Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.

From: TSS ()
Subject: Chronic Wasting-Disease Culprit May Be Tongue
Date: October 5, 2005 at 11:20 am PST

Wasting-Disease Culprit May Be Tongue

Published: October 4, 2005
The mystery of how deer and elk spread chronic wasting disease from one animal to another may be solved: their tongues are infectious.

When the animals lick or slobber on each other - a fairly common occurrence, especially among elk - the agent that causes the fatal disease may be shed from their tongues via saliva. And when they graze, leaving sloughed-off tongue cells and saliva in grass and soil, the disease could be widely transmitted.

Skip to next paragraph

Associated Press
Elk tend to lick and slobber on one another, possibly causing the mad-cow-like chronic wasting disease.

Forum: Wildlife

Dr. Richard Bessen, an associate professor of veterinary molecular biology at Montana State University in Bozeman, discovered the infectious agent, called a prion, in deer and elk tongues. Details of disease transmission still need to be worked out, he said, but he believes the prions in saliva are significant in the growing national epidemic of the disease.

Since it was first identified two decades ago in deer in Colorado, chronic wasting disease has spread to a dozen states (including New York) and two Canadian provinces.

Last month officials in West Virginia and Alberta announced their first cases of the malady in wild deer, an indication that the problem is still spreading. And last week the Colorado Department of Wildlife said it had found it in a wild bull moose for the first time.

Deer, elk and moose are all members of the cervid family and share genetic traits. But unlike deer and elk, moose are solitary animals that roam alone or in cow-calf pairs.

Chronic wasting disease belongs to a group of fatal maladies called transmissible spongiform encephalopathies, which include mad cow disease and sheep scrapie.

Infectious prions are also found in sheep tongues, Dr. Bessen said. He presented his findings at the Second International Chronic Wasting Disease Symposium held in Madison, Wis., in July. Results should be published in the next few months.

The findings "are pretty convincing," said Dr. Patrick Bosque, a neurologist and expert on prion diseases at the Denver Health Medical Center, who added, "Up to now, no one has been able to show how the disease spread from deer to deer."

The United States Department of Agriculture, which provided the tissue samples used by Dr. Bessen, declined to comment until the findings are accepted for publication in a scientific journal.

The details of how prions get into certain animals have been worked out, Dr. Bessen said. When cows, sheep, monkeys or other animals eat feed contaminated with prions, the infectious particles land in their guts. From there they invade lymph tissue and nerves that travel from the gut into the spinal cord and the brain.

But wild deer and elk are not likely to eat contaminated feed. Somehow the disease is spread from animal to animal, via the environment.

The question is how prions move from the brain to peripheral tissues and how are they shed.

"We decided to focus on the tongue," Dr. Bessen said. It is a muscle with extensive nerve connections to the brain and the central nervous system. Some nerves make direct connections with taste cells, which shed into saliva. And a type of tonsil tissue found at the back of the tongue is a potential target for prions.

"Prions love nerves," Dr. Bessen said. "They jump on them and go."

Experiments clearly show that the tongues of elk and deer contain prions, Dr. Bessen said. Nasal tissue is also infected. Other experiments with hamsters show that prions travel specifically to taste buds on the tongue, raising the possibility that the same happens in deer and elk.

British scientists are also concerned about the tongues of cattle infected with mad cow, Dr. Bessen said. In April, Dr. Gerald Wells of the Veterinary Laboratories Agency in Weybridge, England, reported trace amounts of prions found in palantine tonsil, a type of tissue in the pharynx, near the back of the tongue. Slaughterhouses remove tonsils, he said, but they often allow the root of the tongue, which may also be infected, into the food supply.

So far there is no evidence that people exposed to chronic wasting disease are in danger of contracting it or any related prion disease.

Hunters are advised to take whole deer or elk heads to centrally run state laboratories for prion testing. Otherwise they leave the head and entrails in the wild, where scavengers scatter the remains.

Re: Risk of mad cow disease to dental patients investigated
Mon Sep 12, 2005 09:09

----- Original Message -----
From: "Terry S. Singeltary Sr."
Sent: Tuesday, September 06, 2005 9:23 AM
Subject: Prion Infection of Mucosal Tissue


Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: Prion Infection of Mucosal Tissue


Hamir, Amirali
Richt, Juergen

Submitted to: Chronic Wasting Disease Symposium Proceedings
Publication Acceptance Date: June 15, 2005
Publication Date: July 12, 2005
Citation: Bessen, R.A., Dejoia, C., Dlakic, W., Sorg, R., O'Connell, K., Tucker, T., Hamir, A.N., Richt, J.A., Rocke, T. 2005. Prion Infection Of Mucosal Tissue. 2nd International Chronic Wasting Disease Symposium. P. 38.

