Friday, June 3, 2016

The epidemiological evolution of prion infection on bovine in Romania, in the period of 2010 – 2015

PRION 2016 TOKYO JAPAN

 
P-159


The epidemiological evolution of prion infection on bovine in Romania, in the period of 2010 – 2015

 
Florica Barbuceanu1,2, Gabriel Predoi2, Cristina Diaconu1, Theodora Chesnoiu3, Bogdan Georqescu2, Florin Furnaris1, Claudiu Diaconu1

 
1Institute for Diagnosis and Animal Health, Romania; 2Faculty of Veterinary Medicine Bucharest; 3National Sanitary Veterinary and Food Safety Authority

 
The first BSE epidemic began in England in 1986 and progressed steadily until 1992. Implementation of preventive measures materialized by progressive decline of the disease but new cases continued to occur in different European countries.

 
This prion disease in Romania was first diagnosed in 2014, at the Institute for Diagnosis and Animal Health, in the National Reference Laboratory for transmissible spongiform encephalopaties.

 
The epidemiological evolution of BSE in cattle are presented in this paper, with methods used, the results of investigations, the outbreaks and the number of cattle diagnosed with this prion disease.

 
Were subjected to epidemiological investigations and laboratory tests 510166 large ruminants in the period of 2010 - 2015.

 
The whole diagnostic activity were coordinated by the National Reference Laboratory for TSE; the Morphopatology Department of the Institute for Diagnosis and Animal Health.

 
In the frame of passive and active surveillance for BSE on large ruminants, 1720 histological exams, 510166 rapid tests, 2765 immunoblotting tests and 286 imunohistochemical tests were performed and after applying immunoblotting and imunohistochemical tests being confirmed 2 atypical cases of BSE.

 
The differentiation tests were performed by the Eu-RL-TSE of the Animal and Plant Health Agency (APHA) Weybridge, United Kingdom, the atypical L-type BSE being diagnosed at the two cases.

 
Key words: BSE, rapid tests, confirmation tests, atypical form, L-type

 
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http://prion2016.org/

 
Rom J Leg Med [23] 157-161 [2015] DOI: 10.4323/rjlm.2015.157 © 2015 Romanian Society of Legal Medicine 157

 

*** 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

 

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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

 


 


 


 


 


 


 


 

- 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

According to Resolution No. 18 (82nd General Session May 2014)
  • Negligible BSE risk

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
 
 
Previous article Nature | Letter
 
Arithmetic and local circuitry underlying dopamine prediction errors Next article Nature | Letter
 
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, Peter Rudge,2, 4, John Collinge2, 3, 4, & Sebastian Brandner1, 2, 3, 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.
 

Monday, May 2, 2016

France Confirms Case of Classical Mad Cow Disease BSE

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).

 


 


 

Wednesday, July 15, 2015

 

Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?

 


 

***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.

 

***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

 

*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***

 

Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT

 


 

SEE THE DRASTIC REDUCTION OF CONFIRMED BSE CASES IN THE UK ONCE THE FEED BAN TOOK HOLD FROM THE TOP YEAR DOWN TO THE FIRST ZERO YEAR ;

 

1992 36680 SLAUGHTERED SUSPECTS IN WHICH BSE CONFIRMED

 

2013 0 0 0 0 0 0 0 0

 


 


 


 


 


 

10 years post mad cow feed ban August 1997

 

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

 


 

16 years post mad cow feed ban August 1997

 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

17 years post mad cow feed ban August 1997

 

Monday, October 26, 2015

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Thursday, April 07, 2016

 

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

 

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008).

 

***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.

 

snip...

 

For the purpose of the qualitative risk assessment developed here it is necessary to estimate the probability that a 30-ml bottle of lure contains urine from an infected deer. This requires an estimate of the proportion of deer herds in the USA which are infected with CWD together with the within herd prevalence.

 

The distribution map of CWD in US shows it is present mainly in central states (Figure 1). However, Virginia in the east of the country has recorded seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take steps to prevent urine being taken from infected animals eg by sourcing from farms where the deer are randomly tested for CWD (Anon 2015a). However, if disease is already present and testing is not carried out regularly, captive populations are not necessarily disease free (Strausser 2014). Urine-based deer lures have been known to be collected from domestic white-tailed deer herds and therefore there is a recognised risk. This is reflected by 6 US States which have

 

14

 

banned the use of natural deer urine for lures, as the deer urine may be sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For example, the US State of Virginia is banning the use of urine-based deer lures on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned urine-based deer lures and acknowledged that there is no way to detect their use (Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it appears that up to 50% of deer herds can be infected with 80-90% of animals infected within some herds.

 

*** It is therefore assumed that probability that a 30-ml bottle of deer urine lure imported from the USA is sources from an infected deer is medium.

 

SNIP...

 

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. ***For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. ***However, this recommendation is guidance and not a requirement by law.

 

***Animals considered at high risk for CWD include:

 

***1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

***2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

***Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants. The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB cannot be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the very low tonnage of non-fish origin processed animal proteins that were imported from US into GB.

 

*** Overall, therefore, it is considered there is a greater than negligible risk that (non-ruminant) animal feed and pet food containing deer and/or elk protein is imported into GB. There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

SNIP...

 


 

Summary and MORE HERE ;

 

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

 


 

Tuesday, April 12, 2016

 

*** The first detection of Chronic Wasting Disease (CWD) in Europe

 


 

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 

Greetings again FDA and Mr. Pritchett et al, I would kindly like to comment on ; Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 

#158

 

Guidance for Industry

 

Use of Material from Deer and Elk in Animal Feed

 

This version of the guidance replaces the version made available September15, 2003.

 

This document has been revised to update the docket number, contact information, and standard disclosures. Submit comments on this guidance at any time.

 

Submit electronic comments to http://www.regulations.gov. Submit written comments to the Division of Dockets Management (HFA-305), Food and Drug Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).

 

For further information regarding this guidance, contact Burt Pritchett, Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519 Standish Place, Rockville, MD 20855, 240-402-6276, E-mail: burt.pritchett@fda.hhs.gov.

 

Additional copies of this guidance document may be requested from the Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm or http://www.regulations.gov.

 

U.S. Department of Health and Human Services Food and Drug Administration Center for Veterinary Medicine March 2016

 

Contains Nonbinding Recommendations

 

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Guidance for Industry Use of Material from Deer and Elk in Animal Feed

 

This guidance represents the current thinking of the Food and Drug Administration (FDA or Agency) on this topic. It does not establish any rights for any person and is not binding on FDA or the public. You can use an alternative approach if it satisfies the requirements of the applicable statutes and regulations. To discuss an alternative approach, contact the FDA office responsible for this guidance as listed on the title page.

 

I. Introduction

 

Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer and elk is prohibited for use in feed for ruminant animals. This guidance document describes FDA’s recommendations regarding the use in all animal feed of all material from deer and elk that are positive for Chronic Wasting Disease (CWD) or are considered at high risk for CWD. The potential risks from CWD to humans or non-cervid animals such as poultry and swine are not well understood. However, because of recent recognition that CWD is spreading rapidly in white-tailed deer, and because CWD’s route of transmission is poorly understood, FDA is making recommendations regarding the use in animal feed of rendered materials from deer and elk that are CWD-positive or that are at high risk for CWD.

 

In general, FDA’s guidance documents do not establish legally enforceable responsibilities. Instead, guidances describe the Agency’s current thinking on a topic and should be viewed only as recommendations, unless specific regulatory or statutory requirements are cited. The use of the word should in Agency guidances means that something is suggested or recommended, but not required.

