Friday, January 23, 2015

Replacement of soybean meal in compound feed by European protein sources and relaxing the mad cow ban $

Replacement of soybean meal in compound feed by European protein sources

 

Effects on carbon footprint

 

H.C. de Boer1, M.M. van Krimpen1, H. Blonk2, M. Tyszler2 1 Wageningen UR Livestock Research 2 Blonk Consultants Wageningen UR Livestock Research

 

Lelystad, November 2014


SNIP...

 

2.5 Scenario 4: replacement of SBM-SA by poultry meat and bone meal

 

Introduction

 

Animal meal (e.g. blood meal, bone meal, meat meal, meat and bone meal) used to be a valued protein-rich ingredient in animal feed, but was banned from use in the year 2000 because of increased incidences of 'mad cow disease' (Bovine spongiform encephalopathy). However, voices are heard in politics that, under limitations, the use of animal meal should be permitted again. Animal meal has a low CFP because no upstream CFP is allocated, due to its relatively low economic value. Therefore, the inclusion level of animal meal in compound feed could contribute to the replacement of SBM-SA by proteins from European origin, and potentially lower its CFP.

 

Input for compound feed formulation

 

In this scenario, the inclusion level of SBM-SA was not allowed and meat and bone meal could be included in the diet to a maximum of 3%. Because of the species to species ban, indicating that animals should be prevented to consume the remains of their own species, meat meal and meat and bone meal of poultry origin were used in this scenario. Because the inclusion level of poultry meat and

 

Livestock Research Report 819 | 17

 

bone was very low, poultry meat meal was added later to see if this would increase the inclusion level. Poultry meat and bone meal 50 Sonac (Appendix 1) and poultry meal 63 Sonac were used as meat and bone meal and meat meal, respectively. Prices were set at 40 and 61 € 100-1 kg of product, respectively (based on information from Vionfood, Eindhoven, the Netherlands).

 

CFP calculation

 

The CFP of poultry meat and bone meal was calculated with FeedPrint. For this scenario, CFP of poultry meat and bone meal (Category 3 rendering) with a crude fat content of maximal 100 g kg-1 of product was used. This meal was sourced from the Netherlands (default FeedPrint sourcing).

 


 

>>>Animal meal (e.g. blood meal, bone meal, meat meal, meat and bone meal) used to be a valued protein-rich ingredient in animal feed, but was banned from use in the year 2000 because of increased incidences of 'mad cow disease' (Bovine spongiform encephalopathy). *** However, voices are heard in politics that, under limitations, the use of animal meal should be permitted again.<<<

 

American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013

 

BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)

 

Little is known about atypical BSE. The origin and natural routes of transmission, if any, have yet to be determined. Almost all cases have been in older cattle (usually > 8 years of age) that have shown little resemblance to the clinic-pathological picture seen in classical disease. It has been suggested that the disease may be sporadic or be caused by a genetic mutation, but no convincing evidence has been found to support either of these ideas. The correct answer will probably only come by study of the future annual incidence curves of both types of disease. Regardless of the origin of atypical BSE, the possibility of recycling the disease in cattle and other ruminants, as well as the potential for transmission to humans, mandate a continuation of feed and specified-risk materials (SRM) bans, together with diagnostic testing programs for some time to come.

 

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Naturally occurring cases of BSE in species other than cattle have been very limited and have been linked to exposure to contaminated feed or infected carcasses. The majority of cases originated in the UK and like BSE in cattle, have declined with the implementation of feed controls. None of the exotic animals were infected in the wild.

 

 

Experts who may be consulted:

Linda A. Detwiler, DVM

Clinical Professor

Department of Pathobiology and Population Medicine

 

College of Veterinary Medicine

Mississippi State University

732-580-9391

Fax: 732-741-7751


 

 


 

 

Saturday, November 6, 2010

 

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

 

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU

 

© TAFS, Berne, 2010

 

Epidemiological evidence implicated contaminated rendered meat and bone meal as the source of the BSE epidemic in the United Kingdom, continental Europe as well as a few other countries around the world. With the overall global decline of BSE cases, national governments are beginning to explore the possibility of relaxing some of the measures taken to bring the disease under control. This paper will examine the current scientific knowledge and other facets that may impact decisions regarding the feed bans.

 

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Countries outside of Europe

 

After confirming BSE in September 2001, the government of Japan enacted many of the same regulations adopted by the European Union. In regard to feed controls, all meat and bone meal (MBM) is prohibited from being fed to bovines. Porcine and marine mammal derived MBM is banned from the rations of pigs and chickens as well. MBM from poultry produced separately may be fed to pigs and chickens. (Ref. 13)

 

These feed control measures appear to have been effective in Japan. Japan has detected a total of 36 cases of BSE (2001-2009) that seemingly peaked in 2006. In 2008 and 2009, only one case/year has been found. To date, with the exception of one case born in January 2002, all other BSE cases have been born prior to the feed ban.

 

BSE has also been identified in both Canada and the United States (US). The first case of BSE in Canada was reported in May 2003 and the first native-born case in the US was identified in 2004. Both Canada and the US prohibited the feeding of most rendered mammalian proteins to ruminants in 1997. It is evident by the Canadian BSE cases born between 2000-04 that this was not 100% effective.

 

In Canada as of July 12, 2007 SRMs (same list as removed from food for humans) are prohibited from being included in any animal feed including pet food or fertilizer.

 

As of October 2009, the US expanded the 1997 feed ban to prohibit the feeding of certain high risk cattle materials in all animal feed. This list includes: 1) the entire carcass of BSE-positive cattle, 2) the brains and spinal cords from cattle 30 months of age and older, 3) the entire carcass of cattle not inspected and passed for human consumption, unless the cattle are less than 30 months of age or the brains and spinal cords have been effectively removed, 4) tallow derived from BSE-positive cattle, 5) tallow derived from cattle material prohibited in animal feed (CMPAF) that contains more than 0.15% insoluble impurities and 6) mechanically separated beef derived from CMPAF.

 

Many countries not reporting BSE have taken some precautionary feed control measures to prevent an internal recycling of the BSE agent if it were to be introduced into the animal feed chain. The measures usually include a ruminant to ruminant or mammalian to ruminant ban. Some countries have also excluded SRMs from animal feed and set parameters for rendering. For example, as of 2001 Australia prohibits the feeding of any material taken from a vertebrate animal other than tallow, gelatin, milk products or oils extracted from poultry and fish. It includes rendered products such as blood meal, meat meal, meat and bone meal, fish meal, poultry meal, feather meal, and compounded feeds made from these products to be fed to ruminants. In 2002 Argentina enacted a mammalian to ruminant ban.

 

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Evaluation of these possible future developments

 

Disease considerations

 

In Europe there seems to be general support for the opinion that feeding any animal proteins to ruminants2 should remain forbidden to ensure that the BSE epidemic will not be revived and to respect the herbivorous nature of cattle and sheep. That particular feed ban was at the core of the hugely successful control of the BSE epidemic in Europe.

 

2 With the exception of fish meal in milk replacers

 

The inclusion of non-ruminant feed in the BSE feed ban regulations was not a result of a direct and proven TSE risk to, or arising from, non-ruminants, but rather the consequence of the complexity of the rendering and feed industry and the limited diagnostic capabilities.

 

Prior to the total feed ban, the production processes for ruminant and non-ruminant feed were not separated completely. During rendering processes, feed production, storage or transportation there was ample opportunity for ingredients of non-ruminant feed to contaminate ruminant feed and vice-versa. Despite previous feed bans, ruminant feed therefore continued to contain ruminant proteins, and crossfeeding of ruminants with non-ruminant feed containing ruminant proteins remained a possibility. The number of BSE cases born after ruminant-to-ruminant feed bans or mammalian-to-ruminant feed bans clearly demonstrates that in practice such feed bans were not sufficiently effective in preventing new infections. This was true for Europe and seems to be the same at least in Canada. Prior to finding the first case of BSE in Japan there was only a voluntary feed ban. After the initial case, Japan adopted more stringent and broader measures than the ruminant to ruminant or mammalian to ruminant ban.

 

While maintaining the total ban of PAPs in ruminant feed alone would in theory (e.g., under ideal, controlled conditions) be sufficient to protect cattle and sheep from exposure to potentially infected material, erroneous cross-contamination, labeling errors and fraudulent misconduct could lead to some contamination with PAPs in ruminant feed if they were to be allowed for non-ruminants. Inspections and testing (see below) can reduce, but not eliminate such a risk.

 

Even if PAPs would, unlawfully or unintentionally, end up in ruminant feed, they would pose no known TSE risk under the assumption of two important, jointly sufficient conditions:

 

1) That the PAPs stem exclusively from non-ruminants. With the complete ban of ruminant material being rendered into feed for farmed animals this assumption is very likely to be met, although pet feed could be a source of contamination.

 

2) That non-ruminant proteins can under no circumstances trigger the development of TSE diseases in ruminants even if fed to them. According to an EFSA opinion (Ref. 6) there is no evidence to suggest the contrary and EFSA considers the risk of transmitting BSE to pigs utilizing poultry PAPs (and vice versa) as negligible. On the other hand, there is also only weak evidence to actively support the scientific validity of this assumption. Additionally, pigs have been shown to be susceptible to infection with TSE-material of ruminant origin by parenteral challenge, but experimental transmission of BSE to pigs by the oral route has been unsuccessful (Ref 16). Given the current paucity of the experimental evidence, the condition cannot be considered completely satisfied, since the absence of evidence does not constitute evidence of absence.

 

No spontaneous development of TSE-like disease has been observed in pigs, but it is plausible to assume that pigs can develop such diseases as a very rare event and if left alive long enough. Multiplied by the number of live pigs – close to 1 billion worldwide – that would result in a non-negligible number of pigs with TSE. On the other hand by far most, if not all, pigs slaughtered for human consumption do not live to be even 1 year old.

 

TAFS 6

 

If pig-meal is allowed as feed to poultry and vice versa then a closed loop of material could be established provided that undigested pig proteins contained in the gastrointestinal tract of poultry is fed back to pigs or the other way round. This loop can be prevented if all gastrointestinal tracts and their contents are removed and discarded before the rendering of animal by-products. This requirement would be – like all other risk reduction measures – subject to error and fraud, but add to the redundancy of risk management.

 

In the light of the evolving BSE epidemic, the zoonotic potential of BSE and consumer concerns, the authorities were therefore forced to take drastic measures and exclude all animal proteins from all feed for farmed animals, with a few exceptions as outlined above.

 

By 2010, the BSE epidemic appears to be phasing out. In 2001, 2,167 BSE positive cases were detected within the framework of the EU surveillance activities. By 2008, this number had fallen to 125, 17 times less. Also the number of BSE cases detected per 10,000 animals tested had fallen dramatically: 2.55 BSE cases per 10,000 in 2001 against 0.12 BSE cases per 10,000 in 2008, a 21-fold reduction (Ref. 10). This also implies that the probability has diminished significantly that infected cattle erroneously enter the feed production chain.

 

Emerging Disease Considerations

 

Atypical BSE and other TSEs

 

For almost the entire two decades that BSE had been known in the world it was thought that there was only one ?train?that infected cattle and caused disease in other species such as humans (Refs. 17, 18).

 

In 2004, cases of a bovine prion disease molecularly different than those already documented as classical BSE were described by scientists in both Italy (Ref. 18) and France (Ref. 19). In both countries the cattle were over 8 years of age. The Italian cases (11 and 15 years of age) named bovine amyloidotic spongiform encephalopathy (BASE) were characterized by an unglycosylated protein band with a lower molecular mass (thus named L cases) and the predominance of the monoglycosylated band. In addition, immunohistochemical detection of PrPres in these cases found greater deposits in the cerebral cortex and thalamus versus the brain stem, as is characteristic of classical BSE. The French cases found a higher molecular mass associated with the unglycosylated protein band and were called H cases. The different ?trains?are now called atypical BSE.

 

Atypical BSE is a study in progress with more unknowns than knowns. One of the most important of the unknowns is the significance of atypical BSE in regard to human and animal health.

 

Since these two publications, additional cases of atypical BSE have been found in other countries. H cases have been detected in Canada, France, Germany, Japan, the Netherlands, Poland, Sweden, Switzerland, the United Kingdom and the United States. L cases have been diagnosed in Belgium, Canada, Denmark, France, Germany, Italy, Japan and Poland.

 

It has now been shown that both the L and H types of atypical BSE are experimentally transmissible via the intracerebral route. Homogenates from L cases have been transmitted to wild-type mice, bovinized, ovinized and humanized transgenic mice, Cynomolgus monkeys and cattle (Refs. 20, 21, and 22).

 

H cases have been transmitted to bovinized transgenic (Tgbov) and ovinized transgenic mice (Ref. 23) and cattle (personal communication March 2009).

 

TAFS 7

 

Early studies provide some evidence that L type (or BASE) BSE may be more virulent for primates including humans (Refs. 21, 24, and 25).

 

Studies on the oral route are underway. These would provide data to evaluate the potential for natural transmission of the disease.

 

Atypical BSE may arise spontaneously in a small proportion of cattle. The existence of sporadic CJD in humans has led to postulation that disease could arise spontaneously in any animal, but this theory like others has not been proved.

 

In the US one of the H-type BSE case was found to be associated with the novel mutation E211K within the prion protein gene (Prnp) suggesting that this strain may have a genetic origin (Ref. 26).

 

As per the SEAC: „here are too few data to enable an assessment of the natural transmissibility of L- and H-type BSE between cattle, or to sheep or goats. The present feed control measures which prevent feeding of mammalian meat and bone meal to ruminants would limit the spread of these forms of BSE to cattle, sheep and goats should they be transmissible to these species by the oral route.?