Technical Abstract: To investigate the site(s) of prion agent shedding in chronic wasting disease (CWD), we examined the distribution of the prion agent in mucosal tissue from ruminants and rodents with experimental prion disease. We chose the tongue as a peripheral target of prion infection since is a densely innervated tissue at the oral mucosa that we postulate can be a site of CWD agent shedding. The prion agent, PrP**Sc, was present in tongues from elk infected with the CWD agent and sheep infected with the scrapie agent. In hamsters infected with the prion agent, PrP**Sc was found in nerve fibers and skeletal muscle cells as well as in taste cells. In fungiform papillae on the tongue, the distribution of PrP**Sc was consistent with deposition in the taste bud and the surrounding stratified squamous epithelium. These findings suggest that the prion agent can spread from the brain to the tongue along sensory and motor fibers. The presence of the prion agent in the tongue of ruminants and rodents indicates that 1) ingestion of tongue or tongue derived food products can pose a risk to human and animal health, and 2) the localization of the prion agent at the mucosal surface of the tongue could provide a site for prion agent shedding and subsequent transmission to naive hosts.

© SEAC 2003 1




SEAC were asked to advise on the possible BSE risk to the UK population from the

consumption of tonsil present on ox tongue. Although the scientific evidence does not

conclusively prove that tonsil tissue on ox tongue could be infective, SEAC agreed it was

prudent to assume this was the case. SEAC considered that in view of the level of

scientific uncertainty in this area it was not possible to advise precisely on the magnitude

of that risk. However, the committee agreed that any BSE risk from eating tongue was

likely to be very small.


The Committee published a statement in October 2002 when it considered new research

showing BSE infectivity had been found in bovine palatine tonsil. The Committee

recommended that an assessment of BSE risk from bovine tonsil be conducted. This

work was commissioned by the Food Standards Agency, and presented to SEAC at the

June 2003 meeting.

The Committee was asked to advise on two reports

• A Veterinary Laboratories Agency (VLA) report on the presence of tonsil tissue on

ox tongue.

• An assessment of BSE risk from bovine tonsil carried out by DNV consulting

© SEAC 2003 2

Distribution of tonsil tissue in Ox tongue

Bovine tonsil is not a single organ but comprises tissue that is discrete (palatine tonsil)

and tissue organised more diffusely, such as lingual tonsil present on ox tongue. Bovine

tonsil is Specified Risk Material (SRM) from 6 months of age in cattle from the UK and

Portugal, and from 12 months of age in cattle from other EU countries. Ox tongue is not

classified as SRM and is sold for human consumption. The location of palatine tonsil

means that it is unlikely to be removed with ox tongue, but there is a possibility that some

lingual tonsil might be present in tongue prepared for human consumption.

In October 2002, the Committee recommended that it would be prudent to carry out

further examination of the amount and distribution of tonsillar tissue present in ox tongue

prepared for human consumption. Subsequently, an examination of current practices

showed that the majority of tongues prepared for human consumption contained some

lingual tonsil. Twenty four percent (24%) of tongues examined were free of

macroscopically visible lingual tonsil. In 26% of tongues examined, the majority of lingual

tonsil was removed but identifiable tonsillar tissue was still present. However, a

significant amount of tonsillar tissue was present on about 50% of tongues examined. It

was also shown that even when all macroscopically visible tonsil tissue had been

removed from ox tongue, microscopic tonsil tissue could still be present.

The Committee noted the implications of these findings with respect to new EU

legislation due for introduction in October 2003. The research showed that the EU

proposed method of harvesting ox tongue would not exclude all tonsillar tissue from

tongues intended for human consumption.

Infectivity in tonsil tissue

Cattle were experimentally infected with BSE, and pooled palatine tonsil tissue was taken

from animals culled 10 months post inoculation (m.p.i.). Samples of this tissue were

inoculated (intracerebrally) into five calves. The Committee was notified in September

2002 when one animal from this group developed BSE at 45 m.p.i. These assays are

still ongoing and to date the other four animals in this group remain healthy with no

clinical evidence of BSE at 58 m.p.i. Additional groups that received pooled palatine

tonsil taken from animals at different time points after inoculation with BSE (6,18 & 26

m.p.i.) are also still healthy at 51 to 55 m.p.i.

