BOVINE SPONGIFORM ENCEPHALOPATHY BSE CJD TSE PRION DISEASE UPDATE CANADA 2012
Updated monthly. Last updated 2012-03-31
No validated live animal test for BSE currently exists. Accordingly, testing for BSE can only be done on the brains of dead animals. Brain samples are screened using rapid tests that accurately and quickly detect a BSE positive sample nearly 100% of the time. Rapid tests can, in rare cases, react when a sample is not infected with BSE. These are known as "inconclusive" results. All samples that yield inconclusive results using a rapid test are sent to the CFIA laboratory in Lethbridge, Alberta for confirmatory testing.
|Month||Samples Collected||Samples Pending||Negative||Positive|
|Month||Samples Collected||Samples Pending||Negative||Positive|
|Year to date||33458||0||33457||1|
Previously published reports are available in archives maintained by Library and Archives Canada.
Reports for results from 2008 to 2010
"Samples collected" indicates the number of samples submitted or being submitted to provincial or federal laboratories. Each sample represents one animal. Monthly values represent only the number of samples obtained in that month. "Year to date" values represent cumulative samples.
In January 2004, the Government of Canada announced that it would enhance its BSE surveillance testing to at least 8,000 cattle during the first year and to 30,000 per year in subsequent years to calculate the prevalence of BSE in Canadian adult cattle. The level and design of this enhanced program continues to be in full accordance with the guidelines recommended by the OIE.
BSE surveillance samples come from a variety of sources, including the farm, federal, provincial and territorial abattoirs, rendering and deadstock operations, veterinary practitioners, and university and provincial veterinary diagnostic laboratories.
Pending samples are those for which final results are unavailable. This may be because they have yet to be tested, or testing is ongoing. Monthly values represent only the number of samples pending in that month. "Year to date" values represent cumulative pending samples.
Negative samples have been determined negative based on screening results or confirmatory testing. Monthly values represent only the number of samples testing negative in that month. "Year to date" values represent cumulative negative samples.
Positive samples are those that have been confirmed as positive by immunohistochemistry (IHC), or in the case of poor quality samples and IHC negative suspect tests, the SAP immunoblot, both internationally recognized confirmatory tests for BSE. Monthly values represent only the number of samples testing positive in that month. "Year to date" values represent cumulative positive samples.
About this time next month, nine years will have passed since the May 2003 detection of BSE in Canada. Although the numbers continue to decline in terms of detected cases, both in Canada and globally, it will be a few more years before Canada can fully demonstrate the full effectiveness of the control measures in place to eradicate the disease from the national herd.
Dr. Brian Evans, Chief Veterinary officer for Canada, said the BSE surveillance program is the most critical means for Canada to demonstrate just how effective the control measures in place, particularly the feed ban, have been. He is reminding producers that the surveillance program helps Canada to meet the commitments it made to its trading partners as part of the recovery of markets post-BSE.
"While the economic prospects for the sector are looking reasonably good at this point in time, we did make collective commitments on behalf of the industry and government to trading partners in the negotiations that have got us the level of market recovery that we currently have," said Dr. Evans. "We recognize the past nine years have not been easy for producers but if we are to stay the course for a period longer we can achieve what we collectively set out to do."
The stewardship and strong support of producers to date has been an important element in sustaining consumer trust in Canada and noted repeatedly by regulatory officials in other countries in their decision making to restore market access, he said.
During the month of March, a total of 2,593 surveillance samples were tested for BSE, compared with 4,199 samples a year earlier. During the three months between January 1 and March 31, 2012, a total of 7,718 surveillance samples were tested, compared with 10,869 samples last year. About 30,000 samples are required per year, in accordance with World Organization for Animal Health (OIE) guidelines. The surveillance targets have been adjusted to take into account the reduced size of the national herd and changes in the overall age of the herd.
Dr. Evans said Canada is in its fifth year of the enhanced feed ban, and is just at the mean average incubation period. The real proof will come in the next two to three years, he said, and that's what the CFIA is focussing on.
"If we can sustain this effort through to 2015 we should be in a very good position at the international level to adjust our surveillance activities accordingly on the recognition that we've done our due diligence and that the measures we've demonstrated scientifically are effective measures, and then we can then make further programming adjustments as part of the BSE roadmap forward," he said.
