Japan Moves Closer To Raising 20-Month Age Limit For Beef Imports
The Japanese government this week took a new step toward relaxing its
current restrictions on imports of beef from the U.S. and three other countries
when a panel of experts from the country's Food Safety Commission found that
allowing the sale of beef from cattle up to 30 months of age from those
countries instead of the current 20 months poses a "negligible" risk to human
health, according to a Japanese official.1082 words
Japan Moves Closer To Raising 20-Month Age Limit For Beef Imports
The Japanese government this week took a new step toward relaxing its
current restrictions on imports of beef from the U.S. and three other countries
when a panel of experts from the country’s Food Safety Commission found that
allowing the sale of beef from cattle up to 30 months of age from those
countries instead of the current 20 months poses a “negligible” risk to human
health, according to a Japanese official.
The experts also recommended that the Japanese government loosen its
definition of specified risk materials (SRMs) that must be removed from beef
before they can be sold in Japan, a move that would also facilitate U.S. beef
exports to the country, according to the official.
For instance, U.S. exporters cannot currently ship T-bone steaks from
cattle 20 months or under to Japan because that cut of meat includes a portion
of the cow’s spinal column. Japan’s current import rules consider the head,
spinal cord and spinal column from cattle of all ages to be SRMs. The experts
recommended that Japan relax this definition so that these parts of the animal
would only be considered SRMs if they are from cattle older than 30 months. This
is the same definition used by the U.S.
Both of these recommendations were part of a draft risk assessment approved
on Sept. 5 by a subcommittee of the Food Safety Commission that would apply to
imports of beef from U.S., Canada, France and the Netherlands. All of these
countries are considered by the World Organization for Animal Health to pose a
“controlled risk” for bovine spongiform encephalopathy (BSE), also known as mad
cow disease.
A separate risk assessment would be required for other countries looking to
have the BSE age restrictions relaxed for their exports, the official added. But
the draft risk assessment contains recommendations for relaxing BSE restrictions
both for domestic Japanese and imported beef.
For example, the draft risk assessment recommended that the looser
definition of specified risk materials would also apply domestically as well as
for imports.
In addition, while Japan currently requires that domestic cattle over 20
months of age undergo mandatory “blanket” BSE testing at the time of slaughter,
the draft risk assessment recommends that this testing be limited to cattle over
30 months, the official said.
The draft risk assessment still needs to be approved by the entire Food
Safety Commission, which could happen this month, either at its Sept. 10 meeting
or a subsequent one on Sept. 24. This would be followed by a round of public
comments to be submitted within 30 days, which would be analyzed before the
commission would consider a final risk assessment. Once that is approved, the
commission would turn over the issue to the Ministry of Health.
The Office of the U.S. Trade Representative and Sen. Max Baucus (D-MT) on
Sept. 5 praised the action by Japan as a positive step toward greater market
access for U.S. beef exporters.
“We welcome the important step taken by Japan’s risk assessment body and we
look forward to an expeditious conclusion to the risk assessment process,” a
USTR spokeswoman said in an e-mail.
Baucus, who last month met with Japanese officials in Tokyo to discuss the
beef restrictions and other trade issues, said in a statement he was encouraged
by the steps taken today by the Japanese government. “We’re headed in the right
direction,” Baucus said. “U.S. beef — from cattle of all ages — is the safest in
the world and I am confident we will continue to expand exports on the global
market.”
The U.S. Meat Export Federation (USMEF) also praised the subcommittee’s
approval of the draft risk assessment in a separate statement, calling it an
“important step in Japan’s process of bringing its import regimen into
conformance with international standards.” In a Sept. 5 interview, USMEF
spokesman Joe Schuele said it will likely take until late 2012 or early 2013 for
Japan to complete its regulatory process and formally amend its import rules.
The Japanese government first announced in December that it would request a
risk assessment from Food Safety Commission to determine whether the risk of
consuming beef from U.S. cattle up to 30 months in age is higher than the risk
of consuming beef from cattle no older than 20 months (Inside U.S. Trade, Dec.
23). The commission is an independent body under the purview of the Japanese
prime minister’s cabinet.