© SEAC 2003 3

The Committee acknowledged that a single finding supports the evidence for infectivity of

palatine tonsil. They agreed that there was no direct evidence to suggest that lingual

tonsil on ox tongue was infective. However, the positive finding in palatine tonsil meant

that infectivity in the lingual tonsil, which has not been specifically assayed for infectivity,

could not be ruled out. No infectivity was detected in ox tongue in the mouse bioassay

but ox tongue has not been tested in the more sensitive cattle bioassay. The Committee

reiterated their previous opinion that, although the possibility of experimental artefact

could not be excluded, it was prudent to assume that this research suggested evidence

of infectivity in all bovine tonsil tissue.

The Committee recommended that tongue from experimentally challenged animals

should be examined for the presence of prion protein (PrPSc). A positive result would

indicate the potential for infectivity although a negative result would not necessarily

exclude this possibility. A positive result would also help to ascertain if PrPSc was

associated with discrete follicular, diffuse lymphoid tissue or with other structures in

lingual tonsil as this could influence the final evaluation of risk.

Members highlighted the scientific uncertainty over the postulated route of infection for

tonsil. To date, no infectivity has been detected by the mouse bioassay in material from

the tongue, cranial cervical ganglion and lymph nodes of the head from preclinical or

clinical cases of BSE, whether experimental or naturally infected. Pooled lymph nodes

and spleen taken from naturally infected BSE cases did not show evidence of infectivity

in the cattle bioassay. Also, infectivity has not been detected in mesenteric, prescapular

and popliteal lymph nodes (some pooled) in the cattle pathogenesis experiment following

intracerebral inoculation of tissues collected at 6, 18 and 26 month post exposure. The

Committee noted that this assay is ongoing and currently at 52 to 55 m.p.i.

Members noted that if infectivity is detected in bovine tongue it may not necessarily

derive from lymphoid tissue but could reside in the associated nerves. This suggestion

was based on experimental research on scrapie pathogenesis in hamsters, which

showed that the hypoglossal nerve in the tongue could act as a reservoir of prion

infection after direct inoculation into the tongue as well as intracerebral inoculation.

© SEAC 2003 4

Assessment of potential public health implications

The risk assessment considered the possible range of human exposure to BSE infectivity

from the consumption of bovine tonsil present on ox tongue.

As the amount of tonsil that might be consumed with tongue was not defined, one

exposure estimate in the risk assessment was based on the assumption that 100% of the

tonsil tissue, estimated to be 50g, is present on every tongue consumed. The Committee

agreed this was a precautionary estimate. It was likely that tongue would be peeled

before consumption. This would remove the superficial layer, reducing the amount of any

adherent tonsil tissue and thus the exposure. Also, tongue meat is usually served sliced

making it unlikely that one person would consume all the lymphoid tissue remaining on

any one tongue.

The risk assessment also considered a more plausible scenario in which 10% of tonsil

tissue was present on the tongue when consumed.

Estimates of infectivity of tonsil tissue

For the purposes of the risk assessment, the total infectivity of a tonsil was estimated as

0.25 bovine oral ID50 units in an infected animal. It was assumed that infectivity was

present in the tonsil tissue at a similar level over the entire incubation period of the

disease. The quantitative estimate of worst-case exposure to infectivity for a population

(assuming all tonsil was included with the tongue) was calculated as 90 bovine oral ID50

units per year, distributed over the tongue-eating population.

The Committee identified a number of key scientific uncertainties in this estimate. The

main area of uncertainty was the level of infectivity in tonsil tissue. This was estimated by

extrapolation of the BSE incubation period for palatine tonsil (45 m.p.i.) from a dose

response curve based on BSE-infected brain tissue. Members agreed it would have been

preferable to base the estimate of infectivity of tonsil on a dose response curve derived

from lymphoid tissue, but this information was not currently available. The Committee

noted that inter-animal variations in incubation period could also increase the uncertainty

in estimates of tonsil infectivity.

© SEAC 2003 5


This research does not conclusively show that tongue is infective. However, the

Committee agreed that in view of the paucity of data, it was prudent to assume that a risk

existed for those who consumed bovine tongue.

The Committee agreed the risk of human infection was likely to be very small but

concluded that it was not possible to advise the FSA precisely on the magnitude of the

risk due to the uncertainty inherent in the data used for the risk assessment.

The long incubation period of BSE in the animal that developed disease after challenge

with palatine tonsil and the fact that only a single animal has to date developed disease

suggests that the infectivity of this tissue was low. The Committee reiterated its previous

advice that any potential BSE risk was likely to be low given the decline of the BSE

epidemic in the UK and the existing feed controls.


The Committee identified further scientific work that would help refine the risk estimates

and reiterated previous recommendations that further study on lymphoid tissues and

tongue from cattle should be carried out, using the most sensitive assays, as these

become available.

