EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)
• Reasonable worst case assumptions have been used in cases where the available information was not fully adequate. Sources of data • Country dossier (CD) consisting of information provided from the country’s authorities in 1997-2004, including the study entitled “Harvard Risk Assessment” (hereafter abbreviated as HRS). Other sources:
• EUROSTAT data on export of "live bovine animals" and on "flour, meal and pellets of meat or offal, unfit for human consumption; greaves" (customs code 230110), covering the period 1980 to 2003.
• UK-export data (UK) on "live bovine animals", and on "Mammalian Flours, Meals and Pellets" MBM1 , 1980-1996.
• Available export data from other BSE-risk countries.
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 the USA. 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 country dossier, 323 cattle were imported directly from the UK, all between 1980 and 1989, and 10 via Canada in 90, 91 and 92. According to Eurostat, 327 cattle were imported from UK. Of these cattle 96% were beef breeding cattle, 4% were dairy cattle. After 1989 an import stop for UK cattle was in effect. 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) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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• Cattle imported from the UK were traced-back in 1995. This trace back exercise provided the details on which the assessment of the HRS of the import risk assessment is based. The animals still alive in 1995 (117 cattle) have been purchased, diagnostic samples were taken, and the carcasses were incinerated. These animals were not taken into account for the external challenge. All these animals tested negative for BSE (histopathology and IHC). Of these 117 cattle 52 came from UK-herds in which one or more cases of BSE later on developed. • For 173 cattle imported from the UK in the 80s, information on their final use is, according to the HRS, lacking and it is indicated that it is possible that some of these animals could have been rendered. In the HRS it is also noted that these animals were imported before the peak of the epidemic and none came from a birth cohort in which a BSE case is known to be developed. However, based on realistic worst case assumptions it has to be assumed that they created a risk if rendered for feed.
• EU export data show that from the EU (excluding UK), 1,663 cattle were exported to the USA since 1980; according to the CD only 460 cattle have been imported from the EU.
• According to the CD, 162 cattle were imported from Ireland between 1980 and 1988 (according to Eurostat 233). The trace back of these animals showed that 22 were found as being excluded from rendering in the US system and 4 were born in US quarantine and were therefore not taken into account for the external challenge.
• According to the CD, 6 cattle from Belgium (Eurostat also 6), 46 from Germany (Eurostat 430), 3 from Austria (Eurostat 0) and 8 from Italy (Eurostat 21) have been imported. The 40 breeding-cattle imported from these countries in 1996 and 1997 were all traced back and none of them entered the US system.
• According to Eurostat, 12 cattle from Denmark and 558 cattle from the Netherlands were imported to the USA. These imports were not indicated in the CD.
• Additionally according to the CD, 235 cattle have been imported from France (403 according to Eurostat) and 103 cattle from Switzerland (48 according to other sources).
• The discrepancy in the EU export data and the import data in the CD (See table 1) can in some cases, be explained by the use of the fiscal year data (from October to September) in the CD.
• Between 235.000 and 1.7 Million (CD and Other sources) cattle per year are imported to the USA from Canada. According to the CD, feeder/slaughter cattle represent typically more around 80% of the imported cattle from Canada; therefore, only 20% of the imported cattle have been taken into account.
• From Japan, 242 animals from a special beef breed were imported. These animals were traced, and were mostly excluded from the US rendering system. At most 39 of these animals have been rendered.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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Table 1: Live cattle imports into the USA (CD) and corresponding exports from BSE risk countries. Source for export data: Eurostat and UK export statistics and, where available, export statistics from other BSE risk countries. Note: Only imports in risk periods (shaded) are taken into account for assessing the external challenge. Risk periods are defined according to the SSC opinion of January 2002. The numbers shown in the table are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 5 - 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 the USA. 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).
• The CD reports import of 5 tons of MBM from the UK. According to Eurostat, 63 tons have been exported from the UK to the USA between 1980 and 1996; however, according the updated MBM statistics from the UK (August 2001) 24 tons of MBM were exported from the UK to the USA between 1980 and 1996; 39 tons exported in 1989 were not confirmed by the updated UK export statistic and therefore not taken into account. A further 38 tons were exported in 1997-1998 and 39 tons in 1999. As it was illegal to export mammalian meat meal, bone meal and MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. Therefore, these imports were not taken into account.
• According to the CD, MBM was imported from Denmark, France, Italy and the Netherlands. It was claimed but not substantiated that these imports were not from ruminant origin, and therefore did not contribute to the BSE risk of the USA.
• The Eurostat export statistics indicated additional exports from Belgium, Greece, Ireland and Spain.
• Very large amounts of MBM (CD and other sources) between 18.000 and 44.000 tons annually were imported from Canada.
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Last updated: 08 September 2004
Adopted July 2004 (Question N� EFSA-Q-2003-083)
Report
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90�s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases. Publication date: 20 August 2004
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
http://www.efsa.eu.int
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Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of United States of America (USA).
Question N° EFSA-Q-2003-083
Adopted July 2004
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
Key words: BSE, geographical risk assessment, GBR, USA, third countries
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
http://www.efsa.eu.int
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Background
History
In 1998, the EC asked the Scientific Steering Committee (SSC) to perform a risk assessment in order to establish the GBR of a country. In July 2000 the SSC adopted its final opinion on "The Geographical Risk of Bovine Spongiform Encephalopathy (GBR)" (as updated in January 2002). It describes a method and a process for the assessment of the GBR and summarises the outcome of its application. Detailed reports on the GBR-assessments were published on the Internet for each of these countries.
Determination of BSE status
In 2001, Regulation (EC) No 999/20011 established the rules for the determination of BSE status of a country. It determines certain measures concerning the control of BSE and concerning trade and importation of certain live animals and animal products.
Annex II of this Regulation lays down the method for the determination of BSE status. This includes two steps: an initial risk assessment, and the evaluation of additional criteria. The method is similar to that laid down in the International Animal Health Code of the International Animal Health Organisation (OIE).
The categorisation of countries has been deferred until July 2005 awaiting a review of the OIE categorisation system. In the meantime a number of transitional measures are in place, in particular concerning specified risk material and import conditions.
State of play
The Scientific Steering Committee issued an opinion on GBR (using the methodology established by the SSC in June 2000 and updated January 2002) for one third of the countries requesting the determination of their BSE status.