 

Atypical Scrapie

 

In 1998, scientists in Norway discovered a previously uncharacterized strain of scrapie that is now called Nor 98 or atypical scrapie (Ref. 27). Certain epidemiological evidence indicates that atypical scrapie may be a sporadic disease (Ref. 28), however additional research is underway to examine the likelihood of natural transmission and the extent of tissue distribution.

 

As with atypical BSE, there are few data on the potential for natural transmission of the disease to sheep and other species. The disease has been transmitted to sheep however the route was intracerebral (Ref. 29). Studies investigating the possibility of oral transmission are underway.

 

There is some evidence from transmission studies utilizing porcinized transgenic mice that pigs may be susceptible to atypical scrapie and BSE in sheep (Ref. 30). These studies do not involve the natural host or route of transmission so caution may be taken in drawing conclusions.

 

Potential for TSEs in Other Species

 

Studies conducted at the National Institutes of Health Rocky Mountain Laboratory caution against assuming that animals which do not become clinically ill are not infected. There is experimental evidence to indicate that certain species may become carriers (i.e., become infected, shed agent but do not progress to clinical disease) (Ref 31, Ref 32, Ref 33). Specifically, mice inoculated with 263K hamster scrapie demonstrated a phase of inactive persistence. That is, after exposure the mice had a prolonged period (approximately one year), where there was no evidence of infectivity or PrPsc. This was followed by a period of an increasing infectivity and agent adaptation. Many of the mice continued to be devoid of detectable PrPsc.

 

It is important to determine if this persistence and adaptation could occur naturally as it may have significance in feeding programs which continually expose species other than ruminants

 

TAFS 8

 

to TSE infectivity. The results of Race and colleagues, warns that an inactive persistent phase might not produce detectable PrPsc, yet tissues may harbor infectivity (Ref 32).

 

Very recent research provides illustrations of the accumulation of infectivity in tongue and nasal mucosa from terminally diseased field cases and experimentally challenged cases of BSE even when no abnormal PrP was detectable (Ref 34). This same phenomena has also been reported for peripheral tissues collected from sheep with atypical scrapie. (Ref 35).

 

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Key issues to deal with before the feed ban for non-ruminants can be relaxed

 

In our opinion, several key requirements need to be met before the feed ban for non-ruminants can be relaxed:

 

The feed industry needs to ensure the following:

 

Ruminant materials remain excluded completely from the entire feed chain. This requires a complete and reliable traceability system for both ruminant and non-ruminant materials.

 

Intra-species feeding is prevented entirely. This requires that pig and poultry by-products are prevented from mutual cross-contamination by dedicated separate logistical pathways from slaughterhouses through rendering and feed production processes.

 

No animal proteins are included in ruminant feed. This requires that the ingredients for and the production of ruminant feed is completely separate from the ingredients for and the production of non-ruminant feed.

 

Scientific knowledge required:

 

Diagnostic tools must be developed with the capacity to verify compliance with any revised feed ban. These tools must be able to differentiate between PAPs from different animal species, and – in case it is decided to implement a tolerance level for contamination of feed – they must be able to determine if the level of contamination exceeds the defined tolerance levels.

 

More research is needed to support the assumption that non-ruminant proteins cannot induce TSE-like diseases in ruminants, even if these diseases circulated among different non-ruminant species beforehand.

 

The authorities need to ensure the following:

 

Competent authorities have the means and capacity to monitor the feed industry closely and assess their capacity to comply with the remaining feed ban regulations BEFORE any changes are allowed to proceed.

 

Legislation is in place to hold the industry liable in case of breaches of the remaining feed ban.

 

Appropriate diagnostic tools are registered and validated to verify compliance with the feed regulations.

 

In the view of TAFS, taking into consideration all of the scientific and epidemiological knowns and unknowns, the fact that the requirements as listed above are currently not met and acknowledging the potential for fraudulent behavior, a relaxation of the feed ban at the present time would not eliminate all risks. We feel strongly that maintenance of the ban is the only means to drive the level of risk toward zero.

 

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see full text and references here ;

 

 

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

 

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

 


 

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

 

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 Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

 

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

 

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

 

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.

 

 


 

 

Is it more contagious?

 

“There is some evidence in primates and transgenic mice that it seems to spread faster – meaning it maybe more virulent – but we don’t know how representative these models are of the disease in humans,” says Linda Detwiler, a clinical professor at Mississippi State University’s College of Veterinary Medicine. Whether or not L-type could jump species without direct injection into the brain remains unclear, but so far it can transmit to transgenic humanized, ovinized (modified to genetically mimic sheep), bovinized, and normal mice, as well as macaques in the lab.

 

How could this animal have contracted it?

 

“We do know that L-type can transmit from one cow to another through injection in the brain,” says Detwiler. “Long term studies are beginning to look at whether or not it’s capable of transmission orally through feed, but we don’t have the data yet.”

 


 

 

 *** What irks many scientists is the USDA's April 25 statement that the rare disease is "not generally associated with an animal consuming infected feed." The USDA's conclusion is a "gross oversimplification," said Dr. Paul Brown, one of the world's experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement."

 


 




EFSA Journal 2014;12(7):3798 Suggested citation: European Food Safety Authority, 2014.

 

Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE.

 

EFSA Journal 2014;12(7):3798, 55 pp. doi:10.2903/j.efsa.2014.3798 Available online: www.efsa.europa.eu/efsajournal

 

© European Food Safety Authority, 2014 SCIENTIFIC REPORT OF EFSA

 

Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE1 European Food Safety Authority2,3 European Food Safety Authority (EFSA), Parma, Italy

 

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CONCLUSIONS AND RECOMMENDATIONS

 

CONCLUSIONS

 

Data relating to the prevalence and geographical distribution of Atypical BSE are incomplete.

 

The recent cessation of the testing of healthy slaughtered cattle in some EU Member States will lead to a loss of capacity of the monitoring system to detect Atypical BSE cases.

 

For transmission studies, i.c. challenge would be an appropriate proxy for studying the distribution of the agent if the origin of the disease was spontaneous, and originating in the brain, while oral challenge would be more appropriate if the origin of the disease was through ingestion of infected material.

 

The current lack of information on the distribution of infectivity in tissues of Atypical BSE-infected cattle does not allow judgement of whether the current list of bovine SRM, set by EU legislation based on data relating to the pathogenesis and tissue distribution of C-BSE, is fit for the purpose of removing most of the Atypical BSE infectivity from bovine carcasses.

 

Where data exist from both field cases and experimental animals (i.e. for L-BSE only), there is good agreement of the data with regard to abnormal PrP distribution. There are no data for field case H-BSE.

 

Disease-related PrP has been reported consistently in CNS tissues, peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal glands and retina for both H-BSE and L-BSE. All of these tissues are also positive in C-BSE.

 

By contrast with C-BSE, at this stage no lymphoid tissues or gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested positive for PrPSc presence (IHC, WB) or infectivity (bioassay).

 

The reference method for the estimation of prion infectious titre in tissues is endpoint dilution titration in animals. To achieve maximum sensitivity regarding Atypical H-BSE and L-BSE, this bioassay should ideally be done in mouse lines over-expressing bovine PrPC. Several mouse lines over-expressing bovine PrPC are available worldwide.

 

In vitro amplification techniques can be used to determine whether a tissue contains any prion seeding activity. A correlation must be made between the sensitivity achieved by the cell-free assays and bioassays using reference material such as brain tissue from animals at the terminal stage of disease.

 

The application of the proposed protocol would provide elements allowing the assessment of the relative infectious titre, PrPSc accumulation and prion seeding activity in the tissues of cattle that developed H-BSE or L-BSE (using posterior brainstem as a reference).

 

Tissues to be covered by further studies are categorised in three priorities, based on their inclusion in the cattle SRM list, on the presence of infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other TSEs in ruminants, and on the importance in terms of input into the food chain in the EU.

 

Atypical BSE study protocol

 

EFSA Journal 2014;12(7):3798 32

 

Applying the protocol only to the tissues obtained through the EURL study would provide information on some but not all the tissues from the cattle SRM list. It would also provide information on some additional tissues not included in the cattle SRM list, but relevant for the food chain.

 

Material from other studies could be used to augment the range of SRM and non-SRM tissues available.

 

There is no identified source able to provide all the samples necessary to assess infectivity in tissues belonging to the full cattle SRM list in H- and L-BSE-infected animals. Therefore, to complete this objective, new inoculations of cattle would have to be considered.

 

 

RECOMMENDATIONS

 

In accordance with former EFSA recommendations, through the implementation of the protocol information should also be obtained on the performance of currently validated rapid tests for TSE active surveillance in cattle/bioassay for detecting H-BSE and L-BSE agents.

 

If new inoculation experiments are carried out in cattle with H-BSE and L-BSE, the following should be considered:

 

- inoculation through both the i.c. and oral route (despite the potential length of the oral route experiment);

 

- inclusion of C-BSE controls in the i.c. route experiment;

 

- sequential time killing of animals;

 

- collection of all tissues listed in Table 7.

 

DOCUMENTATION PROVIDED TO EFSA

 

1. Summary of the samples available and the tests already carried out by the EURL-TSE. Submitted by the European Commission as Annex 1 to the mandate.

 

2. Information on protocols and tests results provided by the EURL-TSE. Submitted by the European Commission as Annex 2 to the mandate.

 

REFERENCES

 


 

 

Thursday, July 24, 2014

 

Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations

 

 
 

 

 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

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

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

 


 

Friday, April 19, 2013

 

FDA BSE TSE PRION NEWS FEED AND ANNUAL INSPECTION OF FEED MILLS REPORTS HAS CEASED TO EXIST

 


 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations

 


 

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

 


 

Atypical BSE: Transmissibility

 

 BASE (L) transmitted to:  cattle (IC) - inc < 20 mos and oral?)

 

 Cynomolgus macaques (IC)

 

 Mouse lemurs (IC and oral)

 

 wild-type mice (IC)

 

 bovinized transgenic mice (IC and IP)

 

 humanized transgenic mice (IC)

 

 H cases transmitted to:

 

 cattle – IC incubations < 20 months

 

 bovinized transgenic mice (IC)

 

 ovinized transgenic mice (IC)

 

 C57BL mice (IC)

 

 One study did not transmit to humanized PrP Met 129 mice

 

Evaluation of Possibility of Atypical

 

BSE Transmitting to Humans

 

 Possble interpretation:

 

 L type seems to transmit to nonhuman primates with greater ease than classical BSE

 

 L type also transmitted to humanized transgenic mice with higher attack rate and shorter incubation period than classical?

 

 H type did not transmit to Tg Hu transgenic mice

 

 

Linda Detwiller, 5/10/2011

 


 

 

 I ask Professor Kong ;

 

Thursday, December 04, 2008 3:37 PM

 

Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

 

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

 

Professor Kong reply ;

 

.....snip

 

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

 

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

 

 BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.

 

Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.

 

 


 


 

 

P.4.23 Transmission of atypical BSE in humanized mouse models

 

Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA

 

Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were argely undefined.

 

Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice.

 

Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.

 

Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.

 

Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.

 

Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.

 


 


 


 

 

14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

 

18.173 page 189

 

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

 

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

 

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

 

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions. At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

 

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathoge esis and agent distribution for these novel BSE types.

 

Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.

 


 

14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114

 

Session: International Scientific Exchange

 

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary Bacliff, TX, USA

 

 Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

Methods: 12 years independent research of available data

 

Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 


 

Tuesday, November 04, 2014

 

The pathological and molecular but not clinical phenotypes are maintained after second passage of experimental atypical bovine spongiform encephalopathy in cattle

 


 

Saturday, June 12, 2010

 

***PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

 


 

PRODUCT O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 11-oz. bottles, For Animal Use Only.

 

Recall # V-043-2007 CODE A06 RECALLING FIRM/MANUFACTURER Springer Magrath Co., Mc Cook, NE, by telephone on January 2, 2007, fax dated January 9, 2007, by letters on February 22, 2007, March 12, March 14 and March 21, 2007.

 

Firm initiated recall is ongoing.

 

REASON The finished product was manufactured with prohibited bovine blood meal and did not bear the cautionary BSE statement that the product should not be fed to ruminants.

 

VOLUME OF PRODUCT IN COMMERCE

 

Approximately 13,255 bottles DISTRIBUTION

 

Nationwide

 

END OF ENFORCEMENT REPORT FOR JUNE 13, 2007 ###

 


 

PRODUCT

 

Dairy cattle feed blends containing ProLak and/or ProAmino II protein concentrate, Recall # V-020-2007

 

CODE

 

All finished product manufactured from April, 3, 2006 to April 30, 2006

 

RECALLING FIRM/MANUFACTURER

 

Eatonton Co-Op Feed Company, Eatonton, GA, by letter on/about December 12, 2006. Firm initiated recall is complete.

 

REASON

 

Finished feed product was manufactured from raw feed material that may have been contaminated with ruminant derived protein.

 

VOLUME OF PRODUCT IN COMMERCE

 

25 tons

 

DISTRIBUTION

 

GA

 

___________________________________

 

END OF ENFORCEMENT REPORT FOR FEBRUARY 28, 2007

 

###

 


 

PRODUCT

 

O-NO-MORE (Formerly ORPHAN-NO-MORE) Calf Claimer Powder, packaged in 9-oz. bottles, For Animal Use Only, Recall # V-011-2007

 

CODE

 

A07

 

RECALLING FIRM/MANUFACTURER

 

Springer Magrath Co., McCook, NE, by telephone on January 11, 2007 and fax on January 12, 2007. Firm initiated recall is complete.

 

REASON

 

The bovine blood meal which was used to manufacture the finished product was cross-contaminated with prohibited bovine meat and bone meal, and the finished product is not labeled with the cautionary statement that it should not be fed to ruminants.

