Friday, June 10, 2011

Board advises on increase in BSE testing age FSA

The Agency has advised Ministers that it would be acceptable to increase the age at which BSE tests are carried out on healthy cattle slaughtered for human consumption.

http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8HPHBS


Food Standards Agency - 10 Jun 2011 15:15

Board advises on increase in BSE testing age

The Agency has advised Ministers that it would be acceptable to increase the age at which BSE tests are carried out on healthy cattle slaughtered for human consumption.

The advice was given following a discussion on proposed changes to BSE testing held at the Board’s open meeting in Belfast on 25 May. The proposal is that the age threshold for healthy cattle slaughtered for human consumption born in the UK and 24 other member states should be increased from 48 to 72 months.

BSE testing requirements for 'risk' cattle (those most likely to test positive for BSE, but not BSE suspects) would remain largely the same and those for BSE suspects (cattle with clinical symptoms of the disease) would not change.

Commenting on the proposed change, FSA director of food safety Alison Gleadle said: 'Numbers of BSE cases have dropped dramatically since the height of the UK's BSE epidemic. In 1992 there were more than 37,000 clinical cases reported. Last year there were just 11 detected via the testing programme – none of which were in cattle slaughtered for human consumption.

'Subject to effective surveillance for BSE continuing to be in place, the Agency believes that increasing the threshold for BSE testing of healthy slaughtered cattle to 72 months would be acceptable on grounds of food safety. The main protection for consumers is through the removal of specified risk material.'

If Ministers agree to proceed with the change, which could take place from 1 July this year, it will be the third major relaxation in BSE controls in the last six years.

In November 2005, the ban on cattle aged over thirty months (OTM) from entering the food chain was replaced with BSE testing of all OTM cattle entering the food chain.

In January 2009, the age threshold at which cattle had to be tested for BSE was increased from 30 months to 48 months.

The latest change would mean that almost all healthy cattle slaughtered for human consumption will not have to be tested until the age of 72 months.

http://www.wired-gov.net/wg/wg-news-1.nsf/lfi/DNWA-8HPHBS


SEAC

POSITION STATEMENT ON THE REQUIREMENTS FOR BSE TESTING OF HEALTHY CATTLE

SEAC was asked by the Food Standards Agency to consider the change in risk to consumers from exposure to BSE that would result if (a) from 2011, the age threshold for BSE testing healthy slaughter cattle was raised from 48 to 72 months and (b) BSE testing of healthy slaughter cattle was to stop altogether.

FSA presented to SEAC an analysis carried out by the Veterinary Laboratories Agency (VLA) assessing the impact of reducing the level of BSE testing of healthy cattle slaughtered for human consumption, using a mathematical model developed at VLA. The model predicts the number of additional infected cattle that would be consumed if monitoring is reduced and estimates the consequent impact on the amount of infectivity entering the food supply.

SEAC advises that in the short-term there is an insignificant additional risk to human health that would result from raising the age for healthy slaughter cattle from 48 to 72 months. The VLA modelling results concur with the low numbers of cattle now being identified with BSE. However, SEAC notes that this conclusion is only valid if the prevalence of BSE in the UK cattle population remains at or decreases from its current value. The current and future validity of this analysis therefore depends critically on the nature and quality of BSE surveillance within the cattle population, and in particular its capacity to ensure the early detection of any re-emerging epidemic. This assessment would equally apply to any proposal to cease altogether the testing of healthy slaughter cattle. SEAC considers that any change in the incidence of BSE is most likely to be detected in fallen stock and casualty animals because of the currently higher likelihood of detecting BSE in these sub-populations. Provided that surveillance of fallen stock and casualty animals is sufficient to provide the necessary information about disease incidence and prevalence, the additional risk to consumers of reducing testing of healthy cattle will remain small.

In addition, SEAC offers the following observations that the FSA and other interested Government Departments might wish to consider:

(a) Surveillance is the only effective means of monitoring changes in the incidence or prevalence of BSE. It is therefore important that current surveillance protocols are kept under review, to ensure that they are capable of detecting an increase in BSE prevalence both in an appropriate time frame and at a suitable sensitivity to detect an

increase in prevalence that would warrant reintroduction of testing healthy slaughtered cattle.

