various TSE cattle experiments with
intracerebral inoculation of scrapie, CWD and TME are shown in tabular form
(Table 1). Table 1. Comparison of experimental scrapie, chronic wasting
disease (CWD) and transmissible mink encephalopathy (TME) in cattle
inoculated by the intracerebral route during first passage of the inocula.
Abnormal CNS signs: Scrapie. Anorexia, weight loss, leg and back stiffness.
Some showed incoordination and posterior weakness. Eventual severe lethargy.
CWD. Anorexia, weight loss, occasional aimless circling, listlessness and
excited by loud noises. TME. Variable hyperexcitability with occasional
falling to the ground. Some showing circling and aggressive behavior.
Incubation (survival) time: Scrapie. 14 ¿ 18 months. CWD. 23 ¿ 63 months.
TME. 13 ¿ 16 months. Attack rate: Scrapie. 100%. CWD. CWD from mule deer:
38%. CWD from elk: 86%. TME. 100% Histopatholgic lesions: Scrapie. Some
vacuolation and central of chromatolysis of neurons. CWD. Isolated
vacuolated neurons, a few degenerate axons, and a mild astrocytosis. TME.
Extensive vacuolation of neuronal perikarya and neuropil. Presence of mild
multifocal gliosis. Western blot (brainstem): Scrapie. All three isoforms of
PrP**res present. CWD. All three isoforms of PrP**res seen. TME. All three
isoforms of PrP**res seen. Immunohistochemistry: PrP**res in lymphoreticular
tissues: Scrapie. Not present. CWD. Not present. TME. Not present. PrP**res
in CNS: Scrapie. Present within perikaryon and processes of neurons. CWD.
Multifocal distribution with labeling primarily in glial cells (astrocytes).
TME. Diffusely present and usually evenly distributed in neuropil.
Conclusions: 1. All three TSEs agents (scrapie, CWD and TME) are capable of
propagating in cattle tissues when administered intracerebrally. 2. All
three TSEs can be distinguished from each other and from BSE when inoculated
intracerebrally by histopathology, immunohistochemistry and Western blot
techniques.



http://arsserv0.tamu.edu/research/publications/publications.htm?seq_no_115=212439



Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: Pathobiology and diagnosis of animal transmissible spongiform
encephalopathies: current knowledge, research gaps, and opportunities


Authors

Kehrli, Marcus
O`rourke, Katherine
Hamir, Amirali
Richt, Juergen
Nicholson, Eric
Silva, Christopher
Edelman, Daniel - FOOD AND DRUG ADMINISTRAT
Gay, Cyril


Submitted to: Government Publication/Report
Publication Type: Government Publication
Publication Acceptance Date: May 1, 2007
Publication Date: July 1, 2007
Citation: Kehrli, Jr., M.E., O'Rourke, K.I., Hamir, A.N., Richt, J.A.,
Nicholson, E.M., Silva, C.J., Edelman, D., Gay, C.G. 2007. Pathobiology and
diagnosis of animal transmissible spongiform encephalopathies: current
knowledge, research gaps, and opportunities [government white paper].
Beltsville, MD: Interagency Working Group on Prion Science, Subcommittee on
Pathobiology and Diagnostics. USDA, Agriculture Research Service. 33 p.

Technical Abstract: Transmissible spongiform encephalopathies (TSEs) are
fatal neurologic diseases that can affect several animal species and human
beings. There are four animal TSE agents found in the United States: scrapie
of sheep and goats; chronic wasting disease (CWD) of deer, elk, and moose;
transmissible mink encephalopathy (TME) and bovine spongiform encephalopathy
(BSE). Although the animal TSEs do not cause major death losses among US
livestock populations, they are important because of international trade
issues. The experience of the United Kingdom and Europe in dealing with the
vast majority of the world's BSE cases, serves as a reminder of the need for
continuing vigilance in monitoring risks for public health and research to
answer remaining questions around the pathogenesis and transmission of these
diseases. There remain questions on 1) cross-species transmissibility of
TSEs in livestock and wildlife; 2) the pathobiology of TSEs in natural and
secondary hosts; pathogenesis and transmission of CWD; and 4) pathogenesis
and ante mortem detection of typical and atypical BSE. Our understanding of
the pathogenesis and transmission of these diseases continues to evolve as
ongoing, global TSE research efforts focus on defining tissue sites of
abnormal prion accumulation, routes of infection, methods of strain
differentiation, genetics of susceptibility and ante-mortem diagnostics. In
this paper, a Subcommittee on Pathobiology and Diagnostics of TSEs for an
Interagency Working Group on Prion Science summarizes the science of animal
TSEs in order to identify knowledge gaps for the purpose of prioritizing
animal prion research needs. Because of substantial losses involving
international trade and potential risk for interspecies transmission to
susceptible livestock and possibly humans, the presence of BSE, CWD, scrapie
and TME in the United States presents a liability to U.S. domestic and
alternative livestock industries. In addition, the proven risk of BSE to
agriculture and public health from subclinical or clinically sick animals
requires science-based surveillance for any silent, unrecognized epizootic
expansions of these diseases in populations of animals that could either
directly or indirectly affect food animals. CWD is an example of an
uncontrolled expanding epidemic that threatens not only cervids but possibly
other livestock. CWD also has elicited public health surveillance programs
to monitor for scientific evidence of a prion disease in humans that consume
venison. Therefore, some of the research needs are precautionary, but the
risks to animal and human health from being caught unaware are high. Efforts
are being made by both federal and state regulatory agencies to eradicate
scrapie and CWD, and to determine the prevalence of BSE. The effectiveness
of these programs will depend heavily on having accurate information about
the nature of these diseases, not only in the original hosts, but also in
other species that may be in contact with infected animals.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=212488


5. Neuropathological investigations suggest that PrPsc may be more widely
distributed, with a different brain distribution pattern for L- and H-type
BSE, compared with classical BSE. However, these investigations are limited
by the very low number of animals for which a complete brain has been
available for analysis. There are no data on the peripheral distribution of
PrPsc or infectivity of L- and H-type BSE or on the pathogenesis of these
diseases. However, studies to assess the tissue distribution of infectivity
and PrPsc in animals throughout the incubation period following
intracerebral challenge are underway.


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




USA MAD COW CASES IN ALABAMA AND TEXAS


***PLEASE NOTE***


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


TEXAS AND ALABAMA MAD COW CASES

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125



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



***


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


***

If, on the other hand, atypical BSE continues to occur as typical BSE
disappears, this would be a strong indication that it is indeed sporadic,
and if in addition at least 1 form of what is presently considered as
sporadic CJD (such as the type 2 M/V subtype shown to have a Western blot
signature like BASE) were to increase, this would suggest (although not
prove) a causal relationship (Figure 5).


***


http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm



In FY 2007, 331 scrapie cases have been confirmed and reported by the
National Veterinary Services Laboratories (NVSL), including 59* Regulatory
Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY
2007, two field cases, one validation case, and two RSSS cases were
consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks
in California, Minnesota, Colorado, Wyoming and Indiana respectively.
Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6).
The last goat case was reported in September 2007.


snip...



see full report here ;



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



P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E11National
Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of
scrapie was firstdescribed in Norway in 1998. Several features of Nor98 were
shown to be differentfrom classical scrapie including the distribution of
disease associated prion protein(PrPd) accumulation in the brain. The
cerebellum is generally the most affected brainarea in Nor98. The study here
presented aimed at adding information on theneuropathology in the cerebellum
of Nor98 naturally affected sheep of variousgenotypes 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 histologicallesions
and tissue reactions were evaluated. The types of PrPd deposition
werecharacterized. The cerebellar cortex was regularly affected, even though
there was avariation in the severity of the lesions from case to case.
Neuropil vacuolation wasmore marked in the molecular layer, but affected
also the granular cell layer. There wasa loss of granule cells. Punctate
deposition of PrPd was characteristic. It wasmorphologically and in
distribution identical with that of synaptophysin, suggestingthat PrPd
accumulates in the synaptic structures. PrPd was also observed in thegranule
cell layer and in the white matter. The pathology features of Nor98 in
thecerebellum of the affected sheep showed similarities with those of
sporadicCreutzfeldt-Jakob disease in humans.