Prioritisation
The first priority is the re-assessment of GBR I countries, as currently no TSE related import restrictions (certification of absence of specific risk material (SRM)) apply to GBR I countries.
If the preliminary re-assessment indicates that the current GBR I will not be confirmed, any delay might have negative consequences on consumer health protection. Furthermore, the GBR assessment of neighbouring countries with intensive trade contacts should be dealt with at the same time, because the outcomes are interdependent.
The major trading partners with a GBR II classification should be dealt with as second priority, in view of the SSC opinion on tallow derivatives and the draft guidance note of EMEA.
Terms of reference
In view of the above, the European Commission asks the EFSA to advice on the risk assessment for the appearance of BSE in USA.
1
Regulation (EC) No 999/2001 of the European Parliament and of the Council laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies OJ L 147, 31.5.2001 and updates.
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
http://www.efsa.eu.int
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Assessment
EFSA refers to the Working Group Report (annex) prepared by the EFSA Scientific Expert Working Group on GBR for full details on the assessment.
External Challenge
USA was exposed to a moderate external challenge for the period 1980-1990, a very high external challenge for the period 1991-1995, and an extremely high external challenge for period 1996-2003.
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. On the basis of the available information, it has to be concluded that the country's BSE/cattle system was extremely unstable until today, i.e., it would have recycled and amplified BSE-infectivity very fast, should it have entered the system.
Feeding
Until August 1997, ruminant meat and bone meal (RMBM) was legally fed to cattle. Feeding was therefore "not OK". In August 1997, an RMBM-ban was introduced but feeding of nonruminant MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals (farm animals and pets). An RMBM ban is difficult to maintain, as only labels can distinguish the various MMBMs. This makes control of the feed ban very difficult because analytical differentiation between ruminant and non-ruminant MBM is difficult. Due to the highly specialized production system in the USA, various mammalian MBM streams can be separated. Such a feed ban would therefore be assessed as "reasonably OK", for all regions where this highly specialized system exists. However, several areas in the USA do have mixed farming and mixed feed mills, and in such regions an RMBM ban would not suffice. Additionally, official controls for cattle feeds to control for compliance with the ban started in 2002. Thus, for the whole country, the assessment of the feeding after 1997 remains "not OK", but improving.
Rendering
The rendering industry is operating with processes that are not known to reduce 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
Before 1989, the ability of the system to identify (and eliminate) BSE-cases was limited.
Since 1990 this ability is improved, thanks to a specific (passive) BSE surveillance. The initiated introduction of active surveillance in risk populations should improve the system significantly.
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA). http://www.efsa.eu.int
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Conclusions
The European Food Safety Authority concludes:
1. The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. This cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that meat and bone meal (MBM) imported into the USA reached domestic cattle and lead to an internal challenge in the early nineties.
2. A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
3. The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
4. This assessment deviates from the previous assessment (SSC opinion, 2000) because at that time several exporting countries were not considered a potential risk.
5. It is also worth noting that the current GBR conclusions are not dependent on the large exchange of imports between USA and Canada. External challenge due to exports to the USA from European countries varied from moderate to high. These challenges indicate that it was likely that BSE infectivity was introduced into the North American continent.
6. EFSA and its Scientific Expert Working group on GBR are concerned that the available information was not confirmed by inspection missions as performed by the Food and Veterinary office (FVO – DG SANCO) in Member States and other third countries. They recommend including, as far as feasible, BSE-related aspects in future inspection missions.
Expected development of the GBR
As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
A table summarising the reasons for the current assessment is given in the table below Documentation provided to EFSA
• Letter with the ref D (2003) KVD/ip/420722 from the European Commission requesting a geographical risk assessment for the appearance of BSE in a country.
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
http://www.efsa.eu.int
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• Country Dossier as prepared by the country in response to the EC and EFSA data collection request.
• Other sources of data information i.e. exports from third countries and Eurostat data.
• SSC, July 2000. Final opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
• SSC, January 2002. Updated opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
Acknowledgment
Members of the EFSA Scientific Working Group are acknowledged for their valuable contribution to this mandate. The members are: Didier Calavas, Aline De Koeijer, Michael Gravenor, John Griffin, Dagmar Heim, Matthias Kramer, Riitta Maijala, Mo Salman, Vittorio Silano, Emmanuel Vanopdenbosch, and Stig Widell.
Annex
Details of the assessment are presented in the report as prepared by the EFSA Scientific
Expert Working Group on GBR:
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/574_en.html
EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of United States of America (USA).
http://www.efsa.eu.int 6 of 6
USA, Summary of the GBR Assessment, July 2004 GBR Level : III**
EXTERNAL CHALLENGE STABILITY INTERACTION of EXTERNAL CHALLENGE and STABILITY
1980-1990: Moderate
1991-1995: Very High
1996-2003: Extremely high
1980-2003: Extremely unstable
Live Cattle imports MBM imports Feeding Rendering SRM-removal BSE surveillance
Any external challenge would have met the extremely unstable system and infectivity would have been recycled.
INTERNAL CHALLENGE
An internal challenge was possibly present from 1980 to 1990 and was likely to be present and growing from 1991 to 2003
EXPECTED DEVELOPMENT OF THE GBR
From UK: 323 (CD*) or 327 (other sources of data) From other BSE risk countries: 16.656.490 (CD) or 15.496.449 (other sources of data). *CD: country dossier
From UK: 5 tons (CD) or 101 tons (other sources of data) From other BSE risk countries: 406.547 tons (CD) or 229.701 tons (other sources of data)
1980-2003: Not OK. Feeding of ruminant MBM to cattle legally possible until August 1997.
1980-2003: Not OK. No proof of an effective process in reducing BSEinfectivity is given.
1980-2003: Not OK. SRM are still rendered for feed.
Passive but improving with some testing of risk groups.
As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
** GBR level III: ‘it is likely but not confirmed’ that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety
Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
NOTE TO THE READER Independent experts of the EFSA Scientific Expert Working Group on GBR have produced this report, applying an innovative methodology by a complex process to data that were supplied by the responsible country authorities. Both, the methodology and the process are described in detail in the final opinion of the Scientific Steering Committee (SSC) on "the Geographical Risk of Bovine Spongiform Encephalopathy (GBR)" of 6 July 2000 and its update of 11 January 2002. These opinions are available at the following Internet address: Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 2 - 1. DATA • The available information was sufficient to carry out the qualitative assessment of the GBR.
