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Do you STILL feel safe?

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Mike

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From the U.S. Food and Drug (FDA) website:

An Evaluation of the Risk of Variant Creutzfeldt-Jakob Disease from Exposure to Cattle-Derived Protein Used in Cosmetics
Introduction

The discovery of a cow with bovine spongiform encephalopathy (BSE) in Washington State in December 2003 triggered action to put in place additional safeguards against BSE. Even though the cow was born in Canada, the fact that the cow was discovered in the U.S. and had been sent to slaughter and rendering before it was identified as positive indicates a vulnerability in the U.S. BSE protective net.

While BSE is usually identified with either food safety or animal health, cosmetics, because of the ways they are used, provide another route for BSE infectivity to enter the human system. Cosmetics may contain a wide range of cattle-derived ingredients, many of which may carry the BSE agent. FDA prepared this assessment of the risks to public health if cattle-derived ingredients are used in cosmetics.

This qualitative risk assessment follows the generally accepted framework for risk assessments endorsed by the Codex Alimentarious Commission, the U.S. National Academy of Sciences, and other authoritative bodies. The framework divides risk assessment into four components: (1) hazard identification, (2) exposure assessment, (3) hazard characterization (or dose-response assessment), and (4) risk characterization. The risk assessment uses scientific evidence to the extent that it exists. The agency has determined that this qualitative risk assessment is appropriate to the circumstances.
Risk Assessment
Hazard Identification

In April 1996, British scientists reported a previously undetected new variant of Creutzfeldt-Jakob disease (vCJD) in young patients, with symptoms somewhat different from sporadic CJD (Refs. 1 and 2). All cases of vCJD had histopathologic evidence of spongiform changes in the brain, but also showed formation of "florid" plaques (a core of amyloid protein with surrounding halos of vacuoles) not typically seen in other forms of CJD (Ref. 3). Clinically, vCJD usually begins with a psychiatric presentation, such as depression, anxiety, nightmares or hallucinations. These symptoms are followed by memory impairment, then dementia in the late stages. The clinical course may last up to two years before death occurs (Ref. 4). Because scientific evidence suggests that the presence and infectivity of abnormal prion proteins in vCJD share characteristics with abnormal prion proteins found in cattle with BSE, scientists have concluded that exposure to the BSE agent is the most plausible explanation for the occurrence of vCJD (Refs. 5 - 8). Monkeys (genetically the closest animal model to humans) inoculated with samples of brain from BSE-infected cattle have been found to develop a TSE that is histopathologically similar to vCJD (Ref. 9), as have mice inoculated or fed with BSE-infected tissue (Ref. 10). In addition, studies have shown that abnormal prion proteins from vCJD patients are molecularly similar to abnormal prion proteins from BSE-infected cattle and different from abnormal prion proteins from patients with CJD and other spongiform encephalopathies (Ref. 4).

Prions are predominantly found in the central nervous system, portions of the intestine, and tonsils of cattle with BSE. Cosmetic ingredients can be derived from some of these tissues. Although large prion doses are known to have a shorter incubation period before the disease develops, even low doses may cause vCJD if infectious prions survive digestion and the host survives long enough to complete a longer incubation period. Although most scientists believe that vCJD in humans is caused by consumption of cattle-derived food products contaminated with the agent that causes BSE (Refs. 11-14), exposure from cosmetics derived from cattle protein is another potential route of exposure.
Exposure Assessment

BSE in the United States
On December 23, 2003, USDA diagnosed a positive case of BSE in an adult Holstein cow in the State of Washington.

Use of Cattle Protein in Cosmetics
Cosmetics may be made from a variety of cattle-derived ingredients. These ingredients include albumin, brain extract, brain lipid, cholesterol, fibronectin, sphingolipids, collagen, keratin, and tallow and tallow derivatives. However, tallow derivatives, particularly fatty acids and glycerin, are the predominant bovine ingredient used by the cosmetic industry and contain very little protein, and are therefore unlikely vehicles for the transmission of prions. Cattle-derived ingredients serve many functions and may be used as skin conditioning agents, emollients, binders, and hair and nail conditioning agents.

Absorption of Prions from Cosmetics
There are several routes through which cosmetics contaminated with the agent that causes BSE could transmit disease to humans. Transmission of the BSE agent to humans through intact skin is believed to be unlikely; however, cosmetics may be ingested or applied to cut or abraded skin or to conjunctival tissues that can provide direct routes for infection.

It is well-documented that central nervous system tissue, including the optic nerve, carries infectivity in animals with TSEs and humans with vCJD, and serves as an efficient route of transmission. In mice, intraocular injection of scrapie caused infection along the optic nerve, which eventually spread into non-neural tissue via the lymphatic system (Ref. 15). In addition to intraocular injection, infectivity has been transmitted to animals via the conjunctiva of the eye (mucosal tissue). Scott et al. (Ref. 16) found that scrapie was induced in 42 percent of rodents by dropping a high concentration of infectivity onto the conjunctiva. Klitzman et al. (Ref. 17) suggested that kuru, a human TSE disease found only among the Fore people of New Guinea, might have been transmitted by rubbing infected human brain into eyes or cut skin, while handling and consuming infected brain during funeral rituals.

Cut or abraded skin also has been proposed as a route for contracting TSE diseases. The transmission of kuru through cut skin has been suggested and was mentioned previously. Taylor et al. (Ref. 18) and Ingrosso et al. (Ref. 19) demonstrated increased transmission of scrapie via oral mucosal tissue. In one study, 100 percent of mice with experimentally damaged oral mucosal tissue developed scrapie through ingestion of infected material, while only 71 percent of mice with intact mucosa developed the disease (Ref. 18). In addition, Pammer et al. (Ref. 20) and Sugaya et al. (Ref. 21) noted that epithelial cells, dendritic cells, and keratinocytes (the primary cell types found in the epidermis) have been found to contain infectious prion protein, indicating that these cells are potential targets for peripheral infection with a TSE disease.

Use of BSE-contaminated cosmetics could provide a means of human infection via several routes discussed above. Many cosmetics are typically applied in the area of the eye (mascara, eye brow pencil, eyeliner, eye lotion, and eye makeup remover) and almost any cosmetic, including shampoo, can get into the eye via eye rubbing or incorrect application. Any cosmetic product, but particularly shaving creams and gels and lotions, may be applied to cut or abraded skin. Cosmetics that are ingested, such as lipstick, dentifrices, mouthwash, and breath fresheners, would have an oral route of infection, and the ingested fraction would have the same risk as prion-contaminated meat and other food products derived form cattle. Furthermore, the presence of cattle derived ingredients is not generally obvious to the consumer, since the source of the ingredient (i.e. cattle derived) does not need to be placed on the label.
Hazard Characterization

Prions with a particular abnormal tertiary structure are apparently able to generate a similar misconformation in normal proteins, which can in turn cause further misconformations. This allows propagation of the disease and is also important for understanding the relationship between dose, response, and the incubation required for the disease to develop. Once the prions have entered the brain, the prion concentration grows with a relationship that has been described as exponential (Ref. 14).

In cattle, there is a minimal incubation period of six months to a year required for the development of the disease, regardless of the size of the initial dose, although incubation periods of 4 or more years appear to be more common (Refs. 11 and 12). The lag period may reflect the fact that transmission from food to brain may be preceded by symptomless amplification of infectious prions in the intestine and lymphoreticular tissues. While cattle at this stage would be clinically normal and may have negative BSE test results, various tissues could be infectious (Refs. 11 and 12).

Despite widespread exposure in the U.K. to BSE-contaminated meat products, only a very small percentage of the exposed population has been diagnosed with vCJD to date. However, ongoing experiments indicate that the infectious dose for cattle is very low. One gram of affected bovine brain homogenate is sufficient to cause BSE in more than 50 percent of calves exposed by mouth. Five years after oral consumption of lower doses of brain material, 2 of 15 calves fed 0.1 gram had onset of BSE, and 1 of 15 fed 0.01 gram had developed the disease. This experiment is ongoing (Ref. 22). There is thought to be a 10- to 10,000-fold increase in the amount of infectious material needed to cause illness in humans as compared with cattle, because of the species barrier (Ref. 23).
Risk Characterization

This is not a quantitative risk assessment. However, it does sketch out the logical structure that a quantitative model could use if one were constructed. Some conclusions can be drawn without a quantitative analysis. Since there is considerable uncertainty associated with the premises outlined in the present analysis, it follows that there will also be considerable uncertainty associated with the risk estimate. In the exposure assessment, there are considerable uncertainties associated with the origin of protein used in making cosmetics, the effect of processing on prion concentration, and the transmission rates for dermal and ocular exposure. Particularly large uncertainties associated with the dose response assessment include the magnitude of the species barrier and the length of the incubation period.

With exception of the uncertainty associated with estimates of the dermal and ocular transmission rates, most of the uncertainties associated with a risk assessment of BSE prions in cosmetics are also associated with the risk from food consumption. For example, the number of BSE-affected cattle and the variability in human susceptibility will impact the risk of both food- and cosmetic-associated vCJD.

Some of these uncertainties may concomitantly affect both sides of a cost-benefit analysis. In particular, if there is not substantial use of cattle-derived protein in making cosmetics, then there will be little exposure, and also little economic consequence from regulating use. Conversely, high use would require substantial substitution and alternative means of animal-by-product disposal.
Conclusions

A form of spongiform encephalopathy that occurs in humans (vCJD) is thought to result from the same protein (a prion) that causes BSE in cattle. Although the primary source of exposure is likely to be due to the ingestion of beef and other food derived from cattle, other routes of exposure may also be important. Although small doses require longer incubation periods for clinical signs to develop, small doses of infectious prions can potentially cause disease. Cosmetics that contain protein derived from bovine sources are a potential source of exposure. It has been demonstrated experimentally that TSEs may result from ocular absorption of protein, and systemic absorption of protein may also occur when cosmetics are applied to lacerated or abraded skin. As a result, it may be concluded that there is some risk of occurrence of vCJD from the use of cattle-derived protein in cosmetics. However, since there are large uncertainties associated with the quantitative estimates of many of the important variables, any quantitative estimate of the risk or rate at which the disease may be expected to occur would be correspondingly imprecise.

The risk of BSE from cosmetics may be reduced through the control of exposure. Aside from the derivation processes used on tallow, the effectiveness of cosmetic manufacturing processes for inactivating BSE prions is unknown. The surest way to prevent transmission of BSE-prion through cosmetics is to avoid the use of high-risk cattle-derived protein in the manufacture of cosmetics.
 

Mike

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My lawyer was trying to convince me to take supplements comprised of bovine colostrum -

Think your lawyer might have been building a class action case for him to take to trial? :wink:
 

Mike

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Looks like the FDA is more worried about Cosmetic By Products than they are Food Products:

TYPE OF ALERT: DETENTION WITHOUT PHYSICAL EXAMINATION

(NOTE: This import Alert contains guidance to FDA field
personnel only. It does not establish any requirements, or
create any rights or obligations on FDA or on regulated
entities.)

PRODUCT: Bulk shipments of high-risk bovine tissues and
tissue-derived ingredients (see Attachment A for a list of
affected products).

PRODUCT CODE: 17Y--99, meat and meat products, N.E.C.
53P--01, Bovine (bovine amniotic fluid), cosmetic raw
materials. (Review of EEPS entry data indicates that this
code may also be used for bovine placenta)
53P--02, Collagen, cosmetic raw materials
54G--01, Bovine, animal byproducts/extracts
54G--99, Animal byproducts/extracts, N.E.C.

PROBLEM: POISONOUS/DELETERIOUS SUBSTANCE - N.E.C. (PSNC)

OASIS CHARGE
CODES: DIET INGRE; INGRED FIL; COSMETIC; BSE FILTH; INSAN BSE.

PAC: 03819C for product codes 17Y--99, 54G--01,
54G--99
29002 for product codes 53P--01, 53P--02

PAF: MIC (microbiological hazards)

COUNTRIES: ALBANIA (AL), ANDORRA (AD), AUSTRIA (AT), BELGIUM (BE),
BOSNIA-HERZEGOVINA (BA), BULGARIA (BG), CANADA (CA), CROATIA
(HR), the CZECH REPUBLIC (CS), DENMARK (DK), the FEDERAL
REPUBLIC OF YUGOSLAVIA (YU), FINLAND (FI), FRANCE (FR),
GERMANY (DE), GREECE (GR), HUNGARY (HU), IRELAND, REPUBLIC
of (IE), ISRAEL (IL), ITALY (IT), JAPAN (JP), LEICHSTENSTEIN
(LI), LUXEMBOURG (LU), the former YUGOSLAV REPUBLIC OF
MACEDONIA (MK), MONACO (MC), NETHERLANDS (NL), NORWAY (NO),
OMAN (OM), POLAND (PL), PORTUGAL (PT), ROMANIA (RO), SAN
MARINO (SM), the SLOVAK REPUBLIC (SLOVAKIA) (SK), SLOVENIA
(SI), SPAIN (ES), SWEDEN (SE), SWITZERLAND (CH) UNITED
KINGDOM (Great Britain & Northern Ireland, and Falkland
Islands) (GB)

NOTE: The United States Department of Agriculture issued an
interim rule on January 6, 1998. The interim rule restricts
the importation of ruminants, meat and meat products from
ruminants, and certain ruminant products and byproducts not
only from countries and other regions in which BSE is known
to exist, but also from countries and other regions which,
because of import requirements less restrictive than those
that would be acceptable for import into the United States
and/or because of inadequate surveillance, present a
significant risk. Countries listed above are BSE affected
countries and/or have less restrictive import requirements
than those that would be acceptable in the U.S. The list of
countries may change and the Import Alert will be revised
accordingly.

MANUFACTURER/
SHIPPER: All, from the designated countries
 

TimH

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Mike said:
From the U.S. Food and Drug (FDA) website:

An Evaluation of the Risk of Variant Creutzfeldt-Jakob Disease from Exposure to Cattle-Derived Protein Used in Cosmetics
Introduction

The discovery of a cow with bovine spongiform encephalopathy (BSE) in Washington State in December 2003 triggered action to put in place additional safeguards against BSE. Even though the cow was born in Canada, the fact that the cow was discovered in the U.S. and had been sent to slaughter and rendering before it was identified as positive indicates a vulnerability in the U.S. BSE protective net.

While BSE is usually identified with either food safety or animal health, cosmetics, because of the ways they are used, provide another route for BSE infectivity to enter the human system. Cosmetics may contain a wide range of cattle-derived ingredients, many of which may carry the BSE agent. FDA prepared this assessment of the risks to public health if cattle-derived ingredients are used in cosmetics.

This qualitative risk assessment follows the generally accepted framework for risk assessments endorsed by the Codex Alimentarious Commission, the U.S. National Academy of Sciences, and other authoritative bodies. The framework divides risk assessment into four components: (1) hazard identification, (2) exposure assessment, (3) hazard characterization (or dose-response assessment), and (4) risk characterization. The risk assessment uses scientific evidence to the extent that it exists. The agency has determined that this qualitative risk assessment is appropriate to the circumstances.
Risk Assessment
Hazard Identification

In April 1996, British scientists reported a previously undetected new variant of Creutzfeldt-Jakob disease (vCJD) in young patients, with symptoms somewhat different from sporadic CJD (Refs. 1 and 2). All cases of vCJD had histopathologic evidence of spongiform changes in the brain, but also showed formation of "florid" plaques (a core of amyloid protein with surrounding halos of vacuoles) not typically seen in other forms of CJD (Ref. 3). Clinically, vCJD usually begins with a psychiatric presentation, such as depression, anxiety, nightmares or hallucinations. These symptoms are followed by memory impairment, then dementia in the late stages. The clinical course may last up to two years before death occurs (Ref. 4). Because scientific evidence suggests that the presence and infectivity of abnormal prion proteins in vCJD share characteristics with abnormal prion proteins found in cattle with BSE, scientists have concluded that exposure to the BSE agent is the most plausible explanation for the occurrence of vCJD (Refs. 5 - 8). Monkeys (genetically the closest animal model to humans) inoculated with samples of brain from BSE-infected cattle have been found to develop a TSE that is histopathologically similar to vCJD (Ref. 9), as have mice inoculated or fed with BSE-infected tissue (Ref. 10). In addition, studies have shown that abnormal prion proteins from vCJD patients are molecularly similar to abnormal prion proteins from BSE-infected cattle and different from abnormal prion proteins from patients with CJD and other spongiform encephalopathies (Ref. 4).

Prions are predominantly found in the central nervous system, portions of the intestine, and tonsils of cattle with BSE. Cosmetic ingredients can be derived from some of these tissues. Although large prion doses are known to have a shorter incubation period before the disease develops, even low doses may cause vCJD if infectious prions survive digestion and the host survives long enough to complete a longer incubation period. Although most scientists believe that vCJD in humans is caused by consumption of cattle-derived food products contaminated with the agent that causes BSE (Refs. 11-14), exposure from cosmetics derived from cattle protein is another potential route of exposure.
Exposure Assessment

BSE in the United States
On December 23, 2003, USDA diagnosed a positive case of BSE in an adult Holstein cow in the State of Washington.

Use of Cattle Protein in Cosmetics
Cosmetics may be made from a variety of cattle-derived ingredients. These ingredients include albumin, brain extract, brain lipid, cholesterol, fibronectin, sphingolipids, collagen, keratin, and tallow and tallow derivatives. However, tallow derivatives, particularly fatty acids and glycerin, are the predominant bovine ingredient used by the cosmetic industry and contain very little protein, and are therefore unlikely vehicles for the transmission of prions. Cattle-derived ingredients serve many functions and may be used as skin conditioning agents, emollients, binders, and hair and nail conditioning agents.

Absorption of Prions from Cosmetics
There are several routes through which cosmetics contaminated with the agent that causes BSE could transmit disease to humans. Transmission of the BSE agent to humans through intact skin is believed to be unlikely; however, cosmetics may be ingested or applied to cut or abraded skin or to conjunctival tissues that can provide direct routes for infection.

It is well-documented that central nervous system tissue, including the optic nerve, carries infectivity in animals with TSEs and humans with vCJD, and serves as an efficient route of transmission. In mice, intraocular injection of scrapie caused infection along the optic nerve, which eventually spread into non-neural tissue via the lymphatic system (Ref. 15). In addition to intraocular injection, infectivity has been transmitted to animals via the conjunctiva of the eye (mucosal tissue). Scott et al. (Ref. 16) found that scrapie was induced in 42 percent of rodents by dropping a high concentration of infectivity onto the conjunctiva. Klitzman et al. (Ref. 17) suggested that kuru, a human TSE disease found only among the Fore people of New Guinea, might have been transmitted by rubbing infected human brain into eyes or cut skin, while handling and consuming infected brain during funeral rituals.

Cut or abraded skin also has been proposed as a route for contracting TSE diseases. The transmission of kuru through cut skin has been suggested and was mentioned previously. Taylor et al. (Ref. 18) and Ingrosso et al. (Ref. 19) demonstrated increased transmission of scrapie via oral mucosal tissue. In one study, 100 percent of mice with experimentally damaged oral mucosal tissue developed scrapie through ingestion of infected material, while only 71 percent of mice with intact mucosa developed the disease (Ref. 18). In addition, Pammer et al. (Ref. 20) and Sugaya et al. (Ref. 21) noted that epithelial cells, dendritic cells, and keratinocytes (the primary cell types found in the epidermis) have been found to contain infectious prion protein, indicating that these cells are potential targets for peripheral infection with a TSE disease.

Use of BSE-contaminated cosmetics could provide a means of human infection via several routes discussed above. Many cosmetics are typically applied in the area of the eye (mascara, eye brow pencil, eyeliner, eye lotion, and eye makeup remover) and almost any cosmetic, including shampoo, can get into the eye via eye rubbing or incorrect application. Any cosmetic product, but particularly shaving creams and gels and lotions, may be applied to cut or abraded skin. Cosmetics that are ingested, such as lipstick, dentifrices, mouthwash, and breath fresheners, would have an oral route of infection, and the ingested fraction would have the same risk as prion-contaminated meat and other food products derived form cattle. Furthermore, the presence of cattle derived ingredients is not generally obvious to the consumer, since the source of the ingredient (i.e. cattle derived) does not need to be placed on the label.
Hazard Characterization

Prions with a particular abnormal tertiary structure are apparently able to generate a similar misconformation in normal proteins, which can in turn cause further misconformations. This allows propagation of the disease and is also important for understanding the relationship between dose, response, and the incubation required for the disease to develop. Once the prions have entered the brain, the prion concentration grows with a relationship that has been described as exponential (Ref. 14).

In cattle, there is a minimal incubation period of six months to a year required for the development of the disease, regardless of the size of the initial dose, although incubation periods of 4 or more years appear to be more common (Refs. 11 and 12). The lag period may reflect the fact that transmission from food to brain may be preceded by symptomless amplification of infectious prions in the intestine and lymphoreticular tissues. While cattle at this stage would be clinically normal and may have negative BSE test results, various tissues could be infectious (Refs. 11 and 12). This is exactly why SRM removal,not testing, insures food safety!!Despite widespread exposure in the U.K. to BSE-contaminated meat products, only a very small percentage of the exposed population has been diagnosed with vCJD to date. However, ongoing experiments indicate that the infectious dose for cattle is very low. One gram of affected bovine brain homogenate is sufficient to cause BSE in more than 50 percent of calves exposed by mouth. Five years after oral consumption of lower doses of brain material, 2 of 15 calves fed 0.1 gram had onset of BSE, and 1 of 15 fed 0.01 gram had developed the disease. This experiment is ongoing (Ref. 22). There is thought to be a 10- to 10,000-fold increase in the amount of infectious material needed to cause illness in humans as compared with cattle, because of the species barrier (Ref. 23).
Risk Characterization

This is not a quantitative risk assessment. However, it does sketch out the logical structure that a quantitative model could use if one were constructed. Some conclusions can be drawn without a quantitative analysis. Since there is considerable uncertainty associated with the premises outlined in the present analysis, it follows that there will also be considerable uncertainty associated with the risk estimate. In the exposure assessment, there are considerable uncertainties associated with the origin of protein used in making cosmetics, the effect of processing on prion concentration, and the transmission rates for dermal and ocular exposure. Particularly large uncertainties associated with the dose response assessment include the magnitude of the species barrier and the length of the incubation period.
With exception of the uncertainty associated with estimates of the dermal and ocular transmission rates, most of the uncertainties associated with a risk assessment of BSE prions in cosmetics are also associated with the risk from food consumption. For example, the number of BSE-affected cattle and the variability in human susceptibility will impact the risk of both food- and cosmetic-associated vCJD.

Some of these uncertainties may concomitantly affect both sides of a cost-benefit analysis. In particular, if there is not substantial use of cattle-derived protein in making cosmetics, then there will be little exposure, and also little economic consequence from regulating use. Conversely, high use would require substantial substitution and alternative means of animal-by-product disposal.
Conclusions

A form of spongiform encephalopathy that occurs in humans (vCJD) is thought to result from the same protein (a prion) that causes BSE in cattle. Although the primary source of exposure is likely to be due to the ingestion of beef and other food derived from cattle, other routes of exposure may also be important. Although small doses require longer incubation periods for clinical signs to develop, small doses of infectious prions can potentially cause disease. Cosmetics that contain protein derived from bovine sources are a potential source of exposure. It has been demonstrated experimentally that TSEs may result from ocular absorption of protein, and systemic absorption of protein may also occur when cosmetics are applied to lacerated or abraded skin. As a result, it may be concluded that there is some risk of occurrence of vCJD from the use of cattle-derived protein in cosmetics. However, since there are large uncertainties associated with the quantitative estimates of many of the important variables, any quantitative estimate of the risk or rate at which the disease may be expected to occur would be correspondingly imprecise.

The risk of BSE from cosmetics may be reduced through the control of exposure. Aside from the derivation processes used on tallow, the effectiveness of cosmetic manufacturing processes for inactivating BSE prions is unknown. The surest way to prevent transmission of BSE-prion through cosmetics is to avoid the use of high-risk cattle-derived protein in the manufacture of cosmetics.

If there is any definite scientific evidence, presented in this article,which shows that vCJD in humans is ,without a doubt, caused by beef consumption, I must have missed it.
Perhaps Mike or R2 would be kind enough to point it out for those of us with such piss-poor reading comprehension. :roll: :roll: :roll:
 

Mike

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One gram of affected bovine brain homogenate is sufficient to cause BSE in more than 50 percent of calves exposed by mouth. Five years after oral consumption of lower doses of brain material, 2 of 15 calves fed 0.1 gram had onset of BSE, and 1 of 15 fed 0.01 gram had developed the disease. This experiment is ongoing (Ref. 22). There is thought to be a 10- to 10,000-fold increase in the amount of infectious material needed to cause illness in humans as compared with cattle, because of the species barrier

Poor Tim, I hate to let you in on a secret but the only things that are

"WITHOUT A DOUBT" are Death and Taxes.

Do you not think it kind of strange that the FDA warns us about cosmetics (of all things) and the potential for BSE, and the USDA on the other hand assures us that beef in the U.S. is positively safe? Don't you get it? The Japs do!
 

TimH

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Mike- "Poor Tim, I hate to let you in on a secret but the only things that are

"WITHOUT A DOUBT" are Death and Taxes.

Do you not think it kind of strange that the FDA warns us about cosmetics (of all things) and the potential for BSE, and the USDA on the other hand assures us that beef in the U.S. is positively safe? Don't you get it? The Japs do!"

Poor Tim???? :???:(thinly disguised personal attack) Ya Ok. :roll: Why don't you just go ahead and point out the scientific evidence which shows that vCJD is definitely caused by consuming beef........I'll wait.......
:roll: :roll: :roll: :roll: :roll: :roll: :roll: :roll: :roll: :roll: :roll:
 

Bill

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In answer to the original question of this thread, YES I still feel safe. Death and taxes may be the only certainty to life but I also know that I have a far greater chance of leaving this world due to a multitude of other illnesses, diseases, accidents or risks from other lifestyle choices than from eating healthy nutritious and satisfying North American BEEF! :wink:
 

TimH

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While I'm waiting...... Let's do some math....

