Tuesday, March 5, 2013

FSA notified of BSE control breaches again and again 5 March 2013

Last updated on 5 March 2013




FSA notified of BSE control breaches




The FSA has been notified of a series of BSE control breaches that took place last year. The risk to human health is very low as it is very unlikely that any of the animals would have been infected.



Goats from slaughterhouse in Belgium On 5 July 2012, during a routine inspection at London Central Markets (Smithfield), a goat carcass with spleen attached was discovered. Goat spleen is specified risk material (SRM) and must be removed at the slaughterhouse. SRM consists of the the parts of the animal most likely to carry BSE infection.



The goat was in a consignment of 41 goat and kid carcasses slaughtered at Profoods bvba, a slaughterhouse in Antwerp, Belgium. There were also a significant number of hygiene issues with the consignment. All of the carcasses were detained and none of the meat entered the food supply. There was no public health risk resulting from this incident.



Consignments of beef from a Belgian abattoir On 1 October 2012, the Agency was informed by the Belgian authorities that consignments of beef that may have contained meat from six cattle over 72 months of age, which were not tested for BSE, had been exported to the UK. At the time it was mandatory for all cattle slaughtered for human consumption and aged over 72 months to have a negative BSE test result.



The untested cattle were slaughtered at Slachtgroep Leieland (BE185), an abattoir in Harelbeke, Belgium. Meat from the consignments associated with the untested animals was sent to three businesses in the UK. Investigations revealed that most had already been sold to the final consumer and been eaten, but 11 pallets of meat were traced to a UK coldstore and subsequently destroyed.



It is very unlikely that any of the untested animals would have been infected with BSE. Belgium has not reported a case since 2006. In addition the SRM had been removed so any risk to human health is extremely low.



Breaches in UK-produced meat SRM On 7 December 2012, during a routine inspection by Food Standards Agency staff at Simply Halal (Banham) Ltd, a combined slaughterhouse and cutting premises in Norfolk, it was discovered that 25 beef quarters had left the premises without the vertebral column being removed.



Simply Halal sold the quarters to a meat wholesaler. The wholesaler's records were incomplete and as a result it was only possible to trace and detain one of the quarters. This was destroyed. It is probable that meat from all the other quarters was consumed.



The quarters were from cattle over 30 months of age. The vertebral column of cattle over 30 months is specified risk material (SRM) and must be removed. The risk from the meat that entered the food chain is very low, as it is extremely unlikely that any of the animals involved had BSE. Only three cases of BSE were recorded in the UK in 2012. None of these animals entered the food chain.



BSE testing Meat from a cow over 72 months of age entered the food chain without being tested for BSE.



The animal, aged 73 months and 4 days, was slaughtered on 11 October 2012, at Woolley Bros (Wholesale Meats) Ltd, a combined abattoir and cutting plant in Sheffield. The error was discovered on 4 December 2012 during routine cross-checks of slaughter and BSE testing data.



According to regulations any cattle that have not been tested, along with the animal slaughtered immediately before it and the two immediately after should not enter the food supply.



The four affected carcasses were sold as part of consignment of 90 beef sides to a food business operator in the Netherlands. In addition, cheek meat from the same batch of animals was sold to a business in Germany. No meat from the animals entered the UK food supply and the Agency notified the Dutch and German authorities of the breach of controls and that meat from the affected animals had entered their countries.



It should be noted that since 1 March 2013 there is no longer a requirement to test healthy slaughtered cattle over 72 months of age for BSE before they enter the food supply.
















Thursday, January 17, 2013


FSA notified of two breaches of BSE testing regulations 14 January 2013













EURO QUALITY RECALLS ITS LAMBS' BRAINS



Euro Quality Lambs Ltd is recalling its lambs’ brains, which have entered the food chain without being inspected properly. The Food Standards Agency is asking all local authority enforcement officers to ensure that the product is withdrawn from sale and destroyed. The Agency has issued a Food Alert for Action.










sheep, brains, cow brains, lamb brains, did they make sure this time ???





see the potential for Scrapie transmission to man, see studies here ;






Thursday, January 17, 2013


FSA notified of two breaches of BSE testing regulations 14 January 2013











BREACHES OF BSE CONTROLS IN CONSIGNMENTS OF BEEF


Due to an oversight, four breaches of BSE controls in British beef identified last year were not publicised immediately on the Agency’s website in the normal manner.












COW AGED OVER 72 MONTHS ENTERS FOOD SUPPLY WITHOUT BEING TESTED FOR BSE


The Agency has been notified that meat has entered the food supply from a cow aged over 72 months that had not been tested for BSE. A negative BSE test result is mandatory for cattle slaughtered for human consumption at over 72 months of age.













UNTESTED COW ENTERS THE FOOD SUPPLY


The Agency has been notified that meat from a cow that did not have the required BSE test has entered the food supply. The 62 month old cow had been slaughtered on farm for welfare reasons.











Monday, November 14, 2011


Bullock aged over 72 months enters food supply without being tested for BSE











Monday, February 18, 2013


EU Reauthorisation of non-ruminant processed animal proteins for fish feed and welcomes the likely potential for more TSE prion disease











Friday, November 30, 2012


PROPOSED DECISION TO STOP BSE TESTING OF HEALTHY CATTLE SLAUGHTERED FOR HUMAN CONSUMPTION FSA 12/12/04 Open Board – 11 December 2012











ANY RELAXING OF ANY BSE TESTING RULES WOULD NOT BE BASED ON SOUND SCIENCE, BUT BASED ON INDUSTRY LED SCIENCE AND MONEY $$$




we now know that indeed atypical BSE is transmissible to cattle and other species, and atypical BSE have been documented in older cattle to date. so relaxing any BSE testing on older cattle would be a huge step backwards, and could risk everything that has been done over the past 27 years to try and eradicate BSE. ...





TSS








Wednesday, February 20, 2013


World Organization for Animal Health Recommends United States' BSE Risk Status Be Upgraded


Statement from Agriculture Secretary Tom Vilsack:













Thursday, February 14, 2013


The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease












Monday, February 11, 2013


APHIS USDA Letter to Stakeholders: Trade Accomplishments and failures (BSE, SCRAPIE, TSE, PRION, AKA MAD COW TYPE DISEASE)











Friday, November 23, 2012


sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA










Monday, January 14, 2013


Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe











Thursday, February 21, 2013


National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013












Sunday, February 10, 2013


Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection report/CJD











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...










EFSA Journal 2011 The European Response to BSE: A Success Story




This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;




Monday, October 10, 2011




EFSA Journal 2011 The European Response to BSE: A Success Story




snip...


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.




snip...













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, February 28, 2013

Revision of the Norwegian annual monitoring programme for BSE

EFSA Journal 2013;11(2):3119 [46 pp.]. doi:10.2903/j.efsa.2013.3119
 
European Food Safety AuthorityAcknowledgment Contact
 
Type: Scientific Report of EFSA On request from: European Free Trade Association (EFTA) Surveillance Authority Question number: EFSA-Q-2012-00577 Approved: 20 February 2013 Published: 25 February 2013 Affiliation: European Food Safety Authority (EFSA) Parma Italy
 
Article(1.7 Mb)
 
Abstract
 
This Scientific Report of EFSA provides scientific and technical assistance to the European Free Trade Association (EFTA) Surveillance Authority in evaluating i) if the Norwegian continuous use of fishmeal in feed for ruminants until 30 April 2010 has had an impact on the overall risk of BSE in the country; and ii) if a proposed Norwegian revised annual monitoring programme for BSE allows the detection of BSE with a yearly design prevalence of at least one case per 100,000 in the adult population at a confidence level of 95%. Data related to the implementation of the Norwegian feed ban were collected and assessed. The Cattle TSE Monitoring Model (C-TSEMM) was used in order to answer the second term of reference of the mandate received. It is concluded that the use of fishmeal in feed for ruminants might have had a potential impact on the risk of cattle exposure to BSE in Norway. While it is not possible to quantitatively assess this risk, the lack of detection of BSE cases by the Norwegian monitoring system (in spite of its sensitivity limits) suggests that BSE has not significantly spread in the Norwegian cattle population. The proposed revised Norwegian BSE monitoring regime would not be able to meet a yearly design prevalence of at least one case per 100,000 in the adult cattle population at a confidence level of 95%. Moreover, in statistical terms it is not feasible for Norway to achieve the requested design prevalence. It is furthermore highlighted that passing from a sample-based to an exhaustive monitoring scheme (i.e. testing all animals over a certain age that are slaughtered or dead) would provide the most sensitive BSE surveillance system currently possible.
 
© European Food Safety Authority, 2013
 
 
 
Summary
 
Following a request from the European Free Trade Association (EFTA) Surveillance Authority, the European Food Safety Authority (EFSA) was asked to provide scientific and technical assistance on a revision of the Norwegian annual monitoring programme for Bovine Spongiform Encephalopathy (BSE). The current Norwegian monitoring programme for BSE is based on a specific adaptation of the Agreement on the European Economic Area (EEA) to Regulation (EC) No 999/2001, allowing Norway to test a random sample of 10,000 healthy slaughtered cattle over 30 months of age per year. The Norwegian legislation is currently in line with the European Union’s (EU)5 one as regards to the feedban. However, the use of fishmeal for ruminants was legally allowed in Norway until 30 April 2010. Within this context, and taking into consideration the animal age limits set in Commission Decision 2009/719/EC (72 and 48 months of age, respectively, for healthy slaughtered and at risk animals), Norway requested to the EFTA Surveillance Authority the agreement for a revised annual monitoring programme for BSE prescribing i) the testing of a random sample of 2,000 healthy slaughtered cattle over 72 months of age per year, ii) the testing of all at-risk cattle above 48 months of age and iii) the mandatory notification and examination of any animal clinically suspected of being infected by a TSE. EFTA Surveillance Authority asked EFSA: i) to undertake an assessment of whether Norway’s continuous use of fishmeal in feed for ruminants until 30 April 2010 has had an impact on the overall risk of BSE in the country; and ii) to evaluate whether the design of the proposed annual regime of 2,000 randomly selected samples in the subpopulation of healthy slaughtered animals over 72 months of age allows the detection of BSE with a yearly design prevalence of at least one case per 100,000 in the adult population at a confidence level of 95% in Norway. In case Norway’s proposed regime would fail meeting this criterion, EFSA was requested to propose a minimum annual sample size in the subpopulation of healthy slaughtered animals over 72 months of age allowing to reach the proposed criterion. Data related to the implementation of the Norwegian feed ban were collected and assessed. In Norway the only way by which fishmeal could have represented a risk for BSE infection in ruminants was due to the potential cross-contamination with infected Meat and Bone Meal (MBM). The monitoring of ruminant feed and fishmeal for the presence of MBM in Norway did not give rise to positive results. However, considering the number of tests and the total amount of terrestrial animal feed and fishmeal produced and used in Norway the significance of these results is probably limited. Moreover, according to the reports of the missions carried out by the EFTA Surveillance Authority in Norway there were insufficient measures in place to prevent the potential for cross-contamination of fishmeal with MBM. The results of the BSE monitoring system carried out during the period 2001 – 2011 were considered. Overall 200,165 BSE screening tests were performed in Norway with no positive results. The lack of detection of BSE cases by the Norwegian monitoring system (in spite of its sensitivity limits) suggests that BSE has not significantly spread in the Norwegian cattle population. It was then concluded that the use of fishmeal in feed for ruminants might have had a potential impact on the risk of cattle exposure to BSE in Norway. However, the lack of detection of BSE cases by the Norwegian monitoring system suggests that BSE has not significantly spread in the Norwegian cattle population. The Cattle TSE Monitoring Model (C-TSEMM) was used in order to answer the second term of reference of the mandate. According to C-TSEMM the proposed revised Norwegian BSE monitoring regime would not be able to meet a yearly design prevalence of at least one case per 100,000 in the adult cattle population at a confidence level of 95% in Norway. Moreover, the results of the model indicate that in statistical terms it is not feasible for Norway to achieve the proposed design prevalence. The results of C-TSEMM have to be interpreted in the light of its assumptions, uncertainties and limitations. However, they can be considered to be an overestimation of what is achievable by the Norwegian regimes considered. It is furthermore highlighted that passing from a sample-based to an exhaustive monitoring scheme (i.e. testing all animals over a certain age that are slaughtered or dead) would provide the most sensitive BSE surveillance system currently possible.
 
 
snip...
 
 
CONCLUSIONS
 
 
The use of fishmeal in feed for ruminants might have had a potential impact on the risk of cattle exposure to BSE in Norway. While it is not possible to quantitatively assess this risk, the lack of detection of BSE cases by the Norwegian monitoring system (in spite of its sensitivity limits) suggests that BSE has not significantly spread in the Norwegian cattle population. According to the model applied (C-TSEMM): – the proposed revised Norwegian BSE monitoring regime would not be able to meet a yearly design prevalence of at least one case per 100,000 in the adult cattle population at a confidence level of 95% in Norway; and – even in a scenario in which all healthy slaughtered and all at risk cattle above 72 and 48 months respectively would be tested for BSE, in statistical terms it is not feasible to achieve the design prevalence of one case per 100,000 in the adult cattle population at a confidence level of 95% in Norway. The results of C-TSEMM have to be interpreted in the light of its assumptions, uncertainties and limitations. However, they can be considered to be an overestimation of what is achievable by the Norwegian regimes considered. Passing from a sample-based to an exhaustive monitoring scheme (i.e. testing all animals over a certain age that are slaughtered or dead) would provide the most sensitive BSE surveillance system currently possible.
 
 
 
 
Keywords
BSE, Norway, monitoring, revision, design prevalence
 
 
 
 
2004
 
 
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Norway
doi:10.2903/j.efsa.2004.8r
European Food Safety Authority
 
 
Type: Scientific Report of EFSA Question number: EFSA-Q-2003-083F Approved: 01 July 2004 Published: 20 August 2004 Last updated: 08 September 2004. This version replaces the previous one/s.
 
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 Norway, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Norway. This scientific report addresses the GBR of Norway as assessed in 2004 based on data covering the period 1980-2003.
 
 
Between 1980 and 1990, an extremely unstable system was exposed to a negligible/very low challenge. Between 1991 and 1999, the stability of the system increased to very unstable and then to unstable in 2000, while the challenge increased to moderate and subsequently decreased to negligible in 1996. Under such low/intermediate levels of risk (as judged by challenge/stability alone), the fact that no BSE case was detected by the very extensive surveillance carried out in Norway since 2001, makes the possibility that BSE-infectivity could have been recycled and amplified unlikely although it cannot be excluded.
 
 
EFSA concludes that the current geographical BSE-risk (GBR) level is II, as it is unlikely but can not be excluded that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The Norwegian BSE/cattle system is now regarded to be very stable. This implies that the probability of cattle to become newly infected with the BSE-agent is very low. Assuming that measures in place continue to be appropriately implemented the GBR will decrease over time at the rate at which already infected animals leave the system. If the measures in place are effectively implemented, the import of live animals cannot increase the risk because the infectivity that could theoretically be harbored by them would not reach domestic cattle.
 
 
Since recent improvements in the safety of Meat and Bone Meal (MBM) production in many countries or significant recent reductions in the incidence of BSE have not been taken into account for the assessment of the external challenge in the present report, the external challenge assessed after 2001 could be overestimated and is the worst case assumption. However, all current GBR conclusions are not dependent on these assumptions in any of the countries assessed. For future assessments and when the impact of the production, surveillance and true incidence changes has been fully quantified, these developments should be taken into account. Keywords
 
 
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Norway
 
 
 
 
snip...
 
 
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
 
5.1 The current GBR as function of the past stability and challenge
 
• The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely but can not be excluded that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
 
• This assessment deviates from the previous assessment (SSC opinion, 2000) because at that time several exporting countries were not considered a potential risk.
 
5.2 The expected development of the GBR as a function of the past and present stability and challenge
 
• The Norway BSE/cattle system is now regarded to be very stable. This implies that the probability of cattle to become newly infected with the BSE-agent is very low. Assuming that measures in place continue to be appropriately implemented the GBR will decrease over time at the rate at which already infected animals leave the system.
 
• If the measures in place are effectively implemented, the import of live animals cannot increase the risk because the infectivity that could theoretically be harboured by them would not reach domestic cattle.
 
• Since recent improvements in the safety of MBM production in many countries or significant recent reductions in the incidence of BSE have not been taken into account for the assessment of the external challenge in the present report, the external challenge assessed after 2001 could be overestimated and is the worst case assumption. However, all current GBR conclusions are not dependent on these assumptions in any of the countries assessed. For future assessments and when the impact of the production, surveillance and true incidence changes has been fully quantified, these developments should be taken into account.
 
 
 
2000
Report on the assessment of the Geographical BSE-risk of NORWAY July 2000
OVERALL ASSESSMENT The current geographical BSE-risk (GBR) of Norway is level I, i.e. it is highly unlikely that domestic cattle are infected (clinically or pre-clinically) with the BSE agent.
 
Note: This assessment leading to GBR level I is mainly based on the fact that Norway was not exposed to significant external challenges before 1995 when the system became stable.
 
Should this be proven wrong, a GBR level II would have to be assumed.
 