Table 2: MBM imports into the USA (CD) and corresponding exports from BSE risk countries. Source for export data: Eurostat and UK export statistics and, where available, export statistics from other BSE risk countries. Note:
Only imports in risk periods (shaded) are taken into account for assessing the external risk. Risk periods are defined according to the SSC opinion of January 2002.The numbers shown in the table are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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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 2038 (other sources) or 1128 (CD) live cattle from BSE risk countries other than Canada, of which 327 (other sources) or 323 (CD) came from the UK. From Canada the imports were >500,000 animals per year. 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 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported cattle did not enter the domestic BSE-cattle system, i.e. were not rendered into feed. In the case of the USA, all the animals for which tracing information showed that they were not rendered were excluded from the external challenge.
MBM imports:
In total the country imported 689 tons MBM (CD) or 2,230 tons MBM (other sources) from BSE risk countries other than Canada, of which 5 tons (CD) or 101 tons (other sources) were exported from the UK (UK export data). From Canada, the imports were about 30 000 tons per year. 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 to assume that certain imported MBM did not enter the domestic BSE/cattle system or did not represent an external challenge for other reasons. As it was illegal to export mammalian MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. In the case of the USA imported MBM from UK in 1989 and between 1997 and 1999 was not taken into account.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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External Challenge experienced by the USA
External challenge Reason for this external challenge
Period Overall Level Cattle imports MBM imports Comment
1980 to 1985 Moderate Negligible
1986 to 1990
Moderate
Negligible Low
1991 to 1995 Very high High High
1996 to 2000 Very high
2001 to 2003
Extremely high Very high
Extremely high When Canadian import data are excluded from the assessment, the overall level varies from low to high.
Table 3: External challenge resulting from live cattle and/or MBM imports from the UK and other BSE risk countries. The challenge level is determined according to the SSC-opinion on the GBR of July 2000 (as updated in January 2002).
On the basis of the available information, the overall assessment of the external challenge is as given in table 3.
3. STABILITY
3.1 Overall appreciation of the ability to avoid recycling of BSE infectivity, should it enter processing
Feeding
Use of MBM in cattle feed
• Until 1997 ruminant MBM (RMBM) could legally be included in cattle feed and was indeed commonly fed to cattle of different age and type. Prior to the feed ban the US authorities estimated that 10% of all MBM would deliberately have been fed to cattle.
Feed bans
• A ban to feed (several types of) MMBM to ruminants was put in place in August 1997. Derogation from the ban was granted for pure porcine and equine protein (MBM) coming from designated (single species) rendering plants. This MMBM might still be fed to cattle. Therefore this feed ban is a ruminant to ruminant ban.
• It is planned to prohibit the use of all mammalian and poultry protein in ruminant feed and prohibiting materials from non-ambulatory disabled cattle and dead stock from use in all animal feed.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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Potential for cross-contamination and measures taken against
• The animal production chain in the USA is large-scale industry, which allows for a high level of specialisation and many farm and factories for slaughter, rendering and feed production are dedicated to one species only. This reduces the risk of cross-contamination to a large extend, but this does not apply to regions with a lot of mixed farming.
• Cross-contamination of non-ruminant MBM with RMBM is theoretically possible whenever transport of this material from rendering to feed plants is done in bulk and with the same means of transport. It is unknown if this can be excluded.
• Cross-contamination in feed mills is possible as many feed mills produce compound feeds for different species on the same production line. No data on the structure of the feed industry in the USA were provided by the US authorities that would allow estimating the amount of cattle feed annually produced in mixed feed mills throughout the period 1980-2001. Information on inspection of feed mills shows that this problem is still found, by 2003, in a very small fraction of the industry.
• Since 1997, FDA regulations provide for either the use of separate lines in the production of ruminant feed or specify detailed clean-out procedures to be used between production batches. However, experience in Europe shows that flushing batches etc are not capable to eliminate cross-contamination, even though they reduce it. The efficiency of the required measures cannot be assessed as detailed control data are lacking and samples are not taken for this purpose.
• Feed containing RMBM has labels not to be fed to ruminants, but “on-farm” cross-contamination is regarded to be possible.
• Hence, as reasonable worst case scenario, it is assumed that cattle, in particular dairy cattle, can still be exposed to RMBM and hence to BSE-infectivity, should it enter the feed chain.
• Rendering plants and feed mills are, according to the CD, regularly inspected for compliance with the regulations, throughout the country.
• It is planned to require dedicated equipment or facilities for handling and storing feed and ingredients during manufacturing and transportation, to prevent cross contamination.
Control of Feed bans and cross-contamination
• Since 1997, feed mills that are allowed to use RMBM, and also produce cattle feed (without RMBM), are inspected annually, other may also be inspected. Two types of violations were registered. One type not involving RMBM, the others involving this, this mainly concerns cross-contamination problems. These firms were re-inspected soon. In several cases, products were recalled, sales were closed and/or products were destroyed. Cattle feed is not sampled to test for presence of illegal MBM.
• According to information provided in 1999/2000 by the feed producers, the compliance is assumed by the US authorities to be in the order of magnitude of 70% to ≤90% since 1998, and 30% to ≤70% before. Official control data concerning rendering and feed mill industries were provided and show that action at shortcomings in the production processes (a few percent of the firms) have Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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become severe by the beginning of 2003. However, samples from ruminant feed are not regularly tested for the inclusion of MMBM. Reports from the feed industry in 2000 and 2001 indicate significant shortcomings in the implementation of the ban in that period. This does confirm the known difficulty of implementing and enforcing such a feed ban.
• No examinations are performed to assess cross-contamination with RMBM of the protein (e.g. through non ruminant MBM) that enters cattle feed. Rendering
• The domestic MBM production averages 3 million metric tons per year.
• Almost 60% of the MBM produced originate from ruminants (cattle 59%, sheep 0.6%), 20% from pigs and 20% from poultry.
Raw material used for rendering
• Ruminant material is rendered together with material from other species (approx. 50% of all plants). This is particular significant as SRM will be included. "Free renderers" are known to also process fallen stock.