 

VOLUME OF PRODUCT IN COMMERCE

 

300/9-oz. bottles

 

DISTRIBUTION

 

NE

 

END OF ENFORCEMENT REPORT FOR JANUARY 31, 2007

 

###

 


 

PRODUCT

 

Bulk Darling's 85% Blood Meal, Flash Dried, distributed in totes and in 1-ton bags (for one customer only), Recall # V-012-2007

 

CODE

 

Blood meal distributed between 9/7/2006-2/3/2007.

 

RECALLING FIRM/MANUFACTURER

 

Darling National LLC, Omaha, NB, by telephone on January 12, 2007. Firm initiated recall is ongoing.

 

REASON

 

Some of the exempt bovine blood meal was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and the labeling did not bear the cautionary BSE statement that it should not be fed to ruminants.

 

VOLUME OF PRODUCT IN COMMERCE

 

1,366,128 lbs.

 

DISTRIBUTION

 

WI, TX, NE, TN, CO, and MN

 

 END OF ENFORCEMENT REPORT FOR FEBRUARY 7, 2007

 

 ###

 


 

BANNED MAD COW FEED IN COMMERCE IN ALABAMA

 

______________________________

 

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

 

______________________________

 

PRODUCT

 

a) Dairy feed, custom, Recall # V-134-6;

 

b) Custom Dairy Feed with Monensin, Recall # V-135-6.

 

CODE

 

None. Bulk product

 

RECALLING FIRM/MANUFACTURER

 

Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.

 

Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.

 

REASON

 

Possible contamination of dairy feeds with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

1,484 tons

 

DISTRIBUTION

 

TN and WV

 

END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006

 

###

 


 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-115-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA 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

 

Approximately 2,223 tons

 

DISTRIBUTION

 

KY

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-116-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA 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

 

1,220 tons

 

DISTRIBUTION

 

KY

 

______________________________

 

PRODUCT

 

Bulk custom made dairy feed, Recall # V-117-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.

 

REASON

 

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

40 tons

 

DISTRIBUTION

 

LA and MS

 

______________________________

 

PRODUCT

 

Bulk Dairy Feed, Recall V-118-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.

 

REASON

 

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

 

VOLUME OF PRODUCT IN COMMERCE

 

7,150 tons

 

DISTRIBUTION

 

MS

 

______________________________

 

PRODUCT

 

Bulk custom dairy pre-mixes, Recall # V-119-6

 

CODE

 

None

 

RECALLING FIRM/MANUFACTURER

 

Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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

 

87 tons

 

DISTRIBUTION

 

MS

 

______________________________

 

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

 

###

 


 

 what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE ???

 

Saturday, August 14, 2010

 

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

 

*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)

 

BANNED MAD COW FEED IN COMMERCE IN ALABAMA

 

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

 

______________________________

 


 

 Saturday, July 23, 2011

 

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

 


 

Monday, March 8, 2010

 

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

 


 

Monday, March 1, 2010

 

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

 


 

Thursday, September 3, 2009

 

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

 


 

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

 


 

Tuesday, November 3, 2009

 

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

 


 

>>> The generally older age of the identified H-BSE and L-BSE cases, and their apparently low prevalence in the population, suggest that these Atypical BSE forms could be arising spontaneously. <<<

 

if that is the case, then FRANCE has an exceedingly high rate of spontaneous atypical BSE cases. maybe that’s why France stopped mad cow testing ;

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

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

 


 

LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

 


 


 

Saturday, August 14, 2010

 

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)

 


 

her healthy calf also carried the mutation

 

(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).

 

This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.

 

Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009

 


 

Owens, Julie

 

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

 

Sent: Monday, July 24, 2006 1:09 PM

 

To: FSIS RegulationsComments

 

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98

 


 

> Response to Public Comments on the Harvard Risk Assessment of Bovine > Spongiform Encephalopathy Update, October 31, 2005

 

 > RESPONSE TO COMMENTS FROM TERRY S. SINGELTARY SR.

 

> Comment #1: SINCE the first Harvard BSE Risk Assessment was so flawed and > fraught with error after the PEER REVIEW assessment assessed this fact, > how do you plan on stopping this from happening again, will there be > another peer review with top TSE Scientists, an impartial jury > so-to-speak, to assess this new and updated Harvard BSE/TSE risk > assessment and will this assessment include the Atypical TSE and SRM > issues?

 

> Response: The original (October 2003) and the revised (October 2005) > Harvard BSE risk assessments underwent external peer review. Subsequently, > revisions were made to the analysis. In the most recent review, the most > significant revisions have been: *** 1) the addition of explicit modeling of > the poultry litter pathway for the potential recycling of bovine protein > into cattle feed; and 2) a decrease in the assumed effectiveness of ante > mortem inspection in the identification of animals with BSE.

 

> Comment #2: WITH A RECENT NATION WIDE MAD COW FEED BAN RECALL in the past > few months that consisted of some 10,878.06 TONS, then another Mad Cow > feed ban warning letter in May, IT should seem prudent to ask why our feed > bans continue to fail in 2006, and continue to fail today?

 

> Response: This question about feed bans is a matter for policy. As such, > it is not addressed in this response.

 

FSIS, USDA, REPLY TO SINGELTARY

 


 

What Do We Feed to Food-Production Animals? A Review of Animal Feed Ingredients and Their Potential Impacts on Human Health

 

Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1 1Johns Hopkins Center for a Livable Future, Bloomberg School of Public Health, Baltimore, Maryland, USA; 2Maryland Institute for Applied Environmental Health, College of Health and Human Performance, University of Maryland, College Park, Maryland, USA; 3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA

 

snip...

 

Table 1. Animal feed ingredients that are legally used in U.S. animal feeds

 

Animal

 

Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products

 

snip...

 

Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives

 


 

FDA to add new BSE-related feed rules soon Robert Roos News Editor

 

Sep 22, 2005 (CIDRAP News) – The head of the Food and Drug Administration (FDA) said this week the agency will soon align its rules on animal feed more closely with those in Canada and Europe, signaling a likelihood of new restrictions to prevent the spread of bovine spongiform encephalopathy (BSE), or mad cow disease.

 

The United States and Canada both ban the use of cattle parts in feed for cattle and other ruminant animals but allow cattle parts in feed for other animals such as pigs and poultry. However, Canada plans to ban the use of high-risk cattle parts, such as the brain and spinal cord of cattle older than 30 months, in all animal feeds in the near future. Europe already bans high-risk parts, called specified-risk materials (SRMs), from all animal feeds.

 

In July 2004 the FDA said it had reached a "preliminary" decision to ban SRMs from all animal feed, as recommended by an international panel of experts after the first US BSE case surfaced in December 2003. The agency promised to develop a proposal to that effect. SRMs are the tissues most likely to contain the abnormal proteins associated with BSE in infected animals.

 

FDA Commissioner Lester Crawford's comments in a Sep 19 speech now suggest the agency is about to go ahead with the plan, though he gave no date.

 

Crawford said the new rules will be "quite a bit stronger" than initially planned, according to a Sep 19 Bloomberg News report on his speech to the Consumer Federation of America. He said the rules will be similar to those in Europe and Canada.

 

"Our regulation will mimic theirs and it will supersede earlier considerations," Crawford was quoted as saying.

 

Will D. Hueston, DVM, a University of Minnesota professor who served on the expert panel that advised the US government about responses to the first BSE case, said Crawford's comments probably mean the FDA will ban SRMs from all animal feeds.

 

"I think it means they'll take additional action to remove SRMs from animal feeds—I think they' really targeting the high-risk materials, the brain and spinal cord," Hueston told CIDRAP News. "They're actively collaborating with Canada to try to get a uniform program, because we have a lot of trade with Canada in feed and animals and everything else."

 

"It's the international standard to remove SRMs from animal feed . . . in countries where BSE has been identified," said Hueston, who directs the university's Center for Animal Health and Food Safety.

 

SRMs are banned from human food; they are removed from cattle carcasses at slaughterhouses and taken to rendering plants, where they can currently be used in poultry feed and other nonruminant feeds. Hueston said the main concern is that cattle can be exposed to SRMs if they are accidentally given poultry feed. "So this [proposed ban] reduces the potential for leakage in the system."

 

Another pathway that exposes cattle to poultry feed is the practice of putting poultry litter—spilled bedding, feed, and waste collected underneath poultry cages—in cattle feed. Hueston said Canada has banned that, while the United States still permits it.

 

The FDA said last year it was considering banning the use of poultry litter in cattle feed. Reports on Crawford's speech didn't mention any comments on that issue.

 

"They [the FDA] haven't given a clear indication which way they're going to move on that," Hueston said. He commented that keeping SRMs out of poultry feed would address that concern.

 

According to accounts of his speech, Crawford did not suggest whether the FDA will ban the use of cattle blood and restaurant leftovers in cattle feed—practices that some regard as other risk factors for spreading BSE.

 

The United States has been trying to persuade Japan to reopen its market to US beef ever since BSE turned up here in 2003. According to the Bloomberg story, a draft report issued last week by Japan's Food Safety Commission said US cattle are more exposed to BSE than Japanese cattle because of insufficient feed regulations.

 

Hueston said the FDA is undoubtedly weighing the possible effects of its feed rules on the effort to reopen beef trade with Japan and other countries. "Aso, you don't want to create a brand-new disparity with Canada, when our beef industries are essentially joined at the hip," he added.

 

The Canadian Food Inspection Agency (CFIA) said this week it hopes to ban SRMs from all animal feeds by the end of this year, according to a Sep 20 Reuters report. The story quoted Billy Hewett, the CFIA's policy director, as saying, "I know it seems slow, but it is enormously complex."

 

See also:

 

Jul 9, 2004, CIDRAP News story "FDA sets BSE-related rules but delays action on feed"

 

Overview of Canadian BSE safeguards

 


 


 

*** DO NOT forget what was originally promised years ago !!!

 

Press Release FOR IMMEDIATE RELEASE Monday, Jan. 26, 2004 FDA Press Office 301-827-6242

 

Expanded "Mad Cow" Safeguards Announced to Strengthen Existing Firewalls Against BSE Transmission HHS Secretary Tommy G. Thompson today announced several new public health measures, to be implemented by the Food and Drug Administration (FDA), to strengthen significantly the multiple existing firewalls that protect Americans from exposure to the agent thought to cause bovine spongiform encephalopathy (BSE, also known as mad cow disease) and that help prevent the spread of BSE in U.S. cattle.

 

The existing multiple firewalls, developed by both the U.S. Department of Agriculture (USDA) and HHS, have been extremely effective in protecting the American consumer from exposure to BSE. The first firewall is based on import controls started in 1989. A second firewall is surveillance of the U.S. cattle population for the presence of BSE, a USDA firewall that led to the finding of the BSE cow in December. The third firewall is FDA's 1997 animal feed ban, which is the critical safeguard to help prevent the spread of BSE through cattle herds by prohibiting the feeding of most mammalian protein to ruminant animals, including cattle. The fourth firewall, recently announced by USDA, makes sure that no bovine tissues known to be at high risk for carrying the agent of BSE enter the human food supply regulated by USDA. The fifth firewall is effective response planning to contain the potential for any damage from a BSE positive animal, if one is discovered. This contingency response plan, which had been developed over the past several years, was initiated immediately upon the discovery of a BSE positive cow in Washington State December 23.

 

The new safeguards being announced today are science-based and further bolster these already effective safeguards.

 

Specifically, HHS intends to ban from human food (including dietary supplements), and cosmetics a wide range of bovine-derived material so that the same safeguards that protect Americans from exposure to the agent of BSE through meat products regulated by USDA also apply to food products that FDA regulates.

 

FDA will also prohibit certain currently allowed feeding and manufacturing practices involving feed for cattle and other ruminant animals. These additional measures will further strengthen FDA's 1997 "animal feed" rule.

 

"Today's actions will make strong public health protections against BSE even stronger," Secretary Thompson said. "Although the current animal feed rule provides a strong barrier against the further spread of BSE, we must never be satisfied with the status quo where the health and safety of our animals and our population is at stake. The science and our own experience and knowledge in this area are constantly evolving. Small as the risk may already be, this is the time to make sure the public is protected to the greatest extent possible."

 

"Today we are bolstering our BSE firewalls to protect the public," said FDA Commissioner Mark B. McClellan, M.D., Ph.D. "We are further strengthening our animal feed rule, and we are taking additional steps to further protect the public from being exposed to any potentially risky materials from cattle. FDA's vigorous inspection and enforcement program has helped us achieve a compliance rate of more than 99 percent with the feed ban rule, and we intend to increase our enforcement efforts to assure compliance with our enhanced regulations. Finally, we are continuing to assist in the development of new technologies that will help us in the future improve even further these BSE protections. With today's actions, FDA will be doing more than ever before to protect the public against BSE by eliminating additional potential sources of BSE exposure."

 

To implement these new protections, FDA will publish two interim final rules that will take effect immediately upon publication, although there will be an opportunity for public comment after publication.

 

The first interim final rule will ban the following materials from FDA-regulated human food, (including dietary supplements) and cosmetics:

 

Any material from "downer" cattle. ("Downer" cattle are animals that cannot walk.) Any material from "dead" cattle. ("Dead" cattle are cattle that die on the farm (i.e. before reaching the slaughter plant); Specified Risk Materials (SRMs) that are known to harbor the highest concentrations of the infectious agent for BSE, such as the brain, skull, eyes, and spinal cord of cattle 30 months or older, and a portion of the small intestine and tonsils from all cattle, regardless of their age or health; and The product known as mechanically separated beef, a product which may contain SRMs. Meat obtained by Advanced Meat Recovery (an automated system for cutting meat from bones), may be used since USDA regulations do not allow the presence of SRMs in this product. The second interim final rule is designed to lower even further the risk that cattle will be purposefully or inadvertently fed prohibited protein. It was the feeding of such protein to cattle that was the route of disease transmission that led to the BSE epidemic in United Kingdom cattle in the 1980's and 1990's.