Page 1 of 4



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


• 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.

However, no infectivity was detected in the other tissues tested by the

mouse bioassay.

3. It was recognised that assay of bovine material in mice involves crossing a

species barrier, which may reduce the sensitivity of the assay to detect

infectivity. Subsequent research showed that intracerebral injection in

calves ("cattle bioassay") was several hundred-fold more sensitive than the

mouse bioassay with respect to the detection of putative infectivity in

bovine tissues. Therefore, starting about 6 years ago, a study was initiated

to test a range of cattle tissues that had been tested in the mouse bioassay

using the more sensitive cattle bioassay. The Committee was presented with

recent results from this ongoing cattle bioassay.

Page 2 of 4

Research Findings

4. Early results from the cattle bioassay study confirmed infectivity in the

distal ileum, brain and spinal cord at certain times in the incubation period

to those previously reported in the mouse bioassay. However, new findings

show that one of five cattle that received pooled palatine tonsil tissue, taken

10 months after experimental inoculation with BSE, had shown clinical

evidence of the onset of BSE at 45 months post-inoculation. At present, the

4 remaining animals are still alive (48 months after inoculation), without

confirmed evidence of clinical onset of BSE. The equivalent result in the

original mouse bioassay was negative.

5. The Committee considered that although at present only one of the five

animals has shown evidence of transmission of BSE, the finding was

significant and was unlikely to result from experimental artefact. The

Committee noted that the significance of this finding would be strengthened

if any of the other four animals in the experimental group developed BSE or

if tonsil tissue sampled at 6, 18 or 26 months after inoculation also showed

evidence of infectivity in this study. The Committee noted that these studies

are ongoing.

Assessment of potential public health implications

6. The Committee noted that tonsils from cattle are Specified Risk Material

(SRM) from 6 months of age in cattle from the UK and Portugal, and SRM

from 12 months of age for other EU countries. Bovine tongue is not

classified as SRM and therefore can be sold for human consumption.

Although the location of palatine tonsil is such that it is unlikely to be

removed with tongue, there is a possibility that some lingual tonsil, which is

close to the root of the tongue, might be present in that part of the tongue

removed and intended for human food consumption.

7. The Committee was informed by the FSA that a limited, preliminary

examination of current practices of cutting and removal of the tongue

indicated no visible lingual tonsil was present on tongue as removed. The

Committee was informed that such tissue was not detectable if tongue was

cut in a particular area. The Committee considered, nevertheless, that it

would be prudent to conduct further examination of current practices of

preparing bovine tongue and of the amount and distribution of any tonsil

tissue in tongues prepared for human consumption.

Page 3 of 4

8. Despite the paucity of data on current practices, the Committee considered

that any potential risk was likely to be low as the long incubation period of

the one animal that had developed BSE (45 months post-inoculation) in this

experiment suggested that the level of infectivity was low. Additionally the

Committee considered that the potential for exposure is limited given:

The number of BSE infected cattle entering the food chain is likely to be

very small because of the decline of the BSE epidemic in the UK,

existing feed controls and the over thirty month (OTM) rule.

Tonsil is SRM from the age of 6 months in the UK and Portugal and 12

months in other EU states.

Although the quantity of tonsil tissue attached to tongues is unknown, it

is likely, at most, to be small.

9. On the question of whether tonsil should be made SRM from any age, the

Committee acknowledged this was a risk management issue and thus is

beyond their remit. However they considered that this option should be

examined as part of the overall risk assessment.

10. With respect to bovine lymphatic tissue other than tonsil, the Committee

noted that a previous study on pooled lymph nodes or spleen taken from

naturally infected animals with clinical BSE had not shown evidence of

infectivity by cattle bioassay. The Committee was informed that assay of

specific lymph nodes were included in the ongoing experiment and at

present have not shown evidence of infectivity, but the assay is incomplete.


11. The Committee concluded that although only one of the five animals

inoculated with tonsil tissue has so far succumbed to BSE, this finding is

significant and unlikely to be an experimental artefact. However, the

significance of this finding would be strengthened by:

• the pending results from the other four animals in the experimental

group; which are currently not showing definite clinical signs of BSE

• the results from other experimental groups of animals which received

tonsil tissues sampled at 6, 18 or 26 months after inoculation. .

12. The Committee was not able to assess the magnitude of the potential risk, as

insufficient information on current practices was available at the time of

assessment. In view of this, the Committee made a number of


Page 4 of 4


13. The Committee recommended that a risk assessment be carried out to

establish the potential level of exposure to BSE infectivity that the human

population might be exposed to as a consequence of the possibility of

infectivity in tonsil tissue. The Committee considered that further work was

needed to establish the distribution of tonsillar tissue in tongues prepared

for human consumption. The assessment should include risks associated

with both UK and imported meats. The Committee recommended that it is

also necessary to investigate the food uses of tongues and of tonsils from

young animals that are not classified as SRM.

14. The Committee recommended that, in addition to cattle bioassay, further

studies on lymphoid tissues from cattle should be carried out, using the

most sensitive assays, as these become available. These should include

validation of this interim finding by exploring all available techniques to

detect PrPsc on both the original tonsil tissue material collected, as well as

any lymphoreticular tissue tested in the mouse bioassay that had not been

included in the cattle bioassay.

SEAC Statement 2002/1

Evidence For CJD/TSE Transmission
Via Dental Instruments
From Terry S. Singletary, Sr


J Hosp Infect 2002 Jul;51(3):233-5 Related Articles, Links [Click here to read] Contaminated dental instruments.

Smith A, Dickson M, Aitken J, Bagg J.

Infection Research Group, Glasgow Dental Hospital & School, 378 Sauchiehall Street, Glasgow, UK.

There is current concern in the UK over the possible transmission of prions via contaminated surgical instruments. Some dental instruments (endodontic files) raise particular concerns by virtue of their intimate contact with terminal branches of the trigeminal nerve. A visual assessment using a dissecting light microscope and scanning electron microscopy of endodontic files after clinical use and subsequent decontamination was performed. The instruments examined were collected from general dental practices and from a dental hospital. Seventy-six per cent (22/29) of the files retrieved from general dental practices remained visibly contaminated, compared with 14% (5/37) from the dental hospital. Current methods for decontaminating endodontic instruments used in dentistry may be of an insufficient standard to completely remove biological material. Improved cleaning methods and the feasibility of single use endodontic instruments require further investigation.

PMID: 12144804 [PubMed - indexed for MEDLINE]

J Gen Virol 1999 Nov;80 ( Pt 11):3043-7

Transmission of the 263K scrapie strain by the dental route.

Ingrosso L, Pisani F, Pocchiari M

Laboratory of Virology, lstituto Superiore di Sanita, Viale Regina Elena 299, 00161 Rome, Italy.

Apart from a few cases of iatrogenic and familial human transmissible spongiform encephalopathies (TSEs) or prion diseases, the cause of Creutzfeldt-Jakob disease (CJD) remains unknown. In this paper we investigated the possibility that dental procedures may represent a potential route of infection. This was assessed by using the experimental model of scrapie in hamster. In the first part of this study we found that after intraperitoneal inoculation, oral tissues commonly involved in dental procedures (gingival and pulp tissues) bore a substantial level of infectivity. We also found high scrapie infectivity in the trigeminal ganglia, suggesting that the scrapie agent had reached the oral tissues through the sensitive terminal endings of the trigeminal nerves. In the second part of the study we inoculated a group of hamsters in the tooth pulp and showed that all of them developed scrapie disease. In these animals, we detected both infectivity and the pathological prion protein (PrPsc) in the trigeminal ganglion homolateral to the site of injection but not in the controlateral one. This finding suggests that the scrapie agent, and likely other TSE agents as well, spreads from the buccal tissues to the central nervous system through trigeminal nerves. Although these findings may not apply to humans affected by TSEs, they do raise concerns about the possible risk of transmitting these disorders through dental procedures. Particular consideration should be taken in regard to new variant CJD patients because they may harbour more infectivity in peripheral tissues than sporadic CJD patients.

PMID: 10580068

a simple auto-claving just will not kill this agent, considering the fact this agent can survive ashing to 600 degrees celsius;

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999


One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical waste | incineration


The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious beta -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies.

see full text:

Greetings again,

please believe me when i tell you this goes far far beyond the hamburger/deerburger/elkburger/sheepburger. Pandora's box of the demented has been opened for decades, closing it will be most impossible with current safeguards. until they can perfect a test, not only to confirm TSE agent, but also to differentiate between the many differnt strains (there are over 20 in sheep scrapie, and sheep scrapie is the sole model for CJD studies), they then will have to perfect a test that will differentiate between the many different routes. so, as you can see, this could very well take many more decades to answer these questions. but in the mean time, i will not now or ever accept the 'spontaneous/sporadic' theory without any source and route. i plan to continue to fan the fire until we know what killed our loved ones...


Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary, Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B. Schonberger

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]



Follow Ups:

Post a Followup

E-mail: (optional)


Optional Link URL:
Link Title:
Optional Image URL: