P124 The Present Romanian Epidemiological Context With Regard To The Bovine Spongiform Encephalopathy
Mrs. Florica BARBUCEANU1,2, Mr. Gabriel PREDOl2, Mrs. Cristina DIACONU1, Mr. Bogdan GEORGESCU2, Mrs. loana NEGHIRLA3, Mr. Cristian BELU2, Mrs. Marion Simmons4
1Institute for Diagnosis and Animal Health, Bucharest, Romania, 2University of Agronomical Sciences and Veterinary Medicine Bucharest, Bucharest Romania, 3National Sanitary Veterinary and Food Safety Authority, Bucharest, Romania, 4Animal and Plant Health Agency, EU Reference Laboratory for TSE, Weybridge, New Haw, Addlestone, Surrey, United Kingdom
Aim: The prionic diseases represent, still, a little known area form biological and medical point of view. More studies and research is still necessary in order to establish with accuracy the causes and the mechanism determining the occurrence of these diseases. The numerous variants of this disease, as well as their possible different nature, represent a barrier against the achievement of this goal. Presently, at the world level, the BSE epidemiological situation is a stable one due to the preventing actions and corrective measures applied to reduce the risk represented by the BSE down to an acceptable level; the incidence of the disease - i.e. the classical BSE cases - is constantly diminishing. However, during the last years, atypical BSE cases have been reported in several countries from Europe, USA, Canada and Japan.
Methods: Rapid tests: TeSeE ELISA kit manufactured by Bio-Rad and BSE and scrapie antigen Test kit, EIA manufactured by IDEXX; Confirmatory tests: TeSeE Western Blott kit manufactured by Bio-Rad and BSE antigen test kit, immunohistochemistry manufactured by VMRD, Inc.; Discriminatory test. All diagnosis activities were coordinated by National Reference Laboratory for Transmissible Spongiform Encephalopathies - Department of Pathology from the Institute for Diagnosis and Animal Health. The confirmatory and discriminatory tests for the differentiation of the BSE strain for the two brain samples from cattle that were positive for BSE were carried out by the European Reference Laboratory for TSE.
Results: In Romania, the first BSE case was reported in May 2014 by the Romanian National Reference Laboratory for Transmissible Spongiform Encephalopathies (TSE - NRL) active within the Institute for Diagnosis and Animal Health (IDAH), in a bovine slaughtered normally, after a suspicion notification following a positive rapid test. The sample was subsequently diagnosed with specific confirmatory tests. The discriminatory tests performed by the European Reference Laboratory for TSE for the differentiation of the BSE strain have confirmed our diagnostic of atypical BSE case, the L type. In December 2014, a second BSE case was diagnosed, always the atypical form and the L type in a normally slaughtered bovine.
Conclusion: This study presents data on the implementation of the annual programs co-financed by the European Commission for the eradication and monitoring of the transmissible spongiform encephalopathies and data for the two brain samples from cattle that were positive for BSE in Romania.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
COMMISSION IMPLEMENTING DECISION (EU) 2016/600
of 15 April 2016
amending Decision 2007/453/EC as regards the BSE status of Romania
(notified under document C(2016) 2186)
(Text with EEA relevance)
THE EUROPEAN COMMISSION,
Having regard to the Treaty on the Functioning of the European Union,
Having regard to Regulation (EC) No 999/2001 of the European Parliament and of the Council of 22 May 2001 laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies (1), and in particular the third subparagraph of Article 5(2) thereof,
Whereas:
(1) Regulation (EC) No 999/2001 provides that Member States, third countries or regions thereof (‘countries or regions’) are to be classified according to their bovine spongiform encephalopathy (BSE) status into one of three categories: negligible BSE risk, controlled BSE risk and undetermined BSE risk.
(2) The Annex to Commission Decision 2007/453/EC (2) lists countries or regions according to their BSE status.
(3) The World Organisation for Animal Health (OIE) plays a leading role in the categorisation of countries or regions according to their BSE risk.
(4) In May 2014, the OIE General Assembly decided to grant ‘negligible BSE risk’ status to Romania in its Resolution No 18 — Recognition of the Bovine Spongiform Encephalopathy Risk Status of Member Countries (3). On 27 June 2014, the OIE Scientific Commission for Animal Diseases suspended that negligible BSE risk status due to the notification by Romania on 20 June 2014 of an atypical BSE case.
(5) In May 2015, the OIE General Assembly amended the BSE Chapter of the OIE Terrestrial Animal Health Code (‘the Code’), by adding the following sentence in Article 11.4.1 of the Code: ‘For the purpose of official BSE risk status recognition, BSE excludes “atypical BSE” as a condition believed to occur spontaneously in all cattle populations at a very low rate’ (4).
(6) As the negligible BSE risk status of Romania had been suspended because of the detection of an atypical BSE case and as the new version of the Code excludes atypical BSE for the purpose of official BSE risk status recognition, the OIE Scientific Commission for Animal Diseases decided, with effect as from 8 December 2015, to reinstate the negligible BSE status of Romania.
(7) To reflect that decision, the list of countries in the Annex to Decision 2007/453/EC should therefore be amended.
(8) Decision 2007/453/EC should therefore be amended accordingly.
(9) The measures provided for in this Decision are in accordance with the opinion of the Standing Committee on Plants, Animals, Food and Feed,
HAS ADOPTED THIS DECISION:
Article 1
The Annex to Decision 2007/453/EC is amended as follows:
(1) the entry ‘— Romania’ is inserted in Part ‘A. Countries or regions with a negligible BSE risk’, after ‘— Portugal’ and before ‘— Slovenia’;
(2) the entry ‘— Romania’ is deleted in Part ‘B. Countries or regions with a controlled BSE risk’. Article 2
This Decision is addressed to the Member States.
Done at Brussels, 15 April 2016.
For the Commission
Vytenis ANDRIUKAITIS
Member of the Commission
(1) OJ L 147, 31.5.2001, p. 1.
(2) Commission Decision 2007/453/EC of 29 June 2007 establishing the BSE status of Member States or third countries or regions thereof according to their BSE risk (OJ L 172, 30.6.2007, p. 84).
(3) http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/2014_A_RESO-18_BSE.pdf
In December 2014 Romania confirmed the second case of Bovine Spongiform Encephalopathy (BSE), atypical form, as part of the BSE surveillance program.
According to National Veterinary and Food Safety Authority (ANSVSA), the sick animal came from a backyard farm located in the center of Romania.
The first case was detected in May 2014 and it triggered the suspension of the status “country with negligible BSE risk” granted by the World Organization of Animal Health (OIE).
THIS REPORT CONTAINS ASSESSMENTS OF COMMODITY AND TRADE ISSUES MADE BY USDA STAFF AND NOT NECESSARILY STATEMENTS OF OFFICIAL U.S. GOVERNMENT POLICY - Date: GAIN Report Number:
Post:
Report Categories: Approved By: Prepared By:
Report Highlights: In December 2014 Romania confirmed the second case of Bovine Spongiform Encephalopathy (BSE), atypical form, as part of the BSE surveillance program. According to National Veterinary and Food Safety Authority (ANSVSA), the sick animal came from a backyard farm located in the center of Romania. The first case was detected in May 2014 and it triggered the suspension of the status “country with negligible BSE risk” granted by the World Organization of Animal Health (OIE). Monica Dobrescu Russ Nicely Livestock and Products Sanitary/Phytosanitary/Food Safety
Romania confirms the second case of BSE Bucharest Romania RO1502 1/29/2015 Voluntary Public
General Information: On December 22nd 2014, a sample collected from a bovine slaughtered on December 16th, 2014 in an authorized slaughterhouse in Dambovita County (south of Romania) raised the suspicion of BSE disease (also known as mad cow disease). The origin of the animal, a backyard farm from Covasna County (center of Romania), was identified, along with animal ascendants and descendants. Currently the process of identifying all animals pertaining to the same herd and all animals which came in contact with the infected animal is on-going.
The National Veterinary and Food Safety Authority (ANSVSA) assured consumers that public health has not been put in danger, as meat coming from the positive animal has not entered the food chain. Meat and by-products from the positive animal and the animal slaughtered before the infected one have been seized.
On December 23rd 2014, when the Institute for Diagnosis and Animal Health confirmed the suspicion of the disease, the entire amount of seized meat and products was destroyed into a rendering facility.
