Wednesday, September 16, 2015

Ljubljana Slovenia First Mad Cow Disease Case in Eight Years Confirmed

Bovine spongiform encephalopathy ,Slovenia


Information received on 18/09/2015 from Mrs Simona Salamon, Head of Audit, Administration Directorate, Ministry of Agriculture, forestry and food, Administration of the Republic of Slovenia for food safety, veterinary sector and plant protection, LJUBLJANA, Slovenia

Summary


Report type
Immediate notification
Date of start of the event
16/09/2015
Date of confirmation of the event
16/09/2015
Report date
18/09/2015
Date submitted to OIE
18/09/2015
Reason for notification
Reoccurrence of a listed disease
Date of previous occurrence
2007
Manifestation of disease
Clinical disease
Causal agent
Prion
Nature of diagnosis
Laboratory (advanced)
This event pertains to
the whole country

New outbreaks


Summary of outbreaks
Total outbreaks: 1
Outbreak Location
  • NOVO MESTO ( Adlesici )
Total animals affected
Species
Susceptible
Cases
Deaths
Destroyed
Slaughtered
Cattle
2
1
1

0
Outbreak statistics
Species
Apparent morbidity rate
Apparent mortality rate
Apparent case fatality rate
Proportion susceptible animals lost*
Cattle
50.00%
50.00%
100.00%
**

* Removed from the susceptible population through death, destruction and/or slaughter;

Epidemiology


Source of the outbreak(s) or origin of infection
  • Unknown or inconclusive
Epidemiological comments
The sample will be sent to the European Union Reference Laboratory, Animal and Plant Health Agency (APHA), Weybridge (United Kingdom) for BSE typing.

Control measures


Measures applied
  • Traceability
  • No vaccination
  • No treatment of affected animals
Measures to be applied
  • Stamping out

Diagnostic test results


Laboratory name and type
National Veterinary Institute ( National laboratory )
Tests and results
Species
Test
Test date
Result
Cattle
rapid tests
16/09/2015
Positive
Cattle
western blot
16/09/2015
Positive

Future Reporting


The event is continuing. Weekly follow-up reports will be submitted.



Encéphalopathie spongiforme bovine ,Slovénie


Information reçue le 18/09/2015 de Mrs Simona Salamon, Head of Audit, Administration Directorate, Ministry of Agriculture, forestry and food, Administration of the Republic of Slovenia for food safety, veterinary sector and plant protection, LJUBLJANA, Slovénie

Résumé


Type de rapport
Notification immédiate
Date de début de l’événement
16/09/2015
Date de confirmation de l´événement
16/09/2015
Date du rapport
18/09/2015
Date d'envoi à l'OIE
18/09/2015
Raison de notification
Réapparition d’une maladie listée par l'OIE
Date de la précédente apparition de la maladie
2007
Manifestation de la maladie
Maladie clinique
Agent causal
Prion
Nature du diagnostic
Tests approfondis en laboratoire (i.e. virologie, microscopie électronique, biologie moléculaire, immunologie)
Cet événement se rapporte à
tout le pays

Nouveaux foyers


Récapitulatif des foyers
Nombre total de foyers : 1
Localisation du foyer
  • NOVO MESTO ( Adlesici )
Nombre total d'animaux atteints
Espèce(s)
Sensibles
Cas
Morts
Détruits
Abattus
Bovins
2
1
1

0
Statistiques sur le foyer
Espèce(s)
Taux de morbidité apparent
Taux de mortalité apparent
Taux de fatalité apparent
Proportion d'animaux sensibles perdus*
Bovins
50.00%
50.00%
100.00%
**

* Soustraits de la population sensible suite à la mort, à l´abattage et/ou à la destruction;

Epidémiologie


Source du/des foyer(s) ou origine de l´infection
  • Inconnue ou incertaine
Autres renseignements épidémiologiques / Commentaires
L’échantillon sera envoyé au Laboratoire de référence de l’Union européenne, l’Agence de la santé animale et végétale (APHA), Weybridge (Royaume-Uni) pour le typage de l’ESB.

Mesures de lutte


Mesures de lutte appliquées
  • Traçabilité
  • Pas de vaccination
  • Aucun traitement des animaux atteints
Mesures à appliquer
  • Abattage sanitaire

Résultats des tests de diagnostics


Nom du laboratoire et type
Institut vétérinaire national ( Laboratoire national )
Tests et résultats
Espèce(s)
Test
Date du test
Résultat
Bovins
test de détection rapide
16/09/2015
Positif
Bovins
western blot
16/09/2015
Positif

Rapports futurs


Cet événement se poursuit. Des rapports de suivi hebdomadaires devront être envoyés.



Encefalopatía espongiforme bovina ,Eslovenia


Información recibida el 18/09/2015 desde Mrs Simona Salamon, Head of Audit, Administration Directorate, Ministry of Agriculture, forestry and food, Administration of the Republic of Slovenia for food safety, veterinary sector and plant protection, LJUBLJANA, Eslovenia

Resumen


Tipo de informe
Notificación inmediata
Fecha del inicio del evento
16/09/2015
Fecha de confirmación del evento
16/09/2015
Fecha del informe
18/09/2015
Fecha de envio del informe a la OIE
18/09/2015
Motivo de la notificación
Reaparición de una enfermedad de la Lista de la OIE
Fecha de la anterior aparición de la enfermedad
2007
Manifestación de la enfermedad
Enfermedad clínica
Agente causal
Prion
Naturaleza del diagnóstico
Pruebas de diagnóstico de laboratorio avanzadas (ej. virología, microscopía electrónica, biología molecular e inmunología)
Este evento concierne
todo el país

Nuevos focos


Resumen de los focos
Número total de focos: 1
Localización del foco
  • NOVO MESTO ( Adlesici )
Número total de animales afectados
Especies
Susceptibles
Casos
Muertos
Destruidos
Sacrificados
Bovinos
2
1
1

0
Estadística del foco
Especies
Tasa de morbilidad aparente
Tasa de mortalidad aparente
Tasa de fatalidad aparente
Proporción de animales susceptibles perdidos*
Bovinos
50.00%
50.00%
100.00%
**

* Descontados de la población susceptible a raíz de su muerte, destrucción o sacrificio;

Epidemiología


Fuente del o de los focos u origen de la infección
  • Desconocida o no concluyente
Otros detalles epidemiológicos / comentarios
La muestra será enviada al Laboratorio de referencia de la Unión Europea, la Agencia de sanidad animal y vegetal (APHA), Weybridge (Reino Unido) para la tipificación de la EEB.

