Update from USDA Regarding a Detection of Bovine Spongiform
Encephalopathy (BSE) in the United States WASHINGTON bulletin at 04/26/2012
10:11 PM EDT
Update from USDA
Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United
States
USDA and FDA Continue
to Assure Consumers That Existing Safeguards Protect Food Supply; Reiterates
Safety of Consuming Beef and Dairy Products
WASHINGTON, April 26, 2012 –
USDA’s Animal and Plant Health Inspection Service today released the following
update on the BSE detection announced earlier this week:
On April 24, USDA confirmed the
nation’s 4th case of Bovine Spongiform Encephalopathy (BSE) in an animal that
was sampled for the disease at a rendering facility in central California. This
animal was never presented for slaughter for human consumption, so at no time
presented a risk to the food supply, or to human health in the United States. As
the epidemiological investigation has progressed, USDA has continued to
communicate findings in a timely and transparent manner.
As a result of USDA’s ongoing
epidemiological investigation, more information about the history and age of the
animal is now available.
The animal in question was 10
years and 7 months old and came from a dairy farm in Tulare County, Calif. The
animal was humanely euthanized after it developed lameness and became recumbent.
The animal’s carcass will be destroyed.
It is important to reiterate
that this animal was never presented for slaughter for human consumption, did
not enter food supply channels, and at no time presented any risk to human
health.
USDA is continuing its
epidemiological investigation and will provide additional information as it is
available.
The positive animal was tested
as part of targeted BSE surveillance at rendering facilities. Samples were sent
to the California Animal Health and Food Safety Laboratory for testing and
forwarded to the National Veterinary Services Laboratories (NVSL) on April 20th
for confirmatory testing. APHIS announced the confirmed positive finding April
24th.
The United States has a
longstanding system of three interlocking safeguards against BSE that protects
public and animal health in the United States, the most important of which is
the removal of specified risk materials – or the parts of an animal that would
contain BSE should an animal have the disease – from all animals presented for
slaughter in the United States. The second safeguard is a strong feed ban that
protects cattle from the disease. The third safeguard—which led to this
detection— is our ongoing BSE surveillance program that allows USDA to detect
the disease if it exists at very low levels in the U.S. cattle population and
provides assurances to consumers and our international trading partners that the
interlocking system of safeguards in place to prevent BSE are
working.
#
USDA is an equal opportunity
provider and employer. To file a complaint of discrimination, write: USDA,
Office of the Assistant Secretary for Civil Rights, Office of Adjudication, 1400
Independence Ave., SW, Washington, DC 20250-9410 or call (866) 632-9992
(Toll-free Customer Service), (800) 877-8339 (Local or Federal relay), (866)
377-8642 (Relay voice users).
so, USDA et al accidently find two atypical mad cows in Texas and Alabama
during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut
the testing down to numbers so low, it’s almost impossible to find another mad
cow case, unless your country is to a point that mad cow disease can be found in
1 in 40,000, and STILL FIND MAD COW DISEASE. partial and voluntary BSE mad cow
feed ban of August 4, 1997 was nothing more than ink on paper, with as much as
10,000,000 LBS. of blood laced meat and bone meal MBM going out into commerce 10
years later in 2007. who knows since 2007 breach, fda et al stopped posting
those warning letters. ARS said if atypical BSE was more virulent, SRM removal
would have to change if tissue infectivity was found differently than c-BSE. it
was. more virulent and infectivity was found in more tissues, including skeletal
muscle. HOUSTON, WE HAVE A PROBLEM. ...
I am deeply disturbed about the false and terribly misleading information
that is being handed out by the USDA FDA et al about this recent case of the
atypical L-type BASE BSE case in California. these officials are terribly
misinformed (I was told they are not lying), about the risk factor and
transmissibility of the atypical L-type BASE BSE. these are very disturbing
transmission studies that the CDC PUT OUT IN 2012. I urge officials to come
forward with the rest of this story.
please see ;
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
Nadine Mestre-Francés, Simon Nicot, Sylvie Rouland, Anne-Gaëlle Biacabe,
Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel Verdier
We report transmission of atypical L-type bovine spongiform encephalopathy
to mouse lemurs after oral or intracerebral inoculation with infected bovine
brain tissue. After neurologic symptoms appeared, transmissibility of the
disease by both inoculation routes was confirmed by detection of
disease-associated prion protein in samples of brain tissue.
snip...
Conclusions
We demonstrated that the agent of L-BSE can be transmitted by the oral
route from cattle to mouse lemurs. As expected, orally inoculated animals
survived longer than IC-inoculated animals. Orally inoculated lemurs had less
severe clinical signs and symptoms, with no evidence of motor dysfunction. It
was previously suggested that the agent of L-BSE might be involved in the
foodborne transmission of a prion disease in mink (11,12), a species in which
several outbreaks of transmissible mink encephalopathy had been identified,
notably in the United States (13).
Our study clearly confirms, experimentally, the potential risk for
interspecies oral transmission of the agent of L-BSE. In our model, this risk
appears higher than that for the agent of classical BSE, which could only be
transmitted to mouse lemurs after a first passage in macaques (14). We report
oral transmission of the L-BSE agent in young and adult primates. Transmission
by the IC route has also been reported in young macaques (6,7). A previous study
of L-BSE in transgenic mice expressing human PrP suggested an absence of any
transmission barrier between cattle and humans for this particular strain of the
agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus,
it is imperative to maintain measures that prevent the entry of tissues from
cattle possibly infected with the agent of L-BSE into the food chain.
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim
McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre,
Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of
Calgary, Canada
Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type
and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and
changes in glycosylation similar to other atypical BSE cases. PK digestion under
mild and stringent conditions revealed a reduced protease resistance of the
atypical cases compared to the C-type cases. N terminal- specific antibodies
bound to PrPres from H type but not from C or L type. The C-terminal-specific
antibodies resulted in a shift in the glycoform profile and detected a fourth
band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries.
Subject: Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to
a Primate
Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate
Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1,
Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1,
Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4,
Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4,
Jean-Philippe Deslys1
1 Institute of Emerging Diseases and Innovative Therapies, CEA,
Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del
Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps
Florida, Jupiter, Florida, United States of America, 5 Genetics Division,
Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts,
United States of America
Abstract Top Background
Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne
transmission of prions from slaughtered cattle with classical Bovine Spongiform
Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic
in aging cattle, were recently identified at slaughterhouses throughout Europe
and North America, raising a question about human susceptibility to these new
prion strains.
Methodology/Principal Findings
Brain homogenates from cattle with classical BSE and atypical (BASE)
infections were inoculated intracerebrally into cynomolgus monkeys (Macacca
fascicularis), a non-human primate model previously demonstrated to be
susceptible to the original strain of cBSE. The resulting diseases were compared
in terms of clinical signs, histology and biochemistry of the abnormal prion
protein (PrPres). The single monkey infected with BASE had a shorter survival,
and a different clinical evolution, histopathology, and prion protein (PrPres)
pattern than was observed for either classical BSE or vCJD-inoculated animals.
Also, the biochemical signature of PrPres in the BASE-inoculated animal was
found to have a higher proteinase K sensitivity of the octa-repeat region. We
found the same biochemical signature in three of four human patients with
sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the
infected bovine.
Conclusion/Significance
Our results point to a possibly higher degree of pathogenicity of BASE than
classical BSE in primates and also raise a question about a possible link to one
uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning
epidemic of classical BSE, the occurrence of atypical strains should temper the
urge to relax measures currently in place to protect public health from
accidental contamination by BSE-contaminated products.
Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire
S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle
to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017
Editor: Neil Mabbott, University of Edinburgh, United Kingdom
Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20,
2008
Copyright: © 2008 Comoy et al. This is an open-access article distributed
under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Funding: This work has been supported by the Network of Excellence
NeuroPrion.
Competing interests: CEA owns a patent covering the BSE diagnostic tests
commercialized by the company Bio-Rad.
* E-mail: emmanuel.comoy@cea.fr
snip...
In summary, we have transmitted one atypical form of BSE (BASE) to a
cynomolgus macaque monkey that had a shorter incubation period than monkeys
infected with classical BSE, with distinctive clinical, neuropathological, and
biochemical features; and have shown that the molecular biological signature
resembled that seen in a comparatively uncommon subtype of sporadic CJD. We
cannot yet say whether BASE is more pathogenic for primates (including humans)
than cBSE, nor can we predict whether its molecular biological features
represent a clue to one cause of apparently sporadic human CJD. However, the
evidence presented here and by others justifies concern about a potential human
health hazard from undetected atypical forms of BSE, and despite the waning
epizoonosis of classical BSE, it would be premature to abandon the precautionary
measures that have been so successful in reversing the impact of cBSE. We would
instead urge a gradual, staged reduction that takes into account the evolving
knowledge about atypical ruminant diseases, and both a permanent ban on the use
of bovine central nervous system tissue for either animal or human use, and its
destruction so as to eliminate any risk of environmental contamination.
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set
out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE
which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
October 2009 O.11.3
Infectivity in skeletal muscle of BASE-infected cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1,
Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3,
Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5,
Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological
Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS
Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy
caused by a prion strain distinct from that of BSE. Upon experimental
transmission to cattle, BASE induces a previously unrecognized disease phenotype
marked by mental dullness and progressive atrophy of hind limb musculature.
Whether affected muscles contain infectivity is unknown. This is a critical
issue since the BASE strain is readily transmissible to a variety of hosts
including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral
tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice
expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and
i.p. with 10% homogenates of a variety of tissues including brain, spleen,
cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from
cattle intracerebrally infected with BASE. No PrPres was detectable in the
peripheral tissues used for inoculation either by immunohistochemistry or
Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical signs
of disease with incubation and survival times of 175±15 and 207±12 days. Five
out of seven mice challenged with skeletal muscle developed a similar
neurological disorder, with incubation and survival times of 380±11 and 410±12
days. At present (700 days after inoculation) mice challenged with the other
peripheral tissues are still healthy. The neuropathological phenotype and PrPres
type of the affected mice inoculated either with brain or muscle were
indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle
experimentally infected with BASE contains significant amount of infectivity, at
variance with BSE-affected cattle, raising the issue of intraspecies
transmission and the potential risk for humans. Experiments are in progress to
assess the presence of infectivity in skeletal muscles of natural BASE.
now, what about that mad cow feed and atypical BSE $$$
LET’S see how that mad cow triple firewall aka mad cow feed ban is working
out $$$
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM,
which is illegal, mixed with 85% blood meal, which is still legal, but yet we
know the TSE/BSE agent will transmit blood. we have this l-BSE in North America
that is much more virulent and there is much concern with blood issue and l-BSE
as there is with nvCJD in humans. some are even starting to be concerned with
sporadic CJD and blood, and there are studies showing transmission there as
well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD
COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that
reaches commerce is ever returned via recall, very, very little. this was 2007,
TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN
THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow
feed that was in ALABAMA in one of the links too, this is where the infamous
g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the
USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
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 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
###
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
###
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
###
please see full text ;
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen
Inc 2/11/10 USA
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
Tuesday, September 14, 2010
Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)
Friday, October 8, 2010
Scientific reasons for a feed ban of meat-and-bone meal, applicable to all
farmed animals including cattle, pigs, poultry, farmed fish and pet food
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in
the EU
Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND
FOOD SAFETY a non-profit Swiss Foundation
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject
PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
Sunday, February 5, 2012
February 2012 Update on Feed Enforcement Activities to Limit the Spread of
BSE
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
IMPORT EXPORT BEEF, LIVE, PRODUCTS, CANADA AND USA
America's Mad Cow Crisis by John Stauber
Permission granted to reprint this article:
America's Mad Cow Crisis
John Stauber
Americans might remember that when the first mad cow was confirmed in the
United States in December, 2003, it was major news. The United States Department
of Agriculture (USDA) and the Food and Drug Administration (FDA) had been
petitioned for years by lawyers from farm and consumer groups I worked with to
stop the cannibal feeding practices that transmit this horrible, always fatal,
human and animal dementia. When the first cow was found in Washington state, the
government said it would stop such feeding, and the media went away. But once
the cameras were off and the reporters were gone nothing substantial changed.
In the United States, dairy calves are still taken from their mothers and
fed the blood and fat of dead cattle. This is no doubt a way to infect them with
the mad cow disease that has now been incubating here for decades, spread
through such animal feeding practices. No one knows how the latest dairy cow was
infected, the fourth confirmed in the United States. Maybe it was nursed on
cow's blood. Perhaps it was fed feed containing cattle fat with traces of cattle
protein. Or perhaps there is a mad cow disease in pigs in the United States,
which simply has not been found yet, because pigs are not tested for it at all,
even though pigs are fed both pig and cattle byproducts, and then the blood, fat
and other waste parts of these pigs are fed to cattle.