 

This interim final rule will implement four specific changes in FDA's present animal feed rule. First, the rule will eliminate the present exemption in the feed rule that allows mammalian blood and blood products to be fed to other ruminants as a protein source. Recent scientific evidence suggests that blood can carry some infectivity for BSE.

 

Second, the rule will also ban the use of "poultry litter" as a feed ingredient for ruminant animals. Poultry litter consists of bedding, spilled feed, feathers, and fecal matter that are collected from living quarters where poultry is raised. This material is then used in cattle feed in some areas of the country where cattle and large poultry raising operations are located near each other. Poultry feed may legally contain protein that is prohibited in ruminant feed, such as bovine meat and bone meal. The concern is that spillage of poultry feed in the chicken house occurs and that poultry feed (which may contain protein prohibited in ruminant feed) is then collected as part of the "poultry litter" and added to ruminant feed.

 

Third, the rule will ban the use of "plate waste" as a feed ingredient for ruminants. Plate waste consists of uneaten meat and other meat scraps that are currently collected from some large restaurant operations and rendered into meat and bone meal for animal feed. The use of "plate waste" confounds FDA's ability to analyze ruminant feeds for the presence of prohibited proteins, compromising the Agency's ability to fully enforce the animal feed rule.

 

Fourth, the rule will further minimize the possibility of cross-contamination of ruminant and non-ruminant animal feed by requiring equipment, facilities or production lines to be dedicated to non-ruminant animal feeds if they use protein that is prohibited in ruminant feed. Currently, some equipment, facilities and production lines process or handle prohibited and non-prohibited materials and make both ruminant and non-ruminant feed -- a practice which could lead to cross-contamination.

 

To accompany these new measures designed to provide a further layer of protection against BSE, FDA will in 2004 step up its inspections of feed mills and renderers. FDA will itself conduct 2,800 inspections and will make its resources go even further by continuing to work with state agencies to fund 3,100 contract inspections of feed mill and renderers and other firms that handle animal feed and feed ingredients. Through partnerships with states, FDA will also receive data on 700 additional inspections, for a total of 3,800 state contract and partnership inspections in 2004 alone, including annual inspections of 100 percent of all known renderers and feed mills that process products containing materials prohibited in ruminant feed.

 

"We have worked hard with the rendering and animal feed production industries to try and achieve full compliance with the animal feed rule," said Dr. McClellan, "and through strong education and a vigorous enforcement campaign, backed by additional inspections and resources, we intend to maintain a high level of compliance."

 

Dr. McClellan also noted that, in response to finding a BSE positive cow in Washington state December 23, FDA inspected and traced products at 22 facilities related to that positive cow or products from the cow, including feed mills, farms, dairy farms, calf feeder lots, slaughter houses, meat processors, transfer stations, and shipping terminals. Moreover, FDA has conducted inspections at the rendering facilities that handled materials from the positive cow, and they were found to be fully in compliance with FDA's feed rule.

 

To further strengthen protections for Americans, FDA/HHS intends to work with Congress to consider proposals to assure that these important protective measures will be implemented as effectively as possible.

 

FDA is also continuing its efforts to assist in the development of better BSE science, to achieve the same or greater confidence in BSE protection at a lower cost. For example, to enhance the ability of our public health system to detect prohibited materials in animal feed, FDA will continue to support the development and evaluation of diagnostic tests to identify prohibited materials. These tests would offer a quick and reliable method of testing animal feeds for prohibited materials and for testing other products for contamination with the agent thought to cause BSE.

 

FDA has publicly discussed many of the measures being announced today with stakeholders in workshops, videoconferences, and public meetings. In addition, FDA published an Advance Notice of Proposed Rulemaking in November 2002 (available online at http://www.fda.gov/OHRMS/DOCKETS/98fr/110602c.htm concerning possible changes to the animal feed rule.

 

Comprehensive information about FDA's work on BSE and links to other related websites are available at http://www.fda.gov.

 

###

 


 

For Immediate Release July 9, 2004 FSIS Press Office APHIS Press Office FDA Media Relations

 

(202) 720-9113 (202) 734-7799 (301) 827-6242

 

USDA and HHS Strengthen Safeguards Against Bovine Spongiform Encephalopathy WASHINGTON, July 9, 2004--HHS Secretary Tommy G. Thompson and Agriculture Secretary Ann M. Veneman today announced three actions being taken to further strengthen existing safeguards that protect consumers against the agent that causes bovine spongiform encephalopathy (BSE, also known as "mad cow disease").

 

The three documents on display today include:

 

A joint USDA Food Safety & Inspection Service (FSIS), USDA Animal and Plant Health Inspection Service (APHIS) and Food and Drug Administration (FDA) notice that asks for public comment on additional preventive actions that are being considered concerning BSE; An interim final FDA rule that prohibits the use of certain cattle-derived materials in human food (including dietary supplements) and cosmetics; and A proposed FDA rule on recordkeeping requirements for the interim final rule relating to this ban. "Today's actions continue our strong commitment to public health protections against BSE," Secretary Thompson said. "Although our current rules are strong, when it comes to public health and safety we cannot be content with the status quo. We must continue to make sure the public is protected to the greatest extent possible."

 

"This Administration is committed to science-based measures to enhance and protect public health," Veneman said. "The advance notice of proposed rulemaking will allow the public the opportunity to provide their input."

 

"The series of firewalls already in place offer excellent protection against BSE," said Acting Commissioner of the Food and Drug Administration, Dr. Lester M. Crawford. "With these additional measures, we will make a strong system even stronger by putting into effect the most comprehensive, science-based improvements possible."

 

The steps already taken have been effective in protecting the American consumer from exposure to BSE. Import controls on live cattle and certain ruminant products were put in place more than 15 years ago. In 1997, FDA finalized its animal feed ban, which has been the critical safeguard to stop the spread of BSE through the U.S. cattle population by prohibiting the feeding of most mammalian protein to cattle and other ruminant animals. USDA implemented additional measures in January to ensure that no cattle tissues known to be high risk for carrying the BSE agent are included in USDA-regulated products. Finally, as became evident last December, there is a contingency response plan, developed over the past several years, that is launched immediately to contain any potential damage after a BSE positive animal is found.

 

To allow interested parties and stakeholders the opportunity to comment on the additional regulatory and policy measures under consideration, USDA's APHIS and FSIS, along with the FDA, developed an advance notice of proposed rulemaking that includes several additional actions the federal government is considering regarding BSE.

 

The ANPR also provides the public a succinct report on the work of the international review team (IRT) convened by Secretary Veneman to review the U.S. response to the single case of BSE in the United States (in a cow imported from Canada), along with a summary of the many actions already taken by each agency on BSE.

 

USDA's FSIS continues to seek and address comments on actions taken in relation to the BSE mitigation measures and put in place in January 2004. FSIS is also specifically seeking comments on whether a country's BSE status should be taken into account when determining whether a country's meat inspection system is equivalent to the U.S. regulations including the provisions in the FSIS interim final rules.

 

USDA's APHIS is specifically seeking comments on the implementation of a national animal identification system. In April, USDA announced the availability of $18 million in Commodity Credit Corporation funding to expedite development of a national animal identification system, which is currently underway. APHIS is inviting comments on when and under what circumstances the program should move from voluntary to mandatory, and which species should be covered now and over the long term.

 

The ANPRM also requests comment on the following measures related to animal feed, which is regulated by FDA:

 

removing specified risk materials (SRM's) from all animal feed, including pet food, to control the risks of cross contamination throughout feed manufacture and distribution and on the farm due to misfeeding; requiring dedicated equipment or facilities for handling and storing feed and ingredients during manufacturing and transportation, to prevent cross contamination; prohibiting the use of all mammalian and poultry protein in ruminant feed, to prevent cross contamination; and prohibiting materials from non-ambulatory disabled cattle and dead stock from use in all animal feed. FDA has reached a preliminary conclusion that it should propose to remove SRM's from all animal feed and is currently working on a proposal to accomplish this goal. Comments on these issues raised in the ANPRM are due to FDA next month.

 

FDA today also issued an interim final rule that prohibits the use of cattle-derived materials that can carry the BSE-infectious agent in human foods, including certain meat-based products and dietary supplements, and in cosmetics. These highÇrisk cattle-derived materials include SRM's that are known to harbor concentrations of the infectious agent for BSE, such as the brain, skull, eyes, and spinal cord of cattle 30 months of age or older, and a portion of the small intestine and tonsils from all cattle, regardless of their age. Prohibited high-risk bovine materials also include material from non-ambulatory disabled cattle, the small intestine of all cattle, material from cattle not inspected and passed for human consumption, and mechanically separated beef.

 

This action is consistent with the recent interim final rule issued by USDA declaring these materials to be inedible (unfit for human food) and prohibiting their use as human food.

 

FDA's interim final rule, in conjunction with interim final rules issued by FSIS in January 2004, will minimize human exposure to materials that scientific studies have demonstrated are likely to contain the BSE agent when derived from cattle that are infected with the disease. Consumption of products contaminated with the agent that causes BSE is the likely cause of a similar disease in people called variant Creutzfeldt-Jakob disease.

 

Although FDA's interim final rule has the full force and effect of law and takes effect immediately upon publication in the Federal Register, FDA is also asking for public comment on it.

 

In conjunction with the publication of the interim final rule, FDA is also proposing to require that manufacturers and processors of FDA-regulated human food and cosmetics containing cattle-derived material maintain records showing that prohibited materials are not used in their products. FDA is taking this action because records documenting the absence of such materials are important to ensure compliance with requirements of the interim final rule.

 

Publication of this USDA-FDA notice, as well as the two FDA documents, is scheduled for mid-July in the Federal Register. Comments should be submitted as directed in the addresses section of each document. Each document also provides information about how and where comments received may be viewed.

 

####

 

Note to Reporters: USDA news releases, program announcements and media advisories are available on the Internet. Go to the APHIS home page at www.aphis.usda.gov and click on the "News" button.

 

HHS news releases are available online at www.hhs.gov; FDA news releases can be found at www.fda.gov, which will also provide links to the documents discussed in this release.

 

####

 


 

STATEMENT BY LESTER M. CRAWFORD, D.V.M., PH.D. DEPUTY COMMISSIONER OF FOOD AND DRUGS DEPARTMENT OF HEALTH AND HUMAN SERVICES BEFORE THE COMMITTEE ON AGRICULTURE, NUTRITION, AND FORESTRY UNITED STATES SENATE JANUARY 27, 2004

 

Introduction

 

Mr. Chairman, Members of the Committee, thank you for the opportunity to participate in today’s hearing on measures taken by the Federal government to safeguard human and animal health in the United States from Bovine Spongiform Encephalopathy (BSE) and the response to the finding of a BSE-positive cow in the State of Washington. I am Dr. Lester M. Crawford, Deputy Commissioner, Food and Drug Administration (FDA or the Agency).

 

The mission of FDA is to protect the public health by assuring the safety and efficacy of our nation’s human and veterinary drugs, human biological products, medical devices, human and animal food supply, cosmetics, and radiation emitting products. In fulfilling this mission, FDA is the Agency responsible for assuring that all FDA-regulated products remain safe and uncompromised from BSE and related diseases. Many FDA-regulated products contain bovine ingredients, for example, heart valves, ophthalmic devices, dental products, wound dressings, injectable drugs, vaccines, soups, gravies, sausage casings, and animal feeds.

 

FDA has long been actively involved nationally and internationally in efforts to understand and prevent the spread of BSE. FDA collaborates extensively with the Centers for Disease Control and Prevention (CDC), the National Institutes of Health (NIH), the Animal and Plant Health Inspection Service (APHIS) and the Food Safety and Inspection Service (FSIS) within the U.S. Department of Agriculture (USDA), Customs and Border Protection (CBP), the Environmental Protection Agency (EPA), other Federal agencies, state and local jurisdictions, and with affected industries and consumer groups. Many of these activities fit within the framework of the Department of Health and Human Service’s (HHS or the Department) Bovine Spongiform Encephalopathy/Transmissible Spongiform Encephalopathy (BSE/TSE) Action Plan, which was released in August 2001. This collaboration over many years has enabled FDA to strengthen safeguards for FDA-regulated products and to respond quickly and effectively to the first case of BSE within the U.S.

 

Executive Summary

 

The mission of the Agency is to protect the public health by assuring the safety and efficacy of our nation’s human and veterinary drugs, human biological products, medical devices, human and animal food supply, cosmetics, and radiation emitting products. In fulfilling this mission, FDA is the Agency responsible for assuring that all FDA-regulated products remain safe and uncompromised from BSE and related diseases.

 

BSE is a progressive neurological disorder of cattle that results from infection by an unconventional transmissible agent, and was first diagnosed in the United Kingdom (U.K.) in 1986. Many FDA-regulated products contain bovine ingredients, for example, heart valves, ophthalmic devices, dental products, wound dressings, injectable drugs, vaccines, soups, gravies, sausage casings, and animal feeds and thus must be taken into consideration as part the effort to prevent infectivity by BSE.

 

FDA has a longstanding commitment to protecting consumers from BSE by following multiple measures designed to safeguard FDA-regulated products from possible contamination by the BSE agent. Under the Federal Food, Drug, and Cosmetic (FD&C) Act, FDA has the authority to prevent the adulteration and misbranding of FDA-regulated products. Further, for medical products that require pre-market approval (e.g., drugs under Section 505 and medical devices under Section 513 of the FD&C Act), FDA has addressed safety concerns related to BSE through requirements of the application and approval process.

