Wednesday, November 17, 2010

Meat from three cows aged over 48 months not tested for BSE exported to France, the Netherlands, Italy, Denmark and the Republic of Ireland

Meat from three cows aged over 48 months not tested for BSE

Wednesday 17 November 2010

The Agency has been notified that meat from three cattle over 48 months of age has entered the food chain without being tested for BSE.

It is very unlikely that the animals were infected with BSE and, as specified risk material (SRM) was removed, any risk to human health is now extremely low. However, testing is mandatory for cattle slaughtered for human consumption at over 48 months of age.*

The cows were slaughtered at the Cig Calon Cymru abattoir at Crosshands, Carmarthenshire and were 64 months of age, 71 months of age and 87 months of age. The failure was discovered on 3 November during routine checks of slaughter and BSE test data. All of the affected carcasses and offal had left the premises at the time of discovery and subsequent checks indicated that all meat and edible co-product is no longer in the food supply chain.

Inspections have indicated that some of the affected product has been exported to France, the Netherlands, Italy, Denmark and the Republic of Ireland. The authorities in these countries have been informed.

*SRM is that part of the animal most likely to contain BSE infectivity.

http://www.food.gov.uk/news/newsarchive/2010/nov/bse117nov


Seven main threats for the future linked to prions

The NeuroPrion network has identified 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

In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.

Third threat

The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.

Fourth threat

Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,

whereas other countries, including the US,

Brazil, and Argentine do not have these constraints.

However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.

Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.

Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.

Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.

http://www.neuroprion.org/en/np-neuroprion.html


Thursday, August 12, 2010

Seven main threats for the future linked to prions

http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html


http://prionpathy.blogspot.com/



Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992


http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html



Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation


http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html



TSS

Thursday, April 8, 2010

FINAL REPORT OF A MISSION CARRIED OUT IN THE UNITED KINGDOM FROM 19 TO 29 JANUARY 2010 IN ORDER TO EVALUATE MEASURES CONCERNING BSE

DG(SANCO) 2010-8344 - MR FINAL

FINAL REPORT OF A MISSION CARRIED OUT IN THE UNITED KINGDOM

FROM 19 TO 29 JANUARY 2010

IN ORDER TO EVALUATE MEASURES CONCERNING BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)

In response to information provided by the Competent Authority, any factual error noted in the draft report has been corrected; any clarification appears in the form of a footnote.

Executive Summary

This report describes the outcome of a Food and Veterinary Office specific audit carried out between 19 to 29 January 2010, which formed part of the general audit 2009 of the United Kingdom conducted under the provisions of Regulation (EC) No 882/2004.

As part of the general audit, the objective of this specific audit was to evaluate that official controls are carried out in conformity with the multi-annual national control plan drawn up in accordance within Article 41 of Regulation (EC) No 882/2004. The specific audit evaluated the implementation of certain protective measures against Bovine Spongiform Encephalopathy (BSE).

Overall, the report concludes that active surveillance was satisfactory and that some progress has been made as regards the quality of samples for BSE testing. Passive surveillance was appropriately carried out and measures related to suspect animals and following confirmation of BSE were implemented in line with Community requirements.

The arrangements in place for collection and handling of specified risk material were mainly satisfactory, although there were some weaknesses in commercial documentation.

In Great Britain, the identification of users of fish meal and feed containing fish meal has significantly progressed but the registration and authorisation process of such users was far from being completed. Some important steps have been taken to improve the risk prioritisation of inspections, but it remains affected by an incomplete knowledge of some key feed operators. In Northern Ireland, the identification of users of feed containing fish meal was still on-going. The priorities set for inspections in the national control programme were not complied with, resulting in very few visits to on-farm mixers and mixed species farms, including those using fish meal or feed containing fish meal; moreover, the prioritisation of feed ban controls did not take account of the significant use of bulk feather meal as organic fertilisers on farms. The large majority of the said farms were therefore not visited despite several incidents concerning cross-contamination of feed with feather meal that occurred in the recent past. In addition, limited enforcement actions and sanctions had been taken following a number of breaches of feed ban rules.

The report makes a number of recommendations addressed to the United Kingdom competent authorities aimed at rectifying the shortcoming identified and further enhancing the implementing and control measures in place.

snip...

5.5 FEED BAN

5.5.1 Requirements along the chain

Legal requirements

Art. 7 of Regulation (EC) No 999/2001 prohibits the feeding to farmed animals of products derived from animals in accordance with the conditions laid down in its Annex IV, which establishes a number of derogations from the said prohibition and specific conditions for the application of such derogations.

Findings

The relevant recommendation of report 8316/2006 concerned the authorisation of establishments using fish meal for the production of feed, the use of feed containing fish meal on mixed species farms and the labelling of feed containing fish meal. In response to this recommendation, the CCA undertook to take all necessary actions in the following National Feed Audit (NFA) programmes. Since the last mission, the procedure in place for authorising and registering users of fish meal or other derogated products derived from animals, which is described in detail in report 8316/2006, has been simplified. In Great Britain, authorisations to produce feed containing derogated products derived from animals have replaced registrations as in both cases the requirements to comply with were deemed very similar. Official permission to store or use complete feed containing derogated products derived from animals on premises with ruminants present is granted following a satisfactory official inspection.

According to DARD and DEFRA, there is no evidence of use of dicalcium or tricalcium phosphate of animal origin in the United Kingdom. Concerning the use of blood and blood products, both the CCAs declared their use is very limited, and one industry assurance scheme in the UK includes a voluntary ban on the feeding of blood products to pigs.

Commission Regulation (EC) No 956/2008 has not yet been transposed into BSE domestic legislation, which therefore does not provide for a derogation in relation to the use of fish meal to unweaned farmed animals of the ruminant species. Consultations are on-going or about to be launched by the different CCA in order to amend the different domestic legislations. A few samples on milk replacers have been taken in Great Britain but were tested negative for the presence of fish meal. According to DEFRA, little interest has been expressed by the feed industry and farmers associations as regards the use of fish meal in milk replacers.

The mission team noted that:

• Lists of authorised users of fish meal were being kept by AH and DARD. However, in Northern Ireland, the activities indicated on the list of users did not always reflect the actual activities carried out by the operators.

• In Great Britain, important progress has been made in the identification, authorisation and permitting process of users of fish meal and feed containing fish meal. AH achieved such progress by requesting feed mills to provide the lists of purchasers of fish meal and feed containing fish meal. As a result of this exercise, around 10,000 purchasers were identified. The central operations delivery team of AH, which has taken over the authorisation and permissions database, had already contacted around 5,200 of these premises and 393 had been sent to AHROs and AHDOs for inspections, resulting in 329 of them being authorised or permitted. However, the identification process is still incomplete as one half of the purchasers identified (around 5,000) has still to be contacted.

• The tracing exercise carried out centrally by AH focused on farms purchasing fish meal and feed containing fish meal. According to AH, intermediaries or feed stores present on the lists obtained and possibly supplying such feed to other farms or feed operators have not yet been contacted. In some of the AHOs and AHDOs visited, AH staff requested updates of lists of purchasers of feed containing fish meal from local feed business operators. In some cases, such lists (which contained significant proportions of new purchasers) have been sent to AH central operations delivery team (further delaying their authorisation or permission) while in other cases they have been dealt with at local level.

• AH staff inspecting ABP plants, in particular those handling fish meal, have been requested to forward to the NFA lead veterinary officer any relevant information allowing the identification of users. However, importers, brokers or storage plants have not yet been requested to provide list of purchasers of fish meal and it could be confirmed that a limited feed back has been received from AH staff performing ABP inspections; for instance, not all plants involved in bulk storage of fish meal were known by the NFA lead veterinary officer.