All these U.S. cattle feeding methods are long banned and illegal in other
countries that suffered through but eventually dealt properly with mad cow
disease. Here, rather than stopping the transmission of the disease by stopping
the cannibal feeding, mad cow is simply covered up with inadequate testing and
very adequate public relations. US cattle are still fed mammalian blood, fat and
protein, risking human deaths and threatening the long term safety of human
blood products, simply to provide the U.S. livestock industry with a cheap
protein source and a cheap way to get rid of dead animal waste.
I began researching this issue around 1989, long before the disease was
confirmed to have jumped from cattle to the people eating them, as announced by
the British government in 1996. In 1997 I co-authored <
http://www.prwatch.org/books/madcow.html>
Mad Cow USA, warning that the disease was likely already here and spreading,
since the animal cannibalism that caused its outbreak in Britain and spread it
to other countries was actually more widespread in the United States than
anywhere.
Some years ago responsible U.S. beef companies wanted to test their animals
for mad cow disease and label their beef as being disease free, but they were
forbidden under penalty of law from doing so. Only the USDA can test for mad
cows in America. In 2004 and 2005, after two additional mad cows were discovered
in Texas and Alabama, the United Sates government declared that obviously mad
cow wasn't much of a problem and gutted it's anemic testing program. Today only
about 40,000 cattle a year are tested, out of tens of millions slaughtered. It's
amazing that the California cow was even detected given this pathetic testing
program that seems well designed to hide rather than find mad cows.
The prevention of mad cow disease is relatively simple. If your country has
it, test each animal before it goes to slaughter to keep the diseased animals
out of the food chain. Cheap, accurate and easy tests are now available in other
countries but illegal here. Testing cattle both identifies the true extent of
the disease, and keeps infected animals from being eaten in your sausage or
hamburger. In this manner countries like Britain, Germany, France and Japan have
controlled their problem through testing and a strict ban on cannibal feed.
Once mad cow disease moves into the human population of a country, all bets
are off as to what could happen next. It's a very slow disease, it develops
invisibly over decades in someone who has been infected, and it is always fatal.
We'll know a lot more in fifty years, but the future looks worrisome. In Britain
people are dying from mad cow disease, people who never consumed infected meat.
They used medical products containing human blood, and that blood was infected
because it was from infected people. There is no test to identify infectious
prions, the causal agent, in blood.
Almost none of this information appeared in news stories about the
California mad cow. Instead the headlines and the talking heads fed us the line
that the United States fixed this problem long ago, and the fact that only 4 mad
cows have been detected so far is proof of our success. Oprah Winfrey once tried
via her talk show to warn about this, way back in 1996, but Texas cattlemen
dragged her and her guest Howard Lyman into court and she had to spend many
millions of dollars defending herself from the supposed crime of slandering
meat.
Oprah won her case, which was probably unfortunate for the rest of us
because had she been convicted the ensuing appeals court trial might have gotten
enough attention to wake up Americans to the truth. Instead Oprah learned her
lesson - shut up and you won't get sued. Other media learned too that if the
government and industry can silence Oprah, they can muzzle anyone. (One of the 4
confirmed U.S. mad cows was later found in Texas, appropriately enough.)
There are a handful of dedicated activists such as Howard Lyman who have
been sounding the alarm on this. They include the ecologist Dr. Michael Hansen
of Consumers Union and Dr. Michael Greger, a physician. Terry Singeltary Sr.,
whose mom died of a version of the human form of mad cow disease, has been a
relentless, unpaid activist on this issue.
Despite their dedicated work, there is no indication that anything is going
to change here in America. The U.S. government refuses to implement the feed ban
and the animal testing necessary. It doesn't matter if the President is named
Clinton, Bush or Obama because their bureaucrats in the USDA and FDA stay the
course and keep the cover up going. Docile, eating what they are fed, trusting
the rancher all the way to the slaughterhouse. Is that just the cows, or is it
us too?
Tell the USDA to Stop the Spread of Mad Cow Disease!