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


It will be critical to see whether the atypical BSE isolates behave
similarly to typical BSE isolates in terms of transmissibility and disease
pathogenesis. If transmission occurs, tissue distribution comparisons will
be made between cattle infected with the atypical BSE isolate and the U.S.
BSE isolate. Differences in tissue distribution could require new
regulations regarding specific risk material (SRM) removal.

http://www.ars.usda.gov/research/projects/projects.htm?accn_no=408490



In sheep experimentally infected with BSE, the distribution of the
infectious agent (prion) in tissues is wide-spread as the prion can be found
in secondary lymphoid tissue, skeletal muscle and blood. In considering more
recent attempts at quantifying the risk specifically from this experimental
ovine BSE, and in reviewing biochemical approaches to quantify titres in
affected animals, a major stumbling block to quantification was identified
to be the fact that the influence of age and genotype on the distribution of
BSE infectivity in sheep is only defined qualitatively. The BIOHAZ panel
agreed that absolute quantification of prions by biochemical methods was
difficult. However, in the absence of comprehensive infectivity data to
facilitate a QRA, it was concluded that Specified Risk Materials (SRM)
removal alone was unlikely to be sufficient to eliminate the residual BSE
risk to the consumer from a BSE-infected sheep carcass.


http://www.efsa.europa.eu/en/science/biohaz/biohaz_opinions/ej442_qra_bse_sheep.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: [email protected]

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

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


SEAC 99th meeting on Friday 14th December 2007

snip...


SEAC 99th meeting on Friday 14th December 2007

DECEMBER 14, 2007, 10 year Anniversary of my Moms death 'confirmed' from
Heidenhain Variant Creutzfeldt Jakob Disease


Greetings,


AS one of them _lay_ folks, one must only ponder ;


"WITH the Nor-98 now documented in five different states so far in the USA
in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama,
with both scrapie and CWD running rampant in the USA, IS there any concern
from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN
PHENOTYPE'', and what concerns if any, in relations to blood donations,
surgery, optical, and dental, do you have with these unknown atypical
phenotypes in both humans and animals in the USA ???"


"Does it concern SEAC, or is it of no concern to SEAC?"

"Should it concern USA animal and human health officials?"


snip...


----- Original Message -----
From: xxxxxxxxxx
To: [email protected]
Sent: Thursday, November 22, 2007 5:39 AM
Subject: QUESTION FOR SEAC


Mr Terry S Singeltary Sr.,
Bacliff,
Texas 77518
USA.

Dear Mr Singeltary,


"Thank you for your e-mail of yesterday with the question for SEAC. I can
confirm that this will be asked at the meeting on your behalf and the
question and answer will appear in the minutes of the meeting which will be
published on the SEAC Internet site."


snip...end...TSS

http://www.seac.gov.uk
http://www.seac.gov.uk/agenda/agen141207.htm


Archive Number 20071105.3602
Published Date 05-NOV-2007
Subject PRO/AH/EDR> Prion disease update 2007 (07)

PRION DISEASE UPDATE 2007 (07)
******************************
A ProMED-mail post



snip...

[2] USA: National Prion Disease Pathology Surveillance Center
Date: June 2007
Source: National Prion Disease Pathology Surveillance Center (USA) [edited]



CJD Cases examined
----------------------
Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD

1996 / 42 / 32 / 26 / 4 / 0 / 0
1997 / 115 / 68 / 57 / 9 / 0 / 0
1998 / 93 / 53 / 45 / 7 / 1 / 0
1999 / 114 / 69 / 61 / 8 / 0 / 0
2000 / 151 / 103 / 89 / 14 / 0 / 0
2001 / 208 / 116 / 106 / 9 / 0 / 0
2002 / 255 / 143 / 118 / 23 / 2 / 0
2003 / 272 / 174 / 132 / 41 / 0 / 0
2004 / 334 / 183 / 157 / 21 / 0 / 1*
2005 / 352 / 195 / 152 / 37 / 1 / 0
2006 / 372 / 186 / 143 / 30 / 0 / 1**
2007 / 120 / 68 / 35 / 7 / 0 / 0
TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2

*Acquired in UK
** Acquired in Saudi Arabia
*** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007.
**** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36
type pending (2 from 2005, 8 from 2006, 26 from 2007).

Notes:

-- Cases are listed based on the year of death when available. If the
year of death is not available, the year of sample receipt is used.

-- Referrals: Cases with possible or probable prion disease from
which brain tissue or blood in the case of familial disease were submitted.

-- Inconclusive: Cases in which the samples were not sufficient to
make a diagnosis.

-- Non-vCJD type unknown are cases in which the tissue submitted was
adequate to establish the presence but not the type; in all cases,
vCJD could be excluded.

--
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]


http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963



SEAC 99th meeting on Friday 14th December 2007

http://seac992007.blogspot.com/



2 January 2000

British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well


http://www.bmj.com/cgi/eletters/320/7226/8/b#6117



15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.


http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


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

http://cjdusa.blogspot.com/


BSE (Mad Cow) Update:


Do Reports of sCJD Clusters Matter?


snip... see full text ;

http://cjdtexas.blogspot.com/


CJD QUESTIONNAIRE

http://cjdquestionnaire.blogspot.com/


SCRAPIE USA

http://scrapie-usa.blogspot.com/


NOR-98 ATYPICAL SCRAPIE CASES USA

http://nor-98.blogspot.com/


CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA

http://cjdmadcowbaseoct2007.blogspot.com/


BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS


http://madcowtesting.blogspot.com/


MADCOW USDA the untold story

http://madcowusda.blogspot.com/


USA NVCJD BLOOD RECALLS ONLY ;

http://www.google.com/search?hl=en&q=CJD+BLOOD+RECALLS+TSS&btnG=Search


vCJD case study highlights blood transfusion risk

http://vcjdblood.blogspot.com/



Transmissible Mink Encephalopathy TME

http://transmissible-mink-encephalopathy.blogspot.com/


CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/


TSS
 

flounder

Well-known member
Q4. Have the EU-wide feed controls been effective?

A. Yes. Over the past years there has been a significant overall decrease in the number of BSE cases in cattle across EU Member States due to the stringent control measures put in place to combat the disease (about 850 BSE cases were reported in 2004 in EU Member States compared to 2129 BSE cases in 2002).


Q5. What are the current feed controls in place?

A. With certain exceptions, the current feed controls prohibits the feeding of:

any animal protein to ruminant animals;
any processed animal protein to ruminant and non-ruminant farmed animals; and
gelatin of ruminant origin to both ruminant animals and non-ruminant farmed animals.
(N.B. See feed controls section for current feed controls at a glance).

Q6. Why is fishmeal still banned from ruminant feed?

A. Although it has been agreed that fishmeal does not in itself present a risk of transmitting TSEs, it can be difficult to reliably differentiate under a microscope between the fragments of fish bone and bone fragments from land animals, meaning that the use of fishmeal may mask the presence of mammalian material in feed. Although testing capabilities have improved and new tests are under development, a political discussion on the ethical question of feeding an animal protein to herbivore animals is needed in the European Parliament for a decision on the future use of fishmeal in ruminant feed.

Q7. Is any guidance on the Animal feeding section of the Transmissible Spongiform Encephalopathies (No.2) Regulations 2006 available?

A. Yes. A full set of Guidance Notes (92 KB) is available on the Defra website

Q8. Why can blood meal only be fed to farmed fish when blood products can be fed to all non-ruminant farmed animals?

A. Whilst blood products can only be produced using blood from animals that have passed both post- and ante-mortem inspection, blood meal may be produced using blood from animals that have passed ante-mortem inspection only. Because of the slightly less stringent production standard for the production of blood meal the scope for its use is consequently limited to farmed fish feed.

Q9. Does permitting the feeding of non-ruminant blood products to non-ruminant animals and hydrolysed proteins to all ruminant animals and non-ruminant farmed animals mean that intra-species re-cycling of these products could occur?

A. Technically – yes. However; initial indications are that commercial and consumer pressures mean that feeding blood products in such a way may not be taken up by the industry. In addition, no-one in the UK is currently approved to produce hydrolysed proteins, either because it is generally not economically viable to do so, or because, for some materials, it is perhaps not technically possible to meet the required production standards.

Q10. What animals do the feed controls in the Transmissible Spongiform Encephalopathies (No.2) Regulations 2006 apply to?

A. The feed ban applies to all ruminant animals including those kept as pets or in zoos or safari parks and to all non-ruminant farmed animals including pigs, poultry and horses.

Q11. What are ruminant animals?

A. Ruminant animals are any various hoofed, even-toed, usually horned mammals of the suborder Ruminantia characteristically having a stomach divided into four compartments and chewing a cud consisting of regurgitated, partially digested food. Ruminant animals include cattle, goats, sheep, camels, llamas, giraffes, bison, buffalos, deer, wildebeest and antelopes.

Q12. Does ‘non-ruminant farmed animals’ only apply to animals kept on farms?

A. No. Apart from pet rabbits and pet or ornamental fish, non-ruminant farmed animals, in addition to any pig, poultry, or horse, means any animal that can be kept, fattened, bred and used for the production of food, wool, feathers, skins or any other product of animal origin.

Q13. Are horses covered by the term ‘non-ruminant farmed animals’?

A. Yes. Because the feed controls in the Transmissible Spongiform Encephalopathies (No.2) Regulations 2006 are part of EU wide measures to combat BSE and because horses are kept, fattened, bred and used for the production of food in some EU Member States horses are covered.


http://www.defra.gov.uk/animalh/bse/controls-eradication/feedban-quanda.html#q4


BSE: Disease control & eradication - The feed ban
Feed ban guidance (183 KB)
Born after ban cases
Methods of analysis
National Feed Audit
Legislation
Questions
Leaflet - Authorisation and Registration Requirements (604 KB)
The aim of our BSE-related feed control policy in the UK is clear – to ensure the continued successful decline and eventual eradication of BSE. Practical experience gained over the years has shown that effective controls on livestock feed are the key to achieving this. And we are getting there. The rate of BSE cases in cattle being reported now is significantly lower than in 1988, when the disease was first made notifiable, and the number of new cases continues to decline yet further.

The crucial factor behind this success has been the very high level of compliance with BSE-related feed controls throughout the feed manufacture, supply, and livestock industries. In addition, industry representative organisations’ own quality assurance schemes have considerably enhanced the official level of controls. Bearing in mind, however, that the actual dose of infective material required to infect a ruminant animal with BSE is very small (currently estimated to be as low as a single exposure through feed of 0.001 of a gram), there can be no room for complacency. There is a need for constant vigilance for everyone involved at all points of the feed chain, from those producing ingredients, to manufacturers and suppliers, right down to end-users, and the on-farm feeding practices used.

Feed controls
In the UK, the original feed ban was introduced in 1988 to prevent ruminant protein being fed to ruminants. In addition, it has been illegal to feed ruminants with all forms of mammalian protein (with specific exceptions) since November 1994 and to feed any farmed livestock, including fish and horses, with mammalian meat and bone meal (mammalian MBM) since 04 April 1996.
EU-wide Feed Controls
Harmonised EU control measures were introduced in 2001 to combat the spread of BSE. The measures included a ban on the feeding of processed animal proteins to animals which are kept, fattened or bred for the production of food. These control measures combined with domestic controls have proved successful and have significantly reduced the number of BSE cases across EU member states.
The Standing Committee on the Food Chain and Animal Health on 5 August 2005 introduced new elements to the controls, whilst still maintaining the ban on the feeding of processed animal proteins to farmed animals. The new elements are contained in the EU Regulation (1292/2005) which amended Annex IV of the Regulation (999/2001) from 1 September 2005.
The amendments are currently implemented by the Transmissible Spongiform Encephalopathies (No.2) Regulations 2006, which came into force on 3 May 2006.
The measures set out in EU Regulation (999/2001) are currently being discussed in the context of the EU TSE Roadmap and possible changes to the controls are being considered.


Feed controls - At a glance


SNIP...


Legislation regarding catering waste and former food stuff and controls on unprocessed animal by-products are in the Animal By-Products Regulations.
The BSE-related feed controls are set out in the Transmissible Spongiform Encephalopathies (No.2) Regulations 2006. Guidance notes (92KB) are available.
Production or use of farmed animal feed containing restricted animal proteins is a leaflet aimed at feed producers and farmers to inform about the authorisation and registration requirements under the new Transmissible Spongiform Encephalopathies Regulations 2006.

Monitoring and enforcement
To monitor compliance with BSE-related livestock feed controls in Great Britain, the State Veterinary Service (SVS) has been taking feed samples for analysis since February 1996. From 2001, previous sampling programmes were replaced by the risk-based National Feed Audit. Responsibility for enforcement in the event of a breach of the ban lies primarily with local authorities.
Page last reviewed: 10 September, 2006
Page last modified: 19 December, 2006


http://www.defra.gov.uk/animalh/bse/controls-eradication/feed-ban.html



BSE: Disease control & eradication - the feed ban - born after the July 1988 ban (BAB) cases
[back to The feed ban]

The July 1988 ban on feeding ruminant-derived protein to ruminants (e.g. cattle, sheep, goats and deer) in Great Britain, significantly reduced the number of cattle exposed to BSE infection. There was a marked decrease in the number of confirmed BSE cases born after the July 1988 ban (BAB cases). The prolonged incubation period of BSE delayed the corresponding effect on the annual confirmation rate by approximately five years. Detailed investigations of the initial BAB cases indicated that the most likely source of infection in these cases was the continued use of feed manufactured before the 1988 ban. In November 1994, GB implemented an EU-wide ban on the feeding of mammalian protein to ruminants.

Reasons for BAB cases
By autumn 1994 the decline in the epidemic, which commenced in early 1993, was occurring more slowly in the northern and eastern regions of England in which the proportion of pigs relative to cattle was highest. At that time pig and poultry feed could legitimately contain ruminant meat and bone meal (MBM), and in such regions there was an increased risk of cross contamination of ruminant feed with MBM, either in the feed mill, during transport, or on farm. Samples of cattle feed taken on a farm in August 1994 were shown to contain ruminant MBM, demonstrating that such cross-contamination could occur. A 1994 case-control study looked closely at possible causes of BSE in BAB animals. This study found no statistical significance of horizontal or vertical transmission of BSE in BAB cases and concluded that a food borne source of infection was the most likely explanation.

The continued presence of BSE infectivity in MBM suggested failings in the Specified Risk Material (SRM), then called Specified Bovine Offals (SBO), controls. The most likely source of this problem came from the practice of splitting bovine skulls. Until August 1995, when the practice was banned, bovine skulls could be split to remove the brain for disposal as SBO, allowing the remaining bone to be sent for rendering to meat and bone meal. Brain material sometimes remained in the skull, providing a significant route by which infectivity could enter MBM. Other SBO may have been inadequately separated from non-SBO material, providing another potential route of infection. Research has since shown that some of the rendering systems in use until December 1994 had little effect on BSE infectivity. Current research indicates that 1 milligram (one thousandth of a gram) of unprocessed brain from a clinically affected cow, fed to calves, can cause infection and eventually disease.

Prevention of Cross Contamination
In August 1995, the controls on the handling of SBOs were strengthened to further protect animal health. They required that the whole skull (with the exception of the tongue) be disposed of as an SBO and that rendering plants use dedicated lines for the processing of SBO tissues. In April 1996 the use of mammalian MBM was banned in all feed for livestock, fish and equine animals. This was not as a result of fears that non-ruminant species may catch BSE by oral exposure, but to remove any possible risk of cross-contamination of cattle rations in feed mills, during transport or on farms with MBM intended for other species. A Voluntary Feed Recall Scheme, launched in June 1996, encouraged removal of residual stocks of mammalian MBM from UK farms, feed mills and feed merchants. The VFR Scheme offered free collection and disposal of residual stocks of feed. From 1 August 1996 it became an offence (except in very tightly defined and controlled circumstances) to hold mammalian MBM on farms or in feed mills and premises where livestock feed is used, produced, prepared or stored.

BSE: Disease Control & Eradication - The Feed Ban - Born After the Reinforced Ban (BARB) Cases
Additional measures to prohibit the feeding of mammalian MBM to all farmed livestock have been in place in the United Kingdom since 1 August 1996. This is regarded as the date the reinforced feed ban became effective. BSE cases born after July 1996 are referred to as born after the reinforced ban (BARB) cases. The State Veterinary Service carries out a detailed epidemiological investigation into all BARB cases in Great Britain.

