OIE WAHIS SPAIN BOVINE SPONGIFORM ENCEPHALOPATHY BSE Atypical H-Type
Spain - Bovine spongiform encephalopathy - Immediate notification
GENERAL INFORMATION
COUNTRY/TERRITORY OR ZONE
ZONE
ANIMAL TYPE
TERRESTRIAL
DISEASE CATEGORY
OIE-listed
EVENT ID
4888
DISEASE
Bovine spongiform encephalopathy
CAUSAL AGENT
Bovine spongiform encephalopathy prion, atypical strain, H-type
GENOTYPE / SEROTYPE / SUBTYPE
START DATE
2023/01/21
REASON FOR NOTIFICATION
Recurrence of an eradicated disease
DATE OF LAST OCCURRENCE
2021/04/16
CONFIRMATION DATE
2023/02/03
EVENT STATUS
Resolved
END DATE
2023/02/06
SELF-DECLARATION
NO
REPORT INFORMATION
REPORT NUMBER
Immediate notification
REPORT ID
IN_159183
REPORT REFERENCE
REPORT DATE
2023/02/07
REPORT STATUS
Validated
NO EVOLUTION REPORT
EPIDEMIOLOGY
SOURCE OF EVENT OR ORIGIN OF INFECTION
Unknown or inconclusive
EPIDEMIOLOGICAL COMMENTS
Point 1 of paragraph 2, Chapter B (Measures following confirmation of a TSE in cattle) of ANNEX VII - CONTROL AND ERADICATION OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES of Regulation (EC) 999/2001 establishes that in case of confirmation of BSE in a bovine animal, all cattle identified in the following cases must be killed and completely destroyed: - in cases where the disease has been confirmed in a female, all her offspring born within two years before or after the clinical onset of the disease, - all animals in the age group of the animal in which the disease has been confirmed, - other animals present on the holding of the animal in which the disease was confirmed, or on other holdings, which may have been infected by the TSE agent or exposed to the same feed or source of contamination. Based on investigations of the two cattle identified on the case farm, they are NOT: - descendants of the affected animal, - cattle that, during their first year of life, were raised with the case so that in their first year of life they have not consumed the same feed, - cattle born during the twelve months before or after the birth of the affected animal, - nor have had access to the same feed while on the farm. So that their slaughter is not considered necessary. However, and as required by European legislation, they were identified for epidemiological investigation as in all cases of BSE.
QUANTITATIVE DATA SUMMARY
MEASURING UNIT
Animal
Species Susceptible Cases Deaths Killed and Disposed of Slaughtered/ Killed for commercial use Vaccinated Cattle (DOMESTIC)NEW11-1--TOTAL11-1--
DIAGNOSTIC DETAILS
CLINICAL SIGNS
NO
METHOD OF DIAGNOSTIC
Diagnostic test
Test name Laboratory Species sampled Outbreaks Result date Result
Antigen detection Western blot (Ag Western blot) Laboratorio Central de Veterinaria de Algete Cattle Pontevedra 2023/02/03 Positive
Immunohistochemistry (IHC) Laboratorio Central de Veterinaria de Algete Cattle Pontevedra 2023/02/03 Positive
CONTROL MEASURES AT EVENT LEVEL
CONTROL MEASURES AT EVENT LEVEL
DOMESTIC ANIMALS
WILD ANIMALS
Traceability
Applied
Official disposal of carcasses, by-products and waste
Applied
Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
see full report;
REPORT OF THE MEETING OF THE OIE AD HOC GROUP ON BOVINE SPONGIFORM ENCEPHALOPATHY RISK ASSESSMENT AND SURVEILLANCE
Paris, 18-21 March 2019
snip...
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below.
With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
The Group acknowledged the challenges in demonstrating the zoonotic transmission of atypical strains of BSE in natural exposure scenarios. Overall, the Group was of the opinion that, at this stage, it would be premature to reach a conclusion other than that atypical BSE poses a potential zoonotic risk that may be different between atypical strains.
snip...
In contrast, there have not been any substantiated reports of the successful oral transmission of H-BSE in cattle. Initial reports from Dudas et al., 2014 based on RT-QuIC pointed to the possibility of oral transmission following a very high dose (100 grams of brain material), although the individual did not display clinical signs and the findings from standard molecular or immunohistochemical assays were all negative. Investigations are ongoing in an attempt to clarify these findings.
Although significant uncertainty remains regarding the origin of C-BSE, several studies involving the serial passage of H-BSE and L-BSE in transgenic and wild-type mice have revealed their potential to lead to the emergence of a C-BSE-like phenotype (Baron et al., 2011; Torres et al., 2011; Bencsik et al., 2013) or other novel strains (Masujin et al., 2016). Whether or not one or both of these atypical strains led to the emergence of C-BSE remains speculative; however, the similarities between transmissible mink encephalopathy (TME), first reported in the USA in 1947 (Hartsough and Burger, 1965), and L-BSE indicate that TME may have been a surrogate indicator for the presence of L-BSE in cattle populations in those countries such as the USA, Canada, Germany, Finland and Russia where outbreaks of TME had been reported decades before C-BSE was first recognised in the United Kingdom in 1986 (Hadlow and Karstad, 1968; Marsh et al., 1991; McKenzie et al., 1996; Baron et al., 2007!
; Comoy et al., 2013). Although TME was originally thought to have occurred as a result of feeding mink with scrapie infected sheep carcases, oral challenge studies did not confirm this (Marsh et al., 1991). Importantly, in an outbreak reported in the USA in 1985, mink had never been fed sheep products; instead they had been fed on products derived from dead and sick dairy cattle (March et al., 1991). Similarly, from an outbreak in Canada in 1963, mink had reportedly been fed with products derived from cattle but not sheep (Hadlow and Karstad, 1968).
Although, as discussed above, the passage of H-BSE or L-BSE has been proposed as a possible explanation for the origin of C-BSE, transformation of L-BSE or H-BSE to C-BSE has not been observed so far in transmission studies in cattle. That being said, it is likely that, compared to various rodent models, an insufficient number of passages have been undertaken.
It is worth noting that sheep and goats are susceptible to L-BSE following intracerebral inoculation without lymphoid involvement in most individuals (Simmons et al., 2016; Gielbert et al., 2018; Vallino-Costassa et al., 2018). As discussed by Houston and Andreoletti (2018), C-BSE appears to increase in virulence for humans if it is first passaged in sheep. Whether or not this is the same for atypical strains remains to be determined.
Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
***> Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
***> As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
Atypical L-type BSE
Emerg Infect Dis. 2017 Feb; 23(2): 284–287. doi: 10.3201/eid2302.161416 PMCID: PMC5324790 PMID: 28098532
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
Hiroyuki Okada, corresponding author Yoshifumi Iwamaru, Morikazu Imamura, Kohtaro Miyazawa, Yuichi Matsuura, Kentaro Masujin, Yuichi Murayama, and Takashi Yokoyama Author information Copyright and License information Disclaimer This article has been cited by other articles in PMC. Go to: Abstract To determine oral transmissibility of the L-type bovine spongiform encephalopathy (BSE) prion, we orally inoculated 16 calves with brain homogenates of the agent. Only 1 animal, given a high dose, showed signs and died at 88 months. These results suggest low risk for oral transmission of the L-BSE agent among cattle.
Keywords: atypical bovine spongiform encephalopathy, cattle, L-type, prion, oral transmission, L-BSE, prions and related diseases, zoonoses The epidemic of bovine spongiform encephalopathy (BSE) in cattle is thought to be caused by oral infection through consumption of feed containing the BSE agent (prion). Since 2003, different neuropathologic and molecular phenotypes of BSE have been identified as causing ≈110 cases of atypical BSE worldwide, mainly in aged cattle. Although the etiology and pathogenesis of atypical BSE are not yet fully understood, atypical BSE prions possibly cause sporadic cases of BSE (1).
The L-type BSE (L-BSE) prion has been experimentally transmitted to cattle by intracerebral challenge, and the incubation period was is shorter than that for classical BSE (C-BSE) prions (2–6). The origin of transmissible mink encephalopathy in ranch-raised mink is thought to be caused by ingestion of L-BSE–infected material (7). Although L-BSE has been orally transmitted to mouse lemurs (8), it remains to be established whether L-BSE can be transmitted to cattle by oral infection. We therefore investigated the transmissibility of L-BSE by the oral route and tissue distribution of disease-associated prion protein (PrPSc) in cattle. All experiments involving animals were performed with the approval of the Animal Ethical Committee and the Animal Care and Use Committee of the National Institute of Animal Health (approval nos. 07–88 and 08–010).
snip...
The neuroanatomical PrPSc distribution pattern of orally challenged cattle differed somewhat from that described in cattle naturally and intracerebrally challenged with L-BSE (2–6,11,13,14), The conspicuous differences between the case we report and cases of natural and experimental infection are 1) higher amounts of PrPSc in the caudal medulla oblongata and the spinal cord coupled with that in the thalamus and the more rostral brainstem and 2) relatively low amounts of PrPSc in the cerebral cortices and the olfactory bulb. Furthermore, fewer PrPSc deposits in the dorsal motor nucleus of the vagus nerve may indicate that the parasympathetic retrogressive neuroinvasion pathway does not contribute to transport of the L-BSE prion from the gut to the brain, which is in contrast to the vagus-associated transport of the agent in C-BSE (15). PrPSc accumulation in the extracerebral tissues may be a result of centrifugal trafficking of the L-BSE prion from the central nervous syste!
m along somatic or autonomic nerve fibers rather than centripetal propagation of the agent (4,6,9). Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
Our study clearly confirms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a first passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
Atypical H-type BSE
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Author item Greenlee, Justin item MOORE, S - Orise Fellow item WEST-GREENLEE, M - Iowa State University
Submitted to: Prion
Publication Type: Abstract Only
Publication Acceptance Date: 5/14/2018
Publication Date: 5/22/2018
Citation: Greenlee, J.J., Moore, S.J., West Greenlee, M.H. 2018.
The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge.
Prion 2018, May 22-25, 2018, Santiago de Compostela, Spain. Paper No. P98, page 116. Interpretive Summary:
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route.
The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure.
Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US H-type BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates.
Cattle were observed daily throughout the course of the experiment for the development of clinical signs.
At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized.
Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain.
Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum.
With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease.
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
ESP 22-02-19 OIE Alert - Alerta - Alerte - Bovine spongiform encephalopathy - Encéphalopathie spongiforme bovine - Encefalopatía espongiforme bovina
Bovine spongiform encephalopathy ,Spain
Information received on 22/02/2019 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 | 24/01/2019 |
Date of confirmation of the event | 19/02/2019 |
Report date | 22/02/2019 |
Date submitted to OIE | 22/02/2019 |
Date event resolved | 22/02/2019 |
Reason for notification | Recurrence of a listed disease |
Date of previous occurrence | 23/11/2017 |
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 |
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Total animals affected |
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Outbreak statistics |
* Removed from the susceptible population through death, destruction and/or slaughter; |
Epidemiology
Source of the outbreak(s) or origin of infection |
|
Epidemiological comments | On January 25th, 2019, the Central Veterinary Laboratory in Algete (National Reference Laboratory for TSEs, accredited under UNE-EN ISO/IEC 17025:2005 standard), received a nerve tissue sample suspected of infection by bovine spongiform encephalopathy (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 EU Regulation No. 1148/2014. The selected combined tests were Bio-Rad TeSeE Wb confirmation Western blot and ELISA (Idexx HerdChek BSE-Scrapie Antigen Test Kit) and positive results were obtained for both tests. Afterwards, tests for BSE strain discrimination were carried out through hybrid immunoblotting with antibodies against PrP, confirming atypical BSE (H type strain). The sample was taken within the national TSE surveillance program (sampling of dead or non-slaughtered for human consumption animals over 48 months old). The animal was a Holstein-like bred cow born on July 30th, 2013. |
Control measures
Measures applied |
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Measures to be applied |
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Diagnostic test results
Laboratory name and type | Central Veterinary Laboratory in Algete ( National laboratory ) | ||||||||
Tests and results |
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Future Reporting
The event is resolved. No more reports will be submitted. |
Encéphalopathie spongiforme bovine ,Espagne
Information reçue le 22/02/2019 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 | 24/01/2019 |
Date de confirmation de l´événement | 19/02/2019 |
Date du rapport | 22/02/2019 |
Date d'envoi à l'OIE | 22/02/2019 |
Date de clôture de l'événement | 22/02/2019 |
Raison de notification | Réapparition d’une maladie listée par l'OIE |
Date de la précédente apparition de la maladie | 23/11/2017 |
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 |
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Nombre total d'animaux atteints |
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Statistiques sur le foyer |
* 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 |
|
Autres renseignements épidémiologiques / Commentaires | Le 25 janvier 2019, 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'être infecté par l’encéphalopathie spongiforme bovine (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 de confirmation Bio-Rad TeSeE Wb 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 immuno-empreintes hybrides avec différents anticorps dirigés contre PrP, qui ont identifié l’ESB atypique (souche de type H). 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 Frisonne, femelle, est né le 30 juillet 2013. |
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 | Laboratoire central vétérinaire d’Algete ( Laboratoire national ) | ||||||||
Tests et résultats |
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Rapports futurs
L’événement est terminé. Aucun autre rapport ne sera envoyé. |
Encefalopatía espongiforme bovina ,España
Información recibida el 22/02/2019 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 | 24/01/2019 |
Fecha de confirmación del evento | 19/02/2019 |
Fecha del informe | 22/02/2019 |
Fecha de envio del informe a la OIE | 22/02/2019 |
Fecha del cierre del evento | 22/02/2019 |
Motivo de la notificación | Recurrencia de una enfermedad de la Lista de la OIE |
Fecha de la anterior aparición de la enfermedad | 23/11/2017 |
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 |
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Número total de animales afectados |
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Estadística del foco |
* 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 | El 25 de enero de 2019 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 resultado positivo a 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 de confirmación Bio-Rad TeSeE Wb y ELISA (Idexx HerdCherk BSE-Scrapie Antigen Test Kit), obteniendo resultados positivos a ambas. Posteriormente procedió a hacer pruebas de discriminación de cepas de EEB a través de inmunotransferencia híbrida con diferentes anticuerpos frente a la PrP, resultando EEB atípica cepa tipo H. 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 frisona, hembra, nació el 30 de julio de 2013. |
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 | Laboratorio Central de Veterinaria, Algete ( Laboratorio nacional ) | ||||||||
Pruebas y resultados |
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Informes futuros
El episodio ha sido resuelto. Ningún otro informe será enviado |
SPAIN OIE Bovine Spongiform Encephalopathy atypical L-type Camargo, CANTABRIA 12/05/2017
Information received on 12/05/2017 from Dr Valentín Almansa, Director General, Sanidad de la Produccion Agraria, Ministerio de Agricultura, Alimentación y Medio Ambiente, Madrid, Spain
Bovine spongiform encephalopathy , Spain |
Information received on 12/05/2017 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 | 27/04/2017 |
Date of confirmation of the event | 05/05/2017 |
Report date | 12/05/2017 |
Date submitted to OIE | 12/05/2017 |
Date event resolved | 10/05/2017 |
Reason for notification | Recurrence of a listed disease |
Date of previous occurrence | 10/03/2017 |
Manifestation of disease | Sub-clinical infection |
Causal agent | Prion (Atypical BSE type L) |
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 |
| ||||||||||||
Total animals affected |
| ||||||||||||
Outbreak statistics |
* Removed from the susceptible population through death, destruction and/or slaughter; |
EPIDEMIOLOGY
Source of the outbreak(s) or origin of infection |
|
Epidemiological comments | On April 28th, 2017, the Central Veterinary Laboratory at Algete (National Reference Laboratory for transmissible spongiform encephalopathies accredited under UNE-EN ISO/IEC 17025:2005) received a brainstem sample suspected to be BSE-positive from the regional accredited animal health laboratory of Cantabria (official regional laboratory) after a positive result was obtained through the Bio-Rad TeSeE SAP rapid test. The National Reference Laboratory undertook the confirmatory tests authorized according to Regulation (EU) No. 1148/2014. The selected assays associated were Western blot (Prionics) and ELISA (TeSeE SAP Bio-Rad). Following positive results to both assays, the National Reference Laboratory performed assays to discriminate the BSE strains by immunoblotting with results for atypical BSE type L on May 5th, 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 (conjunto mestizo) female born on 25 February 2002. |
CONTROL MEASURES
Measures applied |
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Measures to be applied |
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DIAGNOSTIC TEST RESULTS
Laboratory name and type | Central Veterinary Laboratory, Algete ( National laboratory ) | ||||||||||||
Tests and results |
|
FUTURE REPORTING
The event is resolved. No more reports will be submitted. |
Encéphalopathie spongiforme bovine ,Espagne
Information reçue le 12/05/2017 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 | 27/04/2017 |
Date de confirmation de l´événement | 05/05/2017 |
Date du rapport | 12/05/2017 |
Date d'envoi à l'OIE | 12/05/2017 |
Date de clôture de l'événement | 10/05/2017 |
Raison de notification | Réapparition d’une maladie listée par l'OIE |
Date de la précédente apparition de la maladie | 10/03/2017 |
Manifestation de la maladie | Infection sub-clinique |
Agent causal | Prion (ESB atypique de type L) |
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 |
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Nombre total d'animaux atteints |
| ||||||||||||
Statistiques sur le foyer |
* 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 | Le 28 avril 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 tronc cérébral suspecté d'ESB envoyé par le laboratoire régional agréé de santé animale de Cantabrie (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 de Prionics et ELISA (TeSeE SAP Bio-Rad). Suite à l’obtention de résultats positifs pour les deux tests, le LNR a effectué des tests de discrimination de souches de l’ESB via immunoblotting, qui ont identifié l’ESB atypique (type L), le 5 mai 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 25 février 2002. |
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 | Laboratoire central vétérinaire, Algete ( Laboratoire national ) | ||||||||||||
Tests et résultats |
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RAPPORTS FUTURS
L’événement est terminé. Aucun autre rapport ne sera envoyé. |
Encefalopatía espongiforme bovina ,España
Información recibida el 12/05/2017 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 | 27/04/2017 |
Fecha de confirmación del evento | 05/05/2017 |
Fecha del informe | 12/05/2017 |
Fecha de envio del informe a la OIE | 12/05/2017 |
Fecha del cierre del evento | 10/05/2017 |
Motivo de la notificación | Recurrencia de una enfermedad de la Lista de la OIE |
Fecha de la anterior aparición de la enfermedad | 10/03/2017 |
Manifestación de la enfermedad | Infección sub-clínica |
Agente causal | Prión (EEB atípica tipo L) |
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 |
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Número total de animales afectados |
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Estadística del foco |
* 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 | El 28 de abril 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 tronco encefálico sospechosa de EEB desde el laboratorio regional acreditado de Sanidad animal de Cantabria (laboratorio regional oficial), tras haber obtenido resultado positivo a test rápido Bio-Rad TeSeE SAP. El Laboratorio nacional de referencia 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 (TeSeE SAP Bio-Rad), obteniendo resultados positivos a ambas. Posteriormente procedió a hacer pruebas de discriminación de cepas de EEB a través de inmunotransferencia, resultando EEB atípica cepa tipo L el 05/05/2017. La muestra se tomó como parte del programa nacional de vigilancia de EETs (muestreo de animales muertos o no sacrificados para el consume humano mayores de 48 meses de edad). El animal de la raza denominada conjunto mestizo, hembra, nació el 25 de febrero de 2002. |
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 | Laboratorio Central de Veterinaria, Algete ( Laboratorio nacional ) | ||||||||||||
Pruebas y resultados |
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INFORMES FUTUROS
El episodio ha sido resuelto. Ningún otro informe será enviado |
SPAIN CJD CLUSTER
[3] CJD cluster (Spain) Date: Mon 21 May 2012
From: Terry Singeltary <flounder9@verizon.net>
Creutzfeldt-Jakob disease cluster in the health area of Meixoeiro Hospital
——————————————–
(M J Moreno, et al. Acta Neurologica Scandinavica, early view (online version)
Objective ——— Galicia is the Spanish region in which most bovine spongiform encephalopathy cases have been registered. Meixoeiro Hospital is included in the Galician Health Service (SERGAS). The aim of the study was to analyze the clinical and epidemiological characteristics of Creutzfeldt-Jakob disease (CJD) in the health area of Meixoeiro Hospital and to identify possible specific risk factors to the general public.
Methods ——- All incident cases of CJD were identified in the health area of Meixoeiro Hospital (187 877 inhabitants) over a 14 year period, 1997-2010, and classified according to WHO diagnostic criteria. We obtained clinical details and epidemiological information on all cases. Crude and age-specific incidence rates were calculated. A review of surgical or invasive medical procedures was undertaken.
Results ——- We diagnosed 12 patients with CJD, 10 sporadic CJD (sCJD), and 2 genetic CJD (gCJD). No iatrogenic or variant CJD was detected. According to Poisson distribution, 3.9 CJD cases would be expected for our area over the 14 years researched. The average yearly mortality rate from CJD was 4.6 cases per million (3.8 from sCJD and 0.8 from gCJD). Eight patients (67 per cent) underwent at least one surgical or invasive medical procedure. 16 of 27 (59 per cent) of these procedures were undertaken in Meixoeiro Hospital.
Conclusions ———– The incidence of CJD in the health area of Meixoeiro Hospital is 3 times higher than expected. The hypothesis that at least some cases of sCJD are apparently because of covert transmission or zoonosis events should not be formally refuted and might explain the high rate found.
— Terry S Singeltary Sr <flounder9@verizon.net>
[These figures may be no more than a statistical anomaly, but they deserve attention and further investigation and similar analysis extension to other locations. – Mod.CP]
[A ProMED-mail HealthMap for Spain can be found at <http://healthmap.org/r/1zJm>;.] ;
****** [4] RT-QuIC diagnostic test trial Date: 15 Mar 2012
From: Terry Singeltary <flounder9@verizon.net>
RT-QuIC analysis of cerebrospinal fluid in sporadic Creutzfeldt-Jakob disease
————————————————
SNIP...END...SEE;
SUNDAY, MARCH 28, 2010
SPAIN BSE, Nor-98 atypical scrapie, SPORADIC CJD HIGH INCIDENT RATE >2 PER MILLION
FRIDAY, JANUARY 09, 2009
Mad cow disease detected on Madrid farm Friday, January 9, 2009
Monday, September 01, 2008
Two cases of variant Creutzfeldt-Jakob disease reported in Spain in 2007 and 2008
Tuesday, April 21, 2009
Doctor Antonio Ruiz Villaespesa, pathologist and CJD researcher deceased because of Creutzfeldt-Jakob Disease SPAIN
SEAC 102nd Meeting on Wednesday 4 March 2009 (SEE DH risk assessment on sourcing and pooling plasma)SEACAgenda102nd Meeting on Wednesday 4 March 2009Room 808, Nobel House, 17 Smith Square, Defra, London SW1P 3JR10.05 Approval of draft minutes from SEAC 101
snip...
ITEM 3 - CURRENT ISSUES 8.
SEAC was informed about the following issues: .
A mother and son in Spain had died of variant Creutzfeldt-Jakob Disease (vCJD). This is the first recorded instance of more than one case of vCJD within one family. As both the mother and son lived in a region of Spain with a history of BSE, had frequently shared meals of cattle brain, and as no other risk factor has been identified, it seems most likely that both infections were acquired from dietary exposure. Furthermore, the similar times of onset of disease of the cases did not suggest transmission had occurred from one to the other.snip...Thursday, February 26, 2009SEAC 102nd Meeting on Wednesday 4 March 2009 (SEE DH risk assessment on sourcing and pooling plasma)
see full text ;
SEAC 102nd Meeting on Wednesday 4 March 2009 SEAC
Agenda
102nd Meeting on Wednesday 4 March 2009
Room 808, Nobel House, 17 Smith Square, Defra, London SW1P 3JR
10.05 Approval of draft minutes from SEAC 101
snip...
ITEM 3 – CURRENT ISSUES 8. SEAC was informed about the following issues: • A mother and son in Spain had died of variant Creutzfeldt-Jakob Disease (vCJD). This is the first recorded instance of more than one case of vCJD within one family. As both the mother and son lived in a region of Spain with a history of BSE, had frequently shared meals of cattle brain, and as no other risk factor has been identified, it seems most likely that both infections were acquired from dietary exposure. Furthermore, the similar times of onset of disease of the cases did not suggest transmission had occurred from one to the other.
snip...
Published Date: 1999-07-19 23:50:00
Subject: PRO/AH> BSE, beef import restrictions - Spain Archive Number: 19990719.1215 BSE, BEEF IMPORT RESTRICTIONS - SPAIN
MONDAY, NOVEMBER 27, 2017
Spain OIE Bovine Spongiform Encephalopathy Prion atypical BSE type H Confirmed
FRIDAY, MARCH 10, 2017
OIE Spain Prion (Atypical BSE type L) Bovine Spongiform Encephalopathy Mad Cow Disease
FRIDAY, MAY 12, 2017 SPAIN OIE
Bovine Spongiform Encephalopathy atypical L-type Camargo, CANTABRIA
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
FRIDAY, JANUARY 09, 2009
Mad cow disease detected on Madrid farm
Monday, September 01, 2008
Two cases of variant Creutzfeldt-Jakob disease reported in Spain in 2007 and 2008
Spanish woman and son could be first relatives to die of BSE
Submitted by Marina Dimova on Wed, 08/27/2008 - 11:53.
The Spanish health authorities are investigating the death of a woman whose son died earlier of Creutzfeldt-Jakob Disease (CJD), the human variant of bovine spongiform encephalopathy (BSE) or mad cow disease, experts said Wednesday in Madrid.
If it is confirmed that the woman and her son died from the same cause, they would be the first members of the same family in the world to succumb to CJD, neuropathologist Alberto Rabano said.
The woman, who was about 60-years-old, passed away last week in the northern city of Leon. The son died in February. Their identities were not given.
Veterinary experts said the son caught the disease by eating infected meat before 2001, when preventative measures were adopted.
***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.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
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.
==============
PRION 2015 CONFERENCE
***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.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
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.
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
Sunday, January 10, 2021
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with 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. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022
SPECIFIED RISK MATERIALS DOCKET NUMBER DOCKET NO. FSIS-2022-0027 SINGELTARY SUBMISSION ATTACHMENT
SO, WHO'S UP FOR SOME MORE TSE PRION POKER, WHO'S ALL IN $$$
SO, ATYPICAL SCRAPIE ROUGHLY HAS 50 50 CHANCE ATYPICAL SCRAPIE IS CONTAGIOUS, AS NON-CONTAGIOUS, TAKE YOUR PICK, BUT I SAID IT LONG AGO WHEN USDA OIE ET AL MADE ATYPICAL SCRAPIE A LEGAL TRADING COMMODITY, I SAID YOUR PUTTING THE CART BEFORE THE HORSE, AND THAT'S EXACTLY WHAT THEY DID, and it's called in Texas, TEXAS TSE PRION HOLDEM POKER, WHO'S ALL IN $$$
***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.
SNIP...SEE;
THURSDAY, JULY 8, 2021
EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie
TUESDAY, MAY 31, 2022
USA Bovine Spongiform Encephalopathy BSE: description of typical and atypical cases
TUESDAY, SEPTEMBER 07, 2021
Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom
TUESDAY, SEPTEMBER 13, 2022
BSE pathogenesis in the ileal Peyer’s patches and the central and peripheral nervous system of young cattle 8 months post oral BSE challenge
TUESDAY, SEPTEMBER 07, 2021
Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA
WEDNESDAY, JANUARY 12, 2022
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA, what if?
PLOS ONE Journal
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
***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 ***
MONDAY, SEPTEMBER 19, 2022
589.2001 BSE TSE regulations which prohibits the use of high-risk cattle material in feed for all animal species 2022
SATURDAY, SEPTEMBER 24, 2022
Transmission of CH1641 in cattle
FRIDAY, APRIL 1, 2022
USDA TAKES THE C OUT OF COOL, what's up with that?
MONDAY, JUNE 6, 2022
APHIS USDA History Highlight: APHIS Combats Bovine Spongiform Encephalopathy Published Jun 1, 2022
MONDAY, NOVEMBER 30, 2020
***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION
see updated concerns with atypical BSE from feed and zoonosis...terry
WEDNESDAY, DECEMBER 8, 2021
Importation of Sheep, Goats, and Certain Other Ruminants AGENCY: Animal APHIA, USDA, FINAL RULE [Docket No. APHIS–2009–0095] RIN 0579–AD10
WEDNESDAY, MARCH 24, 2021
USDA Animal and Plant Health Inspection Service 2020 IMPACT REPORT BSE TSE Prion Testing and Surveillance MIA
https://animalhealthreportpriontse.blogspot.com/2021/03/usda-animal-and-plant-health-inspection.html
SUNDAY, MARCH 21, 2021
Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005 Singeltary's Regiew 2021
https://animalhealthreportpriontse.blogspot.com/2021/03/investigation-results-of-texas-cow-that.html
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
THURSDAY, JANUARY 23, 2020
USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service
sent this bulletin at 01/23/2020 02:15 PM EST
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
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
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
SATURDAY, OCTOBER 8, 2022
Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation
MONDAY, AUGUST 29, 2022
Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2021 Annual Report
FRIDAY, FEBRUARY 03, 2023
OIE Netherlands Bovine Spongiform Encephalopathy BSE, atypical strain, L-type
Thursday, February 2, 2023
EFSA OIE WOHA UPDATES ON CHRONIC WASTING DISEASE CWD TSE PrP ZOONOSIS
WEDNESDAY, FEBRUARY 8, 2023
NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER SURVEILLANCE TABLES OF CASES EXAMINED January 11th, 2023
Aug. 5, 2001
Mad cow disease: Could it be here?
Man's stubborn crusade attracts experts' notice
Photo of Carol Christian
Carol Christian, Chron.com / Houston Chronicle
Aug. 5, 2001
Like Paul Revere with e-mail, Terry Singeltary Sr. is on a mission to sound an alarm: Beware of mad cow disease.
As is true of many crusaders, however, his pleas often fall on deaf ears. Health officials here and abroad insist that bovine spongiform encephalopathy -- popularly known as mad cow disease, a fatal brain disorder that can make cows shake uncontrollably -- has been kept out of this country through surveillance of the cattle industry.
But since his mother's death in December 1997, the Galveston County man has been obsessed with possible connections between her deadly brain disorder, sporadic Creutzfeldt-Jakob Disease, and mad cow disease.
And after much persistence on his part, people are taking notice of this former machinist and high school dropout who jokes that he has a Ph.D. -- a Pool Hall Degree.
"They called me Chicken Little for four years," he said. "Now they're calling back, asking for more information."
For the past year he has been U.S. co-coordinator of an international monitoring group called CJD Watch. He regularly gets e-mail from scientists and journalists around the world.
Debora MacKenzie, a reporter for the British magazine New Scientist, described Singeltary, 47, as a "dogged unearther and tabulator of government documents."
Singeltary monitors "every word written about CJD/BSE," said Anita Manning of USA Today, also by e-mail.
"He's passionate, opinionated and not always tactful, although I like him because he's such a character and he is so transparent," Manning said. "He is what he appears to be."
Science and environment writer Jonathan Leake of the Sunday Times in London said Singeltary has helped him track down families of people with CJD along with academic research papers.
"I strongly suspect he is right in thinking the USA has had BSE cases," Leake said by e-mail.
"The American government is making the same mistake as the British in putting the short-term commercial interests of its farmers before health considerations," he added.
"It should start formal and widespread testing of cattle plus compulsory autopsies for all human CJD victims at the state's expense. If there is BSE, then leaving it to spread will kill people -- and that would eventually destroy the industry, too."
Texas Department of Health epidemiologist Julie Rawlings said Singeltary's careful monitoring of the disease had proven useful.
"Terry has been helpful in providing contact information regarding suspect CJD cases so that the Health Department can initiate case investigations and learn more about CJD in Texas," she said.
Noting that the department cannot release records on individual patients, she added, "I think we learn more from him than he does from us."
Mad cow disease surfaced in England in 1986 and quickly became an epidemic. It since has been reported in 15 European countries, most recently Greece on July 2, and the Czech Republic on June 14. Two German-born cows tested positive for BSE in November.
Singeltary said he became convinced that BSE is here as he watched his mother, Barbara Poulter of Crystal Beach, dying of sporadic Creutzfeldt-Jakob Disease. The rare, fatal brain disease is sometimes accompanied by severe jerking.
"She would jerk so bad at times, it would take three of us to hold her down," Singeltary said. "They can call it whatever they want, but I know what I saw, and what she went through. `Sporadic' simply means they don't know."
Poulter, a retired telephone-company field worker, had a form of sporadic CJD -- Haidenhain variant -- that is even less common than the typical sporadic case. One of its first symptoms is loss of vision.
She started seeing brown spots in September 1997 and was virtually blind within two weeks. By the eighth week of the illness Poulter was bedridden, and in the 10th week she died. Before that she had been in good health.
In many countries and most U.S. states, physicians are not required to report CJD cases to health officials. Texas made the disease reportable in 1998. Through 2000, there were 17 probable or confirmed cases, according to the Texas Department of Health.
In mid-June, a case of sporadic CJD was confirmed through brain biopsy at Christus Spohn Hospital Shoreline in Corpus Christi, said Jane Bakos, hospital vice president. The patient has since died, the hospital reported.
CJD and mad cow disease leave their victims' brains full of holes like a sponge. Although not contagious, the illnesses are thought to be transmissible through prions, or nearly indestructible abnormal proteins.
Because the prion protein is not killed by standard sterilization, sporadic CJD can be spread by contaminated surgical instruments.
In March 1996, the British government announced the discovery of a new variant of CJD, most likely explained by exposure to bovine spongiform encephalopathy.
Through June, 101 cases of new-variant CJD have been reported in the United Kingdom, three in France and one in Ireland. In contrast to sporadic CJD, the new variant usually affects younger patients and lasts longer.
No cases of new-variant CJD or BSE have been reported in the United States. No relationship has been shown between sporadic CJD and mad cow disease.
There is no indication that new-variant CJD can be spread through blood transfusions, but a U.S. Food and Drug Administration advisory committee voted in June to broaden the categories for excluding potential donors. The recommendations have not yet been approved by the FDA.
The American Red Cross has announced that on Sept. 17 it will begin rejecting potential blood donors who, since 1980, have spent at least three months in the United Kingdom or at least six months in any European country or combination of countries. Those who have received a blood transfusion in Britain since 1980 also will be rejected.
The primary collector of local blood donations is the Gulf Coast Regional Blood Center, which will follow the FDA's guidelines, said Bill Teague, president and chief executive officer.
Singeltary said it's naive to think that U.S. prevention efforts have kept mad cow and new-variant CJD out of the United States.
"They haven't found it," he said, "because they haven't looked."
For one thing, he said, too few cows are tested for the disease. In the first six months of this year, the European Union tested more than 3.2 million cows, David Byrne of the European Commission said in a speech last month.
By contrast, it took the U.S. Department of Agriculture nearly 10 years to analyze about 13,000 cow brains, according to the department's Web site.
With more than 68 million cattle slaughtered since 1990 in the United States, according to the USDA, checking about 13,000 falls far short, Singeltary said.
Though not a scholar, Singeltary has collected voluminous material on mad cow and CJD. Disabled from a neck injury, Singeltary never used a computer until 1998. He now spends hours each day on the Internet while his wife, Bonnie Singeltary, runs a flower shop in their home in Bacliff, in north Galveston County.
His challenge to the CJD/BSE establishment is courageous and refreshing, said Dr. Lynette Dumble, former visiting professor of surgery at University of Texas Medical School at Houston and a former senior research fellow in the history and philosophy of science at the University of Melbourne in Australia.
"I certainly have no problem with Terry's ideas on BSE/CJD," said Dumble, who coordinates the Global Sisterhood Network, a computer service that posts media reports on developments affecting women. "His research skills are excellent, and he is abreast of each and every development in the field."
Among Singeltary's worries now, he said, are widespread violations of an August 1997 ban on feeding animal products to U.S. cattle. The FDA reported in January that hundreds of feed manufacturers were not complying with regulations designed to keep BSE out of this country.
(That same month, a Purina Mills feedlot near San Antonio told the FDA that a "very low level" of cow parts had been found in cattle feed. The company voluntarily removed 1,222 animals who had been fed the prohibited materials.)
He obtained copies of FDA letters to various feed mills that had been found in violation of the regulations and immediately sent them by e-mail to hundreds of people around the world.
Singeltary might not be so zealous in getting the word out if he weren't convinced that someone is covering up the truth.
"They used to say BSE would never transmit to humans," he said, "and it has. They lied about the feed ban being in place.
"I've lost faith in the whole process. I've discovered too many things."
Photo of Carol Christian
Written By Carol Christian
Terry S. Singeltary Sr., Bacliff, Texas, USA, 77518 flounder9@verizon.net
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