 

II. Background

 

CWD is a neurological (brain) disease of farmed and wild deer and elk that belong in the animal family cervidae (cervids). Only deer and elk are known to be susceptible to CWD by natural transmission. The disease has been found in farmed and wild mule deer, white-tailed deer, North American elk, and in farmed black-tailed deer. CWD belongs to a family of animal and human diseases called transmissible spongiform encephalopathies (TSEs). These include bovine spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD) in humans. There is no known treatment for these diseases, and there is no vaccine to prevent them. In addition, although validated postmortem diagnostic tests are available, there are no validated diagnostic tests for CWD that can be used to test for the disease in live animals.

 

Contains Nonbinding Recommendations

 

III. Use in animal feed of material from CWD-positive deer and elk

 

Material from CWD-positive animals may not be used in any animal feed or feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and Cosmetic Act, animal feed and feed ingredients containing material from a CWD-positive animal would be considered adulterated. FDA recommends that any such adulterated feed or feed ingredients be recalled or otherwise removed from the marketplace.

 

IV. Use in animal feed of material from deer and elk considered at high risk for CWD Deer and elk considered at high risk for CWD include:

 

(1) animals from areas declared by State officials to be endemic for CWD and/or to be CWD eradication zones; and

 

(2) deer and elk that at some time during the 60-month period immediately before the time of slaughter were in a captive herd that contained a CWD-positive animal.

 

FDA recommends that materials from deer and elk considered at high risk for CWD no longer be entered into the animal feed system. Under present circumstances, FDA is not recommending that feed made from deer and elk from a non-endemic area be recalled if a State later declares the area endemic for CWD or a CWD eradication zone. In addition, at this time, FDA is not recommending that feed made from deer and elk believed to be from a captive herd that contained no CWD-positive animals be recalled if that herd is subsequently found to contain a CWD-positive animal.

 

V. Use in animal feed of material from deer and elk NOT considered at high risk for CWD FDA continues to consider materials from deer and elk NOT considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and elk not considered at high risk include:

 

(1) deer and elk from areas not declared by State officials to be endemic for CWD and/or to be CWD eradication zones; and

 

(2) deer and elk that were not at some time during the 60-month period immediately before the time of slaughter in a captive herd that contained a CWD-positive animal.

 

3

 


 

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 

Greetings again FDA and Mr. Pritchett et al,

 

MY comments and source reference of sound science on this very important issue are as follows ;

 

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 

I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed.

 

Thank you kindly for allowing me to comment again, ...and again...and again, on a topic so important, why it is ‘NON-BINDING’ is beyond me. this should have been finalized and made ‘BINDING’ or MANDATORY OVER A DECADE AGO.

 

but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still nothing but ink on paper. we have had a mad cow feed ban in place since August 1997, and since then, literally 100s of millions of pounds BANNED MAD COW FEED has been sent out to commerce and fed out (see reference materials). ENFORCEMENT OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.

 

so, in my opinion, any non-binding or voluntary regulations will not work, and to state further, ‘BINDING’ or MANDATORY regulations will not work unless enforced. with that said, we know that Chronic Wasting Disease CWD TSE Prion easily transmits to other cervid through the oral route. the old transmission studies of BSE TSE floored scientist once they figured out what they had, and please don’t forget about those mink that were fed 95%+ dead stock downer cow, that all came down with TME.

 

please see ; It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

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...

 


 

*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***

 

Sunday, March 20, 2016 Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission

 


 


 

Sunday, March 20, 2016

 

UPDATED MARCH 2016 URGENT Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission

 


 

Tuesday, April 19, 2016

 

Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

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 ;

 


 

*** 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 176 of 201 pages...tss

 


 

Saturday, April 16, 2016

 

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

 


 

Sunday, May 1, 2016

 

Center for Biologics Evaluation and Research 25th Meeting of: The Transmissible Spongiform Encephalopathies Advisory Committee June 1, 2015 Transcript

 

AND DRUG ADMINISTRATION

 


 

Terry S. Singeltary Sr.