PRION 2016 TOKYO JAPAN
The epidemiological evolution of prion infection on bovine in Romania, in the period of 2010 – 2015
*** A case of variant Creutzfeldt-Jakob disease in Romania ***
Mihai Ceauşu1, Corneliu Octavian Capatina2, Sorin Hostiuc3,*, Dan
Dermengiu3
Abstract: In humans prion diseases can occur sporadically, through genetic
mutations, or can be transmitted from animal, human (kuru disease), or
iatrogenic sources. Even though transmissible forms are the most well-known, the
sporadic and heritable forms are much more frequent, accounting for about 85% of
all cases. The purpose of this case report is to present an atypical variant CJD
in a 26 years-old woman. The patient died secondary to infectious complications
caused by an acute overdose with alcohol, beta-blockers and oral anti-diabetic
drugs, and had an atypical neuropathology pattern, with absent amyloid plaques,
but present focal, perivascular deposits of amyloid precursor protein and a
positive immunohistochemical reaction for prp. Key Words: variant
Creutzfeldt-Jakob disease, Romania, amyloid precursor protein.
snip...
Discussion This is, to our knowledge, one of the first reported cases of
CJD in Romania. Filip et al described a case of human prion disease (sporadic
CJD) in a 64 years old male[4]. Pop et al described a case of sporadic CJD a 47
years old female [5]. In EUROCJD Surveillance Data, Romania is not present [6].
Clinically our patient had initial psychiatric symptoms, with behavioral changes
- attempted suicide, dysthymic personality disorders, which were primarily
attributed to substance abuse. Neurological signs were identifiable only after
the patient became comatose. The cause of death was not directly prion-related –
the underlying cause of death was considered acute intoxication with
betablockers, alcohol and oral anti-diabetic drugs that lead to coma, finally
complicated with pneumonia. Therefore the neurodegenerative disease was most
likely at the beginning of its course and, due to the predominance of
psychiatric pathology, suggested more likely a clinical diagnose of vCJD
[7].
The presence of the protein 14-3-3 in the CSF in not a definite test for
CJD (or vCJD). However, it currently has a sensibility of 95% and in our case we
excluded other possible causes (tumors, encephalitis, meningitis) [8]. The only
false positive reaction for 14-3-3 that was not excluded clinically was cerebral
ischemia, which was present in our patient. However, corroborating this result
with the neuropathology examination the diagnosis of vCJD was certain.
The histological examination revealed neuronal vacuolar degeneration,
frequent, confluent cysts leading to a spongiform appearance and gliosis,
without inflammation, and amyloid plaques, a pattern suggestive for sporadic CJD
[9, 10].
PrPc is found in normal cells and it suffers a conformation change, turning
its 3-D structure from a α-helix into a β-sheet form, which is highly resistant
and infective. Regarding its normal function, it may play a role in neuronal
development and synaptic plasticity. It is thought it may be required for
neuronal myelin sheath maintenance and sometimes it may play a role in iron
uptake and iron homeostasis. A certain isoform may act as a growth suppressor by
arresting the cell cycle at the G0/G1 phase. Soluble oligomers are toxic to
cultured neuroblastoma cells and induce apoptosis in vitro. PrPSc is found in
high quantity in the brain of humans and animals infected with neurodegenerative
diseases known as transmissible spongiform encephalopathies or prion
diseases.
Ubiquitin is a heat shock protein, required for ATP-dependent non-lysosomal
intracellular protein degradation, which eliminates most intracellular defective
proteins, as well as normal proteins with a rapid turnover.
Degradation involves covalent binding of ubiquitin to the protein to be
degraded and it is believed that in this way, ubiquitin acts to label the
protein for disposal by intracellular proteases.
The family history of the patient was negative for CJD or other
neurodegenerative diseases. Also, the patient did not suffer surgical
interventions, treatment with growth hormone or other treatments known to be
associated with the transmission of iatrogenic CJD. In a report of the Centers
for Disease Control and Prevention from 2005-2006 Romania is presented as one of
the countries that were likely to have Bovine Spongiform Encephalopathy [11],
which subsequently suggests a risk for vCJD. Also, in the late 1990s there were
press articles suggesting illegal import of contaminated cow meat from UK,
during the outburst of mad cow disease. Therefore we can speculate that the most
probable cause is represented by the use of contaminated cow meat.
Conclusion
This is the first report of vCJD in Romania. However, the absence of other
reported cases does not necessarily mean their absence; an increased level of
awareness regarding this disease in clinical environments may reveal additional
cases.
see full text ;
CREUZFELDT-JAKOB’S DISEASE – CASE REPORT
Z. Cofoian-Amet1, B. Rusu1, C. Mitu1, E. Roşianu1, B.O. Popescu1,2,3
1Department of Neurology, Colentina Clinical Hospital, Bucharest, Romania
2Department of Neurology, Psychiatry, Neurosurgery and Psychiatrics, School of
Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania
3Laboratory of Neurosciences and Molecular Medicine, “Victor Babes” National
Institute of Pathology, Bucharest, Romania
ABSTRACT
Creutzfeldt-Jakob disease is a low incidence progressive neurodegenerative
disorder and, meanwhile, the most frequent human prion disease. We report here
the case of a 65 years old female with a 2-month history of rapidly progressive
dementia. The clinical examination identifi ed patent cerebellar and
extrapyramidal signs. Despite the absence of myoclonic jerks and pathological fi
ndings in T2 and FLAIR MRI, the presence of protein 14-3-3 in a signifi cant
amount in cerebrospinal fl uid (CSF) was identifi ed. The patient succumbed to
the illness within 2 month of hospitalization.
Key words: sporadic Creutzfeldt-Jakob; rapidly progressive dementia, 14-3-3
Creutzfeldt-Jakob Disease
ABSTRACT Creutzfeldt-Jakob disease is the most common human prion
pathology. We describe is emblematic of this disease in its form of onset and
progression. We have reported the symptoms and the diagnostic possibilities: a
82 years old man accused suddenly confusion, agitation, memory impairment with
rapid progression of cognitive decline and psychiatric signs and the appearance
of other neurological deficits that led the patient quickly to coma leading to
death. The pathological examination clarified the nature of patient's medical
and it allowed players to make the diagnosis.
Key words: General practitioner, dementia, Creutzfeldt-Jakob disease
Creutzfeldt-Jakob Hastalığı ÖZET Creutzfeldt-Jakob hastalığı en yaygın
insan prion patolojidir. Biz bu olgu sunumunda hastalığın başlangıcı ve
ilerlemesini sembolik olarak sunduk. Biz hastanın semptom ve tanısal işlemlerini
bildirdik. Bunlar; ani gelişen konfüzyon ile gelen 82 yaşında erkek hasta,
ajitasyon , kognitif bozulma ile birlikte hafıza bozukluğu, psikiyatrik
belirtiler ve ölüme neden olacak koma ya götürecek nörolojik defisitlerin
bulunması. Patolojik inceleme ile hastanın tanısı konuldu. Anahtar kelimeler:
Pratisyen hekim, demans, Creutzfeldt-Jakob hastalığı Doctor formed in Medical
General Practice, Rome, Italy Received: 08.12.2012, Accepted: 27.11.2013
Correspondence: Valerio Massimo Magro Doctor formed in Medical General Practice,
Rome, Italy Correspondence to valerio_magro@hotmail.com Valerio Massimo Magro
European Journal of General Medicine
INTRODUCTION Creutzfeldt-Jakob disease is a rare cause of dementia evolving
fatal even more rarely it is observed on the Italian territory. A case related
is observed in a General Practitioner’s (GP) study (1). CASE Male patient.
