Wednesday, September 23, 2009

Scientific Opinion on BSE Risk in Bovine Intestines Question number: EFSA-Q-2009-00226

Scientific Opinion on BSE Risk in Bovine Intestines Question number: EFSA-Q-2009-00226

Adopted: 10 September 2009 Summary (0.1Mb)

Opinion (0.1Mb)


Following a request from the European Commission (EC), the Panel on Biological Hazards (BIOHAZ) was asked to deliver a scientific opinion on the BSE related risk of bovine intestines used for casings. Regulation (EC) No 999/2001 of the European Parliament and of the Council stipulates that certain tissues from bovine, ovine and caprine animals must be considered as Specified Risk Material (SRM) and must be removed from the food and feed chain to protect the health of consumers against the risk of bovine transmissible spongiform encephalopathies (BSE). The intestines, from the duodenum to the rectum, of bovine animals of all ages are currently included in the list of SRM. The “TSE roadmap” prepared by the EC details the short, middle and long term actions on TSE measures such as SRM removal and sets the objectives to ensure and maintain the existing high level of consumer protection. It allows for amendments of the current SRM list based on new evolving scientific knowledge while ensuring and maintaining a high level of consumer protection.

Specifically, the mandate asked the BIOHAZ panel to evaluate the scientific validity of a report prepared by Det Norske Veritas Ltd" (DNV) for the Swiss Cervelas task force. This report provides an assessment of the current potential human exposure to BSE infectivity that could result from eating sausages made with EU bovine casings. The BIOHAZ panel was further requested to evaluate the conclusions of the DNV report and, if it was considered necessary based on the report and any other new relevant scientific information, to provide a re-assessment of the BSE related risk of bovine intestines after processing into natural sausage casings.

The BIOHAZ panel evaluated the risk assessment as described in the DNV report, and took into account the relevant previous EFSA opinions as well as new scientific data on the same subject.

New but limited experimental scientific data demonstrate that in addition to ileum, also jejunum may harbour infectivity when a large BSE inoculum dose was used to experimentally infect cattle. With regard to the DNV Report, the BIOHAZ Panel considers its approach (concept and methodology) scientifically sound, whereas the interpretation of the results as obtained is not shared by the Panel. Its assumptions were based on limited scientific data obtained from a single morphometric study (which was already found to be inadequate in the previous EFSA Opinion on bovine casings) and on limited and earlier data on the presence of PrPsc/infectivity in bovine gut after experimental oral BSE inoculation. There is uncertainty about the relative BSE risk of neural and lymphoid tissues in casings compared to CNS that might have significant impact on the calculated results of the DNV Report. The Panel notes that the DNV Report considers the individual human BSE exposure risk from bovine casings, excluding ileum, to be “very low”. However, when the upper confidence limits are taken into account, along with the uncertainties in key parameter assumptions, the calculated total human exposure per year in the EU from bovine casings, even when ileum is excluded (based on the calculated BSE prevalence in 2007) is 11.000 cattle oral ID50 units per year (when all casings would have been sourced in the UK) and about 1.000 cattle oral ID50 units per year (when all casings would have been sourced in the Netherlands) and therefore cannot be considered negligible. Thus the conclusion in the DNV report that sausage casings sourced from intestines of cattle in EU Member States would lead to a negligible risk for human consumption cannot be considered valid. Moreover, when considering other new relevant scientific information it is concluded that the previous EFSA assessment of the BSE related risk of bovine intestines after processing into natural sausage casings remains valid. The Panel recommends that future considerations on the risk in bovine casings should take into account the BSE prevalence in cattle at that time.

Published: 22 September 2009




6. Overview of current scientific knowledge on BSE risk in Bovine Intestines. The previous EFSA Opinion on BSE risk from bovine intestine summarised the scientific knowledge that was available until early 2007. Since then, additional publications have become available on a natural BSE case in Japan (Kimura and Haritani, 2008) and two experimental studies that examined

presence of PrPsc and/or infectivity in the intestines of cattle challenged orally with 100g (Espinosa et al., 2007; Hoffmann et al., 2007). Moreover, a new study performed by the VLA in the UK on PrPsc in BSE-infected cattle (Stack, 2009) and preliminary results from the German BSE pathogenesis study have recently be made available to EFSA and were also taken into account.

