Monday, November 27, 2017

Spain OIE Bovine Spongiform Encephalopathy Prion atypical BSE type H Confirmed




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Subject: ESP 27-11-17 OIE Alert - Alerta - Alerte - Bovine spongiform encephalopathy - Encéphalopathie spongiforme bovine - Encefalopatía espongiforme bovina

Bovine spongiform encephalopathy ,Spain

Information received on 24/11/2017 from Dr Valentín Almansa, Director General, Sanidad de la Produccion Agraria, Ministerio de Agricultura, Alimentación y Medio Ambiente, Madrid, Spain

Summary

Report type
Immediate notification (Final report)
Date of start of the event
10/11/2017
Date of confirmation of the event
21/11/2017
Report date
24/11/2017
Date submitted to OIE
27/11/2017
Date event resolved
27/11/2017
Reason for notification
Recurrence of a listed disease
Date of previous occurrence
10/05/2017
Manifestation of disease
Sub-clinical infection
Causal agent
Prion (atypical BSE type H)
Nature of diagnosis
Laboratory (advanced)
This event pertains to
a defined zone within the country

New outbreaks

Summary of outbreaks
Total outbreaks: 1
Outbreak Location
  • CASTILLA Y LEON ( EL SAHUGO, SALAMANCA )
Total animals affected
Species
Susceptible
Cases
Deaths
Killed and disposed of
Slaughtered
Cattle
213
1
0
1
0
Outbreak statistics
Species
Apparent morbidity rate
Apparent mortality rate
Apparent case fatality rate
Proportion susceptible animals lost*
Cattle
0.47%
0.00%
0.00%
0.47%

* 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
On 10 November 2017, the Central Veterinary Laboratory in Algete (National Reference Laboratory for TSEs, accredited under UNE-EN ISO/IEC 17025: 2005 standard), received a nervous tissue sample suspected of BSE from the accredited Regional Laboratory for Animal Health in Villaquilambre, León (official regional laboratory), after a positive result was obtained through a Bio-Rad TeSeE SAP rapid test.
The NRL carried out the confirmation tests authorized according to Regulation (EU) No. 1148/2014. The selected combined tests were Western blot (Prionics) and ELISA (Idexx HerdChek BSE-Scrapie Antigen Test Kit) and positive results were obtained for both tests. Afterwards, tests for BSE strain discrimination were made through differential digestion and immunoblotting, confirming atypical BSE strain type H on 21 November 2017.
The sample was taken within the national TSE surveillance program (sampling of dead or non-slaughtered animals for human consumption over 48 months old).
The animal was a crossbred cow born on 14 June 1999.

Control measures

Measures applied
  • Traceability
  • Official disposal of carcasses, by-products and waste
  • Selective killing and disposal
  • Disinfection
  • Vaccination prohibited
  • No treatment of affected animals
Measures to be applied
  • Official destruction of animal products

Diagnostic test results

Laboratory name and type
Central Veterinary Laboratory in Algete ( National laboratory )
Tests and results
Species
Test
Test date
Result
Cattle
western blot
21/11/2017
Positive

Future Reporting

The event is resolved. No more reports will be submitted.

Encéphalopathie spongiforme bovine ,Espagne

Information reçue le 24/11/2017 de Dr Valentín Almansa, Director General, Sanidad de la Produccion Agraria, Ministerio de Agricultura, Alimentación y Medio Ambiente, Madrid, Espagne

Résumé

Type de rapport
Notification immédiate (rapport final)
Date de début de l’événement
10/11/2017
Date de confirmation de l´événement
21/11/2017
Date du rapport
24/11/2017
Date d'envoi à l'OIE
27/11/2017
Date de clôture de l'événement
27/11/2017
Raison de notification
Réapparition d’une maladie listée par l'OIE
Date de la précédente apparition de la maladie
10/05/2017
Manifestation de la maladie
Infection sub-clinique
Agent causal
Prion (ESB atypique de type H)
Nature du diagnostic
Tests approfondis en laboratoire (i.e. virologie, microscopie électronique, biologie moléculaire, immunologie)
Cet événement se rapporte à
une zone définie à l'intérieur du pays

