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
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To: oie-info-web
Sent: Mon, Nov 27, 2017 11:13 am
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
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Immediate notification (Final report)
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Date of start of the event
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10/11/2017
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Date of confirmation of the event
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21/11/2017
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Report date
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24/11/2017
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Date submitted to OIE
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27/11/2017
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Date event resolved
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27/11/2017
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Reason for notification
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Recurrence of a listed disease
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Date of previous occurrence
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10/05/2017
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Manifestation of disease
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Sub-clinical infection
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Causal agent
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Prion (atypical BSE type H)
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Nature of diagnosis
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Laboratory (advanced)
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This event pertains to
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a defined zone within the country
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New outbreaks
Summary of outbreaks
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Total outbreaks: 1
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Outbreak Location
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Total animals affected
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Outbreak statistics
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* Removed from the susceptible population through death, destruction and/or slaughter; |
Epidemiology
Source of the outbreak(s) or origin of infection
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Epidemiological comments
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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
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Measures to be applied
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Diagnostic test results
Laboratory name and type
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Central Veterinary Laboratory in Algete ( National laboratory )
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Tests and results
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Future Reporting
The event is resolved. No more reports will be submitted.
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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
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Notification immédiate (rapport final)
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Date de début de lévénement
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10/11/2017
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Date de confirmation de l´événement
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21/11/2017
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Date du rapport
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24/11/2017
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Date d'envoi à l'OIE
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27/11/2017
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Date de clôture de l'événement
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27/11/2017
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Raison de notification
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Réapparition dune maladie listée par l'OIE
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Date de la précédente apparition de la maladie
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10/05/2017
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Manifestation de la maladie
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Infection sub-clinique
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Agent causal
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Prion (ESB atypique de type H)
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Nature du diagnostic
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Tests approfondis en laboratoire (i.e. virologie, microscopie électronique, biologie moléculaire, immunologie)
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Cet événement se rapporte à
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une zone définie à l'intérieur du pays
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Nouveaux foyers
Récapitulatif des foyers
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Nombre total de foyers : 1
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Localisation du foyer
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Nombre total d'animaux atteints
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Statistiques sur le foyer
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* 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
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Autres renseignements épidémiologiques / Commentaires
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Le 10 novembre 2017, le Laboratoire central vétérinaire dAlgete (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 lobtention dun 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 lESB via digestion différentielle et western blot, qui ont identifié lESB atypique (souche de type H), le 21 novembre 2017. Léchantillon a été prélevé dans le cadre du programme national de surveillance des EST (prélèvement sur animaux morts ou non-sacrifiés pour consommation par lhomme, de plus de 48 mois). Lanimal de race métisse (conjunto mestizo), femelle, est né le 14 juin 1999. |
Mesures de lutte
Mesures de lutte appliquées
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Mesures à appliquer
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Résultats des tests de diagnostics
Nom du laboratoire et type
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Laboratoire central vétérinaire dAlgete ( Laboratoire national )
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Tests et résultats
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Rapports futurs
Lévénement est terminé. Aucun autre rapport ne sera envoyé.
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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
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Notificación inmediata(Informe final)
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Fecha del inicio del evento
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10/11/2017
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Fecha de confirmación del evento
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21/11/2017
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Fecha del informe
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24/11/2017
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Fecha de envio del informe a la OIE
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27/11/2017
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Fecha del cierre del evento
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27/11/2017
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Motivo de la notificación
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Recurrencia de una enfermedad de la Lista de la OIE
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Fecha de la anterior aparición de la enfermedad
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10/05/2017
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Manifestación de la enfermedad
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Infección sub-clínica
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Agente causal
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Prión (EEB atípica tipo H)
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Naturaleza del diagnóstico
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Pruebas de diagnóstico de laboratorio avanzadas (ej. virología, microscopía electrónica, biología molecular e inmunología)
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Este evento concierne
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una zona definida dentro del país
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Nuevos focos
Resumen de los focos
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Número total de focos: 1
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Localización del foco
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Número total de animales afectados
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Estadística del foco
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* 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
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Otros detalles epidemiológicos / comentarios
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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
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Medidas para implementar
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Resultados de las pruebas diagnósticas
Nombre y tipo de laboratorio
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Laboratorio Central de Veterinaria de Algete ( Laboratorio nacional )
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Pruebas y resultados
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Informes futuros
El episodio ha sido resuelto. Ningún otro informe será enviado
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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.
posted by Terry S. Singeltary Sr. at
11:35 AM
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