Medidas de Control


Medidas implementadas
  • Trazabilidad
  • Vacunación: no
  • Ningún tratamiento de los animales afectados
Medidas para implementar
  • Sacrificio sanitario

Resultados de las pruebas diagnósticas


Nombre y tipo de laboratorio
Instituto veterinario nacional ( Laboratorio nacional )
Pruebas y resultados
Especies
Prueba
Fecha de la prueba
Resultados
Bovinos
prueba rápida
16/09/2015
Positivo
Bovinos
western blot
16/09/2015
Positivo

Informes futuros


El episodio continúa. Informes de seguimiento semanales serán enviados



First Mad Cow Disease Case in Eight Years Confirmed Ljubljana, 16 September - A 12-year-old cow that died on a farm in southern Slovenia has tested positive for mad cow disease, or BSE, the veterinary administration said on Wednesday.

 
https://english.sta.si/2176025/first-mad-cow-disease-case-in-eight-years-confirmed

 

Rare mad cow disease case suspected in Slovenia English.news.cn 2015-09-16 22:35:09

 

LJUBLJANA, Sept. 16 (Xinhua) -- The Slovenian veterinary administration disclosed on Wednesday that a 12-year-old cow that died on a farm in southern Slovenia has tested positive for mad cow disease, or BSE.

 

The results of a follow-up confirmation test are expected later Wednesday, and if confirmed, this would be the ninth case of BSE in Slovenia and the first after 2007, according to report by the Slovenian Press Agency.

 

The Administration for Food Safety, Veterinary and Plant Protection said precautionary measures have been taken at the farm such as preventing animal movement to and from the farm and examining the cow's history.

 

Slovenia has since 2013 been classified as a country with negligible BSE risk and the veterinary administration said the case was unlikely to change given that the cow was born 12 years ago.

 


 

NAČRT UKREPOV ZA BSE IN TSE V Načrtu ukrepov so opisani ukrepi, ki jih je v Sloveniji treba izvesti ob pojavu bovine spongiforme encefalopatije (BSE) ali transmisivne spongiformne encefalopatije pri drobnici (TSE), z namenom izkoreninjenja bolezni. V dokumentih so opredeljeni organi, ki pri tem sodelujejo, njihove pristojnosti in odgovornosti ter poti in postopki za izmenjavo informacij med udeleženimi pri izvajanju posameznih ukrepov. Podroben opis postopkov prispeva k ustrezni izmenjavi informacij med pristojnimi organi in vsemi zainteresiranimi skupinami ter k hitremu in učinkovitemu ukrepanju ob sumu oziroma po potrditvi BSE oziroma TSE.

 

 
NAČRT UKREPOV OB POJAVU GOVEJE SPONGIFORMNE ENCEFALOPATIJE (BSE) PRI GOVEDU V REPUBLIKI SLOVENIJI (verzija 4, 26.9.2014)

 

 
CONTINGENCY PLAN FOR BOVINE SPONGIFORM ENCEPFALOPHATY (BSE) IN BOVINE ANIMALS IN THE REPUBLIC OF SLOVENIA

 

NAČRT UKREPOV OB POJAVU TRANSMISIVNIH SPONGIFORMNIH ENCEFALOPATIJ (TSE) PRI DROBNICI V REPUBLIKI SLOVENIJI

 


 


 


 
 

Bovine Spongiform Encephalopathy, Slovenia

Impact Worksheet, November 23, 2001

  Summary: In Slovenia, BSE was confirmed in a five-year old domestically bred cow; this is the first case of BSE in that country. Slovenia identified the cow as a suspected BSE case during mandatory prionic testing in slaughter cattle. The Ljubljana, Slovenia National Veterinary Institute confirmed the BSE test through histopathological and immunohistochemical examinations on 16 November. Positive results were corroborated by the Institute of Animal Neurology at the University of Bern in Switzerland on 20 November.

In December 1997, APHIS prohibited the importation of live ruminants and most ruminant products from all of Europe including Slovenia. In December 2000, import restrictions regarding BSE were expanded by prohibiting all imports of rendered animal protein products, regardless of species, from Europe. Slovenia had less than 0.1 percent of the world’s stocks in cattle, goats, and sheep in 2000. Slovenia’s meat exports were minimal, and destination countries for the live animal exports were not specified. Slovenia exported meat and bone meal to Austria, Bosnia-Hercegovina and Croatia in 1999. The US imported no products from Slovenia during 2000 or 2001 that would be of risk for BSE transmission. In 1998, the US imported small quantities of animal feeds from Slovenia, however, it is not known if these feeds contained ruminant materials. The infected cow came from a farm in northeast Slovenia.
BSE Slovenia
How extensive is the outbreak of BSE in Slovenia?

BSE has been confirmed in a five-year old cow in Slovenia on 16 November. This is the first case of BSE in Slovenia, and the cow was domestically bred. Slovenia first identified the cow as a suspected BSE case during routine and mandatory Western blot prionic testing for BSE in slaughter cattle. The Ljubljana, Slovenia National Veterinary Institute and the Institute of Animal Neurology Laboratory in Switzerland confirmed the BSE test. The infected cow came from a small, extensive farm with nine animals in the Zgornja Savinsjka valley in northeast Slovenia. Veterinary authorities immediately isolated the farm and banned all movement of animals to and from the farm.

Source: Reuters; AgWorldwide Internet news; OIE Weekly Disease Information Reports, 16 and 23 November 2001

What actions has Slovenia taken to protect its livestock from BSE?