*** He was 82 years old. He emigrated young in a country in Eastern Europe
in search of work and then he had lived for a long time in Romania.
snip...see ;
ROMANIA CJD STATISTICS with current CJD surveillance ???
| Romania | 22 | 22,355,5512 |
| Creutzfeldt-Jakob Disease in Eastern Europe (Extrapolated Statistics) | ||
| Azerbaijan | 7 | 7,868,3852 |
| Belarus | 10 | 10,310,5202 |
| Bulgaria | 7 | 7,517,9732 |
| Estonia | 1 | 1,341,6642 |
| Georgia | 4 | 4,693,8922 |
| Kazakhstan | 15 | 15,143,7042 |
| Latvia | 2 | 2,306,3062 |
| Lithuania | 3 | 3,607,8992 |
| Romania | 22 | 22,355,5512 |
| Russia | 143 | 143,974,0592 |
| Slovakia | 5 | 5,423,5672 |
| Slovenia | 2 | 2,011,473 2 |
| Tajikistan | 7 | 7,011,556 2 |
| Ukraine | 47 | 47,732,0792 |
| Uzbekistan | 26 | 26,410,4162 |
THIS REPORT CONTAINS ASSESSMENTS OF COMMODITY AND TRADE ISSUES MADE BY USDA
STAFF AND NOT NECESSARILY STATEMENTS OF OFFICIAL U.S. GOVERNMENT POLICY
Voluntary Public
Date: 1/29/2015
GAIN Report Number: RO1502
Romania
Post: Bucharest
Romania confirms the second case of BSE
Report Categories: Sanitary/Phytosanitary/Food Safety Livestock and
Products
Approved By: Russ Nicely
Prepared By: Monica Dobrescu
Report Highlights:
In December 2014 Romania confirmed the second case of Bovine Spongiform
Encephalopathy (BSE), atypical form, as part of the BSE surveillance program.
According to National Veterinary and Food Safety Authority (ANSVSA), the sick
animal came from a backyard farm located in the center of Romania. The first
case was detected in May 2014 and it triggered the suspension of the status
“country with negligible BSE risk” granted by the World Organization of Animal
Health (OIE).
General Information:
On December 22nd 2014, a sample collected from a bovine slaughtered on
December 16th, 2014 in an authorized slaughterhouse in Dambovita County (south
of Romania) raised the suspicion of BSE disease (also known as mad cow disease).
The origin of the animal, a backyard farm from Covasna County (center of
Romania), was identified, along with animal ascendants and descendants.
Currently the process of identifying all animals pertaining to the same herd and
all animals which came in contact with the infected animal is on-going.
The National Veterinary and Food Safety Authority (ANSVSA) assured
consumers that public health has not been put in danger, as meat coming from the
positive animal has not entered the food chain. Meat and by-products from the
positive animal and the animal slaughtered before the infected one have been
seized.
On December 23rd 2014, when the Institute for Diagnosis and Animal Health
confirmed the suspicion of the disease, the entire amount of seized meat and
products was destroyed into a rendering facility.
On January 7th 2015, the sample was sent for strain determination to the EU
Reference Laboratory in Weybridge, United Kingdom, which later confirmed the
atypical form of BSE. Under such circumstances, the veterinary service started
the procedure of evaluating the health status of all animals which came in
contact with the positive one. The backyard farm has been officially placed
under surveillance for animal and products movement. All animal owners will be
compensated for losses in case their animals are sent for disposal.
Institute for Diagnosis and Animal Health confirmed the first case of
atypical BSE form in May 2014. Following this occurrence, World Organization of
Animal Health (OIE) suspended in June 2014 the status of “country with
negligible BSE risk”.
Unlike the classical cases of mad cow which are caused when cattle are fed
with feeding materials which contain proteins of animal origin, the atypical
cases occur spontaneously, the causes being currently under investigation. In
the context of a second case of BSE atypical form confirmation in Romania,
ANSVSA suggested during the most recent meeting of the Standing Committee on
Plants, Animals, Food and Feed (SCOFCAH) at EU level that the European Food
Safety Authority (EFSA) would consider undertaking studies regarding the causes
of BSE atypical forms.
USDA Announces Preliminary Concurrence with OIE Risk Designations for BSE
in 16 Countries USDA Animal and Plant Health Inspection Service sent this
bulletin at 12/04/2015 11:15 AM EST
Bookmark and Share
USDA Announces Preliminary Concurrence with World Animal Health
Organization Risk Designations for Bovine Spongiform Encephalopathy in 16
Countries
December 4, 2015—The United States Department of Agriculture’s Animal and
Plant Health Inspection Service (APHIS) is preliminarily concurring with the
World Organization for Animal Health’s (OIE) bovine spongiform encephalopathy
(BSE) risk designations for 16 countries. The OIE recognizes these regions as
being of negligible risk for BSE. APHIS reviewed the information supporting the
OIE’s risk designations for these regions and agrees with the OIE designations.
The 16 countries are: Bulgaria, Cyprus, Czech Republic, Estonia, France,
India, Korea (Republic of), Hungary, Latvia, Liechtenstein, Luxembourg, Malta,
Portugal, Romania, Slovakia, and Switzerland.
The OIE recommendations regarding each of the above countries can be viewed
online.
APHIS considers all countries of the world to fall into in one of three BSE
risk categories: negligible risk, controlled risk, or undetermined risk. Any
region that is not classified by APHIS as presenting either negligible risk or
controlled risk for BSE is considered to present an undetermined risk.
Under the regulations, APHIS may classify a region for BSE in one of two
ways. One way is for countries that have not received a risk classification from
the World Organization for Animal Health (OIE) to request classification by
APHIS. The other way is for APHIS to concur with the classification given to a
country by the OIE.
This notice is available for 60 days for review and comment. APHIS will
consider all comments received on or before February 2, 2016. After reviewing
any comments we receive, we will announce our final determination regarding the
BSE classification of these countries in the Federal Register.
snip...see ;
Saturday, December 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Thursday, December 25, 2014
Bovine spongiform encephalopathy, Romania Confirmed
In addition to the countries with indigenous cases of confirmed BSE in
2003, 6 countries previously had reported one or two BSE cases to the OIE; these
countries include Austria, Finland, Greece, Israel, Liechtenstein, and
Luxembourg. The European Union's committees on BSE risk assessment have also
classified 18 other countries as likely to have BSE, including Albania, Andorra,
Belarus, Bulgaria, Croatia, Cyprus, Estonia, Hungary, Latvia, Lithuania,
Macedonia, Malta, Mexico, Romania, San Marino, South Africa, Turkey, and the
United States.
Opinion of the Scientific Steering Committee on the GEOGRAPHICAL RISK OF
BOVINE SPONGIFORM ENCEPHALOPATHY (GBR) in Romania Adopted on 11/05/2001
Opinion of the SSC on the Geographical BSE-risk of Romania 11/05/200
2
Opinion of the Scientific Steering Committee on the GEOGRAPHICAL RISK OF
BOVINE SPONGIFORM ENCEPHALOPATHY (GBR) in Romania
THE QUESTION
The Scientific Steering Committee (SSC) was asked by the Commission to
express its scientific opinion on the Geographical BSE-Risk (GBR), i.e. the
likelihood of the presence of one or more cattle being infected with BSE,
pre-clinically as well as clinically, at a given point in time, in a number of
Third Countries. This opinion addresses the GBR of Romania.
THE BACKGROUND
In December 1997 the SSC expressed its first opinion on Specified Risk
Materials where it stated, inter alia, that the list of SRM could probably be
modulated in the light of the species, the age and the geographical origin of
the animals in question. In June 2000 the European Commission adopted a Decision
on SRM (2000/418/EC), prohibiting the import of SRM from all Third Countries
that have not been "satisfactorily" assessed with regard to their
BSE-Risk.
In July 2000 the SSC adopted its final opinion on "the Geographical Risk of
Bovine Spongiform Encephalopathy (GBR)", which described a method and a process
for the assessment of the GBR and summarised the outcome of its application to
23 countries. Detailed reports on the GBR-assessment were published on the
Internet for each of these countries.
In September 2000 the Commission invited Third Countries, which are
authorised to export products to the EU that are listed in annex II to the above
mentioned SRM-Decision, to provide a dossier for the assessment of their GBR.
Until today 46 dossiers have been received, 28 are already assessed and 18 are
in different states of assessment.
