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From: TSS ()
Subject: Chinese report on possible residual BSE risks in products derived from ruminant materials and used as cosmetics ingredient
Date: March 7, 2006 at 7:21 am PST



Request for a scientific opinion on

Chinese report on possible residual BSE risks in products derived from ruminant

materials and used as cosmetics ingredient

1. Background

The Chinese administration responsible for the surveillance of imported cosmetic

product (AQSIQ) had, in 2002, introduced measures in the light of possible risk of

transmission of TSE through cosmetic products containing certain animal-derived


The EU and China subsequently agreed to organize a joint hearing with scientists from

both regions to assess the actual risk and to propose the appropriate measures. Following

a hearing, a scientific report was adopted in May 2003.

In response to the above report, the Chinese authorities have now provided a further

report entitled “China’s risk evaluation of animal-origin TSE infectious factors in


2. Terms of reference

Does the report “China’s risk evaluation of animal-origin TSE infectious factors in

cosmetics” contain new scientific evidence for a risk of transmission of BSE and related

diseases through cosmetic ingredients derived from ruminant material?

3. Deadline

December 2006

TSS report on possible residual BSE risks in products derived from ruminant November 10, 2000 at 2:06 pm PST

From: TSS (
Date: November 10, 2000 at 2:06 pm PST


the risk from TSE's can best be explained from the research
on kuru. the following is rather gross, but explains the hypothosis;

'Others who attended those feasts were found to have quite varied incubation periods. They could have been infected at other feasts not investigated or received a different dose of the
infective agent by a different route, such as through a wound or a mucous membrane or by ingestion.'


'It has since been found that the most infectious parts of the body are the brain and the spinal cord, both of which were favoured by the women. Their children, milling about and being tended by their mother with their kuru-infected hands, were susceptible to infection.'


also, the fact that during these rituals, some members would
not eat, but would spread blood and other tissues over their
body, which would get into open sores (tropical ulcers or yaws were
very common).

SO, you ask, what does this have to do with cosmetics???
well, know one can say definately, but, as i have said,
my Mom looked like a greased pig (sorry mom), when she went
to bed at night. All her life, she would smear this facial
cream all over her face and especially around the eyes.
also, eye liner and make-up. Now, if the 'accumulation theory'
plays into the picture, we might have something here.
Heidenhain Variant CJD is a strain that destroys the brain,
directly behind the eyes. It's a 'frontal CJD' OOOOOOOOOps,
forgot, it is also sporadic-hvCJD. so, the hypothosis that
cosmetics containing bovine brain and placenta posing a potential
risk, could be in fact, be true.

everything you ever wanted to know about cosmetics/cjd/bse

Volume 7 Medicines and Cosmetics
8. Cosmetics and toiletries
Standard topical products
Collagen implants
How the issue was handled

8.1 In this chapter we consider the Government's response to the risks posed by the use of bovine material in cosmetics. Cosmetics, as defined by the Cosmetics Products (Safety)
Regulations 1996, include:

any substance or preparation intended to be placed in contact with any part of the
external surfaces of the human body (that is to say, the epidermis, hair system,
nails, lips and external genital organs) or with the teeth and the mucous
membranes of the oral cavity with a view exclusively or mainly to cleaning them,
perfuming them, changing their appearance, protecting them, keeping them in
good condition or correcting body odours except where such cleaning, perfuming,
protecting, changing, keeping or correcting is wholly for the purpose of treating or
preventing disease. 1

8.2 Cosmetics using bovine materials fell into three categories: (i) products using lightly treated
high-risk bovine offals: 'exotica'; (ii) standard topically applied products using heavily
processed bovine by-products; and (iii) implants using bovine collagen.


8.3 Concern about a risk of possible BSE contamination focused mainly on those cosmetic
products commonly described as 'exotica'. These included 'premium priced facial skin care
products' such as certain anti-ageing and anti-wrinkle creams. There was no ban on the use in
them of animal material such as 'cellular extracts' that was deemed an unacceptable risk in
food and medicines, and accordingly proscribed under the food safety and medicines safety
legislation. Such material might be only lightly processed or simply chilled. Possible
ingredients identified relatively early on were gangliocides extracted from the brain; and
placental material, spleen and thymus. 2

Standard topical products

8.4 Although never considered a serious risk, questions were also raised about how to ensure
the safety of more standard cosmetic products. These included the full range of topically
applied cosmetics, ie, creams and toiletries applied to the skin, lips and eyelids, and included
soaps, skin creams, shaving sticks and stick deodorants. Many of these used heavily
processed bovine by-products such as collagen, elastin, gelatine and tallow derivatives. 3

Collagen implants

8.5 Concern was also expressed about bovine collagen used in implants. Although not
mentioned in the highly condensed minutes of the CSM/BSC meeting of 2 November 1988, Dr
Pickles's own note at the time records that this came up at the meeting as an area of concern:
'Some collagen implants of bovine origin as used by cosmetic clinics are not even licensed.' 4
Collagen products intended for correction of contour deficiencies of the skin were considered
licensable under the Surgical Materials Order SI 1971 No. 1276. DH has told us that although
collagen implants might have been used for 'cosmetic' reasons, this would have been under
medical supervision as they were 'prescription only' medicines. 5

How the issue was handled

8.6 Although specifically identified in the Tyrrell Report in June 1989 as a small-scale
user that
might not be covered by the regulations and guidelines then in place, 6 the cosmetics industry
was not itself the subject of advice or guidance until February 1990.

8.7 In January of that year Mr Richard Roscoe of the Department of Trade and Industry (DTI),
the Department with policy responsibility for the safety of cosmetics, had on his own initiative
asked DH for advice about the risk from BSE associated with the use of bovine offal in certain
cosmetics. 7 DH's advice was that although the risk of transmission of BSE was remote, it
would be prudent to reformulate, or source bovine material from cattle reared outside the British
Isles. 8 DTI passed this advice on to the cosmetics industry trade association, the Cosmetics,
Toiletries and Perfumery Association (CTPA), which in turn informed its members. 9

8.8 SEAC considered the use of bovine material in non-food products generally in June 1991. 10
By that time, BSE had been identified in countries other than the UK, and it was suggested
that the advice issued to the cosmetics industry in February 1990 should be updated to take
this into account. Updated advice was not sent to the CTPA until April 1992. 11

8.9 One approach that was considered within DH was the introduction of a voluntary ban on
bovine materials from countries in which cases of BSE had been reported. Such a ban, if it
were to be introduced, would have to be implemented at EU level, so as not to fall foul of
European law. The question of BSE and cosmetics was therefore taken forward in the EC
Working Party on Cosmetics (ECWPC). Progress at EC/EU level was slow; by the end of
October 1994 the Scientific Committee on Cosmetology (SCC) had produced only an interim
statement suggesting that material from animals with the potential to transmit infectious agents
should not be used in the manufacture of cosmetics. 12 In February 1995 the ECWPC decided
that the existing Cosmetics Directive did not need alteration. 13 This decision was based in part
on assurance by COLIPA, the European cosmetics trade association, that its members were
following certain approved basic precautions on a voluntary basis. 14

8.10 When, in March 1996, the EU ban on the export from the UK of bovine products destined
for use in cosmetic, medicinal and pharmaceutical products was introduced, 15 the CTPA
conducted a survey of its members and reported that almost all had been using
non-UK-sourced bovine material for some time. 16

8.11 In the sections that follow we look first at the regulatory framework on cosmetics safety,
which was markedly different from that on either food or medicinal products safety. The
sponsoring Department for the industry, which was also responsible for its regulation, was DTI.
As we shall see, there was some confusion at various points in the sequence of events about
the respective responsibilities of DTI and DH for minimising risks to human health from the
production and use of cosmetic products.

8.12 In the final section of the chapter we review some lessons that emerge from the way BSE
was handled.

Volume 7 Medicines and Cosmetics
8. Cosmetics and toiletries
Regulatory framework
DTI handling of cosmetics
DH's role in cosmetics safety

8.13 The regulation of cosmetics is based on the EU Cosmetics Directive (1976), which was
implemented in the UK by regulations made under the Consumer Protection Act 1987. Under
this system, cosmetic products must meet various safety requirements, but, unlike medicinal
products, they do not require a licence.

8.14 The Cosmetics Directive seeks to ensure the safety of cosmetics and their unhindered
trade throughout the EU. In relation to safety, Article 2 provides:

Cosmetic products put on the market within the Community must not be liable to
cause damage to human health when applied under normal conditions of use. 1

8.15 Dr Robin Fielder of DH told us that the Cosmetics Directive places the onus on
manufacturers and suppliers to ensure that the product is safe for the use intended. 2

8.16 Member States have a duty to 'take all necessary measures to ensure that only cosmetic
products which conform to [the Directive] may be put on the market'. 3 The Annexes to the
Cosmetics Directive list substances that must not be used in cosmetics and substances
whose use is regulated. They also contain lists of substances ('the prescribed lists')
for certain uses (preservatives, colourants, sun screens) and only these substances may be
used for those purposes in cosmetic products. 4 The prescribed lists may be amended
following consideration by the European Commission's Cosmetic Products Working Party,
which consists of representatives from the Member States and the industry. DTI led for the
on this with DH also having a role. The final decision is taken by the Committee on the
Adaptation to Technical Progress, which is chaired by the Commission and consists of
representatives from Member States. Both the Working Party and the Commission have
access to the opinions of the Scientific Committee on Cosmetology (SCC), an independent
multidisciplinary body of scientists appointed by the Commission to assess the safety of
cosmetics ingredients, as well as to advice from their own national scientific advisers. 5

8.17 The Cosmetics Directive limits the action individual Member States can take to regulate
cosmetics. 6 If a product complies with the relevant Annex, the UK Government cannot
its use unless, on the basis of a 'substantiated justification', it represents a hazard to
health. 7

8.18 Regulations made, in part, under section 11 of the Consumer Protection Act 1987 give
effect to the Cosmetics Directive in UK law. The Cosmetic Products (Safety) Regulations 1984
(made under a predecessor of the Act) were replaced on 1 January 1990 by the Cosmetic
Products (Safety) Regulations 1989 ('the 1989 Regulations').

8.19 The main provisions of the 1989 Regulations are as follows: 8

1.A cosmetic product shall not be liable to cause damage to human health when it is
applied under normal conditions of use (reg. 3(1)).
2.No cosmetic product may contain any substance listed in column 2 of Schedule 1,
unless it is only a trace that could not reasonably have been removed during or
manufacture (reg. 4(2)).
3.A cosmetic product must not contain any substance listed in column 2 of Schedule
2 unless specified requirements in that schedule are satisfied (reg. 4(3)).
4.The Secretary of State may authorise the use in a cosmetic product of any
substance not listed in either schedule 1 or 2 (reg. 5(1)). In giving authorisation
Secretary of State may impose conditions relating to the use of the substance (reg.
5.There are various conditions and standards for labelling and packaging (reg. 6).

8.20 The Consumer Protection Act imposes a general safety requirement on all consumer
goods. Section 10 of the Act makes it an offence to supply consumer goods that fail to
with the general safety requirement. For this purpose, consumer goods fail to comply with
safety requirement if they are not reasonably safe having regard to all the circumstances.
means that there is no risk (apart from one reduced to a minimum) that the goods will
immediately or later) cause death or personal injury to any person. 9

8.21 The Cosmetics Directive and the 1989 Regulations left only limited scope for the
application of section 10 of the Act. Since the introduction of the General Product Safety
Regulations 1994 10 there has been virtually no scope for its application.

8.22 In practice informal contact and voluntary cooperation played an important part in the
regulation of the cosmetics industry.


8.23 DTI had policy responsibility for the safety of cosmetics in the UK. Day-to-day
enforcement of safety regulations such as the 1989 Regulations fell to the trading standards
departments of local authorities. 11

8.24 Supplying consumer goods that failed to comply with the general safety requirement or
with certain requirements of safety regulations was an offence and punishable in the courts.

8.25 In addition, enforcement authorities (which for these purposes meant DTI and the
standards departments of local authorities) had power to serve a suspension notice
the person on whom it was served from supplying goods for up to six months; power to apply
the court for a forfeiture order; 13 and power for an authorised officer of the enforcement
authority to enter any premises, inspect any goods, or examine any procedure, or in
appropriate circumstances to seize and detain goods. 14

8.26 The Secretary of State also had the power to serve a notice on a person prohibiting the
person from selling consumer goods if the Secretary of State considered them to be unsafe (a
prohibition notice), or requiring the person to publish a warning about such goods (a notice
warn). 15 However, these powers applied only to the person on whom the notice was served or
against whom the order was sought, rather than to a general category of goods, and no power
existed to recall products under these provisions. 16

8.27 DTI told us that it was unaware of any instance in which these powers had been used in
respect of a BSE risk in cosmetics. 17

DTI handling of cosmetics

8.28 Within DTI overall responsibility for the safety of cosmetics lay with the Consumer
Unit (CSU). Within the CSU, the Chemical Hazards Section (CHS) had day-to-day
responsibility for cosmetics. 18

8.29 Mr David Jones, a Grade 5 official, was Head of the CSU until 1995. Mr Roscoe, a Grade
official, was Head of the CHS from 1983 to 1992, with specific responsibility for ensuring
safety of cosmetics sold in the UK. 19 He was succeeded by Mr John Walker. Mrs M L Payne,
a Higher Executive Officer in the CSU from 1990, was responsible for developing policy on
regulation covering chemicals, including ingredients used in cosmetics. 20

8.30 The CTPA was the peak representative body for the UK cosmetics industry and the
channel through which DTI distributed cautionary guidance on BSE to cosmetics

DH's role in cosmetics safety

8.31 Although DTI had overall regulatory responsibility for cosmetics, DH also played a role
DTI's adviser on toxicity. 21 The relevant Division in DH was MED TEP (Medical Toxicology
Environmental Protection), 22 later evolving into the HEF M (Health Aspects of Environment
Food Medical), 23 which would give advice when necessary.

8.32 Mr Roscoe told us that whenever the CHS was alerted to the presence of a potentially
'risky' ingredient in a particular cosmetic product it would refer the matter to DH. 24 Upon
receipt of advice from DH, the CHS would then decide on a course of action. According to Mr
Roscoe, DTI would always act on this advice 'unless there were very strong reasons for not
doing so'. 25

8.33 Mr Roscoe also told the Inquiry that he believed that when DH encountered a new risk it
was its responsibility to pass on the information to DTI. 26

8.34 The DH adviser on toxicology over the period of concern was Dr Fielder, who was
by Dr Dewhurst (1988-90), Dr Gott (1991-93) and Ms Mulholland (1993-97). 27

COSMETICS-further reading from the inquiry on this subject;

8.227 These matters stretch well beyond our remit. However, it appears to us, as it did to
the Tyrrell Committee, that cosmetics were indeed a potential pathway for pathogens, and that
enough was known about this. Future occasions could arise when, as with BSE, there needs to
be a means of turning off the tap at source, rather than catching droplets downstream.
Consideration might usefully be given to what powers and processes would assist this.

9.63 Mr Bradley replied by letter dated 17 June 1990 to Dr Pickles's letter of 11 June. He
in relation to A1d:

I have not got far with this. Where do fetal calves, placenta and uteri go and are any
uses made of lymph nodes? Cosmetics, ointments, oils, indeed anything that is used on the
skin (it could have a lesion) could presen an increased hazard. I have some concern over
mesenteric lymph nodes though they are not eaten, though DOH/MAFF agreed earlier there was no
need to include them in
the offal ban. This is one to discuss in Committee. 34

I understand that there is concern on the Tyrrell Committee recommendation A1d on
pharmaceuticals and cosmetics. This has never been considered a primary responsibility of
MAFF although collaboration with the principals (DOH and
industry) was anticipated.

I suspect the VMD approach will be to avoid or selectively reduce use of bovine tissues
in medicinal products for animals. Presumably the authorities responsible for human medicinal
products and cosmetics have taken similar action. 35
(iii) Non-food uses of bovine material. The Committee asked for a note on the use of
bovine material for cosmetics in particular, although it might make sense to cover all the
non-food uses that we can think of (harp strings, tennis rackets etc).
I think that all that is required is a factual note about the range of uses, and
quantities, together with an assessment of possible risk factors. It looks to me like a job
for Dr Pickles. 1

Annex 2 to Chapter 9: Uses made of the cattle carcass

Item Products derived Additional comments


Brain Human food
Laboratory reagents
Veterinary medicines

4.4 On 10.1.90 I attended the second meeting of the CSM BSE Working
Party. The discussions which took place
and the conclusions reached can be found in the Minutes of the
meeting [YB 90/1.10/1.1-1.24]. I provided
comments to Dr Singh in Med TEH on his draft letter to DTI
which responded to a request for advice on the safety
of the use of bovine offal (in particular, spleen and thymus)
in cosmetics [YB 90/1.29/1.1-1.2]. My briefing notes
were used to accompany the reply to DTI [YB 90/2.1/4.1]. I
indicated I was not happy about the use of bovine
offal from calves under 6 months in cosmetics (in contrast to
foods) because on damaged skin such use could be
close to parenteral administration so the nearest parallel
might be injectable medicines. Besides there were no
compensating benefits.

57. April 1990

57.1 The formation of SEAC was announced by Mr Gummer on
3.4.90 [YB 90/5.24/4.1-4.2]. As requested, I
supplied comments on the draft Agenda prepared by Mr Lowson
for SEAC's first meeting [YB 90/4.6/4.1-4.3] and
I supplied a list of documents to accompany the formal papers
for background information. I offered to put together
a discussion paper on bovine eyeballs and the use of bovine
material in cosmetics. This draft paper entitled Routes
of Possible Transmission into Man was later sent to Mr Lowson
for comment [YB 90/4.12/1.1-1.4]. It met with
the approval of Mr Lowson but it was not submitted to SEAC at
that time as CVO indicated he thought a more
detailed paper was needed [YB 90/4.24/3.1-3.2 and see YB

Re: TSE's -- GELATINE -- SOME CONCERN,or just something to
barf at???
Wed, 18 Oct 2000 09:17:59 -0700
"Terry S. Singeltary Sr."
Bovine Spongiform Encephalopathy
1 , 2

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

Hello Roland and other list members,

I thought i would pass this through, for those that have not read it.
It fits this discussion rather nicely;

Opinion on the Safety of Hides and Skins adopted by Written Procedure by
the Scientific Committee on Medicinal Products and Medical Devices on 24
March 1999

Executive Summary


The DG XXIV has asked the SCMPMD to provide it with comments on the
following publication:

Pammer, J., Weninger, W. and Tschachler, E. : Human keratinocytes
express cellular prion-related proteins in vitro and during inflammatory
skin disease. American Journal of Pathology 153, 1353-1358, 1998.

Context of the question

The question is asked in the frame whether or not it is necessary to
modify the policy regarding the use of hides and skins for the
preparation of gelatine.


Pammer et al. unequivocally demonstrate the presence of PrPc in the
skin. By this finding, they extent the range of tissues known to express
PrPc. The theoretical possibility that skin contains also PrPSc, the
pathologic form of the prion protein, or TSE infectivity in significant
amounts is not supported by the majority of observations. However,
experiments as a search for PrPSc in the skin have not yet been
performed. The methods are easily available. Until those studies are
completed there is no sound justification for a change in policy
regarding the use of hides and skins for the preparation of gelatine.


After a discussion at the plenary meeting of the SCMPMD on 10 February
1999, the comments are summarised as follows:

1. The paper by Pammer et al. describes the detection of the cellular
(non-pathogenic) form of the prion protein (PrPc) in the skin of humans,
mainly in keratinocytes, but also in infiltrating mononuclear cells. The
amount of PrPc is enhanced under certain pathological conditions of the
skin (dermatitis, psoriasis, viral warts, squamous cell carcinomas).
These findings are supported by in vitro studies on keratinocytes.

2. As it is generally accepted that the presence of PrPc is a
prerequisite for the replication of TSE agents, the authors discuss two
possible consequences of their finding:
i) the TSE agent may enter the body via the skin; ii) the TSE agent may
be transmitted via the skin to other individuals.

3. Although TSE agents can be transmitted by skin scarification (Taylor
1996) there is little epidemiological evidence that this route is of
major importance. While some investigators believe that Kuru is
transmitted through small injuries of the skin during the cannibalistic
Committee on Medicinal Products and Medical Devices on 21 October 1998,
p. 12) others argue that the oral route is of greater importance as this
route is the established way of infection in bovine spongiform
encephalopathy (BSE) and transmissible mink encephalopathy (TME). Also,
epidemiological studies did not show that health care personnel with a
high risk for skin injuries during invasive procedures (surgeons,
neuropathologists) is at risk of acquiring CJD (Taylor 1996, van Duijn

4. While the presence of PrPc presents, at least theoretically, a site
for entry of the TSE agent, it does not necessarily mean that there is
also a site of PrPSc accumulation in diseased individuals. PrPc can be
found in many tissues (Bendheim 1992, Horiuchi 1995), also in tissues in
which TSE infectivity cannot be demonstrated (see table). Horiuchi
concludes from his studies in sheep: "The tissue distribution of PrPc
appears to be inconsistent with the tissues which possess scrapie
infectivity, suggesting that factor(s) specific to certain cell types
may be required to support multiplication of the scrapie agent."

5. Up to date, it is assumed that skin does not contain measurable
amounts of infectivity (see table in the CPMP Note for Guidance on
Minimising the Risk of Transmitting Animal Spongiform Encephalopathy
Agents via Medicinal Products). However, at least to the knowledge of
the SCMPMD, there are no experiments published which are aimed todetect
infectivity in skin. Especially, Hadlow (Eklund 1967, Hadlow 1974,
Hadlow 1980, Hadlow 1982, Hadlow 1987) did not report on skin in his
different studies with TSE infected mice, goats, sheep and minks. This
may be partly due to the difficulty to prepare skin homogenates. In
addition, there are no published reports which demonstrate the presence
or the lack of PrPSc in the skin.

6. Pammer et al., seeking for a biological plausibility for the presence
of PrPSc in the skin refer to the pruritus which is characteristic for
scrapie infected sheep. However, unless the presence of PrPSc in the
skin of those sheep is unequivocally shown, a neurological origin of
this pruritus should be continued to be assumed.

7. Recent epidemiological studies (van Duijn 1998) show some unexplained
correlation between the risk for CJD and contacts with skin and skin
derivatives. While work with leather is obviously not a risk factor for
CJD "contact with fur/leather other than through clothes" is. Also the
use of fertilisers containing hoofs and horn seems to be a high risk
factor for CJD, but detailed analysis shows that this correlation only
holds for the years before 1985. As BSE was not existent or at least
very limited before 1985 it is difficult to find a biological
explanation for this observation.

8. Pammer et al. unequivocally demonstrate the presence of PrPc in the
skin. By this finding, they extent the range of tissues known to express
PrPc. The majority of observations seems to support the opinion that
skin does not contain TSE infectivity in significant amounts. However,
as there are still some open questions there is the need for studies
investigating the presence of PrPSc, the pathologic form of the prion
protein, in the skin. The methods are easily available. Until those
studies are completed there is no sound justification for a change in
policy regarding the use of hides and skins for the preparation of


Tissue Presence1 of PrPc Scrapie infectivity2

brain + +
spleen + +
lymph node + +
lung + -
heart + -
kidney + -
skeletal muscle + -
uterus + -
adrenal gland + +
parotid gland + -
intestine + +
liver - -

Data from sheep with scrapie according to 1Horiuchi 1995 and 2Hadlow
1982. Infectivity was measured in mice as indicator animals. In a
scrapie mouse model (Eklund 1967) infectivity could be found also in
tissues like uterus, kidney and liver. In evaluating animal models all
the considerations discussed in the OPINION ON THE RISK QUANTIFICATION
Scientific Committee on Medicinal Products and Medical Devices on 21
October 1998 (pp. 18-19) have to be taken into account.


Bendheim, P.E., Brown, H.R., Rudelli, R.D., Scala, L.J., Goller, N.L.,
Wen, G.Y., Kascsak, R.J., Cashman, N.R., Bolton, D.C.: Nearly ubiquitous
tissue distribution of the scrapie agent precursor protein. Neurology
42, 149,-156, 1992

Eklund, C.M., Kennedy, R.C., Hadlow, W.J.: Pathogenesis of scrapie virus
infection in the mouse. Journal of Infectious Diseases 117, 15-22, 1967

Hadlow, W.J., Eklund, C.M., Kennedy, R.C., Jackson, T.A., Whitford,
H.W., Boyle, C.C.: Course of experimental scrapie virus infection in the
goat. Journal of Infectious Diseases 129, 559 567, 1974

Hadlow, W.J., Kennedy, R.C., Race, R.E., Eklund, C.M.: Virologic and
neurohistologic findings in dairy goats affected with natural scrapie.
Veterinary Pathology 17, 187,-199, 1980

Hadlow, W.J., Kennedy, R.C., Race, R.E.: Natural infection of Suffolk
sheep with scrapie virus. Journal of Infectious Diseases 146, 657-664,

Hadlow, W.J., Race, R.E., Kennedy, R.C.: Temporal distribution of
transmissible mink encephalopathy virus in mink inoculated
subcutaneously. Journal of Virology 61, 3235-3240, 1987

Horiuchi, M., Yamazaki, N., Ikeda, T., Ishiguro, N., Shinagawa, M.: A
cellular form of prion protein (PrPC) exists in many non-neuronal
tissues of sheep. Journal of General Virology 76, 2583-2587, 1995

Pammer, J., Weninger, W. and Tschachler, E.: Human keratinocytes express
cellular prion-related proteins in vitro and during inflammatory skin
disease. American Journal of Pathology 153, 1353-1358, 1998.

Taylor, D.M., McConnel, I., Fraser, H.: Scrapie infection can be
established readily through skin scarification in immunocompetent but
not immunodeficient mice. Journal of General Virology 77, 1595-1599,

van Duijn, C.M., Delasnerie-Lauprêtre, N., Masullo, C., Zerr, I., de
Silva, R., Wientjens, D.P.W.M., Brandel, J.-P., Weber, T., Bonavita, V.,
Zeidler, M., Alpérovitch, A., Poser, S., Granieri, E., Hofman, A., Will,
R.G.: Case-control study of risk factors of Creutzfeldt-Jakob
disease in Europe during 1993-95. Lancet 351, 1081-1085, 1998

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

Subject: Cosmetics, Toiletry and Perfumery Association & B.S.E.

change to;

CJD/COSMETICS INDUSTRY & Opinion concerning Amino Acids Obtained By
Hydrolysis of Human Hair


PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C


BSE Inquiry report criticises ex-Tory ministers

Sat, Sep 2, 2000 PA News

Conservative former ministers and Whitehall officials face strong criticism in the official report into the BSE crisis, it was
reported tonight. The inquiry chairman Lord Phillips is believed to have notified several former health and agriculture ministers
that they are facing criticism in the 13-volume report he is to publish in a few weeks.

Reports in several Sunday newspapers suggested the former ministers would be taken to task for being "too adamant" in their
assurances that British beef was safe, and for failing to react swiftly enough to scientists' findings that the disease could spread
to humans. Scientists first suspected that there was a risk to humans eating BSE-infected offal in the mid-80s, but it was not
until March 1996 that Tory ministers admitted that there was a danger to the public.

But the ex-ministers could come off lightly compared with senior civil servants who ran the two departments as the decade-long
saga unfolded.

Lord Phillips' two-year inquiry is said to have concluded that too much importance was attached to the interests of the livestock
industry, and not enough to those of consumers. The BSE affair led to a worldwide ban on British beef exports which is
estimated to have cost the taxpayer 4.6 billion.

Comment (webmaster): It is unclear why the judge released the findings prior to publication. What purpose is served anyway
with polite criticism (1, 2) of long-departed political figures and retired civil servants? Keith Meldrin, who masterminded the
coverup within MAFF for 10 years, also receives a wrist-slap for a leading role in 82 human deaths. His successor at MAFF
who continued these abominable policies was forced into retirement this year but given a handsome 400,000 pound retirement
package. MAFF itself has spent 7 million pounds of public money on lawyers even and successfully fought the Inquiry practise
of publishing fulltext of government memos on the Internet.

However, these documents can still be obtained in print form. Terry S. Singeltary Sr. of Bacliff, Texas, has obtained many of
the documents alluded to in the Inquiry but never released. These have been optically character read into electronic form and
distributed to the German BSE listserve archive as well as to this web site:

BSE offals used in cosmetics, toiletry and perfume industry

Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas

Miss Marion Kelly
Cosmetic, Toiletry and Perfumery Association
35 Dover Street London W1X3RA

Department of Trade and Industry
10-18 Victoria Street
London SW1H ONN
Enquiries 01-215 5000 Telex 8811074 DTHQ G 01 215 3324 1 February 1990

Dear Marion

As you know there is no record of bovine spongiform encepalopathy crossing to humans, but we need to take precautions to
avoid any risk.