 

The U.S. employs a robust multi-layered approach to preventing the introduction and amplification of BSE. While the goal of this approach is to achieve an extremely high level of compliance with each preventative measure, this multi-layered approach is designed to protect the U.S. consumer from exposure to the BSE infective material, and to date this approach has been working. Since 1989, USDA has prohibited the importation of live animals and animal products from BSE-positive countries. Since 1997, FDA has prohibited the use of certain mammalian proteins in the manufacture of ruminant feed. FDA continues to implement policies to keep safe all FDA-regulated products, including food, food ingredients, dietary supplements, drugs, vaccines, and cosmetics from risk of any BSE-contaminated bovine material. As a result of these multiple regulatory safeguards, the risk of exposure to BSE through products, FDA regulates remains extremely low in the U.S.

 

FDA’s 1997 animal feed regulation forms the basis of the Agency’s efforts to prevent the spread of BSE through animal feed. This rule prohibits the use of most mammalian protein in the manufacture of animal feeds for ruminants. FDA implemented this rule to establish in our country feeding practices consistent with the best science and epidemiological knowledge known at the time to prevent the spread of BSE throughout herds of U.S. cattle. A risk assessment sponsored by USDA and conducted by the Harvard Center for Risk Analysis, released in November 2001, identified FDA’s feed ban as one of the primary safeguards against the spread of BSE in U.S. cattle.

 

To maximize protection afforded by the feed regulation, FDA has developed and implemented a BSE/Ruminant Feed Ban Inspection compliance program and established the goal of 100 percent compliance. FDA’s strategy for achieving uniform compliance with the feed rule focuses on three areas: education, inspection, and enforcement. FDA and its state counterparts conduct, at least annually, targeted BSE inspections of 100 percent of known renderers, protein blenders, and feed mills processing products containing material prohibited from use in ruminant feed. Compliance by these establishments with FDA’s feed rule is estimated to be at better than 99 percent. As of December 20, 2003, FDA had received over 26,000 inspection reports (6,404 for Fiscal Year 2003). The majority of these inspections (around 70 percent) were conducted by state officials for FDA, with the remainder conducted by FDA officials. The total number of inspection reports represents 13,672 firms, 1,949 of which are active and handle materials prohibited from use in ruminant feed. The 1,949 active firms that handle prohibited material have been inspected by FDA and, as of December 31, 2003, only five were found to have significant violations, resulting in official action indicated (OAI). FDA is working with these firms to bring them into compliance.

 

On December 23, 2003, FDA was notified by USDA of a presumptive-positive finding of BSE in a cow in Washington State. FDA immediately initiated its BSE Emergency Response Plan. As part of the plan, FDA has been coordinately closely with USDA so that we can effectively investigate this BSE case, trace the various products involved, and take the appropriate steps to protect the public. FDA investigators and inspectors located the high risk material rendered from the infected cow, and the rendering plants placed a hold on the rendered material, which is being disposed of appropriately. I am happy to report that all of the establishments inspected by FDA during the course of the investigation were in compliance with the feed ban. In addition, to help address the concerns of foreign governments and restore confidence in American products, FDA has participated, along with USDA, in numerous meetings and consultations with foreign governments since USDA surveillance found the BSE-positive cow.

 

In addition to new policies and regulations, new knowledge and tools gained through applied research can greatly help us to be more effective in our regulatory mission, such as protecting the country from BSE. Several of FDA’s Centers, as well as many private laboratories, academic institutions, and other Federal agencies (most notably NIH) are also involved in significant research activities relating to TSEs. Basic areas requiring research include: increasing our understanding of prions, learning how prions are transmitted within a species and potentially between species, developing diagnostic tests for humans and animals, developing detection methods for use on regulated products, developing methods to increase or eliminate infectivity, and designing new treatments. We are optimistic about the promise of new technologies, such as better methods to quickly distinguish the species of proteins and sensors to detect abnormal prions in food. Development of these technologies can contribute significantly to the effort to prevent the spread of BSE and must be considered carefully when evaluating potential regulatory changes to address BSE.

 

At the time that FDA implemented the feed rule in 1997, the Agency also recognized that evolving, complex scientific and public health issues, particularly regarding BSE required the Agency to continue to assess and scrutinize the rule to ensure its integrity as a firewall against the potential for spread of BSE. To further explore ways the animal feed regulation could be improved in November 2002, FDA published an advance notice of proposed rulemaking (ANPR) soliciting information and views from the affected industries and the public on some potential changes to its current feed regulation, including ways that the animal feed regulation could be strengthened. Although the risk of exposure to BSE in the U.S. remains extremely low and the measures in place are working, as a result of the recently discovered infected cow in the state of Washington, the Agency is evaluating the appropriateness of additional science-based measures to further strengthen our current protections.

 

Yesterday, Department Secretary Tommy Thompson and FDA Commissioner Mark McClellan announced several additional public health measures to further strengthen the current robust safeguards that help protect Americans from exposure to the agent that causes BSE and help prevent the spread of BSE in U.S. cattle. These measures relate to both protections for foods intended for human consumption as well as additional measures to strengthen FDA’s 1997 final rule regulating animal feed. With respect to human foods, FDA announced that it will extend to FDA-regulated foods, dietary supplements and cosmetics, restrictions on using specified risk materials that would complement the recent USDA announcements. Concerning animal feed, the Agency announced a series of measures designed to lower even further the risk that cattle will be purposefully or inadvertently fed “ruminant” proteins, including, eliminating an exemption in the feed rule that allows mammalian blood and blood products at slaughter to be fed to ruminants as a protein source; banning the use of “poultry litter” as a feed ingredient for cattle and other ruminants; prohibiting the use of “plate waste” as a feed ingredient for ruminants, including cattle; and taking steps to further minimize the possibility of cross-contamination of animal feed via equipment, facilities or production lines.

 

Finally, FDA is increasing its inspections of feed mills and renderers in 2004. Our 2001 base funding for BSE-related activities was $3.8 million. We shifted resources internally in 2001 and received a substantial increase from Congress in 2002. Our funded level for 2004 is currently approximately $21.5 million, almost a five-fold increase over the 2001 base. FDA will itself conduct 2,800 inspections and will make its resources go even further by working with state agencies to fund 3,100 contract inspections of feed mills and renderers and other firms that handle animal feed and feed ingredients. Through partnerships with states, FDA will also receive data on 700 additional inspections, for a total of 3,800 state contract and partnership inspections in 2004. These inspections would include 100 percent of all known renderers and feed mills that process products containing prohibited materials.

 

The Agency looks forward to continuing to assist Congress as it evaluates the risks associated with BSE, identifies opportunities to promote technologies that will detect and prevent the spread of BSE, and considers science-based approaches to further strengthen regulatory protections and bolster the resources available to assist Federal, state, local and private efforts to assure that BSE does not present a threat to human or animal health in the U.S.

 

see full text ;

 


 

OH, that's right, old lester sold out to the highest bidder $$$

 

 Ex-FDA Chief Faces Fines in Stock Case By ANDREW BRIDGES, Associated Press Writer 1:55 PM PST, January 19, 2007

 

WASHINGTON -- Former FDA Commissioner Lester Crawford would face a $50,000 fine and probation but no jail time as punishment for lying about ownership of illegally held stocks, according to a deal worked out between his attorney and federal prosecutors.

 

Crawford and the government both have agreed to the fine and some form of probation, though his ultimate sentence will be at the discretion of Magistrate Judge Deborah A. Robinson, according to sentencing memoranda filed with the U.S. District Court in Washington.

 

His sentencing is set for Tuesday.

 

Crawford pleaded guilty in October to charges of having a conflict of interest and false reporting of information about stocks he and his wife owned in food, beverage and medical device companies he regulated while head of the Food and Drug Administration.

 

The U.S. Attorney's office recommended the $50,000 fine, saying it would exceed the roughly $39,000 Crawford and his wife, Cathy, made from exercising options and in dividends from the forbidden stocks they held in the FDA-regulated companies.

 

The government also recommended Crawford be sentenced to probation and community service but skip any jail time, according to its sentencing memo filed with the court. Crawford could face up to six months in jail under sentencing guidelines.

 

"Given his early acceptance of responsibility, the defendant's actions merit the stigma of criminal convictions, a fine, and probation, but not incarceration," according to the government memo, signed by assistant U.S. attorneys Howard R. Sklamberg and Timothy G. Lynch. Sklamberg declined to comment Friday.

 

Crawford's attorney, Barbara Van Gelder, said her client agreed to pay the fine, according to her memo to the court. However, Van Gelder specifically requested unsupervised probation, which would allow Crawford to travel overseas for work. Van Gelder did not mention community service in her memo. She did not immediately return a message seeking comment.

 

In October, Crawford admitted to falsely reporting that he had sold or did not own stock when he continued holding shares in the firms governed by rules of the FDA, which is illegal. Beginning in 2002, Crawford filed seven incorrect financial reports with a government ethics office and Congress, leading to the misdemeanor charges.

 

Although Crawford lied about ownership of the stocks -- including under oath before the Senate -- government attorneys acknowledged there is no evidence he was "engaged in a concerted scheme to use his high office for personal gain."

 

Van Gelder, meanwhile, suggested Crawford's wife, secretary and financial adviser prepared and handled the inaccurate financial statements Crawford filed with the government. She acknowledged, however, that Crawford remained ultimately responsible for their accuracy.

 

Crawford, a veterinarian and food-safety expert, abruptly resigned from the FDA in September 2005 but gave no reason for leaving. He had held the job for two months, following his confirmation by the Senate.

 

On the Net:

 

Food and Drug Administration: http://www.fda.gov

 


 

Date: October 18, 2006 at 7:44 am PST

 

Former FDA Commissioner Pleads Guilty to Conflict of Interest and Making False Financial Disclosures

 

WASHINGTON, Oct. 17, 2006 - Lester M. Crawford, a former Commissioner of the Food and Drug Administration (FDA), has pled guilty to a Conflict of Interest charge and Making False Financial Disclosures to the U.S. Senate and the Executive Branch, announced U.S. Attorney Jeffrey A. Taylor and Inspector General Daniel Levinson, U.S. Department of Health and Human Services.

 

Crawford entered his guilty plea to the two misdemeanor charges this afternoon in the U.S. District Court for the District of Columbia before U.S. Magistrate Judge Deborah Robinson. Crawford is scheduled to be sentenced on January 22, 2007. He faces a sentence of up to one year in prison on each charge.

 

"One of the most important principles of our ethics laws is that public officials cannot have a financial interest in any decision that they make,” stated U.S. Attorney Taylor. “Lester Crawford, who held one of the most important jobs in government, blatantly violated these principles. Today, he is being held accountable for his actions."

 

Inspector General Levinson stated, "Any Government official's disregard of the conflict of interest laws undermines the integrity of the rules of conduct established for all those in Government. Taxpayers must have confidence that administrators of Government programs will be objective and free from improper influences in carrying out their official duties."

 

Crawford, 68, of Chevy Chase, Maryland, held some of the most senior positions in the FDA. He served as Deputy Commissioner between February 25, 2002 and March 26, 2004, when he became Acting Commissioner. On February 15, 2005, Crawford was nominated to become Commissioner. On July 18, 2005, the U.S. Senate confirmed Crawford, who remained Commissioner until September 30, 2005.

 

As a senior FDA employee, Crawford was required to file regular Public Financial Disclosure Reports, known as Standard Form SF 278s. Schedule A of the SF 278 required the filer to list all investment assets having a value exceeding $1,000 that were held by the filer or the filer's spouse, as well as sources of income exceeding $200 earned by the filer during the applicable reporting period.

 

Each year, ethics officials at the Department of Health and Human Services reviewed Crawford's SF 278s to ensure that he and his wife were not holding stocks or stock options of companies that were "significantly regulated organizations," which federal regulations defined as organizations for which the sales of products regulated by the FDA constitute ten percent or more of annual gross sales in the organization's previous fiscal year. Any FDA employee who was required to file an SF 278 could not hold a "financial interest," such as stock or stock options, in a significantly regulated organization.

 

Crawford's nomination as Commissioner required confirmation by the U.S. Senate and was considered by the Senate Committee on Health, Education, Labor, and Pensions. As a nominee, Crawford was required to submit two financial disclosure documents to the Committee: an SF 278 and a Statement for Completion by Presidential Nominees. Crawford filed both forms in February 2005.

 

Crawford’s plea to Making False Writings is based on his failure to disclose his and his wife’s ownership of stock in “significantly regulated organizations” to the Senate Committee and to the Executive Branch.

 

During the relevant time periods, Crawford and/or his wife owned forbidden stocks in the following “significantly regulated organizations”: Pepsico, Sysco, Kimberly-Clark, and Embrex.

 

Crawford filed a number of disclosure forms and other false writings in which he did not declare his and his wife’s ownership of forbidden stocks and stock options. Specifically,

 

•July 1, 2004. In this SF 278, Crawford disclosed ownership of Sysco and Kimberly-Clark stock. When an HHS ethics official inquired about Crawford’s ownership of this stock, Crawford responded in a December 28, 2004 email that the stocks in "Sysco and Kimberly-Clark have in fact been sold." That statement was false.

 

• February 23, 2005. Crawford did not disclose on this SF 278 his income from a November 17, 2004 exercise of Embrex stock options or the Crawfords' ownership of Kimberly-Clark or Sysco stock.

 

• February 25, 2005. Crawford failed to disclose in his nominee Statement to the Senate Committee his income from the exercise of Embrex stock options in October 2003 and November 2004. Crawford also did not disclose his remaining Embrex stock options.