This opinion concerns only one country, Romania. It is recommended to read
the opinion and the detailed report on the GBR of Romania in the context of the
GBRopinion of July 2000.
The Commission requested this SSC opinion on the GBR of this, and of all
Third Countries that decided to provide the necessary information, as input into
its Decision concerning the treatment of exports from these countries in view of
BSE in general and SRM in particular.
The SSC is concerned that the available information was not confirmed by
inspection missions as they are performed by the FVO in the Member States. It
recommends that BSE-related aspects are included in the program of future
inspection missions, as far as feasible.
Opinion of the SSC on the Geographical BSE-risk of Romania 11/05/200
3
The Analysis
The external challenge that Romania was exposed to was high between
1980-1990 and between 1994-2000 and moderate between 1991-1993. About 22,000
cattle were imported from BSE-affected countries other than the UK: 8,600 from
DE and IRL during 1980-1987 (mostly in 1981); 6,300 from NL, DK, DE and FR
between 1988 and 1993; and 7,400 from NL, DK, DE, and IT since 1994. MBM imports
from BSE affected countries amounted to 467 tonnes from the UK (in 1995) and
about 10,600 tonnes from other BSE-affected countries, mostly imported before
1990 from DE and to a much smaller extent from IT and IRL. After 1990 smaller
imports of MBM occurred from more countries: NL, DE, BE, IT, and DK. All in all
these imports make it likely that the BSE agent entered Romania, either during
the eighties or after 1994.
The BSE/cattle system of Romania was extremely unstable from 1980 to 1996
and unstable since then. The feed ban that apparently was already adopted in
1982 and the authorised feed recipes that did not include animal protein in
cattle feed are not regarded as sufficient evidence that cattle could not
receive animal proteins because no information was provided on enforcement. In
1997 this feed ban was reconfirmed, the production of concentrates and premixes
for cattle was prohibited, and controls were introduced. This made accidental
feeding of MBM to cattle much more unlikely, but again controls remained
unsatisfactory. Since 1974 rendering was done at 130°C for 90 minutes (pressure
not specified), and since 1997 at 130°C for 20min at 3bar. No information was
provided on the enforcement of the application of the conditions prior to 1997,
since then some regular controls are carried out. Rendering therefore is
assessed as being able to reduce the BSE agent to some extent since 1997. A
partial SRM-ban existed since 1995, when brains and spinal cord and non-edible
bovine offal were withdrawn from the feed chain. Since 29 January 2001, fallen
stock and SRM have to be incinerated. BSE is notifiable since 1993 and passive
and some elements of active BSE surveillance exist. However, the surveillance of
the domestic cattle population is assessed as insufficient to detect low levels
of BSE-incidence. Crosscontamination cannot be excluded. The relatively small
number of ELISA tests annually carried out since 1995 cannot proof the contrary,
also because their stated sensitivity is with 0.5-2% contamination to low.
It is concluded that it is likely, but not confirmed that one or several
cattle that are (pre-clinically or clinically) infected with the BSE agent are
currently present in the domestic herd of Romania (GBR- III).
Given the unstable system and the fact that the BSE agent is likely to be
already present in the country, it is assumed that the GBR is increasing.
A summary of the reasons for the current assessment is given in annex 1 to
this opinion. A detailed report on the assessment of the GBR of Romania is
published separately on the Internet. It was produced by the GBR-task force of
the SSCsecretariat and peer reviewed by the GBR-Peer group. The country had two
opportunities to comment on different drafts of the report before the SSC took
both, the report and the comments, into account for producing this opinion. The
SSC appreciates the good co-operation of the country’s authorities.
ANNEX I
SNIP...SEE ANNEX I
Scrapie, Romania, (Follow-up report No. 4) 12/10/2007
Information received on 12/10/2007 from Dr Stefan Nicolae, Directeur
Général , Direction Générale, Autorité Nationale Sanitaire Vétérinaire pour la
Sécurité des Aliments (ANSVSA), Bucuresti , Romania
Summary
Report type Follow-up report No. 4 Start date 19/01/2007 Date of
confirmation of event 12/06/2007 Report date 12/10/2007 Date submitted to OIE
12/10/2007 Reason for notification Reoccurrence of a listed disease Date of
previous occurrence 08/12/2006 Manifestation of disease Clinical disease Causal
agent Scrapie prion Nature of diagnosis Laboratory (advanced) Report pertains to
Defined zone within the country Related reports Immediate notification
(13/06/2007) Follow-up report No. 1 (09/07/2007) Follow-up report No. 2
(18/07/2007) Follow-up report No. 3 (31/07/2007) Follow-up report No. 4
(12/10/2007)
New outbreaksOutbreak 1 Silistea, Silistea, BRAILA Date of start of
outbreak 19/09/2007 Outbreak status Continuing (or date resolved not submitted)
Epidemiological unit Farm Affected animals Species Susceptible Cases Deaths
Destroyed Slaughtered Sheep 1259 2 0 0 2
Affected population non-professional holding. Two animals were sick and
were slaughtered ; their heads were sent to the laboratory. Summary of outbreaks
Total outbreaks: 1 Outbreak statistics Species Apparent morbidity rate Apparent
mortality rate Apparent case fatality rate Proportion susceptible removed* Sheep
0.16% 0.00% 0.00% 0.16% * Removed from the susceptible population either through
death, destruction or slaughter
EpidemiologySource of infection Unknown or inconclusive
Epidemiological comments Control measures applied in accordance with the
legislative provisions in force.
Control measuresMeasures already applied Movement control inside the
country Screening Vaccination permitted No treatment of affected animals
Measures to be applied None specified
Diagnostic test resultsLaboratory name and type Institute for Diagnosis
and Animal Health (National laboratory) Tests and results Species Test Test date
Result Sheep western blotting 09/10/2007 Positive
Map of outbreak locations Click on map to zoom in.
Greetings BSE-L members,
Confusious is confused again. Confusious ask ;
WHY does OIE not report the 5 cases of Nor-98 reported this year in the USA
???
WHY no data on OIE site on the h-BASE in Alabama and Texas in USA ???
if it's there, i cannot find it.
no wonder OIE gives favorable BSE ratings for USA, they never report
nothing about it. ... snip...end...TSS
THIS REPORT CONTAINS ASSESSMENTS OF COMMODITY AND TRADE ISSUES MADE BY
USDA STAFF AND NOT NECESSARILY STATEMENTS OF OFFICIAL U.S. GOVERNMENT
POLICY
Voluntary Public
Date: 7/15/2011
GAIN Report Number: E60043
EU-27
Post: Brussels USEU
Further decrease in EU BSE cases may lead to end of MBM feed ban
Report Categories: Sanitary/Phytosanitary/Food Safety
Approved By: Maurice House
Prepared By: Yvan Polet
Report Highlights: On July 6, 2011, the European Parliament gave the green
light for a conditional lifting of the EU ban on feeding meat and bone meal
(MBM). MBM will remain excluded in ruminant feed, while feeding MBM to the same
species will also remain banned. However, under this scenario, poultry MBM could
be fed to pigs and pig MBM to poultry as of the second half of 2012. As of July
1, 2011, the age for mandatory BSE testing in 25 Member States has been
increased from 48 to 72 months. These measures have been introduced as part of
the EU TSE Road Map 2, which covers the 2010-2015 period.