6.1. New experimental studies on intestines of BSE infected cattle

Espinosa et al. (2007) examined pooled tissues from 13 cattle inoculated at ages between 4 and 6 months and culled at ages between 24 and 39 months. Infectivity in Tgbov mice but not PrPsc by ELISA/WB was found in Peyer’s patches dissected from distal ileum at all ages. Hoffmann et al (2007) demonstrated PrPsc by IHC in Peyer’s patches of distal ileum in one of two preclinical animals sacrificed at 24 and 28 months post inoculation (mpi). Most recently, Arnold et al. (2009) estimated the titre of infectivity in the distal ileum from the incubation time found by bioassay in wild type mice. Over time, the infectivity in the distal ileum showed an initial increase up to 14-18 months post exposure, followed by a decrease, which was likely to be highly variable between animals. However, these estimates were based on mouse titration of brain material, while the incubation period to dose relationship may differ between brain and intestines (Robinson et al., 1990).

6.2. Infectivity of intestines in cattle with natural BSE infection

Data on presence of PrPsc or infectivity in intestines of natural BSE cases are sparse. The immunohistochemistry (IHC) and Western blot examinations of three BSE infected cattle detected in Japan in the course of active surveillance (but showing locomotor deficits) found PrPsc in distal ileum of two (by IHC confined to the myenteric plexus) (Iwata et al., 2006). No PrPsc was detected in Peyer’s patches of distal ileum, or in samples of other regions of small and large intestine, or in a range of other lymphoid tissues. Labelling of myenteric plexus was also detected in 9/29 confirmed field cases of BSE examined in the UK (Terry et al., 2003). Infectivity by wild-type mouse assay or the presence of PrPsc has not been found in the distal ileum, or other levels of intestine in a total of some six natural BSE cases studied (Fraser and Foster, 1994; Buschmann and Groschup 2005; Iwata et al., 2006). In one of these cases in Germany, however, infectivity was detected in the distal ileum by bioassay in TgBov XV mice (Buschmann and Groschup, 2005). More recently, another BSE case (94 months of age) in Japan showed definite or equivocal immunoreactivity in nerve cells of the myenteric plexus in ileum, caecum and colon, and in Schwann cells of the myenteric plexus in duodenum, jejunum, ileum, caecum and colon (Kimura and Haritani, 2008).

6.3. Study commissioned by ENSCA

This ENSCA commissioned study investigated the presence of BSE PrPsc in small intestines of cattle that had been orally challenged at 4-6 months of age with 100g or 1 g doses of BSE affected brain tissue. These animals were culled and examined 18-30 months post inoculation (p.i.). Three methods to identify PrPsc were applied: a commercial ELISA test, Western immunoblotting, and IHC. Results confirmed previous observations that PrPsc was mainly confined to lymphoid tissue of the ileum, whereas the duodenum was negative and no part of the enteric nervous system tested positive. The lymphoid tissue of the jejunum of one high-dosed animal tested positive. As expected, the low-dosed animals had a much lower frequency of positive ileum samples (1/18 vs. 15/18 in the high-dose group) and some longer incubation times (24 months in the one animal with positive ileum), whereas the high-dose group included animals positive at all ages examined.

As the ENSCA commissioned study was performed retrospectively on archival tissue, sampling was limited by availability, and the study authors themselves concede that “it is possible tissue sampling was not optimal” for duodenum and jejunum of low-dosed animals. The 1g-dosed group included 6 animals sampled at 18 months p.i., 6 at 24 months, and 6 at 30 months. The 100g-dosed group included 6 animals sampled for ileum at 18 months p.i., 6 at 24 months, and 6 at 30 months;

duodenum and jejunum, however, were sampled only in 2 animals each at 18, 24 and 30 months p.i., respectively. From each level of the intestine, three sections were examined by IHC per case. While at least two of the three sections of the ileum per case contained lymphoid follicles, in 36% of the duodenum cases, and in 39% of the jejunum cases lymphoid follicles were absent in any of the examined sections. The frequency of positive follicles per section ranged between 1% and 14% in ileum of the high-dose group, and 0,7% in the one positive ileum of the low-dose group, and was 6,7% and 11,1% in the two positive jejunum sections of one high-dosed animal.