 

Crawford’s ownership of Sysco and Pepsico stock and his role as Chairman of the FDA’s Obesity Working Group (“OWG”) gave rise to the Conflict of Interest charge, to which he has also pled guilty. On February 11, 2004, Crawford and the OWG's Vice Chairman submitted the OWG's final report and recommendations, entitled "Calories Count: Report of the Working Group on Obesity," to then-FDA Commissioner Mark McClellan. The report contained many recommendations, including encouraging manufacturers to re-label serving sizes, noting as an example that "a 20 oz bottle of soda that currently states 110 calories per serving and 2.5 servings per bottle could be labeled as 275 calories per bottle." The FDA publicly released "Calories Count" on March 12, 2004.

 

On June 3, 2004, Crawford testified before the House of Representatives Committee on Government Reform about the government's role in combating obesity. In his testimony, Crawford outlined the OWG's recommendations and again stressed the importance of re-labeling serving sizes for sodas.

 

During the entire period from the formation of the OWG to the date of Crawford's congressional testimony, Crawford and his wife owned 1,400 shares of Pepsico stock, worth a minimum of about $62,000, and 2,500 shares of Sysco stock, worth a minimum of about $78,000. Pepsico, a leading manufacturer of soft drinks and snack foods, and its shareholders had a financial interest in the OWG's conclusions and recommendations. Sysco, a leading manufacturer of food products, and its shareholders had a financial interest in the OWG's conclusions and recommendations.

 

There is no evidence that the OWG's conclusions were altered because of the Crawfords' ownership of Pepsico or Sysco stock.

 

Following the announcement of Crawford’s departure from office, Senators Mike Enzi and Edward Kennedy and Representatives Maurice Hinchey, Marcy Kaptur, Lynn Woolsey, Raúl Grijalva, and Sam Farr asked that the Inspector General investigate this matter.

 

In announcing today’s guilty plea, U.S. Attorney Taylor and Inspector General Levinson commended Inspector Thomas Sowinski of the Inspector General’s office for his outstanding investigation of this case. They also thanked the Senate Legal Counsel’s Office for the help that it provided in the investigation. Finally, they commended Assistant U.S. Attorneys Howard Sklamberg and Timothy Lynch, who prosecuted the case, and intern Vi Do, who assisted in the investigation.

 

For Information, Contact Public Affairs Channing Phillips (202) 514-6

 


 

SO, in essence, the fda simply hung a carrot out in front of the public, and the public bit. i ain't biting. it's all about money, to hell with human health ;

 

reminds me of ;

 

STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

 

snip...END full text ;

 


 

FOR IMMEDIATE RELEASE P07-08 January 19, 2007 Media Inquiries: Kathleen Quinn, 301-827-6242 Consumer Inquiries: 888-INFO-FDA

 

FDA Commissioner Announces Important Personnel Changes

 

U.S. Food and Drug Administration (FDA) Commissioner Dr. Andrew C. von Eschenbach is pleased to announce two new personnel changes at the Agency; the creation of the Office of the Chief Medical Officer which will be overseen by Deputy Commissioner Dr. Janet Woodcock and the appointment of John R. Dyer, MPH, as the agency's Deputy Commissioner for Operations and the Chief Operating Officer (COO).

 

snip...

 

"FDA is a science-based agency and science-led Agency; science provides the foundation for our regulatory decisions and the work we do on a daily basis to promote and protect the nations' health," said Dr. von Eschenbach. "Creation of this office, and position, will better ensure we achieve this mission with the highest scientific quality and effectiveness needed."

 

snip...

 

Mr. Dyer most recently served as the Chief Operating Officer for the Centers for Medicare & Medicaid Services (CMS), a federal agency within the Department of Health and Human Services that is responsible for providing health insurance benefits to the elderly, disabled, and indigent through the Medicare and Medicaid programs. In that capacity, he led the implementation of the Medicare Modernization Act (MMA) and was responsible for the overall day to day operations of the agency. Specifically as COO, he helped develop the program policies and regulations, and stood up the business and systems operations of the prescription drug program in time for the congressionally mandated start of open enrollment on Oct 15, 2005 and start of the drug prescription benefits on January 1, 2006.

 

Prior to CMS, from 2001-2003, Mr. Dyer worked in the private sector for information technology and executive leadership companies. He was involved in entrepreneurial ventures in agriculture, real estate, and industrial enterprises in Latin America from 2003-2004.

 

In his federal career from 1972 to 2000, Mr. Dyer held increasingly responsible executive positions with the Social Security Administration (SSA), including the Chief Information Officer and Principal Deputy Commissioner where he assisted the agency by leading the effort to automate and modernize systems and improve the level of customer service. Other federal positions include the Director for Budget and Management at CMS (then the Health Care Financing Administration) from 1984-1998 and Commerce Branch Chief at the Office of Management and Budget in the Executive Office of the President. While at OMB, Mr. Dyer had budget and policy review of wide-ranging research and development programs ranging from mental health to ocean and atmospheric related.

 

Mr. Dyer has been the recipient of many awards during his federal career including the Presidential Award for Distinguished Executive. He holds a Masters Degree in Public Health from the University of Michigan and obtained his undergraduate Bachelor of Arts in Sociology from Notre Dame.

 

####

 


 

*** UPDATE ON TSE roadmap 2, a road to no where Sunday July 18, 2010 ***

 

 IN reply to ;

 

Saturday, July 17, 2010

 

TSE Road map 2 A Strategy paper on TSE, a road to no where

 

Brussels, 16.7.2010 COM(2010)384 final COMMUNICATION FROM THE COMMISSION TO THE EUROPEAN PARLIAMENT AND THE COUNCIL

 


 

Confucius is confused again. IF BSE was spontaneous, just happens from nothing occasionally, from a funked out twisted protein, that just happens to spontaneously change shapes on it's own, as most officials have had us believe over the years, decades. THEN how is BSE almost eradicated ??? hmm?

 

WHAT about atypical BSE's ?

 

WHAT about IBNC BSE ?

 

SRM's there from all of the above ?

 

WHAT about SRM from pigs, poultry, fish, AND the potential for passing the TSE agent surviving the digestinal track to expose further in feed ?

 

The potential for transmissible spongiform encephalopathies in non-ruminant livestock and fish

 

D. Matthews (1) & B.C. Cooke (2) (1) Transmissible Spongiform Encephalopathy [TSE) Programme Manager, Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone. Surrey KT15 3NB. United Kingdom (2) 1 Jenkins Orchard, Wick St Lawrence. Weston Super Mare. North Somerset, BS22 7YP. United Kingdom

 

Summary

 

Pigs and poultry in the United Kingdom have undeniably been exposed to the bovine spongiform encephalopathy (BSE) agent. They consumed the same ruminant protein that gave rise to the BSE epidemic in cattle, but there has been no evidence of an epidemic in these species. Experimental investigations have shown pigs to be susceptible to infection by multiple parenteral challenge, but resistant to oral exposure with BSE-infected cattle brain. Current but incomplete evidence suggests that they are also resistant to oral challenge with sheep scrapie. Studies in domestic chickens indicate that they are resistant to both parenteral and oral challenge. Unfortunately, no published data exists on the susceptibility of fish to infection. Incidental findings in the brains of unexposed pigs are described that could otherwise give rise to concerns about the presence of a transmissible spongiform encephalopathy in pig populations around the world.

 

Keywords

 

Chicken - Fish - Meat-and-bone meal - Pig - Poultry - Prion - Prion protein ­Transmissible spongiform encephalopathy.

 

Introduction

 

The recognition of bovine spongiform encephalopathy (BSE) in domestic cattle in the United Kingdom (UK) in 1986 inevitably led to concerns about the potential risk to non-ruminant livestock (49). Although the initial focus was on the identification of the causal agent of BSE and confirmation that the disease was transmissible (20), research rapidly investigated the likelihood that pigs and poultry might also be susceptible to infection. lnitial epidemiological investigations into the source of BSE identified the likely vehicle to be the consumption by cattle of rendered animal protein of ruminant origin (51). With time, the decline of the epidemic following the implementation of measures to remove ruminant protein from cattle feed has confirmed that hypothesis. This is distinct from the debate about whether the actual origin of the agent was ovine or bovine. While there has been speculation about whether BSE arose spontaneously in bovines, rather than from transmission of sheep scrapie to cattle, the ban dealt with the vehicle of transmission, irrespective of origin.

 


 

Wednesday, April 02, 2008 In vivo prion protein intestinal uptake in fish

 

1: APMIS. 2008 Mar;116(3):173-80.

 

In vivo prion protein intestinal uptake in fish.

 

Dalla Valle AZ, Iriti M, Faoro F, Berti C, Ciappellano S. Department of Food Science and Microbiology (DISTAM), Section of Human Nutrition, University of Milan, Milan, Italy.

 

Intestinal uptake of abnormal prion protein (PrP(Sc)), the pathological agent involved in transmissible spongiform encephalopathies (TSEs), has been investigated in rainbow trout (Oncorhynchus mykiss). Experimental procedures were conducted in vivo by immunohistological PrP(Sc) localization in intestine and pyloric caeca after forced feeding of infected material. Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the distal intestine. It did not remain longer than 15 days in the fish intestine; furthermore, it did not cross the intestinal barrier.

 

PMID: 18377582 [PubMed - in process]

 


 

Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted

 

in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the

 

distal intestine.

 

It did not remain longer than 15 days in the fish intestine;

 

WOULD this not be a potential risk factor for transmission of the PrPSc agent to cattle and other species via fish by-products and or fish feed ???

 

vCJD in the USA * BSE in U.S.

 

15 November 1999

 

snip...

 

Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows.

 

***I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing.

 

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.

 

snip...

 

full text ;

 


 


 

Research article

 

Scrapie infectivity is quickly cleared in tissues of orally-infected farmed fish

 

Loredana Ingrosso1 , Beatriz Novoa2 , Andrea Z Dalla Valle3 , Franco Cardone1 , Raquel Aranguren2 , Marco Sbriccoli1 , Simona Bevivino1 , Marcello Iriti4 , Quanguo Liu1 , Vito Vetrugno1 , Mei Lu1 , Franco Faoro4 , Salvatore Ciappellano3 , Antonio Figueras2 and Maurizio Pocchiari1

 

1 Istituto Superiore di Sanità, Department of Cellular Biology and Neuroscience, viale Regina Elena,299,00161 Rome, Italy

 

2 Instituto Investigaciones Marinas, CSIC, Eduardo Cabello 6, 36208 Vigo, Spain

 

3 Section of Human Nutrition, Department of Food Science and Microbiology, DiSTAM, University of Milan, via Celoria 2, 20133 Milano, Italy

 

4 Institute of Plant Pathology, University of Milan and Institute of Plant Virology, CNR, Milano, Italy

 

author email corresponding author email

 

BMC Veterinary Research 2006, 2:21doi:10.1186/1746-6148-2-21

 

Published: 15 June 2006

 

Abstract Background Scrapie and bovine spongiform encephalopathy (BSE) belongs to the group of animal transmissible spongiform encephalopathy (TSE). BSE epidemic in the UK and elsewhere in Europe has been linked to the use of bovine meat and bone meals (MBM) in the feeding of cattle. There is concern that pigs, poultry and fish bred for human consumption and fed with infected MBM would eventually develop BSE or carry residual infectivity without disease. Although there has been no evidence of infection in these species, experimental data on the susceptibility to the BSE agent of farm animals other than sheep and cow are limited only to pigs and domestic chicken. In the framework of a EU-granted project we have challenged two species of fish largely used in human food consumption, rainbow trout (Oncorhynchus mykiss) and turbot (Scophthalmus maximus), with a mouse-adapted TSE strain (scrapie 139A), to assess the risk related to oral consumption of TSE contaminated food. In trout, we also checked the "in vitro" ability of the pathological isoform of the mouse prion protein (PrPSc) to cross the intestinal epithelium when added to the mucosal side of everted intestine.

 

Results Fish challenged with a large amount of scrapie mouse brain homogenate by either oral or parenteral routes, showed the ability to clear the majority of infectivity load. None of the fish tissues taken at different time points after oral or parenteral inoculation was able to provoke scrapie disease after intracerebral inoculation in recipient mice. However, a few recipient mice were positive for PrPSc and spongiform lesions in the brain. We also showed a specific binding of PrPSc to the mucosal side of fish intestine in the absence of an active uptake of the prion protein through the intestinal wall.

 

Conclusion These results indicate that scrapie 139A, and possibly BSE, is quickly removed from fish tissues despite evidence of a prion like protein in fish and of a specific binding of PrPSc to the mucosal side of fish intestine.

 


 

>>>However, a few recipient mice were positive for PrPSc and spongiform lesions in the brain. We also showed a specific binding of PrPSc to the mucosal side of fish intestine in the absence of an active uptake of the prion protein through the intestinal wall. <<<

 


 

WOULD this not be further evidence to show that the rendering of such product after ingesting TSE tainted product, would further expose species that consume such product, i.e. even if the fish do not contract a TSE, could not the intestines and the feed that may still be there further expose species eating those by-products ???

 

Competing interests

 

none

 


 

 An evolutionary basis for scrapie disease: identification of a fish prion mRNA

 

References and further reading may be available for this article. To view references and further reading you must purchase this article.

 

Eric Rivera-Milla, Claudia A. O. Stuermer and Edward Málaga-Trillo

 

Department of Biology, University of Konstanz, 78457, Konstanz, Germany

 

Available online 11 December 2002.

 

Abstract Infectious prion proteins cause neurodegenerative disease in mammals owing to the acquisition of an aberrant conformation. We cloned a Fugu rubripes gene that encodes a structurally conserved prion protein, and found rapid rates of molecular divergence among prions from different vertebrate classes, along with molecular stasis within each class. We propose that a directional trend in the evolution of prion sequence motifs associated with pathogenesis and infectivity could account for the origin of scrapie in mammals.