• In Northern Ireland, DARD had recently obtained lists of purchasers of feed containing fish meal from feed mills. Around 70 farms keeping ruminants and non-ruminants and buying such feed have been identified and are in the process of being registered.

• All authorised users of fish meal visited were also producing ruminant feed. Adequate arrangements, including physical separation and dedication of equipments or means of transports, were in place to avoid cross-contamination of ruminant feed except in one onfarm mixer visited, where there was an incomplete physical separation between the storage of bulk feed material used for ruminant feed and the area where feed containing fish meal was manufactured.

• Labelling requirements for fish meal and feed containing fish meal were complied with and in most cases a warning sentence was printed on the bags. In one on-farm mixer visited, bags of fish meal were not properly labelled but this had been identified by AH which had taken immediate corrective actions.

• On a number of consignments of imported fish meal checked during the mission, it was verified that microscopy testing had been carried before they were released for free circulation.

Conclusions

Legal and administrative arrangements are in place in order to ensure that the use of products derived from animals is subject to the requirements of Art. 7 of Regulation (EC) No 999/2001 and there is a good level of compliance amongst the feed operators using derogated products derived from animals. However, even if the authorisation and permission process of such users has made important progress since the last FVO mission, it is still far from being completed. As a consequence, it can not be yet ensured that the use of derogated products derived from animals is always carried out in accordance with the conditions established in Annex IV to Regulation (EC) No 999/2001.

snip...

6 OVERALL CONCLUSIONS

Active surveillance was satisfactory and that some progress has been made as regards the quality of samples for BSE testing. Passive surveillance was appropriately carried out and measures related to suspect animals and following confirmation of BSE were implemented in line with Community requirements.

The arrangements in place for collection and handling of specified risk material were mainly satisfactory, although there were some weaknesses in commercial documentation.

In Great Britain, the identification of users of fish meal and feed containing fish meal has significantly progressed but the registration and authorisation process of such users was far from being completed. Some important steps have been taken to improve the risk prioritisation of inspections, but it remains affected by an incomplete knowledge of some key feed operators.

In Northern Ireland, the identification of users of feed containing fish meal was still on-going. The priorities set for inspections in the national control programme were not complied with, resulting in very few visits to on-farm mixers and mixed species farms, including those using fish meal or feed containing fish meal; moreover, the prioritisation of feed ban controls did not take account of the significant use of bulk feather meal as organic fertilisers on farms. The large majority of the said farms were therefore not visited despite several incidents concerning cross-contamination of feed with feather meal that occurred in the recent past. In addition, limited enforcement actions and sanctions had been taken following a number of breaches of feed ban rules.


5.1 BSE SITUATION

The number of BSE positive cases in Great Britain and Northern Ireland is shown in the table below (data as of 31 December 2009; information provided by the DEFRA).

The last BSE positive case identified by passive surveillance in a herd without previous BSE cases occurred in 2007. In 2009, six BSE positive cases were animals born before 1 August 1996.


Great Britain Northern Ireland

Passive surveillance Active surveillance Passive surveillance Active surveillance


2007 7 46 0 14

2008 2 31 0 4

2009 1 8 0 3


snip...please see full text here ;

http://ec.europa.eu/food/fvo/act_getPDF.cfm?PDF_ID=8070


16 March 2010

Annex 1 – Comments on DG(SANCO) 2010-8344 – MR DRAFT

BSE Measures

Section Reference Page UK Comment Abbreviations III

Amend “Department for Agriculture and Rural Development” to “Department of Agriculture and Rural Development”

1

With regards to the sentence commencing “Representatives of the Food Standard Agency and of the Meat Hygiene Service”, note that there were no representatives of the Food Standards Agency present at the slaughterhouse in England.

5.1 3

The sentence “Since then [2007], BSE cases were notified either in sub-populations of fallen stock or animals slaughtered for human consumption” is incorrect as there were cases detected as clinical suspects, by passive surveillance in 2008 and 2009.

5.1 3

The sentence commencing “In 2009, the last...” should be amended as follows “In 2009, six BSE positive cases were animals born before 1 August 1996”

5.2.1 (Bullet 1) 4

Amend “Cattle Cohort and Offspring System” to “Offspring and Cohort Cull (OCC) System”.

5.2.2 (Bullet 2) 5

Amend “In one of the slaughterhouse visited...” to “In one of the slaughterhouses visited...”

5.2.3 (Findings)

5

In sentence commencing “The relevant recommendations of report...” amend “from being slaughter” to “from being slaughtered”.

5.2.3 (First full paragraph on page) 6

Replace paragraph beginning “According to DARD...” with “According to DARD, several changes have been introduced in procedures concerning the extraction and entry of data from and onto APHIS. The Required Method of Operations (RMOPs) in all slaughterhouses were reviewed and amended to require post slaughter identification checks. These are designed to ensure the correct identification of all animals prior to BSE sampling."

5.2.3 (Fourth full paragraph on page) 6

The facility to check the cattle ID database (i.e. CTS) at slaughterhouses does not apply in GB. GB operates the policy of passport seizure. NI does not use passports.

? Amend the sentence commencing “DEFRA continued the policy which had been implemented...” to “The CCAs in Great Britain continued the policy which had been implemented...”

? Amend the sentence commencing “In addition restricted animals received special status in CTS and APHIS, which allows their identification at slaughterhouses...” to “In Northern Ireland, restricted animals received special status

16 March 2010

2

in APHIS, which allows their identification at slaughterhouses...”

5.2.3 (Bullet 3) 7

Amend the paragraph commencing “According to the OV met in the slaughterhouse...” to “According to the OV met in the slaughterhouse visited in Northern Ireland, animals with clinical signs consistent with BSE would be rejected at ante-mortem inspection, and animals with localized lesions such as distal limb lameness were not recorded as sick at ante-mortem and therefore considered as healthy slaughtered. On the spot checks detected one animal which should have been recorded as sick at ante-mortem but which was recorded as healthy slaughtered. All ante-mortem information was recorded on APHIS and this triggered the BSE testing category on the sample label, however timing of data entry could result in the default printing of the label as healthy slaughtered”.

5.2.3 (Bullet 6) 7

Amend the paragraph commencing “In Northern Ireland, there was...” to “In Northern Ireland, there was one case in 2009 where a bovine animal eligible for testing was slaughtered for human consumption and not tested. According to the CCA, this was due to a human error by the manufacturer of a replacement tag. When this error was identified, the meat from this animal had already been placed on the market. Following that case, an additional document verification procedure was put in place in the lairage for animals of all ages as an obligatory check.” 5.2.3 (Conclusions)

8

DARD considers that the conclusions reached are overstated based on the evidence identified. Further evidence of subpopulation recording can be provided. For example:

? in 2008 in NI, 426 UA (24-30 month sick at ante-mortem animals) category animals were recorded. 101 of these were identified in the slaughterhouse visited;

? in 2009 in NI, 71 TC (O48 emergency slaughter) category animals were recorded. 18 of these were identified in the slaughterhouse visited; and

? in 2009 in NI, 218 TA (O48 sick at ante-mortem animals) were recorded. Further statistics are available at

http://www.defra.gov.uk/vla/science/docs/sci_tse_stats_ireland.pdf


5.2.4 (Findings, second paragraph)

8

The number 54000 in the sentence commencing “According to the CCA...” is incorrect. In the response to the evaluation plan, we advised that as of 30 September 2009, there were around 75000 cattle in GB born before 1 August 1996, of which around 54000 were born before 1 August 1995. As of 1 February 2010, the number of cattle in GB born before 1 August 1996 had reduced to 66834 of which 48275 were born before 1 August 1995.

