Monday, May 5, 2014

Brazil BSE Mad Cow disease confirmed OIE 02/05/2014

 

 

 From: Terry S. Singeltary Sr.

 

Sent: Monday, May 05, 2014 11:54 AM

 

To: BSE-L BSE-L

 

Cc: CJD-L ; CJDVOICE CJDVOICE ; bloodcjd bloodcjd

 

Subject: Brazil BSE Mad Cow disease confirmed OIE 02/05/2014

 

Bovine spongiform encephalopathy, Brazil

 

Information received on 02/05/2014 from Dr Figueiredo Marques Guilherme Henrique , Director, Departamento de Saúde Animal , Ministério da Agricultura, Pecuaria e Abastecimento , Brasilia, Brazil

 

Summary

 

Report type Immediate notification

 

Date of start of the event 19/03/2014

 

Date of pre-confirmation of the event 14/04/2014

 

Report date 02/05/2014

 

Date submitted to OIE 02/05/2014

 

Reason for notification Reoccurrence of a listed disease

 

Date of previous occurrence 19/12/2010

 

Manifestation of disease Sub-clinical infection

 

Causal agent Prion

 

Nature of diagnosis Laboratory (advanced)

 

This event pertains to the whole country

 

 New outbreaks (1)

 

 

 

Outbreak 1 Porto Esperidião, MATO GROSSO

 

Date of start of the outbreak 19/03/2014

 

Outbreak status Resolved (01/05/2014)

 

Epidemiological unit Farm

 

Affected animals

 

Species Susceptible Cases Deaths Destroyed Slaughtered

 

Cattle 1177 1 0 50 0

 

Buffaloes 11 0 0 0 0

 

Affected population A 12-year-old female bovine tested during emergency slaughter at the slaughterhouse. The animal was born and raised on a full-cycle beef farm on extensive grazing, with a population of 1,177 cattle and 11 buffaloes.

 

 Summary of outbreaks Total outbreaks: 1

 

Total animals affected

 

Species Susceptible Cases Deaths Destroyed Slaughtered

 

Cattle 1177 1 0 50 0

 

Buffaloes 11 0 0 0 0

 

Outbreak statistics

 

Species Apparent morbidity rate Apparent mortality rate Apparent case fatality rate Proportion susceptible animals lost*

 

Cattle 0.08% 0.00% 0.00% 4.25%

 

Buffaloes 0.00% 0.00% - 0.00%

 

*Removed from the susceptible population through death, destruction and/or slaughter

 

Epidemiology

 

Source of the outbreak(s) or origin of infection •Unknown or inconclusive

 

Epidemiological comments As part of the Brazilian surveillance system for Bovine Spongiform Encephalopathy (BSE), the prion marker was identified on 14 April 2014 in a 12-year-old female bovine sent for emergency slaughter because she was found fallen at her arrival at the slaughterhouse following some problems during transport. The animal was born and raised in the same full-cycle beef farm on extensive grazing. Meat and other products from this animal did not enter the food chain and there was no risk for human population. Tracing back animal movements since 2000, it was established that some animals from the birth cohort of this animal had been moved to 10 other properties in 3 municipalities in the state of Mato Grosso. During the epidemiological investigation, 49 animals from the cohort, which did not show clinical signs of the disease, were destroyed. Samples of nervous tissue were taken from the cohort animals and tested for BSE at the National Laboratory and all were negative on 1 May 2014. All control measures according to the OIE Terrestrial Animal Health Code have already been applied in order to close the outbreak and only the results of the typing tests carried out at the Reference Laboratory at Weybridge (United Kingdom) are pending.

 

Control measures

 

Measures applied •Quarantine •Screening •Modified stamping out •No vaccination •No treatment of affected animals

 

Measures to be applied •No other measures

 

Diagnostic test results

 

Laboratory name and type Species Test Test date Result

 

National Agricultural Laboratory (LANAGRO/PE) (National laboratory) Cattle immunohistochemical test 14/04/2014 Positive

 

National Agricultural Laboratory (LANAGRO/PE) (National laboratory) Cattle immunohistochemical test 01/05/2014 Negative

 

Animal Health and Veterinary Laboratories Agency (AHVLA), Weybridge, United Kingdom (OIE’s Reference Laboratory) Cattle immunohistochemical test 01/05/2014 Positive

 

Future Reporting

 

The event is continuing. Weekly follow-up reports will be submitted.

 

 Map of outbreak locations

 


 

 

>>>Atypical BSE, or “mad cow” disease, is a form of the prion disease not associated with the animal’s consumption of feed.<<<

 

 

don't you just love it when the officials just make stuff up $$$

 

 

*** What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”

 

 

 The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”

 

 


 

 

The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSE infected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.