Terry Singeltary P.O. Box 42 Bacliff, TX 77518-0042
April 25, 2012
Administrator Gregory Parham
12th & Jefferson Drive, SW Whitten Bldg., Room 313-E Washington, DC
20250 Re: Docket No. APHIS-2008-0010
Dear Administrator Parham:
In order to stop the spread of bovine spongiform encephalopathy (BSE or mad
cow disease), the US Department of Agriculture should adopt and enforce the same
strict standards required by the European Union and Japan:
* Mandatory testing for all cattle brought to slaughter, before they enter
the food chain.
* Ban the feeding of blood, manure, and slaughterhouse waste to animals.
In the meantime, the USDA must stop harassing farmers and food processors
who are interested in independently testing their own beef for mad cow disease.
Ironically, the news that mad cow is still in our food supply comes at a
time that the U.S. Department of Agriculture Animal and Plant Health Inspection
Service (APHIS) is proposing to drop significant protections the U.S. has
against the importation of cattle infected with mad cow disease.
APHIS proposes to open United States' borders to cattle from countries that
have had thousands of cases of BSE, and where new BSE cases continue to be
found. The importation of a single infected cow from Canada in 2001 set in
motion restrictions on U.S. beef exports that cost the beef industry billions of
dollars and that still exist today in several major export markets.
APHIS also proposes to drop important measures that have been used to
protect U.S. consumers from these imported cattle and meat products (which have
a much higher chance of being infected with BSE than U.S.-raised cattle), and
intends to rely almost exclusively on slaughtering techniques, particularly the
removal of specified risk materials (SRMs), which we know on occasion is not
employed fully or effectively, and which has not been practiced long enough to
determine whether it is indeed the panacea APHIS assumes, given the long
gestation time of variant Creutzfeldt-Jakob Disease (vCJD) in humans.
I support the view of R-CALF USA CEO Bill Bullard:
"Seventy-six farm and consumer organizations, representing tens of millions
of U.S. citizens, recently urged Secretary Vilsack to strengthen, not weaken,
our already lax BSE policies by reversing the so-called 'over-thirty-month
rule,' which allows Canadian cattle born during the time the BSE agent was known
to be circulating in Canada's feed system to be imported into the United States.
"Secretary Vilsack has again ignored our concerns and is putting the
self-interests of corporate meatpackers that want access to more meat supplies
regardless of risk to humans and livestock, ahead of the health and safety
concerns of U.S. citizens.
"The USDA is touting its proposed rule as a trade rule, claiming it will
strengthen the United States' negotiating position in trade agreements. This is
the same failed argument the Bush Administration used when it first relaxed our
U.S. BSE policies in 2004, and the result of that failed argument is that many
important export markets imposed long-lasting export restrictions on U.S. beef.
"USDA's proposal amounts to a unilateral disarmament of essential disease
protections for U.S. citizens and livestock. It will disadvantage U.S. producers
in the global market because other major beef exporters, including Brazil,
Australia, and India continue to maintain adequate import standards while the
U.S. relaxes its own. This will create unnecessary and avoidable anxieties among
other beef consuming nations for U.S. beef.
"Exposing U.S. consumers and U.S. livestock to a heightened risk of BSE
introduction is irresponsible and contrary to pledges made by the Obama
Administration during his campaign."
This is no time to relax our essential protections against the introduction
of mad cow disease.
so, USDA et al accidently find two atypical mad cows in Texas and Alabama
during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut
the testing down to numbers so low, it's almost impossible to find another mad
cow case, unless your country is to a point that mad cow disease can be found in
1 in 40,000, and STILL FIND MAD COW DISEASE, HOUSTON, WE HAVE A PROBLEM. ...
PLEASE UNDERSTAND, the USDA et al are lying about atypical BSE being a
spontaneous mutation, NOT caused by feed. spontaneous BSE has NEVER been proven
in any natural field case of BSE. feed is the most likely route. ...tss
As previously stated most of the characteristics of atypical BSE have not
been defined. In addition to the origin, the risk to other cattle by means of
natural transmission, the risk to humans and other animal species suck as
chickens and pigs is still unknown as is the distribution of infectivity
throughout the body of a bovine. There is little information on clinical
manifestation if it occurs at all in certain of the cases. Documented L cases
have been diagnosed from samples taken from older ''healthy'' cattle presented
for routine slaughter.