One gram of affected bovine brain homogenate is sufficient to cause BSE in more than 50 percent of calves exposed by mouth. Five years after oral consumption of lower doses of brain material, 2 of 15 calves fed 0.1 gram had onset of BSE, and 1 of 15 fed 0.01 gram had developed the disease. This experiment is ongoing (Ref. 22). There is thought to be a 10- to 10,000-fold increase in the amount of infectious material needed to cause illness in humans as compared with cattle, because of the species

Since when does 3 out of 15 add up to 50%????
Post the rest of the article Mike so we can see exactly what "(Ref. 22)" is.

"There is thought to be a 10- to 10,000-fold increase in the amount of infectious material needed to cause illness in humans as compared with cattle, because of the species "

Thought to be ??? Now that is some scientific language!!!
If you do the math on that one, even if it was proven that vCJD is caused by eating beef, a person would have to eat somwehere between, approximately, in the neighborhood of, 1 ounce to 22 pounds of SRM(or thereabouts or somewhere in that vicinity, more or less, possibly).

Interesting also that Mike neglected to copy and paste this portion of the article.......

Despite widespread exposure in the U.K. to BSE-contaminated meat products, only a very small percentage of the exposed population has been diagnosed with vCJD to date

Hmmmmmm??????? :roll: :roll: :roll:
 

Big Muddy rancher

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reader (the Second) said:
Bill said:
In answer to the original question of this thread, YES I still feel safe. Death and taxes may be the only certainty to life but I also know that I have a far greater chance of leaving this world due to a multitude of other illnesses, diseases, accidents or risks from other lifestyle choices than from eating healthy nutritious and satisfying North American BEEF! :wink:

Well as the wife of someone who died from a supposedly RARE disease and who now knows many families who have lost someone to this disease, I would not be so glib about BSE. I was talking to someone today whose mother -- a surgical nurse -- died from CJD. I met the wife of a funeral director who died of CJD. My husband was infected via neurosurgery most likely. I know families who have lost someone to vCJD as well. When you're the person or the family member of the person who is the "rare" case, it brings it home to you that an always fatal, untreatable disease being rare is only a consolation if you're not the one affected. I have met and heard about too many people with CJD and seen too many cases in the media of countries now popping up with 26 year olds dying of vCJD to be so sanguine.

Believe me, you can feel safe and 10 or 20 years from now regret in hindsight what precautions you could have taken or supported today. Been there.

Altho I have sympathy for you reader can you tell us how these people contracted CJD and vCJD?
 

Big Muddy rancher

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So eating BEEF is probably safer then walking in Central Park. That's ggod enough for me. I can see avoiding the SRM type meat but even lightening stikes somewhere.
 

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Tim, You can find the entire article of which I posted part of on the FDA website. It is a VERY long article. www.FDA.gov

The reason I posted it was not to persuade the transmission of BSE. I know your stance on BSE and you know mine. Arguing those points would be completely redundant.

It was simply the irony of two separate U.S. Regulatory Agencies telling us almost two entirely different scenarios concerning BSE.

The USDA tells us that beef is completely safe to eat and the FDA warns us that cosmetics contain beef products and may not be safe.
:???:

Do you understand? 8)
 

Big Muddy rancher

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Mike said:
Tim, You can find the entire article of which I posted part of on the FDA website. It is a VERY long article. www.FDA.gov

The reason I posted it was not to persuade the transmission of BSE. I know your stance on BSE and you know mine. Arguing those points would be completely redundant.

It was simply the irony of two separate U.S. Regulatory Agencies telling us almost two entirely different scenarios concerning BSE.

The USDA tells us that beef is completely safe to eat and the FDA warns us that cosmetics contain beef products and may not be safe.
:???:

Do you understand? 8)


Tim is Mike telling you to becareful when putting on your Lipstick? :wink:
 

Bill

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reader (the Second) said:
Bill said:
In answer to the original question of this thread, YES I still feel safe. Death and taxes may be the only certainty to life but I also know that I have a far greater chance of leaving this world due to a multitude of other illnesses, diseases, accidents or risks from other lifestyle choices than from eating healthy nutritious and satisfying North American BEEF! :wink:

Well as the wife of someone who died from a supposedly RARE disease and who now knows many families who have lost someone to this disease, I would not be so glib about BSE. I was talking to someone today whose mother -- a surgical nurse -- died from CJD. I met the wife of a funeral director who died of CJD. My husband was infected via neurosurgery most likely. I know families who have lost someone to vCJD as well. When you're the person or the family member of the person who is the "rare" case, it brings it home to you that an always fatal, untreatable disease being rare is only a consolation if you're not the one affected. I have met and heard about too many people with CJD and seen too many cases in the media of countries now popping up with 26 year olds dying of vCJD to be so sanguine.

Believe me, you can feel safe and 10 or 20 years from now regret in hindsight what precautions you could have taken or supported today. Been there.
This is Ranchers.Net so try to understand if once in a while some of us try to remain positive despite the countless allegations and claims against the safety of the product we produce. As a beef producer I believe the product I raise is safe so excuse me if I don't readily believe every theory or allegation made against our industry. We all feel badly for the loss of your husband, you have mentioned it several times as you continue to promote the link between BSE, vCJD and CJD, but until some one proves that link I will remain skeptical.

A question for you R2 as you seem convinced that organic beef is safer. It has been suggested that prions may be carried in the blood and urine of animals, why is is "Grassfed" or "Organic" beef safer which has been raised on pasture possibly contaminated by urine from wild animals such as deer and elk. Also are those fruits and vegetables you eat perfectly safe or did a deer stop for take a whiz while crossing the field?
 

TimH

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Mike said:
Tim, You can find the entire article of which I posted part of on the FDA website. It is a VERY long article. www.FDA.gov

The reason I posted it was not to persuade the transmission of BSE. I know your stance on BSE and you know mine. Arguing those points would be completely redundant.

It was simply the irony of two separate U.S. Regulatory Agencies telling us almost two entirely different scenarios concerning BSE.

The USDA tells us that beef is completely safe to eat and the FDA warns us that cosmetics contain beef products and may not be safe.
:???:

Do you understand? 8)

And I'm only trying to point out the fact that the supposed "link" between BSE and vCJD is only a theory. And ,in my opinion, a very weak theory. Do you understand? :)
As far as the "irony" in what FDA and USDA is saying.......
SRM's are removed from the food chain , insuring food safety, and USDA informs the consumer of this fact,as is their job.
Some cosmetics "may contain" SRM material, which COULD pose some risk. FDA is informing consumers of this theoretical risk, as is their job.
Sorry Mike, but I'm not seein' the irony !!! :)
 

Bill

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reader (the Second) said:
Bill said:
In answer to the original question of this thread, YES I still feel safe. Death and taxes may be the only certainty to life but I also know that I have a far greater chance of leaving this world due to a multitude of other illnesses, diseases, accidents or risks from other lifestyle choices than from eating healthy nutritious and satisfying North American BEEF! :wink:

Well as the wife of someone who died from a supposedly RARE disease and who now knows many families who have lost someone to this disease, I would not be so glib about BSE. I was talking to someone today whose mother -- a surgical nurse -- died from CJD. I met the wife of a funeral director who died of CJD. My husband was infected via neurosurgery most likely. I know families who have lost someone to vCJD as well. When you're the person or the family member of the person who is the "rare" case, it brings it home to you that an always fatal, untreatable disease being rare is only a consolation if you're not the one affected. I have met and heard about too many people with CJD and seen too many cases in the media of countries now popping up with 26 year olds dying of vCJD to be so sanguine.

Believe me, you can feel safe and 10 or 20 years from now regret in hindsight what precautions you could have taken or supported today. Been there.
Reader2 I see your post as more than a casual link though it may not be intended as such. In regards to your reference to Secretary Chertoff's comment, is Homeland Security the go to agency ahead of USDA? Just make sure you wash all your lettuce, caulilower and strawberries well in case there is any deer excrement or ecoli on it. :wink:
 

mrj

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Mike said:
Tim, You can find the entire article of which I posted part of on the FDA website. It is a VERY long article. www.FDA.gov

The reason I posted it was not to persuade the transmission of BSE. I know your stance on BSE and you know mine. Arguing those points would be completely redundant.

It was simply the irony of two separate U.S. Regulatory Agencies telling us almost two entirely different scenarios concerning BSE.

The USDA tells us that beef is completely safe to eat and the FDA warns us that cosmetics contain beef products and may not be safe.
:???:

Do you understand? 8)

Mike, even when I factor in your ASSUMPTION that I have a reading comprehension problem unrelated to my desperate lack of time and tendency to at times only quickly scan some material presented here, I can see that the FDA mentioned the fact that cosmetics may contain brain material. Isn't it entirely logical that because brain material is removed as SRM from the approved for FOOD parts of the bovine animal, BEEF with the SRM's removed can be considered as BSE free, while some cosmetics might not be? And, yes, I'm ASSUMING (as in taken to be a fact) that there are some countries that do not require brain destruction. Also ASSUMING there are some countries other than the USA from which cosmetics may be imported.

MRJ
 

TimH

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Big Muddy rancher said:
Mike said:
Tim, You can find the entire article of which I posted part of on the FDA website. It is a VERY long article. www.FDA.gov

The reason I posted it was not to persuade the transmission of BSE. I know your stance on BSE and you know mine. Arguing those points would be completely redundant.

It was simply the irony of two separate U.S. Regulatory Agencies telling us almost two entirely different scenarios concerning BSE.

The USDA tells us that beef is completely safe to eat and the FDA warns us that cosmetics contain beef products and may not be safe.
:???:

Do you understand? 8)


Tim is Mike telling you to becareful when putting on your Lipstick? :wink:

You nearly sneaked this one past me BMR!!
I'm don't know exactly what Mike is trying to tell me but I'm pretty sure that if I ever need any tips on makeup application, Mike is probably the wrong person to ask. And besides, I was careful about how and when I put on my lipstick long before BSE was an issue! (smarta$$) :lol: :lol: :wink:
 

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-------- Original Message --------
Subject:
Docket No. 2004N-0081 and or RIN number RIN-0910-AF47 Use of Materials Derived
From Cattle in Human Food and Cosmetics [comment submission]
Date: Tue, 13 Jul 2004 16:08:38 -0500
From: "Terry S. Singeltary Sr."
To: [email protected]
CC: [email protected], [email protected]

COMMENT SUBMISSION
[Docket No. 2004N-O081]
RIN-0910--AF47
Use of Materials Derived From Cattle in Human Food and Cosmetics
http://www.fda.gov/OHRMS/DOCKETS/98fr/04n-0081-nir0001.pdf

Greetings FDA,

I would kindly like to comment on the potential for TSE transmission from
cosmetics to humans and why I think that ALL animal by-products should be
excluded from cosmetics. IF we look at the TSE 'KURU'. Kuru is a
transmissible spongiform encephalopathy that was identified in Papua New
Guinea in the late 1950s. Several thousand cases of the disease occurred
during a period of several decades. Epidemiologic investigations
implicated ritual endocannibalistic funeral feasts as the likely route
through which the infectious agent was spread. The incubation period in
females was estimated to be shorter than that in males. The shortest
incubation periods were estimated in adult women, who may have been
exposed to the largest doses of infectious material.
MY question is, was the woman exposed to larger doses, are was it the
route of the
agent that may have been the factor of shorter incubation in woman, or both?

What is Kuru?
Kuru is a rare and fatal brain disorder that occurred at epidemic levels
during the 1950s-60s among the Fore people in the highlands of New
Guinea. The disease was the result of the practice of ritualistic
cannibalism among the Fore, in which relatives prepared and consumed the
tissues (including brain) of deceased family members. Brain tissue from
individuals with kuru was highly infectious, and the disease was
transmitted either through eating or by contact with open sores or
wounds. Government discouragement of the practice of cannibalism led to
a continuing decline in the disease, which has now mostly disappeared.

snip...

PLEASE NOTE the later ''or by contact with open sores or wounds.''

> and the disease was transmitted either through eating or by contact
> with open sores or wounds.


http://www.ninds.nih.gov/health_and_medical/disorders/kuru.htm

> the Fore women would scoop the brains of their dead relatives out of
> their skulls by hand before cooking. They then wiped the residual
> liquid and cadaver tissue over their paint-daubed bodies, leaving it
> caked in their hair and on their bodies for weeks after a mortuary feast.


Jennifer Cooke: kuru deaths continue in 1999

Sydney Morning Herald, Saturday, August 28, 1999


TSE INFECTION does takes place when the skin surface has been broken by
scarification (Taylor et al, 1996).

The transmission of KURU into animals supported the belief that the
disease had
been transmitted through ceremonial cannibalistic rituals in New Guinea
with a
possible route of spread involving handling fresh tissue and inoculation
through
mucous membranes and wounds including skin abrasions (Gajdusek, 1977)

Masters, C.J., Gajdusek, D.C. and Gibbs, C.J., (1980). The spongiform
encephalopathies: the natural history of CJD and its relationship to
kuru and scrapie.


* Gajdusek D.C. (1996). Kuru: From the New Guinea field journals
1957-1962. Grand Street, 15:6-33


* Gajdusek D.C. (1973). Kuru in the New Guinea Highlands. In
Spillane JD (ed): Tropical Neurology. New York, Oxford University
Press.


* Gajdusek D.C., Gibbs C.J., and M. Alpers (1966). Experimental
transmission of a kuru-like syndrome to chimpanzees. Nature, 209:794.


* Lindenbaum S. (1979). Kuru Sorcery. Mountain View, Ca, Mayfield
Publishing Company.

SCCNFP/0724/03, final
THE SCIENTIFIC COMMITTEE ON COSMETIC PRODUCTS AND NON-FOOD PRODUCTS
INTENDED FOR CONSUMERS
OPINION
CONCERNING
USE OF SPECIFIED RISK MATERIAL IN COSMETICS
CLARIFICATION FOR TALLOW DERIVATIVES
adopted by the SCCNFP on 30 July 2003
by means of the written procedure
SCCNFP/0724/03, final
Opinion on the Use of specified risk material in cosmetics -
Clarification for tallow derivatives
_____________________________________________________________________________________________
2
1. Background

snip...FULL TEXT;

http://www.vegsource.com/talk/madcow/messages/92820.html

THE following was posted the next day by FDA;

July 14, 2004

horizontal rule


An Evaluation of the Risk of Variant Creutzfeldt-Jakob Disease from
Exposure to Cattle-Derived Protein Used in Cosmetics


Introduction

The discovery of a cow with bovine spongiform encephalopathy (BSE) in
Washington State in December 2003 triggered action to put in place
additional safeguards against BSE. Even though the cow was born in
Canada, the fact that the cow was discovered in the U.S. and had been
sent to slaughter and rendering before it was identified as positive
indicates a vulnerability in the U.S. BSE protective net.

While BSE is usually identified with either food safety or animal
health, cosmetics, because of the ways they are used, provide another
route for BSE infectivity to enter the human system. Cosmetics may
contain a wide range of cattle-derived ingredients, many of which may
carry the BSE agent. FDA prepared this assessment of the risks to public
health if cattle-derived ingredients are used in cosmetics.

This qualitative risk assessment follows the generally accepted
framework for risk assessments endorsed by the Codex Alimentarious
Commission, the U.S. National Academy of Sciences, and other
authoritative bodies. The framework divides risk assessment into four
components: (1) hazard identification, (2) exposure assessment, (3)
hazard characterization (or dose-response assessment), and (4) risk
characterization. The risk assessment uses scientific evidence to the
extent that it exists. The agency has determined that this qualitative
risk assessment is appropriate to the circumstances.


Risk Assessment


Hazard Identification

In April 1996, British scientists reported a previously undetected new
variant of Creutzfeldt-Jakob disease (vCJD) in young patients, with
symptoms somewhat different from sporadic CJD (Refs. 1 and 2). All cases
of vCJD had histopathologic evidence of spongiform changes in the brain,
but also showed formation of "florid" plaques (a core of amyloid protein
with surrounding halos of vacuoles) not typically seen in other forms of
CJD (Ref. 3). Clinically, vCJD usually begins with a psychiatric
presentation, such as depression, anxiety, nightmares or hallucinations.
These symptoms are followed by memory impairment, then dementia in the
late stages. The clinical course may last up to two years before death
occurs (Ref. 4). Because scientific evidence suggests that the presence
and infectivity of abnormal prion proteins in vCJD share characteristics
with abnormal prion proteins found in cattle with BSE, scientists have
concluded that exposure to the BSE agent is the most plausible
explanation for the occurrence of vCJD (Refs. 5 - 8). Monkeys
(genetically the closest animal model to humans) inoculated with samples
of brain from BSE-infected cattle have been found to develop a TSE that
is histopathologically similar to vCJD (Ref. 9), as have mice inoculated
or fed with BSE-infected tissue (Ref. 10). In addition, studies have
shown that abnormal prion proteins from vCJD patients are molecularly
similar to abnormal prion proteins from BSE-infected cattle and
different from abnormal prion proteins from patients with CJD and other
spongiform encephalopathies (Ref. 4).

Prions are predominantly found in the central nervous system, portions
of the intestine, and tonsils of cattle with BSE. Cosmetic ingredients
can be derived from some of these tissues. Although large prion doses
are known to have a shorter incubation period before the disease
develops, even low doses may cause vCJD if infectious prions survive
digestion and the host survives long enough to complete a longer
incubation period. Although most scientists believe that vCJD in humans
is caused by consumption of cattle-derived food products contaminated
with the agent that causes BSE (Refs. 11-14), exposure from cosmetics
derived from cattle protein is another potential route of exposure.


Exposure Assessment

BSE in the United States
On December 23, 2003, USDA diagnosed a positive case of BSE in an adult
Holstein cow in the State of Washington.

Use of Cattle Protein in Cosmetics
Cosmetics may be made from a variety of cattle-derived ingredients.
These ingredients include albumin, brain extract, brain lipid,
cholesterol, fibronectin, sphingolipids, collagen, keratin, and tallow
and tallow derivatives. However, tallow derivatives, particularly fatty
acids and glycerin, are the predominant bovine ingredient used by the
cosmetic industry and contain very little protein, and are therefore
unlikely vehicles for the transmission of prions. Cattle-derived
ingredients serve many functions and may be used as skin conditioning
agents, emollients, binders, and hair and nail conditioning agents.

Absorption of Prions from Cosmetics
There are several routes through which cosmetics contaminated with the
agent that causes BSE could transmit disease to humans. Transmission of
the BSE agent to humans through intact skin is believed to be unlikely;
however, cosmetics may be ingested or applied to cut or abraded skin or
to conjunctival tissues that can provide direct routes for infection.

It is well-documented that central nervous system tissue, including the
optic nerve, carries infectivity in animals with TSEs and humans with
vCJD, and serves as an efficient route of transmission. In mice,
intraocular injection of scrapie caused infection along the optic nerve,
which eventually spread into non-neural tissue via the lymphatic system
(Ref. 15). In addition to intraocular injection, infectivity has been
transmitted to animals via the conjunctiva of the eye (mucosal tissue).
Scott et al. (Ref. 16) found that scrapie was induced in 42 percent of
rodents by dropping a high concentration of infectivity onto the
conjunctiva. Klitzman et al. (Ref. 17) suggested that kuru, a human TSE
disease found only among the Fore people of New Guinea, might have been
transmitted by rubbing infected human brain into eyes or cut skin, while
handling and consuming infected brain during funeral rituals.

Cut or abraded skin also has been proposed as a route for contracting
TSE diseases. The transmission of kuru through cut skin has been
suggested and was mentioned previously. Taylor et al. (Ref. 18) and
Ingrosso et al. (Ref. 19) demonstrated increased transmission of scrapie
via oral mucosal tissue. In one study, 100 percent of mice with
experimentally damaged oral mucosal tissue developed scrapie through
ingestion of infected material, while only 71 percent of mice with
intact mucosa developed the disease (Ref. 18). In addition, Pammer et
al. (Ref. 20) and Sugaya et al. (Ref. 21) noted that epithelial cells,
dendritic cells, and keratinocytes (the primary cell types found in the
epidermis) have been found to contain infectious prion protein,
indicating that these cells are potential targets for peripheral
infection with a TSE disease.

Use of BSE-contaminated cosmetics could provide a means of human
infection via several routes discussed above. Many cosmetics are
typically applied in the area of the eye (mascara, eye brow pencil,
eyeliner, eye lotion, and eye makeup remover) and almost any cosmetic,
including shampoo, can get into the eye via eye rubbing or incorrect
application. Any cosmetic product, but particularly shaving creams and
gels and lotions, may be applied to cut or abraded skin. Cosmetics that
are ingested, such as lipstick, dentifrices, mouthwash, and breath
fresheners, would have an oral route of infection, and the ingested
fraction would have the same risk as prion-contaminated meat and other
food products derived form cattle. Furthermore, the presence of cattle
derived ingredients is not generally obvious to the consumer, since the
source of the ingredient (i.e. cattle derived) does not need to be
placed on the label.


Hazard Characterization

Prions with a particular abnormal tertiary structure are apparently able
to generate a similar misconformation in normal proteins, which can in
turn cause further misconformations. This allows propagation of the
disease and is also important for understanding the relationship between
dose, response, and the incubation required for the disease to develop.
Once the prions have entered the brain, the prion concentration grows
with a relationship that has been described as exponential (Ref. 14).

In cattle, there is a minimal incubation period of six months to a year
required for the development of the disease, regardless of the size of
the initial dose, although incubation periods of 4 or more years appear
to be more common (Refs. 11 and 12). The lag period may reflect the fact
that transmission from food to brain may be preceded by symptomless
amplification of infectious prions in the intestine and lymphoreticular
tissues. While cattle at this stage would be clinically normal and may
have negative BSE test results, various tissues could be infectious
(Refs. 11 and 12).

Despite widespread exposure in the U.K. to BSE-contaminated meat
products, only a very small percentage of the exposed population has
been diagnosed with vCJD to date. However, ongoing experiments indicate
that the infectious dose for cattle is very low. One gram of affected
bovine brain homogenate is sufficient to cause BSE in more than 50
percent of calves exposed by mouth. Five years after oral consumption of
lower doses of brain material, 2 of 15 calves fed 0.1 gram had onset of
BSE, and 1 of 15 fed 0.01 gram had developed the disease. This
experiment is ongoing (Ref. 22). There is thought to be a 10- to
10,000-fold increase in the amount of infectious material needed to
cause illness in humans as compared with cattle, because of the species
barrier (Ref. 23).


Risk Characterization

This is not a quantitative risk assessment. However, it does sketch out
the logical structure that a quantitative model could use if one were
constructed. Some conclusions can be drawn without a quantitative
analysis. Since there is considerable uncertainty associated with the
premises outlined in the present analysis, it follows that there will
also be considerable uncertainty associated with the risk estimate. In
the exposure assessment, there are considerable uncertainties associated
with the origin of protein used in making cosmetics, the effect of
processing on prion concentration, and the transmission rates for dermal
and ocular exposure. Particularly large uncertainties associated with
the dose response assessment include the magnitude of the species
barrier and the length of the incubation period.

With exception of the uncertainty associated with estimates of the
dermal and ocular transmission rates, most of the uncertainties
associated with a risk assessment of BSE prions in cosmetics are also
associated with the risk from food consumption. For example, the number
of BSE-affected cattle and the variability in human susceptibility will
impact the risk of both food- and cosmetic-associated vCJD.

Some of these uncertainties may concomitantly affect both sides of a
cost-benefit analysis. In particular, if there is not substantial use of
cattle-derived protein in making cosmetics, then there will be little
exposure, and also little economic consequence from regulating use.
Conversely, high use would require substantial substitution and
alternative means of animal-by-product disposal.


Conclusions

A form of spongiform encephalopathy that occurs in humans (vCJD) is
thought to result from the same protein (a prion) that causes BSE in
cattle. Although the primary source of exposure is likely to be due to
the ingestion of beef and other food derived from cattle, other routes
of exposure may also be important. Although small doses require longer
incubation periods for clinical signs to develop, small doses of
infectious prions can potentially cause disease. Cosmetics that contain
protein derived from bovine sources are a potential source of exposure.
It has been demonstrated experimentally that TSEs may result from ocular
absorption of protein, and systemic absorption of protein may also occur
when cosmetics are applied to lacerated or abraded skin. As a result, it
may be concluded that there is some risk of occurrence of vCJD from the
use of cattle-derived protein in cosmetics. However, since there are
large uncertainties associated with the quantitative estimates of many
of the important variables, any quantitative estimate of the risk or
rate at which the disease may be expected to occur would be
correspondingly imprecise.

The risk of BSE from cosmetics may be reduced through the control of
exposure. Aside from the derivation processes used on tallow, the
effectiveness of cosmetic manufacturing processes for inactivating BSE
prions is unknown. The surest way to prevent transmission of BSE-prion
through cosmetics is to avoid the use of high-risk cattle-derived
protein in the manufacture of cosmetics.


References

1.

Will, R.G., J.W. Ironside, M. Zeidler, S.N. Cousens, K. Estibeiro,
A. Alperovitch, S. Poser, M. Pocchiari, A. Hofman, and P.G. Smith.
1996. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet
347: 921-25.

2.

Chazot, G., E. Broussolle, C.I. Lapras, T. Blattler, A. Aguzzi,
and N. Kopp. 1996. New variant of Creutzfeldt-Jakob disease in a
26-year-old French man. Lancet 347: 1181.

3.

Prusiner, S.B. 2001. Shattuck Lecture--Neurodegenerative diseases
and prions. N Engl J Med 344 (20): 1516-1526.

4.

Collinge, J. 2001. Prion diseases of humans and animals: Their
causes and molecular basis. Annu. Rev. Neurosci. 24: 519-50.

5.

Almond, J. and J. Pattison. 1997. Human BSE. Nature 389: 437-38.

6.

Scott, M.R., R. Will, J. Ironside, H-O.B Nguyen, P. Tremblay, S.J.
DeArmond, and S.B. Prusiner. 1999. Compelling transgenetic
evidence for transmission of bovine spongiform encephalopathy
prions to humans. Proc. Natl. Acad. Sci. 96 (26): 15137-142.

7.

Hill, A.F., M. Desbruslais, S. Joiner, K.C.L. Sidle, I. Gowland,
J. Collinge L.J. Doey, and P. Lantos. 1997. The same prion strain
causes vCJD and BSE. Nature 389: 448-450.