• Slaughter by-products from different species, including SRM, is the raw material for most rendering plants that are associated with slaughterhouses.
• Some plants process material from one species, e.g. pigs or horses or poultry only.
• The CD does not provide the numbers of plants falling under each category nor of their respective annual production.
Rendering processes
• Four major rendering systems are used in the approximately 280 rendering plants in the USA. All systems operate under atmospheric pressure with temperatures ranging between 100 and 150 °C and different heating times:
- Batch cooker plants (46): 115-125 C°, 30-240 min.
- Continuous tube and disc cooker systems (220): 131-150 °C, 45-90 min.
- Continuous multi-stage evaporator systems (10): 115-125 °C, 20-40 min.
- Continuous preheat/press/evaporator systems (4): 87-120 °C, 240-270 min.
Due to the fact that they operate under atmospheric pressure only, none of the described rendering processes are assumed to reduce BSE-infectivity significantly, should it enter the processing.
SRM and fallen stock
• An SRM-ban for human food has been introduced in 2004. There was however never an SRM ban for the feed chain.
• SRM are rendered together with other slaughter by-products and, in case of independent renderers, together with fallen stock.
• It is planned to remove SRM from all animal feed, including pet-food. Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
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Conclusion on the ability to avoid recycling
• Before 1997, US system would not have been able to avoid recycling of the BSEagent to any measurable extent. If the BSE-agent was introduced into the feed chain, it could have reached cattle.
• After the introduction of the 1997 ban in August 1997, the ability to avoid recycling of BSE-infectivity was somewhat improved. However, the rendering of ruminant material (including SRM and fallen stock) is inadequate (non pressurized), and cross-contamination potentials of cattle feed with other feeds remain.
• Therefore, the system is still unable to avoid recycling of BSE-infectivity if already present in the system or incoming.
3.2 Overall appreciation of the ability to identify BSE-cases and to eliminate animals at risk of being infected before they are processed
Cattle population structure
• The total cattle population of the USA was approximately 111 Million cattle in 1980, 99 Million in 1990, 102.8 Million cattle in 1995 and 99.5 Million cattle in 1998. Of these, approximately 17.6 % (17.5 Million) were dairy cattle and 82.4% beef cattle (based on data 1995-1998). However, the HRS recognised that the official slaughter figures were only compatible with a stable total cattle population of about 140 million.
• Between 17% and 19% of all cattle slaughtered were >2 years of age. The average age at slaughter for dairy cattle is between 4 and 5 years.
Husbandry systems
• According to the country experts it was assumed that mixed farming did exist in the USA, but at a low (and decreasing) level. No figures were provided.
• The two main cattle husbandry systems are beef (82.4%) and dairy (17.6%). Within both systems all levels of intensity are existing, however, both segments are now characterised by large, intensive operations. For dairy cattle a clear trend towards larger, more efficient holdings can be seen.
Maps were presented by the country experts in 1999 that indicate an overlap of intensive cattle, swine and poultry industry in certain geographic regions of the USA.
Cattle identification and monitoring system
• The existing animal identification system is jointly operated by State and Federal representatives and is maintained individually for each State. No centralised USwide animal identification system is in place.
• It was estimated by the country experts that this system ensures that approx. 95% of all cattle are officially tagged and registered in State databases.
• A trace-back of individual animals is possible whenever the animal has not moved several times (through several herds) within a particular State. Intra-State Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 12 -
movements are not recorded in any type of database, and any follow-up would rely on the documentation (records) or the memory of the respective owners.
BSE surveillance
• All foreign animal diseases (exotic diseases) have been and are notifiable by Federal legislation. BSE, as an exotic disease, was notifiable since it first was described as a disease (1986).
• A surveillance targeting animals with clinical signs that could be consistent with BSE is in place since 1989/1990 and operating with larger sample sizes (900-1600 per year) since 1997. This program officially started in 1990 but some samples examined under this system go back to 1986. The samples come from:
- Cattle exhibiting signs of neurological disease;
- Cattle condemned at ante-mortem examination in slaughterhouses for neurological signs;
- Rabies-negative cattle submitted to public-health laboratories (the country experts confirmed that samples were appropriately taken and should have allowed finding BSE if present);
- Neurological cases submitted to veterinary diagnostic laboratories and veterinary schools/teaching hospitals;
- Between 25% and 33% of the animals in the sample were supposed to be aged dairy cattle which are non-ambulatory (“downer cows”) at slaughter. Detailed information on the age distribution of those animals was not available.
• In addition to histopathology, immunhistochemistry is applied since 1994, initially on those animals for which a differential diagnosis could not be established. Since 1997 it is fully incorporated in the surveillance scheme and approx. 900-1.600 samples are examined annually by both tests. In 2000, a total of 2 870 submissions were examined.
• In 2001, the number of submissions doubled, and in 2002 and 2003, submissions totalled 19.777 and 20.277 respectively. The total number of samples examined through April 2004 is more than 72.500.
• A BSE case has been detected in December 2003. Intensive research showed that it was born and raised in Canada, and therefore, it is not a domestic case.
• In addition, since 1 June 2004, an extensive testing of the risk population is initiated. It is planned to test as many cattle from the risk population (the target is 268.000 cattle) in a 12–to–18–month period. The following categories will be tested: non-ambulatory cattle, cattle exhibiting signs of a central nervous system disorder, cattle exhibiting other signs that may be associated with BSE and dead cattle. The surveillance program will also include a limited number of random samples from apparently normal, aged animals.
3.3 Overall assessment of the 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.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 13 -
Feeding
Until August 1997, RMBM was legally fed to cattle. Feeding was therefore "not OK". In August 1997 an RMBM-ban was introduced but feeding of non-ruminant MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals (farm animals and pets). An RMBM ban is difficult to maintain, as only labels can distinguish the various MMBMs. This makes control of the feed ban very difficult because analytical differentiation between ruminant and non-ruminant MBM is difficult if not impossible.
Due to the highly specialised production system in the USA, various mammalian MBM streams can be separated. Such a feed ban would therefore be assessed as "reasonably OK", for all regions where this highly specialised system exists. However, several areas in the USA do have mixed farming and mixed feed mills, and in such regions an RMBM ban would not suffice. Additionally, official controls for cattle feeds to control for compliance with the ban started in 2002. Thus, for the whole country, the assessment of the feeding after 1997 remains "not OK", but improving.
Rendering
The rendering industry is operating with processes that are not known to reduce 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. SRMremoval is therefore regarded as "not OK".
BSE-surveillance
Before 1989, the ability of the system to identify (and eliminate) BSE-cases was limited. Since 1990 this ability is improved, thanks to a specific (passive) BSE surveillance. The initiated introduction of active surveillance in risk populations should improve the system significantly.
Stability of the BSE/cattle system in the USA over time
Stability Reasons
Period Level Feeding Rendering SRM removal BSE surveillance 1980 to 2003
Extremely unstable
Not OK
Not OK
Not OK
Passive but improving with some testing of risk groups
Table 4: Stability resulting from the interaction of the three main stability factors and the BSE surveillance. The stability level is determined according to the SSC-opinion on the GBR of July 2000 (as updated in 2002).
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 14 -
On the basis of the available information, it has to be concluded that the country's BSE/cattle system was extremely unstable until today, i.e., it would have recycled and amplified BSE-infectivity very fast, should it have entered the system. The stability of the BSE/cattle system in the USA overtime is as given in table 4.
The present assessment modifies the stability assessment of the previous GBR report in 2000 mainly due to a different perception of the impact of BSE surveillance on stability and of the efficiency of the RMBM feed ban.
4. CONCLUSION ON THE RESULTING RISKS
4.1 Interaction of stability and challenges
In conclusion, the stability of the USA BSE/cattle system in the past and the external challenge the system has coped with, are summarised in table 5 below. From the interaction of the two parameters “stability” and “external challenge” a conclusion is drawn on the level of “internal challenge” that emerged and had to be met by the system, in addition to external challenges that occurred.
Interaction of stability and external challenge in the USA
Period Stability External Challenge Internal challenge
1980 to 1985 1986 to 1990 Moderate Possibly present 1991 to 1995 Very high 1996 to 2000 2001 to 2003
Extremely unstable
Extremely high
Likely to be present and growing
Table 5: Internal challenge resulting from the interaction of the external challenge and stability. The internal challenge level is determined according to guidance given in the SSC-opinion on the GBR of July 2000 (as updated in 2002).
An external challenge resulting from cattle import could only lead to an internal challenge once imported infected cattle were rendered for feed and this contaminated feed reached domestic cattle. Cattle imported for slaughter would normally be slaughtered at an age too young to harbour plenty of BSE infectivity or to show signs, even if infected prior to import. Breeding cattle, however, would normally live much longer and only animals having problems would be slaughtered younger. If being 4-6 years old when slaughtered, they could suffer from early signs of BSE, being approaching the end of the BSE-incubation period. In that case, they would harbour, while being pre-clinical, as much infectivity as a clinical BSE case. Hence cattle imports could have led to an internal challenge about 3 years after the import of Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 15 -
breeding cattle (that are normally imported at 20-24 months of age) that could have been infected prior to import.
In the case of the USA a few potentially infected cattle were imported from the UK and more from other BSE-risk countries. Furthermore, large numbers of imported animals came from Canada. This implies that cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s.
On the other hand imports of contaminated MBM would lead to an internal challenge in the year of import, if fed to cattle. The feeding system is of utmost importance in this context. If it could be excluded that imported, potentially contaminated feed stuffs reached cattle, such imports might not lead to an internal challenge at all.
In case of the USA this implies that it was possible that imported MBM reached domestic cattle and lead to an internal challenge in the early 90s.
If Canadian imports would be excluded from this assessment, we find that the USA receives a moderate challenge for all 5-year intervals since 1980, a high challenge between 1985 and 2000 and a low challenge thereafter. If combining these moderate to high challenges due to imports with the extremely unstable system, the conclusion would still be that the occurrence of an internal challenge is possible during the early 80s and likely in the late 80s.
4.2 Risk that BSE infectivity entered processing
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
4.3 Risk that BSE infectivity was recycled and propagated
A risk that BSE-infectivity was recycled and propagated exists since a processing risk first appeared, i.e. in the early 90s. Until today this risk persists and increases fast because of the extremely/very unstable BSE/cattle system in the USA.
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
5.1 The current GBR as function of the past stability and challenge
• The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
Note1: It is also worth noting that the current GBR conclusions are not dependent on the large exchange of imports between USA and Canada. External challenge due to exports to the USA from European countries varied from moderate to high. These Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 16 -
challenges indicate that it was likely that BSE infectivity was introduced into the North American continent.
Note2: This assessment deviates from the previous assessment (SSC opinion, 2000) because at that time several exporting countries were not considered a potential risk.
5.2 The expected development of the GBR as a function of the past and present stability and challenge
• As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (preclinically or clinically) infected with the BSE-agent persistently increases.
• Since recent improvements in the safety of MBM production in many countries or significant recent reductions in the incidence of BSE are not taken into account for the assessment of the external challenge, the external challenge assessed after 2001 could be overestimated and is the worst case assumption. However all current GBR conclusions are not dependent on these assumptions in any of the countries assessed. For future assessments and when the impact of the production, surveillance and true incidence changes have been fully quantified, these developments should be taken into account.
5.3 Recommendations for influencing the future GBR
• Measures that improve the stability of the system, will, over time, reduce the probability that cattle could get infected with the BSE-agent. Possible actions include
- removal of SRM and/or fallen stock from rendering of animal by-products into feed,
- high pressure standards in rendering processes,
- significant improvement of ban on use of ruminant MBM in cattle feed, supported by regular sampling of feed for the occurrence of such MBM.
• Improved passive and active surveillance, i.e. sampling of animals not showing signs compatible with BSE from “at-risk” cattle populations, such as adult cattle in fallen stock and emergency slaughter, by means of rapid screening, would allow monitoring the efficiency of stability enhancing measures.
Documentation provided to EFSA
• Letter with the ref D (2003) KVD/ip/420722 from the European Commission requesting a geographical risk assessment for the appearance of BSE in a country.
• Country Dossier as prepared by the country in response to the EC and EFSA data collection request.
• Other sources of data information i.e. exports from third countries and Eurostat data.