While additional surveillance and research is being conducted, it is
important for policy make to consider the implications of atypical BSE. They may
need to rethink what populations are appropriate targets. It would probably be
unwise to prematurely lessen or discontinue the current BSE protection measures.
SNIP...
Atypical BSE: What is it and what is the significance
Linda A. Detwiler, Paul Brown, Lisa M. McShane, and Gianluigi Zanusso
When atypical cases were first reported there was some speculation that
these may merely be protein accumulation disorders associated with old age. It
has now been shown that both the Land H types of atypical BSE are at least
experimentally transmissible. Homogenates from L cases have been transmitted to
bovinized transgenic mice, humanized transgenic mice, Cynomolgus monkeys and 1
breed of cattle (Buschmann et al. 2006; Book of abstracts (2006), International
Conference on Prion Diseases, Turin, Italy). H cases have been transmitted to
bovinized transgenic (Tgbov) and ovinized transgenic mice (Béringue et al.
2006). The incubation times for atypical L cases of BSE were shorter in the
Tgbov mice than classical BSE inoculated into Tgbov mice and the H cases had
longer incubations.
A variation or mutation of the classical BSE strain A different route of
exposure or exposure at an older age A strain of Scrapie transmitted to
cattle Sporadic or a spontaneous occurrence of BSE At his point in time,
there is no evidence to conclude that any of the theories are or are not a
possibility. There is considerable interest in the sporadic theory. If a form of
BSE were to ocnaturally, this may suggest that certain control and prevention
measure would have to remain in place indefinitely. Proving or disproving the
occurrence of a relatively rare sporadic disease poses a significant challenge.
It would require between 3 and 4.5 million tests performed on brain samples
randomly taken from cattle over 7 years of age in a country with no evidencrisk
from orally acquired BSE. It is unlikely that any country would have the will or
resources to perform such a study. Lacking this type of evidence, systematic
surveillance over a long time period may provide evidence about the nature of
atypical BSE.
snip...see full text ;
When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
Wednesday, April 25, 2012
ACTUALITY - USDA Chief Veterinary Officer On Surveillance And Milk Safety
and BSE aka MAD COW DISEASE
Thursday, April 26, 2012
Maternal Transmission of the BSE and Birth Cohorts
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update,
October 31, 2005 INTRODUCTION The United States Department of Agriculture’s Food
Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in
Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine
Spongiform Encephalopathy Update, October 31, 2005 (report and model located on
the FSIS website:
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
Owens, Julie From: Terry S. Singeltary Sr.
[mailto:flounder9%40verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
Sunday, November 13, 2011
California BSE mad cow beef recall, QFC, CJD, and dead stock downer
livestock
> > > Ackerman says downed cattle are 50 times more likely to have
mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than
ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of
mad cow disease in North America since 1993, at least 16 have involved downer
cattle, he said. < < <
don’t forget the children...
PLEASE be aware, for 4 years, the USDA fed our children all across the
Nation (including TEXAS) dead stock downer cows, the most high risk cattle for
BSE aka mad cow disease and other dangerous pathogens.
who will watch our children for CJD for the next 5+ decades ???
WAS your child exposed to mad cow disease via the NSLP ???
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH
RISK FOR MAD COW DISEASE ???
you can check and see here ;
ATYPICAL L-TYPE BASE BSE AND TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TME,
is there a link ???
4.6.1. Epidemiology TME is a disease that affected mink ranches, decimating
the herds, in the frame of five to eleven isolated outbreaks, from 1947 to 1985,
mainly in USA (Wisconsin was the main affected State since it is where mink
ranches where mainly located) (Robinson et al., 1994). Moreover, eastern
European countries (East Germany, Finland and USSR) also reported outbreaks in
the mid-sixties.
According to its rare occurrence associated with a massive rate of
infection, and in the absence of probing horizontal or vertical transmission,
the hypothesis of a food-borne infection is the most convincing explanation.
This theory is enforced by the fact that three of those outbreaks occurred in
large mink production facilities that prepared on-site feed involving the use of
non-ambulatory (i.e. animal unable to stand alone) cattle (Hartsoug and Burger,
1965; Marsh et al.,
1991).
SNIP...
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
In April of 1985, a mink rancher in Wisconsin reported a debilitating
neurologic disease in his herd which we diagnosed as TME by histopathologic
findings confirmed by experimental transmission to mink and squirrel monkeys.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead
dairy cattle and a few horses. She had never been fed.
We believe that these findings may indicate the presence of a previously
unrecognized scrapie-like disease in cattle and wish to alert dairy
practitioners to this possibility.
snip...
PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL
VETERINARY MEDICINE, University of Arizona, March 17-19, 1986
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Volume 13, Number 12–December 2007 Research
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and
L-type Bovine Spongiform Encephalopathy in a Mouse Model
Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,*
andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon,
Lyon, France; and†Montana State University, Bozeman, Montana, USA
Abstract
Transmissible mink encepholapathy (TME) is a foodborne transmissible
spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant
TSE has been proposed as the cause, but the precise origin of TME is unknown. To
compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct
natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE,
and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4).
Transgenic mice were susceptible to infection with bovine-passaged TME, typical
BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain
lesions profiles, disease-associated prion protein brain distribution, and
biochemical properties of protease-resistant prion protein, typical BSE had a
distint phenotype in ovine transgenic mice compared to L-type BSE and bovine
TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4
mice suggest that L-type BSE is a much more likely candidate for the origin of
TME than is typical BSE.
snip...
Conclusion
These studies provide experimental evidence that the Stetsonville TME agent
is distinct from typical BSE but has phenotypic similarities to L-type BSE in
TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for
a bovine source of TME infection than typical BSE. In the scenario that a
ruminant TSE is the source for TME infection in mink, this would be a second
example of transmission of a TSE from ruminants to non-ruminants under natural
conditions or farming practices in addition to transmission of typical BSE to
humans, domestic cats, and exotic zoo animals(37). The potential importance of
this finding is relevant to L-type BSE, which based on experimental transmission
into humanized PrP transgenic mice and macaques, suggests that L-type BSE is
more pathogenic for humans than typical BSE (24,38).
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1
Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and
Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State
University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain;
5Health Canada; Ottawa, ON Canada†Presenting author; Email:
emmanuel.comoy@cea.fr
The epidemiology of Transmissible mink encephalopathy (TME) indicates an
alimentary origin. Several inter-species transmission experiments have not
succeeded in establishing with certainty any natural reservoir of this prion
strain, although both ovine and bovine sources have been suspected. Cattle
exposed to TME develop a spongiform encephalopathy that is distinct from
classical Bovine Spongiform Encephalopathy (c-BSE).
Inoculation of c-BSE to cynomolgus macaque provided early evidence of a
possible risk to humans, and remains an important model to define the risk of
both primary (oral transmission from cattle to primate) and secondary
(intravenous intra-species transmission) exposures. We have also evaluated the
transmissibility of other cattle prion strains to macaques, including L- and H-
atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.
BSE-L induced a neurological disease distinct from c-BSE. Peripheral
exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and
intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted
TME also induced a rapid disease in cynomolgus macaque. The clinical features,
lesion profile, and biochemical signature of the induced disease was similar to
the features observed in animals exposed to BSE-L, suggesting a link between the
two prion strains. Secondary transmissions to a common host (transgenic mouse
overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in
primates induced diseases with similar incubation periods: like the c-BSE
strain, these cattle strains maintained their distinctive features regardless of
the donor species and passages.
If the link between TME and BSE-L is confirmed, our results would suggest
that BSE-L in North America may have existed for decades, and highlight a
possible preferential transmission of animal prion strains to primates after
passage in cattle.
=====================end...tss====================
link url not available, please see PRION 2011 ;
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
snip...
PAGE 31
Appendix I
VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE
1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:-
i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BSE-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason given for
not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally- (and naturally) infected sheep by ET. He had
found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).
3. Prof. A Robertson gave a brief account of BSE. The US approach was to
PAGE 32
accord it a very low profile indeed. Dr A Thiermann showed the picture in
the "Independent" with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. BSE was not reported in USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP} shows some promise.
7. Results of a questionnaire sent to 33 states on the subject of the
national sheep scrapie programme survey indicated;
17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and
were neutral
Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
please see ;
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
SNIP...