8.

Collinge, J. 1999. Variant Creutzfeldt-Jakob disease. Lancet 354:
317-323.

9.

Lasmezas, C.I., J-G. Fournier, V. Nouvel, H. Boe, D. Marce, F.
Lamoury, N. Kopp, J-J. Hauw, J. Ironside, M. Bruce, D. Dormont and
J-P. Deslys. 2001. Adaptation of the bovine spongiform
encephalopathy agent to primates and comparison with
Creutzfeldt-Jakob disease: Implications for human health. Proc.
Natl. Acad. Sci. 98 (7): 4142-4147.

10.

Bruce, M.E., R.G. Will, J. W. Ironside, I. McConnell, D. Drummond,
A. Suttie, L. McCardle, A. Chree, J. Hope, C. Birkett, S. Cousens,
H. Fraser, and C.J. Bostock. 1997. Transmissions to mice indicate
that 'new variant' CJD is caused by the BSE agent. Nature 389:
498-501.

11.

Brown, P. 1997. The risk of bovine spongiform encephalopathy ('mad
cow disease') to human health. J. Am. Med. Assn. 278 (12): 1008-1011.

12.

Brown, P., R.G. Will, R. Bradley, D.M. Asher, and L. Detwiler.
2001. Bovine spongiform encephalopathy and variant
Creutzfeldt-Jakob disease: Background, evolution, and current
concerns. Emerging Infect. Dis. 7 (1): 6-16.

13.

Scientific Steering Committee, European Commission. 1999. Opinion
of the Scientific Steering Committee on the Human Exposure Risk
(HER) via food with respect to BSE. Accessed online at
http://europa.eu.int/comm/food/fs/bse/scientific_advice08_en.html.

14.

Harvard Center for Risk Analysis, Harvard School of Public Health.
2003. Evaluation of the potential for bovine spongiform
encephalopathy in the United States. Accessed online at
http://www.hcra.harvard.edu/pdf/madcow.pdf.

15.

Fraser, J.R. 1996. Infectivity in extraneural tissues following
intraocular scrapie infection. J. Gen. Virol. 77: 2663-68.

16.

Scott, J.R., J. D. Foster and H. Fraser. 1993. Conjunctival
instillation of scrapie in mice can produce disease. Vet Microbiol
34 (4): 305-309.

17.

Klitzman R.L., M.P. Alpers, and D.C. Gajdusek. 1984. The natural
incubation period of kuru and the episodes of transmission in
three clusters of patients. Neuroepidemiology 3 (1): 3-20.

18.

Taylor, D.M., I. McConnell, and H. Fraser. 1996. Scrapie infection
can be established readily through skin scarification in
immunocompetent but not immunodeficient mice. J. Gen. Virol. 77:
1595-99.

19.

Ingrosso, L., F. Pisani, and M. Pocchiari. 1999. Transmission of
the 263K scrapie strain by the dental route. J. Gen. Virol. 80:
3043-47.

20.

Pammer, J., W. Weninger, and E. Tschachler. 1998. Human
keratinocytes express cellular prion-related protein in vitro and
during inflammatory skin diseases. Am. J. Pathol. 153: 1353-58.

21.

Sugaya, M., K. Nakamura, T. Watanabe, A. Asahina, N. Yasaka, Y.
Koyama, M. Kusubata, Y. Ushiki, K. Kimura, A. Morooka, S. Irie, T.
Yokoyama, K. Inoue, S. Itohara, and K. Tamaki. 2002. Expression of
cellular prion-related protein by murine Langerhans cells and
keratinocytes. J. Dermato. Sci. 28: 126-134.

22.

Vossen, P., J. Kreysa, and M. Goll. 2003. Overview of the BSE risk
assessment of the European Commission's Scientific Steering
Committee (SSC) and it TSE/BSE ad hoc group. Accessed online at
http://europa.eu.int/comm/food/fs/sc/ssc/out364_en.pdf.

23.

Scientific Steering Committee, European Commission. 2000. Oral
exposure of humans to the BSE agent: Infective dose and species
barrier. Accessed online at
http://europa.eu.int/comm/food/fs/sc/ssc/out79_en.pdf.


http://www.cfsan.fda.gov/~comm/bse-ra.html

THIS was just published ;

Scrapie transmission following exposure through the skin is
dependent on follicular dendritic cells in lymphoid tissues

Joanne Mohan, Karen L. Brown, Christine F. Farquhar, Moira E. Bruce and
Neil A. MabbottCorresponding Author Contact Information
,

E-mail The Corresponding Author

Institute for Animal Health, Ogston Building, West Mains Road, Edinburgh
EH9 3JF, UK

Received 9 March 2004; Revised 22 April 2004; accepted 12 May 2004.
Available online 8 July 2004.


Abstract

Background: Transmissible spongiform encephalopathies (TSEs) are chronic
infectious neurodegenerative diseases that are characterized by the
accumulation in affected tissues of PrPSc, an abnormal isoform of the
host prion protein (PrPc). Following peripheral exposure, PrPSc usually
accumulates on follicular dendritic cells (FDCS) in lymphoid tissues
before neuroinvasion. Studies in mice have shown that TSE exposure
through scarified skin is an effective means of transmission. Following
inoculation via the skin, a functional immune system is critical for the
transmission of scrapie to the brain as severe combined immunodeficiency
(SCID) mice are refractory to infection. Until now, it was not known
which components of the immune system are required for efficient scrapie
neuroinvasion following skin scarification. Objective: To determine
which cells are critical for the transmission of scrapie to the brain
following inoculation via the skin. Methods: A chimeric mouse model was
used, which had a mismatch in PrPc expression between FDCs and other
bone marrow-derived cells within lymphoid tissues. These chimeric mice
were challenged with scrapie by skin scarification to allow the separate
roles of FDCs and lymphocytes in peripheral scrapie pathogenesis to be
determined. Results: We show that mature FDCs are essential for the
accumulation of scrapie within lymphoid tissues and the subsequent
transmission of infection to the brain following TSE exposure by this
route. Furthermore, we show that the accumulation of PrPSc and
infectivity in the spleen is independent of PrP expression by
lymphocytes or other bone marrow-derived cells. Conclusion: Following
inoculation with scrapie by skin scarification, replication in the
spleen and subsequent neuroinvasion is critically dependent upon mature
FDCs.

Author Keywords: Transmissible spongiform encephalopathy; Scrapie; Skin;
Follicular dendritic cell; Prion protein; Spleen


Corresponding Author Contact Information
Corresponding

author. Tel.: +44 131 667 5204; fax: +44 131 668 3872.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T87-4CTD13F-3&_coverDate=08%2F31%2F2004&_alid=189125137&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=5079&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=8878b345dd3743a8fe239a820e6aea0b


TSS




----- Original Message -----
From: Terry S. Singeltary Sr.
To: [email protected]
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. <<<


TSE science is emerging and the old testing techniques for TSEs are becoming much more sensitive than when some of these old BSE tissue bio-assays were done in the distant past. I urge once again for the FDA and the USDA to put forth sound science instead of the political and corporate science they have floundered with for the last 3 decades. THERE is much new data out that dispute the position the FDA/USDA have taken on SRMs.


STATEMENT ON INFECTIVITY IN BOVINE TONSIL

Background

1. The views of the Committee were sought on unpublished results from an

ongoing long-term study of the pathogenesis of BSE in cattle. This study is

being carried out by the Veterinary Laboratory Agency and is funded by the

Food Standards Agency (FSA).

2. In this study, cattle were orally dosed with 100g of BSE-infected bovine

brain material. At various times after oral dosing, cattle were killed and

different tissues tested for infectivity. In the first instance, the presence of

infectivity was assessed by injection of various tissues into inbred mice

("mouse bioassay "). In this research infectivity was detected in:

• distal ileum (the earliest infectivity was detected at 6 months after

inoculation.)

• brain and spinal cord and closely associated nervous tissue

(infectivity was detected in the months just prior to the clinical onset

of BSE in cattle)

• at a single time point (around the time of clinical onset) bone marrow

was also found to contain infectivity. ...snip


http://www.seac.gov.uk/statements/tonsil211002.pdf


UPDATE OF THE OPINION ON

TSE INFECTIVITY DISTRIBUTION IN RUMINANT TISSUES

INITIALLY ADOPTED BY

THE SCIENTIFIC STEERING COMMITTEE

AT ITS MEETING OF 10-11 JANUARY 2002

AND AMENDED AT ITS MEETING OF 7-8 NOVEMBER 2002

following the submission of (1) a risk assessment by the German Federal Ministry of

Consumer Protection, food and Agriculture and (2) new scientific evidence

regarding BSE infectivity distribution in tonsils


http://europa.eu.int/comm/food/fs/sc/ssc/out296_en.pdf


3. New work, work still in progress and future work

The infectivity of neural and non-neural tissues by intracerebral inoculation of cattle is being

assayed in projects M03006 and M03007. These studies are important since it is possible

that some tissues may not yet have been found to be infective, due to the fact that

infectivity in these tissues is below the detection limits of the tests applied so far. To date,

this study has shown infectivity in CNS tissues, the distal ileum, tonsil tissue and the

nictitating membrane (the nictitating membrane is also known as the third eyelid). Other

challenged and control cattle continue to be closely monitored for clinical signs of BSE.

Research is ongoing to determine the susceptibility of other food animal species to TSEs.

These include a project to determine the susceptibility of pigs to scrapie through oral

exposure (M03005) and a project to further study the transmission of BSE to pigs (M03010).

Project M03024 aims to determine whether UK red deer are susceptible to BSE by oral

exposure. These studies are important since it is highly probable that pigs and deer were

historically exposed to ruminant derived meat and bone meal (MBM). ...


http://www.food.gov.uk/multimedia/pdfs/annualresearchrpt04.pdf


TSEs And The Environment

The LANCET
Volume 351, Number 9110 18 April 1998

BSE: the final resting place

snip...


The first matter to consider is the distribution of infectivity in the
bodies of infected animals. The brain (and more generally, the central
nervous system) is the primary target in all transmissible spongiform
encephalopathies (TSE), and it contains by far the highest concentration
of the infectious agent. In naturally occuring disease, infectivity may
reach levels of up to about one million lethal doses per gram of brain
tissue, whether the disease be kuru, CJD, scrapie, or BSE. The
infectious agent in BSE-infected cattle has so far been found only in
brain, spinal cord, cervical and thoracic dorsal root ganglia,
trigeminal ganglia, distal ileum, and bone marrow.4 However, the much
more widespread distribution of low levels of infectivity in human
beings with kuru or CJD, and in sheep and goats with scrapie, suggests
that caution is advisable in prematurely dismissing as harmless other
tissues of BSE-infected cattle.


snip...end...TSS


TRANSMISSIBLE SPONGIFORM

ENCEPHALOPATHY AS A

ZOONOTIC DISEASE

WRITTEN BY

PAUL BROWN

WITH CONTRIBUTIONS BY:

RAYMOND BRADLEY

LINDA DETWILER

DOMINIQUE DORMONT

NORA HUNTER

GERALD A.H. WELLS

JOHN WILESMITH

ROBERT WILL

ELIZABETH WILLIAMS

PREPARED UNDER THE RESPONSIBILITY OF THE ILSI EUROPE EMERGING PATHOGEN TASK FORCE

WITH THE ENDORSEMENT OF THE INTERNATIONAL FORUM FOR TSE AND FOOD SAFETY (TAFS)

March 2003

snip...

Despite the issuance by many governments of a package of prohibitions that could reasonably be

expected to eliminate the veterinary and public health risks of BSE, loopholes often exist that

could allow the spread of disease. The situation in the US is illustrative:

• No rules exist that require the rendering process to be capable of sterilizing BSE infectivity.

Most feed mills render carcasses under conditions that cannot be guaranteed to sterilize.

• Feed for ruminants and non-ruminants can be processed in the same feed mills, creating

the potential for cross-contamination. Thus, rendered carcasses of deer and elk with

chronic wasting disease could conceivably be fed to cattle.

• If farmers or ranchers mistakenly or deliberately use non-ruminant feed for ruminants, the

mammalian to ruminant feed ban would be bypassed. Spontaneous TSE occurring in nonmammalian

species, if it occurs, would also escape the mammalian to ruminant feed ban.


1 With the advent of BSE, safe sourcing has been practiced by avoiding tissues that are known to harbour

or replicate TSE agents, eliminating ruminant materials, or where there is no satisfactory alternative,

sourcing them from countries, herds and animals with an acceptably low geographical BSE risk

assessment. This is therefore not a table of risk, but rather a reminder of the extent to which humans are

exposed to products of bovine origin.

2 Some bone material, such as skull and vertebral column (excluding the tail) from cattle over certain

ages are classified as specified risk materials (SRM) in the EU.

3 SRM include skull, brain, ganglia, eyes, tonsils, intestines and spinal cord, and in the EU and some

other countries these are compulsorily removed for destruction.

4 Some fat (e.g. mesenteric fat) is classified as SRM in the EU.

5 Production of mechanically recovered meat from ruminant animals in the EU is banned. Elsewhere, its

inclusion in meat products usually does not exceed 5–10% by weight.

6 Tallow (bovine rendered fat) is one of the two major end products from rendering bovine carcass waste.

Tallow is not used in regulated medicines, but can be used in soaps, topical creams, cosmetics, and

suppositories. Tallow from SRM is not permitted for use except under license as a fuel.

7 Tallow derivatives include glycerol, fatty acids and their esters, stearates, polysorbates, and sorbitan

esters. Tallow derivatives are produced from tallow by hydrolysis at temperatures and pressures that have

been shown to sterilize TSE infectivity. They are used in the manufacture of some medicines and

cosmetics and may also be used in plastics (food wrappers).

8 Glucagons (replaced by recombinant technology in some countries), corticosterol,chondroitin sulfate,

vitamin D3, cholesterol, and cholic acid.

9 Liver, thymus, heart, mammary glands, placenta, ovary, and spleen.

http://europe.ilsi.org/file/TSE.pdf


From: TSS ()
Subject: PrPSc distribution of a natural case of bovine spongiform encephalopathy
Date: August 8, 2005 at 12:28 pm PST

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 [email protected]

Abstract

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


snip...



"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; [email protected]
Symposium Secretariat
Kyomi Sasaki
TEL +81-22-717-8233 FAX +81-22-717-7656
e-mail: [email protected]


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


107

Vet Pathol 42:107–108 (2005)

Letters to the Editor

Editor:

Absence of evidence is not always evidence of absence.

In the article ‘‘Failure to detect prion protein (PrPres) by

immunohistochemistry in striated muscle tissues of animals

experimentally inoculated with agents of transmissible spongiform

encephalopathy,’’ recently published in Veterinary

Pathology (41:78–81, 2004), PrPres was not detected in striated

muscle of experimentally infected elk, cattle, sheep, and

raccoons by immunohistochemistry (IHC). Negative IHC,

however, does not exclude the presence of PrPSc. For example,

PrPres was detected in skeletal muscle in 8 of 32

humans with the prion disease, sporadic Creutzfeldt-Jakob

disease (CJD), using sodium phosphotungstic acid (NaPTA)

precipitation and western blot.1 The NaPTA precipitation,

described by Wadsworth et al.,3 concentrates the abnormal

isoform of the prion, PrPres, from a large tissue homogenate

volume before western blotting. This technique has increased

the sensitivity of the western blot up to three orders

of magnitude and could be included in assays to detect

PrPres. Extremely conspicuous deposits of PrPres in muscle

were detected by IHC in a recent case report of an individual

with inclusion body myositis and CJD.2 Here, PrPres was

detected in the muscle by immunoblotting, IHC, and paraf-

fin-embedded tissue blot. We would therefore caution that,

in addition to IHC, highly sensitive biochemical assays and

bioassays of muscle are needed to assess the presence or

absence of prions from muscle in experimental and natural

TSE cases.

Christina Sigurdson, Markus Glatzel, and Adriano Aguzzi

Institute of Neuropathology

University Hospital of Zurich

Zurich, Switzerland

References

1 Glatzel M, Abela E, et al: Extraneural pathologic prion

protein in sporadic Creutzfeldt-Jakob disease. N Engl J

Med 349(19):1812–1820, 2003

2 Kovacs GG, Lindeck-Pozza E, et al: Creutzfeldt-Jakob

disease and inclusion body myositis: abundant diseaseassociated

prion protein in muscle. Ann Neurol 55(1):

121–125, 2004

3 Wadsworth JDF, Joiner S, et al: Tissue distribution of protease

resistant prion protein in variant CJD using a highly

sensitive immuno-blotting assay. Lancet 358:171–180,

2001


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


Volume 349:1812-1820 November 6, 2003 Number 19


Extraneural Pathologic Prion Protein in Sporadic Creutzfeldt-Jakob Disease


Background In patients with sporadic Creutzfeldt–Jakob disease, pathologic disease-associated prion protein (PrPSc) has been identified only in the central nervous system and olfactory-nerve tissue. Understanding the distribution of PrPSc in Creutzfeldt–Jakob disease is important for classification and diagnosis and perhaps even for prevention.

Methods We used a highly sensitive method of detection — involving the concentration of PrPSc by differential precipitation with sodium phosphotungstic acid, which increased the sensitivity of Western blot analysis by up to three orders of magnitude — to search for PrPSc in extraneural organs of 36 patients with sporadic Creutzfeldt–Jakob disease who died between 1996 and 2002.

Results PrPSc was present in the brain tissue of all patients. In addition, we found PrPSc in 10 of 28 spleen specimens and in 8 of 32 skeletal-muscle samples. Three patients had PrPSc in both spleen and muscle specimens. Patients with extraneural PrPSc had a significantly longer duration of disease and were more likely to have uncommon molecular variants of sporadic Creutzfeldt–Jakob disease than were patients without extraneural PrPSc.

Conclusions Using sensitive techniques, we identified extraneural deposition of PrPSc in spleen and muscle samples from approximately one third of patients who died with sporadic Creutzfeldt–Jakob disease. Extraneural PrPSc appears to correlate with a long duration of disease.


Source Information

From the Institute of Neuropathology and National Reference Center for Prion Diseases, University Hospital of Zurich, Zurich, Switzerland.

Dr. Glatzel and Mr. Abela contributed equally to the article.

Address reprint requests to Dr. Aguzzi at the Institute of Neuropathology, University Hospital of Zurich, Schmelzbergstr. 12, CH-8091 Zurich, Switzerland, or at [email protected] .


http://content.nejm.org/cgi/


Creutzfeldt-Jakob disease and inclusion body myositis: Abundant disease-associated prion protein in muscle

Gabor G. Kovacs, MD PhD 1 2, Elisabeth Lindeck-Pozza, MD 1, Leila Chimelli, MD, PhD 3, Abelardo Q. C. Araújo, MD, PhD 4, Alberto A. Gabbai, MD, PhD 5, Thomas Ströbel, PhD 1, Markus Glatzel, MD 6, Adriano Aguzzi, MD, PhD 6, Herbert Budka, MD 1 *
1Institute of Neurology, University of Vienna, and Austrian Reference Centre for Human Prion Diseases, Vienna, Austria
2National Institute of Psychiatry and Neurology, Budapest, Hungary
3Department of Pathology, School of Medicine, Federal University of Rio de Janeiro
4Department of Neurology, School of Medicine, Federal University of Rio de Janeiro
5Department of Neurology, School of Medicine, Federal University of Sao Paulo, Brazil
6Institute of Neuropathology, University Hospital of Zürich, Zürich, Switzerland
email: Herbert Budka ([email protected] )

*Correspondence to Herbert Budka, Institute of Neurology, AKH 4J, Wühringer Gürtel 18-20, POB 48, A-1097 Vienna, Austria

Funded by:
European Union (EU) Project; Grant Number: TSELAB QLK2-CT-2002-81523
EU Concerted Action PRIONET; Grant Number: QLK2-2000-CT-00837

Abstract

Pathologicalprion protein (PrPSc) is the hallmark of prion diseases affecting primarily the central nervous system. Using immunohistochemistry, paraffin-embedded tissue blot, and Western blot, we demonstrated abundant PrPSc in the muscle of a patient with sporadic Creutzfeldt-Jakob disease and inclusion body myositis. Extraneural PrPC-PrPSc conversion in Creutzfeldt-Jakob disease appears to become prominent when PrPC is abundantly available as substrate, as in inclusion body myositis muscle.

--------------

Received: 16 June 2003; Revised: 11 September 2003; Accepted: 11 September 2003
Digital Object Identifier (DOI)


10.1002/ana.10813 About DOI

http://www3.interscience.wiley.com/


EMBO reports AOP Published online: 11 April 2003


Widespread PrPSc accumulation in muscles of hamsters orally infected with scrapie

http://www.emboreports.org/



Watson Meldrum et al Scrapie agent in muscle - Pattison I A (1990)
Veterinary record, 20 January 1990. p.68

http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdf


SADLY, it's all about money, to hell with human health;


The Economic Impact of BSE

on the U.S. Beef Industry:

Product Value Losses, Regulatory

Costs, and Consumer Reactions

snip...


5.4 Expanded Definition of SRM

The definition of SRM in other countries

with BSE does not typically recognize a 30-

month age cut-off for tissues such as brain

and spinal cord. When SRM controls were

first introduced in the United Kingdom in

1989, the definition included the brain, spinal

cord, spleen, thymus, tonsils and intestines of

bovine animals aged 6 months or over. Since

then, the definition has been expanded many

times as more was learned about the disease.

As of October 2000, SRM is defined in all

European Union countries to include the following

tissues (DEFRA):

Skull including the brains and eyes, the

tonsils, the spinal cord of animals aged

over 12 months and the intestines from

the duodenum to the rectum of bovine

animals of all ages.

The following tissues are also designated as

SRMs in the United Kingdom and Portugal:

The entire head, excluding the tongue,

including the brains, eyes, trigeminal

ganglia and tonsils; the thymus; the

spleen and spinal cord of animals aged

over 6 months; and the vertebral column,

including dorsal root ganglia, of animals

aged over 30 months.

A possible extension of current U.S. regulations

would be to eliminate or reduce the

30-month age limit in the current definition

of SRM. As noted above, the International

Review Team recommended that the SRM

definition be expanded "unless aggressive surveillance

showed the BSE risk to be minimal."

If indigenous BSE cases are discovered, it

seems likely that this change would occur.

Assuming SRM is banned from all animal

feed, an expanded SRM definition would

increase the cost of the regulation for under

30-month animals – i.e., from $2.16 per head

to the estimate of $6.77 per head applicable

for older animals.23

http://fss.k-state.edu/research/reports/CoffeyMintertFoxSchroederValentin200504.pdf


BY reducing or weakening the SRM list due to the Economic Impact of BSE on the U.S. Beef Industry and while doing so, ignoring all 'sound science', again the FDA/USDA et al are willing to put every human and animal out there at risk to further exposure to this TSE agent, all for a buck. this is not 'sound science' this is what i call 'corporate science', and it is and will continue to expose people. some of these people will die from this agent either directly or indirectly via a multitude of scientific proven routes and sources. WE must remove all political and corporate science from TSE research.


I find it disturbing that products that carry SRMs are still on the market for humans such as nutritional supplements ;


ODD, I just picked up a catalog from STANDARD PROCESS INC. 2003 - 2004 Product Catalog
(a chiropractor had just left this catalog in my wife's foot doctors office 4/5/05)
and it's full of THOSE SRMS FOR HUMANS. I wonder how much is still left on the market,
and how much is still in production, how much crosses the borders? 5 pages of products
full of SRMs for humans. THIS is a really fine catalog, i am just now going over.
LOADED with SRMs for humans. NO wonder my neighbors mom died from CJD while taking
these damn mad cow pills. THEY even have a candy bars loaded with SRMs. HERE is one ;

NATURAL COCOA STANDARDBAR (mad cow candy bar)
(i will just list animal organs)

bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...

NATURAL PEANUT BUTTER STANDARDBAR

bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...

USF (MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ;

bovine orhic glandular extract

UTROPHIN PMG

bovine uterus PMG

VASCULIN

bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine duodenum,
bovine adrenal Cytosol extract, bovine spleen, ovine spleen (some yummy stuff)

IPLEX (neighbors mom died from CJD while taking these pills for years)

bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach, bovine adrenal,
bovine kidney, bovine adrenal Cytosol extract, BOVINE BRAIN, bovine bone, veal bone
meal

MYO-PLUS

bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract, bovine
spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN

NEUROPLEX

bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT,
BOVINE ANTERIOR PITUITARY, bovine liver, BOVINE PITUITARY PMG EXTRACT,
AND MORE BOVINE BRAIN... HOLY MAD COW IN A PILL !!!

NEUROTROPHIN PMG

BOVINE BRAIN PMG

NIACINAMIDE B6 VM

bovine liver, porcine stomach, bovine spleen ovine spleen,
BOVINE BRAIN

OCULOTROPHIN PMG
BOVINE EYE PMG

ORCHEX

bovine liver, bovine orchic Cytosol extract, porcine stomch,
bovine spleen, ovine spleen, BOVINE BRAIN

OSTARPLEX

veal bone PMG extract, veal bone PMG extract, bovine liver,
porcine stomach, bovine adrenal, bovine spleen, ovine spleen,
BOVINE BRAIN

PARAPLEX

bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG,
BOVINE PITUITARY PMG EXTRACT, bovine thyroid PMG extract

PITUITROPHIN PMG

RUMAPLEX

BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate
Cytosol extract, veal bone meal, bovine liver PMG extract, bovine spleen,
ovine spleen, bovine liver

SENAPLEX

bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal, bovine
kidney, bovine orchic extract, bovine spleen, ovine spleen ..........

THESE are just a few of MANY of just this ONE COMPANY.

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7


253 1 DR. BOLTON:

I have an additional question about 2 that. What is the assurance that additional locally sourced 3 tracheas are not added into that manufacturing process, thus 4 boosting the yield, if you will, but being returned to the 5 U.S. as being produced from U.S.-sourced raw material? 6 DR. McCURDY: Are there data to indicate how many 7 grams, or whatever, of infected brain are likely to infect 8 an organism, either animal or man, when taken orally? 9 DR. BROWN: If I am not mistaken, and I can be 10 corrected, I think a half a gram is enough in a cow, orally; 11 in other words, one good dietary-supplement pill. 12 DR. McCURDY: What I am driving at is the question 13 we are asked is really not do we wish to regulate these 14 things coming in. I think the statements about difficulties 15 in regulating things in the future or near future for new 16 regulations were probably accurate. 17 But I think that we could exhibit some quite 18 reasonable concern about blood donors who are taking dietary 19 supplements that contain a certain amount of unspecified- 20 origin brain, brain-related, brain and pituitary material. 21 If they have done this for more than a sniff or something 22 like that, then, perhaps, they should be deferred as blood 23 donors. 24 That is probably worse than spending six months in 25 the U.K. 254 1 DR. BROWN: That is exactly right. I think that 2 is why the discussion has apparently been on things that are 3 not directly related to these questions because, in order to 4 think about deferrals for blood donors who are taking 5 dietary supplements with things like bovine brain in them, 6 it is very important that we know that those products are 7 safe. 8 I think we have heard enough to suggest that they 9 may not be. 10 DR. McCURDY: There is one other item that needs 11 to be considered and that is what proportion of blood donors 12 are doing this; that is, how many blood donors would you 13 lose, and I don't know what the demographics--there is 14 fairly good information on the demography of blood donors. 15 I have no idea what the demography of people who take these 16 supplements is. Maybe they are old men like me and aren't 17 going to be blood donors anymore. 18 DR. BROWN: The wording of the question is not as 19 demanding as the wording of other deferral questions; that 20 is, the question here is consider recommending. We are 21 not even recommending at this point. We are saying to the 22 FDA, please think about this. It is worth thinking about. 23 DR. DETWILER: One point about brain from Europe, 24 and Jean Philippe is still here, those are considered 25 specified risk material and it is not correct to be 255 1 incinerated; correct? Or destroyed? Brain and spinal cord 2 and other high-risk tissues in Europe? 3 DR. NORTON: In tomorrow morning's British Medical 4 Journal, which has appeared on-line today, there is an 5 article called U.S. Takes Precautions against BSE. One 6 paragraph says, Even though the U.S. and U.K. governments 7 ban the practice of feeding cattle products to cows, in the 8 early 1990s, some U.K. renderers continued to manufacture 9 and ship contaminated meat and bonemeal around the world. 10 British export statistics show that thirty-seven tons of 11 meal made from offal was sent to the United States in 1997, 12 well after the U.S. government banned imports of such risky 13 meat. The ultimate use of these imports has not been 14 identified. 15 That will appear tomorrow morning. 16 DR. DETWILER: That actually was in The New York 17 Times. That is a direct quote out of The New York Times 18 article. We called the reporter on that. That statement, 19 the thirty-seven tons, was taken out of the U.S. 20 Geographical BSE Risk Assessment. What they didn't put in 21 there, in the statement, was the remainder of the GBR is at 22 that time, the big labeling for that category in the U.K., 23 because it was illegal for them to ship it to us from their 24 own regs. It is illegal for us to get that. 25 We did go and try and trace that so that wasn't [FULL TEXT ABOUT 600 PAGES] 3681t2.rtf http://www.fda.gov/ohrms/dockets/ac/cber01.htm

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm


IN fact, we are now finding that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE ;


Published online

January 27, 2005

Risk of oral infection with bovine spongiform

encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,

Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys

The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant

Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral infection

and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral

transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a

BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the

other remained free of disease at 76 months. On the basis of these .ndings and data from other studies, we made a

preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public

health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the .rst positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


snip...end


www.thelancet.com Published online January 27, 2005


THEN you must consider cross contamination at feed mills and such. this has been well proven in both the UK and the USA to date via r-to-r feed ban violations. IT was proven in the UK that they indeed put profits before human health;



[PDF] The BSE Inquiry / Statement No. 14 Issued 20 March 1998 THE ...


The BSE Inquiry / Statement No. 14. Issued 20 March 1998 ... number of feed
compounders and it became clear that cross contamination of feeds could occur. ...

http://www.bseinquiry.gov.uk/files/ws/s014.pdf

[PDF] The BSE Inquiry / Statement No 76F (Supplementary) Mr Alan ...


But the mainbut the main problem was probably cross-contamination. ...

http://www.bseinquiry.gov.uk/files/ws/s076f.pdf


STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

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

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

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

snip...

THE FUTURE

4..........

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

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

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

SEE full text ;

http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf



----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Friday, August 19, 2005 10:24 AM
Subject: Re: 1,000 CITATIONS ISSUED ON MAD COW REGULATIONS


> ##################### Bovine Spongiform Encephalopathy #####################
>
> From: TSS ()
> Subject: Re: 9,200 USA POTENTIAL MAD COWS IN JUNE 2004 ENHANCED COVER-UP
> SURVEILLANCE PROGRAM NO WB
> Date: August 19, 2005 at 8:14 am PST
>
> Hello Dr. Vogel,
>
> thank you for your kind reply.
>
> Dr. Vogel answers;
>
> > WHY was this not reported in the feed enforcement updates?"
> >
> > The answer is because they were NOT feed discrepancies. These were
> > noncompliance reports issued by USDA Food Safety and Inspection Service
> > employees to meat processing establishments.
> >
>
>
> WOULD it not be likely that from some of these noncompliance reports that
> indeed some breaches led to some potential tainted materials to enter the
> animal/human feed chain?
>
> ALL we have heard about in the last 7 years or better, well, since the
> 12/14/97 partial and voluntary ruminant-to-ruminant feed ban is that the
> feed ban is working, tripple fire walls, no ruminant protein entering the
> animal feed chain. along with this was a constant barage of 'no mad cow
> disease in the USA'. then we find this 12 year old TEXAS cow that was
> infected from tainted feed some time in that 12 year period. so, the NE
> TEXAS CJD cluster, where it was stated that NO mad cow was in the USA or
> TEXAS at that time frame, was in fact not true.
>
> SINCE some 460 of these occurred because slaughter plants did not have an
> adequate plan for dealing with BSE in their plant's food safety plan, as
> required by the USDA, the analysis showed, and of those 460 violations, 60
> percent described plans that contained no mention of BSE at all. then again,
> would it not be very possible that indeed some potentially tainted material
> of a BSE or atypical TSE DID enter the animal feed chain, thus later some of
> those animals entering the human food chain.
>
> WHAT about the SRM violations? Violations of rules about the removal and
> handling of specified risk material (SRMs) occurred at 131 plants in at
> least 35 states. SRMs are the high-risk materials, such as brains and spinal
> cords, most likely to be infectious. More than 30 percent of the NRs
> analyzed were due to either improperly handling or removing SRMs. Could this
> not have also led to potentially BSE/TSE tainted materials entering the
> animal/human food chain?
>
> In 10 percent of the NRs analyzed, plants incorrectly identified the age of
> cattle. THIS also could have led to tainted BSE/TSE SRM materials entering
> the animal/human food chain.
>
> IN my opinion, this could have led to many feed discrepancies and should
> HAVE been reported to the public, without the media having to request this
> data via FOIA. I think in the future it would be best if the NRs
> (non-compliance reports) were made easily available to the public in there
> feed enforement reports. ...
>
>
> FOR IMMEDIATE RELEASE
> AUGUST 18, 2005
> 5:25 PM CONTACT: Public Citizen
> (202) 588-1000
>
>
> Evidence of Weak Meat Inspection Program Found in Nearly a Thousand
> Violations of Mad Cow Rules at Slaughter Plants
> Noncompliance Records Show Plants Failed to Follow Regulations
>
> WASHINGTON - August 18 - In stark contrast to the public relations message
> touted by the U.S. Department of Agriculture (USDA) and the beef industry
> that the U.S. regulatory system is adequate to prevent the spread of mad cow
> disease, an analysis released today by the consumer group Public Citizen
> found significant lapses in the industry's compliance with federal rules.
> The analysis stems from a December 2004 Freedom of Information Act (FOIA)
> request from Public Citizen to the USDA for all "noncompliance records"
> (NRs) related to bovine spongiform encephalopathy (BSE). Public Citizen
> received copies of 829 records on Aug. 15.
>
> More than half the violations (460) occurred because slaughter plants did
> not have an adequate plan for dea
 

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----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Friday, August 19, 2005 10:24 AM
Subject: Re: 1,000 CITATIONS ISSUED ON MAD COW REGULATIONS