(b) It is not clear that testing a sample of healthy slaughter cattle older than 72 months would provide much useful information: this age group might be sub-optimal. The arguments for random testing of healthy slaughter cattle at this age, compared to other ages, should be considered carefully, taking account of the purpose of this sampling, the sample size and test sensitivity (by incubation period) amongst other considerations.

(c) UK data should continue to be used to demonstrate a decline in the prevalence of BSE in the UK herd, rather than relying on EU-wide figures.

(d) It is instructive to use the VLA model to examine a range of hypothetical rates of increase in BSE infection and the ability of current surveillance measures to detect the change, and this should be repeated as necessary when significant changes to current practices are envisaged.

(e) Changing one BSE control measure can have knock-on effects on other control measures and it is important that the possibility of such interactions is fully taken into account when a proposal such as this is considered.

30 MARCH 2011

http://www.food.gov.uk/multimedia/pdfs/seacstatment.pdf



Related links

BSE

http://www.food.gov.uk/safereating/animaldiseases/bse/



Chair's letters to ministers

http://www.food.gov.uk/multimedia/pdfs/letterstominst.pdf


(pdf 696KB)

Letter from the Chief Medical Officer

http://www.food.gov.uk/multimedia/pdfs/lettermedpfficer.pdf


(pdf 110KB)

Paper considered by SEAC

http://www.food.gov.uk/multimedia/pdfs/paperseac.pdf



(pdf 250KB)

SEAC position statement

http://www.food.gov.uk/multimedia/pdfs/seacstatment.pdf


(pdf 23KB)

END...TSS



Monday, May 12, 2008

BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS

http://bseyoungestage.blogspot.com/


Wednesday, March 31, 2010

Atypical BSE in Cattle

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2


Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

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.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html


Friday, May 13,

2011 EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/efsa-joint-scientific-opinion-on-any.html


Monday, May 23, 2011

Atypical Prion Diseases in Humans and Animals 2011

Top Curr Chem (2011)

DOI: 10.1007/128_2011_161

# Springer-Verlag Berlin Heidelberg 2011

Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar

Abstract

Although prion diseases, such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the "scrapie form" (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.

M.A. Tranulis (*)

Norwegian School of Veterinary Science, Oslo, Norway

e-mail: Michael.Tranulis@nvh.no

S.L. Benestad

Norwegian Veterinary Institute, Oslo, Norway

T. Baron

Agence Nationale de Se´curite´ Sanitaire, ANSES, Lyon, France

H. Kretzschmar

Ludwig-Maximilians University of Munich, Munich, Germany

Keywords Animal Atypical Atypical/Nor98 scrapie BSE-H BSE-L Human Prion disease Prion strain Prion type

http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest


snip...SEE MORE HERE ;

http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html


Thursday, June 2, 2011

USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California

http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html


Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083

Adopted: 1 July 2004

Summary

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm


Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004

http://www.efsa.europa.eu/en/scdocs/doc/3rax1.pdf


Sunday, May 01, 2011

STUDY OF ATYPICAL BSE 2010 Annual Report May 2011

http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html


What is the potential cost of pre- and post-slaughter testing? The estimated cost of post-mortem testing is $40 per head. This amount is comprised almost entirely of the cost of the test kit and sample analysis. It is expected that ante-mortem tests (live animal), if a test is developed, will reduce BSE testing costs to approximately $15 per head.

http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293720&app=70&cat1=211&tp=12&lk=no


Monday, May 23, 2011

CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/cdc-assesses-potential-human-exposure.html


Wednesday, July 28, 2010

Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report

http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html


IBNC

"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."

Saturday, February 28, 2009

NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009

SEAC 102/2

http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html


2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html


Tuesday, April 26, 2011

sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)

http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html


Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html


Tuesday, April 26, 2011

sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)

http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html


something that disturbs me very much, iatrogenic prion TSE exposure and accumulation there from all of the above ???

Tuesday, March 29, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html


TSS