On January 7th 2015, the sample was sent for strain determination to the EU Reference Laboratory in Weybridge, United Kingdom, which later confirmed the atypical form of BSE. Under such circumstances, the veterinary service started the procedure of evaluating the health status of all animals which came in contact with the positive one. The backyard farm has been officially placed under surveillance for animal and products movement. All animal owners will be compensated for losses in case their animals are sent for disposal.
Institute for Diagnosis and Animal Health confirmed the first case of atypical BSE form in May 2014. Following this occurrence, World Organization of Animal Health (OIE) suspended in June 2014 the status of “country with negligible BSE risk”.
Unlike the classical cases of mad cow which are caused when cattle are fed with feeding materials which contain proteins of animal origin, the atypical cases occur spontaneously, the causes being currently under investigation. In the context of a second case of BSE atypical form confirmation in Romania, ANSVSA suggested during the most recent meeting of the Standing Committee on Plants, Animals, Food and Feed (SCOFCAH) at EU level that the European Food Safety Authority (EFSA) would consider undertaking studies regarding the causes of BSE atypical forms.
This Decision followed a favorable opinion [4] from the European Food Safety Authority (EFSA) from December 2010.
Only Bulgaria and Romania failed to propose an updated monitoring regime, but both countries had no BSE cases in recent years.
FINAL REPORT OF AN AUDIT CARRIED OUT IN ROMANIA FROM 07 TO 18 FEBRUARY 2011 IN ORDER TO EVALUATE MEASURES CONCERNING BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)
Executive Summary This report describes the outcome of an audit carried out by the Food and Veterinary Office (FVO) in Romania, from 7 to 18 February 2011.
The objective of the audit was to evaluate the implementation of requirements concerning Bovine Spongiform Encephalopathy (BSE), as laid down in Regulation (EC) No 999/2001.
In terms of scope, the audit concentrated on BSE epidemio-surveillance in bovines, measures taken after suspicion/confirmation of BSE, removal and handling of specified risk material (SRM) from bovines, and the prohibition of feeding products of animal origin to farmed animals and exceptions applicable to this ban. The evaluation included measures taken in response to the recommendations made in a previous FVO audit regarding the afore-mentioned issues.
Overall, the report concludes that very limited progress has been made in order to address the recommendations of the previous FVO audit. In particular, BSE active epidemio-surveillance and compliance with SRM rules are significantly affected by the lack of arrangements for the collection of brain samples and SRM at backyard farms, where the majority of the bovine population is kept. There are also weaknesses concerning feed-ban controls.
The report makes a number of recommendations addressed to the Romanian competent authorities, aimed at rectifying the shortcomings identified and further enhancing the implementing and control measures in place.
Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy
A Notice by the Animal and Plant Health Inspection Service on 08/10/2016
snip...
In the December 2015 notice, we mistakenly announced our intent to recognize Romania as a region of negligible risk for BSE.
In December 2014, the OIE suspended Romania's status as a negligible risk region because Romania reported a case of atypical BSE.
Since then, the OIE has announced its intent to reinstate Romania's status as a region of negligible risk for BSE.
We will be seeking information to verify Romania's status and will announce our intent to concur with the OIE's designation in a future notice.
Also in the December 2015 notice, we announced our intent to recognize France as a region of negligible risk for BSE in concurrence with the OIE.
Since then, France has confirmed a case of classical BSE in a 5-year-old cow.
Accordingly, the OIE has suspended France's status as a region of negligible risk for BSE and reinstated its status as a region of controlled risk effective March 25, 2016.
For this reason we have removed France from the list of regions of negligible risk for BSE in this document.
We will continue to recognize France as a region of controlled risk for BSE.
MONDAY, MAY 2, 2016
France Confirms Case of Classical Mad Cow Disease BSE
The affected bovine, a Salers female born on April, 8th 2011, showed paresis and was euthanized on March, 1st 2016. Samples made on March, 4th 2016 during rendering were analyzed at the Department Laboratory of La Somme. The rapid test proved positive on March, 8th 2016 and the samples were then sent for further analysis to the National Reference Laboratory, ANSES, which confirmed a case of classical BSE on March, 21st 2016. The European Union Reference Laboratory confirmed those results on the basis of documentation on March, 23rd 2016.