 


 


 

AS the crow flies, so do TSE...feces

 

Could Crows Play a Role in Spreading CWD was presented by Dr. Kurt VerCauteren, NWRC, WS-APHIS- USDA. From the first observations (40 years ago) of CWD in mule deer (Odocoileus hemionus) and Rocky Mountain elk (Cervus elaphus nelsoni) in Northern Colorado, the disease has been identified in an increasing geographic area. Mechanisms for the spread of CWD are incompletely understood. Birds have been identified as potential vectors for a number of diseases, where infected material is ingested and the disease agent is later shed in new areas after flying substantial distances. We hypothesized that avian scavengers have the potential to disseminate prions associated with transmissible spongiform encephalopathies (TSEs), like CWD, by a similar process. As prions are resistant to destruction, it is reasonable that infectious material could pass through the digestive tract of scavenging birds. Our objective was to determine if TSE-positive brain material from mice (i.e., mouse-adapted scrapie) could pass through the digestive tract of American crows (Corvus brachyrhynchos) and still be infectious to mice. Our experimental design included treatment groups of mice inoculated intraperitoneally with: 1) normal mouse brain, 2) infected mouse brain, 3) gamma-irradiated feces from crows gavaged with normal mouse brain, and 4) gamma-irradiated feces from crows gavaged with infected mouse brain. Our preliminary results indicate feces from each of 20 crows gavaged with infected mouse brain were infectious for mice (proportion of crows=1.00, 95% CI: 0.83-1.00) and average longevity for mice was 213 days (95% CI: 210-216). Longevity of mice inoculated with infected mouse brain was slightly less (198 days, 95% CI: 188-207). Most mice inoculated with normal brain, or feces from crows gavaged with normal brain, were still alive 1 year post inoculation with no evident clinical signs of TSE disease in any control mice. Our results demonstrate that a common, migratory North American scavenger, the American crow, can pass infective prions in feces and, therefore, could play a role in the spatial dissemination of prion disease.

 


 

 Sunday, November 01, 2009

 

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

 

snip...

 

PLUS, this goes back to what the late Dr. Gibbs told me, and what the late Harash Narang book showed, Dr. Gibbs stating that the TSE agent could spread through the digestinal track, and survive, and could still have the potential to spread, and Harash Narang's book 'The Link', page 135, where a farmers around Kent have chickens with BSE. MAFF was aware of this and was suppose to do some studies? BUT, regardless whether or not these birds become clinical and die, the fact that the above studies showed that the TSE agent survived the digestinal tract, and went on to further infect mice via feces, is very disturbing, and further enhances transmission studies must be done asap. PLUS, this should be the final straw for chicken litter being fed back to cattle and other food producing animals for humans and animals. AND not to forget the Red Necked Ostrich and BSE? ...TSS

 

snip...

 

SEI805 Transmissibility of BSE to domestic fowl by injection with brain homogenate.

 

1 challenged bird died overnight (42 months p.i.) following a period of ataxia ­- histopathological examination pending. 2 further challenged birds are also showing neurological signs of ataxia and tremor (43 months p.i.). All affected birds are cock birds. The remaining 4 challenged hens are clinically normal (43 months p.i.).

 

2 control birds were culled due to intercurrent disease (40 and 43 months p.i.) . No significant lesions were observed in one and histopathological examination is pending on the other.

 

The remaining 6 control birds are clinically normal.

 

SE1806 Transmissibility of BSE to domestic fowl by oral exposure to brain homogenate.

 

1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems.

 

94/01.19/7.1

 

1 other challenged cock bird is also showing ataxia (43 months p.i.). The remaining 2 challenged cocks and 5 hens are clinically normal (43 months p.i.).

 

Ruther examinations are in progress to determine the cause of morbidity in these studies (SE1805 and SE1806).

 

For controls see SE1805.

 

snip...

 

94/01.19/7.1

 


 

 also,

 

TRANSLATION

 

F437/91

 

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY -

 

* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs

 

THE AUTOPSY

 

Date: Mon, 11 Jun 2001 16:24:51 -0700 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'

 

snip...

 

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

 


 

 OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002

 

OPINION

 

1. Necrophagous birds as possible transmitters of BSE. The SSC considers that the evaluation of necrophagous birds as possible transmitters of BSE, should theoretically be approached from a broader perspective of mammals and birds which prey on, or are carrion eaters (scavengers) of mammalian species. Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons, eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could be considered possible vectors of transmission and/or spread of TSE infectivity in the environment. In view also of the occurrence of Chronic Wasting Disease (CWD) in various deer species it should not be accepted that domestic cattle and sheep are necessarily the only source of TSE agent exposure for carnivorous species. While some information is available on the susceptibility of wild/exotic/zoo animals to natural or experimental infection with certain TSE agents, nothing is known of the possibility of occurrence of TSE in wild animal populations, other than among the species of deer affected by CWD in the USA.

 

1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.

 

C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc

 


 

 snip... see full text ;

 


 

 7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE; 1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,

 

Links

 

Click here to read

 

The neuropathology of experimental bovine spongiform encephalopathy in the pig.

 

Ryder SJ, Hawkins SA, Dawson M, Wells GA.

 

Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.

 

In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.

 

PMID: 10684682 [PubMed - indexed for MEDLINE]

 


 

 Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report

 

Authors

 

Greenlee, Justin Kunkle, Robert Hamir, Amirali

 

Submitted to: American Association of Veterinary Laboratory Diagnosticians Publication Type: Abstract Publication Acceptance Date: November 5, 2005 Publication Date: November 5, 2005 Citation: Greenlee, J.J., Kunkle, R.A., Hamir, A.N. 2005. Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report [abstract]. Proceedings of the American Association of Veterinary Laboratory Diagnosticians 48th Annual Conference. P. 38.

 

Technical Abstract: Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids, and a number of laboratory animal models. In a laboratory setting, the host range of a given TSE can be tested by inoculating animals with brain tissue from affected animals through various routes including oral and intracranial. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to bovine spongiform encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility. This study utilized 26 swine randomly divided into three groups: controls (n=6), oral inoculates (n=8), and intracranial inoculates (n=12). Brain homogenate (10%) derived from scrapie-affected sheep was given by a single intracranial injection of 0.75 ml or by oral inoculation of 15 ml on four consecutive days. Scrapie inoculum was derived from clinically ill sheep inoculated with material derived from 13 sheep in seven source flocks. A sample of this material was also inoculated back into sheep to assure infectivity. Necropsies were planned for six months post inoculation, at approximately the time the pigs were expected to reach market weight. Samples collected were examined microscopically after routine staining (hematoxylin and eosin) and staining by standard immunohistochemical methods for prion protein (PrP**Sc). After approximately six months incubation time, no histologic lesions suggestive of spongiform encephalopathy or immunohistochemical evidence of prion infection were obtained. No evidence of scrapie infection was demonstrated in this short-term study, but positive results after an incubation period of only six months would be uncharacteristic. The only TSE with an incubation of six months or less known at this time is transmissible mink encephalopathy in mink, skunk, or raccoon hosts. However, scrapie in the raccoon model has a two-year incubation period. A replicate of littermate pigs has been inoculated and will be studied after long-term (3-7 years) incubation, and a similar study is underway with pigs inoculated with material derived from elk, mule deer, and whitetail deer affected by chronic wasting disease (CWD).

 

Last Modified: 03/19/2006

 


 

 EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

 

2. It was agreed that there was evidence of scrapie in sheep as a result of food borne exposure. This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. As the working hypothesis is that there has been recycling of infected cattle tissues which has augmented the epidemic in cattle the continued infection of sheep with the BSE agent, via the food born source, cannot be excluded. There is therfore also a possibility that the BSE agent may have become endemic in the sheep population, but is is impossible to design any short-term research programme to elucidate this. ...

 


 

 Sunday, April 18, 2010

 

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

 


 

 AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

 

snip...

 


 


 

 FELINE SPONGIFORM ENCEPHALOPATHY FSE

 


 

 STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

 

snip...

 

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

 

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

 

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

 

snip...

 

THE FUTURE

 

4..........

 

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

 

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

 

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

 

SEE full text ;

 


 

 THIS is what happens when you have the industry run the government, and if you think anything has changed in the last 2 decades, well you better think again, junk science and trade policy still rule the day $$$ TSS

 


 

Thursday, November 18, 2010

 

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

 

Dustin Douglass was indicted and charged with making a fraudulent application to the VA, in an effort to obtain benefits from injuries Douglas represented he suffered while deployed in Iraq. Based on his application, the VA provided benefits totaling $22,148.53. Douglass claimed he suffered various injuries and illnesses as a result of his service in combat. The investigation revealed Douglass had, in fact, been deployed to Iraq, but had served as a computer specialist, had never been in combat, and did not suffer the service-related injuries and illnesses he claimed to have suffered. Douglass was placed on supervised release for 3 years, and required to pay $22,148.53 in restitution. Galen Niehues, an inspector for the Nebraska Department of Agriculture, (NDA), was convicted of mail fraud for submitting falsified reports to his employer concerning inspections he was supposed to perform at Nebraska cattle operations. Niehues was tasked with performing inspections of Nebraska ranches, cattle and feed for the presence of neurological diseases in cattle including Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow Disease”. Niehues was to identify cattle producers, perform on-site inspections of the farm sites and cattle operations, ask producers specific questions about feed, and take samples of the feed. Niehues was to then submit feed samples for laboratory analysis, and complete reports of his inspections and submit them to the NDA and to the Federal Food and Drug Administration (FDA). An investigation by the FDA and NDA revealed Niehues had fabricated approximately 100 BSE inspections and inspection reports. When confronted, Niehues admitted his reports were fraudulent, and that had fabricated the reports and feed samples he submitted to the NDA. Niehues received a sentence of 5 years probation, a 3-year term of supervised release, and was required to pay $42,812.10 in restitution.

 


 


 

Date: June 21, 2007 at 2:49 pm PST

 

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

 

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

 

snip...

 

Topics that will be covered in ongoing or planned reviews under Goal 1 include:

 

soundness of BSE maintenance sampling (APHIS),

 

implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),

 

snip...

 

The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.

 

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

 


 

-MORE Office of the United States Attorney District of Arizona

 

FOR IMMEDIATE RELEASE For Information Contact Public Affairs

 

February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681

 

CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASE SURVEILLANCE PROGRAM

 

PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.

 

Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.

 

Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:

 

(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;

 

(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;

 

(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;

 

(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;

 

(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and

 

(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.

 

Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #

 


 

WE can only hope that this is a single incident. BUT i have my doubts. I remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5 grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and the FDA was bragging at the time that the amount of potentially BANNED product was so little and the cattle were so big ;

 

"It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated."

 


 

On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed. ... FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

 


 

WE now know all that was a lie. WE know that literally Thousands of TONS of BANNED and most likely tainted product is still going out to commerce. WE know now and we knew then that .005 to a gram was lethal. WE know that CWD infected deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been rendered and fed back to livestock (including cattle) for human and animal consumption.

 

Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ;

 

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

 

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

 

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

 

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end

 


 

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...

 


 

PAUL BROWN COMMENT TO ME ON THIS ISSUE

 

Tuesday, September 12, 2006 11:10 AM

 

"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."

 

OR, what the Honorable Phyllis Fong of the OIG found ;

 

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain

 


 

Table 1. Animal feed ingredients that are legally used in U.S. animal feeds

 

Animal

 

Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products

 

snip...

 

Conclusions

 

Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibioticresistant bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibioticresistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.

 

REFERENCES...snip...end

 

Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives

 


 

SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012 CALIFORNIA

 

Summary Report BSE 2012

 

Executive Summary

 


 

Saturday, August 4, 2012

 

Final Feed Investigation Summary - California atypical L-type BSE Case - July 2012

 


 

Saturday, August 4, 2012

 

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

 


 

Monday, March 19, 2012

 

*** Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy PLoS One. 2012; 7(2): e31449.

 


 

Sunday, January 11, 2015

 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 


 


 

Sunday, December 28, 2014

 

*** Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014

 


 


 

IN A NUT SHELL ;

 

(Adopted by the International Committee of the OIE on 23 May 2006)

 

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

 


 

Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 

Transmissible Spongiform Encephalopathy TSE Prion Disease have now been discovered in a wide verity of species across North America. typical C-BSE, atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine, typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98 Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD in cervid is slowly spreading without any stopping it in Canada and the USA and now has mutated into many different strains. Transmissible Mink Encephalopathy TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease have been silently mutating and spreading in different species in North America for decades. The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion Firewall, of which we now know without a doubt, that it was nothing but ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of banned mad cow feed has been put out into commerce, never to return, as late as December of 2013, serious, serious breaches in the FDA mad cow feed ban have been documented. The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

 


 

The BSE surveillance and testing have also been proven to be flawed, and the GAO and OIG have both raised serious question as to just how flawed it has been (see GAO and OIG reports). North America has more documented TSE prion disease, in different documented species (excluding the Zoo BSE animals in the EU), then any other place on the Globe. This does not include the very likelihood that TSE prion disease in the domestic feline and canine have been exposed to high doses of the TSE prion disease vid pet food. To date, it’s still legal to include deer from cwd zone into pet food or deer food. Specified Risk Material i.e. SRM bans still being breach, as recently as just last month. nvCJD or what they now call vCJD, another case documented in Texas last month, with very little information being released to the public on about this case? with still the same line of thought from federal officials, ‘it can’t happen here’, so another vCJD blamed on travel of a foreign animal disease from another country, while ignoring all the BSE TSE Prion risk factors we have here in the USA and Canada, and the time that this victim and others, do spend in the USA, and exposed to these risk factors, apparently do not count in any way with regard to risk factor. a flawed process of risk assessment. sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?