General Information:
In a plenary session on July 6, 2011, the European Parliament (EP) approved
a resolution [1] on the EU’s Transposable Spongiform Encephalopathy (TSE) policy
initiated by German Socialist MEP Roth- Behrendt. This resolution supports the
partial lifting of the ban on meat and bone meal (MBM) in feed in the EU; the
ban on feeding MBM to ruminants will still remain. MBM may also not be produced
from ruminants. The new policy will allow the feeding of MBM to pigs, poultry
and fish. MBM from poultry may be fed to pigs and MBM from pigs may be fed to
poultry. In order to control and enforce the separation of species-specific MBM,
a testing method must be validated first. However, validation of such a test is
under review and it is expected that the EC will make a proposal to end the MBM
feed ban in the autumn of 2011. The end to the MBM feed ban could be implemented
in the summer of 2012 if no further obstacles arise. In light of the EU’s
protein shortfall and high prices for soymeal, European feed industries have
been lobbying for this end to the MBM feed ban for several years. With the
resolution on the future TSE policy, the EP supports the execution of the “TSE
Road map 2” that the European Commission (EC) presented in its July 2010
Communication [2] to the European Parliament and the Council. Another measure
from the TSE Road map 2 is the Commission Decision [3] of June 17, 2011 to allow
25 out of 27 Member States (MS) to increase the testing age for BSE in cattle
monitoring from 48 months to 72 months. This increase in the BSE testing age
went into effect on July 1, 2011 and was granted after MS submitted their plans
to the Commission with a updated BSE monitoring plan. This Decision followed a
favorable opinion [4] from the European Food Safety Authority (EFSA) from
December 2010. Only Bulgaria and Romania failed to propose an updated monitoring
regime, but both countries had no BSE cases in recent years.
EU BSE cases continue to decrease
In 2010, the number of BSE cases detected in the EU was 44, indicating a
continued decline from 68 cases in 2009 and 121 in 2008. Spain and the United
Kingdom were the only two remaining MS with more than 10 BSE cases, making up
more than half of all detected BSE cases in the EU. Some industry experts are
already suggesting that most ME should halt systematic BSE testing completely,
as they may be down to a naturally occurring threshold of BSE again and
therefore occasional further BSE finds only serve scaremongers. However, at this
point it is politically still inconceivable that BSE monitoring and eradication
measures in the EU be lifted after they have proven successful in the fight
against BSE.
Total BSE cases in the EU
2005 2006 2007 2008 2009 2010
AUSTRIA 2 2 1 0 0 2
BELGIUM 2 2 0 0 0 0
BULGARIA 0 0 0 0 0 0
CYPRUS 0 0 0 0 0 0
CZECH REPUBLIC 8 3 2 0 2 0
DENMARK 1 0 0 0 1 0
GERMANY 32 16 4 2 2 0
ESTONIA 0 0 0 0 0 0
FINLAND 0 0 0 0 0 0
FRANCE 31 8 9 8 10 5
GREECE 0 0 0 0 0 0
HUNGARY 0 0 1 0 0 0
IRELAND 69 41 25 23 9 2
ITALY 8 7 2 1 2 0
LATVIA 0 0 0 0 0 0
LITHUANIA 0 0 0 0 0 0
LUXEMBURG 1 0 0 0 0 0
NETHERLANDS 3 2 2 1 0 2
POLAND 20 10 9 5 4 2
PORTUGAL 51 33 14 18 8 6
ROMANIA 0 0 0 0 0 0
SLOVENIA 1 1 1 0 0 0
SLOVAKIA 3 0 2 1 0 1
SPAIN 103 68 36 25 18 13
SWEDEN 0 1 0 0 0 0
UNITED KINGDOM 226 129 67 37 12 11
Total EU 561 323 175 121 68 44
Source: OIE [5]
For a wide range of useful information on EU agricultural policies and
direct access to FAS/USEU reports, trade information and other practical
information please visit our website:
http://www.fas.usda.gov/posthome/useu/
or contact our office at aguseubrussels@fas.usda.gov
Related reports from FAS EU
E57008 EC animal disease eradication and monitoring program for 2011
12/12/2010
E50041 EC planning TSE Roadmap 2010-2015 as decrease in BSE cases
continues
06/14/2010
These reports can be accessed through our website http://www.fas.usda.gov/posthome/useu/
or
through the FAS website http://gain.fas.usda.gov/Pages/Default.aspx
- Opinion the
Geographical Risk of Bovine Spongiform Encephalopathy (GBR) in Romania
(Adopted on 11/05/2001) (21KB)
List of Bovine Spongiform Encephalopathy Risk Status of Member Countries
Member Countries
recognised as having a negligible BSE risk in accordance with Chapter
11.4. of the Terrestrial
Code :
Argentina
|
Hungary
|
Norway
|
Australia
|
Iceland
|
Panama
|
Austria
|
India
|
Paraguay
|
Belgium
|
Israel
|
Peru
|
Brazil
|
Italy
|
Portugal
|
Bulgaria
|
Japan
|
Romania
|
Chile
|
Korea (Rep.
of)
|
Singapore
|
Colombia
|
Latvia
|
Slovakia
|
Croatia
|
Luxembourg
|
Slovenia
|
Denmark
|
Malta
|
Sweden
|
Estonia
|
Netherlands
|
United States of
America
|
Finland
|
New
Zealand
|
Uruguay
|
-
Controlled BSE risk
Member Countries
recognised as having a controlled BSE risk in accordance with Chapter
11.4. of the Terrestrial
Code :
Canada
|
Germany
|
Nicaragua
|
Chinese Taipei
|
Greece
|
Poland
|
Costa
Rica
|
Ireland
|
Spain
|
Cyprus
|
Lichtenstein
|
Switzerland
|
Czech Republic
|
Lithuania
|
United
Kingdom
|
France
|
Mexico
|
Zone with a
negligible BSE risk Member Countries recognised as having a zone with a
negligible BSE risk in accordance with Chapter 11.4. of the Terrestrial Code :
China (People’s Rep. of):
A zone designated by the Delegate of China in a document addressed to the
Director General in November 2013, consisting of the People’s Republic of China
with the exclusion of Hong Kong and Macau.
Tuesday, July 5, 2011
Risk Assessment of BSE Introduction in the Russian Federation in Connection
with Importation of Cattle from the European Union in 2005–2010
Risk.40: Risk Assessment of BSE Introduction in the Russian Federation in
Connection with Importation of Cattle from the European Union in 2005–2010
Sergey Rybakov† and Alexander Yegorov
FGI Federal Centre for Animal Health; Vladimir, Russia†Presenting author;
Email: s.s.rybakov@mail.ru
The study is aimed at quantitative assessment of risk of BSE introduction
from the EU countries into Russia with breeding animals imported during
2005–2010.
Within 2005–2010 importation of cattle born in 2003–2008 from the EU into
Russia totally amounted to 363,000 animals. According to the data published in
the EU reports, during 2003–2008 the BSE prevalence in the EU countries reduced
from 125 cases per million bovine animals above 24 months of age in 2003 to 12
cases in 2008. If the imported subpopulation had proportionally represented all
age-groups of cattle from EU25 countries, according to the calculation 19.4
animals in BSE incubation period should have been imported from 2005 until
2010.
The main suppliers of breeding cattle into Russia are the following EU
countries: Austria, Denmark, France, Finland, Germany, Hungary and The
Netherlands. Since 2007 import from these countries has amounted to 67.5% of the
total import. The major suppliers—not the EU member states—are Canada (12.2%),
Australia (12.1%) and the US (5.8%). As for the UK, Poland and Portugal, i.e.
countries having the highest BSE incidence, currently export of live cattle from
there is banned. Calculations demonstrated that limitation of live cattle
importation from the countries with high BSE incidence allows to reduce the risk
of BSE introduction into Russia in 14.5 times.
Risk assessment in relation to BSE in animals born after 2003 was performed
by EFSA in 2009. The EFSA results demonstrated that estimated number of BSE
cases in EU17 countries amounted totally to 32 cases within 2003–2008 and the
highest 95% confidence limit constituted 65 cases. As for seven above mentioned
live cattle importing countries the estimated number of BSE cases within
2003-2008 averaged to 1.8 and upper 95% confidence limit was 3.6.
Given that share of cattle annually exported from these seven countries
into Russia averages to 0.293%, according to calculations, within 2005-2010 the
mean probability of importation of an animal in which BSE can be detected
amounts to 0.0064 and the highest probability amounts to 0.0129.
Results of the risk assessment of BSE introduction with cattle imported
into Russia from the above mentioned seven countries within 2005-2010
demonstrate that the risk of BSE introduction amounts to 0.01 case in six years
and implementation of measures recommended in the OIE Code is sufficient for BSE
risk reduction. More detailed information will be provided in the poster.