Slovenia has a national BSE testing program in place, feeding of meat and bone meal is banned,, and bovine product imports have been restricted. Use of meat and bone meal has been banned since 1996 as a feed for ruminants, and for non-ruminants since late 2000.

Beginning February 2001, quick post mortem prionic testing for all slaughtered animals has been mandatory in Slovenia for all slaughtered animals older than 30 months. In January 2000, Slovenian authorities had conducted 700 histological tests after reports of BSE in Germany and Italy. In February 2000, the government was reportedly performing 250 prionic tests daily. In 1996 a policy of random testing for animals older than 36 months was introduced. Since 1992, Slovenia has routinely performed pathohistologic analysis of bovine brains for cattle exhibiting clinical signs of a central nervous system malady.

Since 1991, Slovenia has incrementally added to the list of European countries from which it bans imports of live bovine animals, semen and embryos, meat products, gelatin, collagen, raw materials for pharmaceutical use, and other bovine products:

Imports banned from
Beginning in year
United Kingdom
1991
Ireland, Switzerland, France, Portugal
1996
Belgium, Netherlands
1998
Germany
2000
Italy
2001

Source: USDA, Foreign Agricultural Service GAIN Report #SI1001, March 27, 2001

What is Slovenia’s production and trade in affected animals and animal products?

Slovenia's stocks of cattle, goats and sheep were less than 0.1 percent of world stocks in 2000 (Table 1). Imports of cattle were 0.35 percent of the world export trade in 1999, but goat and sheep imports were both less than 0.1 percent. Cattle imports were exclusively from Central and Eastern Europe and Hungarian imports dominated the Slovenian market. Slovenia exported only 19 metric tons of cattle in 1999; the number of live animals in this figure was not available. Goat export values were not available, and sheep exports were less than 0.1 percent of world sheep exports.

Table 1. Slovenia’s live animal stocks and exports and imports of live animals.

Live Animal
2000 Stocks
Trade
     
1999 Exports
1999 Imports
 
Head
% World
Head
% World
Head
% World
Cattle
471,425
<0 .1="" font="">
-
-
30,000
.36%
Goats
14,643
<0 .1="" font="">
-
-
19
<0 .1="" font="">
Sheep
72,533
<0 .1="" font="">
1
<0 .1="" font="">
180
<0 .1="" font="">

Slovenian production was less than 0.1 percent of the world's production of beef and veal and mutton and lamb in 2000 (Table 2). Slovenia imported less than 0.1 percent of the world's beef and veal and mutton and lamb in 1999. Slovenia also imported 121 metric tons of meat and bone meal from Austria in 1999. Slovenia exported beef and veal in 2000, accounting for 0.2 percent of world exports; destinations of the beef and veal exports were not specified. Slovenian exports of meat and bone meal in 1999 totaled 1,527 metric tons to Austria, Bosnia-Hercegovina and Croatia. Information on goat imports and exports was not available.

Table 2. Production and trade in relevant products by Slovenia.

Products
2000 Production
Trade
     
1999 Exports
1999 Imports
 
Metric ton
% World
Metric ton
% World
Metric ton
% World
Beef and Veal
42,200
<0 .1="" font="">
3,200
.2%
130
<0 .1="" font="">
Mutton and Lamb1
930
<0 .1="" font="">
-
-
11
<0 .1="" font="">

Source: United Nations FAO; USDA, Foreign Agricultural Service GAIN Report #SI1001, March 27, 2001

1 Sheep were included in Table 1 and Table 2 as ‘affected’ because USDA/APHIS includes all ruminants and ruminant products in its restrictions pertaining to BSE. Goat production and trade information was unavailable.

What are the U.S. imports of affected animals or animal products from Slovenia?

In 2001, 2000 and 1999, no affected animals or animal products were imported from Slovenia. In 1998, the only affected product imported into the US from Slovenia was 260,000 kg of "Preparations Used in Animal Feedings, Not Otherwise Specified." It is not known whether this feed contained ruminant materials.

Source: World Trade Atlas

Did the US have restrictions on ruminant imports from Slovenia prior to this case?

In December 1997, APHIS prohibited the importation of live ruminants and most ruminant products from all of Europe including Slovenia until a thorough assessment of the risks of introduction of BSE into the US could be made. Prior to December 1997, import restrictions were applied only to those countries which had reported cases of BSE in native animals. Also, importation of ruminant meat from BSE-affected countries was permitted if the meat was deboned and free of visually identifiable lymphatic and nervous tissue and if it met other restrictions. Import regulations enacted December 1997 extended the import restrictions to countries which had not had a declared BSE case, yet had risk factors for BSE occurrence.

These regulatory changes also removed provisions that allowed importation of ruminant meat from the restricted countries, and thereby prohibited importation of ruminant meat from all Europe. These import restrictions also applied to bone meal, blood meal, meat meal, offal, fat, glands, and serum from ruminants. In December 2000, APHIS expanded its import restrictions regarding BSE by prohibiting all imports from Europe of rendered animal protein products, regardless of species.

Source: USDA, APHIS, VS

What is the level of passenger traffic arriving in the United States from Slovenia?

There were no direct flights from Slovenia to the US in fiscal year 2000.

APHIS-PPQ’s agriculture quarantine inspection monitoring sampled 27 air passengers from Slovenia for items of agricultural interest in fiscal year 2000. One of these 27 passengers was carrying two kilograms of a meat item that could potentially harbor pathogens that cause BSE. This passenger arrived to Elizabeth, New York, in June 2000 and declared no intention to visit a farm or ranch in the US.

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

CEI’s plans for follow up:

Prior to CEI’s January 2002 quarterly summary of disease events October-December 2001, CEI will review any further developments in this Slovenian outbreak.

If you need more information or wish to comment, you may reply to this message or contact Jennifer Grannis at (970) 490-7844 or David Cummings at (970) 490-7895.