 
Annual Reports 2011
 
The surveillance and control programme for scrapie in Norway 2011
 
Sviland Ståle, Benestad Lafond Sylvie, Eikenæs Olav, Norström Madelaine
In 2011, Nor98 scrapie was diagnosed in 6 sheep coming from 6 different flocks.
 
Introduction
 
 
Scrapie was first diagnosed in indigenous Norwegian sheep in 1981. Increasing numbers of scrapieinfected flocks were identified in the 1990s, culminating with 31 detected flocks in 1996 (Figure 1). By the end of 2009, scrapie had been diagnosed in a total of 148 sheep flocks and one goat herd (1). Scrapie has been a notifiable disease in Norway since 1965, and control measures have involved destruction of all sheep in affected flocks and in close contact flocks until 2004. The Norwegian scrapie surveillance and control programme was launched in 1997 (2). In 1998 a new type of scrapie, Nor98 scrapie, was identified in Norway. The diagnosis of Nor98 scrapie is verified by Western blot. Nor98 scrapie differs from classical scrapie in several aspects, including the Western blot profile, the distribution of protease resistant prion protein (PrPSc) in the brain, and absence of detectable PrPSc in lymphoid tissues (3). The main clinical sign observed in Nor98 scrapie cases has been ataxia. The PrP genotype distribution among Nor98 scrapie cases differs markedly from that of the previous cases with classical scrapie (4). The Norwegian Food Safety Authority is responsible for carrying out the surveillance and control programme for scrapie. The samples are collected at the abattoirs or in the herds by inspectors from the Norwegian Food Safety Authority. The Norwegian Food Safety Authority also carries out inspections of sheep flocks and goat herds, all of which should be inspected every second or third year. The Norwegian Veterinary Institute is performing the laboratory examinations and the reporting of the results.
 
Materials and methods
 
 
In 2011, the surveillance programme was performed according to the European Union Regulations,
Regulation (EC) No. 999/2001 Annex III, with amendments and included examination of the following categories of small ruminants:
 
 
* all small ruminants with clinical signs consistent with scrapie, irrespective of age
 
 
* 10,000 sheep older than 18 months, which had died or been killed on the farm, but not
slaughtered for human consumption (fallen stock)
 
 
* 10,000 randomly sampled healthy sheep older than 18 months slaughtered for human consumption
 
 
* 500 goats older than 18 months which had died or been killed on the farm, but not slaughtered for
human consumption (fallen stock)
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Prevalence
 
 
The classical scrapie and Nor98 scrapie prevalences in the fallen stock and abattoir populations were estimated assuming an exact binominal distribution.
Results
 
Sheep
Nor98 scrapie was diagnosed in 6 sheep from 6 flocks. One Nor98 scrapie case was identified in fallen stock, five cases were apparently healthy animals slaughtered for human consumption (Table 1).
 
The individual age and breed were registered, and the prion protein genotype examined for all six scrapie cases (Table 2). Four sheep had PrP genotypes with at least one allele with polymorphisms at codon 141 (AF141RQ) or 154 (AHQ), whereas two sheep had the PrP genotype ARR/ARR.
 
In total, 13,486 samples from sheep were received. Of these, 13 (0.09%) samples were unsuitable for examination. The numbers of animals examined within each category are presented in Table 1. The prevalence of Nor98 scrapie in the fallen stock of sheep was estimated to 0.02% (0.0-0.12%), (95% confidence interval [CI]) (Figure 2), and the prevalence of Nor98 scrapie in sheep slaughtered for human consumption was estimated to 0.06% (0.0-0.13%), (95% CI) (Figure 3).
 
For 135 (1.0%) samples (111 healthy slaughtered, 22fallen stock and one from the ante mortem control), the flock of origin was not reported. In the event of a positive sample from slaughtered animals, the flock identity could be traced using the carcass number. The remaining 13,352 samples were collected from carcasses originating in 5,596 different sheep flocks. The mean number of animals tested per flock was 2.3 (range 1-29), flocks eradicated due to scrapie are excluded. From 1,746 flocks more than two samples were tested. The samples were obtained throughout the year, with approximately 26% of the samples collected in September and October, which is the main slaughtering season for sheep in Norway.
 
PrP genotyping was performed on 639 sheep randomly sampled from the healthy slaughtered population examined in Harstad. The PrP genotypes are grouped in accordance with the British National Scrapie Plan (NSP) (Table 3).
 
Goat
 
Scrapie was not detected in any goat in 2011.
 
In total, 390 samples from goats were received. In six of these the flock of origin was not reported. None of these were unsuitable for examination. The numbers of animals examined within each category are presented in Table 1.
 
The samples were collected from carcasses originating from 168 different herds. The mean number of animals tested per herd was two (range 1-13). From 51 herds more than two samples were tested.
 
snip...
 
Scrapie was not detected in goats in 2011. The first and only scrapie case in naturally infected goats in Norway was diagnosed in 2006 and originated from a county with a large goat population. Both classical and atypical scrapie in goats has been diagnosed in several countries in Europe (5).
 
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end...
 
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May 15, 2012 – E-mail: postmottak@vetinst.no www.vetinst.no. ISSN 1890-9973. Title: The surveillance and control programme for scrapie in Norway 2011 ...
Atypical scrapie in a swiss goat and implications for transmissible spongiform encephalopathy surveillance
 
Seuberlich T, Botteron C, Benestad SL, Brunisholz H, Wyss R, Kihm U, Schwermer H, Friess M, Nicolier A, Heim D, Zurbriggen A. Atypical scrapie in a swiss goat and implications for transmissible spongiform encephalopathy surveillance. J Vet Diagn Invest 2007; 19: 2-8.
 
Different types of transmissible spongiform encephalopathies (TSEs) affect sheep and goats. In addition to the classical form of scrapie, both species are susceptible to experimental infections with the bovine spongiform encephalopathy (BSE) agent, and in recent years atypical scrapie cases have been reported in sheep from different European countries. Atypical scrapie in sheep is characterized by distinct histopathologic lesions and molecular characteristics of the abnormal scrapie prion protein (PrPsc). Characteristics of atypical scrapie have not yet been described in detail in goats. A goat presenting features of atypical scrapie was identified in Switzerland. Although there was no difference between the molecular characteristics of PrPsc in this animal and those of atypical scrapie in sheep, differences in the distribution of histopathologic lesions and PrPsc deposition were observed. In particular the cerebellar cortex, a major site of PrPsc deposition in atypical scrapie in sheep, was found to be virtually unaffected in this goat. In contrast, severe lesions and PrPsc deposition were detected in more rostral brain structures, such as thalamus and midbrain. Two TSE screening tests and PrPsc immunohistochemistry were either negative or barely positive when applied to cerebellum and obex tissues, the target samples for TSE surveillance in sheep and goats. These findings suggest that such cases may have been missed in the past and could be overlooked in the future if sampling and testing procedures are not adapted. The epidemiological and veterinary public health implications of these atypical cases, however, are not yet known.
 
The surveillance and control programme for Chronic Wasting Disease (CWD) in wild and captive cervids in Norway
 
21.09.2009 11:12
 
Introduction
 
 
Chronic wasting disease (CWD) was not detected in any of the animals tested in 2008.
 
 
CWD is a transmissible spongiform encephalopathy (TSE) of cervids (1, 2, 3). A few species of the family Cervidae are known to be naturally susceptible to the disease: mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), elk (Cervus elaphus), and moose (Alces alces). CWD was first described as a clinical syndrome termed “chronic wasting disease” in captive mule deer in Colorado, USA in the late 1960s and subsequently identified as a TSE in 1978 (1). Chronic wasting disease is so far only diagnosed in free-ranging and captive cervids in North America, and is yet to be diagnosed in cervids in Europe.
 
 
Four cervid species are prevalent in natural populations in Norway: moose (Alces alces), red deer (Cervus elaphus), roe deer (Capreolus capreolus), and reindeer (Rangifer tarandus). Red deer predominate along the west coast, whereas moose and roe deer mainly inhabit other areas of the country. The wild reindeer live in dispersed populations in separate high mountain areas in southern Norway. The number officially hunted in 2008 was: 35,600 moose, 35,700 red deer, 29,800 roe deer, and 5,200 wild reindeer. Additionally, Norway has a semi-domestic reindeer population, mainly kept in the northern parts of the country, presently counting about 200,000 animals.



There are 75 cervid farms in Norway. Most of the farms keep red deer, and only a few keep fallow deer (Dama dama).
 
Based on the fact that Norway has large free-ranging populations of various cervids, a number of them grazing in regions where scrapie is detected, a passive surveillance programme for CWD in Norwegian wild and captive cervids has been running from 2003. In addition, samples from slaughtered semi-domestic reindeer from several regions in the country have been tested for CWD.
 
Norway performed an EC survey for CWD in cervids in 2006 and 2007 according to Commission decision 2007/182/EC. The target species relevant for Norway was wild red deer and the survey implied sampling of a) clinical/sick, euthanized animals, b) traffic killed animals, c) animals found dead, and d) healthy animals shot during hunting. Additionally, for moose, roe deer, reindeer, and farmed deer the categories a) – c) were sampled. All samples were negative for CW
 
 
 
A small population of approximately 200 free-ranging musk ox (Ovibus moschatus, belonging to the Bovidae), inhabits the Dovre high mountain plateau in Mid-Norway. TSE has not been diagnosed in the musk ox, but the species has been included in the programme from 2004.
 
Aim
 
The aim of the programme is to detect the possible occurrence of CWD in the Norwegian cervid population.
 
 
Material and methods
 
Material
 
Tested animals included captive deer and wild cervids older than 18 months that died or were euthanized due to disease or injuries. Additionally, cervids older than 18 months necropsied at the National Veterinary Institute were examined for CWD. Twelve ordinary hunted roe deer from Vestby in the county of Akershus and one musk ox found dead were also tested. The number and species analysed for CWD in 2008 are given in Table 1.
 
 
Methods
 
A rapid test (either TeSeE ® Bio-Rad or TeSeE Sheep & Goat ® ELISA, Bio-Rad) was used to screen brain samples for detection of the PrPCWD. All the samples were analysed at the National Veterinary Institute, which is the National Reference Laboratory for TSEs in Norway.
Results
None of the 47 samples analysed tested positive for CWD in the rapid test (Table 1).
Totally 25 of the tested animals were exclusively examined for CWD, and the majority was healthy hunted and traffic killed roe deer (Table 1). The remaining 22 animals represent cases received at the National Veterinary Institute for routine necropsy.
A total of two of the tested animals were captive red deer. One semi-domestic reindeer was sampled because of showing clinical signs before it dropped dead.
Table 1. The number of cervids tested in the Norwegian surveillance and control programme for Chronic wasting disease (CWD) 2008, distributed by reason for submission.
snip...
Discussion
No animals were positive for CWD in 2008. A large part of the tested animals in 2008 was roe deer collected in Vestby, comprising hunted and traffic killed animals. Very few captive red deer were tested.
Among the Norwegian cervid species, a higher risk for CWD can be assumed for red deer and moose since these species are among those known to be naturally susceptible to the disease (1, 2, 3). Regarding moose, so far, only a few positive CWD cases has been diagnosed in hunted animals in CWD-endemic areas in Colorado, USA (3), thus they probably represent preclinical CWD. Also, the disease has been transmitted experimentally to moose by oral inoculation of brain tissue from a CWD affected mule deer (4). Roe deer, reindeer and musk ox has so far not been found naturally infected with CWD.
 
 
 
 
 
 
 
Monday, June 18, 2012
 
 
natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds captive Korea and Experimental oral transmission to red deer (Cervus elaphus elaphus)
 
 


 
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Abstract
 
Atypical/Nor98 scrapie was first identified in 1998 in Norway. It is now considered as a worldwide disease of small ruminants and currently represents a significant part of the detected transmissible spongiform encephalopathies (TSE) cases in Europe. Atypical/Nor98 scrapie cases were reported in ARR/ARR sheep, which are highly resistant to BSE and other small ruminants TSE agents. The biology and pathogenesis of the Atypical/Nor98 scrapie agent in its natural host is still poorly understood. However, based on the absence of detectable abnormal PrP in peripheral tissues of affected individuals, human and animal exposure risk to this specific TSE agent has been considered low. In this study we demonstrate that infectivity can accumulate, even if no abnormal PrP is detectable, in lymphoid tissues, nerves, and muscles from natural and/or experimental Atypical/Nor98 scrapie cases. Evidence is provided that, in comparison to other TSE agents, samples containing Atypical/Nor98 scrapie infectivity could remain PrPSc negative. This feature will impact detection of Atypical/Nor98 scrapie cases in the field, and highlights the need to review current evaluations of the disease prevalence and potential transmissibility. Finally, an estimate is made of the infectivity loads accumulating in peripheral tissues in both Atypical/Nor98 and classical scrapie cases that currently enter the food chain. The results obtained indicate that dietary exposure risk to small ruminants TSE agents may be higher than commonly believed.
snip...
 
In 1998 an Atypical/Nor98 Scrapie was identified in Norwegian sheep; the PrPSc signature was partially PK resistant and displayed a multi-band pattern as showed by Western Blot (WB) that contrasted with those normally observed in small ruminants TSE cases [5]. After 2001 and the implementation of active TSE surveillance plans, a number of similar cases were identified in most EU members states as well in other countries, like Canada, USA and New Zealand [6]. The transmissibility of Atypical/Nor98 agent has been demonstrated in both rodent models (transgenic animals expressing the ovine Prnp gene) [7] and sheep [8], [9]. Currently Atypical/Nor98 Scrapie represents a significant part of the TSE cases identified in the EU small ruminant population, where its prevalence was estimated to range between 5 to 8 positive small ruminants per 10,000 tested per year [10].
 
snip...
 
Atypical/Nor98 cases are identified in older animals in comparison to classical scrapie [6], [40]. The lack of PrPSc detection in peripheral tissues of reported cases suggested that Atypical/Nor98 scrapie agent could be restricted to CNS. This is supportive of the hypothesis that Atypical/Nor98 scrapie could be a spontaneous disorder of PrP folding and metabolism occurring in aged animals without external cause [6], [38].
 
 
However, this hypothesis is questioned by the evidence reported here that a negative PrPSc testing result could be observed in animals harbouring high infectious titre in their brain and that the infectious agent can be present in peripheral tissues of Atypical/Nor98 scrapie incubating sheep. TSE are considered to be transmitted following oral exposure; initial uptake is followed by a peripheral replication phase which is generally associated with a dissemination of the agent in the lymphoid system and the deposition of large amounts of PrPSc. This peripheral replication phase is later followed by the entry of the infectious agent into the CNS through the autonomic nervous system [25], [27], [35], [36]. However, in several situations, like BSE in cattle [41], [42], [43] or classical scrapie in ARR heterozygote sheep [44], [45], the involvement of secondary lymphoid system is marginal, which does not preclude central neuro-invasion through the autonomic nervous system [46]. It could be proposed that Atypical Scrapie/Nor98 might occur following oral exposure to a TSE agent, which would spread marginally in lymphoid tissues before neuro-invasion. The slow propagation of Atypical Scrapie/Nor98 in its host (long incubation period) and the impaired detection sensitivity level of PrPSc based assays would explain the apparent old age of detected cases.
 
 
The results presented here are insufficient to rule out the hypothesis of a spontaneous/non contagious disorder or to consider this alternative scenario as a plausible hypothesis. Indeed, the presence of Atypical scrapie/Nor98 infectivity in peripheral tissues could be alternatively due to the centripetal spreading of the agent from the CNS. However, our findings point out that further clarifications on Atypical/Nor98 scrapie agent biology are needed before accepting that this TSE is a spontaneous and non contagious disorder of small ruminants. Assessing Atypical/Nor98 scrapie transmissibility through oral route in natural host and presence in placenta and in colostrum/milk (which are considered as major sources for TSE transmission between small ruminants) [28], [32] will provide crucial data.
 
 
The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.
 
 
Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.
 
 
 
please see more transmissions studies here ;
 
 
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
 
 
 
 
 
Tuesday, July 17, 2012
 
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012
 
 
 
 


 
Thursday, December 20, 2012
 
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE
 
 
 
 
 
 
 
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 
 

 
 
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
 
119
 
 
 
 
 
 
*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
 
 
 
 
 
 
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
 
 
 
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
 
 
 
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

 
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

 
 

 
Wednesday, January 18, 2012
 
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie
 
Journal of Neuropathology & Experimental Neurology:
 
February 2012 - Volume 71 - Issue 2 - p 140–147
 

 
 
 
 
Thursday, March 29, 2012
 
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
 
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
 
 


 
Monday, November 30, 2009
 
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
 
 
 
 
Thursday, December 20, 2012
 
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED

 
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
 
snip...
 
R. BRADLEY
 
 
 
 
 
 
Wednesday, February 16, 2011
 
IN CONFIDENCE
 
SCRAPIE TRANSMISSION TO CHIMPANZEES
 
IN CONFIDENCE
 
 
 


 
 
Sunday, December 12, 2010
 
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010
 
 
 
 
 
 
 
 
 
Sunday, April 18, 2010
 
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
 
 
 
 
 
 
 
 
 
Thursday, December 23, 2010
 
Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
 
Volume 17, Number 1 January 2011
 
 
 
 


 
Thursday, November 18, 2010
 
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

 


 
 
Michigan and California have had a high spike in Goat Scrapie cases, compared to elsewhere ???
 
three is a serious problem with scrapie in goats around Michigan, Ohio, and California, that no one can explain, and it’s not because I have not tried to make them aware of it ;
----- Original Message -----
 
 
From: "BioMed Central Comments"
To:
Sent: Wednesday, February 16, 2011 4:13 AM
Subject: Your comment on BMC Veterinary Research 2011, 7:7
Your discussion posting "Scrapie cases Goats from same herd USA Michigan" has been rejected by the moderator as not being appropriate for inclusion on the site.
Dear Mr Singeltary,
Thank you for submitting your comment on BMC Veterinary Research article (2011, 7:7). We have read your comment with interest but we feel that only the authors of the article can answer your question about further investigation of the route of infection of the five goats in Michigan. We advise that you contact the authors directly rather than post a comment on the article.
With best wishes,
Maria
Maria Kowalczuk, PhD Deputy Biology Editor BMC-series Journals
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Any queries about this decision should be sent to comments@biomedcentral.com
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=========END...TSS=========
 
 
 
 
 
 
 
 
 
Tuesday, February 01, 2011

 
Sparse PrP-Sc accumulation in the placentas of goats with naturally acquired scrapie

 
(Figure 6) including five goat cases in FY 2008 that originated from the same herd in Michigan. This is highly unusual for goats, and I strenuously urge that there should be an independent investigation into finding the common denominator for these 5 goats in the same herd in Michigan with Scrapie. ...
 
 
 
 
 
 
 
Wednesday, February 20, 2013
 
World Organization for Animal Health Recommends United States' BSE Risk Status Be Upgraded
 
Statement from Agriculture Secretary Tom Vilsack:
 
 
 


 
 
Thursday, February 14, 2013
 
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease

 
 
 
 
 
Friday, February 08, 2013

 
*** Behavior of Prions in the Environment: Implications for Prion Biology
 
 
 
 
 
 
Friday, November 09, 2012
 
 
 
*** Chronic Wasting Disease CWD in cervidae and transmission to other species

 
 
 
 
 
Sunday, November 11, 2012

 
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012


 
 
 
 
 
Friday, December 14, 2012

 
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012

 
 
 
 
 
 
 
 
>>>There are 75 cervid farms in Norway. Most of the farms keep red deer, and only a few keep fallow deer (Dama dama).<<<<
 



 
Tuesday, December 18, 2012

 
*** A Growing Threat How deer breeding could put public trust wildlife at risk
 
 
 
 
 
 
 
NORWAY HUMAN TSE PRION DISEASE
EUROCJD Surveillance Data
Total Cases of CJD/GSS (Deaths)
All Definite And Probable Cases:
Sporadic, Familial/Genetic, FFI, GSS and Iatrogenic Deaths (excluding vCJD)
Country 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 Total
Norway - - - - 6 2 2 4 6 3 6 8 4 4 5 3 5 2 4 64
All CJD (excluding vCJD): Annual Mortality Rates Per Million
Norway - - - - 1.37 0.45 0.45 0.89 1.33 0.66 1.32 1.75 0.87 0.86 1.07 0.63 1.04 0.41 0.81 0.92
 
 
 
Creutzfeldt-Jacob disease
Incidence / incidence rate 2006
4 / 0.9 per 1 million population
All four cases of Creutzfeldt-Jacob disease (CJD) reported in 2006 were classified as sporadic CJD following autopsies.
Trends
Suspected and confirmed cases of human transmissible spongiform encephalopathies were made notifiable conditions in 1997.
All cases of CJD registered in Norway so far have been sporadic CJD confirmed by autopsy. One of the cases is suspected to be a hereditary case. Cases of iatrogenic or variant CJD have never been registered in Norway. BSE has never been identified in Norwegian cattle.
Table 35. Creutzfeldt-Jakob disease notifications in Norway 2000-2006 by year of death.
2000 2001 2002 2003 2004 2005 2006
3 5 3 5 7 4 4
 
 
 
*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $
 
 
 
OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles
 
 
 
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA
 
 
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.
 
 
Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
 
 
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.
 
 
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.
 
 
Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
 
 
The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
 
 
 
 
 
Wednesday, March 28, 2012

 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $
 
 
 
 
 
Thursday, February 21, 2013
 
 
National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013
 
 
 
 
tss

Thursday, January 17, 2013

FSA notified of two breaches of BSE testing regulations 14 January 2013

14 January 2013
 
 
 
 
FSA notified of two breaches of BSE testing regulations


 
There have been two separate incidents in which cattle aged over 72 months entered the food chain without being tested for BSE. The incidents involved a total of three animals.


 
The risk to human health is very low as it is very unlikely that any of the cattle would have been infected. The specified risk material (SRM), parts of the cattle most likely to carry BSE infection, had been removed in each case.
 
 
 
 
Bridport
 
 
 
 
On 20 August 2012, two cattle over 72 months of age were slaughtered at S J Norman and Sons abattoir in Bridport and were not tested for BSE before leaving the premises. One animal was 332 days over the 72 month age limit; the other by 1,383 days. The error was discovered on 22 October during routine cross-checks of slaughter and BSE data.
 
 
 
 
It is mandatory for all cattle slaughtered for human consumption and aged over 72 months to have a negative BSE test result. According to regulations any cattle that has not been tested, along with the animal slaughtered immediately before it and the two immediately after, should not enter the food supply.
 
 
 
 
In total, seven carcasses had to be traced in this instance, because of the sequence of the two kills. Meat from these animals was mixed up with other consignments. Most of the meat had been processed or sold on to the end consumer and was no longer in the food supply chain. Of the remaining meat, 1,720 kg was traced to a cold storage facility in Essex. It was disposed of and did not enter the food supply. A further 233 kg had been exported to Malta and the Maltese authorities were informed.


 
Nantwich
 
 
 
 
Separately, on 2 March 2012 a bovine that was 89 months and 27 days of age was slaughtered at High Peak Meat Exports abattoir in Nantwich. Again it was not tested before leaving the premises. The error was discovered during routine data checks on 25 May.
 
 
 
 
The investigation found that only three animals were slaughtered on 2 March. The carcasses, along with six others slaughtered later that month, were dispatched to the Netherlands on 6 March. The Dutch authorities were notified of the breach. No edible meat or offal from the animals slaughtered on 2 March was sold as food in the UK.
 
 
 
 
 
 
 
 
Wednesday, December 21, 2011


 
Potential mad cows that entered food supply without being tested for BSE 2011: UK END OF YEAR REVIEW
 
 
 
 
 
 
 
 
Thursday, September 6, 2012


 
UK Breaches of BSE controls in consignments of beef 2011 communications missing four reports
 
 
 
 
 
 
 
 
Friday, December 21, 2012
 
 
 
 
Four BSE cases with an L-BSE molecular profile in cattle from Great Britain Veterinary Record doi:10.1136/vr.101158 Paper
 
 
 
 
 
 
 
 
Friday, November 30, 2012
 
 
 
 
PROPOSED DECISION TO STOP BSE TESTING OF HEALTHY CATTLE SLAUGHTERED FOR HUMAN CONSUMPTION FSA 12/12/04 Open Board – 11 December 2012
 
 
 
 
 
 
 
 
EURO QUALITY RECALLS ITS LAMBS' BRAINS


 
Euro Quality Lambs Ltd is recalling its lambs’ brains, which have entered the food chain without being inspected properly. The Food Standards Agency is asking all local authority enforcement officers to ensure that the product is withdrawn from sale and destroyed. The Agency has issued a Food Alert for Action.
 
 
 
 
 
 
 
 
Wednesday, February 16, 2011
 
 
 
 
IN CONFIDENCE
 
 
 
 
SCRAPIE TRANSMISSION TO CHIMPANZEES
 
 
 
 
IN CONFIDENCE


 
 
 
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
 
 
 
snip...
 
 
 
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.


 
snip...