Last year, there were a total of 29 BSE cases globally in countries that test for it, and a 50 per cent decrease in cases every year over the last four or five years.
While producers may see that as a signal to finally put BSE behind them, Dr. Evans said continued vigilance at home is still required, given the fact that we have restored markets for beef products and live animals.
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
BSE Cases Identified in Canadian-born Cattle
As of March 2011, 19 BSE cases in Canadian-born cattle have been identified, 18 in Canada and 1 in the U.S. Of these 19 cases, 13 were known to have been born after the implementation of the 1997 Canadian feed ban ; 12 of these 13 were born after March 1, 1999. (See Figure above: BSE Cases in North America, by Year and Country of Death, 1993-03/2011). This latter date is particularly relevant to the U.S. because since a USDA rule went into effect on November 19, 2007, Canadian cattle born on or after March 1, 1999 have been legally imported into this country for any use. One of the 19 Canadian-born BSE cases was reported in an animal that was most likely born before or possibly very shortly after implementation of the 1997 feed ban. Based on the known or most likely year of birth, an average of 1.4 cases of BSE occurred among the group of animals born each year in Canada from 1991 through 2004. The highest reported number of cases by birth year in a single year, 3 BSE cases, occurred in 2000, 2001 and 2002. The most recently reported case extends the period of BSE transmission in Canada through at least the latter half of 2004.
Strains of BSE
There is increasing evidence that there are different strains of BSE: the typical BSE strain responsible for the outbreak in the United Kingdom and two atypical strains (H and L strains).
Typical BSE strain -- The BSE strain responsible for most of the BSE cases in Canada is the same classic or typical strain linked to the outbreak in the United Kingdom. It is known to be preventable through elimination of BSE contaminated feed and has been causally linked to vCJD in humans. This typical strain has not yet been identified in any U.S.-born cattle.
Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease
Both of the U.S.-born BSE cases and two of the 19 Canadian-born BSE cases were 10 years of age or older. Of these older North American cases, 3 were linked to an atypical BSE strain known as the H-type. The strain type for the fourth older North American case, a 13 year-old BSE-infected Canadian cow, has been identified as the L-type.
Molecular, Biochemical and Genetic Characteristics of BSE in Canada
Sandor Dudas1, Jianmin Yang1,2,3, Catherine Graham1, Markus Czub4, Tim A. McAllister2, Michael B. Coulthart5, Stefanie Czub1* 1 Canadian and OIE Reference Laboratories for BSE, Canadian Food Inspection Agency Lethbridge Laboratory, Lethbridge, Alberta, Canada, 2 Agriculture and Agri-Food Canada Research Centre, Lethbridge, Alberta, Canada, 3 College of Veterinary Medicine, China Agricultural University, Beijing, China, 4 Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada, 5 Canadian Creutzfeldt-Jakob Disease Surveillance System, Public Health Agency of Canada, Winnipeg, Manitoba, Canada
The epidemiology and possibly the etiology of bovine spongiform encephalopathy (BSE) have recently been recognized to be heterogeneous. In particular, three types [classical (C) and two atypical (H, L)] have been identified, largely on the basis of characteristics of the proteinase K (PK)-resistant core of the misfolded prion protein associated with the disease (PrPres). The present study was conducted to characterize the 17 Canadian BSE cases which occurred prior to November 2009 based on the molecular and biochemical properties of their PrPres, including immunoreactivity, molecular weight, glycoform profile and relative PK sensitivity. Two cases exhibited molecular weight and glycoform profiles similar to those of previously reported atypical cases, one corresponding to H-type BSE (case 6) and the other to L-type BSE (case 11). All other cases were classified as C-type. PK digestion under mild and stringent conditions revealed a reduced protease resistance in both of these cases compared to the C-type cases. With Western immunoblotting, N-terminal-specific antibodies bound to PrPres from case 6 but not to that from case 11 or C-type cases. C-terminal-specific antibodies revealed a shift in the glycoform profile and detected a fourth protein fragment in case 6, indicative of two PrPres subpopulations in H-type BSE. No mutations suggesting a genetic etiology were found in any of the 17 animals by sequencing the full PrP-coding sequence in exon 3 of the PRNP gene. Thus, each of the three known BSE types have been confirmed in Canadian cattle and show molecular characteristics highly similar to those of classical and atypical BSE cases described from Europe, Japan and the USA. The occurrence of atypical cases of BSE in countries such as Canada with low BSE prevalence and transmission risk argues for the occurrence of sporadic forms of BSE worldwide. Citation: Dudas S, Yang J, Graham C, Czub M, McAllister TA, et al. (2010) Molecular, Biochemical and Genetic Characteristics of BSE in Canada. PLoS ONE 5(5): e10638. doi:10.1371/journal.pone.0010638 Editor: Carles Lalueza-Fox, Institute of Evolutionary Biology (CSIC-UPF), Spain Received February 9, 2010; Accepted April 21, 2010; Published May 14, 2010 Copyright: 2010 Dudas et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: Funding for this project was provided by the Canadian Food Inspection Agency. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. * E-mail: email@example.com
The origin of atypical BSE is unknown, but sporadic, infectious and genetic mechanisms have all been suggested. Several groups have argued that these cases may represent the existence of a sporadic prion disease in bovines, perhaps similar in etiology to sporadic Creutzfeldt-Jakob disease in humans , , , . Experimental infection of cattle with an isolate of naturally occurring British sheep scrapie resulted in differences in the PrPres electrophoretic profiles compared to classical C-type BSE which led to the suggestion that atypical BSE may be a result of transmission of a prion disease from a different natural host into cattle . In addition, an American H-type BSE case with a mutation (E211K) in the PRNP gene has been reported . This represents the first case of BSE with a potentially pathogenic mutation within the bovine PRNP gene, and experiments are underway to determine the potential importance of this mutation in the development of prion disease in cattle . We did not observe such mutations in the Canadian BSE cases analyzed as of November 2009, and negative results of a large population survey in US cattle strongly suggest that the E211K allele is not common in North American cattle . However, the intrinsically recurrent nature of genetic mutation, as shown particularly for the homologous E200K mutation known to cause genetic Creutzfeldt-Jakob disease in humans , means that the possibility that a small subpopulation of cattle that carry such mutations exist cannot be eliminated.
Our results indicate that the range of molecular characteristics of misfolded PrP in Canadian BSE cases is very similar to that observed in other countries and suggests a number of criteria to use when typing BSE cases (Table 6). It is also interesting that the Canadian atypical BSE cases match so well with cases from other countries in terms of their epidemiological profiles, including detection in older animals and no definitive cause of disease. Ongoing inoculation studies with Canadian BSE types in cattle and transgenic mice will provide clarification on how similar these isolates are after transmission using defined and controlled experimental inoculations. These studies should help to answer some of the many outstanding questions about atypical BSE and aid in policy development to reduce the risk of atypical BSE transmission to animals and humans.
PLEASE NOTE, spontaneous TSE prion disease has never, ever, been proven in natural field cases of BSE TSE prion disease. ...TSS
bbbut, what about FEED AND ATYPICAL BSE ???
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice.
The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
Tuesday, July 14, 2009 U.S.
Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book
Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: firstname.lastname@example.org Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
P.9.21 Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis. Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
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.
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU
Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
October 2009 O.11.3 Infectivity in skeletal muscle of BASE-infected cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.
Sunday, February 5, 2012
February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE
IMPORT EXPORT BEEF, LIVE, PRODUCTS, CANADA AND USA
Tuesday, January 17, 2012
Canadian Inspectors criticize plan to cut inspections at meat plants Meat inspectors' union warns of cuts to government's food-safety program
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
Thursday, August 12, 2010
Seven main threats for the future linked to prions
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
Thursday, February 23, 2012
Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012
Wednesday, April 4, 2012
20120402 - Breach of quarantine/Violation de la mise en quarantaine of an ongoing Scrapie investigation
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
Wednesday, February 16, 2011
SCRAPIE TRANSMISSION TO CHIMPANZEES
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
WHICH CAME FIRST, THE CART OR THE HORSE ???
CAPTIVE CWD CONFIRMED 2002
FREE RANGING CWD CONFIRMED 2011
Captive CWD discovered 1967
Free ranging CWD discovered 1981
PLEASE STUDY THIS MAP !
SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).
Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD. Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation. Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified, ...
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*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
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Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Thursday, January 26, 2012
The Risk of Prion Zoonoses
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167
Thursday, January 26, 2012
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659
Monday, April 23, 2012
CREUTZFELDT JAKOB DISEASE CJD HUMAN TSE CANADA UPDATE 2012
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas