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Consumption of beef tongue: Human BSE risk UPDATE

flounder

Well-known member
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings -
Scientific Opinion of the Panel on Biological Hazards

Question number: EFSA-Q-2007-110

Adopted date: 17/04/2008

Summary

http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej700_bovine_tongue_summary_en.pdf

Opinion

http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej700_bovine_tongue_en.pdf

Summary

Following a request from the European Commission, the Panel on Biological
Hazards (BIOHAZ) was asked to deliver a scientific opinion on the human BSE
risk associated with exposure to lymphoid tissue in bovine tongue in
consideration of the findings included in a scientific article recently
published on the consumption of beef tongue and the risk for public health.

This scientific article describes the distribution of lymphoid tissue in
bovine tongue and the location of bovine lingual tonsil. In addition, it
concludes that the method currently prescribed for harvesting bovine tongues
in slaughterhouses is not appropriate for removing all specified risk
material (SRM) and proposes an alternative harvesting method.

EFSA was requested (i) to evaluate the design of the study and its
scientific validity in relation to the distribution of lymphoid tissue in
bovine tongue and (ii) to evaluate the conclusions and recommendations of
the study in relation to BSE risk from bovine tonsil following the
harvesting method currently prescribed by EU legislation compared to the
alternative one proposed in the study.

The BIOHAZ Panel reviewed the scientific article and concluded that the
study further confirms and extends observations that the lingual tonsil at
the base of the tongue may not be entirely eliminated when harvesting
tongues by means of the method currently prescribed.

In reply to the second request, the BIOHAZ Panel assessed different
parameters in order to quantify the human exposure risk to BSE from bovine
tonsil associated with the consumption of bovine tongue. It was concluded
that, overall, the level of infectivity in bovine tonsil is low. This,
together with the declining and overall low BSE prevalence and the current
policy on SRM removal, suggests a very low, if not negligible, human BSE
exposure risk associated with exposure to lymphoid tissue in bovine tongue
harvested as currently prescribed by EU legislation. The BIOHAZ Panel
further concluded that currently there are not sufficient quantitative data
available allowing a comparison of the human BSE exposure risk reduction
achieved by the alternative tongue harvesting method proposed by the study
in comparison to the harvesting method currently prescribed. However, it is
likely that the proposed method would only provide a marginal reduction in
the risk from bovine tonsil compared to the one currently prescribed.

Following to this, the BIOHAZ Panel made a series of recommendations on the
topics that might be addressed in future studies on the subject.

http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178704312961.htm

Annex 1

http://www.efsa.europa.eu/EFSA/Scientific_Opinion/annex_1_bovine_tongue_translation.pdf

