Brazil Agriculture Ministry Investigating Suspected Case Of Mad Cow Disease
SAO PAULO, Sept 1 (Reuters) – Brazil’s agriculture ministry said on Wednesday it was investigating a suspected case of mad cow disease in the country, according to a statement.
An industry source told Reuters, on condition of anonymity, that the suspected case occurred in the southeastern state of Minas Gerais.
The ministry said such investigations are commonplace, and pledged to announce its findings as soon as the ongoing probe is concluded.
This is the first potential case since May 2019, when Brazil’s government reported the occurrence of an “atypical” mad cow disease case in an animal in Mato Grosso state.
At that time, the ministry said mad cow disease, or bovine spongiform encephalopathy (BSE), had been detected in a 17-year-old cow, adding that no parts of that animal had entered the food chain.
The source said evidence suggested the current case was also atypical, as it appeared to have been detected in an older cow like in 2019.
Reporting by Roberto Samora and Nayara Figueiredo Writing by Ana Mano Editing by Rosalba O’Brien and Sandra Maler
CASOS EEB ATÍPICA NO BRASIL
1º CASO: de corte – 13 anos Ø Sertanópolis – Paraná; animal em decúbito – negahvo para raiva; sem alterações no histopatológico Ø 15.06.2012 – diagnóshco posihvo Imunohistoquímica – LANAGRO-PE – Nota Técnica 159/2012; Ø Animal Health and Veterinary Laboratories Agency (AHVLA), Weybridge, United Kingdom – 06.12.2012 - EEB a*pica do 0po H Vaca 2º CASO: corte 12 anos – abate 19.03.14 – vigilância abate emergência – decúbito esternal – fadiga muscular - Notas Técnicas DSA 42 e 52/2014 Ø Porto Esperidião, Mato Grosso; Ø CaracterísHcas – EEB aIpica do Hpo H Ambos no(ficados para OIE.
CASOS EEB ATÍPICA NO BRASIL
3º CASO – 2019 Vaca de corte Nelore – 17 anos Ø Vigilância abate de emergência – animal caído – coleta em 05.04.2019 Ø Nova Canaã do Norte, Mato Grosso Ø Diagnóshco posihvo ELISA – 13.05.2019 - LFDA-PE; Ø Laboratório da Agência de Inspeção de Alimentos Canadenses (CFIA) Alberta, Canada (Laboratório de Referência da OIE) – posihvo ELISA 31.05.2019 Ø CFIA – Canadá – Western Blot – EEB aIpica do Hpo H
OFFICIAL NOTE
Update on an atypical BSE case verified in Mato Grosso Share: Published 06/03/2019 5:41 PM 1- After examining the notification of the occurrence by the International Organization for Animal Health (OIE), this body determined today (3) the closure of the case without changing the Brazilian health status, which remains an insignificant risk for the disease.
2 - The OIE also informed that there will be no supplementary reports on the case.
3 - In the case of China, the Ministry of Agriculture, Livestock and Supply of Brazil has temporarily suspended the issuance of health certificates until the Chinese authority completes its assessment of the information already transmitted about the episode, thus complying with the provisions of the protocol bilateral agreement signed in 2015.
OFFICIAL NOTE
Occurrence of an atypical case of Bovine Spongiform Encephalopathy in Mato Grosso
Published on 05/31/2019 5:20 PM Updated on 05/31/2019 5:25 PM
The Agricultural Defense Secretariat of the Ministry of Agriculture, Livestock and Supply (Mapa) confirms the occurrence, in Mato Grosso, of an atypical case of Bovine Spongiform Encephalopathy ( BSE ). This disease occurs spontaneously and sporadically and is not related to the ingestion of contaminated food.
It is a beef cow, aged 17 years. All BSE- specific risk material was removed from the animal during emergency slaughter and incinerated at the slaughterhouse. Other animal-derived products were identified, located and preventively seized, with no entry of any product into the human or ruminant food chain. Therefore, there is no risk for the population.
It should be noted that the Ministry of Agriculture and the Institute of Agricultural Defense of Mato Grosso (INDEA/MT) immediately began field investigations, with a ban on the original property. All sanitary risk mitigation actions were completed even before the issuance of the final result by a reference laboratory of the World Organization for Animal Health (OIE). After confirmation, this Friday (31), Brazil officially notified the OIE and importing countries, as provided for by international standards.
According to OIE rules, there will be no change in Brazil's risk classification for the disease, which will continue as a country with an insignificant risk, the best possible for BSE . In more than 20 years of surveillance for the disease, Brazil registered only three cases of atypical BSE and no cases of classic BSE .
INTERNATIONAL MARKET
Brazil returns to export beef to China Sales were suspended since June 3 due to notification of an unusual case of BSE in Mato Grosso Share: Published 06/13/2019 11:04 AM Updated on 06/13/2019 1:08 PM China will resume beef imports from Brazil, which had been suspended since June 3, due to the notification of an atypical case of Bovine Spongiform Encephalopathy ( BSE ), detected in Mato Grosso.
China is the only country, among Brazil's importers, that has a sanitary protocol that requires the temporary suspension of meat imports when an atypical case of BSE is detected . The minister of Agriculture, Livestock and Supply, Tereza Cristina, received the news of the reopening of the Chinese market this morning. The minister reaffirmed that she will continue negotiating a new protocol with the Chinese health authorities.
The disease was found in a 17-year-old beef cow. All BSE- specific risk material was removed from the animal during emergency slaughter and incinerated at the slaughterhouse. Other animal-derived products were identified, located and preventively seized, with no entry of any product into the human or ruminant food chain. Therefore, there was no risk for the population.
TUESDAY, SEPTEMBER 27, 2016 Classical Scrapie Diagnosis in ARR/ARR Sheep in Brazil Acta Scientiae Veterinariae, 2015. 43(Suppl 1): 69.
CASE REPORT Pub. 69
ISSN 1679-9216
1
Received: 4 August 2014 Accepted: 19 December 2014 Published: 6 February 2015
1Programa de Pós-graduação em Ciências Veterinárias (PPGCV), Faculdade de Veterinária (FaVet), Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil. 2Setor de Patologia Veterinária (SPV), Departamento de Patologia Clínica Veterinária (DPCV), FAVET, UFRGS, Porto Alegre, RS, Brazil. 3Departamento de Ciências Morfológicas, Instituto de Ciências Básicas da Saúde (ICBS), UFRGS, Porto Alegre, RS. CORRESPONDENCE: J.S. Leal [julianoob@gmail.com - Tel.: +55 (51) 3308 3631]. Setor de Patologia Veterinária, FAVET, UFRGS. Av. Bento Gonçalves n. 9090, Bairro Agronomia. CEP 91540-000 Porto Alegre, RS, Brazil.
Classical Scrapie Diagnosis in ARR/ARR Sheep in Brazil
Juliano Souza Leal1,2, Caroline Pinto de Andrade2, Gabriel Laizola Frainer Correa2, Gisele Silva Boos2, Matheus Viezzer Bianchi2, Sergio Ceroni da Silva2, Rui Fernando Felix Lopes3 & David Driemeier2
ABSTRACT
Background: Scrapie is a transmissible spongiform encephalopathy (TSE) that affects sheep flocks and goat herds. The transfer of animals or groups of these between sheep farms is associated with increased numbers of infected animals and with the susceptibility or the resistance to natural or classical scrapie form. Although several aspects linked to the etiology of the natural form of this infection remain unclarified, the role of an important genetic control in scrapie incidence has been proposed. Polymorphisms of the PrP gene (prion protein, or simply prion), mainly in codons 136, 154, and 171, have been associated with the risk of scrapie. Case: One animal from a group of 292 sheep was diagnosed positive for scrapie in the municipality of Valparaíso, state of São Paulo, Brazil. The group was part of a flock of 811 free-range, mixed-breed Suffolk sheep of the two genders and ages between 2 and 7 years from different Brazilian regions. Blood was collected for genotyping (for codons 136, 141, 154 and 171), and the third lid and rectal mucosa were sampled for immunohistochemistry (IHC) for scrapie, from all 292 animals of the group. IHC revealed that seven (2.4%) animals were positive for the disease. Collection of samples was repeated for 90 animals, among which the seven individuals diagnosed positive and 83 other animals that had some degree of kinship with those. These 90 sheep were sacrificed and necropsied, when samples of brain (obex), cerebellum, third eyelid, rectal mucosa, mesenteric lymph node, palatine tonsil, and spleen were collected for IHC. The results of IHC analyses carried out after necropsy of the seven positive animals submitted to the second collection of lymphoreticular tissue and of the 83 animals with some degree of kinship with them confirmed the positive diagnosis obtained in the first analysis, and revealed that three other sheep were also positive for scrapie. Samples of 80 animals (89%) were negative for the disease in all organs and tissues analyzed. In turn, 10 sheep (11%) were positive, presenting immunoreactivity in one or more tissues. Genotyping revealed