 
Terry S. Singeltary Sr. 6/23/09

Bovine Spongiform Encephalopathy (BSE) Inspection 2009 Slovenia and Bulgaria


 


 Spongiform Encephalopathy, Slovenia

 

Impact Worksheet, November 23, 2001

 

Page 64 of 98

 

8/3/2006

 

Summary: In Slovenia, BSE was confirmed in a five-year old domestically bred cow; this is the first case of BSE in that country. Slovenia identified the cow as a suspected BSE case during mandatory prionic testing in slaughter cattle. The Ljubljana, Slovenia National Veterinary Institute confirmed the BSE test through histopathological and immunohistochemical examinations on 16 November. Positive results were corroborated by the Institute of Animal Neurology at the University of Bern in Switzerland on 20 November.

 

In December 1997, APHIS prohibited the importation of live ruminants and most ruminant products from all of Europe including Slovenia. In December 2000, import restrictions regarding BSE were expanded by prohibiting all imports of rendered animal protein products, regardless of species, from Europe. Slovenia had less than 0.1 percent of the world’s stocks in cattle, goats, and sheep in 2000. Slovenia’s meat exports were minimal, and destination countries for the live animal exports were not specified. Slovenia exported meat and bone meal to Austria, Bosnia-Hercegovina and Croatia in 1999. The US imported no products from Slovenia during 2000 or 2001 that would be of risk for BSE transmission. In 1998, the US imported small quantities of animal feeds from Slovenia, however, it is not known if these feeds contained ruminant materials. The infected cow came from a farm in northeast Slovenia.

 

How extensive is the outbreak of BSE in Slovenia?

 

BSE has been confirmed in a five-year old cow in Slovenia on 16 November. This is the first case of BSE in Slovenia, and the cow was domestically bred. Slovenia first identified the cow as a suspected BSE case during routine and mandatory Western blot prionic testing for BSE in slaughter cattle. The Ljubljana, Slovenia National Veterinary Institute and the Institute of Animal Neurology Laboratory in Switzerland confirmed the BSE test. The infected cow came from a small, extensive farm with nine animals in the Zgornja Savinsjka valley in northeast Slovenia. Veterinary authorities immediately isolated the farm and banned all movement of animals to and from the farm.

 

Source: Reuters; AgWorldwide Internet news; OIE Weekly Disease Information Reports, 16 and 23 November 2001 What actions has Slovenia taken to protect its livestock from BSE?

 

Slovenia has a national BSE testing program in place, feeding of meat and bone meal is banned,, and bovine product imports have been restricted. Use of meat and bone meal has been banned since 1996 as a feed for ruminants, and for non-ruminants since late 2000.

 

Beginning February 2001, quick post mortem prionic testing for all slaughtered animals has been mandatory in Slovenia for all slaughtered animals older than 30 months. In January 2000, Slovenian authorities had conducted 700 histological tests after reports of BSE in Germany and Italy. In February 2000, the government was reportedly performing 250 prionic tests daily. In 1996 a policy of random testing for animals older than 36 months was introduced. Since 1992, Slovenia has routinely performed pathohistologic analysis of bovine brains for cattle exhibiting clinical signs of a central nervous system malady.

 

Since 1991, Slovenia has incrementally added to the list of European countries from which it bans imports of live bovine animals, semen and embryos, meat products, gelatin, collagen, raw materials for pharmaceutical use, and other

 

Page 65 of 98 8/3/2006

 

bovine products:

 

Imports banned from Beginning in year

 

United Kingdom

 

1991

 

Ireland, Switzerland, France, Portugal

 

1996

 

Belgium, Netherlands

 

1998

 

Germany

 

2000

 

Italy

 

2001

 

Source: USDA, Foreign Agricultural Service GAIN Report #SI1001, March 27, 2001

 

What is Slovenia’s production and trade in affected animals and animal products?

 

Slovenia's stocks of cattle, goats and sheep were less than 0.1 percent of world stocks in 2000 (Table 1). Imports of cattle were 0.35 percent of the world export trade in 1999, but goat and sheep imports were both less than 0.1 percent. Cattle imports were exclusively from Central and Eastern Europe and Hungarian imports dominated the Slovenian market. Slovenia exported only 19 metric tons of cattle in 1999; the number of live animals in this figure was not available. Goat export values were not available, and sheep exports were less than 0.1 percent of world sheep exports. Table 1. Slovenia’s live animal stocks and exports and imports of live animals.

 

Live Animal 2000 Stocks Trade 1999 Exports 1999 Imports Head % World Head % World Head % World Cattle 471,425 <0 -="" .1="" .36="" 14="" 180="" 19="" 1="" 30="" 66="" 72="" 8="" 98="" div="" goats="" of="" page="" sheep="">
 

Slovenian production was less than 0.1 percent of the world's production of beef and veal and mutton and lamb in 2000 (Table 2). Slovenia imported less than 0.1 percent of the world's beef and veal and mutton and lamb in 1999. Slovenia also imported 121 metric tons of meat and bone meal from Austria in 1999. Slovenia exported beef and veal in 2000, accounting for 0.2 percent of world exports; destinations of the beef and veal exports were not specified. Slovenian exports of meat and bone meal in 1999 totaled 1,527 metric tons to Austria, Bosnia-Hercegovina and Croatia. Information on goat imports and exports was not available. Table 2. Production and trade in relevant products by Slovenia.

 

Products 2000 Production Trade 1999 Exports 1999 Imports Metric ton % World Metric ton % World Metric ton % World Beef and Veal 42,200 <0 -="" .1="" .2="" 11="" 130="" 3="" 67="" 8="" 930="" 98="" and="" div="" lamb1="" mutton="" of="" page="">
 

Source: United Nations FAO; USDA, Foreign Agricultural Service GAIN Report #SI1001, March 27, 2001

 

1 Sheep were included in Table 1 and Table 2 as ‘affected’ because USDA/APHIS includes all ruminants and ruminant products in its restrictions pertaining to BSE. Goat production and trade information was unavailable.

 

What are the U.S. imports of affected animals or animal products from Slovenia?

 

In 2001, 2000 and 1999, no affected animals or animal products were imported from Slovenia. In 1998, the only affected product imported into the US from Slovenia was 260,000 kg of "Preparations Used in Animal Feedings, Not Otherwise Specified." It is not known whether this feed contained ruminant materials.