Incidence
The tables below contain details for the cases in animals born after the reinforced feed ban of August 1996 that have been confirmed during the last 12 months, in Great Britain and in Northern Ireland. Details of previous cases are available in a separate table.



SNIP...


Note:
The table above does not include one confirmed case of BSE in an animal in which the disease was confirmed on 18 January 2007. This case was identified under the compulsory BSE surveillance programme, an aspect of which requires the UK to test all cattle aged 30 months or over before they enter the food chain. The date of birth of this animal is under investigation but it is likely to have been born after July 1996.

A comparison of the number of BSE cases born before and after the 1996 feed ban provides evidence of its impact:

At the end of August 2005 in Great Britain, there were over 44 000 BSE cases in cattle born between July 1988 and July 1996, but only 110 BARB cases born between August 1996 and August 2005;
At the end of August 2005 in Northern Ireland, there were almost 600 BSE cases in cattle born between January 1989 and July 1996, but only 16 BARB cases born between August 1996 and August 2005.·
There have been over 184 000 BSE cases in the UK in total.

Most BARB cases are detected by active surveillance and the majority of those detected by active surveillance have been emergency slaughtered animals presented to the Over Thirty Month Scheme (OTMS) for disposal.

Reasons for BARB Cases
The UK prohibited the use of mammalian MBM in all feed for livestock, fish and equine animals in April 1996. In December 2000 the European Union decided to prohibit the feeding of processed animal protein (PAP) to all farmed animals from January 2001. The ten new Member States joining the EU in 2004 may not have implemented full BSE controls until after January 2001.

One possible reason for BARB cases is the contamination of cattle feed ingredients with mammalian MBM handled, stored and transported outside the UK, prior to the 2001 EU-wide ban. This hypothesis comes from a detailed analysis of epidemiological data on the first 59 cases which has been considered by the EU's Scientific Steering Committee and more recently by the European Food Safety Authority. There is also evidence from epidemiological investigations into BARB cases that some cases result from the persistence of infection in feed stores beyond the dates of the official feed ban.

In November 2004, Defra appointed an independent expert, Professor William Hill FRS of the University of Edinburgh to carry out an independent review of the Department’s work on BARB cases in the UK.

Professor Hill published his review in July 2005. Professor Hill’s review concludes that the UK controls in place to eliminate BSE in cattle are soundly based. The review confirms that the elimination of food-borne sources is key to the eradication of BSE. It recommends that risk-based controls and monitoring should be maintained on animals and feed. The report is available (177 KB) and the Defra response is available here (55KB).

Public Health
The main public health control is the removal of Specified Risk Material (SRM) in abattoirs. This removes over 99% of infectivity from any cattle infected with BSE. However, all healthy cattle aged over 30 months and all emergency slaughtered cattle aged over 24 months must be BSE tested with negative results before they can be sold for human consumption. In March 2005, the UK started culling and incinerating the cohorts of all BSE cases, where the cohort animals were born after July 1996. A cohort is defined as a group of bovine animals born 12 months either side of the BSE case, or reared with it in the first year of their lives. i.e. cattle potentially exposed to the same feed during the period of greatest susceptibility to BSE.

Multiple Cases and the South West Wales Cluster
Eleven herds in Great Britain have generated a total of 24 BARB cases. These include two triple BARB cases (Pembrokeshire and Wiltshire) and nine paired BARB cases (Cornwall, Devon, Dorset, Somerset, Shropshire, Ceredigion and Orkney). Most of these natal herds are located in South West/ West England or South West Wales. The historic management of two of the three Ceredigion paired BARB case herds is such that these two herds can be regarded together as generating one quadruple BARB case: the two natal herds, are based at two premises. The four BARBs were moved to a third premises at approximately 2-months of age for rearing as a single unit, and remained there until approximately 30-months of age, when they returned to their natal premises.

21/24 of the multiple cases succumbed to BSE in their natal herds. 19/24 of the multiple cases have been detected by active surveillance. At least 11/13 of the subsequent BARB cases were cohorts of the index cases. 6/13 of the subsequent BARB cases were detected through the cohort cull which commenced in March 2005.

These findings support a common feed source during the first 12 months of life in each of the affected herds. A statistical analysis of the number of multiple BARB cases, carried out in 2005, provides evidence that BARB cases do not all occur by chance.

There is also an epidemiologically significant cluster of 8 BARB cases born between 1 August 1997 and 31 July 1998 in South West Wales. These cases include the quadruple BARB case and one of the paired BARB cases, and all the animals received feed from two local feed mills.

In 2005, another herd in South West Wales experienced a BSE case born in October 2001. The subsequent cull of the cohorts of this case detected two further cases born in September 2001 and May 2002. Detailed epidemiological investigations of the herd of origin suggested that these three cases were the result of infected feed from a local mill retained in a feed bin. The feed bin had been in use for adult cattle since September 1998, but was moved and filled with calf rearer feed in late July 2002. One or more bulk consignments of imported feed contaminated with infective material, supplied in 1998/99 to several local feed mills, is believed to have produced the South Wales BARB clusters.

A report of the feed investigations into herds generating the cluster of BARB cases in South West Wales and into herds experiencing multiple BARB cases is available below:

Report on Extended feed investigations into herds generating a cluster of BSE cases born after July 1996 in South West Wales & into herds experiencing multiple BSE cases born after July 1996. (112 KB);
Appendix 1: UK BSE cases in animals born after the reinforced feed ban of 31 July 1996. (20 KB);
Appendix 2: Details of multiple BARB BSE cases in Great Britain. (51 KB).
A full report of the epidemiological investigations into the three Pembrokeshire BARB cases born in 2001 and 2002 is available below:

Final report on BSE confirmed in an animal born on 3 October 2001 & 2002 cohort animals born on 28 September 2001 & 1 May 2002 in Pembrokeshire herd. (56 KB).
Persistence of the BSE Agent in Feed Stores
There is evidence from the epidemiological investigations into the herds experiencing multiple BARB cases that some of these cases may have resulted from the persistence of infection in farm feed bins beyond the dates of the official feed ban. We believe that the current risk of BSE infection to cattle as a result of the persistence of the BSE agent in farm feed bins, from feed produced before either the 1996 UK feed ban or the 2001 EU feed ban, is extremely low. Nevertheless we recommend that cattle keepers clean out feed bins routinely and very thoroughly, particularly those feed bins which were in use before August 1996 and have not been cleaned out since. This is especially important for herds in the areas where herds have experienced multiple BARB cases, and any herds which have experienced homebred BSE cases. The design of many feed bins is such that specialist contractors and/or equipment may be required to minimise the health and safety risks of cleaning the inside of feed bins.

Position in Other Member States
The European Union imposed an EU-wide ban on the feeding of mammalian protein to ruminants in 1994, and an EU-wide ban on the feeding of processed animal protein (PAP) to all farmed animals from January 2001.

Most other EU Member States have experienced cases born in or after 1996. By the end of 2004, some Member States reported a higher prevalence of such cases (cases per million adult cattle) than the UK.

Some EU Member States have also had one or more BSE cases confirmed in cattle born in 2000, 2001 and 2002.

Page last modified: 20 December, 2007
Page last reviewed: 10 September, 2006


http://www.defra.gov.uk/animalh/bse/controls-eradication/feedban-bornafterban.html
 

flounder

Well-known member
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA
2007



END OF ENFORCEMENT REPORT FOR MARCH 21, 2007



http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html



MORE 2006 FEED BAN VIOLATIONS BELOW, ''IN COMMERCE'' ;


Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL,
TN, AND WV
Date: September 6, 2006 at 7:58 am PST

PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE
None
RECALLING FIRM/MANUFACTURER
Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone
on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is
complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based
protein.
VOLUME OF PRODUCT IN COMMERCE
477.72 tons
DISTRIBUTION
AL
______________________________
PRODUCT
a) Dairy feed, custom, Recall # V-134-6;
b) Custom Dairy Feed with Monensin, Recall # V-135-6.
CODE
None. Bulk product
RECALLING FIRM/MANUFACTURER
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on
June 28, 2006.
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated
recall is complete.
REASON
Possible contamination of dairy feeds with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
1,484 tons
DISTRIBUTION
TN and WV


http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html




Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,
MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-115-6
CODE
None
RECALLING FIRM/MANUFACTURER
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or
about July 14, 2006. FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
Approximately 2,223 tons
DISTRIBUTION
KY

______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-116-6
CODE
None
RECALLING FIRM/MANUFACTURER
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006.
FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
1,220 tons
DISTRIBUTION
KY

______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-117-6
CODE
None
RECALLING FIRM/MANUFACTURER
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated
recall is completed.
REASON
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
40 tons
DISTRIBUTION
LA and MS

______________________________
PRODUCT
Bulk Dairy Feed, Recall V-118-6
CODE
None
RECALLING FIRM/MANUFACTURER
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA
initiated recall is complete.
REASON
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
7,150 tons
DISTRIBUTION
MS

______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-119-6
CODE
None
RECALLING FIRM/MANUFACTURER
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm
initiated recall is complete.
REASON
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE
87 tons
DISTRIBUTION
MS

______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-120-6
CODE
None
RECALLING FIRM/MANUFACTURER
Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm
initiated recall is complete.
REASON
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE
350 tons
DISTRIBUTION
AL and MS

______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,
50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD
Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags,
Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags,
Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher,
50 lb bags, Recall # V-127-6
CODE
All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit
on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated
recall is ongoing.
REASON
Poultry and fish feeds which were possibly contaminated with ruminant based
protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
7,541-50 lb bags
DISTRIBUTION
AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###


http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html


Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN
COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J.
Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm
initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated
with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ?????
Date: August 6, 2006 at 6:19 pm PST
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated
recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
?????
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


CJD WATCH MESSAGE BOARD
TSS
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22
71.248.128.67


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL
FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER
H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and
by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
10,878.06 tons
DISTRIBUTION
Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###


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


Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST
Public Health Service
Food and Drug Administration

New Orleans District
297 Plus Park Blvd.
Nashville, TN 37217

Telephone: 615-781-5380
Fax: 615-781-5391


May 17, 2006

WARNING LETTER NO. 2006-NOL-06

FEDERAL EXPRESS
OVERNIGHT DELIVERY

Mr. William Shirley, Jr., Owner
Louisiana.DBA Riegel By-Products
2621 State Street
Dallas, Texas 75204

Dear Mr. Shirley:

On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration
(FDA) investigator inspected your rendering plant, located at 509 Fortson
Street, Shreveport, Louisiana. The inspection revealed significant
deviations from the requirements set forth in Title 21, Code of Federal
Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in
Ruminant Feed. This regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE). You failed to
follow the requirements of this regulation; products being manufactured and
distributed by your facility are misbranded within the meaning of Section
403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act
(the Act).

Our investigation found you failed to provide measures, including sufficient
written procedures, to prevent commingling or cross-contamination and to
maintain sufficient written procedures [21 CFR 589.2000(e)] because:

You failed to use clean-out procedures or other means adequate to prevent
carryover of protein derived from mammalian tissues into animal protein or
feeds which may be used for ruminants. For example, your facility uses the
same equipment to process mammalian and poultry tissues. However, you use
only hot water to clean the cookers between processing tissues from each
species. You do not clean the auger, hammer mill, grinder, and spouts after
processing mammalian tissues.

You failed to maintain written procedures specifying the clean-out
procedures or other means to prevent carryover of protein derived from
mammalian tissues into feeds which may be used for ruminants.

As a result . the poultry meal you manufacture may contain protein derived
from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR
589.2000(e)(1)(i), any products containing or may contain protein derived
from mammalian tissues must be labeled, "Do not feed to cattle or other
ruminants." Since you failed to label a product which may contain protein
derived from mammalian tissues with the required cautionary statement. the
poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the
Act.

This letter is not intended as an all-inclusive list of violations at your
facility. As a manufacturer of materials intended for animal feed use, you
are responsible for ensuring your overall operation and the products you
manufacture and distribute are in compliance with the law. You should take
prompt action to correct these violations, and you should establish a system
whereby violations do not recur. Failure to promptly correct these
violations may result in regulatory action, such as seizure and/or
injunction, without further notice.

You should notify this office in writing within 15 working days of receiving
this letter, outlining the specific steps you have taken to bring your firm
into compliance with the law. Your response should include an explanation of
each step taken to correct the violations and prevent their recurrence. If
corrective action cannot be completed within 15 working days, state the
reason for the delay and the date by which the corrections will be
completed. Include copies of any available documentation demonstrating
corrections have been made.

Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S.
Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie,
Louisiana 70001. If you have questions regarding any issue in this letter,
please contact Mr. Rivero at (504) 219-8818, extension 103.

Sincerely,

/S

Carol S. Sanchez
Acting District Director
New Orleans District


http://www.fda.gov/foi/warning_letters/g5883d.htm



USDA FSIS SRM TSE QUARTERLY ENFORCEMENT REPORT UPDATE

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&D=1&H=1&P=10713


http://www.prwatch.org/node/4541


Subject: Experimental BSE Infection of Non-human Primates: Efficacy of the
Oral Route
Date: September 29, 2007 at 12:50 pm PST

P04.27

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


Background:

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.


Aims:

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.


Methods:


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).


Results:


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.


Conclusions:


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
vCJD 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).


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in
primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


LETS start with the UKBSEnvCJD only theory, lets look at UK exports to USA,
Canada, and Mexico.
the imported only theory. ...



1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY
other Countries list in PDF file)

USA -------- TOTALS ''8'' TONS
CANADA -- TOTALS ''29'' TONS

1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA

USA ------- TOTALS ''358'' TONS

CANADA --TOTALS ''24'' TONS

BONE-IN BEEF AND VEAL

USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons
above?)

UK EXPORT OF LIKE CATTLE TO USA AND CANADA

1986 TO 1996 USA TOTAL = 1297

1986 TO 1996 CAN TOTAL = 299

http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf


UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987

CANADA -- 64,526 KG

UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED
OR FROZEN OTHER THAN LIVER DEC 1987 YTD

USA -- 45,943 KG

UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988

CANADA -- 4,163 KG

PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE
TO DEC 1988

USA -------- 28,609 KG
CANADA -- 22,044 KG

MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989

USA -------- 17,880 KG
MEXICO---- 33,444 KG

BONELESS MEAT OF BOVINE 1989

USA --------111,953 KG
CANADA---1,800 KG
MEXICO --- 1,143,387 KG

EDIBLE OFFAL OF BOVINE ANIMALS 1989

USA -------- 19,980 KG
MEXICO--- 31,244 KG

MORE........

MEAT OF BOVINE ANIMALS BONELESS 1990

USA 146,443


http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf




UK Exports of Live Cattle by Value 1986-96

USA 697 LIVE CATTLE

CANADA 299 LIVE CATTLE

http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf



UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995

USA 24 TONS

CANADA 83 TONS

http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf



HOWEVER, my files show 44 tons of greaves for USA. ...TSS



Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: [email protected]
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: [email protected] (Receipt Notification Requested) (Non Receipt
Notification Requested)

Terry Meat and bonemeal is not specifically classified for overseas trade
purposes. The nearest equivalent
is listed as flours and meals of meat or offals (including tankage), unfit
for human consumption; greaves.
UK exports of this to the US are listed below:

Country Tonnes

1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990

Data for exports between 1975 and 1979 are not readily available. These can
be obtained (at a charge)
from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372
463121) or Abacus (01245 252222).

Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C

====================================== END...TSS



BSE GBR RISK ASSESSMENTS, USA, CANADA, AND MEXICO




EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)
of the United States of America (USA)


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group
on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) were asked by the European Commission (EC) to provide an
up-to-date scientific report on the GBR in the United States of America,
i.e. the likelihood of the presence of one or more cattle being infected
with BSE, pre-clinically as well as clinically, in USA. This scientific
report addresses the GBR of USA as assessed in 2004 based on data covering
the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic
cattle in the middle of the eighties. These cattle imported in the mid
eighties could have been rendered in the late eighties and therefore led to
an internal challenge in the early nineties. It is possible that imported
meat and bone meal (MBM) into the USA reached domestic cattle and leads to
an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports
from BSE risk countries were slaughtered or died and were processed (partly)
into feed, together with some imports of MBM. This risk continued to exist,
and grew significantly in the mid 90’s when domestic cattle, infected by
imported MBM, reached processing. Given the low stability of the system, the
risk increased over the years with continued imports of cattle and MBM from
BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely
but not confirmed that domestic cattle are (clinically or pre-clinically)
infected with the BSE-agent. As long as there are no significant changes in
rendering or feeding, the stability remains extremely/very unstable. Thus,
the probability of cattle to be (pre-clinically or clinically) infected with
the BSE-agent persistently increases.


http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/573.html



http://www.efsa.europa.eu/





EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)
of Canada


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group
on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) were asked to provide an up-to-date scientific report on the GBR
in Canada, i.e. the likelihood of the presence of one or more cattle being
infected with BSE, pre-clinically as well as clinically, in Canada. This
scientific report addresses the GBR of Canada as assessed in 2004 based on
data covering the period 1980-2003.