the presence of four of the five alleles of the PrP gene commonly detected in sheep: ARR, ARQ, VRQ and ARH. These allele combinations formed six haplotypes: ARR/ARR, ARR/ARQ, ARH/ARH, ARQ/ARH, ARQ/ARQ and ARQ/VRQ. Animals were classified according to susceptibility to scrapie, when 8.9% of the genotyped sheep were classified into risk group R1 (more resistant, with no restriction to breeding). In turn, 40% of the animals tested ranked in groups R4 and R5 (genetically very susceptible, cannot be used for breeding purposes). Discussion: The susceptibility of sheep flocks depends on the genetic pattern of animals and is determined by the sequence of the gene that codifies protein PrP. Additionally, numerous prion strains are differentiated based on pathological and biochemical characteristics, and may affect animals differently, depending on each individual’s genotype. Most epidemiologic data published to date indicate that animals that carry the ARR/ARR genotype are less susceptible to classical scrapie. However, in the present study, the fact that two scrapie-positive sheep presented the haplotype ARR/ARR indicates that this genotype cannot always be considered an indicator of resistance to the causal agent of the classical manifestation of the disease. The coexistence in the same environment of several crossbred animals from different flocks and farms, which characterizes a new heterogeneous flock, may have promoted a favorable scenario to spread the disease, infecting animals in the most resistant group.
Keywords: biopsy, scrapie, TSEs, immunohistochemistry.
DISCUSSION
The susceptibility of sheep flocks to scrapie depends largely on the genetic pattern of the animal, and is determined mainly by the sequence of the gene that codifies the PrP protein, since there are several polymorphisms that affect the conversion of the cell protein PrPC to its pathological form, PrPSc [8, 9]. Nevertheless, it is not possible to consider the occurrence of only one form of ovine prion, since there are numerous prion strains with different pathological and biochemical characteristics that may affect animals distinctively, depending on their genotypes [1, 30]. In the present study, the frequency of codon VRQ was very low (2.2%), confirming previous findings, which revealed that the alleles ARR and ARQ prevail in Suffolk sheep, and that the allele ARH sometimes is detected [12, 32]. The high sensitivity of homozygous VRQ carriers or of individuals with ARQ haplotypes has also been reported in the literature [24]. This condition raises concerns about susceptibility from the epidemiological perspective, since the allele VRQ, which is rare or absent in breeds like Suffolk, was present in two animals, one of which was positive for scrapie. Most epidemiological and genetic data published indicate that sheep carrying the haplotype ARR/ ARR are less susceptible to classical form, while animals with the haplotype VRQ in homozygosis or with ARQ haplotypes are highly susceptible [24]. This hypothesis is supported by genotyping data for thousands of sheep with the disease around the world. For example, a study carried out in Japan described a classical scrapie case in one ARR/ARR sheep [16]. Sensitivity of ARR/ARR sheep in a scenario of oral exposure to the disease has also been reported [3]. Atypical cases were observed in ARR/ARR animals [11, 42].
Polymorphisms at codon positions 136, 154 and 171 are not the only ones associated with resistance or susceptibility to scrapie [33]. An analysis of the variation of codon positions 136 and 171, for instance, showed that each has several adjacent polymorphic sites and may codify up to four amino acids [7, 50]. The atypical scrapie form, characterized by strain Nor98 [6], is more frequently detected in AHQ animals that carry a polymorphism in codon 141, and has not been described in Suffolk sheep in Brazil [2]. This atypical form expresses phenylalanine (F), instead of leucine (L) in the form L141F [6, 37, 46].
However, although it is generally acceptable that classical scrapie is an infectious and contagious disease [14], contagion with the atypical form is questionable in light of the fact that the specific marker for the atypical manifestation of the disease is detected outside the central nervous system [5, 20, 29], even in cases experimentally transmitted to transgenic mice [35] and sheep [47]. Several studies have demonstrated that susceptibility to the atypical form is consistently associated with PrP codons 141 (L/F) and 154 (R/H) [6, 42]. In fact, studies have proposed the hypothesis that this form may evolve when the animal is not exposed to the infectious agent [5, 18, 29, 48], given the limited knowledge of the physiopathology of this manifestation of the disease [19].