 

 

 In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.

 

 


 

 

 

 *** 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. ***

 

 

 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. ***

 

 

 see page 176 of 201 pages...tss

 

 


 

 

 Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

 

 P.4.23

 

 

 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)

 


 

 

 UPDATE

 

 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 ;

 

 .....snip

 

 ''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 END...TSS

 

 

 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.

 


 


 

 

 please see below from PRION2013 ;

 

 

 *** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.

 

 AD.56: The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice

 

 Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health; Tsukuba, Japan

 

 H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE, and has been detected in several European countries, and North America. Transmission studies of H-type BSE led to the emergence of the classical BSE (C-BSE) phenotypes during passages in inbred wild type and bovinized PrP-overexpressing transgenic mice. In this study, we conducted serial passages of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice (TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage were constant (~= 220 d), no clear differences were observed in their biological and biochemical properties. However, at the forth passage, 2 different BSE phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the other is longer survival times. TgBoPrP mice with longer incubation period showed the H-type phenotype of PrPsc profile and pathology. However, those of shorter incubation period were different phenotypes from previously existed BSE prions (C-BSE, L-type BSE, and H-type BSE).

 

 *** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.

 


 

 www.landesbioscience.com

 

 please see ;

 

 Thursday, August 15, 2013

 

 The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice

 


 

 

 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: maf12@cam.ac.uk 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, 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)

 


 

 

 Sunday, December 15, 2013

 

 FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

 

 kind regards, terry

 

 

UPDATE SEE R-CALF CONCERNS

 

 Brazil's Second Reported BSE Case Raises Food Safety Concerns

 

 Billings, Mont. - On Monday the World Organization for Animal Health (OIE) provided notice that Brazil confirmed its second case of bovine spongiform encephalopathy (BSE), this time in a 12-year-old Brazilian cow. While the notice states that none of the meat or other products from the infected cow entered the food chain, a recent audit report by the U.S. Department of Agriculture (USDA) reveals that Brazil has not been complying with BSE safeguard measures required by the United States.

 

 A recent audit report

 


 

 

 by the USDA Food Safety and Inspection Service (FSIS) sent to the Brazilian government on April 16, 2014, reveals that Brazil has not been consistently implementing the United States' mandatory requirement that all specified risk materials (SRMs) from cattle be excluded from the human food chain as a condition for allowing Brazil to export beef to the United States.

 

 Specifically, the audit found that beginning in early 2007, the Brazilian government relaxed its SRM removal policies by issuing a notice that removed the skull, trigeminal ganglia, vertebral column, and dorsal root ganglia in cattle 30 months of age or older from the list of SRMs that must be removed at slaughter. The tissues improperly removed from the list of SRMs by the Brazilian government are tissues known to harbor the BSE agent in infected cattle.

 

 United States food safety inspectors confirmed that Brazil was not routinely removing all high-risk tissues as required for countries that export to the United States.

 

 Despite Brazil's failure to meet U.S. food safety standards, FSIS officials nevertheless determined that Brazil "continues to meet FSIS equivalence criteria at an adequate level for this component (the SRM removal component)."

 

 R-CALF USA CEO Bill Bullard said these facts demonstrate the need to fully enforce the U.S. country-of-origin labeling (COOL) law. "Only with COOL can consumers choose to avoid purchasing their food from countries with questionable food safety systems," he said.

 

 Bullard also said these facts along with USDA's current plan to begin importing beef from Brazilian states that are not free of foot-and-mouth disease (FMD) is deeply troubling.

 

 "More and more the USDA is demonstrating its unwillingness to prioritize food safety and animal health above its politically motivated trade relations goals," he concluded.

 

 # # #

 

 R-CALF USA (Ranchers-Cattlemen Action Legal Fund, United Stockgrowers of America) is the largest producer-only cattle trade association in the United States. It is a national, nonprofit organization dedicated to ensuring the continued profitability and viability of the U.S. cattle industry. For more information, visit www.r-calfusa.com or, call 406-252-2516.

 

 

Thursday, April 24, 2014

 

Brazil investigates possible BSE mad cow case

 


 

 

Thursday, September 26, 2013

 

Brazil evaluate the implementation of health rules on animal by-products and derived products SRM BST TSE PRION aka MAD COW DISEASE

 


 

 

Friday, December 07, 2012

 

ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012

 


 

 

Wednesday, December 19, 2012

 

Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Brazil

 


 

 

 

 

TSS

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