5.2.4 8

Amend the sentence commencing “A similar situation was not

16 March 2010 3

(Findings, second paragraph) observed...” to “Although the OCDS ended on 31 December 2008, cattle keepers in NI could still avail of the free collection and disposal service for these older fallen cattle until November 2009”.

5.3 (Findings) 9

In the sentence commencing “Following the confirmation of BSE...” delete the words “all cattle on the affected farm (if necessary)” as we only have powers to kill cohorts and offspring in line with Regulation (EC) No.999/2001 5.4.1 (Findings, Bullet 4) 10

The MHS has clarified that at the time of the visit to the slaughterhouse in England, there were five vehicles on site used to transport animal by-products. Three vehicles were in use and two were empty. One vehicle was in the boning hall disposal bay and contained Category 3 material. It was labelled “Category 3” with a temporary paper label which was not strictly compliant with Regulation (EC) No.1774/2002 in that it did not contain the words “not for human consumption”. Two vehicles were in the back yard, contained SRM and were correctly labelled “Category 1 – for disposal only”. Two vehicles were in the front yard, were empty and unlabelled and were awaiting Category 3 material.

Delete the sentence “However, in one of them (England), means of transport used for the collection of SRM were not identified as required as no category nor any warning sentence were mentioned on most of the trailers used.”

5.4.1 (Findings, first paragraph on page)

11 Fat is combusted in the plant in NI at between 1200°C and 1400°C. The figure of 950°C quoted during the mission was the temperature reached in the secondary chamber where vapours from the plant are oxidised.

5.4.1

(Conclusions)

11

With reference to the clarification above (Section 5.4.1 on page 10) regarding identification of vehicles used to transport SRM, amend the sentence commencing “However, the traceability of SRM...” to “However, the traceability of SRM was affected by weaknesses in commercial documentation, which was not in line with the requirement in Art. 7 of Regulation (EC) No 1774/2002”.

5.4.2 (Findings, Bullet 2)

11

Amend the sentence commencing “In was only after several months...” to “It was only after several months”. 5.4.2 (Final sub-bullet)

12

In the paragraph commencing “Validation of Category 1 processing plants visited...” the official has clarified that although the plant was validated based on the particle size after the cooker, the official had since insisted on changes to the plant to allow the particle size to be assessed before the cooker. This historic deficiency regarding visual assessment of the particle size had been rectified by the time of the FVO mission visit. 5.5.1 (Findings, third paragraph)

13

With regards to the sentence commencing “According to DARD and DEFRA, there



To see the Competent Authority comments on the draft report, click here ( (255Kb) -

http://ec.europa.eu/food/fvo/act_getPDFannx.cfm?ANX_ID=6221


To see the Competent Authority response to the report recommendations, click here

http://ec.europa.eu/food/fvo/ap/ap_gb_2010-8344.pdf



FISH AND PRIONS

Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea Bream (Sparus aurata)

In transmissible spongiform encephalopathies (TSEs), a group of fatal neurodegenerative disorders affecting many species, the key event in disease pathogenesis is the accumulation of an abnormal conformational isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). While the precise mechanism of the PrPC to PrPSc conversion is not understood, it is clear that host PrPC expression is a prerequisite for effective infectious prion propagation. Although there have been many studies on TSEs in mammalian species, little is known about TSE pathogenesis in fish. Here we show that while gilthead sea bream (Sparus aurata) orally challenged with brain homogenates prepared either from a BSE infected cow or from scrapie infected sheep developed no clinical prion disease, the brains of TSE-fed fish sampled two years after challenge did show signs of neurodegeneration and accumulation of deposits that reacted positively with antibodies raised against sea bream PrP. The control groups, fed with brains from uninfected animals, showed no such signs. Remarkably, the deposits developed much more rapidly and extensively in fish inoculated with BSE-infected material than in the ones challenged with the scrapie-infected brain homogenate, with numerous deposits being proteinase K-resistant. These plaque-like aggregates exhibited congophilia and birefringence in polarized light, consistent with an amyloid-like component. The neurodegeneration and abnormal deposition in the brains of fish challenged with prion, especially BSE, raises concerns about the potential risk to public health. As fish aquaculture is an economically important industry providing high protein nutrition for humans and other mammalian species, the prospect of farmed fish being contaminated with infectious mammalian PrPSc, or of a prion disease developing in farmed fish is alarming and requires further evaluation.

Article Metrics Related Content Comments: 1 To add a note, highlight some text. Hide notes Make a general comment Jump to

Acknowledgments Author Contributions References Evgenia Salta1#, Cynthia Panagiotidis2#, Konstantinos Teliousis3, Spyros Petrakis1,4, Eleftherios Eleftheriadis5, Fotis Arapoglou5, Nikolaos Grigoriadis6, Anna Nicolaou7, Eleni Kaldrymidou3, Grigorios Krey5, Theodoros Sklaviadis2*

1 Department of Pharmacology, Aristotle University of Thessaloniki, Thessaloniki, Greece, 2 Centre for Research and Technology-Hellas, Institute of Agrobiotechnology, Thessaloniki, Greece, 3 Laboratory of Pathology, School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece, 4 Max Delbruck Center for Molecular Medicine, Department of Neuroproteomics, Berlin-Buch, Germany, 5 National Agricultural Research Foundation, Fisheries Research Institute, Nea Peramos, Greece, 6 B' Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece, 7 Department of Business Administration, University of Macedonia, Thessaloniki, Greece

http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0006175


WONDER where all this fish feed that is not supposed to be fed to ruminants is going ?

PRODUCT a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6; Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6; c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6; d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6 CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags

DISTRIBUTION AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html


Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST

PRODUCT a) CO-OP 32% Sinking Catfish, Recall # V-100-6; Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE Product manufactured from 02/01/2005 until 06/06/2006 RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.

REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 125 tons DISTRIBUTION AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


CJD WATCH MESSAGE BOARD TSS MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II ______________________________ PRODUCT a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6; b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6; c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; d) Feather Meal, Recall # V-082-6 CODE a) Bulk b) None c) Bulk d) Bulk RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing. REASON Possible contamination of animal feeds with ruminent derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons DISTRIBUTION Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html


see ;

http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html



STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf



greetings,

Confucius is confused yet again. how can you be a consultant of something that has not happened yet ???

is this a typo, or what ??? what is R Bradley speaking of in 1983 ??? what is this BSE CONSULTANT in 1983??? i am confused, i thought the first cow documented was 1985, first discovered in 1984, and the diagnosis was rabies or something else besides BSE at first, then later discovered to be BSE, a new strain of TSE in the bovine. ...

BSE CONSULTANT

APPROVAL OF MATERIAL FOR PUBLICATION

All material for publication including written works to be published in scientific journals, books, proceedings of scientific meetings, abstracts of verbally delivered papers and the like should be scrutinized for risk to the Ministry before dispatch to the publisher. ...

snip...

R Bradly Pathology 12 October 1983

http://www.bseinquiry.gov.uk/files/yb/1983/10/12001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1984/12/28001001.pdf


1981 nervous disease in a Hereford calf (calves aged 7-14 days shoring progressive nervous signs of the hind limb weakness progressing to paraplegia. ...

http://www.bseinquiry.gov.uk/files/yb/1984/01/30001001.pdf


Pathologist: Carol Richardson

DIAGNOSIS: 1. Moderat spongiform encephalopathy- acute. 2. Mild renal nephrosis - peracute

REMARKS: These acute changes suggest a toxicity of some description. The non-suppurative reactions are far more chronic, mild and non-specific.

http://www.bseinquiry.gov.uk/files/yb/1985/09/19001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1985/09/19003001.pdf


Owner of animal, Mr. Stent

snip...