In the present study, two (2/8) positive animals presented the haplotype ARR/ARR, which is considered to be the least susceptible and therefore responsible for the lowest risk of scrapie. However, like all sheep that were genotyped, these animals did not present any change in lysine in codon position 141. This change (that is, when lysine is replaced by phenylalanine) has been associated with atypical scrapie in Suffolk sheep [6]. Therefore, these two ARR/ARR sheep do not fit in the genotypic characteristics of sheep that may commonly present the atypical form. It is possible that the presence of several crossbred animals of different flocks and farms in the same environment, which characterizes an heterogeneous flock, has created the favorable conditions for the disease to evolve and spread, infecting the more susceptible animals.
The variation in the frequency of the PrP genotype between flocks has been identified as a real risk factor for the disease [4]. The introduction of adult sheep free of scrapie in contaminated flocks is believed to allow lateral transmission, even between adult animals with less susceptible genotypes [40, 45], although young sheep are more predisposed [43]. Other reasons behind differences in occurrence include the stress caused during husbandry and large population numbers [26]. Additionally, the lack of a defined epidemiological pattern and the different strains of the causal agent play an important role in inter-flock variability [40]. Several models were based on the assumption that outbreak duration is influenced by flock size and by the frequency of the PrP genotype in one flock [25, 26, 38, 51]. Commercial flocks with high genetic diversity, mainly in codons other than 136, 154 and 171, are more consistently affected. In these animals, the onset of clinical manifestations occurs at significantly different ages, with means varying from 2 to 5.7 years, due to noteworthy dissimilarities in age and PrP genotype profiles [40]. The purchase of infected animals has been pointed out as the main scrapie infection mechanism in flocks [27, 41].
*** The diagnosis of scrapie in two homozygous ARR/ARR sheep indicates that the resistance of this genotype to the classical form of the disease is debatable. Although scrapie in these animals is rare, the cases presented in this case report lend strength to the notion that its occurrence depends on a combination of infectious factors, including differences in biological and biochemical properties in the natural hosts to this prion.
MANUFACTURERS 1VMRD Pullman Albion Road. Pullman, WA, USA. 2Qiagen. Hilden, Germany. 3InvitrogenTM. São Paulo, Brazil. 4Life TechnologiesTM. Gaithersburg, MD, USA. 5InvitrogenTM. Carlsbad, CA, USA. 6Applied Biosystems Inc. Foster City, CA, USA. Declaration of interest. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
Scrapie diagnosis in a goat and four Santa Inês sheep from the same herd in Brazil
J.S. LealG.L.F. CorreaG.S. BoosM.V. BianchiF.M. BoabaidR.F.F. LopesD. Driemeier
Diagnóstico de scrapie em um caprino e quatro ovinos Santa Inês de um mesmo rebanho no Brasil
Scrapie is a fatal and progressive transmissible spongiform encephalopathy (TSE) of natural occurrence in sheep and goats. The suspicion of scrapie may be based on clinical signs; however, the detection of pathological features of the prionic protein (PrP) in target tissues is necessary to diagnose the disease. The presence of an abnormal protein form (PrPSc) in lymphoreticular and nervous tissues is an important characteristic in diagnosis. This paper reports a case of scrapie in a flock of 55 Suffolk crossbred sheep, 19 Santa Inês sheep and 21 goats in the Mato Grosso state, midwestern Brazil. The animals were euthanized after the confirmation of a scrapie case with clinical signs in a Suffolk sheep in the same farm. Samples of brainstem at the level of the obex and lymphoid issues like palatine tonsils, mesenteric lymph nodes, third eyelid fixed in formalin 10% were processed for histological examination. Histological examination with hematoxylin and eosin did not show any microscopic changes in samples. Immunohistochemistry (IHC) examination to detect anti-prion PrPSc was performed in lymphoid tissues. Scrapie diagnosis was confirmed based on IHC positive results for PrPSc in lymphoid tissues of a crossbreed goat and four Santa Inês sheep, without any clinical scrapie signs. IHC showed positive staining in at least three lymphoid germinal centers in goat mesenteric lymph node, palatine tonsil, and third eyelid samples. The mesenteric lymph node, and tonsil samples of all sheep showed positive immunostaining, and only one sheep showed positive staining in lymphoid follicles in the third eyelid. Scrapie diagnosis using IHC in fixed samples of lymphoreticular tissue is technically feasible to detect the disease in both goats and sheep, as a form of pre-clinical diagnosis. The results indicate that the herd was infected by a sheep coming from another herd where scrapie had been diagnosed before.
scrapie; prion; diseases of small ruminants; immunohistochemistry; lymphoid tissues
WEDNESDAY, JUNE 12, 2019
FINAL REPORT OF AN AUDIT CONDUCTED IN BRAZIL MAY 15 TO JUNE 2, 2017 EVALUATING THE FOOD SAFETY SYSTEMS GOVERNING MEAT PRODUCTS EXPORTED TO THE UNITED STATES OF AMERICA
TUESDAY, MARCH 26, 2019
Joint Statement from President Donald J. Trump USA and President Jair Bolsonaro Brazil FOREIGN POLICY BSE TSE Prion aka mad cow disease
SATURDAY, JUNE 01, 2019
Brazil reports another cases of mad cow disease atypical BSE TSE Prion
TUESDAY, SEPTEMBER 27, 2016
Classical Scrapie Diagnosis in ARR/ARR Sheep in Brazil
Acta Scientiae Veterinariae, 2015. 43(Suppl 1): 69.
MONDAY, AUGUST 1, 2016
USDA Announces Reopening of Brazilian Market to U.S. Beef Exports and the Potential for Transmissible Spongiform Encephalopathy TSE prion disease
MONDAY, MAY 5, 2014
Brazil BSE Mad Cow disease confirmed OIE 02/05/2014
Monday, May 5, 2014
Brazil 2nd BSE Mad Cow disease confirmed OIE 02/05/2014
Thursday, April 24, 2014
Brazil investigates possible BSE mad cow case
WEDNESDAY, JANUARY 29, 2014
Another Suspect case of Creutzfeldt-Jakob disease investigated in Brazil
THURSDAY, SEPTEMBER 26, 2013
Brazil evaluate the implementation of health rules on animal by-products and derived products SRM BSE TSE PRION aka MAD COW DISEASE
Wednesday, December 19, 2012
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Brazil
***> Friday, December 07, 2012
***> ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012
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. ...
Owens, Julie From: Terry S. Singeltary Sr. [flounder9@verizon.net] Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006 Greetings FSIS, I would kindly like to comment on the following ;
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018- 0087] Singeltary Submission [Federal Register Volume 84, Number 116 (Monday, June 17, 2019)] [Notices] [Pages 28001-28002] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2019-12654]
-----------------------------------------------------------------------
DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service [Docket No. APHIS-2018-0087] Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy AGENCY: Animal and Plant Health Inspection Service, USDA. ACTION: Notice. -----------------------------------------------------------------------
SUMMARY: We are advising the public of our preliminary concurrence with the World Organization for Animal Health's (OIE) bovine spongiform encephalopathy (BSE) risk designation for Nicaragua. The OIE recognizes this region as being of negligible risk for BSE. We are taking this action based on our review of information supporting the OIE's risk designation for this region.
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
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. ...
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
WEDNESDAY, DECEMBER 2, 2020
EFSA Evaluation of public and animal health risks in case of a delayed post-mortem inspection in ungulates EFSA Panel on Biological Hazards (BIOHAZ) ADOPTED: 21 October 2020
i wonder if a 7 month delay on a suspect BSE case in Texas is too long, on a 48 hour turnaround, asking for a friend???
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 23, 2020
BSE research project final report 2005 to 2008 SE1796 SID5
***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.
https://www.nature.com/articles/srep11573
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***
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***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.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
WEDNESDAY, MARCH 24, 2021
USDA Animal and Plant Health Inspection Service 2020 IMPACT REPORT BSE TSE Prion Testing and Surveillance MIA
MONDAY, JUNE 28, 2021
BSE can propagate in sheep co‑infected or pre‑infected with scrapie
THURSDAY, DECEMBER 31, 2020
Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency
WEDNESDAY, MAY 29, 2019
***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures
USDA HERE'S YOUR SIGN!
TUESDAY, JUNE 8, 2021
***> Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle
***> AS is considered more likely (subjective probability range 50–66%) that AS is a non-contagious, rather than a contagious, disease.
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 COMODITY, 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 $$$
THURSDAY, JULY 8, 2021
EFSA Scientific report on the analysis of the 2‐year compulsory intensified monitoring of atypical scrapie
SATURDAY, AUGUST 16, 2008
Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)
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
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS Regulations Comments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Page 1 of 98
8/3/2006
Greetings FSIS,
I would kindly like to comment on the following ;
MONDAY, NOVEMBER 16, 2015
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission Docket No. APHIS-2007-0127
Scrapie in Sheep and Goats SUMMARY: We are reopening the comment period for our proposed rule that would revise completely the scrapie regulations, which concern the risk groups and categories established for individual animals and for flocks, the use of genetic testing as a means of assigning risk levels to animals, movement restrictions for animals found to be genetically less susceptible or resistant to scrapie, and record keeping requirements. This action will allow interested persons additional time to prepare and submit comments. DATES: The comment period for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is reopened. We will consider all comments that we receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on August 21, 2001, when we published in the Federal Register(66 FR 43964, Docket No. 97-093-5) a final rule amending part 79 by imposing additional restrictions on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set up to fail in the first place. If the world does not go back to the ‘BSE RISK ASSESSMENTS’, enhance, and or change that assessment process to include all TSE prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’ PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ... please see ;
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
see my full Docket Submission here;
JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 April 26,2005
Mr. Terry Singeltary
P.O. Box
Bacliff, Texas 77518
Dear Mr. Singeltary:
In response to your recent request for my assistance, I have contacted the National Institutes of Health. I will write you again as soon as I receive a reply. I appreciate having the opportunity to represent you in the United States Senate and to be of service in this matter.
Sincerely,
JOHN CORNYN United States Senator JC:djl
===============
JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305
May 18,2005
Mr. Terry Singeltary
P.O. Box
Bacliff, Texas 77518
Dear Mr. Singeltary:
Enclosed is the reply I received from the Department of Health and Human Services in response to my earlier inquiry on your behalf. I hope this will be useful to you. I appreciate having the opportunity to represent you in the United States Senate. Thank you for taking time to contact me. Sincerely,
JOHN CORNYN United States Senate JC:djl Enclosure
DEPARTMENT OF HEALTH & HUMAN SERVICES National Institutes of Health National Institute of Neurological Disorders and Stroke NINDS Building 31, Room 8A52 31 Center Dr., MSC 2540 Bethesda, Maryland 20892-2540 Phone: 301-496-9746 Fax: 301-496-0296 Email: [log in to unmask]
May 10, 2005
The Honorable John Cornyn United States Senator Occidental Tower5005 LBJ Freeway, Suite 1150Dallas, Texas 75244-6199
Dear Senator Cornyn:
Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about the preservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by the National Institute of Neurological Disorders and Stroke (NINDS) Intramural Research program for many years. I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand his desire that any tissues that could help investigators unravel the puzzle of this deadly disease are preserved. I hope he will be pleased to learn that all the brains and other tissues with potential to help scientists learn about CJD are, and will continue to be, conserved. (The tissues that are discarded are those that have either decayed to an extent that renders them no longer appropriate for research or those for which we do not have sufficient identification.) The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that end, some of the NINDS-held samples are distributed to investigators who can demonstrate that they have a compelling research or public health need for such materials. For example, samples have been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National Prion Diseases Pathology Surveillance Center at Case Western Reserve University in Ohio and works with the Centers for Disease Control and Prevention to monitor all cases of CJD in the United States. Dr. Gambetti studies the tissues to learn about the formation, physical and chemical properties, and pathogenic mechanisms of prion proteins, which are believed to be involved inthe cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food and Drug Administration, for use in assessing a potential diagnostic test for CJD.
Page 2 - The Honorable John Cornyn
in closing, we know that donating organs and tissue from loved ones is a very difficult and personal choice that must often be made at the most stressful of times. We at the NINDS are grateful to those stalwart family members who make this choice in the selfless hope that it will help others afflicted with CJD. We also know the invaluable contribution such donations make to the advancement of medical science, and we are dedicated to the preservation of all of the tissue samples that can help in our efforts to overcome CJD.
I hope this information is helpful to you in responding to Mr. Singeltary. Sincerely,
Story C. Landis, Ph.D. Director, National Institute of Neurological Disorders and Stroke
snip...see full text;
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally..
Terry S. Singeltary, Sr Bacliff, Tex 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Thursday, July 29, 2021
TSE PRION OCCUPATIONAL EXPOSURE VIA ANIMAL OR HUMAN, iatrogenic transmission, nvCJD or sCJD, what if?
Wednesday, July 28, 2021
France issues moratorium on prion research after fatal brain disease strikes two lab workers
TUESDAY, AUGUST 03, 2021
USA Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined July 9th, 2021
Terry S. Singeltary Sr.