Conclusions on the ENSCA commissioned study:

• This study confirms that detectable PrPsc is mainly confined to lymphoid tissue of the ileum in cattle orally challenged with 100g of BSE brain and culled at 18, 24 and 30 months postinoculation (p.i.)

• One out of 18 animals challenged orally with 1g of BSE brain was positive in ileum.

• One out of 18 animals challenged orally with 100g of BSE brain was positive in jejunum.

• The duodenum was always negative.

• However, the sampling in particular of duodenum and jejunum was limited and contained lymphoid tissue only in a part of sections examined.

• In contrast to previous reports on natural BSE cases in older animals, the enteric nervous system was always negative.

• In consideration of the previous EFSA opinion on bovine intestine that gives detailed advice for future studies, in particular concerning the lower frequency of lymphoid follicles in parts of the intestine other than the distal ileum, the present ENSCA commissioned study meets some but not all recommendations; in particular the mostly negative results obtained for jejunum and duodenum should not be over-interpreted when tissue sampling was limited.

6.4. New preliminary data on bovine intestine from the German BSE Pathogenesis study

In the German BSE pathogenesis study performed at the Friedrich-Loeffler-Institute (FLI), 56 Simmental cross-breed calves aged about four months were challenged orally with 100g brainstemhomogenate pooled out of clinically BSE diseased cattle. The infectivity load in the homogenate was about 106.1 ID50 (grams of tissue)-1 as determined by end-point titration in Tgbov XV mice (Buschmann & Groschup, 2005, Hoffmann et al., 2007). Furthermore, as controls, 18 calves were inoculated orally with a BSE-negative brainstem homogenate. Four to five animals were selected randomly and euthanised every four months. More than 150 tissue and body fluid samples were sampled at subsequent necropsies from each animal under TSE-sterile conditions.

After oral exposure with the TSE agent, previous studies had demonstrated consistently early prion accumulation in the gut associated lymphatic tissue, about six months post infection (mpi) in cattle (Terry et al., 2003), and at two mpi in scrapie infected sheep (van Keulen et al., 2002) and in 21 days old lambs (Andreoletti et al., 2002). In contrast to scrapie, the accumulation of PrPd in the distal ileum of BSE-infected cattle was confined to an only minor proportion of follicles respectively neurons/glial cells of the enteric nervous system (Terry et al., 2003).

Normally when performing IHC, a three micrometer section per paraffin block is used, reflecting a very small proportion of the tissue sample. Therefore a serial section procedure was newly established at the FLI to increase the total amounts of tissue structures examined per sample and consequently increasing the probability of detecting PrPsc accumulation. Thereby, five sections per paraffin block with a plane distance of about 25-30 µm were examined. Hence, a tissue depth of about 150-200 µm per block was screened for positive immunosignals. Additionally two different PrP-specific monoclonal antibodies, highly sensitive for the detection of bovine PrPsc were used.

According to this method, representative samples of the small intestine, in particular Peyer’s patches of the distal ileum but also the ileo-caecal junction from most of the infected animals of the German BSE Pathogenesis study were examined by IHC. From 4 mpi until 44 mpi in most animals (38/43), PrPsc was detectable, initially in the follicles of the Peyer’s patches and at later stages of the incubation period in the enteric nervous system too.

Conclusions on the German pathogenesis study

• With improved sampling, nearly all animals dosed with 100 g of BSE brain tissue showed PrPsc in distal ileum between 4 and 44 mpi, first in lymphoid tissue and later in enteric nervous system.

7. Review of the DNV report

7.1. Summary of the report

DNV makes an attempt to quantify the amount of BSE infectious load in bovine sausage casings. This is then extrapolated to the risk carried in an individual sausage, a normal persons risk per year and the overall exposure within the EU in a year. The key points of the DNV Report are as follows:

• The DNV Report assumes that the ileum is not used for the production of casings and is removed and discarded.