3.1.2. Experimental BSE cases after oral challenge. • In a sequential kill
pathogenesis study of BSE in which calves were experimentally infected by
oral exposure to 100g of a pool of BSE affected brainstems (a dose
considered far in excess of most natural exposures (Arnold et al., 2007)),
palatine tonsil was assayed in conventional mouse strains from all time
points (2-40 months post-exposure). No infectivity was detected (Wells et
al., 1998; Wells et al., 2005). • Palatine tonsil from this sequential kill
pathogenesis study was further assayed by intracerebral inoculation of
cattle, which provides a 500 fold (log10 2.7) greater sensitivity of
detection of the BSE agent than the RIII mouse assay (Wells et al., 2005). A
pooled inoculum was prepared from palatine tonsil of cattle (3, 3, 3 and 1
respectively) at each of 6, 10, 18, and 26 month periods post-exposure
(corresponding to 10, 14, 22 and 30 months of age) from the oral challenge
study. One ml of a ten per cent tissue homogenate in saline was injected by
the intracerebral route into groups of 5 calves. Results indicated traces of
infectivity in the palatine tonsil of cattle killed ten months after
experimental oral exposure, with transmission occurring in 1 of the 5
challenged calves (Wells et al., 2005). An infection rate of 1 out of 5
suggests that the infectivity is close to the limit of detection of the
assay and that the titre of infectivity in tonsil is less than 1 cattle i.c.
ID50/g. The study was completed in 2006, without further transmission to any
of the 4 remaining calves (Veterinary Laboratory Agency, unpublished
data). • Palatine tonsil collected from a further sequential-kill
pathogenesis study of BSE in which 100 calves were exposed to 100g of a pool
of BSE affected brainstems (Arnold et al 2007) was also bioassayed. In this
study, Espinosa et al. (2007) inoculated tonsil tissue intracerebrally into
mice expressing bovine PrP (BoPrP-Tg110). The inocula originated from pooled
samples from three cattle at each of five time points (20, 24, 27, 30 and 33
months) after the oral exposure of calves. Infectivity was detected at all
of the time points tested, with infection rates in the mice of 1/6, 1/6,
1/5, 1/6 and 1/6 respectively. Interestingly, this would seem to indicate a
relatively low constant plateau level of infectivity in the tonsil
throughout this largely preclinical period. The low infection rate (1 out of
6) is consistent with a level of infectivity lower than 1 i.c.ID50 in Tgbov
mice. Buschmann and Groschup (2005) provide data on a Tgbov mice model
giving a 1.000-10.000 fold greater sensitivity than the cattle bioassay.
While the Tgbov mice (tg110) in the study of Espinosa et al. (2007) were
different from the TgbovXV mice used by Buschmann and Groschup (2005), their
sensitivity is likely to be similar based on comparable levels of over
expression of the bovine PrP gene in each model. From data provided by
titrations of BSE infectivity in brain by the i.c. and the oral routes in
cattle it has been calculated that one bovine oral ID50 = 105.5 bovine i.c.
ID50 (Wells et al., 2007). On this basis, the titre of infectivity in tonsil
is less than 10-5.5 bovine oral ID50/g; an estimate, using additional data,
that is closely similar to that provided previously (EFSA 2004). Given the
greater sensitivity of the Tgbov mouse assays than the cattle i.c. assay, it
would seem probable that even in cattle after exposure to a 100g oral dose,
the titre in terms of bovine oral ID50/g may be at least one order of
magnitude less (i.e. 10-6.5 bovine oral ID50/g), for at least part of the
incubation period. As the majority of exposures in the epidemic were
probably less than 1g (Arnold et al., 2007), the infectivity in tonsil might
well have occurred at an even lower titre and have peaked later in
incubation. The most optimistic estimate might be that with doses of the
order of less than 1g, tonsil never contains detectable levels at any time
in the disease course. A table summarising the key parameters of the
infectivity studies mentioned in section 3.1 can be found in Appendix A. In
summary, the available data on BSE infectivity in tonsil indicate that: •
The frequency with which detectable infectivity occurs in tonsillar tissue
of a BSE naturally infected animal is difficult to estimate. Although only
two cases have been investigated employing biological assay, infectivity has
not been detected in palatine tonsil from naturally occurring clinical
cases. • From sequential kill pathogenesis studies in experimentally
infected cattle, infectivity associated with tonsil could be detected at 10
months post-exposure and, in the preclinical period, 20-33 months
post-exposure (Wells et al., 2005; Espinosa et al., 2007), suggesting that,
in this model, infectivity in tonsil probably persists throughout the
disease course. • In the experimental exposure to a 100g dose, infectivity
titer can be estimated from the data available to be 10-6.5 bovine oral ID50
per gram of tonsilar lymphoid tissue. • It must also be noted that all
available data on infectivity relate to palatine tonsil. Occurrence and
comparable levels of infectivity in lingual tonsil is an assumption. 3.2.
Amount of lymphoid tissue associated with the tongue intended for human
consumption As mentioned above, the findings of the study from Casteleyn et
al. (2007) are consistent with those of other studies carried out in Great
Britain (Wells et al., 2005) and Germany (Rebmann et al., submitted for
publication), but provide no quantification of lymphoid tissue remaining in
tongues intended for human consumption. Examination of 251 tongues, derived
from 15 abattoirs in Great Britain after removal of SRM and intended for
human consumption, showed that visible identifiable lingual tonsillar
tissue, indicated by fossulae, remained in 76.5% of them (192 out of 251)
(Wells et al., 2005). Even in the tongues in which no visible tonsillar
tissue remained, histological examination revealed lymphoid tissue in more
than 90% of them. Variations in the distribution of the lingual tonsil
suggested that even after the most rigorous trimming of the tongue traces of
tonsillar tissue may remain. However, the histological examination did not
extend rostral to the most caudal of the filiform papillae, which occur
caudal to the most caudal vallate papillae. In Germany (Rebmann et al.,
submitted for publication), specimens of the lingual mucosa were taken from
thirty cattle immediately after slaughter. The main parameter to identify
the lymphoreticular tissue in this study was the immunohistochemical
identification of the follicular dendritic cells (FDC). Lymph follicles were
detected in areas up to 30 mm rostral to a given macroscopic landmark (i.e.
the most caudal of the vallate papilla). This is an area which would not be
removed from the tongue when implementing the measures foreseen by
Regulation (EC) No 999/2001. Alternative technical approaches for the
removal of the lingual tonsil’s tissue, similar to those by Casteleyn et al.
in 2007, are proposed by the authors. These scientific studies did not take
into account the rostral part of the tongue which can harbor solitary
primary lymph nodules or diffuse accumulations of T and B lymphocytes. Some
information on more rostral areas of the tongue was provided in a more
recent study (Kato and Sawada, 2008). In that study, examination of the
bovine tongue was carried out from the tip of the torus linguae to the root
of the tongue. The study confirmed previous results in relation to the
distribution of lymphoid tissue in bovine tongue. In addition, 1 out of the
20 specimens collected rostrally to the most rostral vallate papilla
contained lingual tonsillar tissue. Based on the above data, neither
qualitative nor quantitative estimation of the significance of the lymphoid
formations located rostrally to the most caudal vallate papilla is feasible
at present. In the DNV risk assessment cited in section 3.1 (EFSA, 2004;
SEAC, 2003), a total weight of bovine tonsil of 50g is assumed. However, in
the DNV risk assessment, it is stated that the weights of the various
tissues were taken from the LFRA ruminant products audit (LFRA, 1997). The
total weight of tonsillar tissue in a typical bovine, as given from
literature derived offal weights in the LFRA audit, is estimated at 200g.
This suggests that the value of 50g in the DNV report is in fact referring
to the weight of lingual tonsil. If the largest contribution to the total
weight of tonsillar material is the palatine tonsil, it would be reasonable
to estimate lingual tonsil as approximately 50g. It is further assumed in
the DNV risk assessment that, after removal of all visible tonsillar tissue,
the realistic upper limit of tissue that would remain in the tongue would be
10% i.e. 5g. Since the palatine tonsil is a circumscribed structure and
easily identified, complete removal, compared to the lingual tonsil, is
ensured, so this estimate remains valid as the quantity of tonsillar tissue
that might not be removed. In conclusion, based on the data available:

• it is not possible to know exactly the quantity of lymphoid tissue
remaining in bovine tongue intended for human consumption when harvested
according to the harvesting method currently applied, even if it can be
estimated to be 5g;

• it is not possible to estimate how much lymphoid tissue is removed by the
alternative harvesting method compared with the one currently applied.

snip...full text ;

http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej700_bovine_tongue_en.pdf


SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html


Subject: [madcow] Substances Prohibited From Use in Animal Food or Feed
[Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46 Friday,
April 25, 2008

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or
Italian L-BASE

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html

Tuesday, April 29, 2008

Interference at the EPA - Science and Politics at the U.S. Environmental
Protection Agency

please see full text ;

http://sciencebushwhacked.blogspot.com/


Wednesday, April 30, 2008

Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings


http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html


TSS
 

flounder

Well-known member
RobertMac said:
Keep it up, Terry...one day you will destroy the cattle industry.

your kidding right $

the beef industry is destroying itself. your a perfect example by the stupid comment. the beef industry could have taken care of this a long time ago. what did old barney fife say "Nip it in the bud!" test, test, test. but the usda showed how NOT to do it last time round. did a pretty good job too. and, you can have all the rules and regs in surveillance, feed, etc you want, but if they are not enforced, then you ain't got nothing :? :???: :help: nothing but ink on paper $$$



RobertMac said:
Keep it up, Terry...one day you will destroy the cattle industry.


robert mac, please tell me what i have to do with any of the following ;


SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html

Subject: [madcow] Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46 Friday, April 25, 2008

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html



Wednesday, April 30, 2008

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html

CJD FACT SHEET

What is CJD? Creutzfeldt-Jakob Disease (CJD) is a rare, fatal brain disorder. The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

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

There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf

Center April 3, 2008

Progress Report from the National Prion Disease Pathology Surveillance Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

Dear Member:

Once again we are writing to thank you for your continued support in enhancing surveillance of prion diseases in the United States and to bring you up to date on the National Prion Disease Pathology Surveillance Center (NPDPSC).

In large part because of your support, the number of cases examined by biopsy, autopsy and 14-3-3 protein determination has increased significantly over the years (see Tables 1 and 2). We are now able to establish a definitive diagnosis of prion disease in an estimated 60-70% of the cases in the United States, a percentage which exceeds that in even some major surveillance centers. In addition, we receive from you cerebrospinal fluid (CSF) for 14-3-3 determination, a surrogate protein which is helpful in the diagnosis of prion disease, probably in most if not all cases of suspected Creutzfeldt-Jakob disease (CJD). We are making constant efforts to reach our goal of at least 80% definitively diagnosed cases.

The major obstacle to our further increasing the autopsy rate remains the inadequate reporting of suspected cases of CJD to the NPDPSC or to the State Health Department, which in turn would notify us. Since you are the one likely to request the 14-3-3 test on these cases, please include in your request the information needed to contact you, which we will do if the test proves positive. If your institution uses a referral laboratory to send us the CSF, please provide your name, phone, and fax numbers to the lab, which will in turn submit it to us along with the sample. If this information is missing in the request accompanying the CSF sample (as it happens in about 30% of the cases), we will be unable to contact the caregiving physician. Having your contact information would also allow us to send results directly to you, thus reducing turnaround times. ...

snip...

Prion surveillance in cattle has been reduced by 90% (from about 470,000 to 40,000 in the U.S. in 2007 out of about 35 million cattle slaughtered). Termination of human prion surveillance would therefore remove the second line of surveillance, thereby eliminating prion surveillance in the U.S. entirely. This development would be extremely worrisome in view of recent reports that precautions to limit the spread of the prion infectious agent may not have been followed in some slaughter houses in the U.S. Cattle affected with bovine spongiform encephalopathy (BSE) continue to be discovered in Canada, which has more rigorous BSE surveillance than the U.S. At the same time, Canada imposes few limitations in the trade of potentially prion-infectious cattle with the U.S.

snip...

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

please see full text with additional comments and links @ ;

http://prionunitusaupdate2008.blogspot.com/

JOURNAL OF NEUROLOGY

MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

[email protected]

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?

http://www.neurology.org/cgi/eletters/60/2/176#535

THE PATHOLOGICAL PROTEIN

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

http://www.thepathologicalprotein.com/

i'm just the messenger, and nobody is listening $$$


Tuesday, April 29, 2008

Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency

please see full text ;

http://sciencebushwhacked.blogspot.com/


terry
 

hypocritexposer

Well-known member
Flounder,

Sandhusker has an answer to that question too, in another post.

He says the majority rules, that being the consumer. They want COOL, so they can make an informed decision on food safety.

An informed decision to me would mean letting the consumer know which countries have the higher inspection and safety standards, and then labelling it as such.

I think you have been doing a stellar job of this so far, so just continue.
 

Sandhusker

Well-known member
hypocritexposer said:
Flounder,

Sandhusker has an answer to that question too, in another post.

He says the majority rules, that being the consumer. They want COOL, so they can make an informed decision on food safety.

An informed decision to me would mean letting the consumer know which countries have the higher inspection and safety standards, and then labelling it as such.

I think you have been doing a stellar job of this so far, so just continue.

If any country has inspection or safety standards that they can brag on, it's up to them to get the word out and market their investment.
 

hypocritexposer

Well-known member
If you look at Porker's post/topic about COOL, you will see that other countries are already planning and to a certain degree, are already doing that.

That's why I think COOL will eventually force the adoption of source verification in the US.

There are only a few groups that are resisting the inevitable, and speaking out of both sides of their mouths.
 

Sandhusker

Well-known member
hypocritexposer said:
If you look at Porker's post/topic about COOL, you will see that other countries are already planning and to a certain degree, are already doing that.

That's why I think COOL will eventually force the adoption of source verification in the US.

There are only a few groups that are resisting the inevitable, and speaking out of both sides of their mouths.

You don't need to verify the pasture to verify the country. We can verify every dang bovine and box of beef in this country TODAY as to country of origin. Unless you're intentinally trying to make this difficult, what the heck is the problem?
 

hypocritexposer

Well-known member
Sandhusker said:
hypocritexposer said:
If you look at Porker's post/topic about COOL, you will see that other countries are already planning and to a certain degree, are already doing that.

That's why I think COOL will eventually force the adoption of source verification in the US.

There are only a few groups that are resisting the inevitable, and speaking out of both sides of their mouths.

You don't need to verify the pasture to verify the country. We can verify every dang bovine and box of beef in this country TODAY as to country of origin. Unless you're intentinally trying to make this difficult, what the heck is the problem?

No you don't, but if you are interested in marketing your product with complete transparency, then why not source verify also.

Transparency will go along way to gain consumer loyalty. Whereas COOL will only be part of an incomplete picture.
 

Sandhusker

Well-known member
hypocritexposer said:
Sandhusker said:
hypocritexposer said:
If you look at Porker's post/topic about COOL, you will see that other countries are already planning and to a certain degree, are already doing that.

That's why I think COOL will eventually force the adoption of source verification in the US.

There are only a few groups that are resisting the inevitable, and speaking out of both sides of their mouths.

You don't need to verify the pasture to verify the country. We can verify every dang bovine and box of beef in this country TODAY as to country of origin. Unless you're intentinally trying to make this difficult, what the heck is the problem?

No you don't, but if you are interested in marketing your product with complete transparency, then why not source verify also.

Transparency will go along way to gain consumer loyalty. Whereas COOL will only be part of an incomplete picture.

Because whether the steer came from Duck Brand in Nebraska or the Arrowhead in South Dakota means absolutely nothing to consumers.
 

hypocritexposer

Well-known member
What if it comes from Canada with better inspection and safety attached?

Or is the product being portrayed as being safer if it is domestic?

Do they not care about food safety, or just that it comes from the US, but what does that mean anyway. Nobody has come with a definite definition yet, have they?
 

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