Greetings,
IN my opinion, from the following risk factors i will post below, and the
fact that the OIE and the USDA systematically did away with the BSE GBR system
for the BSE MRR system, for the legal trading all strains of TSE globally, and
the ramifications there from (BSE MRR), MY confidence level of any TSE
regulatory risk assessment is 0...that is ZERO CONFIDENCE LEVEL IN ANY REGARDS
TO THE TSE PRION DISEASES AKA MAD COW DISEASE. The BSE MRR regulations were set
up to fail, and make legal the trading of all strains of TSE prion disease
globally. the consumers were hung out to dry around the globe, and the
ramifications there from will be long and costly thanks to the OIE and the USDA
et al. ...TSS
================================
Scientific Report of the European Food Safety Authority on the Assessment
of the Geographical BSE-Risk (GBR) of United States of America (USA)
Question N° EFSA-Q-2003-083
Adopted July 2004
Summary of scientific report The European Food Safety Authority and its
Scientific Expert Working Group on the Assessment of the Geographical Bovine
Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission
(EC) to provide an up-to-date scientific report on the GBR in the United States
of America, i.e. the likelihood of the presence of one or more cattle being
infected with BSE, pre-clinically as well as clinically, in USA. This scientific
report addresses the GBR of USA as assessed in 2004 based on data covering the
period 1980-2003. The BSE agent was probably imported into USA and could have
reached domestic cattle in the middle of the eighties. These cattle imported in
the mid eighties could have been rendered in the late eighties and therefore led
to an internal challenge in the early nineties. It is possible that imported
meat and bone meal (MBM) into the USA reached domestic cattle and leads to an
internal challenge in the early nineties. A processing risk developed in the
late 80s/early 90s when cattle imports from BSE risk countries were slaughtered
or died and were processed (partly) into feed, together with some imports of
MBM. This risk continued to exist, and grew significantly in the mid 90’s when
domestic cattle, infected by imported MBM, reached processing. Given the low
stability of the system, the risk increased over the years with continued
imports of cattle and MBM from BSE risk countries. EFSA concludes that the
current GBR level of USA is III, i.e. it is likely but not confirmed that
domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
As long as there are no significant changes in rendering or feeding, the
stability remains extremely/very unstable. Thus, the probability of cattle to be
(pre-clinically or clinically) infected with the BSE-agent persistently
increases.
Key words: BSE, geographical risk assessment, GBR, USA, third
countries
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of
the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific
Expert Working Group on GBR Working Group Report on the Assessment of the
Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the
Geographical BSE Risk of USA - 7 - 2.3
Overall assessment of the external challenge
The level of the external challenge that has to be met by the BSE/cattle
system is estimated according to the guidance given by the SSC in its final
opinion on the GBR of July 2000 (as updated in January 2002). Live cattle
imports: In total the country imported 2038 (other sources) or 1128 (CD) live
cattle from BSE risk countries other than Canada, of which 327 (other sources)
or 323 (CD) came from the UK. From Canada the imports were >500,000 animals
per year. The numbers shown in table 1 are the raw import figures and are not
reflecting the adjusted imports for the assessment of the external challenge.
Broken down to 5 year periods the resulting external challenge is as given in
table 3. This assessment takes into account the different aspects discussed
above that allow to assume that certain imported cattle did not enter the
domestic BSE-cattle system, i.e. were not rendered into feed. In the case of the
USA, all the animals for which tracing information showed that they were not
rendered were excluded from the external challenge.
MBM imports:
In total the country imported 689 tons MBM (CD) or 2,230 tons MBM (other
sources) from BSE risk countries other than Canada, of which 5 tons (CD) or 101
tons (other sources) were exported from the UK (UK export data). From Canada,
the imports were about 30 000 tons per year. The numbers shown in table 2 are
the raw import figures and are not reflecting the adjusted imports for the
assessment of the external challenge. Broken down to 5 year periods the
resulting external challenge is as given in table 3. This assessment takes into
account the different aspects discussed above that allow to assume that certain
imported MBM did not enter the domestic BSE/cattle system or did not represent
an external challenge for other reasons. As it was illegal to export mammalian
MBM from UK since 27/03/1996, exports indicated after that date should only have
included non-mammalian MBM. In the case of the USA imported MBM from UK in 1989
and between 1997 and 1999 was not taken into account.
Feeding Use of MBM in cattle feed
• Until 1997 ruminant MBM (RMBM) could legally be included in cattle feed
and was indeed commonly fed to cattle of different age and type. Prior to the
feed ban the US authorities estimated that 10% of all MBM would deliberately
have been fed to cattle. Feed bans
• A ban to feed (several types of) MMBM to ruminants was put in place in
August 1997. Derogation from the ban was granted for pure porcine and equine
protein (MBM) coming from designated (single species) rendering plants. This
MMBM might still be fed to cattle. Therefore this feed ban is a ruminant to
ruminant ban.
• It is planned to prohibit the use of all mammalian and poultry protein in
ruminant feed and prohibiting materials from non-ambulatory disabled cattle and
dead stock from use in all animal feed.
Conclusion on the ability to avoid recycling
• Before 1997, US system would not have been able to avoid recycling of the
BSEagent to any measurable extent. If the BSE-agent was introduced into the feed
chain, it could have reached cattle.
• After the introduction of the 1997 ban in August 1997, the ability to
avoid recycling of BSE-infectivity was somewhat improved. However, the rendering
of ruminant material (including SRM and fallen stock) is inadequate (non
pressurized), and cross-contamination potentials of cattle feed with other feeds
remain.
• Therefore, the system is still unable to avoid recycling of
BSE-infectivity if already present in the system or incoming.
Feeding
Until August 1997, RMBM was legally fed to cattle. Feeding was therefore
"not OK". In August 1997 an RMBM-ban was introduced but feeding of non-ruminant
MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals
(farm animals and pets). An RMBM ban is difficult to maintain, as only labels
can distinguish the various MMBMs. This makes control of the feed ban very
difficult because analytical differentiation between ruminant and non-ruminant
MBM is difficult if not impossible.
Due to the highly specialised production system in the USA, various
mammalian MBM streams can be separated. Such a feed ban would therefore be
assessed as "reasonably OK", for all regions where this highly specialised
system exists. However, several areas in the USA do have mixed farming and mixed
feed mills, and in such regions an RMBM ban would not suffice. Additionally,
official controls for cattle feeds to control for compliance with the ban
started in 2002. Thus, for the whole country, the assessment of the feeding
after 1997 remains "not OK", but improving.
Rendering
The rendering industry is operating with processes that are not known to
reduce
infectivity. It is therefore concluded that rendering was and is "not
OK".
SRM-removal
SRM were and are still rendered for feed, as are (parts of) the fallen
stock. SRMremoval
is therefore regarded as "not OK".
BSE-surveillance
Before 1989, the ability of the system to identify (and eliminate)
BSE-cases was
limited. Since 1990 this ability is improved, thanks to a specific
(passive) BSE
surveillance. The initiated introduction of active surveillance in risk
populations
should improve the system significantly.
On the basis of the available information, it has to be concluded that the
country's
BSE/cattle system was extremely unstable until today, i.e., it would have
recycled and
amplified BSE-infectivity very fast, should it have entered the system. The
stability of
the BSE/cattle system in the USA overtime is as given in table 4.
The present assessment modifies the stability assessment of the previous
GBR report
in 2000 mainly due to a different perception of the impact of BSE
surveillance on
stability and of the efficiency of the RMBM feed ban.
Interaction of stability and external challenge in the USA
Period Stability External Challenge Internal challenge
1980 to
1985
1986 to
1990
Moderate Possibly present
1991 to 1995
Very high
1996 to
2000
2001 to
2003
Extremely unstable Extremely high Likely to be present and growing
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
5.1 The current GBR as function of the past stability and challenge
• The current geographical BSE risk (GBR) level is III, i.e. it is likely
but not
confirmed that domestic cattle are (clinically or pre-clinically) infected
with the
BSE-agent.
Note1: It is also worth noting that the current GBR conclusions are not
dependent on
the large exchange of imports between USA and Canada. External challenge
due to
exports to the USA from European countries varied from moderate to high.
These
challenges indicate that it was likely that BSE infectivity was introduced
into the
North American continent.
snip...please see full text ;
EFSA publishes Geographical BSE-Risk (GBR) assessments for Australia,
Canada, Mexico, Norway, South Africa, Sweden and the United States of
America
Communiqué de presse 20 août 2004
The European Food Safety Authority (EFSA) has issued today seven up-to-date
scientific reports on the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) assessments for Australia, Canada, Mexico, Norway, South Africa
Sweden and the United States of America. While Australia’s GBR level I (i.e.
presence of BSE in domestic cattle is highly unlikely) is maintained, that of
Norway has been raised to level II (presence of BSE unlikely but not excluded),
Sweden remains at GBR level II and those of Canada and the United States have
been raised to level III (presence of BSE likely but not confirmed, or confirmed
at a lower level) following a new assessment taking into account the most recent
evidence. EFSA’s Scientific Expert Working Group on geographic BSE risk
assessment also evaluated the status of Mexico and South Africa which were
classified as level III.
UK EXPORTS OF LIVE CATTLE BY VALUE 1986-96
U.K. EXPORTS OF MEAL OF MEAT AND MEAT OFFAL; GREAVES ;
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: S.J.Pearsall@esg.maff.gsi.gov.uk
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: flounder@wt.net (Receipt Notification Requested) (Non Receipt
Notification Requested)
Terry Meat and bonemeal is not specifically classified for overseas trade
purposes. The nearest equivalent is listed as flours and meals of meat or offals
(including tankage), unfit for human consumption; greaves.
UK exports of this to the US are listed below:
Country Tonnes
1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990
Data for exports between 1975 and 1979 are not readily available. These can
be obtained (at a charge) from data retailers appointed by HM Customs and
Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222).
Best wishes Simon Pearsall
Overseas trade statistics Stats (C&F)C
====================================== END...TSS
BANNED SUSPECT MAD COW FEED IN COMMERCE 2006-2007, SOME 10 YEARS AFTER THE
INFAMOUS PARTIAL AND VOLUNTARY MAD COW FEED BAN or August 4, 1997, that was
nothing more than ink on paper, so really, there was no BSE triple fire wall at
all, and this was improving ???
*** 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
see Alabama banned suspect mad cow feed in commerce ;
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
###
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)
NOW, what about that mad cow feed from atypical BSE in commerce and SRM
regulations ???
Research Project: Study of Atypical Bse Location: Virus and Prion Research
Unit
Project Number: 3625-32000-086-05 Project Type: Specific Cooperative
Agreement
Start Date: Sep 15, 2004 End Date: Sep 14, 2009
Objective: The objective of this cooperative research project with Dr.
Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to
conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE)
isolate and the atypical BSE isolates identified in Italy. The studies will
cover the following areas: 1. Evaluation of present diagnostics tools used in
the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the
U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3.
Studies on transmissibility and tissue distribution of atypical BSE isolates in
cattle and other species.
Approach: This project will be done as a Specific Cooperative Agreement
with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale
del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance
program to analyze the effectiveness of the U.S diagnostic tools for detection
of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with
atypical BSE isolates will provide further characterization of the U.S. BSE
isolate. Transmission studies are already underway using brain homogenates from
atypical BSE cases into mice, cattle and sheep. It will be critical to see
whether the atypical BSE isolates behave similarly to typical BSE isolates in
terms of transmissibility and disease pathogenesis. If transmission occurs,
tissue distribution comparisons will be made between cattle infected with the
atypical BSE isolate and the U.S. BSE isolate. Differences in tissue
distribution could require new regulations regarding specific risk material
(SRM) removal.
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of
Atypical BSE UPDATE July 28, 2010
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)
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
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.
Atypical BSE...Spontaneous...LOL
BSE identified in France
Posted May 2, 2016
A cow in northern France has been confirmed to have bovine spongiform
encephalopathy, according to the World Organisation for Animal Health (OIE).
The cow had developed partial paralysis and was euthanized March 1, a March
25 OIE report states.
BSE is a fatal neurologic prion disease with a typical incubation period of
four to five years. The cow in France was almost 5 years old.
The affected cow had the classic form of BSE, which is most often
associated with feed containing neurologic tissue from infected animals. It is
distinct from atypical BSE, which may develop spontaneously, according to
information from the U.S. Centers for Disease Control and Prevention.
Investigators were trying to identify the source of infection and other
animals at risk for BSE at the time the report was published.
The affected bovine, a Salers female born on April, 8th 2011, showed
paresis and was euthanized on March, 1st 2016. Samples made on March, 4th 2016
during rendering were analyzed at the Department Laboratory of La Somme. The
rapid test proved positive on March, 8th 2016 and the samples were then sent for
further analysis to the National Reference Laboratory, ANSES, which confirmed a
case of classical BSE on March, 21st 2016. The European Union Reference
Laboratory confirmed those results on the basis of documentation on March, 23rd
2016.
>>> It is distinct from atypical BSE, which may develop
spontaneously, according to information from the U.S. Centers for Disease
Control and Prevention.
THIS IS A MYTH $$$
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40
cases in the remaining 12 Countries, divided by the remaining 12 Countries,
about 3+ cases per country, besides Frances 20 cases. you cannot explain this
away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Thursday, March 24, 2016
FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une
vache dans les Ardennes
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
If you Compare France to other Countries with atypical BSE, in my opinion,
you cannot explain this with ‘spontaneous’.
Table 1: Number of Atypical BSE cases reported by EU Member States in the
period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE
databases on 1 July 2014). By 2015, these data might be more comprehensive
following a request from the European Commission to Member States for re-testing
and retrospective classification of all positive bovine isolates in the EU in
the years 2003–2009
BSE type
Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013(a)
2014(a) Total
H-BSE Austria 1 1
France(b) 1 2 3 1 2 2 2 2 15
Germany 1 1 2
Ireland 1 1 2 1 5
The Netherlands 1 1
Poland 1 1 2
Portugal 1 1
Spain 1 1 2
Sweden 1 1
United Kingdom 1 1 1 1 1 5
Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35
L-BSE Austria 1 1 2
Denmark 1 1
France(b) 1 1 1 1 2 1 3 2 1 1 14
Germany 1 1 2
Italy 1 1 1 1 1 5
The Netherlands 1 1 1 3
Poland 1 2 2 1 2 1 2 1 12
Spain 2 2
United Kingdom 1 1 1 1 4
Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45
Total Atypical cases (H + L)
2 8 6 5 4 5 8 5 7 8 8 7 5 2 80
(a): Data for 2013-2014 are incomplete and may not include all
cases/countries reported.
(b): France has performed extensive retrospective testing to classify BSE
cases, which is probably the explanation for the higher number of Atypical BSE
cases reported in this country.
The number of Atypical BSE cases detected in countries that have already
identified them seems to be similar from year to year. In France, a
retrospective study of all TSE-positive cattle identified through the compulsory
EU surveillance between 2001 and 2007 indicated that the prevalence of H-BSE and
L-BSE was 0.35 and 0.41 cases per million adult cattle tested, respectively,
which increased to 1.9 and 1.7 cases per million, respectively, in tested
animals over eight years old (Biacabe et al., 2008). No comprehensive study on
the prevalence of Atypical BSE cases has yet been carried out in other EU Member
States. All cases of Atypical BSE reported in the EU BSE databases have been
identified by active surveillance testing (59 % in fallen stock, 38 % in healthy
slaughtered cattle and 4 % in emergency slaughtered cattle). Cases were reported
in animals over eight years of age, with the exception of two cases (one H-BSE
and one L-BSE) detected in Spain in 2011/2012. One additional case of H-BSE was
detected in Switzerland in 2012 in a cow born in Germany in 2005 (Guldimann et
al., 2012).
SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW
TYPE DISEASE ???
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in breeding
colonies or primate research laboratories, most notably among hundreds of
animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
*** Singeltary reply ; Molecular, Biochemical and Genetic
Characteristics of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
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. ***
see page 17 6 of 201 pages...tss
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Saturday, May 28, 2016
Infection and detection of PrPCWD in soil from CWD infected farm in Korea
Prion 2016 Tokyo
Saturday, April 9, 2016
The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion
disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer
(Rangifer tarandus tarandus)
Department for Environment, Food and Rural Affairs
Saturday, May 28, 2016
TPWD gives in to Breeders again and postponed their decision regarding
proposed changes to state regulations for managing CWD allowing the TSE Prion to
spread further
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.DATES: The comment period
for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is
reopened. We will consider all comments that we receive on or before December 9,
2015. ...
Comment from Terry Singeltary This is a Comment on the Animal and Plant
Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and
Goats
For related information, Open Docket Folder Docket folder icon
Comment View document:Indeed, much science has changed about the Scrapie
TSE prion, including more science linking Scrapie to humans. sadly, politics,
industry, and trade, have not changed, and those usually trump sound science, as
is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease
in livestock producing animals and the OIE. we can look no further at the legal
trading of the Scrapie TSE prion both typical and atypical of all strains, and
CWD all stains. With as much science of old, and now more new science to back
this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and
CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge
APHIS et al and the OIE, and all trading partners to take heed to the latest
science on the TSE prion disease, all of them, and seriously reconsider the
blatant disregards for human and animal health, all in the name of trade, with
the continued relaxing of TSE Prion trade regulations through the 'NEGLIGIBLE
BSE RISK' PROGRAM, which was set up to fail in the first place. If the world
does not go back to the 'BSE RISK ASSESSMENTS', enhance, and or change that
assessment process to include all TSE prion disease, i.e. 'TSE RISK ASSESSMENT',
if we do not do this and if we continue this farce with OIE and the USDA et al,
and the 'NEGLIGIBLE BSE RISK' PROGRAM, we will never eradicate the TSE prion aka
mad cow type disease, they will continue to mutate and spread among species of
human and animal origin, and they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
snip...
please see file attachment for full submission and recent science and my
deep concerns on the TSE Prion disease... No documents available.
AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Wednesday, May 11, 2016
CERVID TO HUMAN PRION TRANSMISSION PRION 2016 TOKYO UPDATE
Friday, May 27, 2016
Canine Prions: A New Form of Prion Disease EP-021 PRION 2016 TOKYO
PRION 2016 TOKYO JAPAN
WS-02
Scrapie in swine: A diagnostic challenge
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
1National Animal Disease Center, US Dept. of Agriculture, Agricultural
Research Service, United States; 2Iowa State University College of Veterinary
Medicine
A naturally occurring prion disease has not been recognized in swine, but
the agent of bovine spongiform encephalopathy does transmit to swine by
experimental routes. Swine are thought to have a robust species barrier when
exposed to the naturally occurring prion diseases of other species, but the
susceptibility of swine to the agent of sheep scrapie has not been thoroughly
tested.
Since swine can be fed rations containing ruminant derived components in
the United States and many other countries, we conducted this experiment to test
the susceptibility of swine to U.S. scrapie isolates by intracranial and oral
inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the
brains of clinically ill sheep from the 4th passage of a serial passage study of
the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous
ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were
inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24)
with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of
animals at approximately six months post inoculation (PI), at the time the pigs
were expected to reach market weight. Remaining pigs were maintained and
monitored for clinical signs of TSE until study termination at 80 months PI or
when removed due to intercurrent disease (primarily lameness). Brain samples
were examined by immunohistochemistry (IHC), western blot (WB), and
enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in
each inoculation group was used for bioassay in mice expressing porcine PRNP.
At six-months PI, no evidence of scrapie infection was noted by any
diagnostic method. However, at 51 months of incubation or greater, 5 animals
were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5).
Interestingly, positive bioassay results were obtained from all inoculated
groups (oral and intracranial; market weight and end of study).
Swine inoculated with the agent of scrapie by the intracranial and oral
routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by
IHC or WB by the time they reach typical market age and weight. However, strong
support for the fact that swine are potential hosts for the agent of scrapie
comes from positive bioassay from both intracranially and orally inoculated pigs
and multiple diagnostic methods demonstrating abnormal prion protein in
intracranially inoculated pigs with long incubation times.
Curriculum Vitae
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion
Research Unit at the National Animal Disease Center, US Department of
Agriculture, Agricultural Research Service. He applies his specialty in
veterinary anatomic pathology to focused research on the intra- and interspecies
transmission of prion diseases in livestock and the development of antemortem
diagnostic assays for prion diseases. In addition, knockout and transgenic mouse
models are used to complement ongoing experiments in livestock species. Dr.
Greenlee has publications in a number of topic areas including prion agent
decontamination, effects of PRNP genotype on susceptibility to the agent of
sheep scrapie, characterization of US scrapie strains, transmission of chronic
wasting disease to cervids and cattle, features of H-BSE associated with the
E211 K polymorphism, and the development of retinal assessment for antemortem
screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM
degree and completed the PhD/residency program in Veterinary Pathology at Iowa
State University. He is a Diplomate of the American College of Veterinary
Pathologists.
Saturday, January 9, 2016
Transmission of sheep-bovine spongiform encephalopathy to pigs
Research article
Tuesday, May 31, 2016
Priority Interim Position Paper PROTECTING THE FOOD CHAIN FROM PRIONS
Perspectives
snip...
5. Proposed Recommendations
a. The question of re-introduction of ruminant protein into the food-chain
The opinion of the members of PRIORITY is that the sustainment of an
absolute feed ban for ruminant protein to ruminants is the essential
requirement, especially since the impact of non-classical forms of scrapie in
sheep and goats is not fully understood or cannot be fully estimated. Therefore,
the consortium strongly recommends prohibiting re-introduction of processed
ruminant protein into the feed-chain. Arguments in support of this opinion are:
the large (and still uncharacterized) diversity of prion agents that
circulate in animal populations;
the uncertainties related to prion epidemiology in animal populations;
the unknown efficacy of industrial processes applied to reduce
microbiological risk during processed animal protein (PAP) production on most
prion agents;
the intrinsic capacity of prions to cross interspecies transmission
barriers;
the lack of sensitive methodology for identifying cross contamination in
food.
The consortium is also hesitant to introduce processed ruminant proteins
into fish food considering the paucity of data on prion infections in fishes and
sea animals, and the risk of establishing an environmental contamination of the
oceans that cannot be controlled.
b. Atypical prion agents
Atypical prion agents will probably in the next future represent the
dominant form of prion diseases. Type L atypical BSE has clear zoonotic
potential. Similarly, there are now some data that seem to indicate that
atypical scrapie agent can cross various species barriers. Moreover, the current
EU policy for eradicating scrapie (genetic selection in affected flocks) is
inefficient to prevent atypical scrapie. In that context it would appear
valuable
to develop knowledge related to pathogenesis and inter-individual
transmission of atypical prion agents in ruminants (both intraspecies and
interspecies)
to investigate for potential PrP resistance allele to the infection by
atypical prion agents
to improve the sensitivity of detection assay that are applied in the field
towards this type of agent
to maintain a robust surveillance of both animal and human populations
c. Species transmission barriers
Intensified search for a molecular signature of the species barrier is
recommended, since this barrier is a key for many important policy areas - risk
assessment, proportional policies, the need for screening of human products and
food.
snip...see full text ;
Tuesday, May 31, 2016
New insights in the transfusional risk assessment of variant
Creutzfeldt-Jakob Disease: Transfusional transmission of vCJD prions in the
absence of detectable abnormal prion protein Prion 2016 Tokyo
O.I.E.
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
I have seen and proven that the USDA et al will do fraudulent deeds with
regards to the TSE Prion aka mad cow type disease, all one has to do is read my
FOIA reports on the mad sheep of mad river valley. I do not trust the USDA et al
at all for this reason, and others...
Monday, April 11, 2016
*** DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN
THE UNITED STATES AND NORTH AMERICA ?
or, how the USDA et al employees out BSE TSE Prion testing, and this is not
the first time either ;
Wednesday, March 2, 2016
*** RANCHO He did not know that they were placing healthy cow heads next to
suspect carcasses BSE TSE Prion ***
or what Dr. Paul Brown of NIH said;
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that." Brown, who is preparing a
scientific paper based on the latest two mad cow cases to estimate the maximum
number of infected cows that occurred in the United States, said he has
"absolutely no confidence in USDA tests before one year ago" because of the
agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector
general.
"Everything they did on the Texas cow makes everything they did before 2005
suspect," Brown said.
or former Ag Secretary Ann Veneman;
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened ***
Thursday, January 14, 2016
*** EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to
Address Future Risks Report to the Chairman, Committee on Energy and Commerce,
House of Representatives December 2015 GAO-16-132
GAO
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
IL-13 Transmission of prions to non human-primates: Implications for human
populations
Jean-Philippe Deslys, Emmanuel E. Comoy
CEW, Institute of Emerging Diseases and Innovative Therapies (iMETI),
Division of Prions and Related Diseases (SEPIA), Fontenay-aux-Roses, France
Prion diseases are the unique neurodegenerative proteinopathies reputed to
be transmissible under field conditions since decades. The transmission of
Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal prion
disease might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, prion diseases, like the other
proteinopathies, are reputed to occur spontaneously (atypical animal prion
strains, sporadic CJD summing 80 % of human prion cases).
Non-human primate models provided the first evidences supporting the
transmissibility of human prion strains and the zoonotic potential of BSE. Among
them, cynomolgus macaques brought major information for BSE risk assessment for
human health1, according to their phylogenetic proximity to humans and extended
lifetime. We used this model to assess the risk of primary (oral) and secondary
(transfusional) risk of BSE, and also the zoonotic potential of other animal
prion diseases from bovine, ovine and cervid origins even after very long silent
incubation periods.
We recently observed the direct transmission of a natural classical scrapie
isolate to macaque after a 10-year silent incubation period, with features
similar to some reported for human cases of sporadic CJD, albeit requiring
fourfold' . longer incubation than BSE2. Scrapie, as recently evoked in
humanized mice3, is the third potentially zoonotic prion disease (with BSE and
L-type BSE4), thus questioning the origin of human sporadic cases. We also
observed hidden prions transmitted by blood transfusion in primate which escape
to the classical diagnostic methods and extend the field of healthy carriers. We
will present an updated panorama of our different long-term transmission studies
and discuss the implications on risk assessment of animal prion diseases for
human health and of the status of healthy carrier5.
1. Chen, C. C. & Wang, Y. H. Estimation of the Exposure of the UK
Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake
During the Period 1980 to 1996. PLoS One 9, e94020 (2014).
2. Comoy, E. E. et al. Transmission of scrapie prions to primate after an
extended silent incubation period. Sci Rep 5, 11573 (2015).
3. Cassard, H. et al. Evidence for zoonotic potential of ovine scrapie
prions. Nat Commun 5, 5821-5830 (2014).
4. Comoy, E. E. et al. Atypical BSE (BASE) transmitted from asymptomatic
aging cattle to a primate. PLoS One 3, e3017 (2008).
5. Gill O. N. et al. Prevalent abnormal prion protein in human appendixes
after bovine spongiform encephalopathy epizootic: large scale survey. BMJ. 347,
f5675 (2013).
Curriculum Vitae
Dr. Deslys co-authored more than one hundred publications in international
scientific journals on main aspects of applied prion research (diagnostic,
decontamination techniques, risk assessment, and therapeutic approaches in
different experimental models) and on underlying pathological mechanisms. He
studied the genetic of the first cases of iatrogenic CJD in France. His work has
led to several patents including the BSE (Bovine Spongiform Encephalopathy)
diagnostic test most widely used worldwide. He also wrote a book on mad cow
disease which can be downloaded here for free (http://www.neuroprion.org/pdf_docs/documentation/madcow_deslys.pdf).
His research group is Associate Laboratory to National Reference Laboratory for
CJD in France and has high security level microbiological installations
(NeuroPrion research platform) with different experimental models (mouse,
hamster, macaque). The primate model of BSE developed by his group with
cynomolgus macaques turned out to mimick remarkably well the human situation and
allows to assess the primary (oral) and secondary (transfusional) risks linked
to animal and human prions even after very long silent incubation periods.
***For several years, his interest has extended to the connections between PrP
and Alzheimer and the prion mechanisms underlying neurodegenerative diseases. He
is coordinating the NeuroPrion international association (initially european
network of excellence now open to all prion researchers).
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer ***
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary: The transmissible spongiform encephalopathies (also
called prion diseases) are fatal neurodegenerative diseases that affect animals
and humans. The agent of prion diseases is a misfolded form of the prion protein
that is resistant to breakdown by the host cells. Since all mammals express
prion protein on the surface of various cells such as neurons, all mammals are,
in theory, capable of replicating prion diseases. One example of a prion
disease, bovine spongiform encephalopathy (BSE; also called mad cow disease),
has been shown to infect cattle, sheep, exotic undulates, cats, non-human
primates, and humans when the new host is exposed to feeds or foods contaminated
with the disease agent. The purpose of this study was to test whether non-human
primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.
After an incubation period of approximately 10 years a macaque developed
progressive clinical signs suggestive of neurologic disease. Upon postmortem
examination and microscopic examination of tissues, there was a widespread
distribution of lesions consistent with a transmissible spongiform
encephalopathy. This information will have a scientific impact since it is the
first study that demonstrates the transmission of scrapie to a non-human primate
with a close genetic relationship to humans. This information is especially
useful to regulatory officials and those involved with risk assessment of the
potential transmission of animal prion diseases to humans. Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease
that also causes variant Creutzfeldt-Jakob disease in humans. Over the past
decades, c-BSE's zoonotic potential has been the driving force in establishing
extensive protective measures for animal and human health.
*** In complement to the recent demonstration that humanized mice are
susceptible to scrapie, we report here the first observation of direct
transmission of a natural classical scrapie isolate to a macaque after a 10-year
incubation period. Neuropathologic examination revealed all of the features of a
prion disease: spongiform change, neuronal loss, and accumulation of PrPres
throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated.
*** Our results underscore the importance of precautionary and protective
measures and the necessity for long-term experimental transmission studies to
assess the zoonotic potential of other animal prion strains.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
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. ...
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult
mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer
or dead dairy cattle...
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of
$298,770 for 228 white-tailed deer killed on farm ***
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
Tuesday, May 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project
and Hunkering Down in the BSE Situation Room USDA 1998
Monday, April 25, 2016
Arkansas AGFC Phase 2 sampling reveals CWD positive deer in Madison and
Pope counties
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL
CONTROL MEASURES
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO ! ***
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA April 1, 2016
***
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
*** Singeltary reply PLoS ; RE-Molecular, Biochemical and Genetic
Characteristics of BSE in Canada Posted by flounder on 19 May 2010 at 21:21 GMT
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
see Singeltary comment ;
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
PLoS
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
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Single-cell messenger RNA sequencing reveals rare intestinal cell types
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy Zane Jaunmuktane,1, Simon Mead,2, 3, 4, Matthew Ellis,3, Jonathan D.
F. Wadsworth,2, 3, Andrew J. Nicoll,2, 3, Joanna Kenny,2, 4, Francesca
Launchbury,3, Jacqueline Linehan,2, Angela Richard-Loendt,3, A. Sarah Walker,5,
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Affiliations Contributions Corresponding authors Journal name: Nature Volume:
525, Pages: 247–250 Date published: (10 September 2015) DOI:
doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published
online 09 September 2015 Updated online 11 September 2015 Erratum (October,
2015)
see Singeltary Comment ;
Alzheimer-type brain pathology may be transmitted by grafts of dura mater
26/01/2016
Singeltary Comment ;
Terry S. Singeltary Sr.
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