 

Two decades have passed since Dr. Ironside first confirmed his first ten nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is transmissible. yet all these TSE prion disease and victims in the USA and Canada are being pawned off as a spontaneous event, yet science has shown, the spontaneous theory has never been proven in any natural case of TSE prion disease, and scientist have warned, that they have now linked some sporadic CJD cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about this in the public domain. We must make all human and animal TSE prion disease reportable in every age group, in ever state and internationally, we must have a serious re-evaluation and testing of the USA cattle herds, and we must ban interstate movement of all cervids. Any voluntary effort to do any of this will fail. Folks, we have let the industry run science far too long with regards to the TSE prion disease. While the industry and their lobbyist continues to funnel junk science to our decision policy makers, Rome burns. ...end

 

REFERENCES

 

Sunday, June 29, 2014

 

Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 


 

Tuesday, December 2, 2014

 

UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease

 

USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$

 


 

Friday, December 5, 2014

 

SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide

 

OIE BSE TSE PRION AKA MAD COW DISEASE ?

 

‘’the silence was deafening’’ ...tss

 


 

who’s kidding whom $$$ i.e. USDA INC AND THE OIE

 

2014

 

***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.

 

***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent. Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].

 

snip...

 


 

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

 

*** Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2.

 

These data suggest that more than one BSEderived prion strain might infect humans;

 

***it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.

 

snip...

 

These studies further strengthen the evidence that vCJD is caused by a BSE-like prion strain.

 

Also, remarkably, the key neuropathological hallmark of vCJD, the presence of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission to these mice.

 

***However, the most surprising aspect of the studies was the finding that an alternate pattern of disease can be induced in 129MM Tg35 mice from primary transmission of BSE, with a molecular phenotype indistinguishable from that of a subtype of sporadic CJD. This finding has important potential implications as it raises the possibility that some humans infected with BSE prions may develop a clinical disease indistinguishable from classical CJD associated with type 2 PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic CJD. In this regard, it is of interest that the reported incidence of sporadic CJD has risen in the UK since the 1970s (Cousens et al., 1997)...

 


 

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

 

***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

 


 

-------- Original Message --------

 

Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD

 

Date: Thu, 28 Nov 2002 10:23:43 -0000

 

From: "Asante, Emmanuel A" e.asante@ic.ac.uk

 

To: "'flounder@wt.net'" flounder@wt.net

 

Dear Terry,

 

I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.

 

Thank you for your interest in the paper.

 

In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.

 

I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.

 

Emmanuel Asante

 

<>

 

____________________________________

 

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)

 

____________________________________

 

Thursday, August 12, 2010

 

Seven main threats for the future linked to prions

 

First threat

 

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

 

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

 

Second threat

 

snip...

 


 

Monday, October 10, 2011

 

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

 

snip...

 

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far

 

*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

 

snip...

 


 


 

*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL CDC ***

 

Sunday, November 23, 2014

 

*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European

 

the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.

 


 

Sunday, December 14, 2014

 

ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report

 


 

Thursday, January 15, 2015

 

41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

 


 

Saturday, January 17, 2015

 

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

 


 


 

Wednesday, January 21, 2015

 

Norway detects "probable" case of mad cow disease

 


 

Friday, November 28, 2014

 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL CONFIRMED

 


 

Monday, December 1, 2014

 

***Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014

 


 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

Monday, May 5, 2014

 

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

 


 

Brazil covered up it’s first mad cow case for two years before it was finally confirmed

 

Friday, December 07, 2012

 

ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012

 


 

“The two year delay in Brazil’s disease notification is a symptom of the failure of the OIE’s global system that erroneously assumes foreign countries, particularly developing countries, have the same means, commitment and capabilities as the United States to control and eradicate diseases, says Max Thornsberry, who chairs R-CALF USA’s Animal Health Committee.

 

 Thornsberry said USDA’s reliance on foreign countries and OIE to protect U.S. citizens from unsafe imports is “absolutely foolish” and again points up the need for country-of-origin labeling.

 


 

Friday, December 5, 2014

 

SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide

 

BSE TSE PRION AKA MAD COW TYPE DISEASE, THE SILENCE WAS DEAFENING $$$

 


 

IN A NUT SHELL ;

 

(Adopted by the International Committee of the OIE on 23 May 2006)

 

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

 


 

‘’LOL LAUGH OUT LOUD’’...TSS

 

IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.

 

I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.

 

JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...

 

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

 


 

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

 

UPDATE May 13, 2014

 

Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing

 

Greetings everyone,

 

Finally, got a confirmation from top official inside OIE.

 

YES!

 

Indeed, CHRONIC WASTING DISEASE CWD has been brought to the OIE table, by more than one country, and WILL BE BROUGHT TO THE TABLE AGAIN, WHEN THE NEXT AD HOC EXPERT GROUP IS CONVENED...tss

 

‘’On more than one occasion our Commission has received a request from a Member Country to list CWD as a disease notifiable to the OIE. However, it is not our practice to specify which Member Countries make specific requests to us. All countries which submit national comments to us at our February and September meetings are listed in the reports of our meetings. However, the country names are not linked to specific comments or requests.’’

 

’’they may also evaluate CWD against the OIE’s CRITERIA.’’

 

‘’That is where the situation stands at present. Next time an ad hoc group is convened to consider issues of listing and delisting, CWD will be evaluated. I have no idea of time frames.’’

 

personal communication with OIE top official...tss

 

Rome was not built overnight I suppose...tss

 

> In response to a _Member Country’s_ detailed justification for listing of chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2., the Code Commission _recommended_ this disease be reconsidered for listing.

 


 

Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013

 

*** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids.

 

page 6;

 


 

REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 19–28 February 2013

 

In response to a Member Country’s detailed justification for listing of chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2., the Code Commission recommended this disease be reconsidered for listing.

 


 

REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 17–26 September 2013

 

Item 5 Criteria for listing diseases (Chapter 1.2.)

 

Comments were received from Australia, EU, Japan, New Zealand, Switzerland, Thailand and AU-IBAR The Code Commission noted a Member Country’s comment suggesting that greater clarity was needed for the term ‘significant morbidity and mortality’. As noted in the February 2013 report, the Code Commission considered that the structured process of listing diseases, first by an expert group whose conclusions are documented and circulated for Member Countries’ review and comment, then consideration by the World Assembly of Delegates before final adoption, is sufficiently rigorous and transparent.

 


 

greetings,

 

what is criteria of Article 1.2.2. ???

 

curious as to what country detailed justification for listing ???

 

kind regards, terry

 

*******UPDATE ON OIE ARTICLE 1.2.2********

 

OIE Article 1.2.2.

 

The criteria for the inclusion of a disease, infection or infestation in the OIE list are as follows:

 

1) International spread of the agent (via live animals or their products, vectors or fomites) has been proven.

 

AND

 

2) At least one country has demonstrated freedom or impending freedom from the disease, infection or infestation in populations of susceptible animals, based on the animal health surveillance provisions of the Terrestrial Code, in particular those contained in Chapter 1.4.

 

AND

 

3)

 

a) Natural transmission to humans has been proven, and human infection is associated with severe consequences.

 

OR

 

b) The disease has been shown to cause significant morbidity or mortality in domestic animals at the level of a

 

country or a zone.

 

OR

 

c) The disease has been shown to, or scientific evidence indicates that it would, cause significant morbidity or

 

mortality in wild animal populations.

 

AND

 

4) A reliable means of detection and diagnosis exists and a precise case definition is available to clearly identify cases

 

and allow them to be distinguished from other diseases, infections and infestations.

 

OR

 

5) The disease or infection is an emerging disease with evidence of zoonotic properties, rapid spread, or significant morbidity or mortality and a case definition is available to clearly identify cases and allow them to be distinguished from other diseases or infections.

 

2 2013 © OIE - Terrestrial Animal Health Code Chapter 1.2.- Criteria for the inclusion of diseases, infections and infestations on the OIE list

 


 

*** URGENT CWD UPDATE Friday, January 17, 2014

 

FINALLY, 12 years later, the OIE becomes concerned with CWD to humans, not that I did not try and warn them 12 years ago. ...kind regards, terry

 

Friday, January 17, 2014

 

Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013

 

*** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids.

 

*** 2002 Singeltary vs O.I.E. on CWD to human risk factor ;

 

Subject: Re: CWD AMERICA ???

 

Date: Fri, 12 Jul 2002 19:10:18 +0200

 

From: "INFORMATION DEPT"

 

Organization: O.I.E

 

To: "Terry S. Singeltary Sr."

 

References: <3d2f0169 .3="" wt.net=""> < 012901c229b2 ad43bb90="" f00000a=""> 3D2F2358.5010700@wt.net

 

I agree with you Dr Terry. The OIE, namely the International Animal Health Code Commission is working on making proposals to Member Countries to change the OIE lists so to avoid some the problems mentioned in you e-mail. This will take at least two years before adoption by the International Committee. For BSE, countries asked the OIE to post information on BSE on the OIE web site.

 

Personally, I am interested in Chronic Wasting Disease and I follow what is distributed through ProMed. Delegates of OIE Member Countries can propose diseases to be added to the list.

 

Kind regards.

 

Karim Ben Jebara

 


 

----- Original Message -----

 

From: "Terry S. Singeltary Sr."

 

To: "INFORMATION DEPT"

 

Sent: Friday, July 12, 2002 8:43 PM

 

Subject: Re: CWD AMERICA ???

 

>>> *** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids. <<<

 

> hello Dr. Jebara,

 

>

 

> many thanks for your swift and kind reply.

 

>

 

> if i am not mistaken, it was the same email address.

 

> it was 3 or 4 weeks ago i wrote, as it is, i don't

 

> save 'sent' emails anymore, unless very important.

 

>

 

> my main concern (besides the fact that a potential TSE

 

> has been in the USA cattle for some time, but the APHIS

 

> do not test to find), is that the CWD could very well be

 

> transmitting to humans, and i just did not see to much

 

> posted about it on OIE site.

 

>

 

> > Coming back to your question, Chronic Wasting Disease is not an OIE

 

>

 

> > listed disease. Please see OIE disease lists at

 

>

 


 

>

 

> why is this TSE (CWD) not listed and followed as with BSE ?

 

>

 

> Article 1.1.3.2.

 

> 1. Countries shall make available to other countries, through the

 

> OIE, whatever information is necessary to minimise the spread of

 

> important animal diseases and to assist in achieving better worldwide

 

> control of these diseases.

 

>

 


 

>

 

> The USA CWD is an important animal disease.

 

>

 

> why is it not followed?

 

>

 

> > The decision to add or delete a disease from the OIE lists, come

 

>

 

> > through proposals made by Member Countries and it has to be adopted by

 

>

 

> > the International Committee.

 

>

 

> i _urgently_ suggest a proposal to the OIE to follow this disease very

 

> closely, and to propose _more_ testing in the USA for TSEs in the USA

 

> cattle...

 

>

 

> kindest regards,

 

> terry

 

>

 

> INFORMATION DEPT wrote:

 

>

 

> > Dear Sir,

 

> >

 

> > This is the first time that I receive your e-mail. To whom have you written

 

> > in the OIE or to which address?

 

> >

 

> > Coming back to your question, Chronic Wasting Disease is not an OIE listed

 

> > disease. Please see OIE disease lists at

 


 

> >

 

> > Countries should report to the OIE any disease even is not listed in the

 

> > OIE's lists in some conditions (example: an exceptional epidemiological

 

> > event). Please read Chapter 1.1.3 of the International animal health code to

 

> > have more information on disease notification and epidemiological

 

> > information agreed by OIE Member Countries at :

 


 

> >

 

> > The decision to add or delete a disease from the OIE lists, come through

 

> > proposals made by Member Countries and it has to be adopted by the

 

> > International Committee.

 

> >

 

> > Hope that I answered to your question.

 

> >

 

> > Best regards.

 

> >

 

> > Dr Karim Ben Jebara

 

> > Head

 

> > Animal Health Information Department

 

> > OIE

 

> >

 

> >

 

> >

 

> > ----- Original Message -----

 

> > From: "Terry S. Singeltary Sr."

 

> > To:

 

> > Sent: Friday, July 12, 2002 6:18 PM

 

> > Subject: CWD AMERICA ???

 

> >

 

> >

 

> >

 

> >>I WROTE TO OIE RECENTLY ASKING 'WHY OIE DOES NOT FOLLOW CWD IN

 

> >>AMERICA' ? with no reply ? i am still seeking an answer ?

 

> >>

 

> >>many thanks,

 

> >>and kind regards,

 

> >>terry

 

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

 


 

 

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 ***

 


 

 

STILL WAITING...TSS

 

 

Sunday, December 28, 2014

 

*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE USDA USAHA INC DECEMBER 28, 2014

 


 

 

SEE FEED ;

 

 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 

snip...

 

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

 

Animals considered at high risk for CWD include:

 

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

snip...

 

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

 

snip...

 

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

 

snip...

 

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

 

snip...

 

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

 

snip...

 

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

 

snip...

 


 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

 


 

 

 

Wednesday, December 4, 2013

 

Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December 4, 2013

 

TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on paper $$$

 

full text ;

 


 

Comment from Terry Singeltary Sr.


Comment

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ;

I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here?

North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC.

typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$

the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper.

for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before.

lets start with the recent notice that beef from Ireland will be coming to America.

Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying.

Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom)

Country/Year

snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS

Attachments

 (1)

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

View Attachment:


 

 

 

Sunday, January 11, 2015

 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 


 


 

 

Terry S. Singeltary Sr.

Bacliff, Texas 77518

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