There a number of cosmetric products on sale in the United Kingdom such as anti-ageing creams that contain extracts of
bovine offal, primarily from spleen and thymus. [Two of the highest risk tissues. Note the epidemic has been raging for 4 years
by the time of the non-binding voluntary suggestions here. -- webmaster]

The purpose of this letter is to ask you to ask your members to eliminate any risk by reformulating such products to eliminate
these extracts, or alternatively to use material derived from cattle reared outside the UK, Eire or the Channel Islands. [Eire,
Channel Islands, and many other countries were thoroughly infected by then -- webmaster]

Please let me know if you have any trouble persuading your members to do so.

Yours sincerely



BSE110/1 0080


1 February 1990

Mr R Roscoe
Consumer Affairs
Department of Trade and Industry
10-18 Victoria Street
London SW1

Dear Richard


I am replying to your request for advice on the safety of the use of extracts of bovine offal in certain cosmetics, such as skin
products claimed to have 'anti-ageing' properties with respect to bovine spongiform encephalopathy (BSE). As you are aware
there are a number of cosmetic products on sale in the UK that contain small amounts of such extracts, primarily from spleen
and thymus.

We accept that the risk of transmission is likely to be remote, but believe that it would be prudent to eliminate any risk by
reformulating such products. Alternatively if the incorporation of bovine extracts is retained, material derived from cattle reared
outside the UK, Eire or the Channel Islands should be used.

We would be grateful if you would transmit these recommendations to industry via the Trade Association CTPA.

I attach background briefing prepared by medical colleagues from those sections most involved with consideration of BSE in
DH, together with a copy of the Southwood report.

Please let me know if you need any further information.

Yours sincerely

BSE110/1 0081


Presence of Bovine Offals in Cosmetics and Bovine Spongiform Encephalopathy

(1) Extracts of bovine spleen and thymus are present at between ca 0.1 and 5% in certain cosmetic preparations, for example
certain products claimed to delay the signs of ageing of skin. The concern about the increasing incidence of BSE in cattle in the
UK has made it necessary to reconsider the safety of such products.

BSE is a progressive neurological disorder in cattle, which results from infection with an "unconventional viral' agent. The first
case was described in cows in 1986. By 19 January 1990 there had been 9436 confirmed cases in the UK on 5474 farms.
There are no confirmed cases outside the British Isles, apart from a case in a cow recently exported from England. BSE is one
of a family of spongiform encephalopathies which also include scrapie in sheep and kuru and Creutzfeldt Jakob disease (CJD)
in man. The infection which leads to BBE appears to have been introduced into cattle from the contaminated feeding stuff, meat
and bone meal, made partly from sheep offal: scrapie is endemic in sheep in the UK.

The causative agents of these diseases are thought to be unconventional transmissible agents (referred to variously as prions,
virinos, filamentous viruses or slow viruses). They are extremely resistant to most denaturing processes eg heat, UV, high salt
concentration, formalin and alkylating agents. The current DH guideline for treating items used on CJD patients is a temperature
of 134-138 C (at 2 atmospheres) held for 18 minutes. They are also not removed by normal microbiological filters. It is thus
unlikely that the mild processing techniques used to obtain the extracts used in cosmetics would remove the causative agents.

(2) Government action to date includes:

a. An expert working party was set up under Sir Richard Southwood and reported in February 1989. All their
recommendations have been acted upon.

b. The disease has been made notifiable in cattle.

c. All suspect animals are slaughtered and carcases destroyed (50% compensation policy but 100% if diagnosis not
confirmed); milk from such animals is also destroyed.

d. Sale or supply of animal protein from ruminants for feeding to ruminants prohibited - hopefully to prevent any new infections
in cattle. This has had a major effect on the rendering industry.

e. Another committee was set up under Dr David Tyrrell to report on research needs. An interim report was published in
January 1990 together with an announcement about additional funding. Much research work into the disease is currently in
progress and additional studies are being planned.

Regulations in November 1989 introduced a ban on various bovine offal for human consumption, going wider than the
Southwood recommendations which were for such a ban to affect baby food only.

The Medicines Control Agency have gathered information from pharmaceutical companies about use of bovine ingredients
in parenteral pharmaceuticals and issued interim guidelines. Many biological products and vaccines use such
ingredients. The MCA are considering whether action on specific products is appropriate.

h. The Health and Safety Executive (HSE) is reviewing its guidance to those who come into direct contact with bovine 'risk'
tissues. A press release for those who handle BSE carcases has been issued and one for abattoir workers is in preparation. The
HSE ara also discussing risks from BSE exposure with the veterinary profession.

i. All UK cases of CJD will be monitored in a study to be conducted by Dr R G Will in Edinburgh, funded by the Department
of Health: this should allow detection of any spread of infection to hummans, although this possibility is considered remote.

(3) Current live issues

Research: Dr Tyrell's interim report identified a large research programme classed as high priority. Almost all of this research
falls to MAFF {Central Veterinary Labs} or the AFRC, although the MRC also has an interest. Substantial money has been
made available for this work but research will be laborious and results will come slowly.