The BSE agent was probably imported into the country middle of the eighties
and could have reached domestic cattle in the early nineties. These cattle
imported in the mid eighties could have been rendered in the late eighties
and therefore led to an internal challenge in the early 90s. It is possible
that imported meat and bone meal (MBM) into Canada reached domestic cattle
and led to an internal challenge in the early 90s.

A certain risk that BSE-infected cattle entered processing in Canada, and
were at least partly rendered for feed, occurred in the early 1990s when
cattle imported from UK in the mid 80s could have been slaughtered. This
risk continued to exist, and grew significantly in the mid 90’s when
domestic cattle, infected by imported MBM, reached processing. Given the low
stability of the system, the risk increased over the years with continued
imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of Canada is III, i.e. it is
confirmed at a lower level that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as the system remains
unstable, it is expected that the GBR continues to grow, even if no
additional external challenges occur.



http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/564.html



http://www.efsa.europa.eu/






EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)
of Mexico


Last updated: 8 September 2004 Publication Date: 20 August 2004

Adopted July 2004 (Question N° EFSA-Q-2003-083)


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group
on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) were asked by the European Commission (EC) to provide an
up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of
the presence of one or more cattle being infected with BSE, pre-clinically
as well as clinically, in Mexico. This scientific report addresses the GBR
of Mexico as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into Mexico and could have reached
domestic cattle. These cattle imported could have been rendered and
therefore led to an internal challenge in the mid to late 1990s. It is
possible that imported meat and bone meal (MBM) into Mexico reached domestic
cattle and leads to an internal challenge around 1993.

It is likely that BSE infectivity entered processing at the time of imported
‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at -
risk’ cattle (mid to late 1990s). The high level of external challenge is
maintained throughout the reference period, and the system has not been made
stable. Thus it is likely that BSE infectivity was recycled and propagated
from approximately 1993. The risk has since grown consistently due to a
maintained internal and external challenge and lack of a stable system.

EFSA concludes that the current geographical BSE risk (GBR) level is III,
i.e. it is likely but not confirmed that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. The GBR is likely to increase
due to continued internal and external challenge, coupled with a very
unstable system.



http://www.efsa.europa.eu/



http://www.efsa.europa.eu/



we'll have to see what 2008 brings us. i'm not holding my breath. ...TSS
 

flounder

Well-known member
flounder said:
snip...

In FY 2007, 331 scrapie cases have been confirmed and reported by the
National Veterinary Services Laboratories (NVSL), including 59* Regulatory
Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY
2007, two field cases, one validation case, and two RSSS cases were
consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks
in California, Minnesota, Colorado, Wyoming and Indiana respectively.
Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6).
The last goat case was reported in September 2007.


snip...



see full report here ;



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



P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E11National
Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of
scrapie was firstdescribed in Norway in 1998. Several features of Nor98 were
shown to be differentfrom classical scrapie including the distribution of
disease associated prion protein(PrPd) accumulation in the brain. The
cerebellum is generally the most affected brainarea in Nor98. The study here
presented aimed at adding information on theneuropathology in the cerebellum
of Nor98 naturally affected sheep of variousgenotypes 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 histologicallesions
and tissue reactions were evaluated. The types of PrPd deposition
werecharacterized. The cerebellar cortex was regularly affected, even though
there was avariation in the severity of the lesions from case to case.
Neuropil vacuolation wasmore marked in the molecular layer, but affected
also the granular cell layer. There wasa loss of granule cells. Punctate
deposition of PrPd was characteristic. It wasmorphologically and in
distribution identical with that of synaptophysin, suggestingthat PrPd
accumulates in the synaptic structures. PrPd was also observed in thegranule
cell layer and in the white matter. The pathology features of Nor98 in
thecerebellum of the affected sheep showed similarities with those of
sporadicCreutzfeldt-Jakob disease in humans.


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


It will be critical to see whether the atypical BSE isolates behave
similarly to typical BSE isolates in terms of transmissibility and disease
pathogenesis. If transmission occurs, tissue distribution comparisons will
be made between cattle infected with the atypical BSE isolate and the U.S.
BSE isolate. Differences in tissue distribution could require new
regulations regarding specific risk material (SRM) removal.

http://www.ars.usda.gov/research/projects/projects.htm?accn_no=408490



snip...



Terry S. Singeltary Sr. [[email protected]]

Monday, January 08, 200l 3:03 PM

[email protected]
CJDIBSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and
Consultants Staff January 2001 Meeting (short version)

Greetings again Dr. Freas and Committee Members,


snip...


with same feeding and rendering practices as that of U.K.
for years and years, same scrapie infected sheep used
in feed, for years and years, 950 scrapie infect FLOCKS
in the U.S. and over 20 different strains of scrapie
known to date. (hmmm, i am thinking why there is not
a variant scrapie, that is totally different than all
the rest)? just being sarcastic. ...



snip...end... see full text Monday, January 08, 200l 3:03 PM ;


http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf



TSS
 

rkaiser

Well-known member
Kind of hard to get the drift of your snips and pastes etc, Terry. Read your document at the bottom of the last post which you apparently wrote in 2001. Are you saying that you have had a recent response from this letter or are you simply trying to show us that even though the USDA accepts the feed transmission theory they continue to ignore your mounds of evidence? (Which I can only say I admire your diligence and passion to produce.)

As always Terry, I support any position that leads to a BSE test, or a TSE test in general, however it seems like you are bashing your head against a brick wall when you post letters from 7 years ago and have got no where.

Yes it is all about money and human greed. But maybe a different approach is needed. Searching for a cause beyond simple transmission which is not seen as crucial by your government or ours due to the lack of human death caused by bovines without a shadow of doubt.

Not looking for a fight Terry, just letting you know that someone is actaully reading part of your posts.
 

Big Muddy rancher

Well-known member
I'm reading parts as well.
What I get from Terry's posts is that the USA has the same risk of BSE as Canada. Not that Terry is happy we are trading in these commodities .
 

flounder

Well-known member
Greetings Ranchers,


Happy New Year ! :? :tiphat:


What will the new year bring us in 2008 ? well, in my opinion, 2008 could produce all the rapid test it wanted, validate old rons urine test, and all the others, but there is one thing that will not happen in the USA in 2008, using any of them to confirm any mad cows in the USA, especially in a way that would locate and document all of them i.e. say testing all, or at least one million in a year, but this time using proper surveillance and testing protocols. THIS my friend will not happen with the current administration, and i am beginning to have my doubts with the next one to follow, in regards to properly documenting and eradicating all TSE in the USA food producing livestock and in the wild. it's just not going to happen. they will keep shooten and shoveling, to keep from documenting. ...TSS


http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.html

http://madcowtesting.blogspot.com/


rkaiser wrote ;


Kind of hard to get the drift of your snips and pastes etc, Terry. Read your document at the bottom of the last post which you apparently wrote in 2001. Are you saying that you have had a recent response from this letter or are you simply trying to show us that even though the USDA accepts the feed transmission theory they continue to ignore your mounds of evidence? (Which I can only say I admire your diligence and passion to produce.)


======


THE point i was trying to make was that in that letter in to the FDA in 2001, i called the atypical scrapie. sadly, it took them almost 7 years later to finally documented it here. NOW, in 2007, they finally documented 5 cases of the NOR-98 in 5 different states. and then i attempted to point out the SRM problem with these atypicals, and the fact they will most likely have to be enhanced in the near future. ...END ...tss


======


As always Terry, I support any position that leads to a BSE test, or a TSE test in general, however it seems like you are bashing your head against a brick wall when you post letters from 7 years ago and have got no where.


======


ACTUALLY, we have gotten somewhere, we have documented 5 different cases, in 5 different states of the atypical NOR-98 TSE in sheep in the USA. This is disturbing, and is a part of the puzzle. sadly though, it seems to have been put on the back burners, along with BSE and or the h-BASE. not enough _documented_ body bags. it's simply an acceptable corporate homicide i.e. FOR PROFIT, and this goes much further than the UKBSEnvCJD hamburger eating adolescents only theory. friendly fire, second, third, fourth passage and so on, will play a huge roll in the spreading of this TSE agent. ...end. ...TSS



NOR-98 ATYPICAL SCRAPIE CASES USA

http://nor-98.blogspot.com/


SCRAPIE USA

http://scrapie-usa.blogspot.com/



ALSO, just today, i read in the paper where old GW is going to revamp the FOIA, and now he will release data :liar:



Jan. 1, 2008, 12:56AM
Bush signs bill to expand Freedom of Information Act


By BEN FELLER
Associated Press

CRAWFORD — President Bush on Monday signed a bill aimed at giving the public and the media greater access to information about what the government is doing.

The new law toughens the Freedom of Information Act, the first such makeover to the signature public-access law in a decade. It amounts to a congressional pushback against the Bush administration's movement to greater secrecy since the terrorist attacks of 2001. ...


http://www.chron.com/disp/story.mpl/nation/5414137.html


:disagree:


I'M STILL WAITING DAMNET. ...tss


F.O.I.A.

http://foiamadsheepmadrivervalley.blogspot.com/


======


Yes it is all about money and human greed. But maybe a different approach is needed. Searching for a cause beyond simple transmission which is not seen as crucial by your government or ours due to the lack of human death caused by bovines without a shadow of doubt.

Not looking for a fight Terry, just letting you know that someone is actually reading part of your posts.


======


I COULD not agree more with you on the part here ''maybe a different approach is needed''.

glad some are at least reading the data, even if you dont agree with it all. we have to keep discussing this, and searching for the
amplification and transmission of the TSE's. Then, we must stop those actions that are amplifying and transmitting the TSE agent. ...end. ...TSS


======


big muddy wrote ;


I'm reading parts as well.
What I get from Terry's posts is that the USA has the same risk of BSE as Canada.


======


CORRECT!. ...TSS


======


Not that Terry is happy we are trading in these commodities .


======


WHAT i am not happy about is the OIE BSE MRR policy, and the junk science used to fabricate it.
it's nothing more than a legal tool to trade all strains of TSE globally. over time, this will be proven to
have been a lethal mistake. for how many ? only time will tell. ...end. ...TSS



Monthly Test Results

APHIS reports ongoing surveillance totals monthly.

The BSE ongoing surveillance program will sample approximately 40,000
animals each year. Under the program, USDA will continue to collect samples
from a variety of sites and from the cattle populations where the disease is
most likely to be detected, similar to the enhanced surveillance program
procedures.

BSE Ongoing Surveillance Program Cumulative Total

From Sep 1, 2006: 46,673

Month Number of Tests
Sep 2007
3,832

Aug 2007
5,433

Jul 2007
4,267

Jun 2007
4,106

May 2007
5,217

Apr 2007
5,104

Mar 2007
4,130

Feb 2007
2,937

Jan 2007
3,075

Dec 2006
2,477

Nov 2006
2,235

Oct 2006
2,068

Sep 2006
1,792


snip...end


http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml


let's see now, from a USA cattle herd of some 95 million head, the expanded
2004 BSE cover-up that suddenly halted after the finding of the 2 BASE cases
i.e. atypical h-BSE documented in Alabama and Texas, this after rendering
another stumbling and staggering mad cow in Texas that was suspect BSE, but
_no_ test at all was given, and after suspect BSE samples sat stored on some
shelf somewhere for months and months, while the OIE BSE MRR was being born,
etc, etc, the USA total figures for BSE testing in this day and time, regardless of the
figures the OIE recommend, are terribly flawed to say the least. ...TSS


BSE OIE USDA

http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html



BOTTOM LINE $$$


(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 the
Central Bureau,

http://www.oie.int/eng/Session2007/RF2006.pdf



THE only difference between the UK poisoning the globe, and the USA, it is
now legal with GWs and OIEs BSE MRR policy ;


IT's O.K. to poison 3rd world countries ;

http://www.bseinquiry.gov.uk/files/yb/1994/05/20002001.pdf


On 20 February 1990, Dr Pickles wrote to Ms Verity
(APS/CMO). Dr Picklesí minute included the following:

1. Mr Meldrum is arguing that MAFF have already taken all the
necessary and responsible steps to warn importing countries
of the BSE dangers in UK meat and bone meal. Yet the action taken
so far overseas suggest the message has not got
through, or where it has this has been late. The first nation
that woke up to the danger did so a year after our own feed
ban. It seems even now several EC countries neither ban our
imports or the general feeding of ruminant protein. It also
seems the OIE and CVO have yet to inform the rest of the world.

2. I do not see how this can be claimed to be responsible. We
do not need an expert group of the Scientific Veterinary
Committee to tell us British meat and bone meal is unsafe for
ruminants. I fail to understand why this cannot be tackled
from the British end which seems to be the only sure way of doing
it, preferably by banning exports. As CMO says in his
letter of 3 January surely it is short sighted for us to risk
being seen in future as having been responsible for the
introduction of BSE to the food chain in other countries.[79]

http://www.bse.org.uk/dfa/dfa25.htm


PLEASE SEE CORRECT URL HERE ;


http://www.bseinquiry.gov.uk/files/yb/1990/02/20010001.pdf


http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh



kind regards,
terry
 

flounder

Well-known member
TAFS1 Position Paper on Specified Risk Materials (May 29, 2007)

Specified Risk Materials, or SRM, are tissues that have been designated for removal from the
carcases of cattle, and excluded from human food. They have been shown, or assumed, to
contain significant amounts of BSE infectivity in infected animals. By prohibiting their
consumption it is considered to provide a substantial reduction in risk to consumers in
countries where BSE has been shown to exist and in countries having a likely BSE-risk. SRM
are also designated in sheep and goats. This was stipulated as a precautionary measure
assuming that sheep and goats may have become infected with BSE. The finding of BSE in
one goat has confirmed this assumption.
SRM are also usually removed from animal feed as well, and this strengthens more general
feed bans that are intended to prevent infection of cattle and small ruminants with BSE and
lead to the elimination of BSE in each country. This document essentially concentrates on
SRM in the context of human health, except in explaining the evolution of definitions and
protective measures.
Considerable confusion surrounds the term “specified risk materials” or SRM. This confusion
ranges from the reasons for designation of such tissues or organs for destruction rather than
consumption, and the extent to which it is necessary to ensure full compliance with
regulations that require their removal from the food chain. This note briefly summarises the
reasons for the designation of SRM, and concludes by listing current rules in the Europe. This
table will be modified as rules change. Although the table includes a list of sheep and goat
tissues that are defined as SRM, the note primarily addresses the background to bovine SRM.

Why are tissues designated as SRM?


snip...


Has BSE infectivity been detected in all SRM listed later in this position paper?

• Yes. research on bovine tissues, from naturally and experimentally infected cattle,
has now progressed to the point where there is a clearer picture of which tissues
are infectious, and those where no infectivity has been found17,20 .
• In naturally infected cattle the brain, spinal cord and retina (eye) have been
shown to be infectious21,23. In addition, positivity or infectivity was detected in
some peripheral nerves that would not normally be removed as SRM3,13,14. The
amount of infectivity present is low, and considered be up to 1000-fold lower than
the brain. Unpublished evidence suggests at the moment that these become
positive only after the brain and spinal cord.
• In experimentally infected cattle, brain and spinal cord were again been
confirmed to be infectious, but in addition the distal ileum (lower small intestine)
also contained significant amounts of infectivity22. Two key ganglia, which are
key intermediate points linking the central and peripheral nervous systems, namely
the trigeminal and dorsal root ganglia (DRG), were also clearly infectious24. This
is not surprising given their close association with central nervous tissue.
• In addition, in experimentally infected cattle, single incomplete results have
indicated the possible presence of infectivity in bone marrow at about the time of
clinical onset24. These studies are incomplete, but it has not been possible to verify
the results at other time points in the incubation so far.
• In addition, a low amount of infectivity was detected in tonsil early in the
incubation and maintained during the time course9,25.
• A similar single, un-interpretable, result also indicates the presence of infectivity
in the third eyelid of naturally infected cows. This study is also still in progress.
Why are other tissues/organs not expected to be infectious included in the list for
exclusion from consumption?
• Some SRM have not been inherently shown to be infected, but with experience it
is clear that their close association with other SRM, especially the central nervous
system, represents a real risk of cross contamination20. Again, a precautionary
approach has been adopted.
• For example, the skull has not been demonstrated to be inherently infectious, but it
is impossible to remove the brain from the skull without leaving traces of brain
tissue behind20. Similarly the eye is also infected. Therefore, the definition of skull
as SRM acknowledges the remaining risk due to the retained brain tissue, or
contamination with brain as a result of the slaughtering process. The designation
of skull means that the practicalities of compliance and enforcement are easier to
handle, and there is less exposure of abattoir operators to brain tissue while it
remains encased within the skull.
• The vertebral column is also designated because of its close association with
dorsal root ganglia (DRG) and due to contamination with spinal cord tissue. DRG
sit just on the outside of the spine where the spinal nerves pass through from the
spinal cord20. If the vertebral column (spine) was left attached to meat, for
example in a T-bone steak, there is therefore a danger that the DRG would be
consumed. The spinal cord contamination arises as a result of the splitting process
as the saw that cuts the carcase in half passes through the cord and contaminates
the cut surface of the spine.
• In both situations described above the use of vertebral column for the production
of mechanically recovered meat, or mechanically separated meat, would strip off
the DRG and contamination, transferring infectivity into the MRM/MSM which is
used in manufactured meat products. Indeed, European legislation has gone further
than just designating vertebral column as an SRM. The use of ruminant bones for
production of mechanically recovered meat (MRM) is prohibited.
Have all tissues been tested for the presence of infectivity?
• No. There are limits to the number of tissues that can be tested. Decisions on
which tissues to test have historically been driven by several factors such as:-
• which represent a risk to consumers because they are eaten,
• which are key tissues in understanding the biology of BSE in cattle, and
• which represent a risk to humans through the manufacture of other
products such as pharmaceuticals and medical devices.
• Nevertheless, based upon evidence from other species (sheep scrapie) and the
results of assays of bovine tissues, and audits of the use of bovine tissues, it is
considered that all key tissues have been assayed.
Will the list be dynamic?
• Yes10. Research is still ongoing, and it is still possible that infectivity will be
detected in tissues that have been negative so far. The use of cattle for infectivity
assays, or technological breakthroughs to produce alternative assay systems (see
above) mean that the analytical sensitivity of current assays is greater than those
used in earlier studies. It is therefore not possible to exclude the possibility that
new positive results will arise. Their significance, in terms of quantifying the
amount of infectivity present, will be critical to risk assessments that will
determine whether authorities define them as SRM.
• Nevertheless, current evidence suggests that this is a theoretical rather than real
scenario. Authorities and expert committees cannot however remain oblivious to
new findings, and may need to take into account consumer confidence as well as
risk assessments in determining whether or not to add new tissues to the SRM list.
• Also it has to be taken into account that new findings of positive tissues may come
at a time when the prevalence of BSE is very low and decreasing and the vast
majority of cattle consumed have to be considered uninfected. In this situation
authorities may conclude that the addition of further tissues to the list may be
disproportionate to the risk.
• In the TSE roadmap of the EU, published in July 2005,
(http://ec.europa.eu/food/food/biosafety/bse/roadmap_en.pdf) next steps in the BSE
policy on different points are evaluated. Concerning SRM it is discussed, that the
list of SRM could be modified in the medium term, based on new and evolving
scientific knowledge and the results of the surveillance programs.
Designated bovine SRM in Europe
• Brain – expected to be infectious by extrapolation from sheep scrapie, and
subsequently confirmed for BSE. Experimental evidence suggests that the brain
becomes infectious in the later stages of incubation.
• Spinal cord – expected to be infectious by extrapolation from sheep scrapie, and
subsequently confirmed for BSE. Experimental evidence suggests that the spinal
cord becomes infectious in the later stages of incubation.
• Tonsil – expected to be infectious by extrapolation from sheep scrapie, but not
subsequently confirmed for BSE from naturally infected cattle, even by bioassay
in cattle. Result from experimentally infected cattle, suggests that the palatine
tonsil becomes infectious in the early stage of the incubation and the very low
infectivity is maintained during the time course5,9,25. Tongue itself is not
considered as SRM. However, according to EU-legislation, “tongue should be
harvested by a transverse cut rostral to the lingual process of the basihoyd bone”,
due to possible contamination of tonsil tissue.
• Intestine – the distal ileum was expected to be infectious by extrapolation from
sheep scrapie, and this was subsequently confirmed for BSE in experimentally
infected cattle especially in the early stages of incubation. Logic suggests that it
must also be infectious in naturally infected cattle in the early stages of incubation.
This infectivity was particularly associated with Peyer’s patches, collections of
lymphoid tissue that form a first line of defence against infection through the
intestinal wall. This result has not been replicated in naturally infected cattle,
although immunostaining methods have shown the presence of abnormal prion
protein in the nervous plexuses of the intestine. This discrepancy is considered to
be most probably due to the fact that the Peyer’s patches regress as cattle reach
maturity, and consequently reduce the likelihood of finding any infectivity that
may remain. The majority of infected cows die of clinical BSE at five to seven
years of age, after the Peyer’s patches have regressed. Nevertheless, the positive
immunostaining of the nervous plexuses, which extend throughout the intestine,
does justify continued listing of intestine as SRM while there is a danger that cattle
will have been exposed to BSE7,19.
• Skull – designated because of association with brain and eye, with resultant
contamination through the slaughtering process or because of residual brain tissue
following removal of the brain.
• Vertebral column – designated because of a combination of close association
with DRG, and the superficial contamination of the cut surface of the spine with
spinal cord during the carcase splitting process.
• Age restrictions4,20 – all of the above tissues will not necessarily be designated for
all ages of cattle consumed. This is because experimental evidence has suggested
that they only represent a risk at particular stages of the incubation. If a tissue is
infectious early in the incubation then it is normal to designate the tissue for all
ages. If infectivity is detected late in the incubation then it is possible to designate
the tissue in older animals only, especially where the designation is a result of
contamination (eg. vertebral column).
Designated ovine SRM
• SRM designated in sheep are based primarily on evidence from the study of sheep
scrapie, but the outcome is consistent with our understanding of the behaviour of
BSE in sheep that are susceptible to infection with BSE2,6,11.
• The designation adopts a cautious balance between significantly reducing the risk
to consumers should BSE be present in the sheep and goat population and the
introduction of extensive SRM removal which would significantly damage sheep
and meat industries in affected countries6,16,18.
• There is no doubt that the confirmation that BSE is present in the sheep population
will result in an immediate revision of this list, or possibly even a prohibition of
the consumption of certain categories of sheep meat. The confirmation of BSE in a
goat8 did not however have this effect on the definition of SRM. The list of SRMs
in small ruminants was not modified as a result of this finding (see position paper
on BSE in small ruminants). ...

snip...see full text ;

http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_SPECIFIED%20RISK%20MATERIALS_070529.pdf



> There is no doubt that the confirmation that BSE is present in the sheep population

> will result in an immediate revision of this list, or possibly even a prohibition of

> the consumption of certain categories of sheep meat


DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]

http://foiamadsheepmadrivervalley.blogspot.com/


CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA

http://cjdmadcowbaseoct2007.blogspot.com/

http://cjdmadcowbaseoct2007.blogspot.com/2007/11/phenotypic-similarity-of-transmissible.html


NOR-98 ATYPICAL SCRAPIE CASES USA

http://nor-98.blogspot.com/


TSS
 

flounder

Well-known member
January 18

CFIA’s position on the contamination of floor waste and waste water materials by Specified Risk Material (SRM)

http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/enhren/srmmrse.shtml


CFIA Position on head hides (face plates) from cattle slaughtered in Canadian abattoirs*


http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/enhren/heatete.shtml



tss
 

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