• SSC, July 2000. Final opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
- 17 -
• SSC, January 2002. Updated opinion on the Geographical Risk of Bovine Spongiform Encephalopathy (GBR).
Acknowledgment
Members of the EFSA Scientific Expert Working Group on GBR are acknowledged for their valuable contribution to this mandate. The members are: Didier Calavas, Aline De Koeijer, Michael Gravenor, John Griffin, Dagmar Heim, Matthias Kramer, Riitta Maijala, Mo Salman, Vittorio Silano, Emmanuel Vanopdenbosch, and Stig Widell.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
SEAC 91/2
MEDICAL IMPLANTS CONTAINING BOVINE MATERIAL ISSUE
TUESDAY, AUGUST 22, 2017
BSE INQUIRY DFA 16 MID 1995 TO THE FINAL DAYS
TUESDAY, AUGUST 1, 2017
BSE INQUIRY DFA 17 Medicines and medical devices
TUESDAY, AUGUST 1, 2017
Could Insulin be contaminated with and potentially spread, Transmissible Spongiform Encephalopathy TSE Prion, what if?
THURSDAY, AUGUST 3, 2017
BSE INQUIRY DFA 18 COSMETICS FDA OVERSIGHT WARNING The Honorable Frank Pallone, Jr.
SATURDAY, AUGUST 26, 2017
BSE Inquiry
DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations
SATURDAY, AUGUST 26, 2017
BSE Inquiry
DFA 14 Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990
2017
Subject: JAVMA NEWS Atypical BSE found in Alabama cow September 01, 2017
Atypical BSE found in Alabama cow
Posted Aug. 16, 2017
Health authorities found in July that an 11-year-old beef cow in Alabama had bovine spongiform encephalopathy, a degenerative prion disease.
"This animal never entered slaughter channels and at no time presented a risk to the food supply, or to human health in the United States," Department of Agriculture officials said in an announcement.
The cow had an atypical—or spontaneously developing—form of the disease, which differs from the classical form that is contracted through infected feed ingredients, according to the announcement from the USDA Animal and Plant Health Inspection Service. The cow is the fifth known to be infected in the U.S., the first one having been discovered in 2003. That cow had a classical form of BSE, and the rest had atypical forms.
BSE spreads among cattle and to some other animals through consumption of transmissible prion proteins. Consumption of BSE-contaminated materials has been linked with a variant of Creutzfeldt-Jakob disease, a prion disease in humans. But APHIS officials have noted that animal tissues that could contain the BSE agent are prohibited from use in human and animal foods.
Atypical forms of BSE have been identified as L-type—the form found in the Alabama cow—or H-type.
Ryan Maddox, PhD, an epidemiologist in the Prion and Public Health Office of the Centers for Disease Control and Prevention, said L-type atypical BSE has been shown in laboratory conditions to infect both primates and humanized transgenic mice more efficiently than H-type atypical BSE or classical BSE. But he noted that there is no evidence of direct transmission of the L-type form to humans.
Dr. Maddox also said that BSE infections since the 1980s have been associated with disease in about 230 people worldwide, so he would not consider the risk to be extremely high. He also noted that the U.S. has regulations to reduce the risk to humans and animals.
Regulations from the Food and Drug Administration and the USDA prohibit inclusion of mammalian protein in ruminant feed or inclusion of high-risk materials in any animal feed. Examples of materials presenting the highest risk of transmission are the brains and spinal cords of cattle ages 2.5 years and older.
The USDA announcement states that atypical BSE occurs at a low rate in all cattle populations, usually in cattle age 8 years and older. At press time, the World Animal Health Organisation (OIE) had received three other reports of atypical BSE in cattle during 2017, two of them in Spain and one in Ireland.
The OIE lists the United States and Spain among countries considered to have a negligible risk of BSE, and Ireland is considered to have a controlled risk.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
''To assess and monitor for compliance with the feed ban, the FDA established the ruminant feed ban inspection program and guidance to assist both the FDA and State investigators. Feed mill and rendering plant inspections conducted since 1998 indicate a very high level of compliance with the feed ban.''
THERE HAS BEEN LITERALLY 100s if not 1000s OF TONNAGE OF BANNED MAD COW FEED FED OUT INTO COMMERCE AS LATE AS 10 YEARS POST FEED BAN 2007, AND AS RECENTLY AS LAST YEAR 2016 the breach of the mad cow feed ban continued. these are the facts...
P56 Detection of classical BSE prions in the ileal Peyer’s patch of unweaned calves from two months after oral challenge
Ivett Ackermann1, Dr. Anne Balkema-Buschmann1, Dr. Reiner Ulrich2, Dr. Kerstin Tauscher2, Dr. Christine Fast1, Dr. Markus Keller1, James C. Shawulu1, Prof. Dr. Martin H. Groschup1 1Friedrich-Loeffler-Institut, INEID, Greifswald-Insel Riems, Germany, 2Friedrich-Loeffler-Institut, ATB, Greifswald-Insel Riems, Germany
Aims: In cattle the ileal Peyer’s patch (IPP) functions as the entry port for classical BSE prions, as these were detectable from 4 months post experimental challenge of cattle that were 4 to 6 months of age at infection. However, the earliest time point of prion detection in bovines may also be a matter of age, as a recently reported experiment indicated that BSE challenged unweaned lambs are more susceptible than older weaned lambs or adults. To prove this hypothesis and to clarify the dynamics of pathological prion protein (PrPSc) spread during the first 8 months of infection, young unweaned calves were challenged orally with classical BSE prions and the progress of the infection was monitored by assessing the ileal Peyer’s patches to determine – as a proxy of their susceptibility - the earliest time point at which pathological prion protein (PrPSc) and prion infectivity are detectable.
Methods: 18 unweaned Simmental calves aged 4 to 6 weeks were orally challenged with classical BSE, while 2 calves served as negative controls. The animals were euthanized and necropsied at predetermined time points of 1 week as well as 2, 4, 6 and 8 months post infection. To serve as positive controls 2 infected cattle were kept until the development of clinical symptoms of BSE. For each of the 18 infected and 2 negative control calves, samples of the ileal Peyer’s patch were examined by immunohistochemistry (IHC), protein misfolding cyclic amplification (PMCA) and transgenic Tgbov XV mouse bioassay.