Nouveaux foyers

Récapitulatif des foyers
Nombre total de foyers : 1
Localisation du foyer
  • CASTILLA Y LEON ( EL SAHUGO, SALAMANCA )
Nombre total d'animaux atteints
Espèce(s)
Sensibles
Cas
Morts
Mis à mort et éliminés
Abattus
Bovins
213
1
0
1
0
Statistiques sur le foyer
Espèce(s)
Taux de morbidité apparent
Taux de mortalité apparent
Taux de létalité apparent
Proportion d'animaux sensibles perdus*
Bovins
0.47%
0.00%
0.00%
0.47%

* 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
Le 10 novembre 2017, le Laboratoire central vétérinaire d’Algete (Laboratoire national de référence pour les EST, accrédité selon la norme UNE-EN ISO/IEC 17025:2005) a reçu un échantillon de tissu nerveux suspecté d'ESB envoyé par le laboratoire régional agréé de santé animale de Villaquilambre, León (laboratoire régional officiel), suite à l’obtention d’un résultat positif au test rapide Bio-Rad TeSeE SAP.
Le Laboratoire national de référence (LNR) a débuté les tests de confirmation autorisés, conformément au Règlement (UE) nº 1148/2014. Combinaison de tests sélectionnés : Western blot (Prionics) et ELISA (Idexx HerdChek BSE-Scrapie Antigen Test Kit). Les deux tests ont donné des résultats positifs.
Le LNR a ensuite effectué des tests de discrimination de souches de l’ESB via digestion différentielle et western blot, qui ont identifié l’ESB atypique (souche de type H), le 21 novembre 2017.
L’échantillon a été prélevé dans le cadre du programme national de surveillance des EST (prélèvement sur animaux morts ou non-sacrifiés pour consommation par l‘homme, de plus de 48 mois). L’animal de race métisse (conjunto mestizo), femelle, est né le 14 juin 1999.

Mesures de lutte

Mesures de lutte appliquées
  • Traçabilité
  • Destruction officielle des carcasses, des sous-produits et des déchets
  • Mise à mort sélective et élimination
  • Désinfection
  • Vaccination interdite
  • Aucun traitement des animaux atteints
Mesures à appliquer
  • Destruction officielle de tous les produits d'origine animale

Résultats des tests de diagnostics

Nom du laboratoire et type
Laboratoire central vétérinaire d’Algete ( Laboratoire national )
Tests et résultats
Espèce(s)
Test
Date du test
Résultat
Bovins
western blot
21/11/2017
Positif

Rapports futurs

L’événement est terminé. Aucun autre rapport ne sera envoyé.

Encefalopatía espongiforme bovina ,España

Información recibida el 24/11/2017 desde Dr Valentín Almansa, Director General, Sanidad de la Produccion Agraria, Ministerio de Agricultura, Alimentación y Medio Ambiente, Madrid, España

Resumen

Tipo de informe
Notificación inmediata(Informe final)
Fecha del inicio del evento
10/11/2017
Fecha de confirmación del evento
21/11/2017
Fecha del informe
24/11/2017
Fecha de envio del informe a la OIE
27/11/2017
Fecha del cierre del evento
27/11/2017
Motivo de la notificación
Recurrencia de una enfermedad de la Lista de la OIE
Fecha de la anterior aparición de la enfermedad
10/05/2017
Manifestación de la enfermedad
Infección sub-clínica
Agente causal
Prión (EEB atípica tipo H)
Naturaleza del diagnóstico
Pruebas de diagnóstico de laboratorio avanzadas (ej. virología, microscopía electrónica, biología molecular e inmunología)
Este evento concierne
una zona definida dentro del país

Nuevos focos

Resumen de los focos
Número total de focos: 1
Localización del foco
  • CASTILLA Y LEON ( EL SAHUGO, SALAMANCA )
Número total de animales afectados
Especies
Susceptibles
Casos
Muertos
Matados y eliminados
Sacrificados
Bovinos
213
1
0
1
0
Estadística del foco
Especies
Tasa de morbilidad aparente
Tasa de mortalidad aparente
Tasa de letalidad aparente
Proporción de animales susceptibles perdidos*
Bovinos
0.47%
0.00%
0.00%
0.47%