FINAL REPORT

Attempts at virus isolation have proved negative.

http://www.bseinquiry.gov.uk/files/yb/1985/09/23001001.pdf


Cases reviewed and discussed, ...No conclusion drawn....

GAH Wells

http://www.bseinquiry.gov.uk/files/yb/1985/09/26001001.pdf


Subject: Carol Richardson $ BSE
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 1 Nov 2000 09:51:39 -0800 Content-Type: text/plain Parts/Attachments: text/plain (345 lines)

######### Bovine Spongiform Encephalopathy #########

Greetings List,

dont know if this will help calm nerves a bit, but you might find what you want here, in one of those reference YB numbers. her hand-written notes on the case would be; YB85/9.10/3.1-3.2

It was not, therefore, immediately apparent from the post-mortem histopathological examination of the brain of one animal in this herd that it was the first and unprecedented case of a new disease. Even though it can now be seen, with hindsight, that such was the case.

kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA

=============================================

The Stent farm cases

12. On 10th September, 1985 specimens (brain, kidney and spinal cord) from a cow owned by a Mr Stent of Pitsham Farm was referred to the CVL by the Winchester VI Centre (Mr J. Watkin-Jones, Veterinary Officer (VO)) for histopathological examination. Referrals from the VI Centres were dealt with on a rota system by the Consultative Pathology Unit (see paragraph 9 above). The veterinary pathologist on duty when the case came in to the Pathology Department was Ms Carol Richardson. At the time both Carol Richardson and I held the position of Senior Research Officer Grade II (SROII), both of us reporting directly to Ray Bradley. Carol Richardson worked in a section of the Department called Ruminant Reproductive Pathology and I believe that she had been working mainly on reproductive disorders in cattle and sheep, with a particular interest in research into infections producing foetal damage. She would, however, have dealt with scrapie cases through some of her previous work with Dr Stanley Terlecki, a former pathologist in the Department.

13. When such diagnostic cases came into CVL from a VI Centre the technician on duty at the time completed a VL99 card summarising the clinical history of the cow and the herd it originated from (based on information provided in the referral letter from the relevant VI Centre). The duty veterinary pathologist prepared the necessary pathological material for histological processing. Sections were then produced from the animal tissues for subsequent examination. The VL99 card for this particular case from Mr Stent's farm is found at YB85/9.10/3.1-3.2. This card and the prepared sections would then have been passed back to the duty veterinary pathologist for examination, which in this instance was Carol Richardson.

14. Carol Richardson conducted the histopathological examination and reported her findings on 19th September, 1985 (YB85/9.10/3.1-3.2). Her hand-written notes on the examination are on the VL99 card (see YB85/9.10/3.1-3.2). The final pathology report prepared by Carol Richardson, which was sent to Mr Watkin-Jones at Winchester VI Centre, is found at YB85/9.19/3.2. It should be noted that the purpose of the pathology reports prepared by the veterinary pathologists for such referrals from VI Centres is to make morphological diagnoses based on an examination of specimens provided. As far as is possible the pathologist then tries to place the diagnosis in the context of the clinical history of the particular animal and its herd or flock to reach conclusions or speculations on an aetiological diagnosis (the cause of the observed changes). This is the purpose of the "Remarks" section of the pathology report. Carol Richardson's examination reported "moderate spongiform encephalopathy" and "mild renal nephrosis" (the morphological diagnoses) and she attributed these observed changes to "a toxicity of some description" (the possible aetiological diagnosis). This was what was reported to the VI Centre. It is notable that nowhere in her report does she mention scrapie or indicate that her observations lead her to suspect any "scrapie-like" disease. The fact that the report mentions "moderate spongiform encephalopathy" is not conclusive in that respect. As highlighted by my short paper on vacuolation previously referred to in paragraph 8, spongiform conditions of the brain can arise from several different causes, including as a reaction to the ingestion of toxic substances, so this observation was consistent with her suggested aetiological diagnosis.

15. At the time this case came in from Mr Stent's farm, I was attending a meeting of the Charles Davis DVM Foundation for Veterinary Pathology in Cheshire. As is often the practice between pathologists in the event of encountering unusual or unexplained findings, Carol Richardson left the specimens and her pathology report for me to examine immediately on my return. A copy of Carol Richardson's report of 19th September, 1985 as annotated in manuscript by myself, is found at YB85/9.19/3.1. When sections are left for colleagues to examine it is not expected that any particular action would be taken by the colleague on his or her own initiative in respect of those sections. The purpose would be simply to offer a view on the material and then return the sections and report to the original examining pathologist, as was the case in this instance. Carol Richardson was absent from the Department on sick leave from 29th December, 1986, and this subsequently became maternity leave on 31st May, 1987. She returned to the Department on 29th December, 1987. Had Carol Richardson felt strongly thatabout the observations she had originally made were those of scrapie in cattle, and my subsequent opinion on her report, I would have expected that she would have come back to me to discuss the matter subsequently or take the matter further herself. in the period between seeing my annotations on her original report on the Stent case in September 1985 and her absence at the end of December 1985.

16. My re-examination of the sections "reinforcedwas consistent with" her original diagnosis in so far as I agreed with her overall observations and that such observations were not artefactual i.e. caused as a result of post-mortem changes or in the preparation of sections. My conclusion was that the brain lesions observed in this case could not in my experience be attributed to a specific disease, but a speculative comment was made that they could possibly be the result of chronic bacteraemia or an endotoxaemia (the production of poisons in the blood due to infection). Whilst the clinical history as described by the referring VI Centre (see YB85/9.10/3.1) describes that seven out of 130 cows were "nervous", this does not equate necessarily to the occurrence of a specific neurological disorder. The history indicated the occurrence of complex metabolic problems within the Stent herd (see paragraph 17 below).

17. Samples from three other cows in the Stent herd which had died or were killed on the farm had been referred to CVL for examination earlier in March, April and May of 1985 (CVL references VLO11453/85/0286, VLO11453/85/0640 and VLO12473/85/0831 respectively). Following, as far as I can recall, a telephone call from Mr J. Watkin-Jones, on 26th September, 1985 I reviewed the history of the submissions from the Stent herd and discussed them with him. This again, was standard practice where the VIS were investigating a persistent herd problem. A copy of my note of this event, together with the VI Centre referral letters and pathology reports for each case from the Stent farm (with manuscript comments made by myself at the time of this review) are found at YB85/9.26/1.1; YB85/9.10/3.1; YB85/9.19/3.1; YB85/4.31/1.1; YB85/5.9/1.1; YB85/4.6/1.1; YB85/4.16/1.1; YB85/2.13/1.1 and YB85/3.1/1.1 respectively. None of the samples for the three earlier cases included brain tissue and the main post-mortem finding in these cases was internal bleeding. Taken in isolation and in the light of these factors, the case in September 1985 did not at that time suggest that a new disease had been identified. Vacuolar changes in the brain of that particular animal were not severe and there was previous, and current, evidence of other disease problems. The herd from which these animals came had clearly experienced a lot of other health problems including haemorrhagic disorder (internal bleeding), hypocalcaemia (lack of calcium), septic arthritis (pus in joints), renal damage, bovine viral diarrhoea and peritonitis (inflammation of the abdominal cavity) associated with foetal death. This was a complex pattern in a dairy herd indicating that a variety of different diseases might be occurring. It was not, therefore, immediately apparent from the post-mortem histopathological examination of the brain of one animal in this herd that it was the first and unprecedented case of a new disease. Even though it can now be seen, with hindsight, that such was the case.

18. Further samples of nervous system tissues and other organs were received at CVL from a cow in the Stent herd on 10th September, 1986 (YB86/9.22/1.1-1.2). These were examined by Dr S. Done, a veterinary pathologist who joined the Pathology Department in 1983. A copy of the VL99 card for this case is found at YB86/9.22/1.1-1.2. Histopathogical examination of the central nervous system (CNS) tissues submitted from this case showed mild spongiform change in the medulla (hind brain). Other brain regions are described as having either no visible lesions or mild focal haemorrhage. See paragraph 31 for further discussion of this case.

http://www.bse.org.uk/witness/htm/stat065.htm


4.The single case of BSE that I examined in September 1985 was the one and only case that I have seen.

5.The first officially reported case of BSE

Memory recalls a sequence of events the importance of which can only be made by informed judgement. The following account of an interesting and exciting event is taken largely from my memory. I have used copies of the original letter,case card, diagnostic report, accession books and my 1985 organiser diary to make this account as accurate as possible.

6.I had returned from annual leave and was on rota as duty pathologist. The senior technician of the diagnostic unit asked me to examine an adult bovine brain; the vet wanted a diagnosis a.s.a.p.

7.The history was of 7/130 cows showing nervous symptoms over the previous 5 months; most had gone for casualty slaughter and no gross abnormality had been seen in the viscera. (YB85/9.10/1.1).The Pathology Department had examined pieces of liver, kidney, heart and lung from three previous cases from this farm (YB85/2.15/1.1; YB85/4.9/1.1; YB85/5.3/1.1) (2 adults and 1 calf)and had found chronic mild hepatitis(1),acute hepatic necrosis (1) moderate pulmonary oedema (1) and chronic mild interstitial nephritis (2).

8.The history of these earlier cases was one of internal haemorrhage and samples had been sent for organic mercurial poisoning assay. There had been metabolic problems in this herd and active BVD infection in the calves. The case card numbers of these three cases can be seen in the cross-reference column on the case card of the September specimen- MS1509/85 (YB85/9.10/2.1). In addition to the nervous signs seen in this cow, abscessation of the stifle was also present. On gross examination, the brain was well fixed and relatively undamaged; pieces of spinal cord and a piece of kidney were included and were grossly unremarkable. The meninges appeared thickened but this was probably normal for an adult cow.

9.In the absence of gross abnormality, I made multiple incisions and took standard blocks (13) for histological processing and the production of H&E (see procedures) sections. Blocks of spinal cord and kidney were also sent for processing (11/9/85).

10.I have a set sequence for examining brain sections; when these sections were returned to me (13/9/85) I examined the frontal cerebrum first and progressed caudally scanning each section from dorsal to ventral surface. In this case there seemed to be a mild vacuolation of the cerebral neuropil. At this time Gerald Wells had been investigating the possibility that prolonged exposure of nervous tissue to 70% alcohol could produce neuropil vacuolation. Such prolonged exposure would occur over the week-end but I checked with the technician to ensure that such exposure had not occurred in this case before resuming my examination. I noted finding a mild multifocal non-suppurative peri-vascular infiltration with some eosinophils and in the caudal cerebrum mild focal gliosis. No abnormality was found in the thalamus (cranial midbrain) but mild neuropil vacuolation of the reticular formation in the colliculi. The medulla (a pathogonomic site for Scrapie in sheep) showed moderate neuronal and neuropil vacuolation. I found no abnormality in the cerebellum but the section of lumbar spinal cord showed mild neuropil vacuolation of the dorsal horns. There were two types of lesion in the section of kidney;a chronic mild /moderate non-suppurative interstitial reaction with tubular regeneration and fibrosis; a peracute reaction of a mild multifocal tubular necrosis with hydropic change (protein reabsorption).

11.These sections were reviewed by Gerald Wells in 1987 with essentially similar findings but more refined. (See case card at YB85/9.10/2.1).

12.Although I had never seen this type of lesion before in a cow I had frequently seen the combination of neuronal and neuropil vacuolation with this distribution in Scrapie. To me,this was Scrapie in a cow.

13.Before writing the report I sought a second opinion; I needed the opinion of a ruminant neuropathologist and therefore placed the sections, my findings and a request for re-examination on Martin Jeffrey’s bench. I was eager to hear his opinion and immediately after lunch went to collect the slides. Martin had left a note on which was written "Bovine scrapie". As I left his room I met him in the doorway. Apparently this was the first case he had seen but he informed me that Gerald had examined two cases and was expecting another two cases.

14.Interestingly, we apparently had more than one case here from different farms but obviously Gerald was dealing with it. In all my experience, there has not been a case of a novel disease in cattle affecting more than one farm initially: this should have caused alarm bells to ring. If there are several cases at different farms, it is important to cross-reference for the purposes of disease surveillance. A site visit to the Pitsham farm would have resulted in further well-preserved specimens, and more background information.

15.On the 17th-18th Sept. I drafted a batch of diagnostic reports including my report to Winchester VIC (YB85/9.19/1.1).

16.The report is a reiteration of my findings except that the histo-anatomical term `reticular formation’ should have been typed in the sentence above and not under the findings in the medulla. When it came to stating a diagnosis I decided that since the pathological term used for the clinical disease Scrapie of sheep is ovine spongiform encephalopathy then this "new" entity must also be classified as a "spongiform encephalopathy". I called it mild because again projecting onto the sheep situation with only a few sites affected the inclusion of mild as a descriptive term seemed correct. Although there was a chronic interstitial nephritis , I decided to highlight the peracute nephrosis which was probably related to a bacterial toxaemia associated with the stifle abcess.

17.From the history of the case on the Stent farm, it seemed as if the clinical course of the disease was fairly rapid in that metabolic disorders of short duration and heavy metal toxicities were being considered on the farm. Therefore, it seemed likely that the cause(s) of the spongiform changes were a result of an acute clinical disease (rather than a chronic illness) and in the absence of a more likely aetiology, toxicity seemed to be the most appropriate catagory that fitted both symptoms and findings.

18.I dismissed the possibility that a bacterial toxaemia had caused the spongiform change; in my limited experience of ruminant neuropathology, toxaemia was likely to produce frank neuronal necrosis rather than degenerative vacuolation (cf. Clostridial toxaemia).

19.The report was sent for typing; returned and despatched on the 19th September. The second copy and the original letter was filed on VlO 12467, the diagnostic file for cattle diseases. I asked the technician, Dorothy Wells (no relation to Gerald) to cross-reference with similar cases. I always asked the technician to do this, to enter the case numbers of similar cases on the pathology card. In this case I asked Dorothy to cross-reference for the two cases that Gerald had appaerntly already seen.

20.I heard nothing further about my 1985 case.

21.I left the CVL at Christmas 1986, on maternity leave.

http://www.bse.org.uk/witness/htm/stat069.htm



############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############



see full discussion here ;



https://lists.aegee.org/cgi-bin/wa?S2=BSE-L&X=4B20CF095582362D95&Y=flounder9@verizon.net&q=&s=Carol+Richardson&f=&a=&b=




TSS




even the late great Dr. Gibbs once told me personally that even if the Chicken did not contract a TSE, IF the chicken had been fed the TSE tainted feed and then slaughtered, the agent survives the digestinal tract to pass on to other species through feed. The same would hold true with marine fish feed. ..tss


http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html



Tuesday, August 18, 2009

BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html



Monday, April 5, 2010

Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010

http://madcowfeed.blogspot.com/2010/04/update-on-feed-enforcement-activities.html


Wednesday, February 24, 2010

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th

ICID International Scientific Exchange Brochure -

http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html


TSE

http://transmissiblespongiformencephalopathy.blogspot.com/


http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html


Sunday, April 4, 2010

USDA AND OIE OUT OF TOUCH WITH RISK FACTOR ON ATYPICAL TSE

position: Post Doctoral Fellow Atypical BSE in Cattle

Closing date: December 24, 2009

Anticipated start date: January/February 2010

Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta

snip...

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.

snip...

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


http://bseusa.blogspot.com/2010/04/usda-and-oie-out-of-touch-with-risk.html


Monday, March 29, 2010

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas


http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8




>>>Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<


http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html




http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html




2008 - 2010

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html


CJD USA RISING, with UNKNOWN PHENOTYPE ;

5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.

http://www.cjdsurveillance.com/pdf/case-table.pdf


Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html


my comments to PLosone here ;

http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd




Friday, February 05, 2010

New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review

http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html





Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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

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

Adopted: 1 July 2004

Summary (0.1 Mb)

Report (0.2 Mb)

Annex (0.3 Mb)

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 Australia, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Australia. This scientific report addresses the GBR of Australia as assessed in 2004 based on data covering the period 1980-2003.

In the case of Australia, an extremely or very unstable system was exposed to a very low or negligible challenge through the import of cattle. Under these conditions, it is highly unlikely that any internal challenge occurred. Given the negligible level of external challenge through meat and bone meal (MBM), it is highly unlikely that any internal challenge occurred.

The risk that BSE-infected cattle entered processing in Australia and were, at least partly, rendered for feed, due to imported cattle from BSE-risk countries has been very low to negligible throughout the considered period. Some imports of cattle in the early 80s from the UK and from the mid-80s onwards from USA, Canada and European countries increased the risk of BSE infectivity entering the feed chain. However, the probability that BSE contaminated material entered processing is seen as being very low.

EFSA concludes that the current GBR Australia level is I, i.e., it is highly unlikely that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the possibility of cross-contamination exists and there are no serious changes in rendering, the system will continue to be very unstable. Thus, the possibility of cattle being (pre-clinically or clinically) infected with the BSE-agent will remain at a low level.

http://www.efsa.europa.eu/en/scdocs/scdoc/6r.htm


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

Question N° EFSA-Q-2003-083 Adopted July 2004

snip...

EFSA Scientific Report (2004) 6, 1-5 on the Assessment of the Geographical BSE Risk of Australia.

http://www.efsa.eu.int


3 of 6

External Challenge

Australia was exposed to a very low external challenge for the period 1980-1985, a negligible external challenge for the period 1986-1995, a very low external challenge for period 1996-2000, and a negligible external challenge for the period 2001-2003.

Stability

For the overall assessment of the stability, the impact of the three main stability factors, (i.e. feeding, rendering and SRM-removal) and of the additional stability factor surveillance has to be estimated. Again, the guidance provided by the SSC in its opinion on the GBR of July 2000 (as updated in 2002) is applied. Taking the above-summarised discussion of the most relevant stability factors into account, it is concluded that the BSE/cattle system of the Australia was extremely unstable at least until 2001, and slightly improved since then, to very unstable.

Feeding

Until October 1997, ruminant Meat and Bone Meal (ruminant-MBM) was legally fed to cattle. Feeding was therefore "not OK". In October 1997, a ruminant MBM-ban was introduced but feeding of non-ruminant mammalian MBM to cattle remained legal as well as feeding of ruminant-MBM to non-ruminant animals (farm animals and pets). This made control of the feed ban very difficult because analytical differentiation between ruminant and non-ruminant MBM is difficult if not impossible. The ban was further strengthened in 1999 and a comprehensive ban on the feeding of vertebrate MBM to ruminants was put in place in 2001. Given that procedures for auditing and enforcing the ban were also in place by that time, it is assumed that the stability of the system in relation to feeding has been “reasonably OK” since 2001, i.e., voluntary feeding is unlikely but cross contamination cannot be excluded.

Rendering

The rendering industry is operating processes that are not tested with regard to their capacity to reduce BSE-infectivity. It is therefore concluded that rendering was and is "not OK".

SRM-removal

SRM were and are still rendered for feed, as are (parts of) the fallen stock. SRM-removal is therefore regarded as "not OK".

BSE surveillance

• From 1990 to 1997 BSE surveillance remained insufficient, even if a TSE-surveillance program was introduced.

• In 1998, the surveillance system became able to detect BSE to the level set out in the OIE code as a result of the introduction of the NTSESP.

Conclusions

The European Food Safety Authority concludes:

1. In the case of Australia, an extremely or very unstable system was exposed to a very low or negligible challenge through the import of cattle. Under these conditions, it is highly unlikely that any internal challenge occurred. Given the negligible level of EFSA Scientific Report (2004) 6, 1-5 on the Assessment of the Geographical BSE Risk of Australia.

http://www.efsa.eu.int


4 of 6

external challenge through MBM, it is highly unlikely that any internal challenge occurred.

2. The risk that BSE-infected cattle entered processing in Australia, and were at least partly rendered for feed, due to imported cattle from BSE-risk countries has been very low to negligible throughout the considered period. Some imports of cattle in the early 80s from the UK and from the mid-80s onwards from USA, Canada and European countries increased the risk of BSE infectivity entering the feed chain. However, the probability that BSE contaminated material entered processing is seen as being very low.

3. The current geographical BSE-risk (GBR) level is I, i.e., it is highly unlikely that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.

snip... see full text ;

http://www.efsa.europa.eu/en/scdocs/doc/6r.pdf


FOR IMPORTS OF LIVE CATTLE, MBM, GREAVES, ETC INTO AUSTRALIA PLEASE SEE ANNEX !

ANNEX

snip...

2. EXTERNAL CHALLENGES

2.1 Import of cattle from BSE-Risk2 countries

An overview of the data on live cattle imports is presented in table 1 and is based on data as provided in the country dossier (CD) and corresponding data on relevant exports as available from BSE risk countries that exported to Australia. Only data from risk periods are indicated, i.e. those periods when exports from a BSE risk country already represented an external challenge, according to the SSC opinion on the GBR (SSC July 2000 and updated January 2002).

• According to the CD, the import of live cattle has been prohibited from the UK and Ireland since 1988 and from all other countries other than New Zealand, New Caledonia, Canada and the USA since 1991. However, consignments of 42

1 For the purpose of the GBR assessment the abbreviation “MBM” refers to rendering products, in particular the commodities Meat and Bone Meal as such; Meat Meal; Bone Meal; and Greaves. With regard to imports it refers to the customs code 230110 “flours, meals and pellets, made from meat or offal, not fit for human consumption; greaves”.

2 BSE-Risk countries are all countries already assessed as GBR III or IV or with at least one confirmed domestic BSE case. Annex to the EFSA Scientific Report (2004) 6, 1-18 on the Assessment of the Geographical BSE Risk of Australia

- 3 -

buffalo and 24 buffalo from Denmark were recorded in Australia’s import statistics for 1995 and 1996, respectively. The Australian authorities stated that the animals imported in 1995 originated in Italy and that the animals imported in 1996 originated in Bulgaria. Imports from New Caledonia were suspended in 1995.

• The CD states that 204 live cattle were imported for breeding purposes from the UK between 1980 and 1988. According to EUROSTAT, however, 194 cattle were imported during the same period.

• A detailed risk assessment was carried out by the Australian authorities on the cattle that were imported from the United Kingdom. Sixty-two of the imported animals were dairy cattle and nine were dual-purpose animals. Details were provided in the CD in relation to the fate of the imported animals. According to the Australian authorities, 127 of these died and were not rendered. Seven animals remain alive. The remaining seventy animals were slaughtered and presumably entered the food and feed chains.

• In addition to cattle imported from the UK, Australia also imported cattle from other BSE risk countries. According to the CD, Australia imported cattle from Canada (31), Denmark (128), France (185), Ireland (1), Japan (24), and the USA (675). Most of these imports occurred between 1988 and 2003.

• The Eurostat figures are reasonably consistent with those of the CD for Denmark, France and Ireland. However, they indicate that cattle were also imported from Austria (33), Cyprus (1), Germany (86), Hungary (35), Netherlands (124) and Switzerland (9) between 1986 and 2002.

• A detailed risk assessment was carried out by Australian authorities on the imports from European countries other than the UK. This assessment indicates lower numbers of imports from European countries than indicated in the Eurostat data, which are currently being cross-checked by the Australian authorities.

• Information from the Austrian authorities indicated that the export of 33 cattle to Australia from Austria did not, in fact, occur; the country of destination was wrongly coded as AU (Australia) rather than UA (Ukraine), the actual destination of the cattle.

• According to the CD, imports from the Netherlands and Hungary did not occur. However, evidence could not be provided.

• The official USA export figures indicate that a total of 1,441 cattle were exported to Australia from the USA during the period 1993 and 2001. However, information subsequently provided by the only pre-USA export quarantine station that was approved during the time period in question indicated that only 493 cattle were exported to the Australia from the USA during that period. According to the Australian authorities, 190 of the animals imported into Australia between 1996 and 2003 were still alive in early 2004. A further 11 of these animals had died but did not enter the rendering system.

• Official export data were not available for Canada. According to the Australian authorities, 16 of the 21 animals imported from Canada between 1996 and 2003 were still alive in early 2004.

• Official export data were not available for Japan. According to the Australian authorities, 22 of the 24 animals imported from Japan in 1988 were still alive in early 2001 and placed in lifetime quarantine and 2 died on farm and did not enter the rendering system.

snip...

2.2 Import of MBM or MBM-containing feedstuffs from BSE-Risk countries

An overview of the data on MBM imports is presented in table 2 and is based on data provided in the country dossier (CD) and corresponding data on relevant exports as available from BSE risk countries that exported to Australia. Only data from risk periods are indicated, i.e. those periods when exports from a BSE risk country already represented an external challenge, according to the SSC opinion on the GBR (SSC, July 2000 and updated January 2002).

• According to the CD, Australia has imported no MBM from any BSE risk country between 1980 to 2001, as the import of MBM from all countries except New Zealand has been prohibited since 1966. The official import records show that 18 tons of MBM material was imported into Australia from the UK in 1988 and 3 tons in 1994 under the customs code 230110. An investigation by the Australian authorities showed that these imports were fishmeal and packaged dog food. The official import records also show that 7 tons of MBM material was imported into Australia from the USA in 1999 and 9 tons in 2001 under the customs code 230110. An investigation by the Australian authorities showed that the figure for 1999 referred to dried bio-flavour and that the figure for 2001 referred to prepared and packaged dog food for market testing.

• According to Eurostat and other data, Australia has imported no MBM from the UK but has imported 1,824 tons of similar material from other BSE risk countries in Europe. Of these, 43 tons were imported from Denmark in 1996 and 1997, 1,615 tons were imported from France between 1983 and 1985, 22 tons were imported from Germany in 2002, 143 tons were imported from Ireland in 1994 and 1 ton was imported from Italy in 1995.

• The official export figures from the USA showed that 857 tons of MBM was exported to Australia between 1996 and 2001. The official export figures from Canada showed that 163 tons of MBM was exported to Australia in 1998.

• According to the CD, the imports of MBM from Denmark did not take place; however, conclusive evidence was not provided.

• The Australian authorities indicated that coding errors were the most likely reason for these discrepancies. This conclusion was supported by information received from the countries of origin. Such coding errors could include misrepresenting Austria (AUT) as Australia (AUS) or misrepresenting fishmeal and pet food flavourings as meat and bone meal. They pointed out that custom code 230110 may also have been mistakenly used instead of custom code 230910; the latter refers to “dog/cat food put up for retail sale”. Another possibility is that the consignments were refused entry into Australia and were therefore diverted to other markets.

snip...

2.3 Overall assessment of the external challenge

The level of the external challenge that has to be met by the BSE/cattle system is estimated according to the guidance given by the SSC in its final opinion on the GBR of July 2000 (as updated in January 2002).

Live cattle imports:

In total, the country imported over the period 1980 to 2003, 1,248 live cattle from BSE-risk countries, of which 204 came from the UK according to the CD or 2,238 live cattle from BSE-risk countries, of which 194 came from the UK according to other sources. The numbers shown in table 1 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5-years periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow us to assume that certain imported cattle did not enter the domestic BSE/cattle system, i.e. were not rendered into feed. Following a review of the Australian data, it was decided to exclude all animals imported from the UK that were born before June 1976 or were still alive. Imported animals that died on farm were also excluded on the basis of an assurance from the Australian authorities that these animals were placed in lifetime quarantine and, consequently, did not enter the feed chain. A trace back by the Australian authorities showed that some of the animals that were imported from the UK were over 10 years of age at the time of slaughter or death. The Australians considered that the likelihood of these animals contaminating the feed chain with the BSE agent was very low. However, such animals were not excluded from the current assessment because of the fact that many BSE cases have been confirmed in animals over ten years of age in Europe. The Australian risk analysis also took into account the history of the UK farm of origin. Animals from herds of origin in which no cases of BSE were recorded were considered to present no risk. For many of the animals from farms in the UK that did subsequently disclose cases of BSE, the Australian authorities considered that the risk was low because there was a long interval between the data of birth of the imported animals and the date of birth of the cases in the herds of origin. However, such animals were not excluded from the current risk assessment, as per the general procedure of this process, because of the possibility of unreported cases in the herds of origin and the fact that the imported animals could have been the only animals infected with the BSE agent in the herd of origin.

The level of the external challenge as a result of animals imported to Australia from the USA was changed from 1,441 to 493 on the basis of data received from the pre- US export quarantine station. In addition, animals that were still alive or that had been slaughtered but not rendered were removed from the external challenge. Sixteen of the twenty-one animals imported from Canada in 1996 to 2001 were excluded from the external challenge on the basis of information received from the Australian authorities that they were still alive in early 2004. Likewise, the animals imported from Austria in 2001 were excluded from the external challenge on the basis of the explanation from the Austrian authorities that these animals were, in fact, exported to the Ukraine rather than Australia.

snip...

MBM imports:

In total the country imported, over the period 1980-2003, 37 tons under the import code 230110 from BSE-risk countries, of which 21 tons came from the UK according to the CD. Other sources, such as EUROSTAT, indicate that the total import of MBM was 2,844 tons none of which came from the UK. The numbers shown in table 2 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5-year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow us to assume that certain imported MBM did not enter the domestic BSE/cattle system or did not represent an external challenge for other reasons. Following a review of the Australian data, the 22 tons said to have been exported from Germany in 2002 was excluded from the external challenge because the export of processed animal proteins was prohibited from European Union countries from 2001 unless a letter agreement was signed by both countries and the Australians claim (letter dated 21 April 2004) that this was not the case. The 21 tons said to have been exported from the UK in 1988 and 1994 were excluded from the external challenge on the basis of evidence from the Australian authorities that these consignments consisted of fishmeal or dog food. The 143 tons said to have been exported from Ireland in 1994 were excluded from the external challenge on the basis of an assurance from the Irish Chief Veterinary Officer that there was no trade of MBM between Ireland and Australia during the relevant period. All of the imports from Canada, France and the USA were also excluded on the basis of similar assurances from the Chief Veterinary Officer from those countries.

snip...please see full text ;

http://www.efsa.europa.eu/en/scdocs/doc/37rax1.pdf


AUSTRALIA

COMMONWEALTH OF AUSTRALIA

Proof Committee Hansard

SENATE RURAL AND REGIONAL AFFAIRS AND TRANSPORT REFERENCES COMMITTEE Reference: Import restrictions on beef

FRIDAY, 5 FEBRUARY 2010 CANBERRA CONDITIONS OF DISTRIBUTION

This is an uncorrected proof of evidence taken before the committee. It is made available under the condition that it is recognised as such. BY AUTHORITY OF THE SENATE [PROOF COPY] TO EXPEDITE DELIVERY, THIS TRANSCRIPT HAS NOT BEEN SUBEDITED

SNIP...

Friday, 5 February 2010 Senate RRA&T 1

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

Committee met at 9.01 am

CHAIR (Senator Nash)—I declare open this public hearing of the Rural and Regional Affairs and Transport References Committee. The committee is hearing evidence on the committee’s inquiry into the impact and consequences of the government’s decision to relax import restrictions on beef. Before the committee starts taking evidence I remind all witnesses that, in giving evidence to the committee, they are protected by parliamentary privilege. It is unlawful for anyone to threaten or disadvantage a witness on account of evidence given to a committee and such action may be treated by the Senate as a contempt. It is also a contempt to give false or misleading evidence to a committee. The committee prefers all evidence to be given in public but, under the Senate’s resolutions, witnesses have the right to request to be heard in private session. It is important that witnesses give the committee notice if they intend to ask to give evidence in camera. If a witness objects to answering a question, the witness should state the ground upon which the objection is taken and the committee will determine whether it will insist on an answer, having regard to the ground which is claimed. If the committee determines to insist on an answer, a witness may request that the answer be given in camera. Such a request may, of course, also been made at any other time. On behalf of the committee, I thank all those who have made submissions and sent representatives here today for their cooperation in this inquiry.

RRA&T 2 Senate Friday, 5 February 2010

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

[9.03 am]

BELLINGER, Mr Brad, Chairman, Australian Beef Association

CARTER, Mr John Edward, Director, Australian Beef Association

CHAIR—Welcome. Would you like to make an opening statement?

Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:

You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heinemann variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:

The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.

Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:

The BSC policy was set up for one purpose only, trade—the illegal trading of all strains of TSE globally throughout North America, which is home to CBSC, IBSC and HBSC, many scrapie strains and two strains of CJD to date. (please note typo error, those should have read cBSE, lBSE, and hBSE...tss)

I would also like, while I have the opportunity, to explain the beef-off-the-shelves myth. At the first Senate hearing on 14 December, it was explained that the reason why they allowed BSC beef into Australia was the beef-off-the-shelves policy, whereby if we found a case of BSC in Australia they would have to recall all—

Friday, 5 February 2010 Senate RRA&T 3

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

Senator HEFFERNAN—Which of course is total BS.

Mr Bellinger—Correct. This is written in the FSANZ document—Food Standards Australia New Zealand. Why isn’t this same policy in New Zealand? It is not—it is only in Australia. We are the only country in the world to have this idiotic policy. So we again call for the tabling of the WTO obligations paperwork. We do not believe that exists.

Mr Carter—We have an additional concern about human health. We are not scientists, but on 18 December, four days after the last hearing here, the BBC reported a new wave of deaths due to variant CJD linked to eating BSE infected beef could be underway. This is based on the work of Professor John Collinge of the National Prion Clinic, who reported that a 2009 death in Scotland was from a different genetic pool to that of the 166 deaths already reported in the UK. Those are all thought to share one gene, but Professor Collinge and his colleagues estimate that up to 350 people in this new group, represented by the person who died in Scotland, could get CJD. He thinks that CJD has moved into a new phase, and the incubation period is a long one. We tender the Australian Red Cross donor policy sheet, which bears out what Senator Back brought up last time, questioning the Chief Medical Officer, and we say that blood from people who were in the UK between 1980 and 1996 is not acceptable. That is the current ruling. We believe this now should be extended to anyone who has visited the UK, and this new evidence should ensure that Australia revisits the science of CJD.

CHAIR—Thank you, Mr Carter. Before we kick off, can I just remind colleagues that we are short of time today, so I ask that we do not traverse ground the we have previously covered and make sure that we stick to new information that is required. Mr Bellinger, when you started you referred to your view that this decision to allow the importation was politically based. I know you are going to go into this in the course of the next 20 minutes or so, but could you just give us a quick outline of what your definition of politically based is and why you think the decision was politically based?

Mr Bellinger—On the lowering of BSE standards: if you go back to 2006, for example, there were five categories for describing countries that had BSE and Australia was in the category for BSE free. Suddenly, by the time the United States got their third instance of BSE, through the influence of Robert Zoellick—who was the trade minister that signed the BSE corresponding side letter in 2004 and was George Bush’s appointment to the WTO—they suddenly changed the five categories to three categories and, instead of being BSE free, Australia became BSE negligible risk. At the time I put out a press release alerting the media to the dangers of this happening, and we are coming to the stage here when suddenly our government is saying, ‘Now let’s allow the importation of beef from BSE affected countries.’ I believe that the WTO has been influenced by large multinational meat processors and retailers to change and allow the trading of BSE beef throughout the world.

CHAIR—Thanks, Mr Bellinger.

Mr Carter—Of course, the side letter that Minister Vaile signed was at the request of Mr Zoellick, who is now in the position that Mr Bellinger has explained.

Senator HEFFERNAN—I just want to put the committee on notice that, if we do not get through what we have got to get through today, I suggest we have another hearing, because this

RRA&T 4 Senate Friday, 5 February 2010

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

is the greatest ambush of Australia’s farmers of all time by a government. The evidence given at the last meeting was deadset lies. The proposition that this whole change of government policy was led by the industry is a deadset lie. While Simon Crean might want to change his mind because of the WTO and his lack of knowledge, the Australian beef industry, as you know, is under great challenge, not only from the currency but also from the undermining of our markets. This is a disgrace.

SNIP...PLEASE SEE FULL TEXT ;

*************

Tuesday, March 16, 2010

COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA

COMMONWEALTH OF AUSTRALIA

Proof Committee Hansard

snip...see full text 110 pages ;

http://www.aph.gov.au/hansard/senate/commttee/S12742.pdf


for those interested, please see much more here ;

http://docket-aphis-2006-0041.blogspot.com/2010/03/commonwealth-of-australia-hansard.html


The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.

http://www.oie.int/boutique/extrait/06heim937950.pdf



USA MAD COW FEED AND SRM IN COMMERCE UPDATE


http://madcowfeed.blogspot.com/2010/04/update-on-feed-enforcement-activities.html


http://madcowfeed.blogspot.com/



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.


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



TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY


http://transmissiblespongiformencephalopathy.blogspot.com/



Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

snip...

I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;

.....snip

''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.

Thanks for your interest.''

Best regards,

Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA

END...TSS

I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS


http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html


Wednesday, March 31, 2010

Atypical BSE in Cattle

http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518