 

Source: World Trade Atlas

 

Did the US have restrictions on ruminant imports from Slovenia prior to this case?

 

In December 1997, APHIS prohibited the importation of live ruminants and most ruminant products from all of Europe including Slovenia until a thorough assessment of the risks of introduction of BSE into the US could be made. Prior to December 1997, import restrictions were applied only to those countries which had reported cases of BSE in native animals. Also, importation of ruminant meat from BSE-affected countries was permitted if the meat was deboned and free of visually identifiable lymphatic and nervous tissue and if it met other restrictions. Import regulations enacted December 1997 extended the import restrictions to countries which had not had a declared BSE case, yet had risk factors for BSE occurrence.

 

These regulatory changes also removed provisions that allowed importation of ruminant meat from the restricted countries, and thereby prohibited importation of ruminant meat from all Europe. These import restrictions also applied to bone meal, blood meal, meat meal, offal, fat, glands, and serum from ruminants. In December 2000, APHIS expanded its import restrictions regarding BSE by prohibiting all imports from Europe of rendered animal protein products, regardless of species.

 

Source: USDA, APHIS, VS

 

What is the level of passenger traffic arriving in the United States from Slovenia?

 

There were no direct flights from Slovenia to the US in fiscal year 2000.

 

APHIS-PPQ’s agriculture quarantine inspection monitoring sampled 27 air passengers from Slovenia for items of agricultural interest in fiscal year 2000. One of these 27 passengers was carrying two kilograms of a meat item that could potentially harbor pathogens that cause BSE. This passenger arrived to Elizabeth, New York, in June 2000 and declared no intention to visit a farm or ranch in the US.

 

Page 68 of 98 8/3/2006

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base CEI’s plans for follow up:

 

Prior to CEI’s January 2002 quarterly summary of disease events October-December 2001, CEI will review any further developments in this Slovenian outbreak.

 

If you need more information or wish to comment, you may reply to this message or contact Jennifer Grannis at (970) 490-7844 or David Cummings at (970) 490-7895.

 


 

Scientific Steering Committee – Opinion on the GBR of SLOVENIA September 2002

 

CONCLUSION ON THE CURRENT GBR

 

The BSE-agent was potentially imported into the country via infected MBM in the mid 90s when MBM imports peaked. This MBM reached cattle via feed. It can be expected that the 1997 birth cohort had a much lower chance to be infected because MBM imports decreased dramatically and the first feed ban was introduced. Although the rendering system was able to reduce BSE infectivity since 1992, some recycling and propagation may have occurred because SRM were not removed and therefore rendered.

 

The first domestic BSE-case in Slovenia was identified in November 2001 and a second case was confirmed in January 2002. It is therefore confirmed (GBR III) that domestic cattle in Slovenia are (clinically or pre-clinically) infected with the BSE-agent at a low incidence.

 


 

see more here ;

 


 

Greetings list members,

 

i just cannot accept this;

 

23 kg of meat in a suitcase (suitcase bomb...TSS)

 

The data do not provide a species of origin code for these

 

products, therefore they may not contain any ruminant product.

 

what kind of statement is this? how stupid do they think we are? it could also very well mean that _all_ of it was ruminant based products !

 

Terry S. Singeltary Sr., Bacliff, Texas USA

 

What is the level of passenger traffic arriving in the United States from Slovenia?

 

There were no direct flights from Slovenia to the US in fiscal year 2000.

 

APHIS-PPQ’s agriculture quarantine inspection monitoring sampled 27 air passengers from Slovenia for items of agricultural interest in fiscal year 2000.

 

One of these 27 passengers was carrying two kilograms of a meat item that could potentially harbor pathogens that cause BSE. This passenger arrived to Elizabeth, New York, in June 2000 and declared no intention to visit a farm or ranch in the US.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base http://www.aphis.usda.gov/vs/ceah/cei/bse_slovenia1101.htm

 

Greetings FDA and public,

 

if you go to the below site, and search all BSE known countries and check out their air traffic illegal meat they have confiscated, and check out the low number checked, compared to actual passenger traffic, would not take too much for some nut to bring in FMD/TSEs into the USA as a 'suitcase bomb'.

 

[[Under APHIS-PPQ's agricultural quarantine inspection monitoring, 284 air passengers from Israel were sampled for items of agricultural interest in fiscal year 2001. Seven of these passengers, or 2 percent, carried a total of 11 kg of meat items that could potentially harbor the pathogen that causes BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the U.S.]]

 

if they were to have questioned the terrorist that bombed the Twin Towers with jets, if they were to have questioned them at flight school in the USA, i am sure that they would have said they did not intend to visit the Twin Towers as a flying bomb either. what am i thinking, they probably did ask this? stupid me.

 

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

 

Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC -254 Accepted - Volume 11

 


 


 


 


 


 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

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...

 

===============

 


 

-------- Original Message --------

 

Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD

 

Date: Thu, 28 Nov 2002 10:23:43 -0000

 

From: "Asante, Emmanuel A" e.asante@ic.ac.uk

 

To: "'flounder@wt.net'" flounder@wt.net

 

Dear Terry,

 

I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.

 

Thank you for your interest in the paper.

 

In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.

 

I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.

 

Emmanuel Asante

 

<>

 

____________________________________

 

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)

 

____________________________________

 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***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.

 

================

 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***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.

 

===============

 


 


 

Saturday, May 30, 2015

 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 


 


 

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.***

 

================

 


 

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...

 


 

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. ...

 


 

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

 


 

Tuesday, August 4, 2015

 

*** FDA U.S. Measures to Protect Against BSE ***

 


 

Saturday, September 12, 2015

 

The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014

 

>>>We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present. <<<

 


 

Thursday, September 10, 2015

 

25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015

 

TSE PRION MAD COW CIRCUS AND TRAVELING ROAD SHOW

 


 

Tuesday, September 15, 2015

 

Texas TAHC Chronic Wasting Disease Confirmed in Lavaca County Captive White-tailed Deer; Linked to Index Herd

 


 

*** RAW, UNCUT, AND UNCENSORED ***

 

Sunday, August 23, 2015

 

TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 


 

Friday, August 14, 2015

 

*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation

 


 

Terry S. Singeltary Sr.