* 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
El 10 de noviembre de 2017 el Laboratorio Central de Veterinaria de Algete (Laboratorio Nacional de Referencia para EETs, acreditado bajo la norma UNE-EN ISO/IEC 17025:2005), recibió una muestra de tejido nervioso sospechosa de EEB desde el laboratorio regional acreditado de Sanidad animal de Villaquilambre, León (laboratorio regional oficial), tras haber obtenido un resultado positivo a un test rápido   Bio-Rad TeSeE SAP.
El LNR inició las pruebas de confirmación autorizadas de acuerdo al Reglamento (UE) nº 1148/2014. La combinación de pruebas seleccionada fue Western Blot (Prionics) y ELISA (Idexx HerdChek BSE-Scrapie Antigen Test Kit), obteniendo resultados positivos a ambas.
Posteriormente procedió a hacer pruebas de discriminación de cepas de EEB a través de digestión diferencial e inmunotransferencia, resultando EEB atípica cepa tipo H el 21 de noviembre del 2017.
La muestra se tomó como parte del programa nacional de vigilancia de EETs (muestreo de animales muertos o no sacrificados para el consumo humano mayores de 48 meses de edad).
El animal de la raza denominada conjunto mestizo, hembra, nació el 14 de junio de 1999.

Medidas de Control

Medidas implementadas
  • Trazabilidad
  • Eliminación oficial de canales, subproductos y desechos de origen animal
  • Matanza selectiva y eliminación
  • Desinfección
  • Vacunación prohibida
  • Ningún tratamiento de los animales afectados
Medidas para implementar
  • Destrucción oficial de los productos de origen animal

Resultados de las pruebas diagnósticas

Nombre y tipo de laboratorio
Laboratorio Central de Veterinaria de Algete ( Laboratorio nacional )
Pruebas y resultados
Especies
Prueba
Fecha de la prueba
Resultados
Bovinos
western blot
21/11/2017
Positivo

Informes futuros

El episodio ha sido resuelto. Ningún otro informe será enviado




FRIDAY, MARCH 10, 2017

OIE Spain Prion (Atypical BSE type L) Bovine Spongiform Encephalopathy Mad Cow Disease



MONDAY, JUNE 19, 2017 

PRION 2017 CONFERENCE ABSTRACT P61 vCJD strain properties in a Spanish mother and son replicate as those of a young UK case



Thursday, November 16, 2017 

Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination



SATURDAY, NOVEMBER 4, 2017 

FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006



FRIDAY, NOVEMBER 3, 2017

BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW

''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''

IN CONFIDENCE



O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
 
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
 
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
 
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
 
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
 
***is the third potentially zoonotic PD (with BSE and L-type BSE),
 
***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
 
===============
 
***thus questioning the origin of human sporadic cases***
 
===============
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
==============
 
 
 Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
 
 
Saturday, April 23, 2016
 
Scrapie ZOONOSIS PRION CONFERENCE TOKYO 2016
 
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***
 
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
 


SUNDAY, JULY 30, 2017 

PRION2017 

Low levels of classical BSE infectivity in rendered fat tissue P169 Low levels of classical BSE infectivity in rendered fat tissue

Dr. Christine Fast1, Dr. Markus Keller2, Dr. Ute Ziegler3, Prof. Dr. Martin Groschup4 1Friedrich-Loeffler-Institut, Greifswald, Germany, 2Friedrich-Loeffler-Institut, Greifswald, Germany, 3Friedrich-Loeffler-Institut, Greifswald, Germany, 4Friedrich-Loeffler-Institut, Greifswald, Germany

Aims: Specified Risk Materials (SRM) are the animal tissues potentially containing the highest levels of Bovine Spongiform Encephalopathy (BSE) prions; and their removal is the most important consumer protection measure against BSE. BSE infectivity in the mesentery fat is most likely associated with embedded nervous tissue. To date, it is unclear if contamination of the rendered fat could have occurred during tallow production at a slaughterhouse.

Methods: Samples were taken from five cattle originating from the German BSE pathogenesis study. Two animals were at preclinical, one at late preclinical and one animal at clinical stage of disease; one control animal was included. For all cattle, mouse bioassay results for the celiac and mesenteric ganglion complex (CMGC) were generated previously, showing either no, mild, moderate or substantial infectivity loads. Fat was rendered from CMGC samples embedded in mesentery fat by incubating for 20 minutes at 95°C, according to standard tallow production methods. Subsequently, the melted fat was 1:5 diluted in physiological saline and thoroughly vortexed. The liquid fat was cleaned by a short centrifugation at 10.000 rpm. Finally, 7-12 bovine prion protein overexpressing transgenic mice (Tgbov XV) were i.c. inoculated with 25-30 μl of the supernatant. Mice were sacrificed after 730 days or when showing clinical symptoms and mouse brains were subsequently examined by biochemical and immunohistochemical methods.

Results: Neither the control and the preclinical nor the late preclinical animals showed signs of infectivity in mouse bioassay of the fat samples after up to 730 days p.i. In contrast, low levels of infectivity were detected in the fat of the clinical animal as one mouse displayed a clear accumulation of pathological prion protein in the brain after an incubation period of 598 days p.i.

Conclusions: Our results clearly indicate the potential contamination of melted mesenteric fat by embedded nervous structures during standard tallow production. However, the BSE infectivity level was weak and detectable only in the fat rendered from one sample with documented high infectivity load in the ganglion itself (Kaatz et al. 2012). Albeit, this study is not representative as only one clinical animal was included, it provides a proof of principle. A broader examination would allow a better insight into temporal and spatial distribution pattern of BSE infectivity in rendered fat tissues of different origins.Such estimates have a critical role in qualitative and quantitative risk assessments and in providing advice on the designation and removal of certain SRM tissues.



THURSDAY, JULY 20, 2017 

USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200



SUNDAY, JULY 23, 2017

atypical L-type BASE Bovine Amyloidotic Spongiform Encephalopathy BSE TSE PRION


SUNDAY, JULY 23, 2017

Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy


SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY

***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.***


Wednesday, December 21, 2016 

TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH 


Tuesday, September 06, 2016

A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation


Saturday, July 23, 2016

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016


TUESDAY, NOVEMBER 7, 2017 

OIE Opens Texas Office Bovine Spongiform Encephalopathy BSE, Scrapie, CWD, TSE Prion


Atypical Creutzfeldt-Jakob disease with PrP-amyloid plaques in white matter: molecular characterization and transmission to bank voles show the M1 strain signature

Marcello Rossi†,Daniela Saverioni†,Michele Di Bari,Simone Baiardi,Afina Willemina Lemstra,Laura Pirisinu,Sabina Capellari,Annemieke Rozemuller,Romolo Nonno andPiero ParchiEmail authorView ORCID ID profile †Contributed equally Acta Neuropathologica CommunicationsNeuroscience of Disease20175:87 https://doi.org/10.1186/s40478-017-0496-7© The Author(s). 2017 Received: 4 October 2017Accepted: 14 November 2017Published: 23 November 2017

Conclusions

The present study further establishes the existence of a rare CJD subtype, occurring in approximately 0.5% of CJD cases, designated as p-CJDMM1. The novel histotype largely overlaps with sCJDMM1 but shows, as a very distinctive feature, the presence of PrP-amyloid plaques of kuru-type in both subcortical and deep nuclei white matter. Likewise typical CJDMM1, p-CJDMM1 can also be observed in sCJD cases showing the co-occurrence of PrPSc types 1 and 2. Moreover, plaque-like PrP deposits in the white matter can be a feature of genetic CJD. Most significantly, p-CJDMM1 share both PrPSc and transmission properties with classic CJDMM1, strongly pointing to an host-dependent causal factor for amyloid plaque formation in this phenotype.


 Re: vCJD in the USA * BSE in U.S.

15 November 1999 Terry S Singeltary

I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age.


 January 8, 2001 Singeltary submission to FDA

There is histopathology reports describing o florid plaques" in CJD victims in the USA and some of these victims are getting younger. I have copies of such autopsies, there has to be more. PLUS, sub-clinical human TSE's will most definitely be a problem. 


MONDAY, NOVEMBER 06, 2017 

Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque

''On secondary and tertiary transmissions, however, the proportion of PrPres positive animals gradually increased to almost 100%. 

''Recent communications suggest that a similar situation might exist in other models of experimental exposure to prions involving swine32 and cattle33.'' 

''Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque''


MONDAY, OCTOBER 02, 2017 

Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species


THURSDAY, AUGUST 17, 2017 

*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017 Singeltary et al


WEDNESDAY, NOVEMBER 1, 2017 

Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies


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. 



Terry S. Singeltary Sr.

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