Food: There has been constant pressure on MAFF about the supposed risk to humans from eating beef and beef products.
Infected animals who are incubating the disease but do not show any abnormalities cannot be detected at present and will be
entering the human food chain. The offal ban removes the highest 'risk' tissues. Some critics may not be satisfied by this.
However, others may argue the action to date is over the top, not demanded by the experts, and illogical since scrapie-infected
sheep can still be eaten and doing so for the last 200 years has not caused harm to humans. We expect BSE agent to be
resistant to irradiation as applied to food, as well as relatively resistant to cooking.

Other animals: There is no evidence that animals other than cattle (and domesticated, deer) have been or could be affected by
BSE, other than experimentally, but there are pressures to extend the ruminant protein ban: at present pigs and poultry receive
this sort of feed. Such action, as well as being hard to justify scientifically, would increase costs for the industry and cause
perhaps insurmountable problems for abattoirs, who would find renderers no longer willing to accept offal. Many 1000's of
tons of offal need to be disposed of daily.

Compensation: This has been set at 50% for BSE, although for some other diseases it is higher. Some critics believe this
encourages evasion, with cows affected minimally being sent for human consumption. Even the current level of compensation is
proving expensive for MAFF.

Exports: Some foreign countries have banned British exports of seman, embryos and livestock. The EC now no longer accepts
live cattle over 6 months of age. The Germans are creating difficulties over beef exports too. The EC are also considering
making BSE notifiable and banning ruminant protein feeding to rminants, as we have done here. At present, British meat and
bone meat can still be exported and might spread infection overseas (MAFF claim importers have been warned that it is not
regarded suitable for feeding to ruminants).

Human transmission: There are some in the media and even the medical profession who are trying to make connections
between BSE and the human disorder CJD. There is _no_ evidence of any association nor would we expect any cases by now
even were BSE to be transmissible to humans. Dr Wills' study (see 2i above) will monitor the situation for the next decade or

I have been asked to provide a draft reply to the attached letter from Sir Richard Southwood to the Minister. The Minister has
indicated that we must meet Sir Richard's points (a} on the need for him to be fully briefed as to developments and (b) on the
urgency of making progress with the transmission study.

On (a), I would suggest that the draft reply should indicate that you will be in touch with Sir Richard regularly to keep him in the
picture. On (b), I hope we can now tell Sir Richard that the arrangements for the purchase and relocation of the animals are
under way.

A R Cruickshank
20 June 1989
Mr A J Lawrence
cc Mr K C Meldrum
Dr W A Watson
Mr R C Lowson


and today we find that;

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

Detection and Localization of PrPSc in the Skeletal Muscle
Thu Mar 2, 2006 10:40

© 2006 American Society for Investigative Pathology

Detection and Localization of PrPSc in the Skeletal Muscle of Patients with Variant, Iatrogenic, and Sporadic Forms of Creutzfeldt-Jakob Disease
Alexander H. Peden, Diane L. Ritchie, Mark W. Head and James W. Ironside
From the National Creutzfeldt-Jakob Disease Surveillance Unit and Division of Pathology, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom

Variant Creutzfeldt-Jakob disease (vCJD) differs from other human prion diseases in that the pathogenic prion protein PrPSc can be detected to a greater extent at extraneuronal sites throughout the body, principally within lymphoid tissues. However, a recent study using a high-sensitivity Western blotting technique revealed low levels of PrPSc in skeletal muscle from a quarter of Swiss patients with sporadic CJD (sCJD). This posed the question of whether PrPSc in muscle could also be detected in vCJD, sCJD, and iatrogenic (iCJD) patients from other populations. Therefore, we have used the same high-sensitivity Western blotting technique, in combination with paraffin-embedded tissue blotting, to screen for PrPSc in muscle tissue specimens taken at autopsy from 49 CJD patients in the United Kingdom. These techniques identified muscle PrPSc in 8 of 17 vCJD, 7 of 26 sCJD, and 2 of 5 iCJD patients. Paraffin-embedded tissue blotting analysis showed PrPSc in skeletal muscle in localized anatomical structures that had the morphological and immunohistochemical characteristics of nerve fibers. The detection of PrPSc in muscle tissue from all forms of CJD indicates the possible presence of infectivity in these tissues, suggesting important implications for assessing the potential risk of iatrogenic spread via contaminated surgical instruments.


#################### ####################


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


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 controversies
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 9/13/2005

Page 10 of 17

BSE cattle may need to be reexamined.

T. Kitamoto (Ed.)
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. 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; Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: ================================= 9/13/2005
Page 11 of 17 From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640,
Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail:

Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold
Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the previous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated.

REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690.
Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J.
(1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501.
Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450.
Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK.
Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel
molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen,
October 8-10.
Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from
basic research to intervention concepts. Gasreig, Munhen, October 8-10.
Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE
prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366.


Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§ 1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA. *These authors contributed equally to this work. †Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA. ‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. §To whom correspondence should be addressed: E-mail: Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD. To test whether skeletal muscle of diseased cervids.........SNIP....END


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