Saturday, September 12, 2015

The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014

The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014
 
Historical Article
 
The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014
 
Alexandra E. Quimbya1 and Michel C.F. Shamya2 c1
 
a1 Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada
 
a2 Department of Medicine (Neurology), University of Ottawa, Ottawa, Ontario, Canada.
 
Abstract
 
On February 11, 2015, the Canadian Food Inspection Agency announced that a cow born and raised in Alberta had tested positive for bovine spongiform encephalopathy (BSE), commonly known as mad cow disease. BSE is a prion disease of cattle that, when transmitted to humans, produces a fatal neurodegenerative disease known as variant Creutzfeldt-Jakob disease. We believe that this latest case of BSE in Canadian cattle suggests the timeliness of a review of the management of BSE in Canada from a historically and scientifically informed perspective. In this article, we ask: how did the Canadian management of BSE between 1990 and 2014 engage with the contemporary understanding of BSE’s human health implications? We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present.
 
RÉSUMÉ
 
Perspective historique et scientifique sur la gestion de l’encéphalopathie spongiforme bovine au Canada de 1990 à 2014. Le 11 février 2015 l’Agence canadienne d’inspection des aliments a annoncé que le test de dépistage de l’encéphalopathie spongiforme bovine (ESB), communément appelée maladie de la vache folle, s’était avéré positif chez une vache née et élevée en Alberta. L’ESB est une maladie à prion chez les bovins qui, quand elle est transmise aux humains, cause une maladie neurodégénérative fatale connue sous le nom de variante de la maladie de Creutzfeldt-Jakob. Nous croyons que ce cas récent d’ESB chez une vache canadienne indique qu’il est temps de revoir la gestion de l’ESB au Canada sous un éclairage historique et scientifique. Dans cet article, nous posons la question suivante : comment la gestion de l’ESB au Canada de 1990 à 2014 s’est-elle adaptée aux connaissances actuelles des répercussions de l’ESB sur la santé humaine? Nous suggérons que les politiques canadiennes ont ignoré dans une large mesure la nature médicale inhérente à l’ESB en la traitant comme un problème purement du domaine de l’agriculture et du domaine vétérinaire. Souvent les politiques destinées à protéger les Canadiens ont donc été tardives et incomplètes, rappelant de façon préoccupante l’échec de la Grande-Bretagne à gérer l’ESB. En dépit d’affirmations contraires, il est prématuré de conclure que l’ESB (et ainsi le risque de contracter la variante de la maladie de Creutzfeldt-Jakob) est chose du passé au Canada : l’ESB y demeure un problème actuel.
 
(Received December 12 2014)
 
(Accepted June 19 2015)
 
Keywords Creutzfeldt-Jakob Disease; Healther Services Research; History; Neurosciences; Prion
 
Correspondence
 
c1 Correspondence to: Michel Shamy, 1053 Carling Avenue, Room C2182a, Ottawa, ON K1Y 4E9, Canada. Email: mshamy@toh.on.ca.
 
 
Friday, July 10, 2015
 
CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE
 
 
Monday, February 23, 2015
 
20th BSE Case Raises New Concerns about Canada's Feeding Practices and Voluntary Testing Program; Highlights Importance of COOL
 
 
Friday, February 20, 2015
 
A BSE CANADIAN COW MAD COW UPDATE Transcript - Briefing (February 18, 2015)
 
 
EDMONTON - Some of former Alberta premier Ralph Klein's most colourful quotes — and the reactions they elicited:
 
SNIP...
 
"This all came about through the discovery of a single, isolated case of mad cow disease in one Alberta cow on May 20th. The farmer — I think he was a Louisiana fish farmer who knew nothing about cattle ranching. I guess any self-respecting rancher would have shot, shovelled and shut up, but he didn't do that." — Klein recalls how the mad cow crisis started and rancher Marwyn Peaster's role. The premier was speaking at the Western Governors Association meeting in Big Sky, Mont. September 2004.
 
"The premier meant that in an ironic or almost a sarcastic way." — Klein spokesman Gordon Turtle.
 
---
 
"You would have to eat 10 billion meals of brains, spinal cords, ganglia, eyeballs and tonsils." — Klein speaking in Montreal in January 2005 on the risk of humans contracting mad cow disease.
 
---
 
"I would offer $5 billion to have a Japanese person to come over here and eat nothing but Alberta beef for a year. And if he gets mad cow disease, I would be glad to give him $5 billion — make it $10 billion — Canadian." — Klein speaking after Japan closed its borders to Canadian beef.
 
---
 
 
 
Thursday, February 10, 2011
 
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
 
 
Wednesday, August 11, 2010
 
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
 
 
Thursday, August 19, 2010
 
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
 
 
Friday, March 4, 2011
 
Alberta dairy cow found with mad cow disease
 
 
Tuesday, May 21, 2013
 
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$
 
 
Thursday, March 29, 2012
 
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
 
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
 
 
Increased Atypical Scrapie Detections
 
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
 
 
Current as of: 2015-01-31
 
Sheep flocks and/or goat herds confirmed to be infected with classical scrapie in Canada in 2015 Date confirmed Location Animal type infected January 5 Ontario Goat
 
 
 
Tuesday, February 10, 2015
 
Alberta Canada First case of chronic wasting disease found in farm elk since 2002
 
 
Saturday, March 21, 2015
 
***Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence Rates Increasing ***
 
 
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss
 
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.
 
please see ;
 
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
 
CJD Deaths Reported by CJDSS1, 1994-20122
 
As of May 31, 2012
 
Deaths of Definite and Probable CJD
 
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
 
1994 2 0 0 1 0 0 3
 
1995 3 0 0 0 0 0 3
 
1996 13 0 0 0 0 0 13
 
1997 16 0 1 1 0 0 18
 
1998 22 1 0 1 0 0 24
 
1999 26 2 2 1 0 0 31
 
2000 32 0 0 3 0 0 35
 
2001 27 0 2 1 0 0 30
 
2002 31 0 2 2 0 1 36
 
2003 27 1 1 0 0 0 29
 
2004 42 0 1 0 0 0 43
 
2005 42 0 0 2 0 0 44
 
2006 39 0 1 3 1 0 44
 
2007 35 0 0 4 0 0 39
 
2008 48 0 1 0 0 0 49
 
2009 48 0 3 2 0 0 53
 
2010 34 0 3 0 0 0 37
 
2011 37 0 2 1 0 1 41
 
2012 1 0 0 0 0 0 1
 
Total 525 4 19 22 1 2 573
 
1. CJDSS began in 1998
 
2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional
 
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
 
CJD Deaths Reported by CJDSS1, 1994-20122
 
As of May 31, 2012
 
 
SEE DECEMBER 2012 CANADA
 
 
Saturday, June 15, 2013
 
Canada Fraser Health Statement on Creutzfeldt-Jakob Disease outbreak
 
 
 
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, Val erie 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...TSS
 
===============
 
 
2014
 
***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
 
***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent.
 
*** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].
 
snip...
 
 
Monday, October 10, 2011
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
snip...
 
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far
 
*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded.
 
*** Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
 
snip...
 
 
 
Thursday, August 12, 2010
 
Seven main threats for the future linked to prions
 
First threat
 
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
 
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
 
*** These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
 
Second threat
 
snip...
 
 
-------- Original Message --------
 
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
 
Date: Thu, 28 Nov 2002 10:23:43 -0000
 
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
 
To: "'flounder@wt.net'" flounder@wt.net
 
Dear Terry,
 
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
 
Thank you for your interest in the paper.
 
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
 
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
 
Emmanuel Asante
 
<>
 
____________________________________
 
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
 
____________________________________
 
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***
 
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
 
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
 
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
 
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
 
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***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.
 
================
 
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
 
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
 
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
 
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
 
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
 
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***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.
 
===============
 
 
 
***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 flounder on 03 Jul 2015 at 16:53 GMT
 
 
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
 
Tuesday, December 23, 2014
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
 
 
Sunday, June 14, 2015
 
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion
 
 
DR. DEHAVEN:
 
snip...
 
*** As far as spontaneous cases, that is a very difficult issue.
 
***There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative.
 
*** We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million.
 
*** We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.
 
“Again, it's a very difficult situation to prove a negative.
 
“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.
 
snip...
 
 
 
What irks many scientists is the USDA?s April 25 statement that the rare disease is ?not generally associated with an animal consuming infected feed.?
 
The USDA?s conclusion is a ?gross oversimplification,? said Dr. Paul Brown, one of the world?s experts on this type of disease who retired recently from the National Institutes of Health.
 
"(The agency) has no foundation on which to base that statement.?
 
?We can?t say it?s not feed related,? agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.
 
In the May 1 email to me, USDA?s Cole backed off a bit. ?No one knows the origins of atypical cases of BSE,? she said
 
Few scientists would argue that the one California cow which never was headed to the U.S. food supply represents a health hazard.
 
But many maintain that the current surveillance is insufficient.
 
Dr. Kurt Giles, an expert in neurogenerative diseases now at the University of California, San Francisco, was at Oxford during the British outbreak.
 
He told me USDA?s assurances about safety today remind him of British statements during the 1980s.
 
?It is so reminiscent of that absolute certainty,? he said.
 
Robert Bazell is NBC's chief science and medical correspondent. Follow him on Facebook and on Twitter @RobertBazellNBC
 
 
 
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
 
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
 
In an article today for United Press International, science reporter Steve Mitchell writes:
 
Analysis: What that mad cow means
 
By STEVE MITCHELL UPI Senior Medical Correspondent
 
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
 
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
 
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
 
"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.
 
SNIP...
 
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
 
SNIP...
 
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
 
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
 
© Copyright 2006 United Press International, Inc. All Rights Reserved
 
 
 
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
 
 
PAUL BROWN COMMENT TO ME ON THIS ISSUE
 
Tuesday, September 12, 2006 11:10 AM
 
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
 
 
OR, what the Honorable Phyllis Fong of the OIG found ;
 
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program ­ Phase II and Food Safety and Inspection Service
 
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
 
Report No. 50601-10-KC January 2006
 
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
 
 
FRANCE HAVE AN EPIDEMIC OF SPONTANEOUS ATYPICAL BSE ‘’LOL’’
 
spontaneous atypical BSE ???
 
if that's the case, then France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$
 
As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.
 
 
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
 
 
spontaneous TSE prion, that's wishful thinking. on the other hand, if spontaneous did ever happen (never once documented in the field), it would be our worst nightmare, due to feed. just saying.
 
*** 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, June 23, 2014
 
PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES
 
***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
 
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada
 
Keywords: Atypical BSE, oral transmission, RT-QuIC
 
The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.
 
The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.
 
Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.
 
P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)
 
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
 
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein
 
Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.
 
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.
 
Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.
 
Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.
 
P.150: Zoonotic potential of L-type BSE prions: A new prion disease in humans?
 
Emilie Jaumain,1 Stéphane Haïk,2 Isabelle Quadrio,3 Laetitia Herzog,1 Fabienne Reine,1 Armand Perret-Liaudet,3 Human Rezaei,1 Hubert Laude,1 Jean-Luc Vilotte,4 and Vincent Béringue1 1INR A (Institut National de la Recherche Agronomique); UR892; Virologie Immunologie Moléculaires; Jouy-en-Josas, France; 2IN SERM; Equipe maladie d’Alzheimer et maladies à Prions; CRicm; UMRS 1127; CNR S; UPMC. R.; ICM, Hôpital de la Salpêtrière; Paris, France; 3Neurobiologie, CMRR , Gériatrie, Hospices Civils de Lyon, Université Lyon 1-CNR S UMR5292-IN SERM U1028; Lyon, France; 3INR A; UMR1313; Génétique Animale et Biologie Intégrative; Jouy-en-Josas, France
 
In summary, L-type prions can be passaged on the human PrP sequence without any obvious transmission barrier. The phenotype obtained differs from the classical CJD prion types known so far. Careful extrapolation would suggest that the zoonotic transmission of this agent could establish a new prion disease type in humans.
 
 
Wednesday, May 30, 2012
 
PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus
 
Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel Verdier1
 
1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils de Lyon; Lyon, France
 
Here, we demonstrate that the L-BSE agent can be transmitted by oral route from cattle to young and adult mouse lemurs. In comparison to IC inoculated animals, orally challenged lemurs were characterized by longer survival periods as expected with this route of infection.
 
 
Australia
 
COMMONWEALTH OF AUSTRALIA Official Committee Hansard SENATE RURAL AND REGIONAL AFFAIRS AND TRANSPORT REFERENCES COMMITTEE Reference: Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 CANBERRA BY AUTHORITY OF THE SENATE
 
RRA&T 2 Senate Friday, 5 February 2010 RURAL AND REGIONAL AFFAIRS AND TRANSPORT
 
[9.03 am]
 
BELLINGER, Mr Brad, Chairman, Australian Beef Association
 
CARTER, Mr John Edward, Director, Australian Beef Association
 
CHAIR—Welcome. Would you like to make an opening statement?
 
Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14
 
December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:
 
snip...end
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
We have shown that cattle-adapted TME is the third cattle prion strain (joining classical and L-type BSE) to be transmissible both to non-human primates and transgenic mice overexpressing human PrP. However, the successful transmission of raccoon TME to primate, inducing a disease with similar features as cattle TME, extends this notion to TME-related strains independent of host origin. Pathological, biochemical and bioassay investigations converged to demonstrate the similarity between cattle-adapted TME and L-BSE.
 
 
CJD toll among farmers `too high for mere chance'
 
August 15, 1997
 
PA News
 
John von Radowitz and Andrew Woodcock Microbiologist Richard Lacey, billed in this story as the first to suggest a link between CJD and BSE seven years ago, was cited in this story as saying that the number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance, adding that, "Where the CJD Surveillance Unit come unstuck is in trying to explain what happened to these six farmers. This is just too many to have occurred by chance. Unfortunately they don't want to consider the possibility that these farmers in this country and other countries were infected by cattle before BSE developed." The story notes that professor Lacey believes sporadic CJD itself originates from a cattle infection - possibly a precursor to BSE that has not yet been detected, adding that,
 
"For years I have suggested that the cause is a rare disease in cattle world wide. Both BSE and the new variant CJD are a new and different disease. What has probably happened is that BSE is a variant of the old type of disease, which could have been missed because it's symptom free. It would explain why such an unusually high number of dairy farmers are being affected by CJD both here and abroad." He also said that cases of sporadic CJD had been recorded as far back as the 1920s. Professor Lacey went on to add that he thought the new variant pattern was alarming, adding, "It's rising, and that is a concern. Unfortunately we can't predict the scale of the problem. If the disease doubled each year up to the year 2020 you'd have hundreds of thousands of cases."
 
 
.195 Among occupational groups exposed to BSE, farmers remain unusual in having such an excess over the incidence of CJD for the population as a whole. No cases of CJD have been reported amount veterinarians exposed to BSE. Four people in the meat industry (butchers, abattoirs, rendering plants, etc) have been reported to have vCJD.386 The present evidence has been accepted by some as reassuring in that such occupations may not pose as serious a risk as might have been expected.
 
 
This was not simply another farmer but the third farmer...
 
 
suspect case of CJD in a farmer who has had a case of BSE in his beef suckler herd.
 
 
cover-up of 4th farm worker ???
 
 
 
CONFIRMATION OF CJD IN FOURTH FARMER
 
 
now story changes from; SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms.
 
to;
 
This is not unexpected... was another farmer expected?
 
 
4th farmer, and 1st teenager
 
 
snip...
 
2. Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES.
 
3. You will recall that the advice provided by Professor Smith in 1993 and by Dr. Gore this month used the sub-population of dairy farm workers who had had a case of BSE on their farms - 63,000, which is approximately half the number of dairy farm workers - as a denominator. If the above sums are repeated using this denominator population, taking an annual incidence in the general population of 1 per million the observed rate in this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population...
 
 
CJD FARMERS WIFE 1989
 
 
 
20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases....
 
 
Monday, May 19, 2008
 
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
 
 
Monday, June 29, 2015
 
*** RESTRICTED – POLICY CJD IN ADOLESCENTS (16 year old Vickey Rimmer), FARMERS WITH BSE HERDS, AND FARMERS WIFE with Sporadic CJD
 
 
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
 
Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice. 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
 
The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein structures on trans-species prion transmission have relied primarily upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species prion conversion.
 
To assess trans-species conversion in the RT-QuIC system, we compared chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions, as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each prion was seeded into each host recombinant PrP (full-length rPrP of white-tailed deer, bovine or feline). We demonstrated that fCWD is a more efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests adaptation to the new host.
 
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.***
 
================
 
 
***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.
 
 
From: Terry S. Singeltary Sr.
 
Sent: Saturday, November 15, 2014 9:29 PM
 
To: Terry S. Singeltary Sr.
 
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
 
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
 
R. G. WILL
 
1984
 
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
 
snip...
 
 
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...
 
 
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. ...
 
 
Thursday, September 10, 2015
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
Tuesday, August 4, 2015
 
FDA U.S. Measures to Protect Against BSE
 
 
Monday, August 17, 2015
 
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
 
I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;
 
 
Alzheimer's, iatrogenic, transmissible, tse, prion, what if ?
 
Wednesday, September 9, 2015
 
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
 
 
Wednesday, September 2, 2015
 
Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database
 
 
Tuesday, September 1, 2015
 
Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism
 
 
*** Creutzfeldt-Jakob Disease *** Public Health Crisis VIDEO
 
 
 
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.
 
 
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kind regards, terry
 
Terry S. Singeltary Sr.
 
Texas Galveston Bay, on the bottom....