• The DNV Report is based on the assumption that potential infectivity in bovine intestine used for sausage casing production would be 2 logs less than in the ileum. Based on experimental data, the infectivity in the distal ileum was considered to be at a titre equivalent to that in the CNS at the late stage of infection. Thus infectivity in non-ileal parts of the intestines used for casings production was assumed to be 100 fold less than in the CNS.

• The DNV Report uses a value of 0.43g/m (obtained from Wijnker et al.) of casing to quantify the amount of lymphoid and neural tissue that might harbour infectivity in a sausage casing,

• The results of the DNV Report calculate that an exposure per person per year from bovine casings produced in the Netherlands “would be very low” even when a high consumption pattern like in Germany is assumed (upper range 7 x 10-6 cattle oral (CO) ID50 units). For casings sourced in the UK, the exposure would be about one log higher.

• When the calculated total amount of cumulative human exposure per year in the EU is considered, the following scenario emerges: 11.000 CO ID50 units per year when all casings would have been sourced in the UK, and about 1.000 CO ID50 units when all casings would have been sourced in the Netherlands, a country with an about average prevalence of BSE in the EU4.

4 How can the output of the DNV calculations be interpreted in terms of potential human infections? If we follow, as in the previously adopted EFSA Opinions on Tallow and MBM (EFSA 2005 a and b) the cautionary advice of the original QRA WG and assume the species barrier is 1 as a worst case scenario, then there would be up to 5500 infected person in the EU per year in the first scenario, and up to about 500 in the second. This would have to assume a linear dose-response curve of infectivity at very low doses. If the species barrier was given a more realistic value obtained from the analysis carried out on the exposure of the British population to the BSE agent (EFSA, 2006) of around 1000 - 4000, this would mean that there might be up to around 1 to 5 infected person in the EU per year in the first scenario, and less than 1 in the second.

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----- Original Message -----
From: Terry S. Singeltary Sr.
Sent: Wednesday, September 07, 2005 9:44 PM
Subject: Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47

Greetings FDA,

I would kindly like to comment on ; Use of Materials Derived From Cattle in Human Food and Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47 SUMMARY: The Food and Drug Administration (FDA) is amending the interim final rule on use of materials derived from cattle in human food and cosmetics published in the Federal Register of July 14, 2004. In the July 14, 2004, interim final rule, FDA designated certain materials from cattle, including the entire small intestine, as ``prohibited cattle materials'' and banned the use of such materials in human food, including dietary supplements, and in cosmetics. FDA is taking this action in response to comments received on the interim final rule. Information was provided in comments that persuaded the agency that the distal ileum, one of three portions of the small intestine, could be consistently and effectively removed from the small intestine, such that the remainder of the small intestine, formerly a prohibited cattle material, could be used for human food or cosmetics. We (FDA) are also clarifying that milk and milk products, hide and hide-derived products, and tallow derivatives are not prohibited cattle materials. Comments also led the agency to reconsider the method cited in the interim final rule for determining insoluble impurities in tallow and to cite instead a method that is less costly to use and requires less specialized equipment. FDA issued the interim final rule to minimize human exposure to materials that scientific studies have demonstrated are highly likely to contain the bovine spongiform encephalopathy (BSE) agent in cattle infected with the disease. FDA believes that the amended provisions of the interim final rule provide the same level of protection from human exposure to the agent that causes BSE as the original provisions. ...

I would kindly like to submit the following ;

I find it very very disturbing that FDA now takes the position;

>>>Information was provided in comments that persuaded the agency that the distal ileum, one of three portions of the small intestine, could be consistently and effectively removed from the small intestine, such that the remainder of the small intestine, formerly a prohibited cattle material, could be used for human food or cosmetics. <<< href="">


The tissue distribution of infectivity in BSE infected cattle has primarily been determinedby 3 studies conducted in the United Kingdom all of which had limitations.In two of the studies, bioassays were done in mice which are at least 1000 fold lesssensitive to BSE infection than cattle themselves. Only higher titers of infectivity can bedetected by this method. These investigations found infectivity in the brain, spinal cord,retina, trigeminal ganglia, dorsal root ganglia, distal ileum and bone marrow (the bonemarrow finding was from one animal). Infectivity was found in distal ileum ofexperimentally infected calves beginning six months after challenge and continuing atother intervals throughout life. (Wells et. al., 1994; 1998). The bioassay study in calveshas produced similar results and in addition infectivity has been found in tonsil. Thestudy is still in progress. Another project has found infectivity in the lymphoid tissue ofthird eyelid from naturally infected animals. (Dr. Danny Matthews, UK DEFRA,personal communication).While bioassay in cattle is far preferable to mice in terms of sensitivity, cattlenevertheless present their own limitations in terms of the long incubation time and thelimited number of animals that can be used for assay compared to rodents. As aconsequence the significance of the negative finding for many tissues is questionable. Infact, by the end of 2004 there was increasing evidence in species other than cattle thatperipheral nerves and muscle have infectivity. (Bosque et al., 2002; Glatzel et al.,2003;Bartz et al., 2002; Androletti et al., 2004; Mulcahy et al., 2004; Thomzig et al.,2003; Thomzig et al., 2004)In some of these species, studies indicate that the agent migrates to the brain and spinalcord, replicates to high levels in the CNS and then spreads centrifugally from the spinalcord back down through the spinal neurons to the junction of the nerves and muscle intothe muscle cells themselves. A recent German study (Buschmann and Groschup, 2005)examined nerves and muscle from a cow naturally infected with BSE and found thatinfectivity was present in several peripheral nerves and one muscle. The method ofdetection was bioassay in bovinized transgenic mice that show the same or greatersensitivity to transmission of BSE as cattle. This research concurs with findings byJapanese scientists that BSE infectivity is present in peripheral nerves at least in theclinical stage of disease.It is our opinion that there is increasing evidence that the pathogenesis of BSE might notbe entirely different from TSEs in other species at the point of clinical disease in thatthere is peripheral involvement. We feel that the studies as reported above have merit.The current studies not only re-enforce the risk of down and deadstock but also appear toprovide additional information that these animals may be a potential source of greaterlevels of infectivity into the feed system.In the event that FDA may confer with USDA about the risks associated with peripheralnerves we want to point out one issue. In the recent publication of the final rule on theDeleted: SRMs, as defined by theUSDA, are tissues which, in a BSEinfected animal, are known to eitherharbor BSE infectivity or to be closelyDeleted: Rendered with other slaughterInserted: pose a risk of BSEDeleted: may introduce BSE infectivityDeleted: aDeleted: source ofDeleted: animal feedDeleted: perfectly balanced animalInserted: perfectly balanced animalDeleted: contaminationDeleted: they were a major source ofDeleted: .Deleted: SRMs include tissues that areDeleted: does not totally eliminate it.Inserted: doesDeleted: This is significantDeleted: This residual infectivity stillInserted: SRMs include tissues that areInserted: , which are bones, areDeleted: which encaseDeleted: the brain and spinal cordDeleted:Inserted: tissue that they encase andDeleted: , respectively, can be assumedDeleted: RenderingDeleted: Conventional renderingDeleted: willDeleted: reduces infectivity fromDeleted: willInserted: Rendered with otherInserted: they were a major source ofInserted: Conventional renderingInserted: sInserted: from contaminated tissuesInserted: This residual infectivity stillDeleted: (four to six years for high titerDeleted:Deleted: alreadyDeleted: Kovacs et al., 2004;Deleted: pDeleted: 14... [25]... [19]... [26]... [24]... [29]... [31]... [33]... [23]... [30]... [32]... [21]... [34]... [22]... [35]... [17]... [27]... [18]... [20]... [28]FDA Proposed Rule December 20, 2005importation of whole cuts of boneless beef from Japan, 9 CFR Part 94 [Docket No. 05-004-2] RIN 0579-AB93, we disagree with the interpretation provided by USDA, APHIS.APHIS seems to discount the studies conducted by Groschup et al. 2005. on the basis thatthe transgenic mouse bioassay that they used may be too sensitive. In taking this positionthey have failed to realize that the point of an assay is to reveal in which tissues theinfectivity resides and its relative concentration to brain or spinal cord. For this purpose,no assay can be too sensitive. Of course, the probability of an actual infection will beaffected by the efficiency of infection which will be a function of dose, route of exposureand any host barrier effects that are present.We would also like to point out a factual error in the conclusion. APHIS states, “Giventhese factors, APHIS has determined that the finding of BSE infectivity in facial and sciatic nervesof the transgenic mice is not directly applicable to cattle naturally infected with BSE. Therefore,we do not consider it necessary to make any adjustments to the risk analysis for this rulemakingor to extend the comment period to solicit additional public comment on this issue.” It is incorrectthat the infectivity was found in the peripheral nerves of transgenic mice. The peripheralnerves were harvested from a cow naturally infected with BSE. Transgenic mice wereused as a bioassay model.From [Docket No. 05-004-2] RIN 0579-AB93:“Peripheral NervesIssue: Two commenters stated that the underlying assumption of the proposed rule, that wholecuts of boneless beef from Japan will not contain tissues that may carry the BSE agent, is nolonger valid because researchers have found peripheral nervous system tissues, including facialand sciatic nerves, that contain BSE infectivity.\2\ One of these commenters requested APHIS toexplain whether and what additional mitigation measures are needed to reduce the risks thatthese tissues may be present in Japanese beef. This commenter further requested an additionalcomment period to obtain public comments to treat this new scientific finding.


Greetings again APHIS ET AL,

THIS is not correct. IN fact, there are several factors i would like to kindly address.

Muscle tissue has recently been detected with PrPSc in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve) of the 11th BSE cow in Japan (Yoshifumi Iwamaru et al). also recently, Aguzzi et al Letter to the Editor Vet Pathol 42:107-108 (2005), Prusiner et al CDI test is another example of detection of the TSE agent in muscle in sCJD, Herbert Budka et al CJD and inclusion body myositis: Abundant Disease-Associated Prion Protein in Muscle, and older studies from Watson Meldrum et al Scrapie agent in muscle - Pattison I A (1990), references as follow ;

PrPSc distribution of a natural case of bovine spongiform encephalopathy

Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000423/!


Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes progressive neurodegeneration of the central nervous system. Infectivity of BSE agent is accompanied with an abnormal isoform of prion protein (PrPSc).

The specified risk materials (SRM) are tissues potentially carrying BSE infectivity. The following tissues are designated as SRM in Japan: the skull including the brain and eyes but excluding the glossa and the masse- ter muscle, the vertebral column excluding the vertebrae of the tail, spinal cord, distal illeum. For a risk management step, the use of SRM in both animal feed or human food has been prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle and it has caused con- troversies about definitions of SRM. Therefore we have examined PrPSc distribution in a BSE cattle by Western blotting to reassess definitions of SRM.

The 11th BSE case in Japan was detected in fallen stock surveillance. The carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of tissue samples were homogenized. Following collagenase treatment, samples were digested with proteinase K. After digestion, PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets were subjected to Western blotting using the standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish peroxidase was used for the detection of PrPSc.

PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve). Our results suggest that the currently accepted definitions of SRM in BSE cattle may need to be reexamined. ...

179 T. Kitamoto (Ed.) PRIONS Food and Drug Safety


ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004;

Bovine spongiform encephalopathy (BSE) in Japan


"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion"

NO. Date conf. Farm Birth place and Date Age at diagnosis

8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23

9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21

Test results

# 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative

b = atypical BSE case

c = case of BSE in a young animal

b,c, No PrPSc on IHC, and no spongiform change on histology

International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004.

The hardback book title is 'PRIONS' Food and Drug Safety

T. Kitamoto (Ed.) Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000423/! Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000423/!


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Response to Public Commentson theHarvard Risk Assessment of Bovine SpongiformEncephalopathy Update,October 31, 2005



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) theaddition of explicit modeling of the poultry litter pathway for the potential recycling ofbovine protein into cattle feed; and

2) a decrease in the assumed effectiveness of antemortem 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.

Comment #3: WHY still now only partial ruminant feed ban, with the fact that now we seem to have 3 cases of nvCJD to humans i.e. human bovine TSE that were responsible from blood, and the fact the last 2 mad cows documented in the USA were that of an Atypical strain, would it not seem prudent to remove blood as well from ruminant feed?WOULD it not seem prudent to improve and expand the SRM list now? as per your ownthinking; If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.

Response: This comment pertains to policy. As such, it is not addressed here.

Comment #4: WHAT does USDA/FDA ET AL intend to do about the risks of atypical BSE/TSE in cattle now that infectivity shows in tissue samples other than CNS in Japan, the fact now that the last Texas mad cow and that last mad cow in Alabama were indeed of the atypical strain, the fact that the studies long ago in Mission, Texas of USA sheep scrapie transmission to the USA bovine, which proved an 'atypical tse' in the USA bovine, the fact also that USDA/FDA are still floundering on the last SRM regulations, but with the BASE strain now in cattle that is not similar to nvCJD, but very similar to the sporadic CJD, and sporadic CJD has tripled in the last few years in the USA. WHAT do you plan to do to protect human health from these atypical strains of TSE, in relations to SRMs ?

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Response: The BSE risk assessment simulation model characterizes the disease history of BSE, including the agent’s spread within the body of the animal over time. It also quantifies the agent’s persistence during the feed manufacture process, and ultimately the agent’s ability to cause disease in other exposed animals. There is no definitive evidence that these properties differ substantially for atypical BSE strains, compared to the typical BSE agent.

Comment #5: THE 2004 Enhanced BSE surveillance program, that tested all those cows, but then we found just how terribly flawed the program was, from testing protocols, to testing the most likely to have BSE i.e. high risk, to the geographical distribution of the testing and high risk areas, to letting the tissue samples of one mad cow sit on a shelf for 7+ months and then having to have an act of Congress to ever get that cow finally confirmed, to that other Texas mad cow they decided to not even bother testing at all, just rendered that very suspect cow, too suspect to test evidently, back to that Alabama madcow that they could only give a guess as to age with dentition where we all know that the age of that cow was so close to 10 years it could have been 9 years 7 months to 10 years 3 months, thus possibly being an BAPB i.e. USA 'born after partial ban', to all those rabies suspect cows that did not have rabies, and DID NOT get tested for BSE/TSE in that June 2004 enhanced surveillance program, even though the common lay person knows the suspect rabies negative cows are suppose to be BSE/TSE tested, how does one correct all these blatant failures and will they be corrected?

Response: This comment pertains to policy. As such, it is not addressed here.

Comment #6: WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported sheep from Belgium that were confiscated and slaughtered from the Faillace's, what sort of TSE did these animals have?

Response: It is not clear how the test results referred to in this comment are relevant to the Harvard BSE Risk Assessment Update. Sheep were not considered in the risk assessment.

Comment #7: WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these farms from Texas and Alabama with Atypical TSE in the Bovine, they have not been quarantined for 5 years, why not, with the real risk of BSE to sheep, whom is to say this was not BSE ?

Response: This comment pertains to policy. As such, it is not addressed here.

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October 31, 2002
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States
Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University

September 13,2004 USDA, FSTS Docket Clerk 300 12* Street, SW Room 102, Cotton Annex Washington, DC 20250 04-021ANPR 04-021ANPR-70 Richard L. Crawford

Re: Docket No: 04-02 1 ANPR Federal Measures to Mitigate BSE Risks: Considerations for Further Action

Dear Sir or Madame:

On behalf of McDonald’s Corporation, which operates more than 13,000 restaurants in the United States, we appreciate the opportunity to submit comments to this very important Advance Notice of Proposed Rulemaking (ANPRM). 69 Fed. Reg. 42288 (July 14,2004).

In previous comments submitted to FSIS regarding the removal of SRI&, McDonalds fully supported this rule and its immediate implementation. The removal of SRMs from human food is the primary firewall to protect the US consumer from being exposed to the BSE agent. While we applaud the requirement for SRM removal, we feel that it is equally important for FSIS to insure that each slaughterplant which processes cattle have systems in place which prevent cross contamination between edible tissue and SRMs. This should include but not be limited to the use of separate equipment, such as knives, blades, etc. where appropriate. In addition, it is also important that appropriate and effective disinfection procedures for equipment used to handle SRMs be developed and approved for use.

It is our opinion that requiring SRM removal without a procedure to prevent cross contamination is inadequate as a protective public health measure. The TSE agents @ions) are sticky and highly resistant to disinfection. If SRMs such as brain and spinal cord are allowed to contact equipment and other surfaces such as deboning tables which then are used to handle and process edible tissue this could allow contamination and negates the intention of the ban. This is true not only in plants slaughtering fed cattle both under and over 30 months but also in plants slaughtering predominately older cattle. It is important that measure be taken to prevent cross contamination between carcasses and SRms in the cull plants. McDonalds requires their suppliers to prevent cross contamination and audits against certain measurable standards such as requiring spinal cord to bc removed on the kill floor. We would be willing to share these standards with FSIS as an example.

FSIS Docket No. 04-02 1 ANPR

McDonalds again recommends that dura (the covering around the brain and spinal cord) be added to the list of SRMs. While skull and vertebral column are included as SRMs, dura is not. If dura is not removed prior to processing on the fabrication floor, it may come loose and be incorporated into ground product. Bovine dura was never tested for infectivity. It was assumed that due to direct contact with spinal cord, it may serve as a vehicle to transmit disease. In addition, human dura has been the source of human to human transmission of Creutzfeldt-Jakob Disease (CJD). (personal communication - Dr. Danny Matthews, UK, VLA) Our ISAC committee recommended that McDonalds add the removal of dura as a specification in the production of our product.

McDonalds urges the USDA to make the appropriate adjustments in the SRM ban if new scientific findings and/or the results of the increased surveillance warrant a change. In regards to imported meat products from other countries, McDonalds suggests that no SRM exemption be made for countries based on BSE risk. The long incubation period and limited surveillance in many countries can limit the ability to accurately determine risk. Also, the risk level of a country could potentially change over night if the trading patterns of a country changed. It seems logistically impossible to maintain a system which could continually monitor the world’s trading patterns. In addition, science has not provided all of the answers in regards to the transmission of BSE. Requiring SRMs to be removed from imported products for human food is prudent. If the US would wait until disease is confirmed the exposure would already have occurred.

Thank you for the opportunity to comment on these very important issues.

Richard L. Crawford Corporat,e Vice President, Government Relations McDonalds Corporation 1 Kroc Drive Oak Brook, Illinois 60523 FSIS Docket No. 04-021ANPR

Dockets Entered on December 22, 20052005D-0330, Guidance for Industry and FDA Review Staff on Collection of Plateletsby Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ...

03-025IF 03-025IF-631 Linda A. Detwiler [PDF]Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4.Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12.

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03-025IF 03-025IF-634 Linda A. Detwiler [PDF]Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2.Page 3. Page 4. Page 5. Page 6. Page 7. Page 8.

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Page 1 of 17 9/13/2005 [PDF]... 2005 6:17 PM To: Subject: [Docket No. 03-025IFA]FSIS Prohibition of the Use of Specified Risk Materials for Human Food ...

- Text Version 03-025IFA 03-025IFA-6 Jason Frost [PDF]... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al [Docket No. 03-025IF] Prohibition of the Use of Specified Risk Materials for Human Food and ...

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In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF]Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone: 732-741-2290Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ...

Page 1 of 17 9/13/2005 [PDF]
... Page 1 of 17 From: Terry S. Singeltary Sr. [] Sent: Thursday,September 08, 2005 6:17 PM To: Subject ...

03-025IF 03-025IF-618 Richard L. Crawford [PDF]Page 1. 03-025IF 03-025IF-618 Richard L. CrawfordPage 2. Page 3. Page 4.

03-038IF 03-038IF-15 Richard L. Crawford [PDF]Page 1. 03-038IF 03-038IF-15 Richard L. CrawfordPage 2. Page 3. Page 4.



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