Results: In the ileal Peyer’s patches newly generated BSE prions were detectable as early as 2 months post infection (mpi) by PMCA and transgenic mouse bioassay. From 4 mpi, PrPSc accumulation was detectable by IHC in tingible body macrophages (TBMs) of the IPP follicles and already in follicular dendritic cells (FDCs). The positive control animals developed clinical signs of BSE after incubation periods of 32 mpi and 36 mpi, respectively.
Conclusions: The earlier detection of BSE prions in the ileal Peyer’s patches may result from using improved assay protocols for the sample analysis. However, the presented data rather indicate an earlier propagation of BSE prions in the ileal Peyer’s patches as a result of challenging unweaned calves. This is also supported by the observation that the 2 BSE-challenged control animals came down after short incubation times.
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE.
We are further examining explanations for the unusual disease presentation in the third challenged animal.
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplifi- cation (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada
Keywords: Atypical BSE, oral transmission, RT-QuIC
The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.
The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.
Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang 1 , Sandor Dudas 2 , Catherine Graham 2 , Markus Czub 3 , Tim McAllister 1 , Stefanie Czub 1 1 Agriculture and Agri-Food Canada Research Centre, Canada; 2 National and OIE BSE Reference Laboratory, Canada; 3 University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal-specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
USDA announces Alabama case of Atypical L-type BASE Bovine Spongiform Encephalopathy and BANNED FEED
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams.
***It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
2) Infectious dose:
To cattle: 1 gram of infected brain material (by oral ingestion)
SUNDAY, JULY 30, 2017
*** PRION2017 Low levels of classical BSE infectivity in rendered fat tissue
***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
The Presence of Disease-Associated Prion Protein in Skeletal Muscle of Cattle Infected with Classical Bovine Spongiform Encephalopathy
Hiroyuki OKADA,1,* Kohtaro MIYAZAWA,1 Shigeo FUKUDA,2 Yoshifumi IWAMARU,1 Morikazu IMAMURA,1 Kentaro MASUJIN,1 Yuichi MATSUURA,1 Takashi FUJII,2 Kei FUJII,2 Soichi KAGEYAMA,2 Miyako YOSHIOKA,1 Yuichi MURAYAMA,1 and Takashi YOKOYAMA1
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy
Silvia Suardi , Chiara Vimercati , Cristina Casalone , Daniela Gelmetti, Cristiano Corona, Barbara Iulini, Maria Mazza, Guerino Lombardi, Fabio Moda, Margherita Ruggerone, Ilaria Campagnani, Elena Piccoli, Marcella Catania, [ ... ], Fabrizio Tagliavini [ view all ] Published: February 21, 2012 https://doi.org/10.1371/journal.pone.0031449
The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.
Scientists investigate origin of isolated BSE cases
The European response to bovine spongiform encephalopathy (BSE) after the crisis of the 1980s has significantly reduced prevalence of the disease in cattle. However, isolated cases are still being reported in the EU and for this reason the European Commission asked EFSA to investigate their origin.
The key measure for controlling BSE in the EU is a ban on the use of animal proteins in livestock feed. This is because BSE can be transmitted to cattle through contaminated feed, mainly in the first year of life.
Sixty cases of classical BSE have been reported in cattle born after the EU ban was enforced in 2001. None of these animals entered the food chain. Classical BSE is the type of BSE transmissible to humans. The Commission asked EFSA to determine if these cases were caused by contaminated feed or whether they occurred spontaneously, i.e. without an apparent cause.
EFSA experts concluded that contaminated feed is the most likely source of infection. This is because the infectious agent that causes BSE has the ability to remain active for many years. Cattle may have been exposed to contaminated feed because the BSE infectious agent was present where feed was stored or handled. A second possibility is that contaminated feed ingredients may have been imported from non-EU countries.
Experts could not rule out other causes due to the difficulty of investigating individual cases. Some constraints are the long incubation period of the disease and the lack of detailed information available from farms at the time of the trace-back investigation.
EFSA experts made a series of recommendations to maintain and strengthen the EU monitoring and reporting system, and to evaluate new scientific data that become available.
The European response to BSE
The coordinated European response to BSE has succeeded in reducing the prevalence of the disease. Between 2005 and 2015 about 73,000,000 cattle were tested for BSE in the EU, out of which 60 born after the ban tested positive for classical BSE. The number of affected animals rises to 1,259 if cattle born before the ban are included. The number of classical BSE cases has dropped significantly in the EU over time, from 554 cases reported in 2005 to just two in 2015 (both animals born after the ban). Moreover the EU food safety system is designed to prevent the entry of BSE-contaminated meat into the food chain.
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT
Custom dairy premix products:
MNM ALL PURPOSE Pellet,
HILLSIDE/CDL Prot- Buffer Meal,
LEE, M.-CLOSE UP PX Pellet,
HIGH DESERT/ GHC LACT Meal,
TATARKA,
M CUST PROT Meal,
SUNRIDGE/CDL PROTEIN Blend,
LOURENZO, K PVM DAIRY Meal,
DOUBLE B DAIRY/GHC LAC Mineral,
WEST PIONT/GHC CLOSEUP Mineral,
WEST POINT/GHC LACT Meal,
JENKS,
J/COMPASS PROTEIN Meal,
COPPINI - 8# SPECIAL DAIRY Mix,
GULICK, L-LACT Meal (Bulk),
TRIPLE J - PROTEIN/LACTATION,
ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN,
BETTENCOURT #1/GHC MILK MINR,
V&C DAIRY/GHC LACT Meal,
VEENSTRA, F/GHC LACT Meal,
SMUTNY, A- BYPASS ML W/SMARTA,
Recall # V-025-2007
CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs.
DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
ALABAMA MAD COW FEED IN COMMERCE 2006
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) 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
______________________________
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
?????
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
=====
PRODUCT
Bulk Whole Barley, Recall # V-256-2009
CODE
No code or lot number.
RECALLING FIRM/MANUFACTURER
Mars Petcare US, Clinton, OK, by telephone on May 21, 2009. Firm initiated recall is complete.
REASON
Product may have contained prohibited materials without cautionary statement on the label.
VOLUME OF PRODUCT IN COMMERCE
208,820 pounds
DISTRIBUTION
TX
END OF ENFORCEMENT REPORT FOR AUGUST 26, 2009
###
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ?????
Date: August 6, 2006 at 6:19 pm PST
PRODUCT Bulk custom made dairy feed, Recall # V-114-6
CODE None
RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006.
Firm initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE ?????
DISTRIBUTION KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
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
###
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.
You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
PLEASE NOTE, THE FDA URLS FOR OLD WARNING LETTERS ARE OBSOLETE AND DO NOT WORK IN MOST CASES. I LOOKED UP THE OLD ONE ABOVE AND FOUND IT, BUT HAVE NOT DONE THAT FOR THE OTHERS TO FOLLOW. THE DATA IS VALID THOUGH!
Subject: MAD COW PROTEIN IN COMMERCE USA 2006 RECALL UPDATE
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Reply-To: SAFETY <[log in to unmask]>
Date: Mon, 9 Oct 2006 14:10:37 -0500
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS
IN COMMERCE AL, TN, AND WV
Date: September 6, 2006 at 7:58 am PST
PRODUCT a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6. CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006.
Firm initiated recall is complete.
REASON Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
snip...
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
snip...
______________________________
PRODUCT Bulk custom dairy pre-mixes, Recall # V-120-6
CODE None
RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.
REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) 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
###
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;
b) 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
###
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
###
Office of Inspector General Semiannual Report to Congress FY 2007 - 2nd Half
Two Texas Companies Sentenced and Fined for Misbranding Meat Products In April 2007, two closely held and related Texas companies pled guilty in Federal court and were sentenced to 12 months of probation and ordered to pay $10,250 in fines for misbranding meat products. One of the companies sold adulterated meat products to a retail store in New Mexico. Additionally, portions of the invoices failed to properly and consistently identify the meat products as being from cattle more than 30 months old at time of slaughter. This information is required to be disclosed because of bovine spongiform encephalopathy (BSE, or "mad cow disease") concerns. No adulterated meat reached consumers.
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
16 years post mad cow feed ban August 1997 2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
cwd to pig, orally ;
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
MONDAY, AUGUST 14, 2017
Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
2017
TUESDAY, JULY 18, 2017
USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
SUNDAY, JULY 23, 2017
atypical L-type BASE Bovine Amyloidotic Spongiform Encephalopathy BSE TSE PRION
SUNDAY, JULY 23, 2017
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Wednesday, December 21, 2016
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH
Tuesday, September 06, 2016
A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
TUESDAY, JULY 18, 2017
MINK FARMING USA TRANSMISSIBLE MINK ENCEPHALOPATHY TSE PRION DISEASE SURVEILLANCE AND TESTING
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Saturday, April 23, 2016
Scrapie ZOONOSIS PRION CONFERENCE TOKYO 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
Thursday, June 9, 2016
Advisory Committee; Transmissible Spongiform Encephalopathies Advisory Committee; Termination
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
TUESDAY, AUGUST 8, 2017
Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2016-0092]
WEDNESDAY, JULY 26, 2017
APHIS USDA Emerging Animal Disease Preparedness and Response Plan July 2017
THURSDAY, JUNE 22, 2017
World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas
MONDAY, JANUARY 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
WEDNESDAY, MARCH 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
MONDAY, MAY 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing
OIE STILL FLOUNDERING WITH TSE PRION DISEASE, letting it spread around the globe with the bse mrr policy, and still ignoring cwd, and making atypical scrapie a legal trading commodity.
THURSDAY, MAY 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
TUESDAY, JULY 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
BSE YOUNGEST DOCUMENTED TO DATE 20 MONTHS
1992 20 26 15.02 16.02
1.6. YOUNGEST AND OLDEST CASES BY YEAR OF ONSET (FOR PASSIVE SURVEILLANCE CASES) AND ON YEAR OF SLAUGHTER (FOR ACTIVE SURVEILLANCE CASES) AS AT 03/09/2007 NB The last case in an animal aged 30 months or less was in 1996
YR OF ONSET AGE YOUNGEST CASE (mths) AGE 2nd YOUNGEST CASE (mths) AGE 2nd OLDEST (yrs.mths) OLDEST CASE (yrs.mths)
1986 30 33 5.03 5.07
1987 30 31 9.09 10
1988 24 27 10.02 11.01(2)
1989 21 24(4) 12(2) 15.04
1990 24(2) 26 13.03 14
1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02
1993 29 30(3) 14.1 18.1
1994 30(2) 31(2) 14.05 16.07
995 24 32 14.09 15.05
1996 29 30 15.07 17.02
1997 37(7) 38(3) 14.09 15.01
1998 34 36 14.07 15.05
1999 39(2) 41 13.07 13.1
2000 40 42 17.08 19.09
2001 45 48 16.01 20.08
2002 47 48(2) 18.04 22.07
2003 46 49 18.07(2) 20.06
2004 49 52 17.04 22.07
2005 36 38 18.01 19.04
2006 48 58 17.05 19.09
2007 81(2) 88 15(02) 17.03
PAGE 5
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
MONDAY, JULY 17, 2017
National Scrapie Eradication Program May 2017 Monthly Report Fiscal Year 2017
TUESDAY, SEPTEMBER 19, 2017
*** USDA APHIS Notice: Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program
Subject: Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis
(see origin of cwd in Colorado debate and evidence there from...tss)
MONDAY, OCTOBER 02, 2017
Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
FRIDAY, AUGUST 11, 2017
Infectivity in bone marrow from sporadic CJD patients
Bioassays in transgenic mice expressing the human prion protein revealed the presence of unexpectedly high levels of infectivity in the bone marrow from seven out of eight sCJD cases. These findings may explain the presence of blood-borne infectivity in sCJD patients. They also suggest that the distribution of prion infectivity in peripheral tissues in sCJD patients could be wider than currently believed, with potential implications for the iatrogenic transmission risk of this disease.
THURSDAY, AUGUST 10, 2017
Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
National Prion Center could lose all funding just as concern about CWD jumping to humans rises
SATURDAY, JULY 15, 2017
*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
Tracking spongiform encephalopathies in North America
Xavier Bosch
Published: August 2003
Summary;
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”
49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.
To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.
"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."
Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited".
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
2 January 2000 British Medical Journal U.S.
Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S.
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Terry S. Singeltary Sr.
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