 
R. BRADLEY
 
 
 
 
 
 
 
 
Friday, February 11, 2011
 
 
 
 
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues


 
 
 
 
 
Monday, April 25, 2011
 
 
 
 
Experimental Oral Transmission of Atypical Scrapie to Sheep


 
Volume 17, Number 5-May 2011
 
 
 
 
 
 
 
 
Sunday, April 18, 2010
 
 
 
 
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
 
 
 
 
 
 
 
 
Thursday, November 18, 2010
 
 
 
 
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
 
 
 
 
 
 
 
 
Wednesday, January 19, 2011
 
 
 
 
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
 
 
 
 
 
 
 
 
Monday, June 27, 2011
 
 
 
 
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease
 
 
 
 
 
 
 
 
Friday, December 14, 2012
 
 
 
 
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
 
 
 
 
 
 
 
 
ANY RELAXING OF ANY BSE TESTING RULES WOULD NOT BE BASED ON SOUND SCIENCE, BUT BASED ON INDUSTRY LED SCIENCE AND MONEY $$$
 
 
 
 
we now know that indeed atypical BSE is transmissible to cattle and other species, and atypical BSE have been documented in older cattle to date. so relaxing any BSE testing on older cattle would be a huge step backwards, and could risk everything that has been done over the past 27 years to try and eradicate BSE. ...
 
 
 
 
on a lighter note, seems anything goes now $$$
 
 
 
 
16 January 2013
 
 
 
 
FSA investigation into horse DNA found in some burgers
 
 
 
 
The Food Standards Agency is investigating urgently how a number of beef products on sale in the UK and Republic of Ireland came to contain some traces of horse and pig DNA.
 
 
 
 
The Food Safety Authority of Ireland reported yesterday (Tuesday, 15 January) that an analysis they carried out into the authenticity, or labelling accuracy, of a number of burger products revealed that some contained horse and pig DNA.
 
 
 
 
In particular, 27 beefburger products were analysed, with 10 of the 27 products (37%) testing positive for horse DNA and 23 (85%) testing positive for pig DNA. In nine of the ten beefburger samples, horse DNA was found at very low levels. In one sample from Tesco, the level of horse DNA indicated that horse meat was present and accounted for approximately 29% of the total meat content of the burger.


 
All of the retailers involved so far have removed potentially affected products from their shelves.
 
 
 
 
The FSA has been in contact overnight with the retailers and producers named in the FSAI survey and has called a meeting this afternoon with a wider range of food industry representatives to discover the extent of the potential problem and to investigate how this contamination might have occurred.
 
 
 
 
 
 
 
 
Thursday, January 5, 2012
 
 
 
 
Horse Meat, slaughter for consumption USA
 
 
 
 
snip...
 
 
 
 
Greetings,
 
 
 
 
for what it’s worth.
 
 
 
 
I am against horse slaughter for consumption or any other purpose i.e. fertilizer, plastic, fuel, etc.
 
 
 
 
I am against the use of primates in scientific studies. because arguments will always persist on proof of human relation from any given study. However, I am for Human use in place of Primates in these studies. I said it long ago. Death Row inmates. compensate the families and do the studies on these death row inmates. it could be the last good thing they ever do. just my opinion.
 
 
 
 
For horses, they should use the same policy they use in the USA for old diseased mad cows, i.e. SSS policy. shoot, shovel, and shut up. either bury them or incinerate them. again, just my opinion.
 
 
 
 
there is no humanity anymore $$$


 
It brings me to the old movie. how many times do old movies come true? strange...
 
 
 
 
'soyent green'.
 
 
 
 
see ;
 
 
 
 
Soylent Green is a 1973 dystopian science fiction movie depicting a future in which overpopulation lead to depleted resources, which in turn leads to widespread unemployment and poverty. Real fruit, vegetables, and meat are rare, commodities are expensive, and much of the population survives on processed food rations, including "soylent green" wafers.
 
 
 
 
The film overlays the science fiction and police procedural genres as it depicts the efforts of New York City police detective Robert Thorn (Charlton Heston) and elderly police researcher Sol Roth (Edward G. Robinson) to investigate the brutal murder of a wealthy businessman named William R. Simonson (Joseph Cotten). Thorn and Roth uncover clues which suggest that it is more than simply a bungled burglary.


 
snip...
 
 
 
 
After Roth dies, Thorn sneaks into the basement of the government-assisted suicide facility, where he sees corpses being loaded onto waste disposal trucks. He secretly hitches a ride on one of the trucks, which is driven to a heavily guarded waste disposal plant. Once inside the plant, Thorn sees how the corpses are processed into Soylent Green wafers. After Thorn escapes from the plant and heads for the supreme exchange with the information, he is ambushed by Fielding and several other gunmen. In the shootout, Thorn kills some of the gunmen, but is himself wounded. He retreats into a cathedral filled with homeless people. After a desperate fight, Thorn stabs and kills Fielding.
 
 
 
 
When police backup arrives, the seriously wounded and nearly hysterical Thorn confides to Hatcher the horrible secret behind Soylent Green and urges him to spread the word: "Soylent Green is people! We've got to stop them somehow!"


don’t believe me, were almost there ;
 
 
 
 
 
 
 
 
IN CONFIDENCE
 
 
 
 
SUSPECT BSE IN A HORSE
 
 
 
 
CYO BSE 1 9
 
 
 
 
IN CONFIDENCE


 
SUSPECT BSE IN A HORSE
 
 
 
 
The Parliamentary Secretary (Mr Maclean) will wish to be aware that, in making his differential diagnosis, a veterinary surgeon in the Reading area has included the possibility of BSE in a horse under his care. Although it is unlikely to be BSE, because of the symptoms exhibited the veterinarian believes that he cannot exclude the possibility. The case was brought to the notice of one of the veterinary staff at the CVL by the owner's veterinary surgeon and liaison is being maintained.
 
 
 
 
The horse in question is a five-year old eventing gelding which was purchased by the present owner about four months ago. Approximately two months after purchase the animal became a little apprehensive, developed mild nervous symptoms and became over-sensitive to noise. The nervous symptoms have increased and the horse is now practically impossible to ride. Investigations by the owner's private veterinary surgeon are continuing but it is likely that the animal will have to be destroyed.
 
 
 
 
If the horse should die or be destroyed, a full post-mortem examination will be required for insurance purposes and will probably be carried out at a non-Ministry laboratory. However, Mr Bradley of the Pathology Department, CVL, has informed the private veterinary surgeon that he is willing to provide a second opinion on the brain histology if requested.


 
I will keep the Parliamentary Secretary informed of any further developments in the case.
 
 
 
 
I CRAWFORD
 
 
 
 
14 May 1990


 
Mr M P H Hill, PS/Parliamentary secretary (Mr Maclean) - by FAX
 
 
 
 
cc:
 
 
 
 
Private Offices
 
 
 
 
Mr K C Meldrum
 
 
 
 
Mrs E A J Attridge D J Evans Mr K C Taylor Mr R Lawson Mr R Bradley. CVL
 
 
 
 
(hand written notes i cannot read all (cut short) as follows...tss)
 
 
 
 
The Parliamentary Secretary (Mr Maclean was grateful for this. He said that we must keep very close to ...on it, and when the horse dies, or is put down we must be told immediately. He also feels it is very important that our veterinary staff be involved in the brain examination. .........(cannot read the rest .............TSS)
 
 
 
 
90/05.14/10.1
 
 
 
 
 
 
 
 
Mr A Huws Principal WOAD2A CP2
 
 
 
 
SUSPECT BSE IN A HORSE


 
You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had ___contracted BSE after having been fed cattle cake___.
 
 
 
 
The clinical symptoms described were similar to those shown by cattle there ___being a similar case some months ago on the same premises___.
 
 
 
 
The owner' s name and address is:
 
 
 
 
Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse Brecon
 
 
 
 
The horse is a 12 year old gelding used for pony trekking.
 
 
 
 
By yesterday evening the horse was in a comatose state and on humane grounds was destroyed by the veterinary Surgeon. At his request a full post mortem and laboratory investigation will be carried out at the Carmarthen Veterinary Investigation Centre this morning to ascertain the exact cause; I have been told this will take at least two weeks. Charges to the veterinary Surgeon have been waived in this instance.


 
I will inform you immediately I receive a diagnosis.
 
 
 
 
26 June 1990
 
 
 
 
D SUMMERS DRVO
 
 
 
 
cc
 
 
 
 
Mr D R Williams, RVO


 
Mr A R Hunter, SVIO
 
 
 
 
90/06.26/10.1
 
 
 
 
 
 
 
 
Mr A Huws Principal WOAD2A CP2
 
 
 
 
SUSPECT BSE IN A HORSE
 
 
 
 
You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had contracted BSE after having been fed cattle cake. The clinical symptoms described were similar to those shown by cattle there being a similar case some months ago on the same premises.
 
 
 
 
The owner' s name and address is:
 
 
 
 
Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse Brecon
 
 
 
 
The horse is a 12 year old gelding used for pony trekking.
 
 
 
 
By yesterday evening the horse was in a comatose state and on humane grounds was destroyed by the veterinary Surgeon. At his request a full post mortem and laboratory investigation will be carried out at the Carmarthen Veterinary Investigation Centre this morning to ascertain the exact cause; I have been told this will take at least two weeks. Charges to the veterinary Surgeon have been waived in this instance.
 
 
 
 
I will inform you immediately I receive a diagnosis.
 
 
 
 
26 June 1990
 
 
 
 
D SUMMERS DRVO
 
 
 
 
cc


 
Mr D R Williams, RVO
 
 
 
 
Mr A R Hunter, SVIO
 
 
 
 
90/06.26/10.1


 
 
 
 
 
full text ;
 
 
 
 
 
 
 
 
we know that horses, especially quarter horses and show horses are fed feed with high animal protein content, and it’s perfectly legal.
 
 
 
 
see ;


 
Nonprohibited Materials:


 
These feed materials CAN be fed to ruminants.


 
A. The following protein products derived from mammals, including ruminants, are exempt from the Ruminant Feed Ban rule and CAN be fed to ruminants:
 
 
 
 
Blood and blood products


 
Milk products (milk and milk protein)
 
 
 
 
Pure porcine (pork) protein
 
 
 
 
Pure equine (horse) protein
 
 
 
 
Gelatin Inspected meat products, such as plate waste, which have been cooked and offered for human food and further heat processed for animal feed.


snip... see full text ;
 
 
 
 
 
 
 
 
From: TSS
 
 
 
 
Subject: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001 USA
 
 
 
 
Date: August 14, 2001 at 11:36 am PST
 
 
 
 
DEPARTMENT OF HEALTH AND HUMAN SERVICE


 
July 20, 2001
 
 
 
 
CERTIFIED MAIL RETURN RECEIPT REQUESTED
 
 
 
 
WARNING LETTER Ref. KAN 2001-028
 
 
 
 
Mr. Eric N. Blomkuist, CEO Farnam Companies, Inc. 301 W. Osborn P.O. Box 34820 Phoenix, AZ 85013
 
 
 
 
Dear Mr. Blomkuist:
 
 
 
 
An inspection of your Council Bluffs, Iowa facility that serves as a manufacturing/repackaging site for animal feed and as a distribution operation for animal drugs and feeds conducted on June 13-20, 2001 by an Investigator representing this office found significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalophathy (BSE) within the borders of the United States. Such deviations cause products being manufactured and/or distributed by your facility to be adulterated within the meaning of Section 402(a)(4) and misbranded within the meaning of Section 403(F) of the Federal Food, Drug, and Cosmetic Act (the Act).
 
 
 
 
The inspection revealed the following:
 
 
 
 
There are no written procedures demonstrating the clean-out process used to prevent the cross- contamination of product. Your firm uses common equipment for product manufactured with prohibited material and for feed and/or drugs that are not.
 
 
 
 
Your firm distributes products that may contain prohibited material, specifically Flex Free, Equinyl, Generation and Max Flex, that are not labeled with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants"


 
The above is not intended to be an all-inclusive list of violations. As a manufacturer of products intended for animal feed use you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. At the conclusion of the inspection Form FDA483, List of Inspectional Observations was issued to Ronald G. Adler, Plant Manager identifying these and other deviations. A copy is enclosed for your information.
 
 
 
 
Our Investigator reported a telephone discussion with Mr. Barry G. Harrison who identified himself as the Corporate Counsel of the Farnam Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed the products in question are exempt from the cautionary statement requirement. This claimed exemption is based on the fact the products are intended only for the equine market and your firm defines horses as pets. We cannot accept this claimed exemption because while some horses may be held as pets, horses are also working animals and in some parts of North America, food animals.
 
 
 
 
Based on our knowledge of working ranches, horse feed is often stored in the same general area as ruminant feed making a conspicuous cautionary statenmit vital on feeds and supplements, containing prohibited materials.
 
 
 
 
You should take prompt action to correct the above violations and to establish procedures whereby such violations do not recur. Failure to make immediate and lasting corrections may result in regulatory actions without further notice including but not limiting to product seizure and/or injunction.


You should respond, in writing, Within 15 working days of the steps you have taken to bring your firm into compliance with the law. Please include all the steps you plan to take, the timeframe for completing these actions and any documentation demonstrating the action's completion.
 
 
 
 
Your response should be directed to Ralph J. Gray, Compliance Officer at the above address.
 
 
 
 
Sincerely, Charles W. Sedgwick District Director Kansas City District Office
 
 
 
 
Cc: Mr. John C. Williams CEO, Manufacturing and Distribution Farnam Companies, Inc, 1302 Law Ross Road Council Bluffs, IA 51501
 
 
 
 
 
 
 
 
Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001
 
 
 
 
Date: Tue, 14 Aug 2001 23:43:26 –0400
 
 
 
 
From: "Robert A. LaBudde"
 
 
 
 
Reply-To: Bovine Spongiform Encephalopathy
 
 
 
 
######## Bovine Spongiform Encephalopathy #########
 
 
 
 
At 01:41 PM 8/14/01 -0700,
 
 
 
 
Terry wrote:


 
>DEPARTMENT OF HEALTH AND HUMAN SERVICE


 
> >July 20, 2001
 
 
 
 
> >Our Investigator reported a telephone discussion with Mr. Barry G.


>Harrison who identified himself as the Corporate Counsel of the Farnam


>Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed


 
>the products in question are exempt from the cautionary statement


>requirement. This claimed exemption is based on the fact the products
 
 
 
 
>are intended only for the equine market and your firm defines horses as
 
 
 
 
>pets. We cannot accept this claimed exemption because while some horses
 
 
 
 
>may be held as pets, horses are also working animals and in some parts


>of North America, food animals.


 
> >Based on our knowledge of working ranches, horse feed is often stored in
 
 
 
 
>the same general area as ruminant feed making a conspicuous cautionary
 
 
 
 
>statenmit vital on feeds and supplements,


 
>containing prohibited materials.
 
 
 
 
Terry:
 
 
 
 
Perhaps you should pester FDA about this "loophole". Apparently, "pet food" does not have to bear the warning labels specified for food animals.
 
 
 
 
I can't see any serious objection to expanding the label requirement to ALL animal food, not just food animals.


 
Also, horses are "ruminants", so it's disturbing that they might escape the feed ban by being classified as "pets". Another good reason to extend the warning labels and regulation to all animal foods.
 
 
 
 
Perhaps you could submit a request for ruling to the FDA on this issue to propose amending the regulation to include all animal foods, including pet foods.


 
================================================================
 
 
 
 
Robert A. LaBudde, PhD, PAS, Dpl. ACAFS e-mail: ral@lcfltd.com Least Cost Formulations, Ltd. URL: http://lcfltd.com/ 824 Timberlake Drive Tel: 757-467-0954 Virginia Beach, VA 23464-3239 Fax: 757-467-2947
 
 
 
 
"Vere scire est per causas scire"
 
 
 
 
================================================================
 
 
 
 
Subject: Re: Horses & ruminants
 
 
 
 
Date: Wed, 15 Aug 2001 12:41:29 +0200
 
 
 
 
From: Roland Heynkes
 
 
 
 
Reply-To: Bovine Spongiform Encephalopathy
 
 
 
 
######## Bovine Spongiform Encephalopathy #########
 
 
 
 
Dear Robert and Oz,


 
>> Also, horses are "ruminants", so it's disturbing that they


 
>> might escape the feed ban by being classified as "pets".


 
>> Another good reason to >extend the warning labels and


 
>> regulation to all animal foods.
 
 
 
 
> > Just a note that horses are NOT ruminants, as I am sure


 
> robert knows from the quotes.
 
 
 
 
> They are however herbivores.


 
> It's also worth noting problems with x-infection found


 
> in the EU.
 
 
 
 
> although horses are not ruminants, it is of course a very poor idea to exclude them from a feed ban. Unfortunately exactly this is the case even in Germany, where horses are still excluded from the ban, if they are not intended to become human food. As Oz mentioned, this opens an absolutely unnecessary possibility for cross contaminations. Of course I repeatedly informed the involved German politicians and authorities about this problem, but they are not interested.


 
This perfectly fits to the fact, that most German authorities are still not prepared to inform the public about the German BSE cases. If you are interested in some information about this cases, you have to visit private Internet sites. Instead most German authorities provide the public with down playing statements and links to meat industry and marketing agencies. Links to sites with scientific information about TSE safety problems are not allowed on this official sites. Official sites with useful information comparable with those that we all know from the UK, are not wanted in Germany.
 
 
 
 
This also perfectly fits to the fact, that it is at least in Germany well known since 5 days for those who are interested in such information, that Dr. Margit Herbst won the Whistleblower-Prize. You may be not surprised to learn, that this prize is from a scientific association, not from politics. She gets it, because she lost her job, just because she informed the public about the fact that her superiors were not prepared to run the necessary pathological examinations with more than 20 cattle, that she had found to show BSE symptoms between 1990 and 1994 in just one German abattoir. At that time this was the political signal for all German vets not to find any German BSE cases. And as you know, the Bavarian vets were not prepared to let my speak about German BSE risks even in May 2001.
 
 
 
 
I was interested to see, if any of the German members of this list would forward this good news about Dr. Margrit Herbst. In my opinion it is absolutely typical that this was not the case and that again I had to do this.


 
By the way, studying the British BSE statistics I found that the risk to become infected, was sharply declining from birth to the age of about 6 months and that for a given period of time the risk of infection was about 5-times as high for a calf in comparison to adult animals. It is therefore clear, that many cattle became infected only as adults. The detailed analysis will be on my site until the end of this week.
 
 
 
 
kind regards
 
 
 
 
Roland



 
 
 
 
 
 
Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER
 
 
 
 
July 20, 200 1 Date: Thu, 16 Aug 2001 13:52:58 –0400
 
 
 
 
From: "Cook, Nancy" Reply-To: Bovine Spongiform Encephalopathy


 
 
 
 
 
######## Bovine Spongiform Encephalopathy #########
 
 
 
 
Robert, just wanted to comment on your request that the "Do not feed to Cattle or other Ruminants" statement be placed on all animal feeds. In 1997, we undertook a broad, five city survey to determine what effect that statement might have in the marketplace if it occurred on pet food labels.
 
 
 
 
Overwhelmingly, and in all locations, an immediate and severe effect was projected, not only into pet food, but into the Meat Counter as well, as people struggled with the idea that "if it's not good for ruminants (whatever they are?), why should I feed it to my pets, and oh, by the way, why should I eat beef at all if it's a problem?"


 
The Office of Management and Budget agreed with our findings and advised FDA that the labeling was not needed on pet food for retail sale or for laboratory animal feed. However, salvage products are required to bear the statement, since those products are often used for swine feed.
 
 
 
 
In most states, pets are classified as dogs and cats. Specialty pets are other caged and "aquariumed" critters. Horses and rabbits are classified as livestock.
 
 
 
 
Hope this is helpful.
 
 
 
 
Nancy K. Cook Pet Food Institute 2025 M Street, Suite 800 Washington, DC 20036 202-367-1120 202-367-2120 (fax)
 
 
 
 
Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001
 
 
 
 
Date: Fri, 17 Aug 2001 14:37:50 –0700
 
 
 
 
From: "Terry S. Singeltary Sr."
 
 
 
 
Reply-To: Bovine Spongiform Encephalopathy
 
 
 
 
To: BSE-L@uni-karlsruhe.de References: 1
 
 
 
 
######## Bovine Spongiform Encephalopathy #########
 
 
 
 
 
Greetings again List Members,
 
 
 
 
here is a bit of what was thought of pet foods and TSEs in the early days of the BSE Inquiry;
 
 
 
 
 
What is meat and other material from scrapie-infected sheep used for - does it include pet food and material for biological products?
 
 
 
 
 
Pet Food
 
 
 
 
 
As initial preclinical multiplication of the agent takes place in the spleen and other parts of the lympho-reticular system (LRS) there is obviously the possibility that scrapie infected material is used for pet food in addition to material from clinically affected sheep. Sheep spleens are used exclusively for pet foods and processed sheep heads are undoubtedly included.



 
Commercial canned pet food is subject to heat treatment. The following treatments are employed by . . .
 
 
 
 
 
[A table has been deleted here for commercial-in-confidence reasons.]
 
 
 
 
 
snip...
 
 
 
 
 
 
 
 
 
 
18. As it will probably be some months before the answer to No. 17 is known, what steps if any would it be prudent to take in the meantime in clinically affected animals covering a) meat, offal and meat products for human consumption, b) milk, c) material used in the preparation of biologicals and d) pet food?



 
snip...
 
 
 
 
 
Given the difficulties in abattoirs of identifying parts of a given carcass it may be prudent to condemn, for any use, the whole carcass of affected animals. This would seem to be politic given the possible fears from the public of the risk of consuming products from affected animals and therefore unfairly bring all animal products into disrepute.
 
 
 
 
 
 
 
 
6. Might there be a human risk from other animals, eg domestic pets?


 
If scrapie-infected sheep offal is the source of infection for cows, and similar material has gone into pet food, what is the chance of dogs/cats also being infected? Even if they do not show symptoms of disease (say because the incubation period is longer than the natural life span) might they still be infectious? Would there be any chance of transmission to humans through scratches or bites?
 
 
 
 
 
 
 
 
snip...see more here;
 
 
 
 
Thursday, January 5, 2012
 
 
 
 
Horse Meat, slaughter for consumption USA


 
 
 
 
 
Saturday, January 05, 2013
 
 
 
 
Immunohistochemical Detection of Disease- Associated Prion Protein in the Peripheral Nervous System in Experimental H-Type Bovine Spongiform Encephalopathy
 
 
 
 
 
 
 
 
Saturday, December 15, 2012
 
 
 
 
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012
 
 
 
 
 
 
 
 
2012 atypical L-type BSE BASE California reports
 
 
 
 
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
 
 
 
 
Summary Report BSE 2012


 
Executive Summary
 
 
 
 
 
 
 
 
Saturday, August 4, 2012
 
 
 
 
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation


 
 
 
 
 
Saturday, August 4, 2012


 
*** Final Feed Investigation Summary - California BSE Case - July 2012
 
 
 
 
http://transmissiblespongiformencephalopathy.blogspot.com/2012/08/final-feed-investigation-summary.html








HISTORY F.O.I.A. PET FOOD






Saturday, August 29, 2009





FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009





http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html









Thursday, September 3, 2009




429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009




http://madcowfeed.blogspot.com/2009/09/429128-lbs-feed-for-ruminant-animals.html








Friday, September 4, 2009





FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009





http://madcowfeed.blogspot.com/2009_09_01_archive.html







Tuesday, November 3, 2009




re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009




http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html







From: Terry S. Singeltary Sr.



To: CVMHomeP@cvm.fda.gov



Cc: FOIASTAFF@oig.usda.gov ; paffairs@oig.hhs.gov ; HHSTips@oig.hhs.gov ; phyllis.fong@oig.usda.gov





FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009




September 4, 2009




TO:




Food and Drug Administration
Division of Freedom of Information (HFI-35)
Office of Shared Services
Office of Public Information and Library Services
5600 Fishers Lane
Rockville, MD 20857




Or requests may be sent via fax to: fax number 301-443-1726 or 301-443-1719. If experience difficulty sending a fax, please call (301) 443-2414.




FROM:

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518






Greetings FDA FOIE, and the Honorable Phyllis Fong et al @ OIG FOIA,




ANOTHER FOIA REQUEST PLEASE !





PLEASE SEE FULL TEXT ;




Canine Spongiform Encephalopathy CSE TSE





>>> Is anybody even looking at the dogs..especially with CWD now so widespread? <<<





NA, na, na........they know what they will find, Canine Spongiform Encephalopathy, and it was documented, but then they decided not to push the issue anymore, they had enough mad cow disease in different species to deal with. so they screwed the brains up with dogs and deer in the UK. then we took a page or two from the UKs testing protocols and USDA screwed the brains up with cattle, again, and again, and again. then played the stupid card. ya can't fix stupid. ... TSS








Monday, March 8, 2010





Canine Spongiform Encephalopathy aka MAD DOG DISEASE





Greetings,





Another Big Myth about Transmissible Spongiform Encephalopathy, is that TSE will not transmit to dogs. This is simply NOT TRUE. IT is perfectly legal to feed dogs and cats here in the USA bovine meat and bone meal. Canine dementia is real. how many dogs and cats here in the USA are tested for mad cow disease ? I just received this F.O.I.A. request, and thought I would post it here with a follow up on MAD DOG DISEASE. This is a follow up with additional data I just received on a FOIA request in 2009 ;






see full text, and be sure to read the BSE Inquiry documents toward the bottom ;





http://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html







Monday, March 8, 2010





UPDATE 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009





http://madcowfeed.blogspot.com/2010/03/update-429128-lbs-feed-for-ruminant.html







Monday, March 1, 2010




ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010




http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html


 
 
 
 
Friday, November 23, 2012
 
 
 
 
 
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA


 
 
 
 
 
Tuesday, June 26, 2012
 
 
 
 
Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012
 
 
 
 
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA
 
 
 
 
 
 
 
 
Monday, December 31, 2012
 
 
 
 
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012
 
 
 
 
 
 
 
 
Monday, January 14, 2013
 
 
 
 
Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
 
 
 
 
 
 
 
 
TSS