>>> It is distinct from atypical BSE, which may develop spontaneously, according to information from the U.S. Centers for Disease Control and Prevention.
THIS IS A MYTH $$$
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Thursday, March 24, 2016
FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une vache dans les Ardennes
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$
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
The epidemiological evolution of prion infection on bovine in Romania, in the period of 2010 – 2015 PRION 2016 TOKYO JAPAN
P-159 The epidemiological evolution of prion infection on bovine in Romania, in the period of 2010 – 2015
Florica Barbuceanu1,2, Gabriel Predoi2, Cristina Diaconu1, Theodora Chesnoiu3, Bogdan Georqescu2, Florin Furnaris1, Claudiu Diaconu1
1Institute for Diagnosis and Animal Health, Romania; 2Faculty of Veterinary Medicine Bucharest; 3National Sanitary Veterinary and Food Safety Authority
The first BSE epidemic began in England in 1986 and progressed steadily until 1992. Implementation of preventive measures materialized by progressive decline of the disease but new cases continued to occur in different European countries.
This prion disease in Romania was first diagnosed in 2014, at the Institute for Diagnosis and Animal Health, in the National Reference Laboratory for transmissible spongiform encephalopaties.
The epidemiological evolution of BSE in cattle are presented in this paper, with methods used, the results of investigations, the outbreaks and the number of cattle diagnosed with this prion disease.
Were subjected to epidemiological investigations and laboratory tests 510166 large ruminants in the period of 2010 - 2015.
The whole diagnostic activity were coordinated by the National Reference Laboratory for TSE; the Morphopatology Department of the Institute for Diagnosis and Animal Health.
In the frame of passive and active surveillance for BSE on large ruminants, 1720 histological exams, 510166 rapid tests, 2765 immunoblotting tests and 286 imunohistochemical tests were performed and after applying immunoblotting and imunohistochemical tests being confirmed 2 atypical cases of BSE.
The differentiation tests were performed by the Eu-RL-TSE of the Animal and Plant Health Agency (APHA) Weybridge, United Kingdom, the atypical L-type BSE being diagnosed at the two cases.
Key words: BSE, rapid tests, confirmation tests, atypical form, L-type
- 286-
Tuesday, August 9, 2016
Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]
BILLING CODE: 3410-34-P DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service
snip...see more ;
Rom J Leg Med [23] 157-161 [2015] DOI: 10.4323/rjlm.2015.157 © 2015 Romanian Society of Legal Medicine 157
*** A case of variant Creutzfeldt-Jakob disease in Romania ***
Mihai Ceauşu1, Corneliu Octavian Capatina2, Sorin Hostiuc3,*, Dan Dermengiu3
Abstract: In humans prion diseases can occur sporadically, through genetic mutations, or can be transmitted from animal, human (kuru disease), or iatrogenic sources. Even though transmissible forms are the most well-known, the sporadic and heritable forms are much more frequent, accounting for about 85% of all cases. The purpose of this case report is to present an atypical variant CJD in a 26 years-old woman. The patient died secondary to infectious complications caused by an acute overdose with alcohol, beta-blockers and oral anti-diabetic drugs, and had an atypical neuropathology pattern, with absent amyloid plaques, but present focal, perivascular deposits of amyloid precursor protein and a positive immunohistochemical reaction for prp. Key Words: variant Creutzfeldt-Jakob disease, Romania, amyloid precursor protein.
snip...
Discussion This is, to our knowledge, one of the first reported cases of CJD in Romania. Filip et al described a case of human prion disease (sporadic CJD) in a 64 years old male[4]. Pop et al described a case of sporadic CJD a 47 years old female [5]. In EUROCJD Surveillance Data, Romania is not present [6]. Clinically our patient had initial psychiatric symptoms, with behavioral changes - attempted suicide, dysthymic personality disorders, which were primarily attributed to substance abuse. Neurological signs were identifiable only after the patient became comatose. The cause of death was not directly prion-related – the underlying cause of death was considered acute intoxication with betablockers, alcohol and oral anti-diabetic drugs that lead to coma, finally complicated with pneumonia. Therefore the neurodegenerative disease was most likely at the beginning of its course and, due to the predominance of psychiatric pathology, suggested more likely a clinical diagnose of vCJD [7].
The presence of the protein 14-3-3 in the CSF in not a definite test for CJD (or vCJD). However, it currently has a sensibility of 95% and in our case we excluded other possible causes (tumors, encephalitis, meningitis) [8]. The only false positive reaction for 14-3-3 that was not excluded clinically was cerebral ischemia, which was present in our patient. However, corroborating this result with the neuropathology examination the diagnosis of vCJD was certain.
The histological examination revealed neuronal vacuolar degeneration, frequent, confluent cysts leading to a spongiform appearance and gliosis, without inflammation, and amyloid plaques, a pattern suggestive for sporadic CJD [9, 10].
PrPc is found in normal cells and it suffers a conformation change, turning its 3-D structure from a α-helix into a β-sheet form, which is highly resistant and infective. Regarding its normal function, it may play a role in neuronal development and synaptic plasticity. It is thought it may be required for neuronal myelin sheath maintenance and sometimes it may play a role in iron uptake and iron homeostasis. A certain isoform may act as a growth suppressor by arresting the cell cycle at the G0/G1 phase. Soluble oligomers are toxic to cultured neuroblastoma cells and induce apoptosis in vitro. PrPSc is found in high quantity in the brain of humans and animals infected with neurodegenerative diseases known as transmissible spongiform encephalopathies or prion diseases.
Ubiquitin is a heat shock protein, required for ATP-dependent non-lysosomal intracellular protein degradation, which eliminates most intracellular defective proteins, as well as normal proteins with a rapid turnover.
Degradation involves covalent binding of ubiquitin to the protein to be degraded and it is believed that in this way, ubiquitin acts to label the protein for disposal by intracellular proteases.
The family history of the patient was negative for CJD or other neurodegenerative diseases. Also, the patient did not suffer surgical interventions, treatment with growth hormone or other treatments known to be associated with the transmission of iatrogenic CJD. In a report of the Centers for Disease Control and Prevention from 2005-2006 Romania is presented as one of the countries that were likely to have Bovine Spongiform Encephalopathy [11], which subsequently suggests a risk for vCJD. Also, in the late 1990s there were press articles suggesting illegal import of contaminated cow meat from UK, during the outburst of mad cow disease. Therefore we can speculate that the most probable cause is represented by the use of contaminated cow meat.
Conclusion
This is the first report of vCJD in Romania. However, the absence of other reported cases does not necessarily mean their absence; an increased level of awareness regarding this disease in clinical environments may reveal additional cases.
see full text ;
CREUZFELDT-JAKOB’S DISEASE – CASE REPORT
Z. Cofoian-Amet1, B. Rusu1, C. Mitu1, E. Roşianu1, B.O. Popescu1,2,3 1Department of Neurology, Colentina Clinical Hospital, Bucharest, Romania 2Department of Neurology, Psychiatry, Neurosurgery and Psychiatrics, School of Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania 3Laboratory of Neurosciences and Molecular Medicine, “Victor Babes” National Institute of Pathology, Bucharest, Romania
ABSTRACT
Creutzfeldt-Jakob disease is a low incidence progressive neurodegenerative disorder and, meanwhile, the most frequent human prion disease. We report here the case of a 65 years old female with a 2-month history of rapidly progressive dementia. The clinical examination identifi ed patent cerebellar and extrapyramidal signs. Despite the absence of myoclonic jerks and pathological fi ndings in T2 and FLAIR MRI, the presence of protein 14-3-3 in a signifi cant amount in cerebrospinal fl uid (CSF) was identifi ed. The patient succumbed to the illness within 2 month of hospitalization.
Key words: sporadic Creutzfeldt-Jakob; rapidly progressive dementia, 14-3-3
Creutzfeldt-Jakob Disease
ABSTRACT Creutzfeldt-Jakob disease is the most common human prion pathology. We describe is emblematic of this disease in its form of onset and progression. We have reported the symptoms and the diagnostic possibilities: a 82 years old man accused suddenly confusion, agitation, memory impairment with rapid progression of cognitive decline and psychiatric signs and the appearance of other neurological deficits that led the patient quickly to coma leading to death. The pathological examination clarified the nature of patient's medical and it allowed players to make the diagnosis.