> ##################### Bovine Spongiform Encephalopathy #####################
>
> From: TSS ()
> Subject: Re: 9,200 USA POTENTIAL MAD COWS IN JUNE 2004 ENHANCED COVER-UP
> SURVEILLANCE PROGRAM NO WB
> Date: August 19, 2005 at 8:14 am PST
>
> Hello Dr. Vogel,
>
> thank you for your kind reply.
>
> Dr. Vogel answers;
>
> > WHY was this not reported in the feed enforcement updates?"
> >
> > The answer is because they were NOT feed discrepancies. These were
> > noncompliance reports issued by USDA Food Safety and Inspection Service
> > employees to meat processing establishments.
> >
>
>
> WOULD it not be likely that from some of these noncompliance reports that
> indeed some breaches led to some potential tainted materials to enter the
> animal/human feed chain?
>
> ALL we have heard about in the last 7 years or better, well, since the
> 12/14/97 partial and voluntary ruminant-to-ruminant feed ban is that the
> feed ban is working, tripple fire walls, no ruminant protein entering the
> animal feed chain. along with this was a constant barage of 'no mad cow
> disease in the USA'. then we find this 12 year old TEXAS cow that was
> infected from tainted feed some time in that 12 year period. so, the NE
> TEXAS CJD cluster, where it was stated that NO mad cow was in the USA or
> TEXAS at that time frame, was in fact not true.
>
> SINCE some 460 of these occurred because slaughter plants did not have an
> adequate plan for dealing with BSE in their plant's food safety plan, as
> required by the USDA, the analysis showed, and of those 460 violations, 60
> percent described plans that contained no mention of BSE at all. then again,
> would it not be very possible that indeed some potentially tainted material
> of a BSE or atypical TSE DID enter the animal feed chain, thus later some of
> those animals entering the human food chain.
>
> WHAT about the SRM violations? Violations of rules about the removal and
> handling of specified risk material (SRMs) occurred at 131 plants in at
> least 35 states. SRMs are the high-risk materials, such as brains and spinal
> cords, most likely to be infectious. More than 30 percent of the NRs
> analyzed were due to either improperly handling or removing SRMs. Could this
> not have also led to potentially BSE/TSE tainted materials entering the
> animal/human food chain?
>
> In 10 percent of the NRs analyzed, plants incorrectly identified the age of
> cattle. THIS also could have led to tainted BSE/TSE SRM materials entering
> the animal/human food chain.
>
> IN my opinion, this could have led to many feed discrepancies and should
> HAVE been reported to the public, without the media having to request this
> data via FOIA. I think in the future it would be best if the NRs
> (non-compliance reports) were made easily available to the public in there
> feed enforement reports. ...
>
>
> FOR IMMEDIATE RELEASE
> AUGUST 18, 2005
> 5:25 PM CONTACT: Public Citizen
> (202) 588-1000
>
>
> Evidence of Weak Meat Inspection Program Found in Nearly a Thousand
> Violations of Mad Cow Rules at Slaughter Plants
> Noncompliance Records Show Plants Failed to Follow Regulations
>
> WASHINGTON - August 18 - In stark contrast to the public relations message
> touted by the U.S. Department of Agriculture (USDA) and the beef industry
> that the U.S. regulatory system is adequate to prevent the spread of mad cow
> disease, an analysis released today by the consumer group Public Citizen
> found significant lapses in the industry's compliance with federal rules.
> The analysis stems from a December 2004 Freedom of Information Act (FOIA)
> request from Public Citizen to the USDA for all "noncompliance records"
> (NRs) related to bovine spongiform encephalopathy (BSE). Public Citizen
> received copies of 829 records on Aug. 15.
>
> More than half the violations (460) occurred because slaughter plants did
> not have an adequate plan for dealing with BSE in their plant's food safety
> plan, as required by the USDA, the analysis shows. Of those 460 violations,
> 60 percent described plans that contained no mention of BSE at all.
>
> "The fact that 60 percent of the violations were due to a failure to even
> mention BSE or risk materials such as brains and spinal cords is
> significant," said Patty Lovera, deputy director of Public Citizen's food
> program. "If officials running a meat plant cannot be bothered to recognize
> the risk of BSE when writing their safety plan, how much of a priority is it
> in daily operations and training of staff?"
>
> The analysis also found that:
>
>
> Violations of rules about the removal and handling of specified risk
> material (SRMs) occurred at 131 plants in at least 35 states. SRMs are the
> high-risk materials, such as brains and spinal cords, most likely to be
> infectious. More than 30 percent of the NRs analyzed were due to either
> improperly handling or removing SRMs. The SRM ban is considered a critical
> firewall in protecting the food supply from BSE.
>
> The violations described in the NRs occurred from January 2004 through March
> 2005. This shows that the problems in the plants persisted long after plants
> should have adapted to new rules issued in January 2004 after the discovery
> of the first case of BSE in the United States.
>
> In 10 percent of the NRs analyzed, plants incorrectly identified the age of
> cattle. Properly determining the age of cattle is a crucial step in proper
> SRM removal because the definition of SRMs is dependent on age; in cattle
> older than 30 months, there is a greater likelihood that SRM will carry BSE
> and therefore must be removed. Accurately identifying the head, spine and
> carcass of cattle by age is necessary to ensure that all SRMs are removed as
> the carcass moves down the slaughter line.
> "These enforcement records only increase our concerns about how easily
> potentially infected cattle are bypassing inspection points at
> slaughterhouses, creating one more opportunity for infected meat to slip
> through the system," said Tony Corbo, legislative representative of Public
> Citizen's food program. "We're approaching the two-year mark of our first
> case of mad cow in the United States, yet the government is still lagging
> behind on protecting consumers."
>
> Public Citizen sent the FOIA request to the USDA in December 2004 after the
> chairman of the USDA meat inspectors union, Stan Painter, raised concerns
> about the agency's policy for ensuring that cattle age is properly
> determined. Instead of investigating whether the policy was adequate, the
> agency opened a misconduct investigation on Painter. The investigation was
> closed this week, shortly after Public Citizen received the documentation,
> which contained more than 80 records of plants improperly identifying cattle
> age.
>
> ###
>
>
> http://www.commondreams.org/news2005/0819-02.htm
>
>
> thank you,
> kind regards,
>
> Terry S. Singeltary Sr.
>
>
> ----- Original Message -----
> From: "Dr. Lyle Vogel"
> To:
> Sent: Thursday, August 18, 2005 3:08 PM
> Subject: Re: 1,000 CITATIONS ISSUED ON MAD COW REGULATIONS
>
>
> > ##################### Bovine Spongiform Encephalopathy
> #####################
> >
> > Terry, you asked:
> >
> > "Greetings,
> >
> > WHY was this not reported in the feed enforcement updates?"
> >
> > The answer is because they were NOT feed discrepancies. These were
> > noncompliance reports issued by USDA Food Safety and Inspection Service
> > employees to meat processing establishments.
> >
> > Lyle P. Vogel, DVM, MPH
> > Director, Scientific Activities Division
> > American Veterinary Medical Association
> >
> > -----Original Message-----
> > From: Bovine Spongiform Encephalopathy [mailto:[email protected]] On
> > Behalf Of Terry S. Singeltary Sr.
> > Sent: Wednesday, August 17, 2005 9:35 AM
> > To: [email protected]
> > Subject: Re: 1,000 CITATIONS ISSUED ON MAD COW REGULATIONS
> >
> >
> > ##################### Bovine Spongiform Encephalopathy
> > #####################
> >
> > Greetings,
> >
> > WHY was this not reported in the feed enforcement updates?
> >
> >
> > BSE -- CVM Updates
> >
> > June 2005 Update on Feed Enforcement Activities to Limit the Spread of
> > BSE (June 20, 2005)
> >
> > http://www.fda.gov/cvm/bse0605.htm
> >
> > or here;
> >
> > March 2005 Update on Feed Enforcement Activities to Limit the Spread of
> > BSE (March 17, 2005)
> >
> > http://www.fda.gov/cvm/BSE0305.htm
> >
> >
> >
> > TSS
> >
> >
> > ----- Original Message -----
> > From: "Terry S. Singeltary Sr."
> > To:
> > Sent: Tuesday, August 16, 2005 8:19 AM
> > Subject: 1,000 CITATIONS ISSUED ON MAD COW REGULATIONS
> >
> >
> > ##################### Bovine Spongiform Encephalopathy
> > #####################
> >
> > From: TSS ()
> > Subject: 1,000 CITATIONS ISSUED ON MAD COW REGULATIONS
> > Date: August 16, 2005 at 6:09 am PST
> >
> > Aug. 15, 2005, 11:39PM
> >
> > 1,000 citations issued on mad cow regulations
> > Meatpackers didn't follow rules on tissue removal
> > By DANIEL GOLDSTEIN
> > Bloomberg News
> >
> > U.S. government inspectors cited meatpackers more than 1,000 times over
> > a 17-month period for violating rules concerning the removal of tissue
> > associated with mad cow disease, the U.S. Department of Agriculture said
> > Monday.
> >
> >
> > Some 1,036 "noncompliance" reports covering the January 2004-May 2005
> > period were released, the USDA said. The reports document instances of
> > meatpackers failing to properly remove "specified risk materials" or
> > SRMs - brains, spinal cord tissue and other tissues that scientists say
> > harbor the disease.
> >
> > "No specified risk materials got into the food supply" as a result of
> > any of the violations, said Lisa Wallenda Picard, a spokeswoman for the
> > USDA's Food Safety and Inspection Service. In all cases, corrective
> > actions were taken or unsafe practices were changed, Picard said.
> >
> > The release of the noncompliance reports comes as Japan, normally the
> > biggest overseas customer for U.S. beef, debates whether to ease the ban
> > on U.S. beef it imposed in December 2003 after the U.S. found its first
> > case of mad cow disease.
> >
> > Many of the violations cited by the USDA were related to paperwork
> > mistakes, according to the American Meat Institute, which represents
> > Tyson Foods, Smithfield Foods and other large U.S. meatpackers. The USDA
> > released the noncompliance reports to news organizations that had sought
> > the information in freedom of information requests, the Washington-based
> > trade group said in a prepared statement.
> >
> > Consumer group Public Citizen said it was still reviewing all the
> > documents and would need several days to summarize the noncompliance
> > reports. "I think there still has to be a concern about meat from an
> > infected animal making it into the food supply," said Tony Corbo,
> > legislative representative for Public Citizen. "It is not a fail-safe
> > system."
> >
> > The meat industry disagreed.
> >
> > "Some groups will no doubt attempt to use this information as evidence
> > of possible operational problems and even a food safety concern, when
> > nothing is further from the truth," said Jim Hodges, president of the
> > AMI Foundation.
> >
> > The USDA ordered that the risk materials be removed from slaughtered
> > cattle Dec. 30, 2003, a week after the first U.S. mad cow case was
> > confirmed.
> >
> > The second case was confirmed in June, at an undisclosed location in
> > Texas.
> >
> > The noncompliance citations generally broke down into five categories:
> > not having sufficient plans to address SRM removal, inadequate SRM
> > removal, cross-contamination, poor record-keeping and inadequate age
> > determination, Tyson Foods spokesman Gary Mickelson said.
> >
> > Reuters News contributed to this report.
> >
> >
> > http://www.chron.com/cs/CDA/ssistory.mpl/business/3311823
> >
> > #################### https://lists.aegee.org/bse-l.html
> ####################
>
> #################### https://lists.aegee.org/bse-l.html ####################
>


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

From: TSS ()
Subject: Inspector to file charges against USDA for them charging him with misconduct on telling the truth about SRM mad cow violations
Date: September 7, 2005 at 1:37 pm PST

Consumer Health


Inspector to file charges against USDA
By Steve Mitchell Sep 6, 2005, 22:46 GMT


WASHINGTON, DC, United States (UPI) -- The federal meat inspector who was charged with misconduct by the U.S. Department of Agriculture after he claimed mad cow disease safeguards were being violated at slaughterhouses told United Press International he plans to file charges against the agency.

Stan Painter, a USDA inspector and chair of the National Joint Council of Food Inspection Locals, the inspectors union, notified the agency`s management in a letter last December he was aware of instances where the riskiest parts of older cows were not being marked or removed from processing.

Painter worried these risky parts -- known as specified risk materials, or SRMs -- could enter the food supply and infect people, causing a fatal brain illness called variant Creutzfeldt Jakob disease.

Two cases of mad cow have been detected in U.S. herds, and some suspect there are more. The USDA put the SRM safeguards in place in 2004 to protect the public from mad cow disease -- also known as bovine spongiform encephalopathy or BSE -- if more cases are detected.

The USDA did not respond to Painter`s concerns until he made his letter known to news outlets.

On Dec. 28, 2004, the agency charged Painter with personal misconduct for not revealing the names of the inspectors who told him of the SRM violations. Officials also told him he was under a formal investigation, which was dropped last month after the release of internal documents revealing more than 1,000 violations of the USDA`s SRM regulations.

Painter said he thinks the USDA was attempting 'to harass and intimidate him (and) to have a chilling effect' on other inspectors.

'I plan to file charges against the agency,' he told UPI, adding he has not yet decided if he will go through the legal system, through internal USDA procedures or another avenue.

Asked about Painter`s intent to bring charges, agency spokesman Steven Cohen told UPI the documents -- called noncompliance reports, or NRs -- demonstrate 'that BSE safeguard regulations are being enforced and prohibited materials did not reach the public.'

Mad cow disease remains a sensitive topic for the USDA because it can have significant economic ramifications. The U.S. beef industry lost billions of dollars because more than 60 nations closed their borders in 2003 to American beef after the report of the first detected case in U.S. herds. Japan, formerly the largest importer of American beef, still has not reopened its borders.

For months, USDA officials denied Painter`s allegations in media reports, saying they had investigated and found no evidence to substantiate his claims. The NRs released last month under the Freedom of Information Act, however, showed 1,036 violations of SRM regulations in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. The USDA delayed releasing the documents for eight months despite a federal law mandating a response within 30 days.

Patty Lovera, of the watchdog group Public Citizen, which requested the USDA documents, said some of the violations cited in the NRs are egregious. In one, an employee at a plant in Michigan was not properly marking older cows to have their SRMs removed because he did not have a pencil. In another, an employee in a Missouri plant was loading cow heads onto his pickup truck to take home to feed to his dog.

Lovera charged the USDA with attempting to silence Painter and failing to address problems with the SRM ban.

'Their behavior through this whole thing is appalling,' she told UPI. 'Stan brought them concerns about a policy and instead of investigating the policy, they investigated him.'

Last December, after Painter made his letter known publicly, the USDA sent an officer to Painter`s house while he was on leave to question him about the allegations in his letter. Later, USDA officials interrogated Painter twice, asking him for the names of the inspectors who told him about the violations.

Painter said he intentionally was kept ignorant of the inspectors` names because he feared the agency would retaliate against them. Painter also said USDA officials did not need the inspectors` names because they could determine where the infractions were occurring by looking at their database of NRs.

Sometime around June the U.S. Embassy in Japan posted a notice on its Web site stating USDA officials had found no evidence to substantiate Painter`s claims and had requested a criminal investigation into his actions. The notice was removed in July after UPI reported its existence.

Although Cohen acknowledged more than 1,000 NRs were written by USDA inspectors, he minimized their significance, saying they 'amount to less than one-half of one percent of the total written for all reasons by (USDA) inspection program personnel.'

Lovera said any infraction of mad cow safeguards should be of concern, because this disease always is fatal in humans and cooking does not destroy the pathogen.

'You have very little margin of error for something you don`t want to get because you can`t cook it away and you can`t disinfect it,' she said.

Painter said his concern now is what the agency will do to fix what he sees as shortcomings in the SRM policy.

'It`s a failed policy,' he said. 'It doesn`t protect the consumer.'

Cohen did not respond to whether the USDA planned to change the SRM regulations.

The USDA`s Office of Inspector General has launched an investigation to determine whether the regulations are being implemented effectively, and results are due out soon.

E-mail: [email protected]

Copyright 2005 by United Press International


http://washingtontimes.com/upi/20050906-050340-6793r.htm

makes no difference, GW will change the SRM rules like he has the BSE GBR risk assessment to the terribly flawed BSE MRR policy, the legal trading of all strains of TSE, the 'gold card'. ...TSS


IN a time when FDA/USDA et al should be strengthening the TSE regulations, it seems corporate interest has won out again over sound science and consumer protection from an agent that is 100% fatal for the ones that go clinical. With the many different atypical TSEs showing up in different parts of the world, and with GWs BSE MRR policy (the legal policy of trading all strains of TSEs), the battle that has waged for the last 25 years to eradicate this agent from this planet will be set back decades, if not lost for good. ...TSS


Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument


Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html


PART 2


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html


PDF]Freas, William TSS SUBMISSION

File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [[email protected]] Monday, January 08,200l 3:03 PM freas ...


http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf


Asante/Collinge et al, 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;


http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm


[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...


http://www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm


Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...


http://www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm


Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html


Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
http://www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003
- Cached


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed



EMC 1
Terry S. Singeltary Sr.
Vol #:
1

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1

2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm

Send Post-Publication Peer Review to journal:


Re: 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


LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD)the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very

limited.



http://infection.thelancet.com/journal/journal.isa



he complained in a letter to the Journal of the American Medical


Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<


actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...


Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama


BRITISH MEDICAL JOURNAL


SOMETHING TO CHEW ON


BMJ


http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2


BMJ


http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1


THE PATHOLOGICAL PROTEIN

BY Philip Yam

Yam Philip Yam News Editor Scientific American www.sciam.com
http://www.thepathologicalprotein.com/

IN light of Asante/Collinge et al findings 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;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:
"'[email protected]'"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.


I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.


Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

[email protected] (until 9/12/02)

New e-mail: [email protected] (active from now)

____________________________________

snip...

full text ;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


AND the new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic

Creutzfeldt-Jakob disease


http://www.pnas.org/cgi/content/abstract/0305777101v1


Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


ALL animals for human/animal consumption must be tested for TSE.

ALL human TSEs must be made reportable Nationally and Internationally,
OF ALL AGES. ...TSS


Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518
 

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