Reasons for Caution There are several reasons for caution with respect to
zoonotic and interspecies CWD transmission. First, there is strong evidence that
distinct CWD strains exist (36). Prion strains are distinguished by varied
incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc
depositions (3,32). Strains have been identified in other natural prion
diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies
transmission of prions from CWD-positive deer and elk isolates resulted in
identification of >2 strains of CWD in rodent models (36), indicating that
CWD strains likely exist in cervids. However, nothing is currently known about
natural distribution and prevalence of CWD strains. Currently, host range and
pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of
CWD may also vary with CWD strain. In addition, diversity in host (cervid) and
target (e.g., human) genotypes further complicates definitive findings of
zoonotic and interspecies transmission potentials of CWD. Intraspecies and
interspecies passage of the CWD agent may also increase the risk for zoonotic
CWD transmission. The CWD prion agent is undergoing serial passage naturally as
the disease continues to emerge. In vitro and in vivo intraspecies transmission
of the CWD agent yields PrPSc with an increased capacity to convert human PrPc
to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and
yield multiple novel prion strains (3,28). The potential for interspecies CWD
transmission (by cohabitating mammals) will only increase as the disease spreads
and CWD prions continue to be shed into the environment. This environmental
passage itself may alter CWD prions or exert selective pressures on CWD strain
mixtures by interactions with soil, which are known to vary with prion strain
(25), or exposure to environmental or gut degradation. Given that prion disease
in humans can be difficult to diagnose and the asymptomatic incubation period
can last decades, continued research, epidemiologic surveillance, and caution in
handling risky material remain prudent as CWD continues to spread and the
opportunity for interspecies transmission increases. Otherwise, similar to what
occurred in the United Kingdom after detection of variant CJD and its subsequent
link to BSE, years of prevention could be lost if zoonotic transmission of CWD
is subsequently identified, SNIP...SEE FULL TEXT ;
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
see much more here ;
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Thursday, January 26, 2012
The Risk of Prion Zoonoses
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI:
10.1126/science.1218167
Thursday, January 26, 2012
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI:
10.1126/science.1215659
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
THIRD CJD REPORT UK 1994
snip...
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats, there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Wednesday, March 14, 2012
PINK SLIME, MRM’s, BSE AKA MAD COW DISEASE, AND THE USDA NSLP
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE
RISE IN NORTH AMERICA
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1
(August 19, 2011) including Texas
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the
prion protein or just more PRIONBALONEY ?
snip...see full text ;
O.K. let's compare some recent cases of this prionpathy in other countries
besides Gambetti's first 10 recently, that he claims is a spontaneous event,
from a genetic disorder, that is not genetic, but sporadic, that is related to
no animal TSE in North America, or the world. ...
Wednesday, October 27, 2010
A novel variant of human disease with a protease-sensitive prion protein
and heterozygosity methionine/valine at codon 129: Case report
Wednesday, March 28, 2012
CJD FOUNDATION CWRU GAMBETTI FAMILIAL FAMILY AFFAIR CONFERENCE 2012
Thursday, April 12, 2012
Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to
2010
Eurosurveillance, Volume 17, Issue 15, 12 April 2012
Research articles
Tuesday, November 08, 2011
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob
Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011
Original Paper
Conclusions:These findings raise doubt about the possibility of a reliable
CJD surveillance only based on mortality data.
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis
full text with source references ;
PLEASE REMEMBER ;
The Akron, Ohio-based CJD Foundation said the Center for Disease Control
revised that number in October of 2004 to about one in 9,000 CJD cases per year
in the population group age 55 and older.
HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO
ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???
if not, why not...
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
Monday, April 16, 2012
Continuing Enhanced National Surveillance for Prion Diseases in the United
States
Wednesday, April 25, 2012
USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 - 2012
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Information released on 2 February
2005
Summary of information
requested
What statistics are available on cattle less than 30 months of age found
to have BSE?
Information
released
VLA has recorded approximately 100 cases of BSE in cattle of 30 months of
age or under during the entire period of the BSE epidemic (1986 - 2005). The
figure is approximate as for 51 of these the age is only estimated. This is
because farmers did not have accurate documentation to confirm birth date. This
was not a requirement at the time.
We can confirm that of the 100 cases, 49 were
under 30 months of age, of these the youngest case was 20 months old.
http://vla.defra.gov.uk/vla/vla_ati_020205.htm
http://bseyoungestage.blogspot.com/2008/05/bse-youngest-age-statistics-under-30.html
layperson