Key words: General practitioner, dementia, Creutzfeldt-Jakob disease
Creutzfeldt-Jakob Hastalığı ÖZET Creutzfeldt-Jakob hastalığı en yaygın insan prion patolojidir. Biz bu olgu sunumunda hastalığın başlangıcı ve ilerlemesini sembolik olarak sunduk. Biz hastanın semptom ve tanısal işlemlerini bildirdik. Bunlar; ani gelişen konfüzyon ile gelen 82 yaşında erkek hasta, ajitasyon , kognitif bozulma ile birlikte hafıza bozukluğu, psikiyatrik belirtiler ve ölüme neden olacak koma ya götürecek nörolojik defisitlerin bulunması. Patolojik inceleme ile hastanın tanısı konuldu. Anahtar kelimeler: Pratisyen hekim, demans, Creutzfeldt-Jakob hastalığı Doctor formed in Medical General Practice, Rome, Italy Received: 08.12.2012, Accepted: 27.11.2013 Correspondence: Valerio Massimo Magro Doctor formed in Medical General Practice, Rome, Italy Correspondence to valerio_magro@hotmail.com Valerio Massimo Magro European Journal of General Medicine
INTRODUCTION
Creutzfeldt-Jakob disease is a rare cause of dementia evolving fatal even more rarely it is observed on the Italian territory. A case related is observed in a General Practitioner’s (GP) study (1). CASE Male patient.
*** He was 82 years old. He emigrated young in a country in Eastern Europe in search of work and then he had lived for a long time in Romania.
snip...see ;
ROMANIA CJD STATISTICS with current CJD surveillance ???
Romania 22 22,355,5512
Creutzfeldt-Jakob Disease in Eastern Europe (Extrapolated Statistics)
Azerbaijan 7 7,868,3852
Belarus 10 10,310,5202
Bulgaria 7 7,517,9732
Estonia 1 1,341,6642
Georgia 4 4,693,8922
Kazakhstan 15 15,143,7042
Latvia 2 2,306,3062
Lithuania 3 3,607,8992
Romania 22 22,355,5512
Russia 143 143,974,0592
Slovakia 5 5,423,5672
Slovenia 2 2,011,473 2
Tajikistan 7 7,011,556 2
Ukraine 47 47,732,0792
Uzbekistan 26 26,410,4162
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THURSDAY, DECEMBER 25, 2014
Bovine spongiform encephalopathy, Romania Confirmed
*** ''Unlike the classical cases of mad cow which are caused when cattle are fed with feeding materials which contain proteins of animal origin,
***the atypical cases occur spontaneously, the causes being currently under investigation.''
LAUGHT OUT LOUD LOL!
atypical BSE has NEVER, EVER, been scientifically proven to occur spontaneously. in fact, evidence points to the same feeding practices that caused typical c-BSE, can cause atypical BSE as well. ...see;
***Trend analysis indicated an ultimate decline to 0 prevalence, suggesting that spontaneous occurrence does not explain the majority of cases.
Is there a decline in bovine spongiform encephalopathy cases born after reinforced feed bans? A modelling study in EU member states
M. E. ARNOLD (a1), R. R. L. SIMONS (a2), J. HOPE (a2), N. GIBBENS (a3) ... DOI: https://doi.org/10.1017/S0950268817001236Published online: 19 June 2017
Summary
Occasional cases of classical bovine spongiform encephalopathy (BSE) still continue to occur within the European Union (EU) for animals born after reinforced feed bans (BARBs), which should in theory have eliminated all risk of infection. The study aimed to determine (i) whether a common rate of decline of BSE infection was evident across EU member states, i.e. to determine whether control measures have been equally effective in all member states, (ii) whether there was any evidence of spontaneous occurrence of BSE in the data and (iii) the expected date for the last BSE case in UK. It was found that there was no significant difference in the rate of decline of BSE prevalence between member states, with a common rate of decline of 33·9% per annum (95% CI 30·9–37%) in successive annual birth cohorts. Trend analysis indicated an ultimate decline to 0 prevalence, suggesting that spontaneous occurrence does not explain the majority of cases. Projecting forward the trends from the back-calculation model indicated that there was approximately a 50% probability of further cases in the UK, and should the current rate of decline continue, there remains the possibility of further occasional cases up until 2026.