The U.S. has pushed for Japan to relax its restrictions on U.S. beef
exports as one confidence-building measure that would facilitate Japan’s entry
into the Trans-Pacific Partnership talks (Inside U.S. Trade, June 15). While
Japan has expressed an interest in joining TPP talks and held consultations with
the U.S. and other TPP partners about that possibility, it has not yet made an
internal decision about whether to join.
After approving a final risk assessment, the Food Safety Commission would
forward it to Japan’s Ministry of Health, which would open negotiations with the
four affected trading partners to discuss import inspection protocols and other
technical measures.
Those negotiations would touch upon issues such as ensuring that each
trading partner has a verification system in place to determine that cattle
slaughtered for shipment to Japan are 30 months or younger. They would also
likely determine what procedure Japan would follow in the event it discovers a
shipment that does not comply with the new age requirements.
After Japan has completed those negotiations with the U.S. and other
trading partners, Japan’s Health Ministry would have to make a final decision on
changing the import rules. It would then inform the general public and an
advisory council of the decision, the official said.
Subsequently, the health and agriculture ministries would formally amend
the import requirements by sending out updated instructions to customs
authorities and posting the changes on their websites, according to the
official.
Sources have said they do not expect eventual U.S.-Japan negotiations over
the new import protocol to be a major challenge given that the U.S. already has
a verification system in place to ensure beef exports to Japan come from cattle
20 months and younger, and has similar system for verifying that beef sent to
South Korea is from cattle 30 months and younger.
Alternative BSE Risk Assessment Methodology for Beef and Beef Offal
Imported into Japan
Yasuhiro YOSHIKAWA1)*, Motohiro HORIUCHI2), Naotaka ISHIGURO3), Mutsuyo
KADOHIRA4), Satoshi KAI5), Hidehiro MIZUSAWA6), Chisato NAGATA7), Takashi
ONODERA8), Tetsutaro SATA9), Toshiyuki TSUTSUI10), Masahito YAMADA11) and
Shigeki YAMAMOTO12)
1)School of Veterinary Medicine, Kitasato University, 23–35–1 Higashi,
Towada, Aomori 034–8628, Japan
2)Laboratory of Veterinary Hygiene, Department of Applied Veterinary
Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo,
Hokkaido 060–0818, Japan
3)Laboratory of Food and Environmental Hygiene, Department of Veterinary
Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu
501–1193, Japan
4)Department of Life Science and Agriculture, Obihiro University of
Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080–8555, Japan
5)Faculty of Business, Marketing and Distribution, Nakamura Gakuen
University, Fukuoka, Fukuoka 814–0198, Japan
6)Department of Neurology and Neurological Science, Tokyo Medical and
Dental University, Yushima, Bunkyo-ku, Tokyo 113–8619, Japan
7)Department of Epidemiology & Preventive Medicine, Graduate School of
Medicine, Gifu University, Gifu 501–1193, Japan
8)Graduate School of Agricultural and Life Sciences, The University of
Tokyo, 1–1–1 Yayoi, Bunkyo-ku, Tokyo 113–8657, Japan
9)Department of Pathology, National Institute of Infectious Diseases,
Toyama, Shinjuku-ku, Tokyo 162–8640, Japan
10)Epidemiological Research Team, National Institute of Animal Health,
Tsukuba, Ibaraki 305–0856, Japan
11)Department of Neurology and Neurobiology of Aging, Graduate School of
Medical Science, Kanazawa University, Kanazawa 920–8640, Japan
12)Division of Biomedical Food Research, National Institute of Health,
Yoga, Setagaya-ku, Tokyo 158–8501, Japan
(Received 11 September 2010/Accepted 31 October 2011/Published online in
J-STAGE 14 November 2011)
snip...
Recently, there have been a few cases of irregular forms of BSE (atypical
BSE) reported apart from classical BSE in Europe, Japan and the U.S.A. These
reports of atypical BSE indicated variation in molecular sizes of abnormal prion
proteins (PrPSc) among cases, and eventually two major sizes of proteins were
designated as the H and L types. Most of the atypical BSE cases were found in
aged cattle over 8 years old, but a remarkable exception exists in Japan, where
a steer only 23 months old was reported to have been infected with atypical BSE
(the 8th BSE case in Japan). When this exception was excluded, the detection
ages of atypical BSE cases ranged from 6.3 to 18 years old. The average
detection ages for the H and L types were 11.8 and 11.6 years old, respectively
[3].
To the best of the authors’ knowledge, there have been about 40 cases of
atypical BSE reported worldwide, yet the OIE does not require distinction
between classical and atypical BSE cases in member countries for their reports,
while the EFSA only recently referred to case reporting by classical/atypical
recognition in its 2009 scientific opinion. These situations seem to further
obscure the clear number of atypical BSE cases occurring in the world.
The origin of atypical BSE has not yet been determined. According to EFSA’s
scientific opinion published in 2008, all the cases of atypical BSE were
reported with birth dates before the real feed ban in January 2001 in Europe.
Therefore, the possibility of these atypical cases being attributed to
contaminated feeds, just as in classical BSE, cannot be completely denied. On
the other hand, data of atypical BSE cases (both the H and L types) in France
did not show any reasonable correlation between birth year and frequency of
occurrence, as was indicated in classical BSE cases, thus raising the possible
interpretation of atypical BSE being sporadic isolated cases of prion disease
[3].
Based on the data accumulated in France, the frequencies of atypical BSE
cases per 1 million tested adult cattle were estimated to be 0.41 and 0.35 cases
for the H and L types, respectively (1.9 and 1.7 cases for the H and L-types,
respectively, when limiting the sampling to tested cattle over 8 years old). In
Japan, a total of 10 million cattle including fallen stock and slaughtered
cattle were tested for BSE, and the results showed no positive cases of the H
type and 2 positive cases (case 8, a 23-month-old steer; case 24, a
169-month-old Japanese black cow) of the L type of atypical BSE. These data
indicate that Japan has prevalence frequencies of 0 and 0.2 cases of the H and L
types of atypical BSE per 1 million cattle including tested fallen stock and
slaughtered cattle (zero and approximately 1.5 cases of the H and L types
respectively, when limiting the sampling to tested slaughtered cattle over 8
years old).
Atypical BSE of both the H and L types was confirmed to be transmissible by
intracerebral inoculation in transgenic mice expressing alleles of bovine or
ovine PrP genes and of inbred mice. However, for transgenic mice expressing
human prion protein, the L type but not the H type could be transmitted
according to the previously published reports (recently, it was reported that H
type also transmissible to the humanized transgenic mice). There have also been
reports of glycosylation pattern transformation from L-type BASE3 PrPSc-like
type to more of the classical BSE PrPSc type. This phenomenon was observed
during passage using inbred and transgenic TgVR2 mice. As for the atypical cases
of BSE confirmed in Japan, the 24th case of BSE was determined to have had the
atypical L type at the detection age of 169 months old, and its sample was
successfully transmitted to transgenic mice expressing bovine prion protein.
However, transmission of a sample from the other case of atypical L-type BSE
confirmed in Japan (the 8th case; detected at the age of 23-month-old) was
reported to be unsuccessful in transgenic mice expressing bovine prion protein.
The reason for this inconsistency is not clear at this time, although the
possible presence of a limitation in the amount of prion protein accumulated in
the subject’s brain sample or that the inoculated volume was too low to reach
the detection limit cannot be excluded.
A recent report has shown that the atypical L type of BSE has a higher
degree of potential for pathogenicity than that its classical counterpart
because incubation periods are shorter in atypical BSE transmitted to transgenic
mice expressing human prion protein, suggesting that atypical BSE possibly has a
higher degree of pathogenicity when compared to its classical counterpart [7].
In contrast to classical BSE, the systemic distribution of abnormal prion
protein in atypical BSE cases is barely known. Therefore, it is unclear whether
the brainstem is truly the optimal part for sampling and testing in H/L type
detection. Likewise, information regarding the infectivity distribution of
atypical BSE is scarce in bovine peripheral tissues and body fluid. All
together, the lack of essential data hinders, to a certain extent, evaluation of
the relative risk-reducing effects of various SRM removal measures for cattle.
Based on the currently available data concerning the potential risks for
humans of atypical BSE and prevalence of atypical BSE, it may be too extreme to
deny the risk of MRM, especially in MRM derived from aged cattle. However, the
degree of influence of the presence of atypical BSE on our concept of the MRM
risk will be limited to a low level under the circumstances with presently
available knowledge and our discussion. In the meantime, one must also be
reminded of the fact that only a limited amount of data is currently available
concerning atypical BSE. A proper amount of dis cretion should be used when
interpreting these data to avoid unnecessary confusion. Further research and
accumulation of data will bring additional insight into the mechanism,
pathogenicity and transmission potential of atypical BSE, for which further
assessment may become necessary in the future.
To gain the final result of this assessment, the periodic BSE risk status
of a country (the sum of invasive BSE risk and domestic stability) and efficacy
of present BSE riskreducing measures at meat processing lines were combined and
used as an indicator of comprehensive likelihood of BSE prion contamination in
beef and beef offal imported into Japan. Surveillance data were used to verify
reliability of the assessment. Finally, a summary of each country was expressed
in schematic figures (an example is shown in Fig. 4). In Fig. 4, a model
country’s invasive risk was ranked as high (from 1986–2005) but was reduced to
the middle level from 2006 onwards. The efficacy of feed ban (domestic
stability) was unstable during 1986–1989 but improved to the middle level
(1990–1996), to the stable level (1997–2000) and then to the very stable level
(2001-until now). Current risk reduction efficacy at meat processing lines,
determined by factors such as the definition of SRM, compulsory removal of SRM
by law, and HACCP/SSOP procedures were good and verified and were therefore
rated as ◎. BSE testing at slaughterhouse (>30 months), proper slaughtering
procedures such as avoidance of air stunning and pithing were verified as ◎. All
together, the overall risk reduction was extremely effective.
The final assessment for this model country was as follows: the domestic
BSE exposure/propagation risk was low, and risk reduction at meat processing
lines was extremely effective; therefore, the risk of BSE contamination of beef
and beef offal imported from this assessed country was considered to be
negligible.
RISK ASSESSMENT OF BEEF AND BEEF OFFAL IMPORTED INTO JAPAN
Tuesday, July 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th
General Session, 20 - 25 May 2012
Monday, September 3, 2012
2012 JAPAN BANS DEER AND ELK MEAT AND ALLOWS SOME BEEF PRODUCTS, what about
TSE prion concerns ?
We can confirm that of the 100 cases, 49 were under 30 months of age, of
these the youngest case was 20 months old.
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
the myth that cattle under 30 months of age are free from BSE/TSE is just
that, a myth, and it's a false myth !
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.
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.
Youngest confirmed case 20 Months, Oldest confirmed case 22 Years, Data
valid to 01 April 2008
BSE Youngest and oldest cases by year of onset - GB 20 months, 21 months,
(8) 24 months, see complete list of younger than 30 month ;
BSE Youngest Japan 21 months, 23 months
The implications of the Swiss result for Britain, which has had the most
BSE, are complex. Only cattle aged 30 months or younger are eaten in Britain, on
the assumption, based on feeding trials, that cattle of that age, even if they
were infected as calves, have not yet accumulated enough prions to be
infectious. But the youngest cow to develop BSE on record in Britain was 20
months old, showing some are fast incubators. Models predict that 200-300 cattle
under 30 months per year are infected with BSE and enter the food chain
currently in Britain. Of these 3-5 could be fast incubators and carrying
detectable quantities of prion.
Feed borne infection (31-34) a) Recent unpublished experiments at the VLA
have shown that feeding exceptionally low doses (0.001g) of infected neural
tissue can cause BSE. b) The working hypothesis of Defra that the major cause of
BSE in BARBs cases has been through the ingestion of contaminated feed, most
likely by young animals, is strongly supported. Thus control of the disease
requires, as it has always required, completely eliminating the agent from the
cattle feed chain. a) There has been a fall in the underlying incidence of BSE
by birth cohort 1996/97 to 99/00 in GB, but the 2001/2 case leaves doubt
subsequently. There has also been a fall in other countries except where feed
controls were introduced later. 34. In view of the exceedingly low doses of
brain material required to infect young cattle, the reductions in incidence
consequent on the feed bans in the UK and elsewhere and the lack of evidence
that other causes are responsible, the strongest hypothesis for BARBs is
infection of animals via ingestion of BSE contaminated material.
url changed to ;
Detection of PrPSc in peripheral tissues of clinically affected cattle
after oral challenge with BSE
Martin Franz1, Martin Eiden1, Anne Balkema-Buschmann1, Justin Greenlee2,
Hermann M Schaetzl3, Christine Fast1, Juergen Richt4, Jan-Peter Hildebrandt5 and
Martin Groschup1,6
+ Author Affiliations
1 Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany; 2 National
Animal Disease Center, ARS-USDA, Ames, IA, USA; 3 Depts of Veterinary Sciences
and Molecular Biology, University of Wyoming, Laramie, WY, USA; 4 Kansas State
University, College of Veterinary Medicine, Manhattan, KS, USA; 5 University
Greifswald, Germany
↵6 E-mail: martin.groschup@fli.bund.de
Received 6 June 2012. Accepted 20 August 2012.
Abstract
Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative prion
disease that mainly affects cattle. Transmission of BSE to humans caused a
variant form of Creutzfeldt-Jakob disease (vCJD). Following infection the
protease-resistant, disease-associated isoform of prion protein (PrPSc)
accumulates in the central nervous system and in other tissues. Many countries
have defined bovine tissues that may contain prions as specified risk materials
(SRMs), which must not enter the human or animal food chains and therefore must
be discarded. Ultrasensitive techniques such as the protein misfolding cyclic
amplification (PMCA) have been developed to detect PrPSc when present in
miniscule amounts that are not readily detected by other diagnostic methods such
as immunohistochemistry or western blot. This study was conducted to determine
when and where PrPSc can be found by PMCA in cattle orally challenged with BSE.
A total of 48 different tissue samples from 4 orally BSE-infected cattle at
clinical stages of disease were examined using a standardized PMCA protocol. The
protocol used brain homogenate from bovine PrP transgenic mice (Tgbov XV) as
substrate and three consecutive rounds of PMCA. Using this protocol PrPSc was
found in brain, spinal cord, nerve ganglia, optic nerve, and Peyer’s patches. We
could confirm the presence of PrPSc in adrenal gland as well as in mesenteric
lymph node – a finding, which was recently reported by another group.
Interestingly, additional positive results were obtained for the first time in
oesophagus, abomasum, rumen, and rectum of clinically affected cattle.
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND
ANIMAL HEALTH
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of
Atypical BSE UPDATE July 28, 2010
Sent: Wednesday, July 28, 2010 11:42 AM
Subject: re-Freedom of Information Act Project Number 3625-32000-086-05,
Study of Atypical BSE UPDATE
Greetings again Ms Williams et al at FOIA USDA,
Thank You again for your kind reply on this important information. However,
I am concerned that you may not be aware of new transmission studies. You (USDA
et al) state Ma'am ;
================================================
The SCA with Italy was mainly to confirm our respective country’s
diagnostic tests would detect the various atypical BSE cases as seen in each
country), in the meantime, the Italians have published their transmissibility
and pathogenesis work on their BASE cases in the following article:
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C,
Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S,
Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of
BASE induces clinical dullness and amyotrophic changes. PLoS Pathog
4:e1000075
The above mentioned paper concludes, “In all experimentally infected
animals, no PrP**TSE was detected in peripheral tissues, including cervical and
mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and
forelimb and limb muscles, either by standard Western blot analysis or following
phosphotungstic acid precipitation.“
It is not necessary to change SRM removal due to any different tissue
infectivity distribution between classical BSE and atypical BSE. At this time,
there is no scientific evidence to suggest a need for expanding the list of
tissues included in the Specified Risk Material (SRM) ban as a result of
published studies on atypical BSE.
snip...
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine
spongiform encephalopathy-sensitive transgenic mice confirm the essential
restriction of infectivity to the nervous system in clinically diseased cattle.
J Infect Dis 192:934-942; the authors, when speaking about the classical BSE
food-borne epidemic in Europe, concluded their “results provide further
indication that the pathogenesis of BSE in cattle is fundamentally different
from that in sheep and mice, due to an exclusive intraneuronal spread of
infectivity from the gut to the central nervous system.”
end...
================================================
Again, in my opinion, the USDA is cherry picking the science they want to
use, and in doing so, I believe they are putting human lives at risk.
I disagree for the following reasons. New studies indeed show that ;
July 10, 2010
see full text ;
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of
Atypical BSE UPDATE July 28, 2010
USDA TRIPLE BSE MAD COW FIREWALL, SRM, FEED, AND SURVEILLANCE
2012
***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...
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE
in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
The present study demonstrated successful intraspecies transmission of
H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc
in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be
minimally defined by oral transmission of different TSE agents (C-type, L-type,
and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected
cattle have been initiated and are underway to provide information regarding the
extent of similarity in the immunohistochemical and molecular features before
and after transmission.
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
Friday, May 11, 2012
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
***support risk assessments in some peripheral tissues derived from cattle
affected with H-type BSE
Thursday, June 21, 2012
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy
Associated with E211K Prion Protein Polymorphism
Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M.
Nicholson1
1 National Animal Disease Center, United States Department of Agriculture,
Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa
State University, Ames, Iowa, United States of America
Abstract
The majority of bovine spongiform encephalopathy (BSE) cases have been
ascribed to the classical form of the disease. Htype and L-type BSE cases have
atypical molecular profiles compared to classical BSE and are thought to arise
spontaneously. However, one case of H-type BSE was associated with a heritable
E211K mutation in the prion protein gene. The purpose of this study was to
describe transmission of this unique isolate of H-type BSE when inoculated into
a calf of the same genotype by the intracranial route. Electroretinograms were
used to demonstrate preclinical deficits in retinal function, and optical
coherence tomography was used to demonstrate an antemortem decrease in retinal
thickness. The calf rapidly progressed to clinical disease (9.4 months) and was
necropsied. Widespread distribution of abnormal prion protein was demonstrated
within neural tissues by western blot and immunohistochemistry. While this
isolate is categorized as BSE-H due to a higher molecular mass of the
unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with
monoclonal antibodies 6H4 and P4, and a second unglycosylated band at
approximately 14 kDa when developed with antibodies that bind in the C-terminal
region, it is unique from other described cases of BSE-H because of an
additional band 23 kDa demonstrated on western blots of the cerebellum. This
work demonstrates that this isolate is transmissible, has a BSE-H phenotype when
transmitted to cattle with the K211 polymorphism, and has molecular features
that distinguish it from other cases of BSE-H described in the literature.
snip...
Most significantly it must be determined if the molecular phenotype of this
cattle TSE remains stable when transmitted to cattle without the E211K
polymorphism as several other isolates of atypical BSE have been shown to adopt
a molecular profile consistent with classical BSE after passage in transgenic
mice expressing bovine PrPC [40] or multiple passages in wild type mice [23].
Results of ongoing studies, namely passage of the E211K Htype isolate into
wild-type cattle, will lend further insight into what role, if any, genetic and
sporadic forms of BSE may have played in the origins of classical BSE. Atypical
cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins
highlight that it may not be possible to eradicate BSE entirely and that it
would be hazardous to remove disease control measures such as prohibiting the
feeding of meat and bone meal to ruminants.
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the
origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger outbreak.
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.
Sunday, August 26, 2012
Detection of PrPSc in peripheral tissues of clinically affected cattle
after oral challenge with BSE
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected
feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the
origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger outbreak.
SNIP...
==============================================
*** 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 ;
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
=============================================
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
in the url that follows, I have posted
SRM breaches first, as late as 2011.
then
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until
2007, when they ceased posting them.
then,
MAD COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy
(BSE) in the United States Friday May 18, 2012
Monday, September 3, 2012
Sale of misbranded and/or non-inspected meat and meat products to Omaha
Public Schools indicted
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...
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and
it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
see follow-up here about North America BSE Mad Cow TSE prion risk factors,
and the ever emerging strains of Transmissible Spongiform Encephalopathy in many
species here in the USA, including humans ;
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE
RISE IN NORTH AMERICA
Wednesday, August 01, 2012
Behavioural and Psychiatric Features of the Human Prion Diseases:
Experience in 368 Prospectively Studied Patients
Monday, August 06, 2012
Atypical neuropathological sCJD-MM phenotype with abundant white matter
Kuru-type plaques sparing the cerebellar cortex
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Friday, August 24, 2012
Iatrogenic prion diseases in humans: an update
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
TSS
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