Export citation Request permission Copyright COPYRIGHT: © Cambridge University Press 2017
Corresponding author
*Author for correspondence: M. E. Arnold, Animal and Plant Health Agency (APHA), The Elms, College Road, Sutton Bonington, Loughborough, LE12 5RB, UK. (Email: mark.arnold@apha.gsi.gov.uk)
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.***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply on Molecular, Biochemical and Genetic Characteristics of BSE in Canada
Monday, January 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle CDC Volume 23, Number 2—February 2017
***Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
Emerg Infect Dis. 2012 Jan; 18(1): 142–145. doi: 10.3201/eid1801.111092 PMCID: PMC3310119
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
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.
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT
ONE DECADE POST MAD COW FEED BAN OF AUGUST 1997...2007
10,000,000 POUNDS 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.
2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
NEW URL LINK;
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
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, 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
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016 Monthly Report Prion 2016 Tokyo Update
Wednesday, December 21, 2016
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH
Thursday, December 08, 2016
USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie
WEDNESDAY, JUNE 21, 2017
Docket No. FDA– 2009–N–0505 Agency Information Collection Activities; Proposed Collection; Recordkeeping and Reporting Requirements for Human Food and Cosmetics Manufactured From, Processed With, or Otherwise Containing Material From Cattle
CWD in cervid has recently shown that CWD transmits to the Macaque and to the Pig orally.
there is, and has been a major loophole in the USA FDA BSE feed ban.
please see;
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
WEDNESDAY, MAY 17, 2017
SHIC FUNDED STUDY SUGGESTS POTENTIAL FOR PATHOGEN TRANSMISSION VIA FEED
WEDNESDAY, MAY 17, 2017
CWD, TSE, PRION, Cattle, Pigs, Sheep, and Humans aka Mad Cow Disease
Subject: PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
http://creutzfeldt-jakob-disease.blogspot.com/2017/06/prion-2017-p20-descriptive-epidemiology.html
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
FRIDAY, JUNE 16, 2017
P55 Susceptibility of human prion protein to in vitro conversion by chronic wasting disease prions
SATURDAY, JUNE 10, 2017
Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?
MONDAY, JUNE 19, 2017
PRION 2017 P20 Descriptive epidemiology of human prion diseases in Japan: a prospective 16-year surveillance study
Japan Prion Disease Increasing Annually to 2.3 patients per 1 million populations in 2014
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
TUESDAY, JUNE 20, 2017
*** Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease ***
Saturday, June 17, 2017
PRION 2017 P115 α- Synuclein prions from MSA patients exhibit similar transmission properties as PrPSc prions
Saturday, April 23, 2016
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
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, Natalia Fernandez-Borges a. and Alba Marin-Moreno a "Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier. To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant. Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
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.
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
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.
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, ***
*** and there may be asymptomatic individuals infected with the CWD equivalent.
*** These circumstances represent a potential threat to blood, blood products, and plasma supplies.
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
TUESDAY, JUNE 20, 2017
Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease
THURSDAY, JUNE 22, 2017
World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas
THURSDAY, JUNE 22, 2017
Perdue: USDA Halting Import of Fresh Brazilian Beef
WEDNESDAY, JUNE 21, 2017
Docket No. FDA– 2009–N–0505 Agency Information Collection Activities; Proposed Collection; Recordkeeping and Reporting Requirements for Human Food and Cosmetics Manufactured From, Processed With, or Otherwise Containing Material From Cattle
MONDAY, JUNE 19, 2017
Transmissible Spongiform Encephalopathies Advisory Committee June 2017 CJD, BSE, Scrapie, CWD, TSE, Prion?
THURSDAY, JUNE 22, 2017
PRION 2017 CONFERENCE P120 Early preclinical detection of prions in blood of macaques peripherally infected with the variant CJD agent
THURSDAY, JUNE 22, 2017
National Prion Disease Pathology Surveillance Center Cases Examined(1) (May 18, 2017)
Terry S. Singeltary Sr.
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